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PostPosted: Mon Apr 07, 2003 8:31 am 

Joined: Sun Apr 06, 2003 10:59 am
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A recent presentation at the American Academy of Neurology 55th Annual Meeting reported on some data from the Honolulu Heart Study of men of Japanese ancestry that suggests a link between high fruit/"fruit drink" consumption and an increased risk of Parkinson's disease. One thing of note is that the dietary surveys on which the results were based apparently (as far as I know) did not attempt to distinguish between organic and conventional fruit consumption. Another is that the higher fresh fruit consumers in the study apparently consumed a lot of local tropical fruits. Yet another is that the "fruit drink" category included beverages like Hawaiian Punch, which often don't contain much fruit juice and do tend to contain preservatives and artificial colors, and that the fruit consumption over the survey period included frozen and canned fruits. Although the data was harvested from a survey that the subjects completed in 1990, the overall heart study began in 1965. One thing I don't know is how accurately that 1990 food consumption survey identified the individuals' fruit consumption from 1965 to today. If there is a pesticide link, that information would be important because pesticide use almost certainly has changed over that 38-year period. One thing to bear in mind is that the information retreived or inferred from mining the survey data does not "prove" the direct causative link, but rather suggests places to look to try to prove causation. That isn't to say that it is trivial; island population studies have benefits and drawbacks.

The researchers cited in the news stories about the presentation focused on pesticides and food-borne agents as a probable cause for the increased risk, which was identified as about double the normal risk of getting the disease. There are (at least) two curious things about the survey data in relation to the pesticide/food-borne agent link idea. First is that they apparently did not identify a similar risk elevation in connection with vegetable consumption. It seems to me that the implied divergence between "fruits" and vegetables might bear further investgation if only because the pesticides used on fruits over last 40 years probably are/were not the same ones that are/were used on vegetables that Hawaiians (or probably anyone else) typically would eat. Second, fruits as a group do tend to carry/produce different agents than do vegetables as a group. I suppose that raises a question as to whether tropical fruits tend to carry/produce different agents or different concentrations of agents than, say, Washington apples or Michigan blueberries.

One curious thing to me was that a Parkinson's research scientist said that he believes food-borne agents, not pesticides, are to blame: "The study found an association between the disease and both fresh fruit and canned juices," he says. "The common denominator here is the fruit, not possible pesticide exposure." Frankly, I don't buy the idea that conventional fresh fruit (particularly over the past 40 years) did/could have pesticide contamination but that juice made from that same conventional fresh fruit did not/could not have pesticide contamination. There may be more behind that researcher's conclusion than is revealed in that short, maybe even edited, statement, but one possibility to me is that he based that pesticide conclusion on a belief that all pesticide residue was/is confined to the peel. That would trouble me for four reasons: (i) I don't believe it is true; (ii) the character of current pesticide contamination is not necessarily the same as it was 40 years ago due to some differences in the pesticides used and in the way that they were/are used (I would wager that the data on pesticide levels in food for at least the first 20 years of the Heart Study either are non-existent or are worthless as a practical matter); (iii) it isn't clear that smaller doses of contamination in the fruit itself could not be enough to cause, or contribute to the cause of, the increased Parkinson's risk, particularly given the variances in pesticide type/usage over the 40-year period; and (iv) it doesn't allow for the possibility of a synergy between pesticides and naturally-occurring food-borne agents with respect to the Parkinson's mechanism(s). If pesticide is involved, it seems to me that whether points (i) and (iii) require a genetic susceptibility to Parkinson's depends on the answers to points (ii) and (iv).

Nonetheless, he could be right about the food-borne agents, which leads me to wonder whether there is a difference in the quantities of the food-borne suspects (isoquinolones were mentioned specifically) between organic fruit and conventional fruit. Particularly, I wonder if conventional growing practices might adversely affect the concentration and/or the variety of the food-borne suspects or the production of other agents that might modulate the effect of the suspected causative agents. One thing I can be fairly certain of is that a verified link, no matter how small, to naturally produced agents will send researchers scurrying to genetically modify fruit trees/vines to restrict the production of the suspected culprit.

For those that are curious, the reports that I read about the study discounted an earlier suspected connection to vitamin C consumption, and did not mention a consideration of fructose consumption. I wonder about the fructose angle in connection with the very large increase in fructose consumption that has occurred since high-fructose corn sweeteners began to replace sugar in the American caloric sweetener market in the 1980s. It may be that the personal consumption surveys that provided the data for the Heart Study compensate for fructose consumption by considering consumption of soft drinks, confections, etc. Perhaps someone reading this knows whether the Hawaiian food processors have used locally-produced cane sugar instead of HFCS as a sweetener, but the dramatic decline in cane sugar acreage there and the corresponding closing of Hawaii sugar mills would seem to argue against that sugar preference. It may be that the period over which HFCS substituted for cane sugar there was longer than the rapid and near-total conversion we had on the mainland, and I also don't know how much sweetened product would have been produced domestically in Hawaii as opposed to being imported from the mainland.

If anyone has insight into the Study or is a participant or a researcher in it, please chime in.

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