I know fructose is like all sugars and can cause insulin spikes leading to fat gain. I haven't found any studies done on fruit specifically so I was wondering if anyone knew of any.
asked byApril_S_ (10663)
Get FREE instant access to our Paleo For Beginners Guide & 15 FREE Recipes!
on February 05, 2012
at 12:19 PM
Unlike glucose, fructose can only be processed by the liver. There seems to be a limit to how much fructose the liver can process at a time, and it can exhaust the liver. It converts it to glycogen, until the glycogen stores are full, then it converts it to triglycerides instead.
After a while, a chronic flow of fructose to the liver causes it to become filled with fat, and scarred. This is the beginning of NASH, Nonalcoholic Steatohepatitis.
Lustig calls it a hepatotoxin, because in large amounts it does cause damage, and because it is processed in almost the same way as alcohol.
Also, fructose is a 10x higher glycator (fructation in this case), than glucose, so table sugar, which is similar to HFCS, depending on which form of HFCS we're talking about, is just as bad.
It's true that fructose, unlike sucrose or glucose, will not raise trigger insulin spikes, nor raise blood sugar levels, so things like Agave syrup is advertised as diabetic friendly, but it's the devil's bargain in the long term.
That said, if you've heavily worked an hour or two ago, so that your glycogen levels are low, it's ok to eat a little bit of fruit, maybe a cup of berries, to refill your glycogen stores, as it's not likely to lead to NASH. The dose makes the poison, so consuming things like soft drinks, or foods that are loaded with the stuff, made with Agave syrup is where the danger lies.
(Me, I'd rather have tequila than agave syrup - at least I'd get a nice buzz in exchange for the liver damage.)
From Fructose: Metabolic, Hedonic, and Societal Parallels with Ethanol by Robert Lustig (in the 3rd link above), shows how liver enzymes are depleted by this process, why there's a limit to how fast it can be processed, and how it leads to fatty liver. Some choice quotes:
Excess accumulation of metabolites of DNL is seen in both human and rat models of steatosis (72,73). For in- stance, tracer studies in obese subjects with steatosis show that 26.1% of the intrahepatic lipid pool occurs through the process of DNL (74).
Fructose is able to induce the transcription of the enzyme JNK-1 (105) via activation of mitogen-activated protein kinase kinase 7 (106). In addition, the DNL product DAG can also induce JNK-1 via activation of protein kinase C-epsilon (22). JNK-1 is the bridge between hepatic energy metabolism and inflammation and, once induced, begins the inflammatory cascade (107). As part of its inflammatory action, JNK-1 activation induces serine phosphorylation of insulin receptor substrate-1 (IRS-1) in the liver (108), thereby preventing normal insulin-mediated tyrosine phosphorylation of IRS-1 and promoting hepatic insulin resistance.
Animal studies demonstrate increased hepatic lipid deposition in response to high-fructose feeding (92,100). In human studies, eucaloric replacement of glucose with fructose increased intrahepatic lipid levels by 38% within 8 days, as measured by magnetic resonance spectroscopy (81).
Excessive FFA exported from the liver leads to increased uptake into skeletal muscle. There, DAG reassembled from FFA, reduces glucose transport, resulting in skeletal muscle insulin resistance (119). FFA, liberated from circulating VLDL by insulin stimulation of lipoprotein lipase, also contributes to increased storage of intramyocellular lipid, which perpetuates the insulin resistant state in skeletal muscle (120). In rodent models, high-fructose feeding increases skeletal muscle lipid deposition and oxidative stress (121) and reduces IRS-1 phosphorylation and PI3-kinase activation in skeletal muscle (112). Similarly, in obese children, intramyocellular lipid correlates with insulin resistance (122); although the primacy of intramyocellular lipid in the genesis of the metabolic syndrome remains controversial (123).
on February 05, 2012
at 09:51 AM
As far as I know, fructose doesn't spike insulin as much as the other sugars, which is why it's considered low glycemic.
on February 05, 2012
at 01:28 PM
The following is more of a quip than an article, but it might be helpful:
Fatty liver is induced by overfeeding carbs of all kinds, both sugars and starches. Whether force feeding corn to ducks (glucose via starch) or massive consumption of fruit juice and pop by humans (HFCS, fructose, glucose, or sucrose), the effect is the same.