DNA AND SKIN AGING

A GENETIC APPROACH TO SKIN CARE SCIENCE

iDDNA® Skin Care is the only non-invasive, regenerative skin care regimen based on your true biological age:

The most effective ingredients (cosmeceuticals and nutraceuticals). Epigenetics ingredients clinically tested to work on genes expression.

A personalized regimen according to your particular needs. The right ingredients, the right formulas, in the right order.

Potentiation, dosage and frequence adjusted according to the genes to work at a cellular level, respecting your skin's hormonal identity

Personal, individualized, actionable information daily on your smartphone, making the science work for you.

THE iDDNA® SKIN CARE PROGRAMPROMOTES
DURABLE AND LONG-LASTING NATURAL CORRECTIONS
THAT PERFORMS SIMULTANEOUSLY ON:

Skin Firmness, Elasticity and Density
(Chrono-aging, collagen synthesis, elastin, emilin)

Skin Moisturization
(Hyaluronic acid synthesis and degradation, skin barrier homeostasis, transepidermal wl)

Collagen Breakdown
(Collagen degradation, glycation and AGEs)

Free Radical Damage
(DNA Damage, ROS)

Photo-Aging
(Technological aging, Pigmentation, UV-induced DNA-damage)

Skin Regeneration
(Cell renewal, vascolarization and oxygenation)

Skin Sensitivity
(Redness, reactive skin, inflammation).

REGENERATIVE NATURAL CORRECTION FOR ALL TYPES OF WRINKLES AND SKIN CONCERNS.

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What really causes skin aging?

Skin surface dehydration affects up to 98% of the population in varying degrees, and dehydrated skin is more prone to signs of premature aging.

With aging your skin becomes thinner, with decreased elasticity, increased wrinkling, and dryness. Fine lines, dark circles, puffy or swollen eyes, sagging skin, impaired pigmentation, redness, and rough patches are among the most common age-related skin problems.

Current scientific evidence indicates that skin quality and premature aging are caused by various factors, but mainly regulated at the genetic level. These specific genetic markers enable Suisse Life Science to identify the gene(s) involved in your skin aging process

Skin aging facts

The skin is composed of 3 different, interacting layers that intersect to bring the smoothness and elasticity that characterize young, healthy skin:

EPIDERMIS: the outermost layer of the skin, provides an efficient barrier against external agents (Ultraviolet -UV- radiations,microbes, toxins…), promotes a well-moisturized skin by avoiding the loss of water, and createsyour skin tone.

DERMIS: deeper, contains all the connective tissue (collagen, elastic fibers…) that allows the firmness and flexibility of your skin.

HYPODERMIS: the deepest subcutaneous layer contains fat cells (for insulation) and connective tissue as well, supplying the upper compartments with blood vessels and nerves. It promotes a plump and wrinkle-free skin.

The secret of anti-aging
is in our genes

Depending upon ones genetic makeup and lifestyle, normal physiological functions within the skin may decline by 50% by middle age.

Up to 60% of the skin aging variation between individuals can be attributed to genetic factors, while the remaining 40% is due to non-genetic factors.

Individuals can be divided into genetic clusters defined by genotypic variables. These genotypic variables are linked with polymorphisms in one or more genes associated with certain properties of the skin that contribute to a person’s perceived age.

Therefore, by using this classification, it is possible to characterize human skin care and anti-aging needs on the basis of an individual’s genetic signature, thus opening the door to personalized treatments addressed at specific populations.

A recent study led by Dr. Alexa Kimball, Professor of Dermatology, Harvard Medical School/ Massachusetts General Hospital, and other leading scientific and analytical research partners in the fields of systems biology, skin biology, and 3D imaging and hormone mapping, confirms that the secret of people who look younger than their actual age depends on a limited group of genes responsible for a range of key biochemical pathways, including those involved in cellular energy production, cell junction and adhesion processes, skin and moisture barrier formation, DNA repair and replication, and anti-oxidant production. There are distinct gene expression “tipping points” that occur in each decade as we age (Kimball et al., Multi-decade and Ethnicity, 2015).

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Learn how your genes
can make your look better

real people natural result

70-YEAR-OLD

Before

After 7 weeks application

41-YEAR-OLD

Before

After 5 weeks application

51-YEAR-OLD

Before

After 5 weeks application

48-YEAR-OLD

Before

After 3 weeks application

iDDNA® LUXURY ANTI-AGING CLINICALLY TESTED EFFICACY

Experienced dermatologists of Skin Test Institute in Neuchatel, Switzerland, assessed, independently, a group of 44 caucasian women aged 35-60 years (phototype I-III), in 2 separated studies, over 12 weeks assessing the partecipants’ iDDNA® ultra-custom results.

For 71% of the partecipants their own iDDNA® is their best non invasive treatment ever,
with outcomes not comparable to any other treatments

Skin firmeness

+42.9% (after just 60 days) up to +100% tactile tirmness

Wrinkle depth

-16.8% maximum wrinkle depth
(after just 60 days)
up to -36% maximum wrinkle depth

skin density

+16.1% epidermis + dermis density
(after just 60 days)
up to +59% skin density thickness
in 60 days

Skin moisturization

+14.0% (after just 30 days) +23.1% forearms up to +65% moisturization in 60 days

Skin roughness

-19.1% (after just 60 days) up to -45% roughness in 60 days

skin elasticity

+14.0% (after just 30 days) up to +59% face net elasticity in 60 days
Positive results in 90% of the panel.
No irritation at any timepoints.
  • (1)Skin moisture (F, VF, Corneometer® CM 825, t0,t1,t2,t3);

  • (2)Skin roughness (F, VF, Visioscan® VC 98, roughness parameter Rz = CR3, t0,t1,t2,t3);

  • (3)Skin elasticity (F, temple area, VF, Cutometer® SEM 575, net elasticity parameter R5=Ur/Ue, t0,t1,t2,t3);

  • (4)Skin firmness (F, temple area, Reviscometer® RVM 600, parameter RRT = resonance running time, 7 measurement angles: 0°, 30°, 60°, 90°, 120°, 150°, 180°, t0,t1,t2,t3);

  • (5)Wrinkle depth (F, right crow's feet area, PRIMOS® lite, parameter maximum wrinkle depth expressed in microns, t0,t1,t2,t3);

  • (6)Epidermal+dermal thickness & density (F, VF , DermaScan® C, t0,t1,t2,t3)

Before (t0)

After (t2)

Before (t0)

After (t2)

Before (t0)

After (t2)

After (t2)

To ask for the full study please apply here

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iDDNA® Skin Care made to measure from DNA
has been further challenged with Visia biometric measurements
on Asian skins.

49-YEAR-OLD

Visia Complexion Analysis - Wrinkles

Before

After 8 weeks application

49-YEAR-OLD

Visia Complexion Analysis - Red Areas

Before

After 8 weeks application

49-YEAR-OLD

Visia Complexion Analysis - Spots

Before

After 8 weeks application

49-YEAR-OLD

Visia Complexion Analysis - Brown Spots

Before

After 8 weeks application

49-YEAR-OLD

Visia Complexion Analysis - Texture

Before

After 8 weeks application

49-YEAR-OLD

Visia Complexion Analysis - Porphyrins

Before

After 8 weeks application

49-YEAR-OLD

Visia Complexion Analysis - UV Spots

Before

After 8 weeks application

49-YEAR-OLD

Visia Complexion Analysis - Pors

Before

After 8 weeks application

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Genetic approach to skin aging

COLLAGEN

The COL3a1 gene encodes the Type III Collagen, the primary component of the dermis extracellular matrix. The Type III Collagen is mainly associated with the Type I Collagen, acting together to promote endurance, strength, and flexibility to the underlying tissues of the skin. Variations linked to this gene may expose an impaired fibrillogenesis (the formation of effective fiber network), leading to defects in the physiological requirements of the skin and in its progressive atrophy. A loss of firmness and definition would be visible, as well as a premature and/or more pronounced wrinkling (Liu et al., 1997; Uitto, 2008).

COLLAGEN BREAKDOWN (GLYCATION)

The PPARG gene encodes the cellular Peroxysome Proliferator-Activated Receptor Gamma which is involved in a variety of biological activities including cell proliferation and differentiation, glucose and lipid metabolisms, insulin sensitivity and inflammation. In the skin, it inhibits the expression of different inflammatory genes and regulates sugar metabolism (glycation). Variations linked to this gene may involve an chronic inflammatory state, an increased cross-linking of elastic fibers, an impaired regulation of the hydrolipid film which is often linked to dryness, or conversely to oily skin and acne (Briganti et al., 2014; Kim et al., 2012; Mastrofrancesco et al., 2014; Rosenfield et al., 2000; Smith et al., 2001).

COLLAGEN BREAKDOWN/EXTRACELLULAR MATRIX

Matrix MetalloProteinases (MMPs) are a group of enzymes involved in the degradation of the extracellular matrix and in various physiological processes related to tissue remodeling such as wound healing or embryonic development. The MMP3 gene encodes one of those proteins more specifically involved in the degradation of the major components of the dermis, such as collagen, laminin, fibronectin or elastin. Its role is essential for proper skin regeneration after sun exposure for example. Variations linked to this gene expose a possible accelerated turnover of the dermis matrix and abnormal degradation of elastic fibers, reducing the elasticity and density of the skin, which may promote a loss of firmness and resilience (Flament et al., 2013; Quan et al., 2013; Souslova et al., 2010; Van Doren, 2015).

ELASTIN

The ELN gene encodes the protein Elastin. In the skin, this protein is mainly secreted by the fibroblasts and the principal cells constituting the dermis, but also by endothelial cells which form the vascularization network. Elastin is a key component of elastic fibers and its function, purely structural, is to ensure elasticity and strength when the skin is subjected to mechanical stress and facial movements. Variations linked to this gene may influence both the vascular and the cutaneous tissues, modifying the proprietes of the skin and of the capillaries, reducing their extensibility, flexibility and adaptability to external constraints. It would promote a premature and accelerated sagging, increasing the appearance of fine lines (Halper and Kjaer, 2014; He et al., 2012; Uitto, 1989).

EMILIN

Emilin 1 is an important component of elastic fibers, particularly abundant in vascularization and skin constitution. It is involved in elastogenesis, in keratinocyte proliferation, as well as in the integrity of blood and lymphatic vessels, ensuring the link between elastic and collagen fibers. Variations linked to the gene encoding for Emilin 1 may influence the proper junction between dermis and epidermis, but also could lead to alterations of elastic fibers. This would induce a premature lack of firmness and the appearance of expression lines (Zanetti et al., 2004).

SKIN BARRIER

The FLG gene encodes the protein Filaggrin, which is secreted by the keratinocytes, principal cells constituting the epidermis. The top layer of this epidermis is called stratum corneum and is actually the first and most important skin barrier. Filaggrin promotes the formation of the stratum corneum by aggregating the keratin filaments produced by the keratinocytes. The cells can keep an appropriate adhesion and assembly, conferring to the epidermis its mechanical strength and protection from external agents, as well as a proper water homeostasis. Variations linked to this gene expose a possible loss of water molecules and an augmented risk of inflammation, as well as a stratum corneum, showing irregular desquamation. These changes may promote a premature formation of fine lines and wrinkles (de Jongh et al., 2008; Sandilands et al., 2009; van Smeden et al., 2014).

HYALURONIC ACID

The HAS1 gene encodes the Hyaluronic Acid Synthase 1 enzyme, one of the proteins synthetizing the Hyaluronic Acid (also know as Hyaluronan). This is last expressed by the keratinocytes (epidermis) as well as by the fibroblasts (dermis), being a major component of the cutaneous extracellular matrix. Hyaluronic Acid is an important regulator of skin homeostasis, gives compressive strength for tissues, acts as an ideal lubricant thanks to its moisturizing ability, and accelerates growth and healing of the skin cells. Variations linked to the gene of HAS1 may contribute to disturbing the appropriate equilibrium in the hhyaluronic acid synthesis (Siiskonen et al., 2015; Tammi and Tammi, 2009).

FREE RADICALS DAMAGE/PHOTO-DAMAGE

The SOD2 gene encodes manganese SuperOxide Dismutase (MnSOD), an enzyme localized inside cells in the mitochondrial matrix, which is the first line of defense against free radicals. MnSOD catalyzes the dismutation of superoxide (highly damaging free radical) into non-reactive entities, protecting the surronding cells from oxidative stress. These free radicals, mainly issued from Reactive Oxygen Species (ROS), are responsible for the disruption of collagen Type I and III, as well as numerous elastic fibers. Variations linked to this gene may promote an accumulation of free radicals leading to a loss of radiance of the skin and an increased appearance of fine lines, especially around the eyes (Treiber et al., 2012).

The gene GPx encodes the Glutathione Peroxidase, an enzyme playing a key role in the regulation of cellular redox balance. Its antioxidant function helps to protect the cells, counteracting the accumulation of free radicals and fighting oxidative stress in skin. An optimum antioxidant barrier may protect against damage caused by environmental pollution, ultraviolet radiations, tobacco smoke, chronical stress and poor nutrition. Variations linked to this gene may reduce the detoxifying abilities of cells, increasing accumulation of free radicals to oxidative stress. It may accelerate lipid oxidation and collagen cross-linking, finally promoting premature aging (Bastaki et al., 2006; Shuvalova et al., 2010; Yang et al., 2013).

The genes GSTM1 and GSTT1 encode Glutathione S-Transferase proteins, enzymes involved in the detoxification of a variety of reactive and mutagenic compounds, including the products of ultraviolet-induced oxidative damage. Their role is therefore to protect cells and their extracellular matrix from harmful factors, preventing their accumulation into the skin (Board and Menon, 2013; De Luca et al., 2010; Fortes et al., 2011).

SUN DAMAGE / PIGMENTATION

The gene ASIP encodes a secreted protein that may affect the regulation of melanogenesis and the quality of hair pigmentation. The binding of ASIP to MC1R leads to a dow-regulation of eumelanogenesis (brown/black pigment) and thus increasing synthesis of pheomelanin. The ASIP regulates MC1R-related pigmentation pathways, so the SNPs may influence the pigmentation production. AG and GG variants are exposed to 2-4x higher risk of skin sensitivity. KITLG (KIT Ligand) is a Protein Coding gene. Diseases associated with KITLG include hyperpigmentation, familial progressive with or without hypopigmentation. The genetic variation AA has been favored by natural selection to become common in light-skinned people as it might aid the tanning of their skin in response to sunlight, protecting it from UV radiation, which can burn and cause cancer (Zeron-Medina et al., 2013).

CELL RENEWAL/TELOMERE PROTECTION

The gene NOS3 encodes the Nitric Oxide Synthase 3, also known as endothelial Nitric Oxide Synthase (eNOS), which produces one of the most important signaling molecules of the vascularization system: the nitric oxide (NO). It stimulates vasodilation, regulates blood flow and pressure, and is also involved in many wound healing processes. Furthermore, eNOS-derived NO prevents telomere shortening and counteracting the senescence of endothelial cells. Variations linked to this gene may induce cells to proliferate slowly, synthetize a lower amount of proteins and extracellular matrix, and finally display a lower regeneration power to the skin (Bruning et al., 2012; Cals-Grierson and Ormerod, 2004; Forstermann and Sessa, 2012; Valerio and Nisoli, 2015)

SKIN INFLAMMATION

Tumor Necrosis Factor-alpha is a pro-inflammatory cytokine that modulates cells growth and differentiation (skin barrier formation), initiate the death of degenerated cells (after sun exposure as well), but its principal role is to recruit immune cells on the inflammatory site, leading to local redness or chronic sensitivity of the skin. Indeed, TNF-a is secreted in response to endogenous stimuli such as collagen disruption or damaged cells, and to exogenous stimuli such as toxins, allergen or irritant factors. Through its diverses funsctions, this cytokine plays an important role in skin sensitivity, reactivity and inflammatory responses. Variations linked to this gene may induce a deregulation of inflammation process, promoting an hypersensitivity and reactivity of the skin (Banerjee et al., 2011; Bashir et al., 2008; Giacomoni and Rein, 2001; Werth et al., 2000).

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