Study Indicates Prostate Cancer Is Reversible By Diet

According to the National Cancer Institute, each year in the U.S., 240,890 men get diagnosed with prostate cancer, and 33,720 men die from it.

According to the American Cancer Society,

"About 1 man in 6 will be diagnosed with prostate cancer during his lifetime. More than 2 million men in the United States who have been diagnosed with prostate cancer at some point are still alive today.

"Prostate cancer is the second leading cause of cancer death in American men, behind only lung cancer. About 1 man in 36 will die of prostate cancer."

I have a family history of prostate cancer, so I have a personal interest in prevention and remedy for this disease of civilization.

According to some people, whole grains and legumes cause or promote the diseases of civilization, including cancer.

If this disease is caused by eating grains and legumes, then any diet based on grains and legumes should promote cancer.  If you give men living with prostate cancer a diet rich in whole grains and legumes, you should see a promotion of the cancer.

My friend, Gordon Saxe, M.P.H., Ph.D., M.D., professor of medicine at U.C.S.D.,  has actually tested this hypothesis, albeit unintentionally.

Gordon has lead pilot research in which men with diagnosed with prostate cancer were taught to eat a diet consisting of whole grains, legumes, vegetables, fruits, nuts, and seeds, while eliminating animal  products, based on evidence [discussed here] that this dietary pattern may reduce the risk or progression of prostate cancer.

If whole grains and legumes promote prostate cancer then these men should have had an accelerated progression of their cancers.  However, in the first study, over six months, this intervention produced just the opposite effect:  a 100-fold reduction in the rate of rise of their disease, as measured by the rate of change in levels of prostate-specific antigen (PSA).  As stated by Saxe et al:

"The rate of PSA increase decreased in 8 of 10 men, while 3 had a decrease in absolute PSA. Results of the signed rank test indicated a significant decrease in the rate of increase in the intervention period (p = 0.01). Estimated median doubling time increased from 6.5 months (95% confidence interval 3.7 to 10.1) before to 17.7 months (95% confidence interval 7.8 to infinity) after the intervention. Nine of 10 participants in the study had reduction in the rate of rise of their PSA, a marker for progression of disease."

When 9 of 10 people respond in the very same way to an intervention, in this case with a reduction in rate of rise of PSA, this tends to suggest that the effect is no accident and most likely indicates a definite therapeutic effect of the intervention.

In the second study, involving 14 men, Saxe et al produced a similar result.  In this second study they explored the biological mechanisms involved:

"During the first 3 months of the intervention, as both median WHR and body weight declined significantly, the median rate of PSA rise not only declined but became negative, reflecting a slight reduction in absolute PSA and possibly disease regression in patients with absolute reductions. Conversely, during the second 3 months of the intervention, when median body weight increased (though not significantly), median PSA began to rise again, albeit more slowly than during the period prior to Baseline."

This second study suggested that weight-related metabolic changes may have mediated the reduction in rate of PSA increase.  In other words, the intervention resulted in a loss of body fat and concommitant metabolic changes related to reduction of body fatness, including an increase in sex hormone binding globulin, that influence prostate cancer.

"Assuming that the attenuation of PC progression was mediated by weight-related metabolic changes, a question arises as to what aspect of intervention brought about the observed reduction in adiposity. Earlier ⁵³, we described large increases during months 0–3 in intake of whole grains and vegetables, food groups which are fiber and water-rich, very low in fat, and therefore of low energy density. However, intake of these foods declined slightly during months 3–6. Weight loss during the first three months may possibly have resulted from replacing energy-rich foods with energy-poor foods, and the slight increase in body weight during the second three months may have resulted from a small degree of dietary recidivism." 

So this intervention, based on increasing intake of whole grains, legumes, etc., resulted in body fat reduction during the period when the subjects ate the most of these foods, and body weight increased during the period when these subjects ate less of these foods.  This clearly undermines the idea that diets rich in grains and legumes cause two of the major diseases of civilization, i.e. obesity and cancer.

Saxe et al consider the possibility that any diet that induces weight loss may reduce cancer progression.

"A second question that naturally arises regarding the reduction in adiposity is whether it matters, in terms of effects on prostate cancer progression, how it is achieved. One aspect of this question has to do with the preferred dietary strategy for reducing energy intake. Another facet regards whether it is more desirable to increase energy expenditure or decrease intake to achieve this end. Although our study and its findings did not address these issues, they remain important ones that warrant consideration in the planning and design of future behavioral approaches to the management of progressive PC. What can be said is that while both a plant-based diet and a high-protein, low-carbohydrate diet high in foods of animal origin (such as the popular Atkins diet) may both result in weight loss, the former is far more consistent with the dietary cancer prevention guidelines of various agencies (69).⁵⁴ "

Some people reject those cancer prevention guidelines of various agencies, which emphasize increased consumption of whole plant foods and decreased consumption of animal products, claiming that whole grains and legumes are the true causes of diseases of civilization.   These two studies, among others, weaken that claim. 

So far, the only studies I can find testing the effect of a low-carbohydrate diet on prostate cancer were done with mice, not men.  In this one, researchers from Duke Prostate Center fed mice with prostate cancer either a "Western" diet,  "low-fat high-carbohydrate" diet, or a zero-carbohydrate diet.  The results:

"Fifty-one days after injection [with xenograft tumors], NCKD mice tumor volumes were 33% smaller than Western mice (rank-sum, P = 0.009). There were no differences in tumor volume between low-fat and NCKD mice. Dietary treatment was significantly associated with survival (log-rank, P = 0.006), with the longest survival among the NCKD mice, followed by the low-fat mice."

I don't have access to the full text, but if done in a typical fashion, all diets would have been pellets made from isolated nutrients (e.g. casein, starch, sugar, etc.) so this can't tell us much about what would happen in humans if we compared a whole foods vegan diet (whole grains, legumes, vegetables, fruits, nuts, seeds) to a zero-carbohydrate diet (meat and fat only).  The effects of a casein-based zero-carbohydrate diet on mice might be very different from the effects of a meat-based zero-carbohydrate diet on humans.

In a second study, Masko et al fed mice diets containing 0, 10, or 20 percent carbohydrate and again injected them with prostate cancer cells.  As a 'control' they fed a group of mice a 12% fat diet, but they did not inject cancer cells into these mice--which to me means they weren't much of a control group, because they differed from the others not only in dietary composition but also in absence of tumor injection.

The full text of this study tells us the components of all diets:  corn oil, lard, milk fat, casein, dl-methionine, dextrine, maltodextrine, corn starch, sucrose, and isolated vitamins and minerals. 

In the low-fat arm, 72% of calories came from carbohydrate, and 50% of total calories came from sucrose, which means that about 25% of total calories came from refined fructose.  Meanwhile, in the 10% and 20% carbohydrate arms, all of the carbohydrate was provided in the form of corn starch. 

This makes me wonder again about diet composition in the other Duke University study cited above.  Were those mice on the low fat diet also eating a 50% sucrose/25% fructose diet?  If so, did this rig the study, intentionally or not, so that the low fat group would have more body fat and shorter lifespan than the zero-carbohydrate group? 

Moving on, all the mice got all of their protein from casein-plus-methionine, none ate any meat.  Most people eating low carbohydrate diets eat cooked meats, not isolated casein, as their main protein source.  Meat is nutritionally complex, and affected by cooking process, in ways that may result in it having a different effect on prostate cancer than casein-plus-methionine.  For example, unlike the casein-methionine mix fed to these mice, meat contains heme iron and if cooked at high heat, heterocyclic amines, all of which have been linked to prostate cancer causation or promotion [e.g. Sinha et al full text].  So it is not clear how a study of mice eating a low carbohydrate diet wherein casein is the main protein will apply to people eating low carbohydrate diets wherein cooked meat, poultry, and fish are the main protein sources.

Masko et al found that the survival rates of the mice in the 0, 10, and 20 percent carbohydrate groups were similar.  They liked this finding because, as they say, people find it extremely difficult to follow zero-carbohdyrate diets, so now they are ready to test the 20 percent carbohydrate diet on human prostate cancer patients. 

Masko et al also found that the mice in the 20% carbohydrate group had the lowest insulin level, about which they comment:

"It was unexpected that the lowest levels of insulin were observed in mice fed with 20% carbohydrate, but there are possible explanations for this phenomenon. First, there is always the possibility for a type I error in the analysis. Second, it is known that low-carbohydrate diets promote insulin sensitivity in animals (38) and humans (39, 40). Thus, it is possible that a diet containing a small amount of carbohydrates may actually improve insulin sensitivity compared with a diet completely lacking of carbohydrates."

Perhaps unknown to Masko et al, it is also 'possible' that a diet containing an even large amount of carbohydrate may actually improve insulin sensitivity compared to a diet with only 20% carbohydrate. In 1971, Brunzell et al [abstract only] evaluated the effect of increased dietary carbohydrate at the expense of fat in humans, both non-diabetic and mildly diabetic.  In the New England Journal of Medicine they reported that after feeding these subjects a diet providing 85 percent of energy as carbohydrate for 10 days,

"Fasting plasma glucose levels fell in all subjects and oral glucose tolerance (0 to 120-minute area) significantly improved ..... Fasting insulin levels also were lower on the high carbohydrate diet; however, insulin responses to oral glucose did not significantly change. These data suggest that the high carbohydrate diet increased the sensitivity of peripheral tissues to insulin."

 An diet supplying 85 percent of energy as carbohydrate is by necessity very low in fat, so perhaps Brunzell et al could have emphasized that this very low fat diet increased insulin sensitivity.  The mice of Masko et al that got the 20 percent carbohydrate diet had a lower fat intake than the mice on the zero-carbohydrate diet; rather than increasing carbohydrate being responsible for promoting insulin sensitivity, perhaps it is reducing fat (replacing it with starch) that does the trick. 

Anyway, the Masko et al study has a few features that make me skeptical that they will have similar results in humans.  I feel curious to see if their approach will have results as good as those found by Saxe et al.