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Which of the dirty dozen of supplements and foodstuffs in todays SuppVersity review can really help you to make sure, youre not the one out of those nine men who develops prostate cancer?

Supplements that are supposed to protect you from developing prostate cancer and/or agents that may help patients with existing prostate issues are - obviously - in high demand. And as W. Merkle points out in a recent article in the German science journal Urologe using them - even if they may not be as effective as some patients may believe - makes sense: from a psychological perspective, alone (Merkle. 2014).

Taking a pill with selenium, for example, has been shown to alleviate some of the side effects of chemotherapy. General protective effects against prostate cancer, on the other hand, have not been established. In fact, the most recent studies rather suggest that "supplementation did not benefit men with low selenium status but increased the risk of high-grade PCa among men with high selenium status" (Kristal. 2014).
Luckily, there are other supplements with more promising data. Supplements that will actually complement, a healthy diet and active lifestyle, the two pillars of all (not just prostate) cancer protection. Supplements like...

• Curcumin - As a SuppVersity reader youve probably already expected to see the curcumin on the list. Its potent anti-inflammatory effects and more specifically its ability to target multiple inflammatory pathways, which include NF-KappaB, COX2, STAT3 and high levels of CRP, Prostaglandins and TNF-alpha make it a particularly valuable anti-tumor agent of which Guo et al. observed in a recent study that it will induce cell cycle arrest and apoptosis of prostate cancer cells by regulation the expression of IkappaBalpha, c-Jun and androgen receptor (Guo. 2013)
• Genistein - Just like curcumin, genistein acts on NF-KappaB (Adjakly. 2013). In addition it will upregulate a protein called miR-574- 3p that will have cancer cells "kill themselves" (go into apopotosis; Chiyomaru. 2013). In addition scientists have found genistein to support the efficiacy of Cabazitaxel which is used for the treatment of hormone-refractory prostate cancer.
• Pomegranate - Pomegranate extracts or rather its ingredients, i.e. ellagic acid, caffeic acid, luteolin and punicic acic, have been shown to inhibit the proliferation and induce apoptosis in prostate cancer cells (NCI. 2013).

  Figure 1: If you look at the actual increase in apoptotic cancer cells in response to the pomegranate treatment, it is obvious that some patients (e.g. #53) benefited more than others (Pantuck et al. 2006)

  A clinical trial by Pantuck et al. (2006) was also able to show that the time it takes for the PSA levels, an albeit debatable marker of prostate cancer risk, to double decreased significantly, when the subjects, men with rising PSA after surgery or radiotherapy, were treated with 8 ounces of pomegranate juice daily (Wonderful variety, 570 mg total polyphenol gallic acid equivalents) until disease progression. Unfortunately, a more recent study by Stenner-Liewen et al. (2013) could not confirm these effects. 
• Brassica vegetables (cruciferous vegetables) - While general vegetable intake is already associated with a -39% reduced risk of developing extraprostatic prostate cancer (cancer, eating tons of cruciferous vegetable, it was the intake of broccoli and cauliflower that made the biggest impact in a 2007 study by Kirsh et al.
  
  

  Even if they dont protect you from prostate cancer broccoli & co will inhibit myostatin and could help you to grow more muscle... well, at least theoretically, you know about the difference between the petri dish and the real world, so dont expect monster gains | more.

  As it is usually the case the evidence is yet ambiguous. In a 2002 review of the evidence, Kristal, et al. found that of the six studies they could clearly interpret, only three reported statistically significant reduced risks (P < 0.05), while one reported a borderline significant reduced risk (P = 0.06). Against that background Verhoeven et al. are right, when they say: " Further epidemiological research should separate the anticarcinogenic effect of brassica vegetables from the effect of vegetables in general" (Verhoeven. 1996).
  
  More recently, Joseph et al. found that the existing differences in the epidemiological data may be due to genetic polymorphisms due to which only men with a certain genetic polymorphisms in glutathione S-transferases M1 and T1 will benefit from eating tons of cruciferous veggies (Joseph. 2004).
• Green tea - Green tea is good for everything, right? Well unless its not loaded with toxic molecules (see previous SuppVersity article) this may in fact be right. Convincing evidence from human trials is albeit scarce. What we do have are rodent studies like the ones that were conducted with TRAMP mice, which model closely mirrors the pathogenesis of human prostate cancer.
  
  In these mice EGCG, one of the main catechins in green tea, decreased the proliferation of prostate cancer cells and reduced the PSA levels. Scientists believe that these effects are mainly mediated by the effects EGCG has on the growth promoting proteins ERK1/2. Unfortunately, the same rodent studies also suggest that it is probably too late for many of you to start drinking green tea, now, because said beneficial effects are only observed in young, not in old TRAMP mice (Donald. 2012).

• Coffee is for the ladies, too! Studies show significantly reduced risks of breast cancer with 5+ cups of coffee. Tee and cacao help, as well | more

  Coffee - Obviously I am biased, when it comes to coffee. I still hope you believe me when I say that drinking 5+ cups of coffee per day has been associated with significantly reduced risk of prostate cancer in what is probably the most large-scale meta-analysis of the topic today.
  
  In their meta-analsis of 12 peer-reviewed case-control studies, Lu et al. calculated a 4% risk reduction for Europeans who consumed five or more cups of coffee and Americans who consumed 4 or more regular cups of coffee (equ. to approximately 400-500mg of caffeine). Moreover, the scientist found "a significant inverse association in all categories of prostate cancer except Gleason <7 grade" in both the "fixed-effects model" and the "random-effects model" (Lu. 2014).
  
  Wilson et al. also report an inverse association between coffee consumption and the incidence of highly malignant prostate cancer (Wilson. 2013). This means that drinking coffee is not only going to reduce your overall risk of developing prostate and other cancers (Geybels. 2013), it will also increase your chance that in the unfortunate case you still develop cancer, its going to be a benign and treatable form of prostate cancer.
• Lignans (e.g. from flaxseed) - While many of you will probably know them as "bad anti-androgens", there is little doubt that lignans from flax and other foodstuff inhibit cancer growth. What is particularly interesting about these agents is that they dont work via the "regular" NF-kappaB pathway but inhibit the expression of the vascular endothelial growth favtor (VEGF; cf. Azrad. 2013).
• Lycopene - Its the bright red carotene and carotenoid pigment and phytochemical that gives tomatoes and other red fruits and vegetables, such as red carrots, watermelons, gac, and papayas, although not in strawberries, red bell peppers, or cherries their color.
  
  Based on the currently available evidence it appears to help not just with prostate, but also with pancreatic, intestinal and lung cancer (Giovannucci. 1999). In that, it makes a particularly effective adjunct to classic cancer therapy (Tang. 2011).

  Figure 2: Prostate cancer risk w/ high vs. low intakes of the given antioxidants according to XRCC1 genotype (Goodman. 2006)

  Unfortunately, the data is ambigious... as usual. Unlike for other agents, it does yet appear as if scientists have already identified a certain gene, i.e. XRCC1, which appears to determine whether you do or do not benefit from the consumption of increased amounts of tomato lycopene (Goodman. 2006).
  
  In view of the fact that certain genotypes actually increase their prostate cancer risk specifically if they are consuming both, a high amount of lycopene and vitamin E (alpha-tocopherol), the latest Cochrane Review on the protective effects of lycopene against prostate cancer considers the evidence for "preliminary" and "insufficient" (Ilic. 2011).
• Fish oil / omega-3 - In spite of the fact that the media jumped at the finding of the SELECT trial (learn more) that claimed that selenium would be bad, while a high fish consumption or rather a high amount of omega-3s in the blood would protect you against prostate cancer, a close re-analysis of the data you can read up on at the website of the Life Extension Foundation indicates that this was all media hype.
  
  With a de facto difference of only 0.18% the difference was... well, youd say a joke, scientists would say "within the margin of statistical error" and thus by no means significant. If you take an even closer look at the data, it would even seem as if omega-3 fatty acids would increase the risk of prostate cancer.
• Resveratrol - If you look at the existing evidence you will be surprised to find studies that indicate that resveratrol increases (Klink. 2013) and studies that show that it inhibits prostate cancer growth (Iguchi. 2012; Kai. 2011).
  
  Again, it took a closer look at the data and another experiment to find out what really was going on: a dose-dependent effect with increased risk with low and decreased risk with high doses of resveratrol (Benitez. 2007). Bad news: With the current low biovailable oral resveratrol preparations youre likely to end up in the "increased risk" resveratrol exposure zone.
• Selenium - While I have mentioned it in the introduction already, its certainly worth taking a closer look at what selenium is actually supposed to do.
  
  In their 2011 review of the literature, Rizky Abdulah et al. didnt just highlight the many different molecular pathways, by which selenium could protect you from developing cancer, they also point out that the type of selenium supplement used could be of critical importance with respect to the success of your efforts to avoid the development of cancer. In that,...

  In rodents selenium acts as corrosion inhibitor in the brain | learn more

  "[...] methylselenol is believed to be the critical metabolite in selenium chemoprevention. Since methylselenol is highly reactive, methylselenol precursors such as Semet and Se-mSC are important both in in vitro and in vivo experiments. Semet and Se-mSC conversion to methylselenol, however, requires enzymatic conversion by the enzyme ?-lyase, which is 800 times less prevalent in human tissues than in mouse tissues.

  This may explain why the results of Semet and Se-mSC anticancer studies in humans were not as impressive as in vivo experiments. Although researchers have now turned to other Se compounds such as mSeA, which do not need enzymatic conversion to methylselenol, or selenite, which does not need to be converted to methylselenol for its anticancer properties, more substantial research on selenium compound metabolism in human tissues is necessary." (Abdulah. 2011)

  In other words, as of now, we dont know which form of selenium we actually have to use in human trials to generate similar impressive results as they have been observed in rodents.
  
  And as if that wasnt already "bad" enough, a meta-analysis of intervention studies by Hurst et al. (2012) indicates that there is a very narrow "band" of serum concentrations, where selenium is actually good for you! When your selenium level passes 170 ng/ml the tumor-protective effect disappears and - worst case scenario - your risk increases. So remember: More does certainly not help more!
• Silibin (from milk thistle) - You probably think of milk thistle as a "liver supplement". In fact, its main active constituent will yet also reduce the efficacy of osteoclast cytokines and reduce the concentration of RANKL-ligands. Thus it will regulate the NF-?B und AP1 levels in cells and inhibit the proliferation, invasion and migration of metastatic prostate cancer (Ting. 2011; Chen. 2012) 
• Vitamin D - Believe it or not: There are things vitamin D3 cannot do! One of this things is to protect you prostate cancer. Thats the prerogative of active vitamin D aka calciferol. In rodent studies and studies on human cell lines calciferol and multiple analogs of active vitamin D have shown to be promising drugs for prostate cancer protection, though (Tokar. 2005).
  
  

  Underestimated Vitamin D Sources: Eggs, Chicken, Pork, Fish & Dairy Contain Ready-Made 25OHD | more

  Since simply popping tons of vitamin D3 is (luckily) without effect on the levels of calciferol (otherwise you would run the risk of being calcified from the currently prevalent abuse of vitamin D3 supplements), using vitamin D3 is less effective, but not useless.
  
  In 2010, for example, Woo et al. observed that the time it took for the PSA levels of prostate cancer patients to double was significantly reduced, when the subjects received 2,000 IU of vitamin D3 per day (Woo. 2005) - an effect of which previous in vitro studies suggest that it could be due to the local conversion of D3 to active vitamin D in prostate cancer cells (Tokar. 2005).
• Vitamin E - Needless to say that vitamin E has gotten a bad rep ever since scientists observed an increased risk when they gave the subjects of the SELECT trial vitamin E (learn more). Still, as long as you stay away from "classic" vitamin E and buy one of the still expensive tocotrienol supplements (or eat red palm oil), you can expect an anti-proliferative effect of the vitamins E (Conte. 2004; Srivastava. 2006)

References:

• Abdulah, Rizky, et al. "Molecular targets of selenium in prostate cancer prevention (Review)." International journal of oncology 39.2 (2011): 301-309. 
• Andersson, Swen-Olof, et al. "Lifestyle factors and prostate cancer risk: a case-control study in Sweden." Cancer Epidemiology Biomarkers & Prevention 5.7 (1996): 509-513.
• Azrad, Maria, et al. "Flaxseed-derived enterolactone is inversely associated with tumor cell proliferation in men with localized prostate cancer." Journal of medicinal food 16.4 (2013): 357-360.
• Benitez, Dixan A., et al. "Mechanisms Involved in Resveratrol?Induced Apoptosis and Cell Cycle Arrest in Prostate Cancer—Derived Cell Lines." Journal of andrology 28.2 (2007): 282-293. 
• Chen, Rongxin, et al. "The significance of MMP-9 over MMP-2 in HCC invasiveness and recurrence of hepatocellular carcinoma after curative resection." Annals of surgical oncology 19.3 (2012): 375-384.
• Chiyomaru, Takeshi, et al. "Genistein up-regulates tumor suppressor microRNA-574-3p in prostate cancer." PloS one 8.3 (2013): e58929. 
• Conte, Carmela, et al. "??Tocotrienol Metabolism and Antiproliferative Effect in Prostate Cancer Cells." Annals of the New York Academy of Sciences 1031.1 (2004): 391-394.
• Donald, J. L. "Plasma metabolic profiling reveals age-dependency of systemic effects of green tea polyphenols in mice with and without prostate cancer." Molecular BioSystems 6.10 (2010): 1911-1916.
• Geybels, Milan S., et al. "Coffee and tea consumption in relation to prostate cancer prognosis." Cancer Causes & Control 24.11 (2013): 1947-1954. 
• Giovannucci, Edward. "Tomatoes, tomato-based products, lycopene, and cancer: review of the epidemiologic literature." Journal of the National Cancer Institute 91.4 (1999): 317-331.
• Guo H, Xu YM, Ye ZQ, Yu JH, Hu XY. "Curcumin induces cell cycle arrest and apoptosis of prostate cancer cells by regulating the expression of IkappaBalpha, c-Jun and androgen receptor." Pharmazie 68.6 (2013):431-4.
• Hurst, Rachel, et al. "Selenium and prostate cancer: systematic review and meta-analysis." The American journal of clinical nutrition 96.1 (2012): 111-122.
• Iguchi, Kazuhiro, et al. "Antiandrogenic activity of resveratrol analogs in prostate cancer LNCaP cells." Journal of andrology 33.6 (2012): 1208-1215. 
• Joseph, Michael A., et al. "Cruciferous vegetables, genetic polymorphisms in glutathione S-transferases M1 and T1, and prostate cancer risk." Nutrition and cancer 50.2 (2004): 206-213.
• Kai, Li, and Anait S. Levenson. "Combination of resveratrol and antiandrogen flutamide has synergistic effect on androgen receptor inhibition in prostate cancer cells." Anticancer research 31.10 (2011): 3323-3330.
• Kirsh, Victoria A., et al. "Prospective study of fruit and vegetable intake and risk of prostate cancer." Journal of the National Cancer Institute 99.15 (2007): 1200-1209.
• Klink, Joseph C., et al. "Resveratrol worsens survival in SCID mice with prostate cancer xenografts in a cell?line specific manner, through paradoxical effects on oncogenic pathways." The Prostate 73.7 (2013): 754-762.
• Kristal, Alan R., et al. "Baseline selenium status and effects of selenium and vitamin E supplementation on prostate cancer risk." Journal of the National Cancer Institute 106.3 (2014): djt456.
• Lu, Yu, et al. "Coffee consumption and prostate cancer risk: an updated meta-analysis." Cancer Causes & Control 25.5 (2014): 591-604. 
• Merkle, W. "Prostatakarzinomprophylaxe durch Nahrungsergänzungsmittel." Der Urologe (2014): 1-7.
• NCI (2013) Pomegranate: prostate cancer, nutrition and dietary supplements (PDQ). NCI, Bethesda. http://www.cancer.gov
• Ornish, Dean, et al. "Intensive lifestyle changes may affect the progression of prostate cancer." The Journal of urology 174.3 (2005): 1065-1070.
• Pantuck, Allan J., et al. "Phase II study of pomegranate juice for men with rising prostate-specific antigen following surgery or radiation for prostate cancer." Clinical Cancer Research 12.13 (2006): 4018-4026.
• Putnam, Shannon D., et al. "Lifestyle and anthropometric risk factors for prostate cancer in a cohort of Iowa men." Annals of epidemiology 10.6 (2000): 361-369.
• Stenner-Liewen, Frank, et al. "Daily Pomegranate Intake Has No Impact on PSA Levels in Patients with Advanced Prostate Cancer-Results of a Phase IIb Randomized Controlled Trial." Journal of Cancer 4.7 (2013): 597. 
• Srivastava, Janmejai K., and Sanjay Gupta. "Tocotrienol-rich fraction of palm oil induces cell cycle arrest and apoptosis selectively in human prostate cancer cells." Biochemical and biophysical research communications 346.2 (2006): 447-453.
• Tang, Yaxiong, et al. "Lycopene enhances docetaxels effect in castration-resistant prostate cancer associated with insulin-like growth factor I receptor levels." Neoplasia 13.2 (2011): 108-119. 
• Ting, Harold, Gagan Deep, and Rajesh Agarwal. "Molecular mechanisms of silibinin-mediated cancer chemoprevention with major emphasis on prostate cancer." The AAPS journal 15.3 (2013): 707-716. 
• Tokar, Erik J., and Mukta M. Webber. "Chemoprevention of prostate cancer by cholecalciferol (vitamin D3): 25-hydroxylase (CYP27A1) in human prostate epithelial cells." Clinical & experimental metastasis 22.3 (2005): 265-273.
• Verhoeven, Dorette T., et al. "Epidemiological studies on brassica vegetables and cancer risk." Cancer Epidemiology Biomarkers & Prevention 5.9 (1996): 733-748.
• Wilson, Kathryn M., et al. "Coffee and risk of prostate cancer incidence and mortality in the Cancer of the Prostate in Sweden Study." Cancer Causes & Control 24.8 (2013): 1575-1581.
• Woo, Tony Choon Seng, et al. "Pilot study: potential role of vitamin D (cholecalciferol) in patients with PSA relapse after definitive therapy." Nutrition and cancer 51.1 (2005): 32-36.

Eggs or Flakes? Not 30% vs. 25% protein! A brief reminder of the fact that the stuff you eat is still food.

I am not quite sure when or why this happened, but I know that more and more people are thinking in terms of "macros" instead of foods. What I do know, though, is that the recent publication of studies from the Pennington Biomedical Research Center at the Louisiana State University System (Bayham. 2014) and an ostensibly unrelated study that was conducted by researchers from the Alimentary Pharmabiotic Centre, Biosciences Institute in Cork and scientists working at the local university and the University of Pittsburgh School of Medicine (Patterson. 2014) confirms - once again (!) - how futile this ignorant approach to nutrition actually is.

Eggs vs. cereals - not the best example, but...

In that, I am well aware that the "battle" between an egg- and a cereal-based breakfast in the Patterson study is not exactly a good model of whats currently going on in the health and fitness community. With cereals being labeled as "the devil" (its always nice to be "anti", isnt it?), no one would after all consider having ...

• One-and-a-half cup of Special K® RTE cereal, 200 ml Silk® original soymilk, one slice of Natural Grain “Wheat n’ Fiber”® bread, 13 g of butter, and 10 g of sugar-free strawberry jam (CG)

... for breakfast. In view of the fact that the same can be said for the calorie- and mocronutrient matched "high quality protein" breakfast, i.e.

• Two scrambled eggs, 120 mL skim milk, two slices of Holsum® thin white  bread, 5 g of butter, and 18 g of Smuckers® strawberry jam

... I still believe that the consequences of "breaking the fast" (learn why I am calling breakfast thus in "Breakfast or Breaking the Fast" | read more) with eggs vs. Special K are still relevant to the previously introduced context. And if you know that the acetylated form of ghrelin and PYY are "satiety hormones", it does not take a rocket scientists to interpret the data in Figure 1.

Figure 1: Level(s) of "satiety hormones" after the different breakfasts (Bayham. 2014)

What is difficult to tell, though, is whether the increased satiety after the egg breakfast would actually lead to a reduced intake at the subsequent meal.

• On an individual basis, i.e. on just one of the two eating occasions, the higher levels of acetylated ghrelin and PYY did not suppress the 20 healthy overweight or obese subjects energy intake during the subsequent lunch
• For day 1 and day 7, together, on the other hand, the 64kcal the egg eaters consumed less than the cereal eaters did reach statistical significance.

If we throw overboard all the things we (believe) we know about the fallacy of calorie counting, this would translate into a ~448kcal difference for one week and a whopping difference of 23,360kcal for a year, which should shed ~3.3kg of body fat a year.
Whether or not similar concrete weight loss vs. gain effects can be achieved with different types of fat is nothing study #2 in todays science mash-up here at the SuppVersity could answer. What it can tell you though, is that protein and obviously carbohydrates, where even Mr. Average Joe thinks in terms of "low GI" = good and "high GI" = bad carbs, these days, is by no means the only food component, where unspecifically counting macros is not going to cut it (or get you cut, if thats what you want to achieve).

This is not just about fish oil

"Of course, the bad omega-6s" ... I know that this is what youre thinking right now, but lets be honest, isnt that a bit narrow-minded?  It sure is and still, the results Ellaine Petterson and her Irish and American colleagues present in their most recent paper demonstrate quite clearly that the ingestion of fish and flax seed oil has pretty unique effects that go beyond its ability to increase the tissue concentrations of DHA to levels way beyond what youd see in low fat or high fat diets with palm, olive or safflower oil powered high fat diets.
In addition it lead to an increase in the relative abundance of bifidobacteria, a gut tenant that has been linked to all sorts of beneficial health effects, but has recently been outshadowed by various strains of lactobacilli (0.95% vs. more than 2% in all other groups), which - and this is an important information - were the lowest in the rodents who were kept on diets with 45% of the energy from fish and flaxseed oils.

Whether or not, the negative effects of fish oil on the lactobacillacea count in the guts of the lab animals is also partly responsible for the more or less disappointing effects the fish and flax seed diet had on the body composition (Figure 2) of the wild-type C57BL/6J male mice (21 d old) in the study at hand is questionable.

Figure 2: Body composition analysis at the end of the study (Patterson. 2014)

Its not impossible, though. A brief glance at the insulin levels and leptin levels in Figure 3 reveals that neither of them looks anyway close to what someone whos religiously taking his fish oil caps on a daily basis would be expecting. In the end, it is thus not really that surprising that only the palm oil diet group ended up with an inferior lean-to-fat mass ratio of 1.17 (vs. 1.33 in the omega-3 group).

Figure 3: Changes (%) in relevant metabolic markers in response to the different diets (Patterson. 2014)

The results of the study at hand, i.e. the effects on body composition (Figure 2), as well as blood glucose and lipid metabolism (Figure 3) are thus clearly not in line with the ubiquitously placated message that "fish oil is good for you" - a message, the indoctrinated average supplement junkie will still discern from the abstract of the study:

"[...] Ingestion of the HF-flaxseed/fish oil diet for 16 weeks led to significantly increased tissue concentrations of EPA, docosapentaenoic acid and DHA compared with ingestion of all the other diets (P< 0·05); furthermore, the diet significantly increased the intestinal population of Bifidobacterium at the genus level compared with the LF-high-maize starch diet (P< 0·05). These data indicate that both the quantity and quality of fat have an impact on host physiology with further downstream alterations to the intestinal microbiota population, with a HF diet supplemented with flaxseed/fish oil positively shaping the host microbial ecosystem." (Petterson. 2014).

Neither the "loss" of lactobacilli, nor the - if anything - negative effects of the high omega-3 diet on the lean-to-fat-mass ratio and the amount of insulin thats floating around in the rodents blood are mentioned in said abstract.

Fat = Diabetes - A FAT Mistake?

If you go take a look at the actual study data, we are thus left with the question, whether the purported benefits of having high amounts of omega-3 fatty acids in our cells (see red info box a couple of paragraphs above) are real enough (or really enough - whatever you prefer) to discard the fact that the study at hand would actually suggest that olive and not fish + flaxseed oil should be your go-to source of dietary fat on a high fat diet.

Moreover, if we abandon any paradigmatic believes, we would even have to concede that - within the current context, i.e. a rodent study and a diet with protein contents of only 19.2% (low fat) and 23% (high fat), the low fat mix of 1.25% of palm, 1.25% olive, 1.25% safflower oil, 0.625% fish and 0.625% flaxseed oil the rodents in the starch and sucrose groups received is superior to any of the high fat variants.

You may say that this is "rodent shit" (and it is, because this is what the scientists analyzed to access the SFCA metabolism of the mice) and a mere coincidence, but wouldnt you agree that this oil mix looks a little too much like the mixture youd get on a low-to-moderate fat diet with olive oil as a staple for everything, where you add oils, palm and safflower oil from processed foods on your cheat days and fish oil / omega-3s from your once or twice a week serving of salmon... ?
References: 

• Bayham, Brooke E., et al. "A Randomized Trial to Manipulate the Quality Instead of Quantity of Dietary Proteins to Influence the Markers of Satiety." Journal of Diabetes and its Complications (2014).
• Filaire, Edith, et al. "Effect of 6 Weeks of n-3 fatty-acid supplementation on oxidative stress in Judo athletes." International journal of sport nutrition 20.6 (2010): 496.
• Danthiir, Vanessa, et al. "Cognitive Performance in Older Adults Is Inversely Associated with Fish Consumption but Not Erythrocyte Membrane n–3 Fatty Acids." The Journal of nutrition (2014): jn-113.
• Patterson, E., et al. "Impact of dietary fatty acids on metabolic activity and host intestinal microbiota composition in C57BL/6J mice." The British journal of nutrition (2014): 1-13.