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Omega-3s: “The Triple Threat” or “The Dynamic Duo”?

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The popularity of the essential polyunsaturated omega-3 fatty acids (O3FA) is on the rise. In 2017, O3FA achieved a spot on the top 20 foods and ingredients list that Americans are adding to their diets (The Hartman Group). In addition, the global fish oil market is expected to reach a whopping 4.08 billion dollars in the next four years!  The proposed health benefits are likely the driving force behind the increasing demand.

Despite their booming popularity, a large percentage of adults are not meeting the O3FA recommended intake. There are three primary O3FAs with distinct characteristics: alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Although commonly grouped under the umbrella term O3FAs, are all O3FAs created equal?

Unique Characteristics of O3FAs

Omega-3 fatty acids cannot be sufficiently produced in the body earning them the title of “essential fatty acids.” The plant-derived omega-3, ALA, is the parent precursor to EPA and DHA. Unfortunately, the conversion rate in our bodies is very low.  It is important to realize that in the process of metabolizing ALA to EPA and DHA, a series of anti-inflammatory markers are produced (leukotrienes, prostaglandins and thromboxane). As these anti-inflammatory metabolites are beneficial, direct EPA and DHA consumption is needed to meet bodily requirements.

Independent and Complementary Health Benefits

The majority of current research focuses on the health benefits of marine fatty acids.  DHA and EPA consumption portray an array of shared and complementary benefits related to the treatment of cardiovascular disease, depression diabetes, sleep disorders and more. DHA is more significantly associated with decreases in resting heart rate, blood pressure and with improvements in cellular membrane health due to its additional double bond and longer carbon chain. Increased cellular levels of EPA have been shown to benefit coronary heart disease, hypertension and to decrease inflammation. EPA and DHA are both associated with reduced gene expression related to fatty acid metabolism, reduced inflammation and oxidative stress.

Specific supplementation of ALA is not consistently associated with cardiovascular health. Although plant-derived ALA can be easily substituted in for excess omega-6 fatty acids (O6FAs). Research has shown that by reducing the O3FA:O6FA ratio, you can decrease bodily inflammation, increase anti-inflammatory markers and more efficiently utilize EPA and DHA.

An ALA, EPA and DHA-Rich Diet

The 2015-2020 Dietary Guidelines for Americans recommends that healthy adults consume at least 8 ounces of a variety of non-fried fatty seafood per week. For EPA and DHA requirements, the American Heart Association recommends fatty marine sources containing 500 mg or more of EPA and DHA per 3oz cooked serving (e.g., salmon and tuna).   ALA is the most commonly consumed O3FA in the Western diet as it is found in plant-based foods (e.g., dark green leafy vegetables, walnuts, canola oil, flax seed). Unlike EPA and DHA, an Adequate Intake (AI) level is established at 1.6 g/day and 1.1 g/day for men and women respectively.

The Final Verdict 

The wide range of benefits stemming from marine O3FAs indicates the importance of regular consumption of fatty seafood and EPA and DHA-containing products.  The incorporation of plant-derived ALA may serve more importantly as a substitute for omega-6 fatty acids to reduce bodily inflammation, decrease the high O3FA:O6FA ratio typically observed in the Western diet, and to help elevate EPA and DHA levels in the body. EPA and DHA may be featured as the health promoting “dynamic duo,” but ALA is still invited to the party!

 

References

1.         Yanni Papanikolaou JB, Carroll Reider and Victor L Fulgoni. U.S. adults are not meeting recommended levels for fish and omega-3 fatty acid intake: results of an analysis using observational data from NHANES 2003–2008. Nutrition Journal 2014.

2.         Harris WS, Mozaffarian D, Lefevre M, Toner CD, Colombo J, Cunnane SC, Holden JM, Klurfeld DM, Morris MC, Whelan J. Towards establishing dietary reference intakes for eicosapentaenoic and docosahexaenoic acids. J Nutr 2009;139(4):804S-19S. doi: 10.3945/jn.108.101329.

3.         Frits A. J. Muskiet MRF, Anne Schaafsma, E. Rudy Boersma and Michael A. Crawford. Is Docosahexaenoic Acid (DHA) Essential? Lessons from DHA Status Regulation, Our Ancient Diet, Epidemiology and Randomized Controlled Trials. Journal of nutrition 2004;134.

4.         Mozaffarian D, Wu JH. (n-3) fatty acids and cardiovascular health: are effects of EPA and DHA shared or complementary? J Nutr 2012;142(3):614S-25S. doi: 10.3945/jn.111.149633.

5.         Bork CS, Veno SK, Lundbye-Christensen S, Jakobsen MU, Tjonneland A, Schmidt EB, Overvad K. Dietary Intake of Alpha-Linolenic Acid Is Not Appreciably Associated with the Risk of Ischemic Stroke among Middle-Aged Danish Men and Women. J Nutr 2018. doi: 10.1093/jn/nxy056.

6.         Evangeline Mantzioris MJJ, Robert A Gibson and Leslie G Cleland Differences exist in the relationships between dietary linoleic and alpha-linolenic acids and their respective long-chain metabolites. Am J Clin Nutr 1995;61:320-4.

7.         Agriculture. USDoHaHSaUSDo. 2015 – 2020 Dietary Guidelines for Americans. 8th Edition. December 2015.

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Sarah Purcell
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How can we implement better health behaviors in cancer survivors?

Lifestyle interventions targeted at obtaining/maintaining a healthy body weight and/or incorporating physical activity and healthy eating habits have great potential in improving outcomes in cancer survivors. Cancer diagnosis is a “teachable moment” wherein many patients are highly motivated to make changes (1). Furthermore, a balanced diet and moderate exercise can improve prognosis, quality of life, physical function, and survival across the cancer continuum. As such, groups such as the Amercian Cancer Society, National Comprehensive Cancer Network and the American College of Sports Medicine have released lifestyle guidelines for cancer survivors.

However, implementing changes in individuals and healthcare systems is challenging, to say the least. This is a recent topic covered by Karen Basen-Engquist and a number of colleagues as part of a special Issue of Obesity (Transdisciplinary Research on Energetics and Cancer)(2). Their article provides a 6-point agenda for translating research into clinical and community action, as follows:

  1. Increase the availability of different types of activities for weight management, nutrition counseling, and physical activity. One size will never fit all when it comes to improving health. Individual goals/preference, resources, and logistics all come into play, and cancer-specific programs may be needed.
  2. Improve screening and referral to lifestyle interventions. A system for evaluating and triaging patients for health programs should be developed. Importantly, an individual’s physical status, health needs, and goals should be considered.
  3. Improve the health care provider’s ability to screen, assess, and refer survivors for lifestyle programs. Oncology providers have a powerful role in helping cancer survivors; however, they often do not feel confident in screening, giving advice, or administering recommendations for lifestyle-related constructs. Implementation of processes such as the 5As (Ask, Advise, Assess, Assist, Arrange), which has been successful in tobacco cessation (3) and obesity management (4) might prove beneficial.
  4. Expand the support of oncology-specific professional training and certification. Professional organizations of dietitians, exercise professionals, psychiatrists, and physical therapists have additional certification programs for oncology or are working on developing one for its members. However, professionals with specific expertise in oncology are still greatly needed to address the unique needs of this population.
  5. Expand dissemination and implementation research. Many research programs do not address how a program could be implemented in a real-world setting (external validity). Dissemination of research findings with consideration of the sustainability and generalizability of programs is essential for broader impact.
  6. Advocate for health care policies that support lifestyle services for cancer survivors. Coverage for health programs is highly variable and often has barriers such as large co-payments, no coverage in grandfathered plans, and cost sharing. A potential solution could be incentivizing nutrition and exercise services, although more research is needed to determine the effectiveness of such actions.

As the authors eloquently articulate, the time has come to enable research into action for optimal healthcare in all cancer survivors.

References:

  1. Demark-Wahnefried W, Aziz NM, Rowland JH, Pinto BM. Riding the crest of the teachable moment: promoting long-term health after the diagnosis of cancer. J Clin Oncol 2005;23:5814–30.
  2. Basen-Engquist K, Alfano CM, Maitin-Shepard M, Thomas CA, Schmitz KH, Pinto BM, et al. Agenda for Translating Physical Activity, Nutrition,and Weight Management Interventions for Cancer Survivors into Clinical and Community Practice. Obesity 2017; 25, S9-S22.
  3. Siu AL, Force USPST. Behavioral and pharmacotherapy interventions for tobacco smoking cessation in adults, including pregnant women: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2015;163:622-634.
  4. Rueda-Clausen CF, Benterud E, Bond T, Olszowka R, Vallis MT, Sharma AM. Effect of implementing the 5As of Obesity Management framework on provider-patient interactions in primary care. Clin Obes 2013; 4, 39-44.

 

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Colby Vorland
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Alkaline Diets and Kidney Disease

Many dangerous fad diets exist that purport to treat diseases such as cancer by manipulating the pH of blood with different foods. While there is no good evidence that acidic foods alter the body’s pH and promote disease, the hypothesis that “dietary acid load” relates to disease should not be completely dismissed. The kidney serves to regulate blood pH, but if kidney function declines and other tissues catabolize to maintain pH, then it is very plausible that manipulating the diet to reduce the acid load could spare tissues and improve outcomes in chronic kidney disease (CKD). After all, for example, the metabolism of amino acids yields hydrogen ions, whereas fruits and vegetables contain organic salts that generally reduce acid load when metabolized. Recently, a growing number of human studies that manipulate diet acid load using fruits and vegetables and sodium bicarbonate support this hypothesis. Let’s take a look at some of them.

The first randomized controlled trial on bicarbonate supplementation and CKD progression was published in 2009 by de Brito-Ashurst and colleagues. Bicarbonate is produced by the kidneys and serves to neutralize acid. Supplementation of bicarbonate for 1 year in CKD patients slowed the progression of kidney disease as suggested by creatinine clearance and reduced the need for dialysis. The next year, in 2010, a 5-year trial was published by Donald Wesson’s group that found a slowed kidney decline as measured by estimated glomerular filtration rate (eGFR) with bicarbonate supplementation. Several subsequent studies by his group have used bicarbonate or fruits and vegetables to achieve beneficial outcomes. Goraya et al. gave oral bicarbonate or enough fruits and vegetables that were estimated to reduce dietary acid load by 50% to CKD patients for 30 days and also observed a slowed reduction in eGFR in patients at moderate, but not mild, stages of the disease. In patients with more advanced stages of CKD, one year of bicarbonate or fruits and vegetables did not slow the decrease in eGFR, though several urinary markers of kidney injury were reduced. Their most recent trial tested if kidney function might be preserved through a reduction in angiotensin II in moderate stage CKD patients. Three years of bicarbonate or increased fruits and vegetables lessened the decline in eGFR and resulted in a corresponding decrease in the marker angiotensin II. Other studies using bicarbonate from six months to two years have provided strong evidence that reducing acid load consistently slows the decline of eGFR, and improves markers of bone health and muscle function.

Each of the studies described provided fruits and vegetables to patients free of charge to increase adherence. It will be important to test if adherence can be maintained through education alone. Additionally, it may be that “prescribing” fruits and vegetables is effective at improving outcomes and reducing health care costs more so than bicarbonate since they also reduce blood pressure. While “alkaline diets” in general should be viewed skeptically, there is accumulating evidence that fruits and vegetables as dietary alkali do indeed help in kidney disease.

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Sarah Purcell
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Multimodal interventions: Combining nutrition with exercise in clinical populations

nutrition and exercise

Nutrition provides the building blocks our body needs, including energy to move for physical activity and metabolic adaptations that occur after exercise. Similarly, those who are physically active are more likely to eat a healthier diet [1]. As an athlete, it’s easy to see this reciprocal relationship; but can we simultaneously administer physical activity and nutrition interventions in populations that are not athletes? More specifically, can we use these modalities together in clinical populations?

The answer is yes. Multimodal interventions constitute two or more modalities aimed at improving outcomes. While these types of interventions do not necessarily have to include nutrition and exercise, this approach is highly effective, especially when the goal outcome is increasing or maintaining muscle. Exercise has anabolic and anti-catabolic effects, but a net protein balance occurs only when sufficient energy and protein is consumed after exercise [2]. The theoretical rationale for using these interventions in clinical populations is that many patients have systemic inflammation, insulin resistance, and muscular disuse – all of which can be ameliorated through physical activity and nutritional strategies (especially those with high calories and protein). Indeed, studies in older individuals, individuals who are obese or have HIV/AIDs or chronic obstructive pulmonary disease, and healthy adults undergoing prolonged bedrest show that while nutrition supplementation might promote muscle anabolism and strength, adding exercise is even more effective [3].

Clearly, clinical populations have diverse nutrition needs, functional limitations, and disease status that might impact the feasibility and efficacy of such integrative interventions. Inclusion criteria must be carefully selected in order to observe any statistical impact. For example, in critically ill patients, there is a possibility that inclusion of “severely ill” individuals might make statistical or clinical impact impossible to detect, since these patients experience such high mortality because of their condition. Conversely, if a patient’s hospital stay is short (i.e. <4 days), then muscle atrophy might not develop, again negating the benefits of an intervention [3]. Like a clinical trial in any population, the primary outcome must be carefully selected, the intervention should be clear and feasible, and statistical tests must be robust.

Interventions like the MENAC trial are implementing nutrition, exercise, and anti-inflammatory interventions in individuals with cancer cachexia, a population that is likely to lose muscle and have significant nutrition impact symptoms. In the pilot phase II study, patients on the intervention arm gained weight while the control group lost weight (p<0.001); there was also a trend indicating the control arm might have lost more muscle [4]. The phase III trial is currently underway in multiple sites across Europe, Canada, and Australia.

Dietitians will play a crucial role in these trials by working with patients and colleagues in other fields to design and implement optimal nutrition throughout the disease trajectory. Future research should highlight the role of the dietitian and elucidate the ideal amount and quality of nutrition to recommend, the mechanisms and outcomes of such interventions, and the patient experience.

References:
1. Loprinzi PD, Smit W, Mahoney S. Physical Activity and Dietary Behavior in US Adults and Their Combined Influence on Health. Mayo Clin Proc. 2014 Feb;89(2):190-8.
2. Poole C, Willborn C, Taylor L, Kerksick C. The role of post-exercise nutrient administration on muscle protein synthesis and glycogen synthesis. J Sports Sci Med. 2010 Sep 1;9(3):354-63
3. Heyland DK, Stapleton RD, Mourtzakis M, Hough CL, Morris P, Deutz NE, Colantuoni E, Day A, Prado CM, Needham DM. Combining nutrition and exercise to optimize survival and recovery from critical illness: Conceptual and methodological issues. Clin Nutr. 2016 Oct;35(5):1196-206.
4. Kaasa S, Solheim T, Laird BJA, Balstad T, Stene G, Bye A, Fallon MT, Fayers P, Kearon K. A randomised, open-label trial of a multimodal intervention (exercise, nutrition, and anti-inflammatory medication) plus standard of cares versus standard of care alone to prevent/attenuate cachexia in advanced cancer patients undergoing chemotherapy. J Clin Oncol. 2015; 33(suppl; abstr 9628)

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Revisiting Fiber and Colorectal Cancer

By Kevin Klatt

Colorectal cancers are the third most common worldwide, and represent one of the major areas of prevention research. Rates of these cancers increase with industrialization, and are uncommon in Africa and much of Asia. A number of potential nutritional targets have been posited, based on preclinical and epidemiological data; however, these remain controversial. The American Institute of Cancer Research’s 2011 report (1) on Colorectal Cancer states that there is convincing evidence that foods high in fiber decrease risk and red and processed meats increase risk of colon cancer. However, there are few controlled feeding studies in humans have corroborated these associations; indeed, a large body of literature (2-7) focusing on dietary fiber supplementation back in the late 90’s and early 2000’s did not show any support for any positive effects of high fiber/low-fat diets on recurrent adenomas . However, these studies can/have been criticized for: 1. not being long enough 2. fail to capture of a window of true prevention (as subjects already had adenomas) 3. The dose/type of fiber. Since these trials, considerable experimental data (8,9) has been generated to suggest that the type of fiber, its dose, and the type/amount of short chain fatty acid fermentation products likely add some complexity to the inconsistent epidemiological associations between fiber intake and colorectal cancer risk.

A recent study published in Nature Communications (10) provides a novel perspective on this contentious topic of high-fiber diets and colon. The study employed a food-based dietary intervention in 2 populations: African Americans and rural South Africans (a sensible population to study given Burkitt’s original observations that rural Africans are nearly free of large bowel diseases). Twenty healthy, middle-aged African Americans and 20 rural Africans were first examine in their home environments for 2 weeks, to examine their normal food intake, before being housed in their respective research facilities for the 2 weeks of the dietary intervention (to ensure compliance). African Americans were given the ‘African style’ diet that was low in fat (16% kcals) and high in fiber (55g/day). Participants from Africa were given a western style diet that was higher in fat (52% kcals) and lower in fiber (12g/day). Notably, the high fiber diet was achieved using HiMaize, a purified resistant starch product. The authors look at outcomes related to mucosal epithelial cell proliferation (Ki67 staining) and markers of inflammation (CD3+ intraepithelial lymphocyte and CD68+ lamina propria macrophage staining), to examine the effect of diet on predicted neoplastic change and increased risk of colon cancer. They further look at alterations in microbial composition, highlighting changes in microbes with the baiCD gene, responsible for the deconjugation of bile acids and production of their carcinogenic, secondary metabolites. Their results quite nicely show that the high fiber intervention alters biomarkers in directions that suggest a protective effect against colorectal cancer, while also finding some interesting nuances related to amino acid and choline metabolism.

While providing encouraging results for the role of nutrition in colorectal cancer development, the study leaves us with more hypotheses to test, and a renewed interest in the way in which fiber and its fermentative products might act to buffer against colorectal cancer. Without hard clinical outcomes, it’s difficult to get too excited about the results in light of the multiple fiber interventions that have failed in the past. The biomarkers chosen are not without their scrutiny, as it has been noted that decreases in apoptosis rather than increased cell proliferation better predict tumorigenesis in animal models of colorectal cancer (11). Regardless of one’s enthusiasm about biomarker changes over 2 weeks, it does force us to critically think about previous study designs that have cast doubt on fiber’s role in colon cancer. The authors in this current study employ highly butyrogenic starches, at doses not tested in the trials that have failed before. There is consistent molecular evidence that butyrate works in a paradoxical manner, both stimulating cell proliferation at low concentrations and inhibiting it at high (12), leaving open the possibility that the previous doses of fiber were too low to see a beneficial effect.

Given the Western diets low concentrations of dietary fiber, particularly resistant starches (13), as well as the increased enthusiasm to fortify the food supply with added fibers, further research examining the role of particular fibers, their appropriate doses, and their relationship to clinical outcomes appear warranted. The type 2 resistant starch utilized in this study is uncommon in the food supply, coming largely from raw potatoes, unripe bananas, and some legumes and represents a potential area for food technologists to significantly alter the food supply for better health (14).

References
1. http://www.aicr.org/continuous-update-project/colorectal-cancer.html
2. http://www.ncbi.nlm.nih.gov/pubmed/11073017
3. http://www.ncbi.nlm.nih.gov/pubmed/10770979
4. http://www.ncbi.nlm.nih.gov/pubmed/10770980
5. http://www.ncbi.nlm.nih.gov/pubmed/7730878
6. http://www.ncbi.nlm.nih.gov/pubmed/7473832
7. http://www.nejm.org/doi/pdf/10.1056/NEJM199901213400301
8. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3926973/
9. http://www.ncbi.nlm.nih.gov/pubmed/20937167
10. http://www.nature.com/ncomms/2015/150428/ncomms7342/full/ncomms7342.html
11. http://carcin.oxfordjournals.org/content/18/4/721.abstract
12. http://jn.nutrition.org/content/134/2/479.full
13. http://linkinghub.elsevier.com/retrieve/pii/S0002-8223(07)01932-3
14. http://advances.nutrition.org/content/4/3/351S.full

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Nutrition Superstition – How Your Grandma’s Tales Could Actually Be True

By Brett Loman

Nutrition may be a relatively young science, but perhaps the intuition of our elders has informed us more than we realize. Food superstitions are as old as culture itself and essentially every civilization has added its share to the ever-growing list of dos and don’ts. In respect to two months in a row with Friday the 13ths this year, I investigated how some long-standing tales about what we eat might actually be grounded in truth.

Spilling salt brings bad luck. This widely recognized superstition originating in ancient Greece may hold some hidden truths. One of the most commonly believed concepts about sodium (salt) today is that eating too much can aggravate conditions such as hypertension, cardiovascular disease, and chronic kidney disease. The American Heart Association and National Kidney Foundation recommend limiting salt consumption to about 1,500 mg/d. So whether you believe the superstition or modern medicine, you will think twice and shake the habit of spilling salt onto your meal.

Eating garlic, onions, and mustard seeds is good luck by granting blessings or warding off evil. This superstition is rooted in many proverbs, and it just so happens that vegetables in the Amaryllis (onions, garlic, etc) and Brassicaceae (mustard, broccoli, etc) families are being investigated as anticarcinogens. Many of the naturally occurring phytochemicals in these plants may serve to halt the formation of cancer causing compounds, enhance repair of damaged DNA, and induce apoptosis of tumor cells. Chowing down on these luckily talismans could ward off disease, but don’t forget that those same beneficial compounds may also scare off your friends with the odors they leave lingering behind.

Bringing bananas on a boat will cause fishermen ill will and a bad catch. Green bananas, coincidentally, may just cause some unwanted symptoms of illness. Un-ripened bananas are a good source of resistant starch. Depending on your personal disposition, fermentation of resistant starch could either provide a healthy dose of short-chain fatty acids to the intestines, or a healthy dose of gas and diarrhea. Any angler would have difficulty landing the big one between frequent trips to the loo, and that’s no fish tale.

Planting parsley will help a woman become pregnant. Of course having good nutrition is important for increasing chances of beginning a pregnancy, but parsley is specifically of interest for the health of the newly developing fetus. This ubiquitous herb is a good source of many vitamins and minerals, including folic acid. In the first few weeks, adequate folate is especially important for preventing neural tube defects in the rapidly growing baby. Consider sowing seeds of parsley before sowing your wild oats.

Every day we find out more and more about how our eating habits affect our bodies, but in some cases we shouldn’t overlook what prior generations have already provided us. Tell the researchers and your grandma thanks for the advice.

References
1. Cobb, L.K., Anderson, C.A.M., Elliott, P., et al. Methodological issues in cohort studies that relate sodium intake to cardiovascular disease outcomes: A science advisory from the American Heart Association (2014) Circulation, 129 (10), pp. 1173-1186. http://www.scopus.com/inward/record.url?eid=2-s2.0-84895928005&partnerID=40&md5=75ecd90a4f86d73a8c200d300b4ca6c8
2. https://www.heart.org/HEARTORG/GettingHealthy/NutritionCenter/HealthyEating/About-Sodium-Salt_UCM_463416_Article.jsp
3. https://www.kidney.org/atoz/content/sodiumckd
4. http://www.cancer.gov/cancertopics/factsheet/prevention/garlic-and-cancer-prevention#r18
5. http://www.cancer.org/treatment/treatmentsandsideeffects/complementaryandalternativemedicine/dietandnutrition/broccoli
6. http://digestivehealthinstitute.org/2013/05/10/resistant-starch-friend-or-foe/
7. http://ndb.nal.usda.gov/ndb/foods/show/3080?fg=&man=&lfacet=&format=&count=&max=25&offset=&sort=&qlookup=parsley
8. http://www.cdc.gov/features/folicacidbenefits/

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