Many thanks to Stan for pointing me to this BBC article and the study it relates to.
Obviously anyone making a habit of soft drink consumption, be that sucrose or HFCS sweetened, is in trouble metabolically. The joy of this report is the association between not only orange juice and gout, but also with apples and oranges as whole fruit. Observational perhaps, but the biochemistry is all there to support causality.
Ultimately fructose is fructose is fructose. Eat an orange and your liver will immediately set about defending you as best it can. When it fails or goes wrong, you get gout.
I like the BBC's picture. The chap with metabolic syndrome and gout is probably wealthy enough in the 1700s to buy sugar and to drink port, possibly the sweetest bulk consumption form of alcohol. Obesity and gout.
A few choice fruity quotes:
"I can think of some situations, for example in severe treatment failure gout, where reducing sweet fruits, such as oranges and apples could help," he added.
Translation, take drugs, more drugs and even more drugs. In absolutely dire straits, dump fruit. Why not just dump the fruit in the first place? Gout drugs do not look to be much fun.
"But this finding needs to be balanced against the benefit of fruit and vegetables in preventing other chronic disorders like heart disease and stroke."
Show me the data!
"...and fructose rich fruits (apples and oranges) were associated with a higher risk, the researchers said."
Quite a lot of fructose in grapes and plums and and kiwis and peaches and bananas and and and...
The nice thing about science is that eventually the truth will out.
Eventually.
Peter
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Peter
Did you see the article in the Guardian on the "myth of fruit"? I pointed to it at the post below
http://conditioningresearch.blogspot.com/2008/01/myth-of-fruit-and-more-taubes.html
Great post, Peter. Fructose and the misconceptions about what it is and what it isn't have been giving me fits lately.
I've got a friend who is predisposed to gout-like symptoms (her parents both have diabetes and her dad gets gout). What does she do? Avoid red meat and cut down on red wine, yet she guzzles orange juice. She doesn't want to hear anything possibly negative about her "healthy" fruit consumption. My tongue is about an inch shorter from biting it all the time.
I don't know if it has hit the market it the UK yet, but the alternative sugar darling of the moment in the US is Agave Syrup (sometimes called Agave Nectar). Initially only available in bottles in "natural foods" stores, it is moving into the processed "organic junk food" and mainstream stores (Trader Joe's now how their own private label agave syrup. You can read more about agave syrup at http://en.wikipedia.org/wiki/Agave_syrup .
Until recently granulated fructose was often recommended to diabetics (talk about a bad recommendation!). Now agave syrup is recommended to diabetics and anyone with high or low blood sugar issues because it has a lower glycemic index (low glucose %). It's also very popular with folks who want to avoid "refined" white sugar, etc. Raw foodists like the "made without heat" claims from some brands. "Nutrient-oriented" people like agave syrup because it still contains trace minerals and such. Certain "natural food" stores make headlines because they no longer stock foods containing HFCS, yet every week there seems to be a new product on the shelf with agave syrup as an ingredient. So people don't want to consume HFCS but they are flocking to agave syrup ... well, it isn't full of fructose from corn, but it sure is full of fructose, usually in a much higher percentage than HFCS.
As much as 92% of sugars are fructose in some agave syrup brands according to wikipedia, so that is much, much worse than the 55% fructose in HFCS. So sure, it doesn't cause a blood glucose spike because the glucose content has been mostly removed, but it sure will send the triglycerides into the stratosphere and fatten up the liver nicely. People who have been using agave syrup (sometimes liberally because it's healthy, ya know) are really surprised when I tell them this, yet some of the labels even indicate that agave syrup is very high in fructose, implying a benefit. And the ones who want raw unprocessed foods are surprised that it is made with enyzmatic action. I don't call that unprocessed. It isn't some thing our great grandmothers could have made.
As you probably know, concentrated fructose (and agave syrup certainly is highly concentrated) is a train wreck waiting to happen for the liver and especially for diabetics, who already have enough AGEs (advanced glycation endproducts) damaging their proteins and cells. Your readers can learn more about cell damaging AGEs at wikipedia if they want: http://en.wikipedia.org/wiki/Advanced_glycation_endproduct
Ah, fructose, the supposedly healthy sugar because it makes us think of fruit. Is it any wonder that young kids have foie gras forming inside them already?
When I tell people what I have learned about agave syrup, AGEs, etc., they are gobsmacked, then desolate or in denial. They say, "what do I use then?" or "they wouldn't sell it in "X" store if it wasn't healthy". It seems few are willing to reduce their sugary intake or accept that food manufacturers don't have their best interests in mind, just their wallets. They've gotta have their sugar.
Cheers,
Anna
Hi Chris,
Thanks for that. I really ought to read the Grauniad, but there's too much depression from Radio 4 without having it in print! So I do miss occasional gems like that one. Nutritionists KNOW. They really do, but 5 a day it is...
PS Emma is getting in to hows and whys and genetics of salicylate and amine intolerances. Much more interesting that "avoid this, this and that..." on most sites for this problem.
PPS need more Cairns pictures!
Hi Anna,
That Agave "nectar" looks like scary stuff. Makes molasses and even HFCS look like health foods! As you say, people have to have their sugar.
We had a beef casserole with parsnips included as the carbs for our meal last night. By the time you're adapted to LC, casseroled parsnips taste overwhelmingly sweet! Goodness knows what a 90% fructose based syrup tastes like!
Love that comment about Fois Gras...
Peter
I do not know if fruit juice can be blamed for gout. Most people aren't drinking 100% fruit juice. They are drinking fruit juice sweetened with sugar or HFCS. What about the claim that cherries prevent or cure gout? Do they have a lot of fructose?
The value of observational studies is very poor, IMO. As a kid, I must have drank a quart (~liter) of O.J. (frozen), and a quart of milk (2%?) every day. I was thin, until I went to college, drank sodas frequently, and gained the "Freshman 15."
Fruit may not be good for somebody who is already obese, or unhealthy. But I don't believe it would cause disease in a healthy person eating natural food and avoiding the junk like most vegetable oils and sugar or flour laden snack foods. I have no doubt that a fruitarian type of diet would be harmful to everybody in the long term. But based on my experience, I think refined sugars are at least 10 times worse.
Anna, I would like to point out it has not been proven that glucose or fructose cause AGEs. Some like Ray Peat argue that it's the PUFAs that cause AGEs. If you don't eat PUFAs much, you have little or no protein damage from glycation. Blaming the carbs for glycation is simply guilt by association. Unless you isolate PUFAs in the experiment, there's no way to prove causality. Here are a couple of articles discussing this.
http://preview.tinyurl.com/3447ur
"when tested in a controlled experiment, lipid peroxidation of polyunsaturated fatty acids produces the protein damage about 23 times faster than the simple sugars do."
http://raypeat.com/articles/articles/unsaturatedfats.shtml
Regards,
Bruce
It keeps occurring to me that going to a LC high sat fat diet does far more than you expect, it's not just LC and low fructose but low PUFA as well. Which is most important is not obvious when you start. Exactly how important the LC aspect is overall is open to negotiation too.
Can't say I've got any time for HFCS, sucrose or fructose. Ultimately fructose is fructose wherever it comes from. Mind you, in healthy people not much fructose ever gets in to the systemic circulation either, so this needs factoring in.
Peter
Hi Bruce,
That's very interesting. Sally Fallon is always talking about the dangers of polyunsaturated oils.
Of course, I'm sure you'll agree it's a leap to go from that JBC article and generalize that PUFAs are toxic to an intact organism.
For example, Indians in the Pacific NW of the US ate salmon year-round as a staple food. They even collected the oil that dribbled out of the very fatty fish as they cooked in front of the fire and used it in their cooking. They also used the unsaturated oils of other marine organisms like the candlefish liberally.
They were very robust people, physically strong and resistant to all but the nastiest zoonotic diseases the Europeans brought over. And as far as their lifespan, chief Sealth, after whom Seattle is named, lived to 80 years old. Not too bad for a hunter-gatherer living on a high-fat polyunsaturated diet. Check out his skin in this picture, taken just a few years before his death:
http://en.wikipedia.org/wiki/Chief_Seattle
Of course, those were mostly omega-3s, so maybe that's the distinction.
Hi Bruce,
What do you feel was happening in the DART study and the Lyon study? The increase in PUFA (omega 6 probably) in the DART study was neutral and increased fish intake (presumably replacing a standard meal protein source of some sort) was beneficial. Only have the abstract for this one. In the Lyon study there was a drop in PUFA intake (total PUFA, ignoring 3-6 ratio) of about 1.5g/d. Would a drop of this much produce the CVS/neoplasia benefits they found? Most of their other interventions look pretty rubbish.
Peter
I do notice from studies back in the 50s that corn oil was added to otherwise fat free rat diets at 50g/kg to "prevent EFA deficiency" without any ref being cited. That does make it look like a belief structure rather than hard data.
I've sent an email to my husband's colleague asking him about the formation AGEs & PUFA involvment (he's a glycobiologist). When I talked to him at a party about AGEs and diabetes a month or so ago, PUFAs didn't come up as part of our discussion (he did a great job explaining dinstictions between glycation and glycosylation to me, though). I'll report back when I hear from him.
Also, I don't think that weight is always an indication of what is happening with the glucose metabolism. Cellular damage can be occuring for many years while someone is thin and consuming excess sugars and starches, especially if there are genetic tendencies.
Hi Anna,
I looked at this study, cited by Dr Briffa,
"When women were categorized by baseline menopausal status and body mass index (BMI; in kg/m(2)), the increased risk of dietary GL was confined to those who were premenopausal (RR = 3.89; 95% CI: 1.81, 8.34) and who had normal BMI (ie, <25) (RR = 5.79; 95% CI: 2.60, 12.90) (P for trend = 0.001 for both). CONCLUSIONS: A high-GL diet may increase the risk of breast cancer in Italian women. The effect is particularly evident in premenopausal women and those with BMI < 25."
and my general feeling was that one hypothesis you could generate from the LOW BMI, high GL group's high cancer incidence was that effective metabolisers of carbs push more glucose in to their cellular machinery.
Once the glycation process starts it generates lots of free radicals. Those double bonds of PUFA are sitting ducks for peroxidation reactions. Whether reducing glucose or PUFA is the best route seems open to negotiation. Reducing both seems a good start! There's plenty of lab rat information and some human studies to suggest omega 6s are carcinogenic, mostly I think looking at mammary neoplasia. Of course very few studies have looked at omega 3 outside observational stuff on unusual populations, Eskimo etc...
I have a paper (somewhere) by a medic in Sweden arguing that the common neoplasms are just an aspect of metabolic syndrome. No help if you get one. The other thought is that as it's not anyone's BMI that matters but how they deal with glucose in a high PUFA environment. Usually people on high GL diets tend to high BMI, but elevated glucose/insulin often produce the high BMI and also produce neoplasia... I also think there also needs to be some level of insulin resistance involved. Appropriate insulin release per unit carb intake seems much less of a problem. Insulin resistance and hyperinsulinaemia not need obesity, so still fit in with the hypothesis generated by the cited study.
It's all very interesting and interlinked methinks.
Peter
I got a quick response this morning from our glycobiologist acquaintence (pasted below). I won't be able to get my husband to get that paper for me for at least a week or so. I am running late so I will digest your last comment later tonight, Peter. But I'm pretty sure that overall, my PUFA intake is relatively low now that I have given up industrial seed oils and nearly all grains, at least compared to most Westerners. But I hadn't ever considered PUFAs relation to glycation. No matter how much I learn I realize there's so much more that I still don't understand or see (sigh)...
Hi Anna-
I would not give sugars a pass. I can see where PUFA could contribute based on the Fu et al article. A lot of that study was done in vitro and the single protein they studied may not be representative of everything, plus the availability of the free PUFA in the blood is very low. Most in lipoproteins and not easily accessible. Of course your body needs and makes PUFA, its not only in the diet. While it might contribute some, hard to know how much—but I would think glucose is the main driver.
Have Guy print out the Fu article from the JBC, and take a look.
Sasquatch, wild salmon is not about half as fatty as farm-raised. Also, the Indians were probably hunting a lot of wild animals which would not have as much PUFAs. I've heard that even Eskimos only ate about 10% of their calories as PUFA, which might be the maximum safe amount. I have also read that they had problems in relation to those PUFAs, like long bleeding times (nose bleeds lasting for days), bleeding strokes, organ failure in old age, etc. And their diet had other factors that helped protect them, like high iodine and organ meats that increased thyroid function and metabolism.
Ray Peat said the Eskimos actually had hyperthyroid. 25% faster than a normal person. This helped them to burn off a lot of the PUFAs rather than store them. Also, they didn't have a constant food supply, so we can add intermittent fasting as a possible factor. I've heard that IF increases membrane saturation, and reduces the stored PUFAs. Eskimos also ate high protein, which might help make saturated fat.
The availability of free PUFAs goes up with age and body weight - also associated with many diseases, like like Alzheimer's. Combining a high carb and high PUFA diet seems like the worst possible diet to me. But as carbs are reduced, PUFAs should be reduced with them IMO. This will happen naturally to some extent as Peter noted, since most of the junk foods are loaded with PUFAs.
I would aim for no more than 10% of calories from PUFAs on any diet and preferably more like 1-4% calories. PUFA vegetable oils, I avoid 100%. Acceptable oils are coconut, cocoa butter, macadamia, palm kernel, red palm, and maybe hazelnut (in small amounts). Duck and goose are better than most chicken or turkey, which is what JK advises. I would prefer shellfish to salmon, also.
Avocados and olive oil are also OK, but I would use them more sparingly than the more saturated, lower PUFA vegetable fats mentioned. It's not wise to eat a lot of nuts or seeds, IMO. Coconut is the most stable of the solid oils and macadamia's the most stable liquid oil.
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