Beware the Myths of Feedlot Marketeers

An article which first appeared on the web back in January is doing the rounds again. This time it’s being used by the National Beef Packing Company to promote its “natural” beef.

The National Beef Packing Company has a lot to say about the benefits of its feedlot-raised, grain-fed beef versus grassfed beef, and is currently using an edited version of an article by James E. McWilliams, entitled “Beware the Myths of Grassfed Beef,” to support its argument.

I’m not sure if the editing of this newer version was done by McWilliams himself, or if National realized that if they printed the original article in its entirety they would at the very least find themselves promoting the animal welfare and health benefits of grassfed over feedlot beef. Because in his original article, McWilliams states that “the comparative health benefits of grass-fed beef are well documented” and that “scores of studies indicate that it’s higher in omega 3s and lower in saturated fat.” He also says that grassfed systems are “kinder to the animals” – all points which have miraculously disappeared from the National Beef Packing Company’s current version. But let’s not worry about that now, and go straight to the “meat” of the article.

My initial reaction to McWilliams report was utter disappointment. How can someone who wants to refute claims that grassfed beef is safer – and who actually promotes the view that grassfed beef could be a public health hazard – have missed so much evidence to the contrary? Indeed, the biggest problem in pointing out the mass of scientific evidence that supports the health-giving benefits of grassfed beef both in terms of its beneficial nutritional composition (unaccountably overlooked in this newer version of the article) and the lower risks of food borne illness is this:  exactly where should I begin?

Well, let’s start by looking at some of the references that McWilliams uses to support his article. Sadly, he doesn’t actually give a full list of references which would allow an interested reader to look up the particular studies to which he has referred. (For the record, you’ll find all my references at the end of this article.) Nevertheless, McWilliams does provide the occasional weblink to research, or at least a place and a year where the research was carried out. So I’ve done my best to track down his references to assess their relevance. Let’s take this one to start with. McWilliams states that:

“An Australian study actually found a higher prevalence of O157:H7 in the feces of grass-fed rather than grain-fed cows.”

McWilliams provides no clear reference to substantiate this claim. A review of online scientific journals drew a blank. However, another piece written on the topic of the comparative food safety of cattle fed hay vs. cattle fed grain (Hancock and Besser 2006) makes the following statement:

One study (Fegan et al, 2004a) found that a higher prevalence among pastured cattle and, among positive cattle, similar concentrations of E. coli O157:H7 in feces.

Fegan is Australian, so this must be the study referred to in McWilliams article. But if you read this particular piece from Fegan et al you also find the following statement:

There was no significant difference (P = 0.06) between the numbers of E. coli O157 in pasture-fed or grain-fed cattle feces, although the geometric mean (antilog of the mean of log10 transformed MPN values) was higher in grain-fed (130 MPN g-1) than in pasture-fed (13 MPN g-1).

Leaving out all the “MPN g-1” jargon, this statement directly contradicts both Hancock and Besser – and McWilliams’ assertions. The level of E. Coli O157 is higher in grain-fed than in pasture-fed cattle. Are the two misleading references to this research related, I wonder?

There’s another Australian study which McWilliams’ “Beware the Myths of Grassfed Beef,” article links to – and it’s Fegan et al again, this time with a different piece of research (Fegan et al 2004b). McWilliams uses it to back up his claim that grassfed cattle do become colonized with E. coli O157:H7 at rates nearly the same as grain-fed cattle.  That’s what the abstract of the original research article says.  Yet, when you read the full report – and it’s always worth finding out what particular researchers define as being “grassfed” when it comes to cattle – you find the following statement:

“It was observed that on some occasions, the feces of grass-fed cattle contained remnants of grain. This could indicate supplemental feeding of such animals or changes in the husbandry of these animals during transport and/or holding before slaughter. However, such animals would not have fit the definition of lot-fed (60 days on grain) applied to animals defined as lot-fed in the study. This survey was conducted during a period of widespread drought in Australia, and it is possible that some husbandry practices (e.g. supplemental feeding) may have changed in some areas and that this influenced the results of the survey”.

So it is clear from this statement that the “grassfed” cattle in this study may have been fed supplemental grain at a time when pasture quality and quantity was low due to a widespread drought. Is this therefore a true comparison of grassfed and grain-fed? I don’t think so.

Here’s another Australian study that McWilliams doesn’t consider. Barlow and Mellor (2010) investigated the concentration of E. coli and the prevalence of non-O157 E. coli in grassfed and grain-fed cattle fecal samples. They found that “feed type was shown to have an effect on mean E. coli counts with grain-fed cattle significantly more likely to have a higher concentration of E. coli in their feces than grass-fed cattle.”

OK, so Barlow and Mellor looked at non-O157 E. coli. But O157 is not the only pathogenic type of E. coli: it’s just the one we hear about most, and any system that has reduced the overall levels of E. coli is better than one with high levels.

In another study – again with a wider focus than just E. coli O157 – Bailey and Vantelow in 2003 looked at food borne pathogens and found that, among truck loads of feedlot and grassfed cattle, 58 percent of the feedlot cattle carried the campylobacter bacteria. Only 2 percent of cattle raised on pasture had these food poisoning bacteria, which can cause symptoms including fever, upset stomach, headache and muscle pain.

So, I hope you will agree that that the situation is not quite what McWilliams would have us believe. But there are other points that we also need to examine. The piece of work that started to show that grassfed beef could be less risky in terms of food borne illness was Diez-Gonzalez et al 1998. This study showed that grain-fed beef had far greater numbers of acid resistant E. coli than grassfed beef. Yes, they only looked at a limited sample size of animals in that study, but the important point is that this isn’t the only piece of scientific research that Diez-Gonzalez was involved in on this topic. He also worked with Russell et al (2000), which summarized research to date and provided some updated graphs from the original research which confirmed the original finding that grassfed beef presented less of a risk in terms of E. coli.

Further references to support the point that grain-fed cattle have a far higher load of E. coli include Scott et al (1999) who switched cattle from grain-based diets to hay and found that acid-resistant E.coli decreased from 10,000 to 20 viable cells per gram in 7 days. Scott et al did not specifically look at E. coli O157 but Keen et al (1999) did. They noted that a similar diet shift (grain to hay for 7 days) caused a large decrease (53 percent to 18 percent) in the number of cattle that were E. coli O157:H7 positive.

And there’s so much more: Dargatz et al (1997) and Buchko et al (2000) both showed that grain feeding – particularly barley – was linked to increased shedding of E. coli O157:H7 by feedlot cattle. All I’m interested in is grassfed versus grain – as far as I am concerned, the grain could be corn or wheat or barley. But it’s interesting to note that some grains may actually be worse than corn for providing an environment in the cattle gut for E. coli to thrive. This fact was clearly demonstrated by Berg et al (2004) in their study, while Bach et al (2005) showed that survival of E. coli O157:H7 in manure from corn- and barley-fed cattle is approximately equal, and that simple survival in the feces is not responsible for the increased prevalence of E. coli O157:H7 in barley-fed cattle. To summarize all of the points above, the scientific consensus when comparing grain-fed to forage-fed cattle still indicates that more E. coli (including O157:H7) are present in the feces of cattle fed grain diets.

As stated at the beginning of this report, while McWilliams disputes the “food safety” claims of grassfed beef over feedlot beef, in his original article he accepts that “the comparative health benefits of grass-fed beef are well documented.” Yet in the more recent version of his article which is being promoted by the National Beef Program, it seems that someone has apparently chosen to remove this particular argument entirely. So I will summarize just a few of the many published scientific studies which show that meat and milk from grassfed animals is better for us.

Firstly, let’s consider the omega-3 content of grassfed meat. Studies from around the world – including the European Union’s “Healthy Beef” project and Ponnampalem (2006) – have shown that meat from grassfed animals has two to four times more omega-3 fatty acids than meat from grain-fed animals. Omega-3s are often called good fats because they play a vital role in every cell and system in the body. It might surprise you to know that, of all the fats, they are also the most heart-friendly. Indeed, people who have ample amounts of omega-3s in their diet are less likely to have high blood pressure or an irregular heartbeat.

Let’s look at another good fat – this time conjugated linoleic acid (or CLA for short). When ruminants are raised on fresh pasture alone, their meat and milk contain from three to five times more CLA than similar products from animals fed a conventional grain-based diet. Scientists now believe that CLA may be one of our most potent defenses against cancer. In laboratory animals, a very small percentage of CLA—a mere 0.1 percent of total calories—greatly reduced tumor growth. In addition, other studies have shown that a study group of hamsters fed a diet of CLA had lower amounts of LDL (low density lipoprotein) in the blood, as well as a reduced risk of developing early aortic atherosclerosis (Wilson et al 2002). Another study from Iran (Aryaeian et al 2008) found that adults with rheumatoid arthritis showed a significant decrease in blood pressure after CLA additions to their diet.

Finally, scientists have shown that grassfed meat is higher in vitamin E than either grain-fed animals or, surprisingly, grain-fed animals that were given high doses of synthetic vitamin E (Smith and Realini 2003). In humans, we know that vitamin E is linked with a lower risk of heart disease and cancer.

As a final note, I wonder whether McWilliams is aware of the irony of the situation when his article is being used by the National Beef Packing Company to promote meat from systems that, aside from the potential E. coli risks, have an appalling record when it comes to environmental management. The irony being that McWilliams is a vegetarian who promotes the virtues of this lifestyle choice in terms of its environmental benefits.

Perhaps Mc Williams hasn’t read our extensive blogs on this topic, “Beware of Bad Science” or “The Bigger Picture,” which refute other articles which have also attempted to paint grassfed beef in a similar bad light. Our fully referenced reports clearly show that if the whole system of meat production is taken into account – and not some selected part of the cycle – then grassfed beef has a huge role to play in assuaging climate change. While McWilliams rightly points out that feeding ruminants on grain that could be supporting humans is neither right nor sustainable, he fails to develop this concept further in recognizing that we can move to grass-based livestock systems that are not directly competing with humans for food and which have a vital role to play in carbon sequestration, too – aside from the proven animal welfare and human health benefits that he acknowledges such systems already offer.

But sadly McWilliams is of the view that: “Issues of animal welfare are equally implicated in all forms of meat production.” I’m sorry, Mr. McWilliams, but I simply cannot agree. We must not lump all meat production – feedlot and industrial and pasture-based and grassfed –together. You may well oppose livestock production in any form, but I know that pasture-based systems can deliver high animal welfare, environmental sustainability, and improved nutritional qualities – and present a much lower risk of E. coli, too.

References

Aryaeian N, Shahram F, Djalali M, Eshragian M R, and Djazayeri A 2008. Effect of conjugated linoleic acid, vitamin E and their combination on lipid profiles and blood pressure of Iranian adults with active rheumatoid arthritis. Vascular Health and Risk Management volume 4(6)  1423 – 1432.

Bach, S.J., K. Stanford and T.A. McAllister. 2005b. Survival of Escherichia coli O157:H7 in feces from corn- and barley-fed steers. FEMS Microbiol. Lett. 252:25-33.

Bailey, G.D., B.A. Vantelow et al. (2003) A study of the food borne pathogens Campylobacter, Listeria and Yersinia, in faeces from slaughter-age cattle and sheep. Australia. Commun Dis Intell. 2003; 27(2): 249-57.

Barlow R, S., Mellor, G. E. YEAR. Prevalence of Enterohemorrhagic Escherichia coli Serotypes. Australian Beef Cattle. Foodborne Pathogens and Disease 7(10): 1239-1245.

Berg, J.L., T.A. McAllister, S.J. Bach, R.P. Stillborn, D.D. Hancock and J.T. LeJeune. 2004. Escherichia coli
O157:H7 excretion by commerical feedlot cattle fed either barley- or corn-based finishing diets. J. Food Prot. 67:666-671.

Buchko, S.J., R.A. Holley, W.O. Olson, V.P.J. Gannon and D.M. Veira. 2000a. The effect of different grain diets on fecal shedding of Escherichia coli O157:H7 by steers. J. Food Prot. 63:1467-1474.

Dargatz, D.A., S.J. Wells, L.A. Thomas, D.D. Hancock and L.P. Garber. 1997. Factors associated with the presence of Escherichia coli O157 in feces of feedlot cattle. J. Food Prot. 60:466-470.

Dewhurst, R.J., Shingfield, K.J., Lee, M.R.F., and Scollan, N.D. 2006. Increasing the concentrations of beneficial polyunsaturated fatty acids in milk produced by dairy cows in high-forage systems. Animal Feed Science and Technology 131:168–206.

Diez-Gonzalez, F., T. R. Callaway, M. G. Kizoulis, and J. B. Russell. 1998. Grain feeding and the dissemination of acid-resistant Escherichia coli from cattle. Science 281:1666–1668.

Fegan N, Higgs G, Vanderlinde P, Desmarchelier P.  2004a Enumeration of Escherichia coli O157 in cattle faeces using most probable number technique and automated immunomagnetic separation. Lett Appl Microbiol. 38(1):56-9.

Fegan N, Vanderline P, Higgs G, and Desmarchelier P. 2004b The prevalence and concentration of Escherichia coli O157 in faeces of cattle from different production systems at slaughter. Journal of Applied Microbiology 97 (2)  362-370

Hancock D and Besser T 2006 E. coli O157:H7 in hay- or grain-fed cattle College of Veterinary Medicine  Washington State University. at: http://www.puyallup.wsu.edu/dairy/nutrient-management/data/publications/E%20coli%20O157%20in%20hay-%20or%20grain-fed%20cattle%20Hancock%20and%20Besser%2011%2006.pdf Accessed on 16 October 2010

Keen, J. E., G. A. Urlich, and R. O. Elder. 1999. Effects of hay and grain-based diets on the fecal shedding of naturally-acquired enterohemorrhagic E. coli (EHEC) 157:H7 in beef feedlot cattle. 80th Conference of Research Workers in Animal Diseases, Abstract #86, November 7–9, 1999. Chicago, IL.

Noziere, P., Graulet, B., Lucas, A., Martin, B., Grolier, P., and Doreau, M. 2006. Carotenoids for ruminants: From forages to dairy products. Animal Feed Science and Technology 131:418–450.

Ponnammpalam E N, Mann N J and Sinclair A J 2006. Effect of feeding systems on omega-3 fatty acids, conjugated linoleic acid and trans fatty acids in Australian beef cuts: potential impact on human health. Asia Pacific Journal of Clinical Nutrition 15(1):21-9

Realini C E, Duckett S K, Brito G W, Dalla Rizza M and De Mattos D (2003)Effect of pasture vs. concentrate feeding with or without antioxidants on carcass characteristics, fatty acid composition, and quality of Uruguayan beef. Meat Science 66 (2004) 567–577

Russell J B, Diez-Gonzalez F, and Jarvis G N 2000. Effects of Diet Shifts on Escherichia coli in Cattle. Journal of Dairy Science Vol. 83, No. 4

Scollan, N., Hocquette, J., Nuernberg, K., Dannenberger, D., Richardson, I., and Moloney, A. 2006. Innovations in beef production systems that enhance the nutritional and health value of beef lipids and their relationship with meat quality. Meat Science 74:17–33.

Scott, T., C. Wilson, D. Bailey, T. Klopfenstein, T. Milton, R. Moxley, D. Smith, J. Gray, and L. Hungerford. 1999. Influence of diet on total and acid-resistant E. coli and colonic pH. Nebraska Beef Rep. 2000:39–41.

Smith, G.C. Dietary supplementation of vitamin E to cattle to improve shelf life and case life of beef for domestic and international markets.” Colorado State University, Fort Collins, Colorado

Wilson T.A,  Nicolosi R.J,  Chrysam M and Kritchevsky, D 2002. Conjugated linoleic acid reduces early arotic atherosclerosis greater than linoleic acid in hypercholesterolemic hamsters. Nutr-res. New York, N.Y v. 20 (12) p. 1795-1805.