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Le concept du luxe

PARTIE I: APPROCHE THEORIQUE
Chapitre 1 Introduction de luxe
1.1. Le concept du luxe
Qu’est-ce que le luxe? Le mot LUXE provient du latin « luxus » qui veut dire somptuosité excessive et ostentatoire. Il signifie, selon le petit Larousse: «somptuosité excessive, faste, richesse». Cette notion a connu plusieurs changements dés le 17e Siècle, et à l’aube du 21e Siècle, le luxe n’est plus nécessairement somptueux, ni même réservé à certains privilégiés, selon Michel GODET, dans son ouvrage «le luxe dans tous ses états». Le luxe se banalise et se démode de plus en plus vite, par rapport au passé.
Le mot luxe défini par Le PETIT ROBERT est «un mode de vie caractérisé par de grandes dépenses consacrées à l’acquisition de biens superflus, par gout de l’ostentation et du plus grand bien-être.»
En réalité, il est difficile de lui donner une définition unique et précise. Beaucoup de professionnels du luxe, économistes, chercheurs, sociologues, les clients du luxe, essaient de lui donner une définition précise, mais pour l’instant il reste un concept subjectif. Comme l’affirme Jean-Noël Kapferer dans son ouvrage «luxe oblige» en écrivant que le concept de luxe n’est pas une catégorie dans l’absolue, mais un ensemble relatif qui ne peut être dissocié de la structure politique et sociale du siècle auquel il appartient[1]. Si on demande à la population ce que luxe signifie selon eux, les réponses seront très différents, parce qu’à chacun son luxe[2]! D’ailleurs, les frontières du luxe se déplacent avec les conditions de vie, les classes et les cultures, présentées dans la lecture de Jean – Philippe Antoine.
Michel GODET, «le luxe dans tous ses états», le luxe se définit d’abord comme un mode de vie généralement associé à des dépenses importantes pour l’acquisition de biens superflus. Donc le luxe est tout d’abord se traduit par un rôle sociologique: un mode de vie. Le mot superflu signifie Satisfaire des besoins dont on n’a pas besoin[3], et que celui ci n’est pas indispensable et qu’il n’est pas un besoin ordinaire de la vie.
1.2 Les caractéristique d’un produit de luxe
Malgré les nombreuses définitions proposées par différentes personnes telles que des professionnels du luxe, économistes, chercheurs, sociologues, les consommateurs, le luxe se caractérise toujours par les 5 critèresdéfinis ci-dessous:
La qualité
L’industrie du luxe est basée sur une qualité supérieure des ces produits ou de ces services. La meilleure qualité est la principale caractéristique du luxe. Pour devenir un luxe, il doit y avoir des différences nettes par rapport aux produits de la consommation de masse. Parmi les composantes d’un objet de luxe, on trouve toujours une véritable supériorité technique qualitative ou technologique[4].
Par exemple, chez Rolls-Royce, chaque partie de leurs véhicules sont uniquement fabriquées à la main, donc les voitures de la production industrielle ne peuvent pas remplacer sa position unique. Rolls-Royce se distingue donc par sa qualité supérieure et cette caractéristique le démarquant clairement des autres marques. La haute couture de luxe se distingue particulièrement par leur design, la texture de haute qualité. Le luxe est présent aussi dans le secteur des services. Par exemple, dans un l’hôtel de luxe dont le service est de haute qualité proposant un trés grand confort et plaisir. Donc l’atout et la principale caractéristiques de luxe du luxe est forcément supérieur aux les produits ordinaires.
La rareté
Selon Vincent Bastien, la rareté est centrale dans l’identité du luxe. La Rareté est un caractère très essentiel pour le luxe ce qui le distingue des produits de masse. Le PDG de cartier international, Bernard Fornas, a dit que « Je dois gérer la désirabilité de cette maison, il faut maintenir le ratio entre disponibilité et rareté».
Vincent Bastien distingue deux grands types de rareté dans son ouvrage «luxe oblige»: un coté la rareté physique qui comprend les ingrédients, les processus de production comme par exemple dans la haute couture où les habits sont fabriqués à la main par un grand couturier et donc chaque pièce est unique dans le monde. D’un autre coté il y a une rareté virtuelle ou impression de rareté, signifiée, créée et entretenue par la communication elle-même.
Si un produit de luxe perd de sa rareté, si un jour on le trouve dans n’importe quel magasin, et tout le monde peut donc posséder ce produit, alors il ne sera pas classé et reconnu comme un produit de luxe, mais un produit de grande consommation. C’est pourquoi les entreprise de luxe font des efforts pour préserver la rareté de son produit: Cartier a réduit le nombre de références dans sa ligne, « Must», diminué le nombre de ses points de vente en particulier chez les opérateurs « Duty Free », et lancé un département « Private Collection » pour les montres de prestige[5].
Le prix
Quand on pense le mot «luxe», on pense tout de suite à «cher».
Saphia Richou a dit dans son ouvrage «le luxe dans tous ses états» que le produit de luxe est forcément cher et il est cher parce qu’il est rare et de qualité[6]. C’est la rareté, la production en nombre limité, et la qualité qui rend le produit de luxe distinctif par rapport aux produits de masse.
D’ailleurs, il faut prendre en compte de la valeur imaginaire de luxe. D’après Vincent Bastien dans son ouvrage «luxe oblige», le prix indique la valeur d’échange d’un produit, mais ce qui fait le luxe est la valeur symbolique. Cela signifie qu’une marque de luxe peut demander un prix d’autant plus élevé que sa valeur symbolique est plus forte.[7]
Pour l’auteur de la Théorie de la classe de loisir datée de 1899, l’objet de luxe est cher parce que tout ce qui «est absolument ravissant est synonyme de pécuniairement honorifique». [8]
Donc sans ce prix élevé, les produits de luxe n’existeraient pas.
Le superflu
Comme présenté dans la définition de luxe, «Le mot superflu signifie Satisfaire des besoins dont on n’a pas besoin[9], et que celui ci n’est pas indispensable et qu’il n’est pas un besoin ordinaire de la vie.».
Raconte une histoire
1.3 Les trois cercles du luxe
Jean Castarède, dans on ouvrage «le luxe», classifie le secteur du luxe selon trois cercles présentés au dessous:
– Le Superluxe accessible à quelques-uns. D’après Jean Castarède, Les produits sont alors uniques et sur mesure. Par exemple, celui de la haute de coutume, les moyens de transport (les voiture de luxe, les avions privés..), la joaillerie de luxe, les œuvre d’art. Son Chiffre d’affaire estimé est de 35,5 milliards d’euros[10].
– Le deuxième cercle est plus abordable, qui sont plutôt des déclinaisons du luxe[11].Ce cercle correspond aux secteurs traditionnels du luxe. Par exemples, les prêts à porter, les bagages, les accessoires, les montres, les stylos. Son Chiffre d’affaire est de 45 milliards d’euros[12].
– Le troisième cercle correspond aux produits particuliers par rapport aux produits de masse, comme les parfums, les cosmétiques haut de gamme, les spiritueux de luxe. Son Chiffre d’affaire dans le monde est environ 98,5 milliards d’euros.[13]
Source: «Le luxe», Jean Castarède, 1992, P62
1.4 Les trois niveaux de luxe
Danielle Allérès, dans son ouvrage «LUXE….Stratégies Marketing», distingue trois niveaux de luxe: Luxe inaccessible, luxe intermédiaire et luxe accessible qui correspondent bien aux 3 cercles de Jean Castarède. Je vais retirer l’essentiel de ces définitions pour qu’on puisse mieux comprendre les spécificités de chaque niveau des produits de luxe.
* Le luxe inaccessible
Le luxe des modèles exclusifs, parfois réalisés à la main et à l’unité. Il correspond à des produits de qualité inégalée et exceptionnelle, rare, voire unique, et précieux possédant une certaine perfection de réalisation, par exemple, la haute couture de Chanel. Son prix est extrêmement élevé et sa méthode de communication est très sélective, prestigieuse et intimiste. Le luxe inaccessible utilise beaucoup en hors média les événements sportifs et culturels et en média une presse très sélective, comme les magazines de mode très «select».
* Le luxe intermédiaire
Le luxe intermédiaire est de très grande qualité mais moins parfait et moins rare que le luxe inaccessible. Par rapport au luxe inaccessible, son prix est déjà plus accessible mais fait néanmoins l’objet d’une réflexion très poussée. Son cible de consommateurs est plus large par rapport à celui de luxe inaccessible. Daniel Allérès nous a dit que, le luxe intermédiaire correspond à une classe sociale intermédiaire qui souhaite conserver ses distances par rapport aux autres classes sociales. Les consommateurs de luxe intermédiaire souhaitent se distinguer des autres.
* Le luxe accessible
Les produits de luxe accessibles sont fabriqués en série et plus rapidement. On peut citer, par exemple, les parfums et les cosmétique. C’est un marché très concurrentiel. Dans ce marché, les consommateurs n’ont pas suffisamment de connaissances sur les produits, par exemple, les fonctions d’un produit soin de la peau, ou un nouvel odorat d’un parfum, donc ils sont beaucoup influencés par la publicité. La communication repose sur tous les médias.
Source: «LUXE….Stratégies Marketing», Danielle Allérès, P169 – 207
1.5 Etude de marché du secteur du luxe
1.5.1 Le Chiffre d’affaire depuis 2000
Touché par la crise financière de 2009, le secteur du luxe dans sa globalité à connu une forte récession.
Quelle est la taille du marché du luxeactuellement ? Si nous prenons le luxe dans sa forme la plus reduite: mode, accessoires y compris la maroquinerie, produits cosmétiques et parfums, vins et spiritueux, etc, les ventes sont de 175 milliards d’euros, comme on peut le constater sur le graphique ci dessous. Touchée par la crise financière de 2008, en 2009, le marché du luxe a chuté de 10%, soit 157 milliards d’euros, après 5 ans de croissance constante depuis 2003. C’est surtout le marché européen qui est plus touché par la crise; par contre, les Etats-Unis et surtout l’Asie sont moins influencés.
Si nous prenons compte les voitures et les voyages de luxe, la taille du marché serait proche de 250 milliards d’euros[14], selon l’estimation en 2007.
Ces chiffres nous permettent d’avoir une idée générale de la taille du marché du luxe.
Source:
Traitement Xerfi Global: données primaires sources national et Bain

The Role of Oxidative Stress in Ageing

“Evidence for and against the role of oxidative stress in ageing.”
Ageing is defined as the progressive accumulation of changes, characterised by changes over time in physiological function and increased probability of pathological diseases and death.(1)It is of the general consensus that ageing begins with molecular damage that leads to cell, tissue, and eventual organ dysfunction.(1) Many theories have been put forward to explain ageing process. One of the most examined theory is the oxidative stress theory of ageing. This idea was first proposed by Denham Harman in 1956 as the free radical theory of ageing, suggesting that oxygen free radicals are related to ageing process.(2)In 1972, he published a refinement of his theory by highlighting mitochondria as most of reactive oxygen species (ROS) are produced here.(3) This theory postulates that oxidative stress is caused by an imbalance between prooxidants and antioxidants, leading to accumulation of oxidative damage to the cellular macromoleculecules over time. Under this framework, theoretically a long-lived organism should have a reduced oxidative stress.
A free radical is a molecule that has one or more unpaired valence electrons on its outer shell. As such, it is unstable and is highly reactive in order seek electrons to pair. Reactive Oxygen Species (ROS) include free radicals which contain oxygen, such as superoxide anion (•O2) and hydroxyl radical (•OH), and nonradical molecules that contribute to their formation, such as hydrogen peroxide (H2O2). In an effort to stabilize its bond, ROS can take away an electron from a target molecule in a process called oxidation, leading to a chain reaction which produce even more free radicals and causing deterioration to the targets. These targets can be DNA, protein, and lipid.(2,4)
ROS is produced by several processes in the body. It is a by-product of a normal metabolism. It is also produced in other enzymatic reactions such as xanthine oxidase, cytochrome P45, secretion of activated leukocytes, etc.(1) However, it is mainly produced by mitochondria, most of which are generated from the electron transport system as they consume aproximately 85% of the oxygen utilized in the cell.(4)
The production of ROS in mitochondria happens during oxidative phosphorylation occuring in the inner mitochondrial membrane, specificially in complexes I and III.(1,5) In this process, ROS are continuously produced in the mitochondrial electron transport chain where O2 is reduced to water H2O2. Unfortunately, this system is imperfect, causing electrons to leak from the electron transport chain to form •O2– instead. •O2– is short-lived and cannnot pass through the membrane. However, it can be converted to hydrogen peroxide (H2O2) either spontaneously or catalyzed by superoxide dismutase (SOD). H2O2 is membrane permeable and relatively stable, thus able to pass to the cytosol and damage other components. It has been estimated that about 2% of oxygen consumed in the mitochondria is turned into superoxide.(6)•OH, the most reactive ROS, is produced from Haber Weiss reaction, Fenton reaction, and reaction between hypochlorous acid and •O2–.(1)
Antioxidants function to limit the oxidative damage. There are three different mechanisms in which they may work: inhibiting the generation of ROS, scavenging the free radicals in an enzymatic way, and elevating the endogenous antioxidant defences.(1) Antioxidants consist of enzymatic and non-enzymatic types. The main enzymatic antioxidants are superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPX). SOD catalyse the dismutation of superoxide to hydrogen peroxide. It is thought to be the primary antioxidant as it limits the further generation of free radicals.(1) SOD1 is located in the mitochondrial intermembrane space, SOD2 is located in the mitochondrial matrix, while SOD3 is located extracellularly.(7) Catalase works by catalysing the conversion hydrogen peroxide to water. It is mainly found in the peroxisomes, but it also found in lesser amount in mitochondria.(1) GPX functions in the same way, but it requires glutathione as a cofactor. GPX also prevent lipid peroxidation, thus maintaining the structure and function of biological membranes. It is located in mitochondria and cytosol.(1)
Non-enzymatic antioxidant, also known as small molecule antioxidants, are especially important extracellularly where enzymatic antioxidants are not present.(1) It consists of lipid-soluble and water-soluble components.(1) The lipid-soluble antioxidants are present in cellular membranes and lipoproteins while water-soluble antioxidants are present in aqueous fluid such as in the blood.(1)
Generation and of ROS and its metabolism by antioxidants are summarized in Figure 1.

Figure 1. Generation of ROS and metabolism by antioxidants. von Zglinicki T. Aging at the molecular level. Netherlands: Kluwer Academic Publisher; 2003.
As mentioned before, oxidative stress can cause damage to DNA, protein, and lipids. DNA lesions are divided into five types: oxidised purines, oxidised pyrimidines, abasic sites, single-strand breaks, and double strands breaks.(1)The most important repair mechanism for DNA is base excision repair (BER) (Figure 2).(1)BER begins with DNA glycosylase that recognizes the modified base and subsequently removes it, forming an abasic (AP) site.(1) This abasic site can be acted upon by two types of enzyme: AP lyase that cleaves the DNA strand 3’ or AP endonuclease that hydrolises the phosphodiester bond 5’.(1) Many glycosylase has an intrinsic lyase activity and is thus bifunctional.(1) The choice between these two is based on what damage is going to be repaired.(1) Removal of oxidised purines and pyrimides in involve DNA glycolylase, while repair of abasic sites is primarily acted on by AP endonucleases.(1) Action of AP lyase or AP endonuclease results in the formation of one-nucleotide gap, which may be further extended by Flap Endonuclease I (FEN1) and later the gap will be filled by DNA polymerase.(1) Single strand repair protein complex includes of POLB, XRCC1, ADPRT, LIG3, and PNK while double strand protein repair occurs by homologous recombination of RAD50/51/52/54 or nonhomologous end rejoining involving DNA-dependent protein kinase, KU70, KU80, LIG4, etc.(8) Repair of mitochondrial DNA adepends on the repair proteins being transported into the mitochondria and through BER mechanism.(1) Nucleotide excision repair (NER) also exist to repair bulky DNA lesions. It is shown that DNA in aged liver cells of mice contain a higher amount of 8-Oxo-2’-deoxyguanosine (oxo8dG) (Figure 3).(9)

Figure 2. Base Excision Repair. von Zglinicki T. Aging at the molecular level. Netherlands: Kluwer Academic Publisher; 2003.

Figure 3. Comparison of oxidative DNA damage from livers of young and old rats. Ames BN, Shigenaga MK, Hagen TM. Mitochondrial decay in aging. BBA – Molecular Basis of Disease. 1995;1271(1):165-70.
There are several ways in which oxidative pathways can damage protein: oxidation of the the protein backbone, formation of protein cross-linkages, oxidation of amino acid side chains, and protein fragmentation.(1) Indirect damage can also occur by ROS oxidising lipids and carbohydrates to form derivatives that can form protein carbonyl adducts or oxidising glycated proteins.(1) Repair of oxidative protein damage can occur directly or indirectly.(1) One of the most important process in direct repair systems is the re-reduction of oxidised sulfhydryl groups.(1) Another process that can involves methionine sulfoxide reductase (MsrA) which can regenerate methionine residues.(1) The indirect repair system consists of two steps: the recognition, removal, and degradation of the damaged protein molecule, followed by de novo synthesis of the removed protein.(1)
Damaged proteins are recognized by chaperones that can either repair or degrade the damaged protein.(10) However, as cells get older, there is a chaperone overload, thus causing the damaged proteins to accumulate intracellularly.(10)The two major proteolytic system involved in intracellular protein turnover are the lysosomal system and the ubiquitin-proteasome system (UPS).(10) The lysosomal system is associated with autophagy which consists macroautophagy, microautophagy, and chaperone-mediated autophagy.(10) Each of these types differ in the way in which they deliver substrates to the lysosomes, the type of substrates, and their regulation.(10)UPS consists of two steps: ubiquitylation and degradation.(10)Attachment ubiquitin molecules is the “tagging” of the damaged protein for proteasome to recognize and degrade.(10)
Oxidative lipid damage results in decreasing fluidity of cellular membranes with age.(11)This change is associated with changes in the composition of lipid membrane.(12) In the liver microsomal and mitochondrial membrane isolated from rodents, there is a decline in the amount of linoleic acid accompanied by an increase in the amount of long chain polyunsaturated fatty acids (PUFA), which are more sensitive to oxidative reactions.(12)Phospholipids which contain a high amount of PUFA make them prime target of oxidation, resulting in lipid peroxides.(1) MDA is a marker for lipid peroxidation, and it is shown that malondialdehyde accumulation is higher in aged liver and brain tissues (Figure 4).(9)Oxidatively damaged lipids are repaired by phospolipase A2.(4) Phospholipase A2 is located in the inner mitochondrial membrane and increase in activity when there is an increased oxidant production.(13)It catalyzes the removal of oxidised lipid in the membrane.(4)

Figure 4. Comparison of malondialdehyde accumulation in young (3 months) and old (26-31) rats. Ames BN, Shigenaga MK, Hagen TM. Mitochondrial decay in aging. BBA – Molecular Basis of Disease. 1995;1271(1):165-70.
In addition to mitochondria being the major producer of ROS, mitochondrial DNA (mtDNA) is also close in proximity to ROS.(14) Thus, mtDNA is more prone to oxidative damage than the nuclear DNA, as also shown in Figure 3.(4) As mitochondria is both the producer and the target of ROS, the mitochondrial theory of ageing postulates that the oxidative damage generated produce the most damage to mitochondrial macromolecules, including its mtDNA, proteins, and lipids.(14) Therefore, this damage leads to impaired oxidative phosphorylation and protein synthesis machinery, creating an even more imperfect system which will lead to further accumulation of ROS.(14) This is called the vicious cycle hypothesis.(14) If this continues, eventually the cell will be deprived of energy and eventually die.(14)
In trying to prove oxidative stress theory, most literatures try to prove the notion that long-lived animals has reduced oxidative damage or increased oxidative resistance. These interventions include caloric restriction (CR), genetic mutation, and pharmacological intervention such as metformin.
CR, an intervention consisting of reducing caloric intake without causing malnutrition, is one of the most examined intervention and is the most robust. For more than 80 years, it has produced reproducible results that it can increase lifespan up to 50% and decelerate the onset of age-associated pathologic and biologic changes in rodent and primate models.(15)This increase in lifespan is associated with reduced oxidative damage, shown by reduced levels of oxidised protein, lipid, and DNA, decreased production of ROS from the mitochondria, and increased oxidative resistance compared to rodents that are fed ad libitum.(7)Studies of CR in humans support the notion that CR remains the cornerstone to a healthy ageing, prevention of obesity and its complications, and is able to decrease mortality rate.(16)For example, in World War I and II, the CR imposed on them managed to reduce mortality rates by around 30% compared to pre-war level.(17) A study by Civitarese et al.(18)regarding CR in humans confirmed that it is accompanied by a decline of oxidative stress markers, consistent with the animal models.
As antioxidants can limit oxidative damage, theoretically organisms with long life-span should have an increased concentration of antioxidants to provide protection to oxidative resistance. However, several models of antioxidant knockdown and transgenic mice have not supported this concept.(7)It does, however, increase healthspan, the period in which an organism remain free of disease.(7)For example, a mice knockdown model of SOD2 /-, despite showing increased oxidative damage markes, have no change in lifespan compared to control mice, but has an increased incidence of cancer.(19)Transgenic mice studies provide results that antioxidants can reduce oxidative damage accumulation and provide resistance to oxidative, but the majority of the studies produce no effect on the lifespan, thus putting the oxidative damage theory to doubt.(7)An example of this is a transgenic mice that overexpress SOD1 and SOD2, shown to have increased resistance to superoxide toxicity but no effect in lifespan.(20)In fact, from this same study, out of 18 genetic manipulations they have done, only the deletion of SOD1 gene had an effect on lifespan.(20) Another potential explanation to this gap in theory is associated with the environment.(7)The environment contributes in ageing in which it differs in the amount of stress. In an environment with minimal stress, oxidative damage will play minimal role thus no enhanced antioxidant defense is needed.(7) In terms of these mice models, the environment is translated to the husbandry, as proven by the contradicting results of study between Moskovitz et al.(21)and Salmon et al.(22) Moskovitz et al.(21) observed a shorter lifespan in MsrA-/- mice while Salmon et al.(22) observed no change, suggesting that the mice used by Moskovitz et al.(21) may be kept at a less optimal husbandry.
A drug that has been most intensely examined as a geroprotective agent is metformin. Metformin is an insulin sensitizer widely used as a drug for diabetes type II. A meta-analysis shows that metformin can increase lifespan indepeendent of diabetes, as shown by it being able to reduce all-mortality cause, especially related to age-related diseases.(23)
Ageing has been closely associated such as sarcopenia, Alzheimer’s disease (AD), several types of cancer, cardiovascular diseases, etc. Several genetic mice models of AD have been developed. One of the most commonly used is the one that overexpresses a mutation of amyloid precursor protein (APP TG).(24) Reduction of SOD2 in these mice is shown to accelerate AD-like pathology such as amyloid deposition and nerodegeneration, conferring a positive association between decrease oxidative defense and AD.(25) In a similar manner, reduction of GPX4 also increase amyloid plaque burden and increases amyloid-β deposition.(26) Overexpression of SOD1 can increase lifespan of these mice.(27) However, this extension does not change the pathology of AD, thus it is thought that it either only protect against AD side effect or just give an oxidative stress protection in general which improves health.(7)As opposed to AD, there is a significant association between increased oxidative protein damage with lowered grip strength among older women.(28)
Nevertheless, a study in human oxidative stress marker in age-related disease support the oxidative stress theory. In a study by Schottker et al.(29)examining derivatives of reactive oxygen metabolite (D-ROM) levels and total thiol levels (TTL) in a population-based cohort from four countries, these serum markers are all strongly associated all-cause and cardiovascular mortality.(29) D-ROM levels even have an additional strong association with cancer mortality.(29)
In conclusion, researches regarding oxidative stress have produced conflicting results. In regards to oxidative stress theory itself, it can be tested either by modulating the oxidative stress or the antioxidant defenses. Interventions supporting the role of decreased oxidative stress, such as CR and metformin, have produced supporting results towards the oxidative stress theory and is now still being investigated more intensively, which is good especially since these interventions can be applied to humans with seemingly favorable results. Interventions regarding genetic modification of antioxidant defenses, however, seems to point towards changes in healthspan rather in lifespan. Therefore, I think further research in this area should focus more on healthspan. Moreover, this conflicting results is probably due to the presence of more factors at play. Oxidative stress theory is only one example of the single-cause molecular theories. It is highly unlikely that each of the molecular theories work alone and only by understanding all these theories can ageing be fully understood. In addition, I personally think that this theory need more clinical studies in humans as the majority are now done in animal models. However, I realize that in some cases it may be impossible to do. For example, examination of antioxidant defences which are done by genetic alteration is of course impossible to be done in human. Therefore, I think as of now, the most promising oxidative damage modification is CR as it has been proven over and over again to be able to increase lifespan and delay age-related conditions.
References
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