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Spotty labeling confused this customer…the lesson I learned about rBST labeling

By Mary Scourboutakos

Living in Canada, I was never worried about recombinant bovine somatotropin hormone, aka rBST. This synthetic hormone, which mimics a natural hormone that causes cows to produce more milk, was banned in Canada in the 1990s. So North of the 49th parallel, most people have never heard of it.

Meanwhile in the United States, the situation is a little different. rBST is legal in the US because technically, there’s no evidence that it causes harm to humans. Meanwhile in Canada, the rationale for its ban is that it may pose risks for the cows that are treated with it.

With that in mind, whenever I visit the US, I always explore the milk on grocery store shelves to see if it contains rBST. To my surprise, on nearly every occasion, I’ve been hard pressed to find a jug of milk that didn’t say “from cows not treated with rBST”.

This was reassuring. But then I noticed something…while every jug of milk said “no rBST” I couldn’t find a single block of cheese, or container of yogurt declaring this.

This got me thinking…are they using the rBST-treated milk in yogurt and cheese? Could it be that consumers are so far removed from the food chain that they would think to look for “no rBST” on their milk, but wouldn’t think to look for it on their cheese?

It didn’t make sense…were the labels missing? Or was the industry using rBST milk in places where people would be less likely to look for it? I wanted to get to the bottom of this, so I started asking people about it. No one really knew the answer until I spoke with a representative from the food industry who told me that it takes so much effort to change labels, the industry won’t label something unless there is extremely consumer demand. She predicted that the yogurts and cheese are probably made with rBST-free milk, they’re just not advertising it.

Lo and behold, after doing some reading I found that in fact, many brands have removed rBST from ALL of their products, they’re just not stating it on their label, or they’re doing so haphazardly on some products but not others.

Perhaps I’m an over informed consumer who is paying attention to details that nearly no one else even knows or cares about, nevertheless, it’s interesting to consider that a product could in fact be potentially healthier—or at least kinder to the animal it’s coming from—than expected. I guess sometimes the food industry doesn’t show off everything it could.


Are All Sugars Created Equal? Let’s Talk Fructose Metabolism

By Chris Radlicz

According to NHANES (National Health and Nutrition Examination Survey) 2005-2010 the average American consumes about 20 teaspoons of sugar per day, with sugar consumption being the highest in teens and men (1). Interestingly, 33% of calories from added sugars come from beverages, and the majority of those beverages are sweetened with high fructose corn syrup (HFCS) (1).

But what is the novelty of HFCS? Aren’t the grams of sugar on the package all that matters? Although calorically equivalent, not all sugars are metabolized the same way.

Previous papers have established epidemiological links between fructose consumption, obesity, and metabolic disease. To take this further, recent literature has indicated that fructose, particularly in high concentrations, as present in high fructose corn syrup and sucrose, are proving to be toxic. HFCS is composed of about 60% fructose and 40% glucose (2). Prior to the processing of sugars, it was nearly impossible to find such high concentrations of sugar in the diet, but it now seems to be commonplace.

Dr. Kimber Stanhope out of University of California Davis published a recent review paper that touched on the metabolic dysregulation that occurs with high consumption of fructose.

Dr. Stanhope’s group has previously shown that subjects consuming fructose-sweetened beverages for 10 weeks, in addition to their normal diet, had increased de novo lipogenesis, dyslipidemia, circulating uric acid levels, visceral adiposity, reduced fatty acid oxidation, and insulin resistance. In contrast, subjects who consumed glucose-sweetened beverages, had comparable weight gain to the fructose group, but did not exhibit the aforementioned metabolic changes (3). These adverse effects seen in the fructose group all increase the likelihood of chronic diseases such as obesity, fatty liver, type-2 diabetes, and cardiovascular disease.

When consuming glucose, the liver is initially bypassed and the glucose reaches systemic circulation to be used by tissues such as the brain and muscles. If excess glucose is consumed in the diet, it will first be stored as glycogen, and secondarily as fat. Fructose on the other hand, takes a different path. When fructose is consumed, it is exclusively metabolized in the liver, where a particular enzyme, fructokinase, will allow for the uptake of fructose (3). Fructose metabolism as a whole lacks many of the cellular controls that are present in the glucose metabolism, which allows for unrestrained lipid synthesis (2).

Significant metabolic issues arise when a high concentration of fructose is consumed, such as in HFCS. An overload of fructose in the liver will lead to de novo lipogenesis and subsequent lipid droplet accumulation in the liver. With these high levels of fructose, the increase in lipid accumulation consequently decreases the breakdown of fat in the liver (3).

This intra-hepatic lipid will promote the production and secretion of very low-density lipoprotein 1 (VLDL1) leading to an increase in post-prandial triglycerides. A vicious cycle occurs effecting insulin resistance as well. The lipid in the liver will increase insulin resistance resulting in increases in circulating diacylglycerol. Additionally, the insulin resistance will lead to further lipid deposit in the liver with sugar having a greater propensity to turn to fat (3). A downstream effect of increased apoCIII and apoB will lead to muscle lipid accumulation, and end in whole body insulin resistance. All of this metabolic dysregulation results from the direct route fructose initially takes to the liver.

Although there is this well-defined and unique pathway for fructose metabolism, many industry-funded studies, haven’t shown the negative metabolic outcomes of consuming HFCS or sucrose (3). More research is certainly needed, but it is best to remember that added sugar in such high concentrations, no matter the culprit monosaccharide, is not favorable for overall health.

It is interesting to note a possible evolutionary perspective, which proposes the advantage of enhanced fructose to fat conversion. At the end of a growing season, ripened fruit will tend to have high levels of fructose. Therefore the fruit consumed at the end of the season may allow for increased fat storage, which would have been beneficial because of the low food availability in the ensuing months (2).

1.U.S. adults, 2005– 2010. NCHS data brief, no 122. Hyattsville, MD: National Center for Health Statistics. 2013.

2.Lyssiotis CA, Cantley LC. F stands for fructose and fat. Nature. 2013; 508:181-182.

3.Stanhope KL. Sugar consumption, metabolic disease and obesity: The state of the controversy. Crit Rev Clin Lab Sci. 2015;1-16.