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.

By Mary Scourboutakos

Living in Canada, I was never worried about recombinant bovine somatotropin hormone, aka rBST. This synthetic hormone, which mimics a natural hormone that causes cows to produce more milk, was banned in Canada in the 1990s. So North of the 49th parallel, most people have never heard of it.

Meanwhile in the United States, the situation is a little different. rBST is legal in the US because technically, there’s no evidence that it causes harm to humans. Meanwhile in Canada, the rationale for its ban is that it may pose risks for the cows that are treated with it.

With that in mind, whenever I visit the US, I always explore the milk on grocery store shelves to see if it contains rBST. To my surprise, on nearly every occasion, I’ve been hard pressed to find a jug of milk that didn’t say “from cows not treated with rBST”.

This was reassuring. But then I noticed something…while every jug of milk said “no rBST” I couldn’t find a single block of cheese, or container of yogurt declaring this.

This got me thinking…are they using the rBST-treated milk in yogurt and cheese? Could it be that consumers are so far removed from the food chain that they would think to look for “no rBST” on their milk, but wouldn’t think to look for it on their cheese?

It didn’t make sense…were the labels missing? Or was the industry using rBST milk in places where people would be less likely to look for it? I wanted to get to the bottom of this, so I started asking people about it. No one really knew the answer until I spoke with a representative from the food industry who told me that it takes so much effort to change labels, the industry won’t label something unless there is extremely consumer demand. She predicted that the yogurts and cheese are probably made with rBST-free milk, they’re just not advertising it.

Lo and behold, after doing some reading I found that in fact, many brands have removed rBST from ALL of their products, they’re just not stating it on their label, or they’re doing so haphazardly on some products but not others.

Perhaps I’m an over informed consumer who is paying attention to details that nearly no one else even knows or cares about, nevertheless, it’s interesting to consider that a product could in fact be potentially healthier—or at least kinder to the animal it’s coming from—than expected. I guess sometimes the food industry doesn’t show off everything it could.

By Chris Radlicz

According to NHANES (National Health and Nutrition Examination Survey) 2005-2010 the average American consumes about 20 teaspoons of sugar per day, with sugar consumption being the highest in teens and men (1). Interestingly, 33% of calories from added sugars come from beverages, and the majority of those beverages are sweetened with high fructose corn syrup (HFCS) (1).

But what is the novelty of HFCS? Aren’t the grams of sugar on the package all that matters? Although calorically equivalent, not all sugars are metabolized the same way.

Previous papers have established epidemiological links between fructose consumption, obesity, and metabolic disease. To take this further, recent literature has indicated that fructose, particularly in high concentrations, as present in high fructose corn syrup and sucrose, are proving to be toxic. HFCS is composed of about 60% fructose and 40% glucose (2). Prior to the processing of sugars, it was nearly impossible to find such high concentrations of sugar in the diet, but it now seems to be commonplace.

Dr. Kimber Stanhope out of University of California Davis published a recent review paper that touched on the metabolic dysregulation that occurs with high consumption of fructose.

Dr. Stanhope’s group has previously shown that subjects consuming fructose-sweetened beverages for 10 weeks, in addition to their normal diet, had increased de novo lipogenesis, dyslipidemia, circulating uric acid levels, visceral adiposity, reduced fatty acid oxidation, and insulin resistance. In contrast, subjects who consumed glucose-sweetened beverages, had comparable weight gain to the fructose group, but did not exhibit the aforementioned metabolic changes (3). These adverse effects seen in the fructose group all increase the likelihood of chronic diseases such as obesity, fatty liver, type-2 diabetes, and cardiovascular disease.

When consuming glucose, the liver is initially bypassed and the glucose reaches systemic circulation to be used by tissues such as the brain and muscles. If excess glucose is consumed in the diet, it will first be stored as glycogen, and secondarily as fat. Fructose on the other hand, takes a different path. When fructose is consumed, it is exclusively metabolized in the liver, where a particular enzyme, fructokinase, will allow for the uptake of fructose (3). Fructose metabolism as a whole lacks many of the cellular controls that are present in the glucose metabolism, which allows for unrestrained lipid synthesis (2).

Significant metabolic issues arise when a high concentration of fructose is consumed, such as in HFCS. An overload of fructose in the liver will lead to de novo lipogenesis and subsequent lipid droplet accumulation in the liver. With these high levels of fructose, the increase in lipid accumulation consequently decreases the breakdown of fat in the liver (3).

This intra-hepatic lipid will promote the production and secretion of very low-density lipoprotein 1 (VLDL1) leading to an increase in post-prandial triglycerides. A vicious cycle occurs effecting insulin resistance as well. The lipid in the liver will increase insulin resistance resulting in increases in circulating diacylglycerol. Additionally, the insulin resistance will lead to further lipid deposit in the liver with sugar having a greater propensity to turn to fat (3). A downstream effect of increased apoCIII and apoB will lead to muscle lipid accumulation, and end in whole body insulin resistance. All of this metabolic dysregulation results from the direct route fructose initially takes to the liver.

Although there is this well-defined and unique pathway for fructose metabolism, many industry-funded studies, haven’t shown the negative metabolic outcomes of consuming HFCS or sucrose (3). More research is certainly needed, but it is best to remember that added sugar in such high concentrations, no matter the culprit monosaccharide, is not favorable for overall health.

It is interesting to note a possible evolutionary perspective, which proposes the advantage of enhanced fructose to fat conversion. At the end of a growing season, ripened fruit will tend to have high levels of fructose. Therefore the fruit consumed at the end of the season may allow for increased fat storage, which would have been beneficial because of the low food availability in the ensuing months (2).

1.U.S. adults, 2005– 2010. NCHS data brief, no 122. Hyattsville, MD: National Center for Health Statistics. 2013.

2.Lyssiotis CA, Cantley LC. F stands for fructose and fat. Nature. 2013; 508:181-182.

3.Stanhope KL. Sugar consumption, metabolic disease and obesity: The state of the controversy. Crit Rev Clin Lab Sci. 2015;1-16.