L’Arabe n’est pas international, il est arabe

Ce modeste article intitulé des paroles du Sage (Robert Mauvy) fait suite à celui traitant de la consanguinité : « Ah cet embreeding », ainsi qu’en réponse au questionnement de Monsieur R.J. Cadranell.

Il fallait lire : « (…) la dure vie nomade, alliée à l’environnement hostile ainsi qu’aux conditions climatiques implacables joueraient leur rôle de régulateur éliminant du même coup sujets et gènes récessifs indésirables (…) »

Dans de telles conditions de survie, un sujet affligé du moindre handicap n’a que peu de chance de salut, et, par voie de conséquences, n’engendre aucune descendance. Le sujet éliminé ne peut donc être porteur ni parasiter de quelque manière que ce soit le reste du cheptel.

Il est reproché très souvent à la pratique de la consanguinité d’infliger une diminution de la vitalité ainsi que de la fertilité et pousser à l’hypernervosité ; pour tout dire conduire à une dégénérescence.

Nous nous trouvons donc au fait de la question : « le sursum des hérédités entre elles et la possibilité de leur faire atteindre leur maximum d’intensité » avec ce dilemme entre l’hérédité saine … ou morbide.

Mais encore une fois, la race chevaline la plus aboutie qu’est le Cheval Arabe de Sang Pur nous a apporté des géniteurs dotés des plus grandes qualités zootechniques ; façonnées depuis plus de quinze siècles par les hérédités de Race, de Famille et d’Individu à individu, filtrées de surcroît par les sélections Dirigée et Naturelle.

L’affection que vous mentionnez (SCID) se porterait sur 3% des poulains et 30% de la population adulte étudiée serait hétérozygote porteur. La cause de cette immunodéficience primaire serait un gène autosomique récessif (ir) dont la responsabilité incomberait à une sélection inintentionelle…

 Cette étude, ce constat, fut réalisée en premier lieu aux Etats-Unis et, de toute évidence, sur des néo-arabes occidentaux ! Des recherches similaires ont-elles été entreprises sur une population représentative de chevaux Orientaux Bédouins ?

 Sachant que l’accouplement entre porteurs donne 30% de pertes, ajoutant à cela la multiplication de ces derniers, de telles proportions, additionnées aux pertes énormes dues aux conditions de vie extrêmes, si ce syndrome était imputable au mode de vie nomade, la race Noble se trouverait certainement éradiquée depuis fort longtemps.

La prophylaxie telle que nous la concevons, devenue indispensable en nos pays, est absolument ignorée du bédouin !

Je suis convaincu que, malgré et grâce à cette forme d’existence, il est évident que si le problème cité s’était présenté, il se serait vu stoppé par la création d’un gène protecteur.

Mais le voile n’est jamais complètement levé car l’histoire, tout comme la nature, gardent toujours une part de mystère qu’il nous faut respecter.

Miracle de Dieu ou pas, les tribus bédouines de la péninsule Arabique ne seront jamais assez glorifiées pour avoir permit au monde de connaître ce joyau !

Une fois de plus, preuve est faite, s’il en était besoin, que l’Arabe élevé hors de son berceau de race dégénère et perd ses qualités d’améliorateur et… de « mainteneur ».

L’homme moderne, civilisé, n’a pas vu, lui, que cet être était parfait… mais le pouvait-il ?! alors notre « Buveur d’Air » est magnifisé, idéalisé, détourné. Lui, nanti de toutes les qualités dont celle de les transmettre, il se retrouve avili par des fonctions qui ne sont pas siennes. Puis vidé de sa substance, abâtardi, devenu animal curieux, adipeux à souhait, affligé d’une silhouette ridicule et affublé de titres ronflants ne voulant rien dire et surtout ne prouvant rien si ce n’est l’inconscience et la faiblesse humaines.

La barre d’acier trempé arrachée des mains de son artisan et loin de son brasier, du bain glacé de la nuit, se métamorphose en plomb.

Je signerais ces quelques phrases rebattues comme je les ai titrées ; avec une autre citation de Robert Mauvy : «La Race Massacrée ! ».

13 Replies to “L’Arabe n’est pas international, il est arabe

  1. I’ll make three points here, in English, and maybe translate into French later if I have time.

    First, every individual of every species carries genetic defects. That is simply a biological fact of life, whether we are talking about wild animals, domestic animals, or human beings. I am not prepared to believe that Arabian horses exist outside the laws of biology and heredity that govern all other animal life.

    Second, the gene responsible for SCIDS that is now found in Western populations of Arabian horses must have come from the 19th century ancestral Arabian horse population in the Middle East. We know this because SCIDS turned up in Arabian horses in Australia in the 1970s and has been found more recently in 100% Davenport horses in the U.S. There was no Davenport blood in the affected Australian Arabian horses of the 1970s, and hardly any Davenport blood at all in Australia. However, the Davenport horses and the ancestors of the Australian Arabians had a common origin with the 19th century horses of the Anazah and Shammar tribes of Bedouin, which must be where the gene originated. The alternative explanation, that the exact same mutation occurred in horses in both Australia and the U.S. during the same century, is practically impossible.

    Third, I don’t follow your math. Matings of two carriers will produce 25% affected foals, not 30%. However, most adults are not carriers.

    If for sake of argument we assume a population with 25% carriers and random mating, then only 21.88% of foals will be carriers and just 1.56% of foals will die from SCIDS. That is hardly enough mortality to eradicate the race. If only 10% of parents are carriers and with random mating, 9.5% of foals will be carriers and just 0.25% of foals will die from SCIDS.

    Thus under random mating, the percentage of carriers will get lower and lower with each generation until it reaches 1%. With only 1% of the parents carriers, there will be 1% carrier offspring and essentially 0% foals dead from SCIDS. Thus a population of 1% carriers would perpetuate itself generation after generation, undetected and undetectable (absent modern genetic testing), with no or almost no dead foals. This would go on indefinitely in spite of a harsh environment and in spite of strict selection for the toughest individuals.

    If you want to argue that Western breeders have selected toward SCIDS carriers and Bedouin breeders selected away from them, that’s fine. You might be right. But to argue that SCIDS never existed in the Middle East, or if it did it would have been eradicated, is not mathematically or biologically tenable.

  2. The important point about SCIDS is that it is potentially present in every Arabian bloodline. But because a gene test is now available, the status of any individual breeding horse can be known (carrier or clear).

    Different breeders use different approaches. One person I know makes sure that every stallion she uses tests clear for SCIDS. That way, she doesn’t even have to worry whether any of the mares are carriers, because if the breeding stallions are all clear, she will never have a SCIDS foal. Other breeders will use a SCIDS carrier stallion, but only on mares that test clear. Again, no SCIDS foals will be produced. This way, the trait can be intelligently managed in a breeding program like any other fault.

  3. Easier than most faults, as it is just one gene, and not an interaction between genes, like conformation faults.

  4. Here is an English translation of the Louis Bauduin posting, “L’Arabe n’est pas international, il est arabe” (or in English, “The Arab is not international; it is Arab”).

    This modest article with the words of the Sage (Robert Mauvy) made following the one dealing with consanguinity: “Ah this inbreeding”, as an answer to the questioning of Mr R.J. Cadranell.

    It was necessary to read: “(…) the harsh nomad life, together with a hostile environment including relentless climatic conditions would play their part together in eliminating undesirable recessive genes (…) ”

    Under such conditions of survival, an individual afflicted with the least handicap has little chance of survival, and, consequently, does not leave any descendants. The eliminated individual thus cannot be carrying nor weaken in any manner the remainder of the population of livestock.

    The practice of inbreeding is often criticized for inflicting a reduction in vitality as well as fertility and for creating excessively nervous animals; when all is said, it leads to degeneration.

    We are thus faced with the question: “the sum of heredities between them and the possibility of making them reach their maximum of intensity.” With this dilemma comes either healthy heredity… or fatal heredity.

    But once again, the most successful equine race, which is the Arab Horse of Pure Blood, brought to us breeding stock equipped with the greatest zootechnical qualities; developed over more than fifteen centuries by heredities of Race, Family, and Individual, filtered in addition by controlled selection and natural selection.

    The affliction that you mention (SCID) would affect 3% of the foals. Also, 30% of the studied adult population would be heterozygous (carriers). The cause of this primary immunodeficiency would be an autosomal recessive gene for which the responsibility would fall on an unintentional selection.

    This study, this report, was carried out initially in the United States and, obviously, on Western neo-Arabs! Was similar research undertaken on a population representative of Bedouin Oriental horses?

    Knowing that the mating between carriers gives 30% of losses, adding to that the multiplication of the latter, such proportions, added with the enormous losses due to the extreme living conditions – if this syndrome were ascribable with the Bedouin lifestyle, the Noble race would certainly be eradicated before much time passed.

    Disease prevention and veterinary care such as we have, which has become essential in our countries, is absolutely unknown to the Bedouin!

    I am convinced that, in spite of and thanks to this Bedouin form of existence, it is obvious that if the SCID problem had arisen, it would have been seen stopped by the creation of a protective gene.

    But the veil is never completely raised because history, just like nature, always keeps a share of mystery that it is necessary for us to respect.

    Miracle of God or not, the Bedouin tribes of the Arab peninsula never will be glorified enough for having allowed the world to know their jewel!

    Once more, proof is made, if it were needed, that the Arab horse raised away from the cradle of his race degenerates and loses his good and maintaining qualities.

    Modern civilized man did not see him that was perfect… but could he?! Therefore our “Drinker of Air” is over glorified, idealized, diverted. He, secured by all transmittable qualities, is degraded by functions which are not his. Then, emptied of his substance, debased, he becomes a curious animal, bloated with wishes, afflicted with a ridiculous silhouette and fancy titles, not wanting to say anything and especially not proving anything but that this is human unconscionableness and weakness.

    The tempered steel bar torn off with the hands of its craftsman and far from the blazing inferno, of the frozen bath of the night, is metamorphosed out of lead.

    I would close these sentences of rebuttal as I titled them, with another quotation of Robert Mauvy: “The Massacred Race! ”.

  5. Cher Monsieur,
    Il n’est point courtois de taxer certaines de mes lignes d’irrecevabilité alors que visiblement vous ne les avez pas toujours correctement interprétées, à moins peut être que je ne me sois mal fait comprendre ?
    Par le fait, nous ne parlons plus tout à fait de la même chose, ce qui peut avoir pour effet de dérouter nos amis lecteurs.
    Pour exemple :
    En 1980, messieurs Perryman et Torbeck ont durant 3 années de monte fait saillir 26 juments ayant auparavant produit des sujets malades par un étalon qui, lui aussi, avait donné des poulains victimes de la même altération : sur 53 poulains, 15 (soit 28,3%) avaient la maladie !
    Etant entendu que vos 25% sont le résultat d’un calcul théorique tiré d’un schéma où il n’est pas tenu compte, entre bien d’autres choses, de la fertilité et de ses caprices.
    Si j’ai arrondi à 30% c’est dans un esprit de simplicité et ne point non enferrer dans un cours de génétique.
    Une expérience similaire aurait pu donner un pourcentage différent. De plus, une jument à forte tendance (c’est-à-dire plus prompt à transmettre cette maladie) peut très bien ne pas remplir certaines années, alors qu’une autre à plus faible tendance pourra faire ses 3 poulains, et à l’inverse, etc.
    Ceci dit, au risque de me répéter, bien que voulant faire court, on n’élève pas des chevaux (ou autres) avec une calculatrice ni une pharmacie. Et, si la génétique est une chose, il ne faut pas en oublier pour autant le reste et surtout l’environnement et le mode d’élevage souvent liés, ces derniers pouvant être réparateurs comme destructeurs suivant dans quel sens on l’entend. Mais ceci n’est que puzzle mouvant formant un tout.
    Quant aux « arabes australiens » auxquels vous faites allusion, vous allez en mon sens ! En effet, eux aussi sont des néo-arabes avec plus d’un siècle de dégénérescence hors du berceau de race…
    Je veux bien croire que les difficultés de langage, leurs interprétations, ainsi que les subtilités de chaque langue compliquent nos échanges. Aussi faut-il veiller à une certaine prudence quant à la teneur de nos réponses. Quoi qu’à votre crédit, je suis incapable de manipuler l’anglais comme vous le français.
    Par respect pour le fondateur de ce blog, ainsi que pour ses lecteurs, nous sommes en devoir de préserver cet outil formidable et ne point en faire une arme de polémiques du : « dernier qui a parlé a raison ».
    Aussi n’ayant pas l’esprit chagrin et, si ce sujet pour moi est clos, j’espère vous retrouver sur d’autres par des échanges de bon aloi.
    Avec tous mes respects,
    Louis Bauduin

  6. Dear R J Cadranell,
    Considering your excellent translation of Louis Bauduin’s article, it is obvious that there is no language misunderstanding for you. But, I would like to make a point about his article and your very interesting initial comment as a biologist.
    The genetic numbers that you present are certainly correct, although I did not double check your calculations. I assume you used Mendel’s laws to count genetic percentages you edited in this comment.
    Nevertheless, as you seem to know about genetics, you should also know that Mendel’s laws are not completely true (it was very strongly suggested years ago that he actually cheated on his experiment results to establish this basal concept, very useful for present science). Even a monogenic disease will never entirely go along this line of percentage, as you also probably know that there are elaborated statistic calculations (Khi 2 test, for technical terms!) that enable to verify if the studied population corresponds to the theorical percentages expected.
    Moreover, it is now more and more accepted in the scientific community that the theory of the “all is pure genetics” is over. And, maybe you should know that the environment influences significantly the maintenance of gene expression and further mutations.
    Louis Bauduin approximated the percentages, and on that we do agree. For my part, I understood that the 30% is just an approximation that came from a published study.
    I think the important point in his article was, as he mentioned initially, that the environment and breeding conditions are crucial factors impacting on the maintenance, or not, of some genetic mutation(s). Especially in Middle East where conditions are so drastic we understand that DNA transmitted from the parents is not all that save, or suppress, an individual. During his life, the animal, here the horse, sometimes goes through adversity thus modifying his own genome. Just out of curiosity, it has actually been publish very recently for other animal species!
    Finally, between theory and practical facts, there will always be this huge gap that should be filled in with the breeding science.
    Respectfully,
    Margot

  7. So how exactly does adversity modify genes? Do they catch a cold and then decide they don’t like colds,and then reach into their chromosomes, grab the offending gene or gene locus and change it for another one?
    Respectfully
    Bruce Peek

  8. Certainly yes, the environment is always a factor, and yes, the mathematical probabilities do not always play out exactly as expected. For example, the six foals by Tripoli and out of Dharebah should have been half chestnuts and half greys. After all, Dharebah produced non-grey foals by other non-grey stallions. Instead, her foals by Tripoli were all six of them grey!

    One must also take into account the size of the sample. If Dharebah could have had 1000 foals by Tripoli instead of just six, we would expect to see results closer to what is mathematically predicted, although again, probably not exactly 500 foals of each color.

    The case of *Jazaan was well publicized about 30 years ago. His importer advertised to lease known SCIDS carrier mares to breed to him to test his SCIDS carrier status. He sired some SCIDS foals out of these mares, and so his importer gelded him. How could both *Jazaan and one of my own straight Davenport mares, who have no recorded common ancestors, both be SCIDS carriers unless the gene existed in the ancestral population of 19th century Arabian horses in the Middle East?

    If the SCIDS gene is “created” by the non-desert environment in Britain and parts of the U.S., why is the trait confined to horses of Arabian ancestry and not general among all horse populations in these two countries?

    I still take issue with the idea that the harsh desert environment would eliminate all genetic faults. Certainly that environment would eliminate weaker individuals, but living organisms are not chemicals that can be refined to the point of chemical purity. Some faults can be lived with.

    At the end of the day, the Arabian horse is a domesticated animal. The wild animals in the desert arguably have an even more difficult existence than the domesticated animals. Are the wild animals also clear of all genetic defects? Of course not — every individual of every species has genetic defects. In the case of SCIDS, a recessive trait, the carrier animals themselves show no ill effects, and the proportion of affected foals (which die), even if somewhat higher than the proportion predicted mathematically, would still be small enough that SCIDS is not going to eradicate the race.

    I think we would all agree that one of the amazing things about the Arabian horse is how the desert environment and hard life created a breed with toughness and endurance beyond all other horses. To state that such horses have no genetic defects at all, I am afraid, is carrying the argument too far.

    Respectfully,
    R.J. Cadranell

  9. Dear Bruce Peek,

    I answered for Margot due to the fact we wrote the mail together.
    We did not want to use too many genetic technical terms because it is important that in this excellent blog, most of the readers understand the different points.
    The dogmatic point of view that leads to think that genetic is all should be confronted to Darwinism. It is then obvious that environnement plays a major role in the evolution process. You seem to be ironic but we have so many things to discover and to learn. We are all students.
    If a proof is needed that “adversity” (called also “environment”) modify our genome, the recent publication we talked about is here :
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2713434/?tool=pubmed
    Of course, the way how environment modify our genes is not know for the moment. Life is so complicated…

    I can tell you, just as geneticists we are (Margot and I), that the genetic commonly presented for non scientific people is so simplified.
    We could talk about penetrancy, expressivity of the mutation for example. But it is not the good place (in this blog) to do that.
    As a conlusion of this part, it is important to know that Mendel’s laws have been discovered and are used as a tool for geneticists only in a controlled environment. And even in this controlled environment, using in general animals or plants with the same genetic background, and in a huge population, we are currently observing percentages differents of the expected ones coming from Mendel’s laws.
    We should be humble because we have so little knowledge.
    Concerning arabian horses breeding, it is important to listen and be aware of the knowledge of breeders and not to follow dogmatic point of views.

    I want to thank the maker of this blog (which is a real fantastic tool for arabian horses lovers we are) and to finish as Louis said : This fantastic blog is not a polemic weapon and I prefer to close this debate in my case.

    Respectfully,

    Guillaume.

  10. Guillaume! Welcome! I did not realize who (the above) Margot was until I read your post just now. It is such a relief to have you both post in English as I was hard put to understand Louis’ post (until RJ translated it). I would not DARE to make a comment on this thread..except to say (meekly and humbly) that from a psychological POV I very much believe that environment influences genetics in the long run. In psychology it is at least hypothesized for instance that an environment which either creates or contributes to depression in a person, for example, can eventually become genetic if the depressive environment is then recreated over generations. This makes perfect sense because we know that behavior and environment affect brain chemistry and neuronal pathways. Once those pathways become hardwired what would prevent them from being passed on to offspring?

    I hope you and Margot will continue to come here, especially with your double backgrounds in asil Arabians and genetics.

    Mandour is still a secret, but will be announced upon arrival. 🙂

    Elena

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