When I was five, my brother and I used to sneak into our father’s library, tug open the doors of the heavy, musty-smelling breakfront and explore what we called “the sugar drawer.” A treasure chest to us, the drawer overflowed with hundreds of little packets of sugar that bore the names of the eateries we had visited together – Joseph’s Aquarium Restaurant, Friendly’s, Mug n’ Muffin. Although Dad didn’t sweeten his coffee, he felt entitled to the sugar that was provided for that purpose. So whenever it was offered, he accepted, and squirreled it away for eventual visitors to our home.
Those sugar packets were irresistible to my brother and me. We used to sort, stack, build and eventually consume them, carefully tearing open the packages and pouring their entire contents into our mouths. The sugar granules audibly crunched between our teeth before dissolving into syrupy swallows.
For the most part, making mischief with my brother was a highlight of my childhood. But the sugar-eating part of this particular memory makes me wince. And it begs the question: Does eating too much sugar cause diabetes? It’s not entirely clear, but a population-based study published February 27 in the peer-reviewed, online journal PLoS One identifies a relevant correlation.
So Does Sugar Cause Diabetes?
In the study, researchers from Stanford University School of Medicine, the University of California, San Francisco, and the University of California, Berkeley examined the availability of sugar and prevalence of diabetes in 175 countries over a recent ten-year period. They relied on data from the United Nations Food and Agricultural Organization and the International Diabetes Federation as well as economic indicators from the World Bank. The study considered the difference between calories derived from added sugar (cane sugar, high fructose corn syrup and other sweeteners) and calories derived from other sources. For each additional 150 sugar-calories per person, per day (what’s in a 12-oz can of Coke), the prevalence of diabetes rose 1.1%. That’s more than ten times the prevalence when the additional calories came from other (non-sugar) sources.
It is important to note that the PLoS study is an epidemiological – or population-based – study. By design, such studies seek to demonstrate correlation, not causation. Does that limitation in scope make the PLoS study less valuable? I don’t think so. I imagine the study is doing exactly what its authors intended – getting people’s attention and putting a spotlight on the need for more targeted research. “The bottom line,” concludes the study’s lead author Dr. Sanjay Basu, “is that… some calories may be more metabolically harmful than others, and sugar calories appear to have remarkably potent properties that make us concerned about their long-term metabolic effects.”
Another of the study’s authors is Dr. Robert Lustig, a pediatric endocrinologist at UCSF Benioff Children’s Hospital and author of the recently published book Fat Chance: The Bitter Truth About Sugar (HarperCollins Publishers, 2012). Dr. Lustig has been railing against sugar for years. His 2009 lecture Sugar: The Bitter Truth has over three million views on YouTube and formed the basis of Gary Taubes’s 2011 New York Times Magazine cover article Is Sugar Toxic? Dr. Lustig is specifically concerned with the fructose in processed sweeteners (e.g., sucrose and high fructose corn syrup) as opposed to fructose in its natural state (say, in an apple) where the sugary content may be mitigated by fiber. According to Dr. Lustig, excessive intake of added fructose increases insulin production and crashes our blood sugar, causing acute hunger. The insulin dump also disables the satiety hormone whose job it is to signal our brains when we’re full. As the cycle repeats, we feel hungry, we eat more, we gain weight.
Central to Dr. Lustig’s argument is his claim that while glucose can be metabolized by any cell in the body, fructose is metabolized exclusively by the liver. He claims that prolonged, excessive fructose consumption overwhelms the liver, leading to fatty liver disease and a host of other chronic metabolic afflictions including metabolic syndrome, obesity, hypertension, heart disease and type 2 diabetes. Again, more research is needed. Plenty of experts feel strongly that Dr. Lustig should look beyond fructose to carbohydrates in general. Regardless, the message is clear that the 22 teaspoons of added sugar the average American consumes daily is not benefitting our collective health.
For our part, my husband and I strive to keep our family on a whole-foods oriented diet that is low in both refined carbohydrates and added sugar. We minimize packaged foods to ensure that heaps of sugar – like the ones I poured down my throat in the seventies – don’t sneak into our diet through bottled salad dressings, ketchup, peanut butter, crackers, flavored yogurt, and myriad other hidden sources. Because while we may not know for sure whether excess sugar causes diabetes, if there’s a reasonable chance that it does, limiting its intake can’t hurt.
These statistically-based health studies are important, but if one is looking for causality, one need look no further than the structure of fructose itself. Fructose is sufficiently similar to the sugar of our DNA backbone that it can substitute into our DNA, but not without disrupting the structure. I found almost 2000 studied linking fructose to cancer. But because of the mechanism of substitution, I am quite confident in pointing to fructose as the villian. Dr. David K. Teertstra http://TheInsulinProject.ca
Yes, Maureen, the causes of obesity and diabetes are really very complicated. Interestingly, however, a simple diet based on simple science is impressively effective in reversing obesity and diabetes in a significant proportion of cases. Here is is: (scroll down) http://www.australianparadox.com/pdf/why-we-get-fat.pdf Emily, the problem with obviously faulty “peer reviewed” papers such as Australian Paradox – self-published by highly influential “scientists” – is that it means we cannot trust or take seriously anything published in Australian nutrition science. The evident lack of competent quality control in our universities means we have to do our own due diligence on each paper. Accordingly,… Read more »
Thank you, Maureen. I am not suggesting that sugar is the only food associated with (certain forms of) diabetes risk – there are other refined carbohydrates (e.g., white rice and bread) that have also been implicated. And you will get no argument from me that genetic, environmental, and behavioral factors, also appear to be factors.
Thank you, Jennifer
Thank you for your comments, Rory.
In fairness to the University of Sydney, I must confess that I have not read the Australian Paradox study, although I am aware of it, the surrounding controversy, and your wager.
You’re welcome, Maxine.
It is overly simplistic—and misleading—to suggest that reducing or eliminating one specific ingredient from the diet will lower the risk of type 2 diabetes. It’s a complex health condition with numerous risk factors such as age, genetics and obesity, according to the American Diabetes Association (http://www.diabetes.org/diabetes-basics/prevention/risk-factors/). As for high-fructose corn syrup, the American Medical Association has concluded it is so similar in structure to sucrose (table sugar) that your body can’t tell the difference and processes both in the same way (LetsClearItUp.org).
Very interesting and important piece.
Thanks for your piece, Emily. Awkwardly, you are barking up the wrong tree, according to high-profile University of Sydney scientists.
In case you haven’t noticed, “There is absolute consensus that sugar in food does not cause diabetes”.
Furthermore, in Australia, there is “an inverse relationship” between the consumption of added sugar and obesity. This is the “Australian Paradox”, a formally published “peer reviewed” scientific “finding”.
Can you believe it, Emily? Let me know what you think.
Check these and other amazing “facts” at http://www.australianparadox.com/pdf/22Slideshowaustraliangoestoparadoxcanberrafinal.pdf
Thank you for your informative article and for references to further reading sources.