Summary: Fructose, Sucrose and High Fructose Corn Syrup: Relevant Scientific Findings and Health Implications

The Experimental Bio 2012 session, Fructose, Sucrose and High Fructose Corn Syrup: Relevant Scientific Findings and Health Implications, provided me with some important takeaways which I have listed here.

Each of the five speakers had a chance to present their take on the biochemistry and potential health implications of fructose, sucrose and HFCS.

Just the Facts

The first speaker was biochemist Dr. John White. He’s spent the last 30 years in study of the biochemistry of sugars. I’d call him a sugar expert. He clearly presented the biochemistry of both sucrose and HFCS, and described how the controversy over HFCS began – around the year 2000 – when a hypothesis was made that the consumption of HFCS in beverages may play a role in the epidemic of obesity (this suggestion was a simple observation that obesity rates began to increase at about the same time HFCS came into the market in the 1970s). That issue is now put to rest, according to White:

“There is now scientific agreement that HFCS and sucrose are metabolically equivalent. Studies from 3 separate laboratories (Havel, Soenen, Rippe) comparing HFCS with sugar (sucrose) demonstrate that many metabolic markers for obesity (glucose, insulin, triglycerides, uric acid, leptin, ghrelin, blood pressure, muscle fat deposition, hunger, satiety) are virtually identical.”  ~White

White states that the current issues surrounding fructose lacks perspective:

“Contemporary fructose experimentation exaggerates dietary intake levels and patterns and distorts metabolic consequences.”  ~White

In other words, many studies experiment with pure fructose, which doesn’t correlate to our food supply, nor metabolism. We aren’t consuming fructose without glucose. This is a key point – fructose metabolized on its own, differs from fructose metabolized when glucose is present.

As a registered dietitian, I’m interested in study methodologies that can deliver results proving a dietary link to disease that is based in reality. Study participants must consume foods and beverages in a way that humans actually consume them for study conclusions to apply to the population.

To counterpoint the idea that sugar itself is leading to obesity, Dr. White shared USDA data showing that overall calorie intake has increased by an average of 425 kilocalories per day, while added sugars has decreased (19% to 17% from 1970 to 2009). Of course, more calories, coming from any source, will result in weight gain over time.

“There’s also no correlation between the obesity trend and total fructose since obesity is rising and overall fructose intake has remained the same.” ~White

Data is only as good as its Source

Dr. George Bray’s presentation primarily focused on soft drink consumption and what he perceives as the health issues related to this behavior. His theory is simply that soft drinks increase fat. Bray’s studies just don’t stick with me as he attempted to suggest that soft drink consumption itself is responsible for diabetes, metabolic syndrome and fatty liver (in rats, of course). His sugar consumption data is also inconsistent. While Bray tells us that soft drink consumption was 50 gallons per person per year in 2003 compared to 11 gallons in 1955, Klurfeld later offers NHANES data where 50% of Americans over the age of 2 do not drink any soft drinks daily, and young men consume the highest amounts. Bray’s data of both sugar and soft drink consumption is inconsistent with USDA data which you can see here. You can also find data on added sugars and sweeteners at the USDA website.

 

A Man on a Theatrical Mission

Dr. Robert Lustig, fairly well-known in nutrition circles for his “sugar is toxic” mantra and his recent 60 Minutes piece, began his lecture: “Metabolic Consequences of Fructose: Alcohol without the Buzz,” with some in-your-face slides about sugar and obesity, comparing some foods to killers:

“Honey Smacks (cereal) is …. a top killer of children” ~Lustig

He then lunged into a few complex biochemical slides, that he noted included unpublished data (and open for discussion and attack – which did surface during Q&A. He spoke so quickly (I’d call it speed-talking) that many in the audience may not have realized that these slides were unproven models, if one gentleman hadn’t smartly pointed this out during Q&A.

These hypothetical pathways he draws up are essentially his whole case for his idea that fructose metabolism is similar to ethanol metabolism and that chronic fructose intake leads to the same health issues that alcohol abuse does (fatty liver disease, heart disease, addiction). Lustig also believes that sugar is addictive (his conclusions are drawn from research in rats in which the opioid receptors went up when rats were fed sugar-spiked chow, but Dr. Rippe later clarified that rat brains have no prefrontal cortex, therefore comparing the brain activity in rats can not be translated to humans).  Lustig admits there is no human data to support his theory, but shows a clip of the movie “Super Size Me” (you know, the movie where the guy decides to eat nothing but fast food and purposely overeats to gain weight):

“…no data yet, but we do have the movie “Super Size Me” By “day 18 the guy felt withdrawal.” ~Lustig

Fructose VS Glucose

Much discussion during the session revolved around how fructose metabolism differs from glucose metabolism. The big, fat hole in Lustig’s hypothesis is that fructose is rarely, or never, consumed in the absence of glucose, thereby taking a different pathway. According to White, fructose metabolic flow results in offering up 50% to glucose, >15% to glycogen, 25% to lactate, and <3% to fats via de novo lipogenesis. Unlike the theory that Lustig dreamed up, this information is gleaned from actually tracing radio-labeled fructose.

Reality VS Alternate Universe

In contrast to Bray and Lustig, Dr. James Rippe provided useable facts based on human studies using typical intakes. He asks this simple question: Is comparing pure fructose to pure glucose relevant to human nutrition?  He provides this example: When an additional 1,500 calories of carbohydrates are supplied to a diet, only 3 grams of fat is generated. Is this significant? The answer: No.

Regulating Food

Finally, Dr. David Klurfeld, who is a program leader for the USDA, offered information about the role government agencies play in this debate. Klurfeld shared that the FDA is currently in discussion about sugar labeling, but noted that an “added sugars” section on labels can be challenging for some products (there’s the issue of proprietary information – not wanting to share a secret recipe, for example). The FDA considers many criteria when making regulatory decisions: The totality of evidence; the strength of relationship; overall diet and health patterns; and the public health factor.

Klurfeld also points out that the whole diet and dietary pattern should not be overlooked for only the sake of sugar.  Suggesting that we could also overdo many healthy nutrients, Klurfeld offers this poignant quote from Paracelsus, (1493-1541, the first toxicologist):

“The dose makes the poison…The claim that sugar is toxic doesn’t pass the toxicology face value test.” ~Klurfeld

Similar to myself, Dr. John White and Dr. James Rippe, two of the five expert panelists from the symposium, are consultants to the Corn Refiners, but all opinions and statements are our own.

Share This:


Comments

Summary: Fructose, Sucrose and High Fructose Corn Syrup: Relevant Scientific Findings and Health Implications — 1 Comment

  1. Pingback: Take-Away Points from Sugar Session at EB2012 | Chew The Facts

Leave a Reply

Your email address will not be published. Required fields are marked *