It’s enough to make a vegan cry

The full text of a review entitled “Fruit and vegetables and cancer risk” is available on the web site of the British Journal of Cancer, and it is not good news.

According to Professor Key, after many years of study there is minimal evidence that a diet high in fruit and vegetables will reduce risk for cancer in general (or for prostate cancer in particular). The article was also discussed on the Los Angeles Times Booster Shots blog yesterday.

In discussing the effect of diet on prostate cancer risk, specifically, Prof. Key writes as follows:

Risk [for prostate cancer] is increased in men with relatively high plasma concentrations of insulin-like growth factor-I, and levels of this growth factor can be affected by diet, but more research on this pathway is needed (Roddam et al., 2008). … recent large prospective studies suggest that there is little or no association between total fruit and vegetable intake and prostate cancer risk (Kirsh et al., 2007). There has been much interest in the possibility that fruits and vegetables, such as tomatoes, which are rich in the carotenoid lycopene might reduce the risk for prostate cancer, but overall the data do not support this hypothesis (Kavanaugh et al., 2007). Studies of soyabeans and prostate cancer have suggested that this vegetable may help to reduce risk, but the results are not conclusive (Hwang et al., 2009).

Having noted this, however, The “New” Prostate Cancer InfoLink believes that part of the problem in studying the impact of diet on all health risk has to do with time.

Most significant scientific study of the impact of diet on health risks dates back to little earlier than the late 1960s. This means that anyone of 50 or more today was born before any such significant research began, and that anyone over about 40 years of age, even if an organic food compulsive today, probably spent his or her childhood eating things that weren’t necessarily the best for their health.

Any really serious analysis of the impact of diet on risk for cancer (and other chronic health conditions) needs to be able to track diet back to infancy — and perhaps even maternal diet for (at least) the 9 months prior to birth. Why? Because we know that our development over time can be profoundly impacted by what we do when we are very young indeed, and there is at least a reasonable possibility that many of our risks for cancer are affected by things we do and eat in our formative years (e.g., growing up near to a chemical plant).

The bottom line is not that diet has no impact on cancer risk today. It is that we really don’t know whether diet has a significant impact on cancer risk. For the time being, however, as Prof. Keys concludes in his review:

Currently, advice in relation to diet and cancer should include the recommendation to consume adequate amounts of fruit and vegetables, but should put more emphasis on the well-established adverse effects of obesity and high alcohol intakes on cancer risk.

Of course when it comes to prostate cancer specifically, even the evidence of significantly increased risk as a consequence of high alcohol intake and obesity are less compelling that they are in some other cancers. But then again, these two particular problems are associated with much bigger risks than prostate cancer, and are a bad idea for a multitude of reasons — as is a poor diet.

3 Responses

  1. As I have seen Mark Moyad say, eating a heart healthy is prudent. You are more likely to die of something else than prostate cancer and a heart healthy diet addresses a bigger threat to men. We don’t know that it will prevent the cancer progression or even onset, but if it does, you can thank him later because then you would live longer either way.

  2. I continue to make diet, nutrition, and supplements a major part of my program to combat the disease, even though I’m aware that some of the tactics may eventually prove useless, and some may even prove to be adverse. I do this because, on balance, the evidence looks encouraging to me.

    I’m skeptical of studies that are too general, and that includes an abudance of published studies. For instance, for green tea it is well known that a few drops of an acidic substance, such as lemon juice, preserves potency. It is also known that stirring the tea bags while brewing enhances potency, as does duration of brewing time. Yet, many studies involving green tea consumption and cancer do not address any of these aspects, particularly the addition of an acid.

    Other well-known examples involve vitamin E and selenium. While there is still debate, it looks quite likely to me that the wrong dose and form of vitamin E were used in the study, and that the wrong form of selenium was used.

    Selenium is in the forefront of my attention based on the work that the Kantoff group is doing up in Boston. It looks like they are homing in on some genetic characteristics that will help identify who will benefit from selenium and who will not. Their work is an example of the awesome contribution that genetic research should soon be making on a large scale to disease prevention, control and cure.

    The Roddam study relates mainly to IGF-1. We already know that some vegetables (potatoes, for example) have a high glycemic index, promoting IGF-1 as I understand it, whereas other vegetables do not. Therefore, we need to look deeper than just at the overall “vegetable” level to understand how nutrition affects IGF-1. My impression is that we already have a pretty good handle on this knowledge, though it is not employed as well as it should be.

    The Kirsh (2007) study found little association of total fruit and vegetable intake, but it found an impressive reduction in risk associated with cruciferous vegetables (broccoli, cauliflower mentioned), which I strive to include in each lunch, cooked as research suggested a higher benefit, and with lycopene included as seasoning in the form of catsup or cocktail sauce. I’m thinking, building on Sitemaster’s reflections on the diets of our youth, that the overall fruit and vegetable intake reflected in the Kirsh study probably included ample potatotes and corn, neither of which look sound, in substantial amounts, for us as patients (high glycemic index for potatoes, high Omega 6 for corn).

    Regarding the Kavanaugh study of tomatoes (lycopene) and prostate cancer, there is actually some mild encouraging data, which is consistent with the way I’m viewing this nutrient. I looked at parts of the complete article that pertained to prostate cancer, including the table that listed studies reviewed by the FDA and impacts.

    Here’s a summary from the FDA that I find encouraging: “After reviewing the evidence summarized above, FDA found that there was limited credible evidence for a qualified health claim about tomato consumption and a reduced risk of prostate cancer. The strongest evidence for an association between tomatoes and prostate cancer risk came from the two large prospective cohort studies … that reported statistically significant inverse associations between tomato consumption and risk. The eight case–control, one case–cohort, and two ecologic studies reported mixed results on the association. FDA therefore concluded that there was a very low level of comfort that a relationship exists between the consumption of tomatoes and/or tomato sauce and prostate cancer risk.” I believe the level of comfort will increase as time goes by.

    I’m looking forward to checking the soy article also.

  3. The article addresses the link (or lack thereof) between fruits and vegetables and prostate cancer, but does not address the link between diary consumption and prostate cancer, which has been demonstrated in numerous studies to show a positive correlation. A plants-only (vegan) diet is still the recommended diet to halt, reverse, and prevent prostate cancer.

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