Saturday, November 26, 2011

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.


Duffman said...

What about the China study in which high protein consumption was protective against cancer (less mice developed cancer) but lead to cancer growth (mice that had developed cancer were worse off with high protein consumption), in relation to mice that had low protein consumption before and after cancer was established, in which there was a higher chance of cancer but cancer growth was slower? By the way, the obvious solution, hp diet before cancer and lp diet after cancer growth did produce the best results. You keep an interesting blog, keep on challenging predisposed notions.

Sorry for my english, greetings from greece.

Peter said...

Dead Ornish stopped completely the progression of prostate cancer on his patients.

"The diet was predominantly fruits, vegetables,whole grains (complex carbohydrates), legumes and soy products, low in simple carbohydrates and with approximately 10% of calories from fat.The diet is intensive but palatable and practical. In earlier studies most patients were
able to adhere to this diet for at least 5 years"


serega said...

From the linked study: "The strongest protective effects were seen for beans and legumes, nuts, carrots, leafy greens, cruciferous (cabbage family) vegetables , and tomatoes.[17] Cruciferous vegetables have been found in two population-based studies to be associated with a reduction in PC incidence".

Cruciferous vegetables, tomatoes, and leafy greens and known to have cancer protective effect. In fact the study emphasizes vegetables and not "beans and whole grains" if you read carefully. Inclusions of vegetables in the diet is a must regardless whether meat is consumed on not. Diet consisting of just whole grains is not healthy diet, and the same can be said about meat only diet.

Don said...


In the human world, cancer is most prevalent in nations with high protein intake (e.g. U.S.A.) and least prevalent in nations with low protein intake (e.g. China). This suggests that for humans, low protein intake prevents cancer occurence.


Thanks for that, I wanted to mention it.


Since the participants in this study ate grains and legumes in addition to vegetables etc. and they saw a reduction in the rate of progression of their cancers, this suggests that grains and legumes either a) protect against cancer or b) neither protect against nor promote cancer.

However, as discussed in my post on phytate

at least one component of whole grains and legumes (phytate) has distinct and strong anti-cancer properties.

vladex said...

In the human world, cancer is most prevalent in nations with high protein intake (e.g. U.S.A.) and least prevalent in nations with low protein intake (e.g. China).

It's far more likely to do with limited calories and fasting than simple proteins. Besides proteins are self limiting whereas fats and carbs much less so.

jaime said...

Hi, Don:

Would you consider eating all those nuts on daily basis could cause to much omega 6 become imbalance?, or you think omega 6 coming from nuts is totally different from the ones coming from vegetable oil?
In TCM nuts are consider to be very heating if eaten in large quantities.
Im also curious about your daily protein intake, what´s your aprox. range?
Thanks so much for giving another view on food. My blood work and glucose tolerance has been affected negatively on a high fat (paleo style)diet.Now Im trying to heal my liver with a similar approach as the one you´re currently in.



Don said...


Any data to support your view? Like, show me that those nations have limited caloric intake or fast a lot. Also show me that protein intake has nothing to do with it (human studies only).

To support my view, in humans, high protein raises IGF-1, a promoter for breast, prostate,and colon cancers. In fact, high protein with caloric restriction produces a ~20% higher IGF-1 level than low protein without caloric restriction.

Don said...


Regarding omega-6, no, I don't think so, and have seen no evidence to support that idea. The evidence I have seen shows nuts and seeds reduce inflammation (probably due to other components of those foods).

Nuts may be heating but most other plant foods are cooling. Its all about quantity and context. A plant-dominated diet with too little nuts could for some people be too cooling.

I would estimate my protein intake at 60 to 90 g per day.

Sonnenschein said...

sionMay I ask you what protein intake you recommend in relation to body weight? I am 5"8' tall and weight 127 pounds (I am a female). Would you recommend "protein cycling" (around 80 g of protein on strength training days and around 40-50 g the remaining days?
Thank you!

Peter said...

In Japan year 1950 only 18 people died with prostate cancer. I don't have the source but it's the Esselstyns book.

Basically a diet rich in vegeterian whole-foods, low in (animal)protein and fat, makes you pretty much immune to prostate cancer. Oils were basically not consumed at that in Japan. It was an ultra carbohydrate diet where the bulk of the calories came from grains.

marco said...

"IGF-1, a promoter for breast, prostate,and colon cancers.".

Hi Don, any ideas on why so many babies survive to LARGE quantities of IGF-1 and don't get cancer?

Malibu said...

Don said...


No, I wouldn't recommend protein cycling. I don't believe you need more than 50 g of protein. At 127 pounds, if you are very lean (15% fat) you have a LBM of ~49 kg, and a protein requirement of 39 g per day.

Don said...


1. Babies who have higher than normal IGF-1 do have more cancer than others, but not as babies, later in adult life. High IGF-1 brings on earlier puberty and increased stature, and both of these increase the risk of breast and prostate cancer.

2. A cancer takes more than 6 years to reach a detectible size by current methods. Babies are not alive long enough to experience cancer, in most cases.

3. In a baby, normal cells are rapidly dividing, so IGF-1 has its effect on accelerating normal growth and development, so long as the individual's immune system is competent. After puberty, high IGF-1 will mainly act on and promote abnormal growth and development i.e. tumors, skin tags, etc.

4. Cancer involves 3 stages: initiation, promotion, and growth. Initiation involves genetic damage. A healthy body repairs genetic damage as it occurs, but as we age, we are exposed to more carcinogenic events, so the longer we are alive, the more likely an incipient cancer will escape the immune system's surveillance and destruction. In other words, the odds of a baby getting a cancer are much much lower than the odds of an 80 year old getting cancer, simply because the longer you are alive, the more cell replications your cells have been through, raising the odds that there will be an error induced by a carcinogen.

Don said...


That is a hypothesis paper, providing a rationale for a low-carb approach to prostate cancer. It is not a human trial. So far as I know, the only human trials demonstrating dietary control of prostate cancer are those done by Gordon Saxe's team and Dean Ornish's team, both of which move the subjects toward a vegan diet.

Evolutionary knowledge may support the vegan approach better than the meat-based approach.

"A study of evolution indicates that the prostate and breast appeared at the same time 65 million years ago
with the development of mammals. All male mammals have a prostate; however, the seminal vesicles are
variable and are determined by the diet so that species primarily eating meat do not have seminal vesicles. The exception is the human, who has seminal vesicles and consumes meat, although this is a recent dietary change. Human lineage departed from other higher primates 8 million years ago. The closest existing
primate to humans is the bonobo (pigmy chimpanzee), which does not eat meat but exists primarily on a high fruit and fresh vegetable diet.... All current epidemiologic evidence and suggestions for preventing prostate and breast
cancer in humans indicates that we should return to the original diets under which our ancestors evolved."

UROLOGY 57 (Suppl 4A): 31–38, 2001.

marco said...

Is cheese protective?


Don said...


"A higher risk of prostate cancer was observed among subjects with higher dairy product (relative risk (RR; 95 % CI), 4th quartile v. 1st: 1.35 (1.02, 1.78), P = 0.04) and Ca intake (RR (95 % CI), 4th quartile v. 1st: 2.43 (1.05, 5.62), P = 0.04). Nevertheless, we identified a harmful effect of yoghurt consumption upon the risk of prostate cancer (RR (95 % CI), increment 125 g/d: 1.61 (1.07, 2.43), P = 0.02) independently of the Ca content. Our data support the hypothesis that dairy products have a harmful effect with respect to the risk of prostate cancer, largely related to Ca content."

"Stepwise-multiple-regression analysis revealed that milk + cheese was a factor contributing to mortality from prostatic cancer (R = 0.580). The results of our study suggest a role of milk and dairy products in the development and growth of testicular and prostatic cancers. The close correlation between cheese and testicular cancer and between milk and prostatic cancer suggests that further mechanistic studies should be undertaken concerning the development of male genital organ cancers."

Don said...

"In the present study, further meta-analysis was conducted to estimate the summary relative risk (RR) between the consumption of milk and dairy products and prostate cancer from cohort studies published between 1966- 2006. We found 18 relevant articles and 13 independent studies were available for our analysis. The summary RR was 1.13 (95% confidence interval = 1.02-1.24) when comparing the highest with the lowest quantile of consumption. The summary RRs by study stratification showed a positive association."

"Men with the highest intake of dairy products (RR =1.11 [95% CI = 1.00 to 1.22], P = .047) and calcium (RR = 1.39 [95% CI = 1.09 to 1.77], P = .018) were more likely to develop prostate cancer than men with the lowest intake. Dose-response analyses suggested that dairy product and calcium intakes were each positively associated with the risk of prostate cancer (Ptrend = .029 and .014, respectively)."

"A meta-analysis method was conducted to estimate the combined odds ratio (OR) between milk consumption and prostate cancer from case-control studies published between 1984 and 2003 using commercial software (comprehensive meta-analysis). The combined OR was 1.68 (95% confidence interval = 1.34-2.12) in the 11 published case-control studies. The combined OR varied little by study stratification."

"Suggestive positive associations were also seen between fatal prostate cancer and the consumption of milk, cheese, eggs, and meat. There was an orderly dose-response between each of the four animal products and risk. The predicted relative risk of fatal prostate cancer was 3.6 for those who heavily consumed all four animal products. The results of this study and others suggest that animal product consumption and obesity may be risk factors for fatal prostate cancer."

From this PubMed search:

I would estimate that studies showing milk and cheese consumption positively associated (i.e. possibly promoting) with prostate cancer outnumber those showing a negative or neutral association by 2:! at least. Of interest, the positive associations are strongest when looking at populations where cheese consumption ranges from zero up (e.g. Asian nations) and weaker in nations (e.g. Northern Europe) where regular cheese consumption is common. When everyone does something (eats cheese) it is very hard to detect a negative effect of this practice. For example, if nearly everyone smoked, it would be difficult to find a negative effect of smoking on lung health; with everyone smoking, and some having better and some worse lung health, there would appear little relationship between smoking and lung health, because so many people exceeded the dose of smoking that causes lung pathology.

The same with diet. The only way to detect the effect of a substance on health is to start with zero consumption as the standard. We have to compare the prostate cancer risk of cheese eaters to people consuming no dairy at all to see the effect of dairy on prostate health, because it might be that any regular consumption of cheese exceeds the 'toxic' dose with respect to prostate cancer.

vladex said...

Talking about cancer is just a fear mongering strategy to prove or promote somthing tenous No one knows the clear cause of cancer so it's counter productive to fight it because you maybe making it bigger than it is . I think fear and various promotions of cancer are making it more than it is. If you say something stimulates cancer you have to explain why and what would be the strategy of the body to grow that cancer?

As for IGF, it's just a growth promoter, it can't start a cancer . Cancers are started by transcription genes when they receive appropriate stimulation. When nucleus can't respond properly to an outside stimuli, then comes a mutation period in order for the cell to respond to that stimuli. Mutations happen only because of outside stimuli which is controlled by perceptions of the brain on the environment. If the brain believes that there is death or cancer, than it will probably start making real cancer and grow them faster.

Don said...


There is no way to stop initiation of cancer. We are all exposed to mutagens, and over a long lifespan, given the number of cell divisions required to maintain continuity of the body for 60+ years, it is unavoidable that some cells will go awry. That's in part why we have an immune system, to control and eliminate dysfunctional cell growth.

Therefore, it is logical to focus our efforts on the promotion and growth minimize promoters and maximize immune function against cancers, so that we can control growth or reverse it.

This research and that of Ornish both indicate that we can stop the growth of cancer and reverse it well past the initiation stage. Rather than fear-mongering, I would see this as hope-mongering.

vladex said...

There is no way for the human body to know what is normal especially today in a civilized environment where people live removed from nature, all living things depend on nature for survival.Labs and hospitals are static, nature and livings things are not.It's going to do with what it has and what it perceives in the environment. If it perceives death/cancer in it , it's going to react to it but since it probably can't react properly to such a death threat, it will stimulate proteins to activate mutation of genes which will lead to cancer growth.

Genes can not start themselves, they have to be stimulated by an outside environment or more precisely by someone's perception of environment. Be careful of spreading death/cancer fears. As they say be caferul what you wish for.With that said cancer is not something I nor anyone should fear .
This post is negative because it's saying that we need to save ourselves which only encourages negative perceptions and remember that perceptions most of them unconcious is what starts disease processes including cancer. Then when these "anti cancer diets" don't work as they never do, this only makes person even more hopeless and resigned to death.

Don said...


You are saying that 'these anticancer diets' never work, after reading this study that shows clearly that this approach does work?

Cancer is nothing to fear.