Forums des énergies : société, écologie et technologies propres

For their study, Séralini et al. used ‘Sprague-Dawley rats’. This is a laboratory strain that is known for its propensity to the spontaneous development of tumors (see www.harlaneurope.com under ‘lifespan and disease’). The number of tumors that the rats develop spontaneously depends on the amount of food that they are given3. The number of spontaneous tumors is highest when these rats are allowed to consume calories without any restriction4. Various figures for spontaneous tumors are reported. There are publications that mention 42 to 72% among female animals5-6. Among male animals these figures are slightly lower, but there is a study that mentions over 86%

The rats can also develop tumors at a very early stage. Schardein et al. (1968)8 reported that 6 out of 3,000 rats spontaneously develop tumors within three months, 10 out of 700 within 6 months, 20 out of 400 within 9 months, etc., increasing within 18 months

Mais que les lobbys se rassurent, il y a bon espoir que les humains dans quelques générations, à manger toute sortes de cochonneries, OGM, herbicides, pesticides, chimique, radioactif, etc.. sans limites, seront aussi fragiles et souffreteux que ces rats à vie raccourcie !!

There is no data about the quality of the maize that was used. When grown in damp conditions, maize can be plagued by fungi that can produce mycotoxins which are known to be hepatotoxic, toxic to the kidneys, carcinogenic and that can mimic the effects of estrogen.
There is no indication whatsoever of whether the genetically modified maize originating from the land that was sprayed with Roundup contained traces of the degradation products of Roundup and, if so, how much there was, and how this compared to the amount of Roundup that was fed to all the animals. Moreover, Roundup consists of various components: the active ingredient, glyphosate, and a few other substances (among others a substance that promotes distribution of the spray over the leaves). These various components and their degradation products may have been on the treated maize that was fed to the animals in completely different proportions than in ‘pure’ Roundup. Some break down very quickly. In other words, Roundup in the ‘Roundup’ treatment could be completely different to Roundup in the ‘GMO maize + Roundup’.

It is not clear whether the NK603 maize that was sprayed with Roundup was also treated with other herbicides and, if so, which

Sprague-Dawley rats, like many other laboratory rats, develop relatively speaking many pathologies and that, as a consequence of this, many of the animals do not reach two years of age. But we have known this since the 1960s.

LE PLUS. L'étude choc sur la nocivité des OGM, à l'initiative du professeur Séralini et de son équipe, suscite des réactions houleuses : les détracteurs sont en effet nombreux à remettre en cause la validité méthodologique de ces recherches. Paul Deheuvels, membre de l'Académie des Sciences et statisticien renommé, nous explique pourquoi l'étude de Séralini est fiable.
L'objet de cette tribune est d'apporter mon soutien le plus ferme à G.E Séralini, professeur à l'Université de Caen. J’ai pris connaissance du fait que le professeur Séralini avait réalisé des études comparatives ayant eu, récemment, un considérable retentissement.
À ma connaissance, ces enquêtes ont été conçues et analysées en conformité aux meilleures normes professionnelles en vigueur, et devraient être appréciées comme telles.
La durée de l'expérience : un gage de fiabilité
L'un des points les plus intéressants et innovants de ces études est qu’elles ont été menées sur des durées inhabituellement longues. C’est un fait notoire, connu des expérimentateurs, que les analyses du même genre réalisées au cours de périodes plus courtes ne sont pas aptes à détecter des effets toxiques à long terme.
Le cas particulier du développement de tumeurs relève de cette catégorie, et il n'est donc pas surprenant que les études existantes, ayant été développées sur des durées plus courtes que celle des travaux de G.E. Séralini, n'aient pas révélé, jusqu’ici, de différences significatives entre les effets des traitements.
Je considère donc que le professeur Séralini a fourni des indices très solides, propres à établir l'existence de certains effets toxiques inattendus de la part de produits considérés auparavant comme sûrs.
Bien sûr, il se trouvera toujours des personnes pour contester ces résultats, du fait même qu'ils sont susceptibles d'avoir d'importantes conséquences industrielles.
Leur point de vue ne pourra être soutenu qu’à la lumière de résultats d’expérience nouveaux, puisqu’il n’y a pas de doute sur le sérieux et la fiabilité des conclusions actuelles du Professeur Séralini.
Des reproches statistiques infondés : explications concrètes
On reproche, par exemple, à G.E. Seralini d'avoir réalisé son étude avec des blocs de 10 animaux cobayes, alors que l'usage le plus courant est d'en utiliser 50.
Cette critique est infondée. En effet, dans une étude statistique, on peut chercher soit à démontrer l'innocuité d'un produit, soit à mettre en évidence sa nocivité.
Prenons l'exemple d'un produit qu'on soupçonne être un poison. Si on l'administre à 5 patients et s'il y a 5 morts, il n'y a pas besoin d'aller plus loin pour décider qu'il est toxique. Si, par contre, les 5 patients survivent, cela ne veut pas dire pour autant que le produit soit inoffensif, car les 5 patients
ne sont pas nécessairement représentatifs de toute la population.
C'est pour cette raison que les études commanditées par les entreprises qui souhaitent qu'on admette l'innocuité de leurs produits imposent que les échantillons utilisés soient d'une importance minimale.
Dans le cas présent, il est naturel d'imposer un minimum de 50 cobayes (ici, des rats) pour les analyses comparatives. C'est tout à fait différent si on recherche des effets toxiques. Dans ce cas, le fait de déceler des différences significatives sur des petits groupes (10 dans le cas de l'étude de G.E.Seralini) renforce la conclusion, au lieu de l'affaiblir.
Deux types d'erreurs dans les études statistiques
Je conclus en insistant sur le principe suivant. Dans une étude statistique, si on décèle des effets toxiques, il y a toujours un risque de se tromper, mais l'erreur, s'il y a, peut facilement être dissipée par des analyses ultérieures. En revanche, si des études ne décèlent pas d'effets, on commet généralement une faute en en déduisant que ces effets n'existent pas. Car il y a deux types d'erreurs:
1. Déceler une toxicité alors que celle-ci n'existe pas;
2. Admettre l'innocuité alors que la toxicité existe.
La plupart du temps, on contrôle le risque (1) (le standard est de fixer les règles de décision de sorte que sa probabilité soit fixée à 5%). En revanche, le risque (2) dépend de la taille de l'étude, et est souvent très important (40% voire 60% ou plus).
C'est pour limiter le risque (2) qu'on cherche à imposer des études faisant intervenir beaucoup d'expériences individuelles (ou de cobayes). Par contre, lorsqu'on décèle la toxicité, il n'y a que 5% de probabilité d'erreur, quel que soit le nombre de cobayes utilisés.

janic a écrit :C'est d'ailleurs pourquoi ces essais sur des rats au mode de vie "humain" réagissent ainsi

Christophe a écrit :On peut lire la lettre quelque part?

The health effects of a Roundup-tolerant genetically modified maize (from 11% in the diet), cultivated
with or without Roundup, and Roundup alone (from 0.1 ppb in water), were studied 2 years in rats. In
females, all treated groups died 2–3 times more than controls, and more rapidly. This difference was visible
in 3 male groups fed GMOs. All results were hormone and sex dependent, and the pathological profiles
were comparable. Females developed large mammary tumors almost always more often than and
before controls, the pituitary was the second most disabled organ; the sex hormonal balance was modified
by GMO and Roundup treatments. In treated males, liver congestions and necrosis were 2.5–5.5
times higher. This pathology was confirmed by optic and transmission electron microscopy. Marked
and severe kidney nephropathies were also generally 1.3–2.3 greater. Males presented 4 times more large
palpable tumors than controls which occurred up to 600 days earlier. Biochemistry data confirmed very
significant kidney chronic deficiencies; for all treatments and both sexes, 76% of the altered parameters
were kidney related. These results can be explained by the non linear endocrine-disrupting effects of
Roundup, but also by the overexpression of the transgene in the GMO and its metabolic consequences.

3. Results
3.1. Mortality
Control male animals survived on average 624 ± 21 days, whilst
females lived for 701 ± 20, during the experiment, plus in each case
5 weeks of age at the beginning and 3 weeks of stabilization period.
After mean survival time had elapsed, any deaths that occurred
were considered to be largely due to aging. Before this period,
30% control males (three in total) and 20% females (only two) died
spontaneously, while up to 50% males and 70% females died in
some groups on diets containing the GM maize (Fig. 1). However,
the rate of mortality was not proportional to the treatment dose,
reaching a threshold at the lowest (11%) or intermediate (22%)
amounts of GM maize in the equilibrated diet, with or without
the R application on the plant. It is noteworthy that the first two
male rats that died in both GM treated groups had to be euthanized
due to kidney Wilm’s tumors that were over 25% of body weight.
This was at approximately a year before the first control animal
died. The first female death occurred in the 22% GM maize feeding
group and resulted from a mammary fibroadenoma 246 days before
the first control. The maximum difference in males was 5
times more deaths occurring during the 17th month in the group
consuming 11% GM maize, and in females 6 times greater mortality
during the 21st month on the 22% GM maize diet with and
without R. In the female cohorts, there were 2–3 times more
deaths in all treated groups compared to controls by the end of
the experiment and earlier in general. Females were more sensitive
to the presence of R in drinking water than males, as evidenced by
a shorter lifespan. The general causes of death represented in histogram
format (Fig. 1) are linked mostly to large mammary tumors
in females, and other organic problems in males.

Up to 14 months, no animals in the control groups showed any
signs of tumors whilst 10–30% of treated females per group developed
tumors, with the exception of one group (33% GMO + R). By
the beginning of the 24th month, 50–80% of female animals had
developed tumors in all treated groups, with up to 3 tumors per
animal, whereas only 30% of controls were affected. The R treatment
groups showed the greatest rates of tumor incidence with
80% of animals affected with up to 3 tumors for one female, in each
group. A summary of all mammary tumors at the end of the experiment,
independent of the size, is presented in Table 2. The same
trend was observed in the groups receiving R in their drinking
water; all females except one (with metastatic ovarian carcinoma)
presented, in addition mammary hypertrophies and in some cases
hyperplasia with atypia (Table 2).

The lifespan of the control group of animals corresponded to the
mean rat lifespan, but as is frequently the case with most mammals
including humans (WHO, 2012), males on average died before
females, except for some female treatment groups. All treatments
in both sexes enhanced large tumor incidence by 2–3-fold in com parison to our controls but also for the number of mammary tumors
in comparison to the same Harlan Sprague Dawley strain
(Brix et al., 2005), and overall around 3-fold in comparison to the
largest study with 1329 Sprague Dawley female rats (Chandra
et al., 1992). In our study the tumors also developed considerably
faster than the controls, even though the majority of tumors were
observed after 18 months. The first large detectable tumors occurred
at 4 and 7 months into the study in males and females
respectively, underlining the inadequacy of the standard 90 day
feeding trials for evaluating GM crop and food toxicity (Séralini
et al., 2011).

In conclusion, it was previously known that glyphosate consumption
in water above authorized limits may provoke hepatic
and kidney failures (EPA). The results of the study presented here
clearly demonstrate that lower levels of complete agricultural glyphosate
herbicide formulations, at concentrations well below officially
set safety limits, induce severe hormone-dependent
mammary, hepatic and kidney disturbances. Similarly, disruption
of biosynthetic pathways that may result from overexpression of
the EPSPS transgene in the GM NK603 maize can give rise to comparable
pathologies that may be linked to abnormal or unbalanced
phenolic acids metabolites, or related compounds. Other mutagenic
and metabolic effects of the edible GMO cannot be excluded.
This will be the subject of future studies, including transgene and
glyphosate presence in rat tissues. Reproductive and multigenerational
studies will also provide novel insights into these problems.
This study represents the first detailed documentation of longterm
deleterious effects arising from the consumption of a GM Rtolerant
maize and of R, the most used herbicide worldwide.
Altogether, the significant biochemical disturbances and physiological failures documented in this work confirm the pathological
effects of these GMO and R treatments in both sexes, with different
amplitudes. We propose that agricultural edible GMOs and formulated pesticides must be evaluated very carefully by long term
studies to measure their potential toxic effects