Saturday 20 July 2013

Response to Ena Valikov Comments 2

The reason I do not give charts and figures is because my blog is called the everyday scientist, to present the researchers findings in that manner would mean little to my audience. I try to read the literature, examine the data and reiterate those findings to my audience in an easy to read manner. I do however include all of my references, so if I have made a mistake anyone can read them and then comment. I do not need to copy and paste the results; anyone can read them for themselves. That being said I can miss things, I am not perfect, if I had overlooked something I would appreciate the insight.


There are large differences from the control and reference groups. There reference groups were feed conventional dies, whereas the control/treatment groups had altered diets.


You have still ignoring my criticisms of the Malatesta papers; their findings are irrelevant because they are so flawed.


In your comments you make is seem like they are hiding results but that is not the case. In their explanation they clearly say, “Blood was collected via the jugular vein from the first 10 surviving rats/sex/group during week 5 and again at terminal sacrifice after week 13”. That means that they tested 10 rats for each parameter. I do agree that it would have been better if they tested all the rats in each group. This is a flaw of this study. I am by no means saying these findings are perfect. Considering they had two groups (11% and 33%) there is still a large number of rats being tested for each parameter. I would assume they were trying to reduce the work load, and save money. In the end I do however agree that this is a flaw of this study.
Malatesta however only had 12 rats in each group making his conclusions much less significant.


I would have liked to see the data for the urine analysis (the numbers that is) however they do comment on their findings. They explain all statically significant differences in paragraph form. You would have to accuse them of lying to discount this. They could have also put together a table with fraudulent information just as easily.


Your comment on the rats dying is not accurate. They clearly state that they were only going to take readings from 10 rats in each group, it wasn’t because they died. There were a few incidental deaths; one on the MON 863 diet, one from the control group and two from the reference groups.


I do agree that the statistics on rages of rats is a little puzzling however that is not always the case. Table 2, 4, 5. All had an exact number of rats 10.


In regard to your comments on “advanced inflammatory kidney disease”, here is what the article said. “There were small increases in the incidences of focal inflammation and tubular regenerative changes in the kidneys of 33% MON 863 males when compared to their controls. In contrast, the incidence of cardiomyopathy was decreased in 33% MON 863 males when compared to controls. These findings illustrate the variability in the incidence of common microscopic changes that occur in rats of this age and strain. Most of the microscopic findings were of minimal severity and none of the aforementioned pathology findings were considered by the study pathologist to be test article related.” 1 There was not “advance inflammatory kidney disease” as you indicated.


In the end when talking about sample size Hammond’s sample size is 10 rats from each sex for each group (11% and 33%). Meaning 20 rats for 11% and 20 rats for 33%.That leads to 40 rats on GMO crops and 40 rats on non GMO. This is much larger than Malatestas sample size, and yet you still have not acknowledged that fact. If you believe “It wouldn't just be nice to have larger sample sizes, it is mandatory” I would suggest having the same criticism for your references.


Isogenic lines not doable? This is simply not the case, do a DNA analysis on the two varieties and determine if they are analogous. That is a requirement if your results are going to be valid.


In explaining why they chose to use a reference group this is what they said: “Six conventional corn varieties representing a diversity of corn germplasm were also planted to serve as reference controls for the rat feeding study”. In this instance they wanted to have rats on multiple types of corn to see any differences in that respect. They wanted reference values for rats on normal diets, a legitimate endeavor.


All that being said, I did not just reference the Hammond papers. I referenced a review article that looked at 12 long-term studies and 12 multigenerational studies. To discount their findings you would have to go through each article and show why they are invalid. I have provided a plethora of DATA, and all you have provided is the Malatesta studies, which have been heavily criticized by UK Advisory Committee on Novel Foods and Processes. Your argument is not supported by credible data.

If you decide to comment again please to not swear, I would like this to be a professional discussion without such language.



References


1. Hammond, B., Lemen, J., Dudek, R., Ward, D., Jiang, C., Nemeth, M., Burns, J., 2006a. Results of a 90-day safety assurance study with rats fed grain from corn rootworm-protected corn. Food Chem. Toxicol. 44, 147–160.

Wednesday 10 July 2013

Response to Ena Valikov Comments

Thank you again for responding. I really appreciate when people choose to comment and provide references. If you decide to post again I would appreciate if you make specific criticisms on any studies you disagree with. When you make statements such as “the Hammond studies cited: see if you reach the same conclusions” you are not telling me why their conclusions are invalid. Please be specific in your comments so you can indicate where the authors went wrong.

Now I will address your 2 points:

1)

In regards to the studies conducted by Hammond et al, I have found them to be of high quality and I agree with the conclusions of the authors. I will include a few quotes from these studies to illustrate this point.

(Hammond et al, 2006a)

This quote is found in the conclusion where they indicate that the EFSA (European Food Safety Authority) endorses their results and their conclusions.

“The summary prepared by the GMO Panel of the European Food Safety Authority best captures the prevailing scientific conclusion regarding the findings from this study. EFSA concluded that the results of the 90-day rodent study do not indicate adverse effects from consumption of maize line MON 863 (EFSA, 2004b)”.1

(Hammond et al, 2006b)

Here I will simply include a section from the results where some differences between the control and experimental groups are explained.

“Compositional, contaminant, and nutritional content of the experimental diets met the specifications for Certified Rodent LabDiet 5002 established by PMI. The levels of heavy metals, aflatoxins, and chlorinated and organophosphate insecticides were below detection limits. For chlordane, the analytical limit of detection was higher (250 ppb) than the maximum allowable concentration of 50 ppb, but was not considered to have an impact on the study. PCR analysis confirmed that the test diet contained MON 810 as it tested positive for the Cry1Ab transformation event. The control and reference diets did not test positive for the Cry1Ab transformation event. All of the 400 animals were healthy and appeared normal during the course of the study with the exception of one reference male that had to be sacrificed a few weeks prior to study termination due to injury. There were no changes noted during the duration of the study in behavior, activity, posture, gait, or external appearance that were considered to be test article related (data not shown).

3.1. Body weight and food consumption

Overall, body weight and weight gain were comparable for MON 810, control and reference groups (Figs. 1 and 2). Food consumption was generally similar between MON 810, control, and reference groups throughout the course of the study (Figs. 3 and 4).

3.2. Clinical pathology parameters

Clinical pathology parameters (hematology, blood chemistry, urinalysis) were generally comparable for all groups. There were a few statistically significant differences between the MON 810 and the control groups after 4 weeks and at study termination. None of these differences were considered test article related since they were of small magnitude and within ±2SD of the mean for the population of reference groups, and were either different from the control or the reference group but not both, or were not dose related (observed at the low dose but not at the high dose), and/or occurred after 4 weeks but not at study termination.

3.2.1. Hematology

Results for males and females, measured at study termination (week 13), are contained in Tables 2 and 3, respectively. There were no statistically significant differences between male and female MON 810 groups and the controls and reference groups for most of the parameters measured. There were two statistically significant differences (MCHC, PLT) observed in females that were not dose related and therefore not considered to be test article related.

3.2.2. Serum chemistry

Results for males and females, measured at study termination (week 13), are contained in Tables 4 and 5, respectively. There were no statistically significant differences between male and female MON 810 groups and their control and reference groups for most of the parameters measured. The few statistically significant differences observed were not considered to be test article related as they were of small magnitude and fell within ±2SD of the mean of the reference groups (Hammond et al., 2004b). The slight reduction in A/G (albumin/globulin) ratio for high dose MON 810 males was attributed to the slightly lower albumin and slightly higher globulin levels for MON 810 males, neither of which were individually statistically different from controls. The A/G ratio for MON 810 males also fell within ±2SD of the mean (1.79 ± 0.34) of the reference groups (Hammond et al., 2004b) even though it was slightly, but statistically significantly lower that both the control and reference groups. There were no differences in A/G ratio for females. This finding was not considered to be test article related.

3.2.3. Urine chemistry

There were a few statistically significant differences, but these occurred only in the males at the interim sampling period and none occurred at study termination (data not presented). None of the differences were concluded to be test article related.
3.3. Organ weights

There were no statistically significant differences noted in absolute or relative organ weights between treated and control animals. Table 6 presents organ weight data relative to body weights (absolute organ weights and organ weight relative to brain weight data are not shown).
3.4. Pathology

At necropsy, no gross or microscopic lesions were observed that were considered to be test article related(Table 7). The few spontaneous findings that were observed were generally of minimal to slight/mild severity, were randomly distributed among all groups and were the type commonly observed in control rats of this age and strain.”.2

(Hammond et al, 2004)

In regards to this study I would also like to refer you to the results section. In the results they give explanations of any statistically significant differences between treatment and control groups.

To reiterate my earlier point, if you want to criticize their conclusions you must specifically state what they did wrong.

2)

In regards to the papers produced by Malatesta et al., I would like to refer to the comments of the UK Advisory Committee on Novel Foods and Processes. This is what they had to say about their findings:

“The Committee was invited to consider a series of papers published by Italian researchers which examined the differences between the cells from mice given genetically modified (GM) and non-GM soya. Members were asked to identify any conclusions that could be drawn regarding the safety of GM herbicide-resistant soya.

Members noted that the papers did not state the origin of the GM and non-GM soya used in the feeding studies. There were no details of whether the soya had been grown in a field or under controlled conditions and whether or not the GM and non-GM soya were grown, handled and processed under similar conditions. It was also not clear whether the soya used in the control and GM experiments had a similar genetic background.

The Committee was unable to determine whether or not the GM and non-GM soya crops had been treated with the herbicide glyphosate, although the authors had suggested that differences in residual levels of glyphosate might be responsible for the observed differences.”3

Another paper was written in 2010 that further criticized the Malatesta paper that was written in 2008. They came up with 6 methodological problems that make this study invalid. They are as follows:

‘‘controlling for potential litter effect’’,

‘‘using an appropriate number of experimental animals per group and acquiring a sufficiently robust sample of independent observations’’,

‘‘establishing the representativeness of observations’’,

‘‘adhering to the principles for stereologic morphometry’’,

‘‘using appropriate statistical methods (for study design as well as for data analysis)’’,

‘‘controlling for potential confounding factors, including those related to differences in diet phytoestrogen contents’’.4

Considering all the criticism these studies have received and the obvious flaws they have; they do not indicate that GMO’s have metabolic harm. As you have said “The key to this, though, is to step back and examine the DATA to see if it supports the hypothesis”, I would suggest looking closer at the literature before you cite it in your argument.

Now I would like to address your comments in regards to the length of the triticale studies. I would agree that 90 days may not be long enough to examine all of the potential health impacts. I think that longer studies are needed so that we can truly know what effects GM foods have. I would also like to see a study done in human populations (although the logistics could be a nightmare). As I stated in my blog the most reliable evidence we have says that they are safe, that does not mean that more experiments wouldn't be helpful.

I do have institutional access to the primary literature, I could not comment on these issues without it.

Thank you again for commenting, I appreciate the discussion.

References

1. Hammond, B., Lemen, J., Dudek, R., Ward, D., Jiang, C., Nemeth, M., Burns, J., 2006a. Results of a 90-day safety assurance study with rats fed grain from corn rootworm-protected corn. Food Chem. Toxicol. 44, 147–160.

2. Hammond, B., Dudek, R., Lemen, J., Nemeth, M., 2006b. Results of a 90-day safety assurance study with rats fed grain from corn borer protected corn. Food Chem. Toxicol. 44, 1092–1099.

3. UK Advisory Committee on Novel Foods and Processes, 2006. Committee Paper for Discussion ACNFP/78/7 Advisory Committee on Novel Foods and Processes Ultrastructural Changes in Organs of Mice Fed GM and Non-GM Soya. Available at: <http://www.food.gov.uk/multimedia/pdfs/acnfp_78_7_.pdf>. Minutes of the Meeting Held on 20 July 2006, London, UK. Available at: <http://acnfp.food.gov.uk/meetings/acnfpmeet2006/acnfpjul06/acnfpminsjuly2006>.

4. Williams, A.L., DeSesso J.M. 2010. Genetically-modified soybeans. A critical evaluation of studies addressing potential changes associated with ingestion. The Toxicologist. 114, 1, 1154. Annual Meeting of the Society of Toxicology Salt Lake City, Utah March 7–11, 2010.

Saturday 6 July 2013

The Truth Behind GMO's

Before I begin I want to clarify that I am not talking about the politics of genetically modified organisms (GMO’s), nor the licencing of patent’s, nor am I justifying or supporting large agricultural companies. All I want to talk about is, given what we know now, are genetically modified foods safe to eat?

I get riled up every time I read an article bashing GMO’s not because of what they said but because they provide no evidence. I have never come across an article that bashes GMO’s that gives any references. No primary data to support their claims. As I mentioned earlier, science does not care what you think, it only matters what you can prove. Without randomized control trials to support your claims, your thoughts are useless in determining the safety of GMO’s.

It’s almost become popular to create paranoia about GMO’s. People refer to them as “Frankin Foods” and use phrases that encourage people to be afraid of them. The picture I have included illustrates this type of propaganda. Creating fear might be somewhat justifiable if they ever supported their claims with real results, but they usually don’t. If there are real reasons to be concerned about GMO’s then provide the scientific data to prove it. If we are going to have a scientific discussion then use scientific evidence. I don’t mean to sound unkind but I don’t care about your opinion on GMO’s, all I want to know is if they're safe. The way we determine that is through randomized controlled trials.

So let’s look at the scientific data. A study conducted in 2012 looked at the safety of GM maize, potato, soybean, rice, and triticale1.  They reviewed 12 long term studies and compiled their results to come to a conclusion. Their conclusion was that GM plants are nutritionally equivalent to their non-GM counterparts and can be safely used in food and feed. So the most reliable evidence shows that GMO’s are safe.
Just because something is new does not mean that it’s bad or scary. If done correctly advances in science can lengthen our lives and lead to a better world. The next time you come across an anti GMO article see if they give any references. Did they cite any primary research? If the answer is no, what they have said is meaningless.

Now to anyone that believes GMO’s are not safe I have a challenge for you. Please comment and give me references to support your claims. If I have overlooked some important data I will retract what I have said and re-write the article. I don’t have an opinion on the issue; all I care about is what’s true. If I am presented with new evidence that shows that GMO’s are not safe I will change my mind in a second.
I encourage comments and would greatly appreciate them.


References

1.      Snell, Chelsea, et al. "Assessment of the health impact of GM plant diets in long-term and multigenerational animal feeding trials: a literature review." Food and Chemical Toxicology 50.3 (2012): 1134-1148.