Est-ce à dire que la génétique ne joue aucun rôle dans l'obésité humaine ? Certainement pas. De nombreuses études portant sur des jumeaux ainsi que sur des familles d'obèses l'ont prouvé : de façon incontestable, la variabilité du poids corporel des hommes dépend pour une part de facteurs génétiques. Le problème est qu'il ne s'agit pas d'un mécanisme simple. On estime actuellement qu'au moins une vingtaine de gènes seraient « associés » à l'obésité, ce qui ne signifie pas qu'ils en sont responsables. Et les mutations fonctionnelles n'ont, semble-t-il, rien à y voir. Utilisant les méthodes de la génomique contemporaine, qui permettent de lire (« séquencer ») les gènes et de repérer les variantes, des équipes de chercheurs scrutent des banques d'ADN recueillies auprès de populations d'obèses et de témoins. Il est ainsi apparu que le gène normal de la leptine serait statistiquement « lié » à l'obésité extrême (indice corporel supérieur à quarante), mais qu'il n'en va pas de même avec l'obésité courante. Une autre de ces études a montré qu'un gène codant le récepteur d'un neurotransmetteur impliqué dans la régulation de la dépense énergétique est muté chez un homme sur dix... qu'il soit obèse ou non. Il semble cependant que, parmi les sujets atteints d'obésité massive, les porteurs de la mutation soient encore plus gros que les non-porteurs. Reste que la mutation est tellement minime qu'on ne comprend pas encore comment elle pourrait affecter le fonctionnement du récepteur...
De fait, si l'on excepte certaines formes rares de la maladie, l'obésité pourrait bien être la conséquence d'une combinaison malencontreuse de gènes parfaitement « normaux », qui rend certains individus plus sensibles à un environnement pathogène. En clair : la principale cause de l'obésité reste bien la conjugaison d'une alimentation inadaptée et d'une activité physique insuffisante. L'« injustice génétique » tient à ce qu'un excès, même léger, de l'apport nutritionnel peut selon les individus n'avoir aucun effet pathologique ou, au contraire, mener au fil des années à une accumulation de tissu adipeux. Les découvertes actuelles mèneront certainement à la mise au point de molécules à l'efficacité partielle pour certaines obésités, mais il n'existera probablement jamais de traitement uniquement médicamenteux de cette maladie.
Enfants : un bilan préoccupant
Les résultats d'enquêtes s'accumulent, plus alarmistes les uns que les autres. Partout la proportion d'enfants obèses dépasse celle des adultes, et les dix dernières années ont vu une véritable explosion du phénomène : augmentation de 50 à 60 % au Japon, aux États-Unis et en Grande-Bretagne, voire doublement à Singapour... Même en France, pays traditionnellement épargné, l'augmentation atteint 30 %. Plus grave : elle concerne surtout les formes massives de l'obésité.
Pas question d'invoquer une brusque évolution génétique : cette flambée s'explique par une modification des modes de vie. La déstructuration des repas, la consommation incessante de friandises et de boissons sucrées, ainsi que la baisse d'activité physique due à la télévision et aux consoles vidéo en sont les causes premières. Les remèdes passent donc par une éducation alimentaire, délicate pour des sujets en croissance qui ont besoin de manger, et par l'activité physique.
Beaucoup de praticiens insistent : un enfant n'est pas un adulte en miniature. Il doit même paraître maigre, au moins jusqu'à six ans. C'est à cet âge que se produit le « rebond adipeux » et que l'enfant commence à évoluer vers sa corpulence d'adulte, même si les cartes sont en partie redistribuées à l'adolescence. Il faut donc agir très tôt si l'on veut éviter plus tard des complications médicales...
Patrick Philipon
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