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Walnuts, cacao and beans, 3 superfoods that are super only in super-high quantities.

Today's waredownloadsoft Food Science Research Update is all about three so-called "superfoods". It's an article from which you cannot just learn that walnuts, beans and cacao are "superfoods" as they protect you from cancer, improve your gut health and ameliorate diabetes.

It's yet also an article that puts the (rodent) science into perspective. A perspective you won't see taken very often, because it has the "superfoods" look much less "super" than they appear to be without a reality check.

• Dietary walnut suppression of colorectal cancer in mice: Mediation by miRNA patterns and fatty acid incorporation - As a waredownloadsoft reader you are well aware of the beneficial health effects of regular walnut consumption. As far as the mechanisms are concerned, many of you may have speculated that it is related to omega-3s, but do walnuts even have enough omega-3s to make a difference? A recent study from the Beth Israel Deaconess Medical Center at the Harvard Medical School (Tsoukas. 2015) seems to have found the answer is "yes", but it takes some serious walnut eating.
  
  To investigate the protective effects of a high walnut diet, the scientists injected rodents with HT-29 colon cancer cells. 7 days after the injection, the mice were randomized to either control or walnut diets for 25 days of diet treatment. After the study period, thirty samples of tumor and of omental adipose were analyzed to determine changes in lipid composition in each dietary group in response to diets containing either no or 10% (of weight) walnuts.
  

  Figure 1: Gas chromatography analysis of fatty acids in colorectal tumors (left) and omental adipose tissue (right) in 30 mouse samples (Tsoukas. 2015). *P<.05.

  In the tumors of the walnut-containing diet, the scientists found significant increases in α-linolenic, eicosapentaenoic, docosahexaenoic and total omega-3 acids, and a decrease in arachidonic acid, as compared to the control diet.
• More importantly, however, the final tumor size measured at sacrifice was negatively associated with percentage of total omega-3 fatty acid composition (r=−0.641, P=.001). MicroRNA expression analysis of colorectal tumor tissue revealed decreased expression of miRNAs 1903, 467c and 3068 (P<.05) and increased expression of miRNA 297a* (P=.0059) in the walnut-treated group as compared to control diet... and YES! This is the epigenetic "magic" everyone is talking about.
• Beans are SFCA-precursors and colon protectors - Short-chain fatty acids are all the rage these days. SFCAs are the fatty acids that are produced by our bacterial subtenants when we eat resistant starches.
  
  Beans are an excellent source of resistant starches and, according to a recent study from the Agriculture and Agri-Food Canada (Monk. 2015), both cooked white (WK) or dark red kidney (DK) bean flour can, when it is added at 20% to a rodent diet  for 3 weeks, can protect rodents from the pro-colitic assault of dextran sodium sulfate.
  

  Figure 1: Effect of kidney bean diets on (A) SCFA concentrations, (B) cecum size and (C) colon histomorphology in healthy mice + representative images (40×) of  stained colon sections stained highlighting the increased crypt height in the bean-fed mice are shown (scale bar=50μm | Monk. 2015).

  Not only did the "bean preload" (a) reduce the disease severity. It did also ameliorate (b) the colonic histological damage and (c) increase the mRNA expression of antimicrobial and barrier integrity-promoting genes (Toll-like Receptor 4 (TLR4), MUC1–3, Relmβ and Trefoil Factor 3 (TFF3)) and reduce proinflammatory mediator expression [interleukin (IL)-1β, IL-6, interferon (IFN)γ, tumor necrosis factor (TNF)α and monocyte chemoattractant protein-1], which correlated with reduced colon tissue protein levels.
  
  In conjunction with their beneficial effects on IL-17A, IFNγ, TNFα, IL-1β and IL-6, there's little doubt that bean floor can enhance the microbial-derived SCFA metabolite production, gut barrier integrity and the microbial defensive response in the healthy colon, this making it more resilient to artificial and natural assaults.
• Cocoa-rich diet ameliorates hepatic insulin resistance by modulating insulin signaling and glucose homeostasis in Zucker diabetic fatty rats  - While the latest "eat chocolate to lose weigh" paper has been busted, findings of a recent study from the Ciudad Universitaria suggest that cocoa, not chocolate, has the potential to alleviate both hyperglycemia and hepatic insulin resistance in type 2 diabetics - in rats, it already works (Cordero-Herrera. 2015).
  
  In the study, male Zucker diabetic fatty (ZDF) rats which are a common model for "lifestyle" diabetes were fed a control or cocoa-rich diet (10%), and Zucker lean animals received the control diet. ZDF rats supplemented with cocoa (ZDF-Co) showed a significant decrease in body weight gain, glucose and insulin levels, as well as an improved glucose tolerance and insulin resistance.
  

  Figure 1: Effect of the cocoa-rich diet on glucose tolerance and insulin resistance in ZDF rats. (A) Time-course changes in the basal level and after glucose loading (1 g/kg) of blood glucose. (B) AUC calculated from GTT data. (C) Time-course changes in the basal level and after glucose loading (1 g/kg) of serum insulin. Each point represents the mean±S.D. from 8 determinations. (D) HOMA-IR was determined as described in Materials and Methods (p < 0.05 | Cordero-Herrera. 2015).

  The cocoa-rich diet also ameliorated the hepatic insulin resistance by abolishing the increased serine-phosphorylated levels of the insulin receptor substrate 1 and preventing the inactivation of the glycogen synthase kinase 3/glycogen synthase pathway in the liver of cocoa-fed ZDF rats - or put simply, it kept the glycogen storage (and thus another way to store glucose and normalize the blood glucose levels) in the liver intact.
  
  The authors believe that this anti-hyperglycemic effect of cocoa must at least partly be mediated through the decreased levels of hepatic phosphoenolpyruvate carboxykinase which will have the liver pump out more glucose (made mostly from amino acids) although the glucose levels in the blood are already in the red zone while increasing the values of the previously mentioned glucokinase and glucose transporter 2 in the liver which will allow cacao aficionados to store the superfluous glucose as glycogen, not fat. The additional suppression of the c-Jun N-terminal kinase and p38 activation which is usually elevated in response to insulin resistance may also protect you against cancer.

I guess if someone finally dared to do this study, there would be a linear or exponential association between the number of processing steps red meat has undergone and the increase in cancer risk from regular consumption. Stay away from cheap bacon, sausages & co.

The potential relationship between red meat consumption and colorectal cancer (CRC) has been the subject of scientific debate. In fact, you will remember that I have addressed the issue repeatedly and in various articles. If you read all or at least some of the articles you will also be aware of the fact that the evidence against red meat is of observational nature and has a high degree of resulting uncertainty.

Dominik D. Alexander's and his colleagues's objective was thus to conduct a systematic quantitative assessment of the epidemiologic literature. Specifically, they updated and expanded their previous meta-analysis by integrating data from new prospective cohort studies and conducting a broader evaluation of the relative risk estimates by specific intake categories.
Data from 27 independent prospective cohort studies were meta-analyzed using random-effects models, and sources of potential heterogeneity were examined through subgroup and sensitivity analyses. In addition, a comprehensive evaluation of potential dose-response patterns was conducted.

Table 1: Meta-analysis of prospective studies of red meat consumption and colorectal cancer (Alexander. 2015)

In the meta-analysis of all cohorts, a weakly elevated summary relative risk was observed (1.11, 95% CI: 1.03–1.19); however, statistically significant heterogeneity was present. Furthermore

However, in the model that included studies of fresh red meat (n D 17 studies independent of processed meat items), the SRRE dropped to 1.05 and was no longer statistically significant (95% CI: 0.98–1.12), and the model was less heterogeneous (p-H D 0.328). Of 13 of these studies that explicitly defined red meat, the SRRE was 1.04 (95% CI: 0.98–1.14, p-H D 0.263). [...] Stronger (and more heterogeneous) associations were observed in meta-analyses of studies conducted in North America (SRRE D 1.18, 95% CI: 1.05–1.32), compared with studies published in other countries (SRRE D 1.07, 95% CI: 0.98–1.16). The model of studies conducted in China and Japan had the weakest SRRE (1.01, 95% CI: 0.92–1.12; Chen et al. and Khan et al. excluded). Interestingly, the summary associations were modified by publication date, with the SRREs becoming monotonically weaker over time. For example, meta-analysis of 8 studies published prior to the year 2000 resulted in an SRRE of 1.30 (95% CI: 1.06–1.59), while the SRRE for the studies published in the past 5 years was 1.09 (95% CI: 0.98–1.21)" (Alexander. 2015).

So, if sub-analysis using models that looked for the isolated effects of fresh red meat (from processed meat), adjusted for more relevant factors, analyzed women only, and were conducted in countries outside of the United States showed once again that the allegedly "deadly" association between "red meat" and cancer is in fact one between the bacon, burger and overall junkfood laden diet the average American still considers "food", what's the conclusion then? Right, it's the same conclusion researchers have drawn based on the 2007 World Cancer Research Fund Report:

"One of the 10 universal guidelines for healthy nutrition in a report of the World Cancer Research Fund released at the end of 2007 is to “limit intake of red meat and avoid processed meat”, as a result of the “convincing evidence” for an association with an increased risk of colorectal cancer development" (Demeyer. 2008). 

In addition Daniël Demeyer, Karl Honikel, and Stefaan De Smet rightly demand that the food industry takes steps to develop "improved processed meats using new ingredients" by omitting or lowering the use of nitrite and nitrate (a real problem for bacon and sausages), reducing the exuberant salt content and taking measures to inhibit the damaging nitros(yl)ation reactions by haem and nitrite/nitrate present in the digestive tract and of the ensuing carcinogenic effects.

Table 2: Relative risk (RR)* of colorectal cancer in relation to animal food cooking method | all number > 1.00 indicate an increased risk, all number < 1.00 indicate a decreased risk (Lee. 2005).

In the end, all the efforts of the industry will yet be in vain, if you keep buying high nitrite bacon, and deep frying previously benign fresh meats to turn them into colorectal and cancer promoting agents (Lee. 2009 | note: Stir-fried meats are not associated with increased cancer risk in the same study).
References:

• Alexander, Dominik D., et al. "Red Meat and Colorectal Cancer: A Quantitative Update on the State of the Epidemiologic Science." Journal of the American College of Nutrition ahead-of-print (2015): 1-23.
• Chen, Kun, et al. "Nested case-control study on the risk factors of colorectal cancer." World Journal of Gastroenterology 9.1 (2003): 99-103.
• Demeyer, Daniël, Karl Honikel, and Stefaan De Smet. "The World Cancer Research Fund report 2007: A challenge for the meat processing industry." Meat science 80.4 (2008): 953-959.
• Khan, M. M. H., et al. "Dietary habits and cancer mortality among middle aged and older Japanese living in hokkaido, Japan by cancer sites and sex." Asian Pacific Journal of Cancer Prevention 5.1 (2004): 58-65.
• Lee, Sang-Ah, et al. "Animal origin foods and colorectal cancer risk: a report from the Shanghai Women's Health Study." Nutrition and cancer 61.2 (2009): 194-205.