Ashton Kutcher has been in the news a lot recently. Normally this is something well worth ignoring, but in this instance it’s interesting: He’s been promoting the new Steve Jobs movie (in which he plays Steve Jobs) by explaining how he was hospitalized after following Steve Jobs’ diet for some time. Steve Jobs apparently ate nothing but fruit.
So what happened to poor Ashton? Well, the details are quite thin: “I was doubled over in pain […] my pancreas levels were completely out of wack.” Media reports that he spent time in the hospital. The exact nature of his affliction and the treatment for it remain undisclosed.
Not really much to go on there, but since it’s in the news, I thought it worth mentioning a fructose-pancreatic cancer connection described back in 2010.
In the paper, Fructose Induces Transketolase Flux to Promote Pancreatic Cancer Growth, the lead researchers to state, “fructose provides an alternative substrate to induce pancreatic cancer cell proliferation.” Of course, we’re acutely aware of the connection between cancer and glucose, but this paper suggests that even though glucose and fructose have long been considered interchangeable in terms of cancer cell metabolism (aerobic glycolosis), in actuality they are metabolized quite differently by pancreatic cancer cells:
…our data indicate that the contribution of fructose to nucleic acid synthesis is considerably greater than glucose and that cancer cells preferentially use fructose via TKT-mediated metabolism to synthesize additional nucleic acids to facilitate increased proliferative capacity. Synthesis of nucleic acids and nucleotides is of utmost importance for proliferating tissues and especially cancers.
The authors go on to describe the precise metabolic pathways at play and assert that their findings are critical in understanding the etiology of pancreatic cancer in light of the massive (over)consumption of sucrose and HFCS we’ve undertaken in modern times.
While not as sexy as a sensationalist movie promotion, it’s heady and important stuff to pay attention to. If you don’t feel like wading through the research, you might find this BBC Interview with Dr. Anthony Heaney (one of the authors of the paper) to be an accessible source.
Research
- Fructose Induces Transketolase Flux to Promote Pancreatic Cancer Growth, Nissen, Heany et al. Cancer Research August 1, 2010 70; 6368
- Pancreatic Cancers Use Fructose, Common in a Western Diet, to Fuel Growth, UCLA Jonsson Comprehensive Cancer Center press release.
- BBC Interview With Dr. Anthony Heaney, Audio/MP3
- Ashton Kutcher Suffers Health Scare Prepping for ‘Jobs’, USA Today, Jan 29, 2013
The fructose/pancreatic cancer paper posted this morning on Ketpoia is interesting and provides good data on fructose metabolism – especially concerning the pentose pathway. However, the following quote from the paper makes us wonder about their source of information on the biochemistry of glucose/fructose relationship:
“Conventionally, fructose and glucose have been considered as interchangeable monosaccharides that are both metabolized equivalently in aerobic glycolysis and in the TCA cycle, …”
On page 86 of 1st ed. MND (2002), Figure 5-1 shows that dietary fructose bypasses glycolysis and goes to pyruvate and then on through the Krebs cycle. This is not new – it has been known for decades.
Dietary fructose and glucose have long been known as NOT interchangeable (for all practical purposes). The first step in glycolysis is formation of fructose, but this fructose and dietary fructose apparently do not commingle. The only way dietary fructose can become glucose is by conversion to pyruvate and then by reversal of glycolysis.