Diet and Risk of Prostate Cancer Recurrence
by Jacob Schor, ND, FABNO
Prostate cancer is the most common non-skin malignancy and the third leading cause of cancer death among men in the United States. The American Cancer Society estimated that in 2017, 161,360 men would be diagnosed with, and 26,730 would die from, prostate cancer. The majority of these men, about 92%, were diagnosed with low-grade, localized disease. Globally prostate cancer incidence varies 60-fold suggesting that lifestyle and dietary factors may have a large impact.(1)
We frequently see these men in practice at some point after diagnosis when they come seeking advice on how to reduce risk of recurrence. In the last ten years or so significant strides have been made that suggest a number of dietary characteristics are associated with significant impacts on recurrence risk. This article will review some of the more significant data that should now inform the advice we give to patients who have been diagnosed with prostate cancer.
Eggs and Chicken
In 2010, a paper by Erin Richman was among the first to catch our attention. Richman prospectively tracked consumption of processed and unprocessed red meat, fish, poultry, and eggs to see whether risk of prostate cancer recurrence or progression was affected by eating these foods. Her initial assumption was that processed and red meat, then assumed to increase initial diagnosis, would be the culprits that increased risk of recurrence as well. Chicken and eggs were tracked only because it was thought they were safe and would have no effect. Richman and colleagues followed 1,294 men diagnosed with prostate cancer for an average of 2 years. Though a short trial, their data added up to 2,610 person-years during which time 127 events occurred, defined as either prostate cancer death, metastasis, elevated prostate-specific antigen (PSA) or secondary treatment.
The results surprised us (and we assume Richman et al as well). Men who ate the most eggs or poultry with skin were at double the risk of recurrence or progression during the trial compared to men who ate smaller amounts. For eggs, comparing the highest and lowest quartiles of consumption, or an average of 5.5 eggs per week against, 0.4 eggs, the hazard ratio was 2.02 [95% CI: 1.10, 3.72; P for trend = 0.05]. Comparing highest and lowest quartiles of poultry consumption yielded a non-significant hazard ratio of 1.55. A comparison, though, between the upper and lower tertiles of those eating poultry with skin on yielded a statistically significant hazard ratio of 2.26. (95% CI: 1.36, 3.76; P for trend = 0.003). Men with higher prognostic risk and a high poultry intake had a four-fold increase in risk compared with men with low/intermediate prognostic risk and a low poultry intake (P for interaction = 0.003). Eating processed or unprocessed red meat, fish, or skinless poultry was not associated with prostate cancer recurrence or progression; it was only consumption of eggs and poultry with skin that significantly increased risk.
This was not what we would have guessed, and our focus on shifting men away from eating red meat and processed meat suddenly seemed trivial compared to reducing consumption of eggs and chicken skin.(2)
Erin Richman has gone on, in the years since, to author a number of important research studies on the impact diet and lifestyle have on prostate cancer recurrence. During the intervening years she has gotten married, and her recent work is published under her married name, Erin L. Van Blarigan
Richman's chicken and egg study was something of a turning point. Prior to its publication, we had scant data about primary prevention and assumed that after diagnosis we should tell men pretty much the same things we told them before they were diagnosed. We typically suggested that a, "… diet low in fat, high in vegetables and fruits, …. avoiding high energy intake, excessive meat, excessive dairy products and calcium intake, … [would be] possibly effective in preventing PC."(3)
The factors that cause prostate cancer do not necessarily promote recurrence or progression.
Richman's chicken and egg results were important because men with prostate cancer in their attempts to follow a ‘healthier diet' often decrease red meat and increase egg and poultry consumption to compensate for a reduction in protein. Richman turned what we thought was a smart plan into a dumb plan.
It is worth noting that eggs and poultry do not increase risk of getting prostate cancer.(4) Harvard researchers Willard, Giovannucci, Liu et al (who would later mentor Richman) had suggested that different factors promote prostate cancer progression after diagnosis in contrast to those that initiate the cancer. Still other factors may increase how aggressive the cancer is. [The same Giovannucci paper reported that increased levels of alpha-linolenic acid were associated with higher risk of prostate progression, a troubling thought for adherents of the Budwig diet](5)
Erin's 2010 paper was not the first to associate poultry with prostate cancer. A 2001 paper by Michaud et al reported an association between poultry skin and metastatic prostate cancer risk.(6) The American Institute of Cancer Research suggested a possible association between total poultry and prostate cancer in their 2007 report.(7)
So how have we explained this link between chicken, eggs and prostate cancer? In hindsight it seems obvious. With the chicken, it's probably the heterocyclic amines, the same family of chemicals blamed for why high meat consumption increases prostate cancer risk.(8) Cooked poultry skin contains more heterocyclic amines (HCA) than any other type of cooked meat; crispy chicken skin contains more HCA than barbecued beef or even fried bacon. Eggs contain the highest amount of choline of any food; choline, it seems, strongly promotes prostate cancer growth. There is a risk of being perceived as racist for quoting Bogen and Keating, who suggested in 2001 that African American men were at higher risk of prostate cancer simply because of their higher chicken consumption:
[Heterocyclic amine]...intakes were estimated to be greatest for African American males, who were estimated to consume approximately 2- and approximately 3-fold more [heterocyclic amines] than white males.... This difference...may at least partly explain why prostate cancer (PC) kills approximately 2-fold more African American than white men….(9)
Eating eggs raises serum choline levels. Johansson et al reported in 2009 that high plasma choline is associated with greater risk of prostate cancer.(10) Prostate cancer cells take up far more choline than healthy prostate cells.(11) In fact, radio-labeled choline is used for PET scan imaging of prostate tumors rather than the radioactive glucose used in standard PET scans.(12) Prostate cancers eat up choline with a passion. Erin, as Richman, reported in 2012 that dietary choline was correlated with risk of prostate cancer death.(13)
Van Blarigan was lead author of a 2015 study that compared consumption of saturated fat versus vegetable fats after prostate cancer diagnosis with the risk of dying from prostate cancer. This was a prospective study (n=926) of men diagnosed with prostate cancer from the Physicians' Health Study. During follow-up, 333 deaths (56 prostate cancer deaths) occurred. Even slight shifts in type of fat and percentage of calories sourced from fats and carbohydrates made significant differences. Men who obtained five percent more of their daily calories from saturated fat and five percent less of their daily calories from carbohydrate after diagnosis had a 1.8-fold increased risk of all-cause mortality (HR 1.81; 95 % CI 1.20, 2.74; p= 0.005) and a 2.8-fold increased risk of prostate cancer-specific mortality (HR 2.78; 95 % CI 1.01, 7.64; p= 0.05). Men who obtained ten percent more of their daily calories from vegetable fats and ten percent less of their daily calories from carbohydrates had a 33 % lower risk of all-cause mortality (HR 0.67; 95 % CI 0.47, 0.96; p=0.03). Saturated fat intake may increase risk of death, and vegetable fat intake may lower risk of death.(14)
Milk and Dairy Foods
The paper that alerted me to the name change was published in January 2018.(15) Erin Van Blarigan and colleagues had conducted a prospective study comparing consumption of dairy foods with prostate cancer recurrence, following 1,334 men with non-metastatic prostate cancer who were part of the CAPSURE cohort. The men were followed for a mean of eight years starting about two years after diagnosis.
Men who consumed more than four servings of whole milk per week compared to those who consumed 0-3 servings per month had a 73% increased risk of recurrence of prostate cancer (HR: 1.73; 95%CI: 1.00, 2.98; p=0.04). Higher body mass index (BMI) tended to worsen the association (p=0.01). For men with a BMI ≥27, making the same comparison of >4 servings/week versus 0-3 servings/month of whole milk, tripled risk of reoccurrence (HR: 2.96; 95%CI: 1.58, 5.54; p≤ 0.001). Whole milk consumption was not associated with increased risk in men with BMI of less than 27.
There is little new about the idea that milk might be a problem. A number (but not all) studies published over the years have suggested that dairy products increase risk of prostate cancer.(16-24)
Yet data about dairy consumption after diagnosis has been limited. The authors of this current study, Van Blarigan and her coauthors, reported in 2012 that among the 3,918 men in the Health Professionals Follow-up Study, those who consumed whole milk more than four times per week after diagnosis had double the risk of dying from prostate cancer and a 51% increased risk of prostate cancer recurrence compared to those drinking whole milk less than three times per month.(25)
These same authors also analyzed data from the 926 men in the Physicians Health Study and reported in 2015 that consuming more than three servings a day of dairy products was associated with a 2.4-fold increased risk of prostate cancer specific mortality compared to men consuming less than one serving per day.(26)
A 2017 Swedish study by Downer et al, looked at dairy consumption among 230 men diagnosed with localized prostate cancer. Drinking 3 or more servings per day of high fat milk increased prostate cancer mortality 6.1-fold over men who drank less than 1 serving per day.(27)
The bottom line is that consuming dairy, in particular whole milk, puts men at greater risk of recurrence. We should assume that men who have chosen a wait and watch approach rather than treatment, should be even more concerned about dairy consumption. This current study suggests that we may be able to segregate those most at risk by BMI.
Several possible mechanisms have been suggested why milk is a problem:
• High calcium intake decreases vitamin D(28);
• Milk proteins increase igf-1(29);
• Fluctuating phosphorous levels modify vitamin D concentration(30);
• Elevated saturated fat may modulate immune responses.(31)
As mentioned, Erin and her colleagues have already reported that saturated fat intake is associated with increased risk of prostate cancer mortality; and now this data, that whole milk has a greater effect, suggests that the fat content of whole milk increases risk.(32) This clearly should raise concern about other high-fat dairy products such as half & half, cream, butter, and especially that glorious triple-cream brie sold at Costco.
Several other earlier studies have looked at whole milk and prostate cancer recurrence. Pettersson et al reported that men who had the highest whole milk intake (>4 servings/week) had about a two-fold increased risk of prostate cancer mortality (HR: 2.15; 95%CI: 1.28, 3.60; P-trend) compared to men with low intake (0-3 servings /month). In their study there was no association between total dairy consumption and risk of lethal prostate cancer, biochemical or clinical recurrence.(33)
We should add whole milk and probably other high-fat dairy products to our lists of foods that men with a history of prostate cancer should avoid. I've often joked about how patients lump all foods found in the dairy case of the grocery store into one category so that when you tell them to avoid "dairy foods," they ask if that "means eggs?" My response has been, "Do cows lay eggs?" In a way though these people are right. For men who have had prostate cancer, both eggs and dairy increase risk dramatically.
This BMI information from the new milk study puts something of a new twist into the story. Up until this study we were not thinking that the impact of foods would vary significantly with BMI. Van Blarigan was part of a team that reported in 2015 that pre-diagnostic obesity was associated with shorter telomere lengths in prostate stroma cells and overweight (n=596) had higher Gleason scores. Telomere length also varied with physical activity; more active men had significantly longer telomeres in their prostate cells and the least active men tended toward shorter lengths.(34)
Whether a man is overweight also affects prostate cancer prognosis. If he is overweight, we want him to lose weight. In a study of 2,546 men with localized prostate cancer in the Physician's Health Study (PHS), a one-unit higher BMI before cancer diagnosis was associated with about a 10% increase in the risk of prostate cancer specific mortality. A BMI of ≥30 kg/m2 was associated with nearly double the risk of prostate cancer death compared to normal weight men.(35)
Men who gain >2.2 Kg between five years before to one year after prostate cancer surgery have a 94% increased risk of recurrence.(36) Gaining weight after diagnosis is associated with increased risk of biochemical recurrence and prostate cancer specific mortality.(37) Metabolic syndrome is strongly associated with "increased risk of high-grade and advanced prostate cancer."(38,39)
Prospective cohort studies suggest that vigorous exercise is associated with lower risk of prostate cancer specific mortality. This means doing things that make the heart pound, the lungs breath hard, and the skin sweat. If you think in terms of metabolic equivalent task (MET) values, this means MET >6. In simpler terms, we are talkingabout jogging, biking, or swimming or exercise of similar intensity. After analyzing data from the Health Professionals Follow-up (HPFS) (n=2705), Kenfield and other Harvard researchers reported in 2011 that men who performed 3+ hours/week of vigorous activity had a 61% lower risk of dying from prostate cancer when compared to men who exercised less than one hour per week.(40)
Erin Richman, working with this Harvard team, reported similar results in 2011 after analyzing data from the CAPSURE cohort: men who walked briskly (≥3 mph) three or more hours per week had a 57% lower risk of prostate cancer recurrence compared with men who walked less than three hours a week at a easy pace (< 2 mph).(41)
Bonn reported similar effects on prognosis in 2015 from a cohort of 4,623 men with localized prostate cancer. Men who either walked or biked ≥20 min/day versus doing either for less than 20 minutes a day was associated with a 36% decrease in prostate cancer mortality.(42)
In a 2015 paper, again with this Harvard group, Erin (as Van Blarigan) explained in part why exercise might be so beneficial in prostate cancer. Exercise affects tumor morphology, it literally changes the architecture of the tumors, leading to more regularly shaped blood vessels in the tumors. Microvessel morphology was examined in men with prostate cancer and compared to activity levels (n=571). Vigorous walking was associated with "… larger, more regularly shaped blood vessels compared with those of men who walked at a less than brisk pace."(43)
While not smoking might seem to be a no-brainer, many men who have had prostate cancer live in denial and find reasons to rationalize continuing to smoke. Smoking increases prostate cancer aggressiveness and the risk of dying from prostate cancer. For smokers, every aspect of prostate cancer prognosis is worse. They have a higher risk of progression, including biochemical recurrence, metastasis, and development of hormone resistant disease.(44,45)
In the first of these two studies, 5,366 men with prostate cancer, those who smoked prior to diagnosis had a 61% higher risk of biochemical recurrence. Risk decreased in men who stopped smoking for ten or more years to about the same level as those who had never smoked. In the second study (n=6538) current smokers had a 80% higher risk of biochemical recurrence compared with non-smokers [HR 1.80, 95% CI 1.45-2.24; p<0.001)]. Former smokers had a 63% increased risk [HR 1.63, [CI] 1.30-2.04; p<0.001)].
In some studies men who eat more fish have lower risk of death from prostate cancer than men who eat little fish. While some meta-analyses have not found significant associations, others have. A 2010 pooled analysis of four cohort studies by Szymanski reported a significant 63% reduction in prostate cancer mortality among the fish eaters (n = 49,661), RR: 0.37; 95% CI: 0.18, 0.74].(46)
It is thought that oily fish that are high in omega-3 fatty acids, such as salmon, sardines, mackerel and herring may have the most benefit. Yet there are some discrepancies. Brasky reported in 2013 that men with higher omega-3 blood levels are actually at higher risk of being diagnosed with prostate cancer by PSA testing.(47)
Coffee Is Good
Several observational studies report that coffee consumption pre-diagnosis is associated with less lethal prostate cancer and reduced risk of recurrence. Wilson et al in 2011 seems to be the largest of these studies.(48) In 47,911 men in the Health Professionals Follow-up Study, 5,035 cases of prostate cancer were diagnosed, 642 of which proved lethal. Men who drank six or more cups of coffee per day compared with nondrinkers had an 18% lower risk of prostate cancer RR = 0.82, 95% [CI] = 0.68 to 0.98, P= .10) [note p-value. These were non-significant results]. The association was stronger and significant for lethal prostate cancer (consumers of more than six cups of coffee per day [RR = 0.40, 95% CI = 0.22 to 0.75, P(trend) = .03)].
Geybels et al reported in 2013 that in a group of 630 men treated for prostate cancer, drinking four or more cups per day pre-diagnosis versus one or less was associated with a 59% reduced risk of recurrence or progression (HR 0.41, 95 % CI 0.20–0.81; P for trend = 0.01). It didn't matter if they were drinking caffeinated coffee or de-cafe.(49) At this point we have not seen any research about starting to drink coffee post-diagnosis.
Everyone has heard that cruciferous vegetables contain chemicals whose metabolites stop cancer cells from growing and encourage apoptosis. Consuming these vegetables is associated with lower risk of developing advanced prostate cancer, stage III and IV disease. Eating more than one serving of broccoli per week versus less than one serving per month was associated with a 45% decrease in risk (RR = 0.55, 95% CI = 0.34 to 0.89, P(trend) = .02). The same frequency of consumption for cauliflower was associated with a 52% drop in risk [RR = 0.48, 95% CI = 0.25 to 0.89] P(trend) = .03).(50)
A 2012 paper by Erin Richman's group looked at cruciferous consumption after diagnosis.(51) Erin and colleagues examined whether intake of vegetables, in particular cruciferous vegetables, tomato sauce, and beans after diagnosis would shift prostate cancer progression in 1,560 men diagnosed with non-metastatic prostate cancer.
They reported that men in the highest quartile of cruciferous vegetable intake, who were eating almost six servings per day, after diagnosis had a 59% lower risk of progression compared with men in the lowest quartile. Consumption of other vegetable groups was not associated with risk. Trends toward lower risk associated with consumption of other cruciferous vegetable types did not reach statistical significance. No benefit was seen in this particular study for tomato sauce. Six servings a day though seems like a lot to eat.
Laboratory and epidemiology research suggests soy isoflavones may inhibit prostate cancer growth. A 2009 meta-analysis looking at soy and prostate cancer risk reported findings that should trouble us. The studies on soy intake yielded a combined relative risk that was 26% lower in men who ate soy [RR= 0.74 (95% CI: 0.63, 0.89; P = 0.01)]. That is good news but when the data was separated between those eating non-fermented versus fermented soy foods, the benefit was solely from the non-fermented soy. Non-fermented soy foods lowered risk of prostate cancer by 30% [RR/OR of 0.70 (95% CI: 0.56, 0.88; P = 0.01)]. Fermented soy food consumption had no significant effect [1.02 (95% CI: 0.73, 1.42; P = 0.92)].(52) We assume the data for soy and prostate is strong in support, but actually it is relatively weak.
Studies have associated consumption of cooked tomatoes and tomato-based products with reduction in risk of lethal prostate cancer; it is unclear whether these same foods offer benefit post-diagnosis. Two studies have looked at tomato products and prostate cancer progression, and results are not consistent. One suggested a benefit. Chan et al reported an inverse linear relationship for tomato sauce and risk of progression for those consuming two-servings/week increase in tomato sauce.(53) The second, a 2009 review concluded that the data examined in their "… systematic review do not provide sufficient evidence to recommend the use of lycopene supplements in routine clinical practice for patients diagnosed with prostate cancer, although the studies do indicate that lycopene is unlikely to be harmful to such patients. However, no study has been conducted with an adequately sound methodology."(54)
In another 2014 paper published with former associates from Harvard, Erin (still Richman) reported that although closer adherence to a Mediterranean diet did not lower risk of dying from prostate cancer, it did lower overall mortality risk. Erin et al had prospectively followed 47,867 men from 1986 to 2010. This included 4,538 men diagnosed with non-metastatic prostate cancer, followed from diagnosis to lethal outcome or to January 2010. During that time, 6,220 prostate cancer cases were confirmed. The Mediterranean diet was not associated with risk of advanced or lethal prostate cancer. However, there was a 22% lower risk of overall mortality (hazard ratio: 0.78; 95% confidence interval, 0.67-0.90; p=0.0007) among men with greater adherence to the Med-Diet after diagnosis.(55)
Observational studies initially suggested an inverse association exists between vitamin E and risk of prostate cancer, leading to vitamin E frequently being suggested as treatment. Three large randomized controlled trials reported conflicting results, that is higher vitamin E was associated with worse disease risk. In 2013 Richman was part of the group that sorted out and possibly explained this vitamin E phenomenon.
They measured circulating α- and γ-tocopherol and genotyped 30 SNPs among 573 men with prostate cancer. They compared circulating vitamin E, genotypes, and risk of high-grade prostate cancer, and risk of recurrence (56 events; 3.7 years median follow-up). Circulating γ-tocopherol was associated with an 87% increase in risk of high-grade prostate cancer (Q4 v. Q1 odds ratio [OR] = 1.87; [CI]: 0.97-3.58; p=0.02). The less common allele in SOD3 rs699473 was associated with an increased risk of high-grade disease (T > C: OR = 1.40, 95% CI: 1.04-1.89). However, two independent SNPs in SOD1 were inversely associated with prostate cancer recurrence (rs17884057 hazard ratio [HR] = 0.49, 95%CI: 0.25-0.96; rs9967983 HR = 0.62, 95% CI: 0.40-0.95). Genetic variation in SOD may be associated with risk of high-grade disease at diagnosis and disease recurrence. Circulating γ-tocopherol levels may also be associated with an increased risk of high-grade disease. This in effect should put an end to across the board recommendations that men with prostate cancer should take vitamin E.(56)
In 2014 as lead author and under her new name, Erin Van Blarigan pursued these genetic variations a step further. Circulating pre-diagnostic α-tocopherol, γ-tocopherol, and lycopene were analyzed along with various SNPs and the risk of lethal prostate cancer in 2,439 men with prostate cancer in the Health Professionals Follow-up Study and Physicians' Health Study.
They observed 223 events over 10 years of follow-up. Risks varied with different alleles. High α-tocopherol levels were in general associated with lower risk of lethal prostate. Men homozygous for the less common allele [rs3746165 in GPX4] had a 35% lower risk of lethal prostate cancer compared with men homozygous for the more common allele. However, men who were homozygous for the less common allele in rs3746165, and who had high γ-tocopherol levels were at 3.5-fold increased risk of lethal prostate. Thus it looks like we should be testing genetic snps prior to using vitamin E supplements.(57)
Selenium is another supplement that was commonly suggested to men with a history of prostate cancer that has been questioned by prospective human trials. Recall the 2003 van den Brandt study that associated low toenail selenium levels with higher risk of prostate cancer.(58) Even Hurst's 2012 meta-analysis furthered this belief.(59) Yet this notion was countered by the results reported in the SELECT cohort that found supplementation with selenium had no significant impact on disease risk.(60)
Van Blarigan and colleagues reported in 2014 after following 4,459 men diagnosed with prostate cancer for 22 years that those who took selenium supplements had a higher risk of dying from prostate cancer. During 7.8 years of follow up, recurrence rates were 5.6/1000 person-years for those not taking selenium supplements and 10.5/1000 person-years for those who took 140 μg/day or more. Rates of biochemical recurrence were 28.4 vs. 29.3/1000 person-years comparing non-selenium users with users. Risk of dying from prostate cancer increased with selenium doses. Men consuming low-dose selenium (1 to 24 μg/day of selenium) had an 18% higher risk than non-users. Those consuming 25 to 139 μg/day had a 33% increased risk and those taking 140 or more had a 2.60-fold greater risk of prostate cancer mortality. This clearly contradicted the general belief that every man who had prostate cancer should take 200 mcg or more of selenium per day.(61)
In a 2015 Van Blarigan was part of a team that identified specific polymorphisms in selenoprotein coding genes that were associated with higher-grade disease that might affect prostate cancer recurrence.(62)
In 2014 Richman had an important paper on folate published. She prospectively examined the association between post-diagnostic folate consumption and the risk of prostate cancer recurrence after radical prostatectomy, external beam radiation therapy, and brachytherapy. Prior to starting this study, a randomized, placebo controlled clinical trial of folic acid supplementation for the chemoprevention of colorectal adenoma had revealed an increased incidence of prostate cancer in the treatment group. Erin's study was done with 1,153 men who had been treated with radical prostatectomy, external beam radiation therapy and brachytherapy and participated in the CaPSURE Diet and Lifestyle study.
Prostate cancer progressed in 101 men (8.76%) during a mean 34-month follow-up. Though initially no evidence of folate intake and recurrence was seen, on secondary analysis by treatment type, after radical prostatectomy, patients in the lowest decile of dietary folate intake had a 2.6-fold increase in the risk of recurrence (HR 2.56, 95% CI 1.23-5.29, p = 0.01). In patients treated with external beam radiation and brachytherapy, no evidence of an association between prostate cancer progression and increased folate intake was seen.
Though it is rare to see low folate levels in patients, this paper would suggest we should not worry about folate supplementation in men who have had prostate cancer, in fact we should consider supplementation if a man's levels are low post initial treatment with surgery.(63)
Taking a multivitamin is safe and probably useful. The Physicians Health Study randomized trial of a regular multivitamin reported a modest but significant (8%) reduction in total cancer incidence in men (HR, 0.92; 95% CI, 0.86-0.998; P=.04). The men with a history of prior cancer had a 27% reduction in total cancer during the study (HR, 0.73; 95% CI, 0.56-0.96; p=0.02). There was no significant affect on risk of prostate cancer.(64) There is still no strong evidence that any single supplement offers protection against prostate cancer (neither development nor progression).
In a 2016 paper, Nordström, Van Blarigan, Ngo, et al reported that circulating carotenoids, "were inversely associated with the risk of high-grade prostate cancer…odds ratios (OR)… highest versus lowest quartiles were: 0.34 (95% CI: 0.18-0.66) for α-carotene, 0.31 (95% CI: 0.15-0.63) for β-carotene, 0.55 (0.28-1.08) for lycopene and 0.37 (0.18-0.75) for total carotenoids." Once again, these effects were modified by various SNPs. Thus, the argument that we should be doing genetic testing in prostate cancer patients continues to strengthen.(65)
So, what is the current bottom line for men diagnosed with prostate cancer?
If BMI is 27 or higher, lose weight;
Exercise rigorously, do something to sweat;
Eat lots of vegetables (particularly tomato sauce and cruciferous vegetables);
Eat more vegetable fats (i.e. fish, nuts, vegetable oils, soybeans, avocados, and flaxseed) and fewer saturated fats. Eat less carbohydrates;
Drink coffee – regular or de-cafe doesn't seem to matter;
Limit eggs and poultry with skin on;
Limit whole milk if your BMI is high, probably should even if it isn't; and
Limit refined grains, sugars, processed meat, and high-fat dairy.(66,67)
We should probably be testing SNPs before making suggestions for vitamin E, selenium or lycopene.
Granted at this point we do not have the sort of randomized human clinical trials implementing these recommendations that we would prefer. Still this is a great deal more information than we had just a few years ago. A good bit of it is the result of Erin Van Blarigan's research. Hopefully at some future date she will be able to link the earlier research published under her maiden name to her current list. We'll keep our fingers crossed that she keeps this married name for a long, long time and does so with much happiness. Congratulations Erin!