Friday, May 27, 2011

Going hormonal over beef

The mention of hormone use in beef often stirs visceral reactions. Uncomfortable with a seemingly “unnatural” production method, consumers may seek relief in USDA Organic brands or Reserve programs where such a practice is shunned. Although synthetic hormone use carries a heavy stigma (yeah, thanks, baseball players), its actual use in livestock production is far more simple, safe, and even beneficial than you’d think.

Beef producers choose to use hormones to increase efficiency by 20% (Wileman et al., 2009): cattle gain more lean muscle on less feed. Remember the carpool effect discussed in the blog post Food Routing: Local or HOV? The more lean muscle material (lean meat) that can be piled onto fewer body frames means less maintenance energy wastage, less fecal/urinary excretion, smaller carbon footprint, less environmental impact per pound of beef. Some are concerned that animal bodies are weighing down too heavily onto their skeletal frames, causing lameness and breakage, but this is impossible given that estrogen improves bone density and strength, and in some cases causes bones to continue growing (Felson et al., 1994). Consumers derive most of their fear from the inaccurate suspicion that they ingest the hormones that the animals are given; they fear that the substances given to live animals linger in meat.

We’ll get one thing straight: hormones are never injected. The dose from a dissolvable pellet per animal immediately begins to signal for muscle building and breaks down after it “delivers its message”. There is no hormone blood-pooling, no accidental over-dosing; it’s just not possible, nor profitable (cattleman common sense: implanting with more than one is a waste of money, does not amount to increased growth, and could get you jailed). Growth promotants are implanted as a slowly-dissolving pellet in the ear, or they are fed in trace amounts. Animals are not allowed to be slaughtered until the compounds have had more than enough time to decompose and reduce down where they reach an equilibrium at a natural blood concentration. This is why, over and over, the FDA and USDA report that beef from implanted cattle are insignificantly different than non-implanted cattle. Despite the following reasons why, on a most basic biochemical level, there is nothing to fear, the FDA and USDA stringently regulate growth promotant use and routinely test for residues in meat. Secondly, the beef industry excels at self-regulation and mutual accountability through the Beef Quality Assurance program.

Beef producers use two kinds of growth promotants:
1.      Hormones (low-dose ear implants, usually a form of estrogen) signal for continued lean tissue development after the animal reaches sexual maturity (Trenkle, 1997).
2.      Beta agonists (mixed in feed) block amino acid breakdown so that the same weight isn’t maintained as the body "idles" and generates heat, but increases as the animal eats dietary protein (Borohov et al., 1987; Dawson et al., 1988).
Both chemicals are naturally occurring in us and in cattle. Being chemically unstable and having limited half-lives, they degrade all the way down until they reach a normal equilibrium concentration in the animal’s body.

A meta-analysis of ten studies by Taylor et al. (2009) summarized that no significant relationship between conventional beef consumption and breast cancer (mammary tissue being most sensitive to estrogen intake) could be alleged.

Let’s put things into perspective (Preston et al., 1997):
1.      Milk estrogen concentration: 0.12 parts per billion (nanograms/gram)
2.      Unimplanted beef: 0.16 ppb
3.      Implanted beef: 0.22 ppb
4.      Eggs: 35 ppb
5.      Soy flour: 1,510,000 ppb !!
6.      Female daily production: 5,000,000 ng
7.      Male daily production: 100,000 ng

Consequently, vegetarians have repeatedly tested positive for higher circulating androgens because of high consumption of soy products (Armstrong et al., 1981; Thomas et al., 1999).

You’ve heard the rumor about precocious development in females (recent generations of girls hitting puberty earlier)? Blaming this on milk and meat consumption doesn’t make sense, but blaming it on diets higher in starch and sugars does. These simple carbohydrates cause insulin levels to rise, which sets off this chemical chain reaction in the body: Insulin --> GnRH (gonadotropin releasing hormone) --> LH (luteinizing hormone) & FSH (follicle stimulating hormone) --> increased estrogen production (Poretsky et al., 1999; Ultrianen et al., 2009; Rosenfield et al., 2009). In starch and sugar, I believe, you have the culprits for early puberty and possibly even ovarian cysts. Similarly, there are  several beef cattle studies that use  high energy diets to increase blood sugar (--> blood insulin) to ultimately decrease the age of puberty in heifers (Corah et al., 1977; Moseley et al., 1977; 1982; Randel & Rhodes, 1980…).

For more information on why growth promotant use in beef production is safe, refer to Avery & Avery’s 2007 study.

What do you Think?   

2 comments:

  1. This is one of the conversations I have with consumers most often when I start discussing chemical usage in agriculture. The female puberty issue is always brought up. It is astonishing how little people know about their own bodies and the bodies of their children.

    Do you have any information on economics of implanted vs unimplanted beef? Maybe average price per pound and average weight per animal?

    Fantastic write-up as always.

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