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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
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