The Dirt on Clean Eating

Introduction

by Alan Aragon

Everyone knows the difference between dirty and clean foods, so I don’t have to explain the obvious…or do I? My favorite response to questions about how to eat clean is, “Wash your food.” The biggest problem with discussing foods in these terms is that there’s no clear definition of clean or dirty. The difference might seem obvious, but a closer look shows that it’s far from clear-cut. The confusion is compounded when clean eating is preached as the best way to optimal health and body composition. In this article, I’ll use research and field experience to shed some light on these muddy issues.

The Fickle Nature of Clean

To illustrate the inconsistency of clean through decades, I’ll begin with the 1980’s, widely regarded as the start of the fitness revolution. Through much of the decade, fat (regardless of type) was portrayed by both the academic and lay press as the bad guy. Eating clean in the 80’s was largely characterized by avoiding fat, whether through the plethora of fat-free products, or the vigilant avoidance of all forms of added and naturally occurring fats within foods. Toward the end of the decade, whole grain products were regarded as the foundation of optimal health.

The 1990’s was a decade that dichotomized unsaturated fats as good, and saturated fats as bad. Red meat, egg yolks, and pretty much all sources of dietary cholesterol were to be avoided. Abundant grain consumption was still encouraged, and even more so if the grain product had a low glycemic index (GI). High insulin elevations were considered harmful to health and body composition. Therefore, multiple small meals around the clock was recommended not only to control insulin levels, but also to supposedly raise metabolism.


burgers-junk-food-870-820x518
Moderation is the key. Gorging on fast foods is most certainly not the way…
 

Clean in the 2000’s was characterized by the beginnings of amnesty toward saturated fat and cholesterol. They no longer were considered as dirty as previously thought; now hydrogenated vegetable oil was the poison. Omega-3 fatty acids from fish and flaxseed were placed on a heavenly pedestal, receiving the more-is-better stamp. Carbohydrate was now seen as a potentially greater threat to dieters than fat. Sugar was particularly unclean, as evidenced by the boom of artificially sweetened, low-carb products.

The present decade has just begun, and eating clean has taken some interesting directions. One is an appeal to imagination about Paleolithic eating habits, which eliminates the consumption of grains, legumes, dairy, added salt, sugar, alcohol, and even certain vegetables. This definition of clean is perhaps the most logically inconsistent one. It emphasizes a prehistoric model, yet many of its proponents take an array of cutting-edge nutritional supplements, and use satellite technology to navigate their drive to the closest parking spot at the gym. Fruits and vegetables have always been a mainstay of clean eating, but pesticide-free produce is now somehow cleaner, pests and all. Another twist in the carbohydrate saga has snowballed as well. Insulin spikes from high-GI carbs were the bane of the 90’s. But now, fructose, a low-GI carbohydrate with minimal effects on insulin response, is now one of the top public enemies.

As you can see, the definition of clean is an elusive target. Are there any common threads among the decades with respect to eating clean? Is there any way to objectively label foods as clean or dirty? Before I get to that, let’s take a look at the concept as it’s been traditionally applied to bodybuilding.

Bodybuilding Clean

Clean eating in the bodybuilding sense deserves its own discussion. Much of its ‘rules’ are adaptations of dogma from the 80’s and 90’s with a healthy dose of contradiction. Many bodybuilders who consider themselves hardcore will avoid (among other things) dairy and fruit, regardless of training season. Why? Nobody really knows, but I’d speculate that fruit & dairy phobia among bodybuilders originated from the pre-contest leaning-out process, which typically involves the reduction of carbohydrate. Milk and fruit are both carb-dominant foods, and are thus prime candidates for reduction or elimination.

But still, my example above is speculative. This dogma could just as easily have come about by someone cutting milk and/or fruit out of the diet and experiencing further fat loss from the re-creation of an energy deficit, and declaring those foods barriers to fat loss. Nevertheless, in some pre-contest cases, carbohydrate restriction to extreme degrees is called for, and this nullifies the possibility of including milk & fruit (or any carb source, for that matter), at least cyclically. So, milk and fruit got blamed as bad for all occasions, when their omission only potentially applies to certain aggressively carb-restricted dieting phases. Bodybuilders often pride themselves on having nutrient-rich diets, yet many of them opt for a significant portion of their day’s carbohydrate allotment as dextrose (or some other empty-calorie carb source) instead of fruit.

fruit-images-16

Fruits should not be avoided

 

Attempts at Objectively Defining Clean

Scientific investigations of the nutritional status of bodybuilders have shown some interesting results, and here are some of the highlights. Kleiner and colleagues examined the pre-contest dietary habits of male & female junior national & national-level competitors,15-40% of whom admitted to using various drugs [1]. Despite consuming adequate total calories, women were “remarkably deficient” in calcium intake, which is not surprising given the widespread milk-phobia among bodybuilders. In subsequent work led by Kleiner on female & male competitors at the first drug-tested USA Championship, men consumed only 46% of the RDA for vitamin D. Women consumed 0% of the RDA for vitamin D, and 52% of the RDA for calcium [2]. Zinc, copper, and chromium were also underconsumed by the women. Despite dietary magnesium intakes above the RDA, serum magnesium levels in females were low. Serum zinc levels were high in men and women. It’s notable that not all research on bodybuilders has found nutrient deficiencies. Intakes in significant excess of the RDA in both offseason and pre-contest conditions have also been seen [3,4]. Still, the potential for nutrient deficiencies in this population is strong due to the elimination of food groups combined with a high training volume and lowered caloric intake overall.

The two most commonly cited characteristics of foods considered clean are a lack of processing and a high nutrient density. Let’s look at processing first. Foods in their whole, naturally occurring state are often deemed clean. In contrast, foods that are altered or removed from their original state are stripped of the clean stamp. Is this demerit warranted? As we’ll see, this is not a reliable method of judgment for all foods. By this definition, most supplements are dirty, since they often undergo extensive processing and are far-removed from their original source.

To use a common example, whey is doubly processed in the sense that it’s not only a powdered form of milk protein, but it’s a separated fraction of milk protein. Yet, when combining the results of standard ranking methods (biological value, protein efficiency ratio, net protein utilization, and protein digestibility corrected amino acid score), whey has a higher total than all other proteins tested, including beef, egg, milk, and soy [5]. Furthermore, research has shown not only its benefits for training applications [6], but whey has a surprisingly wide range of potential for clinical applications as well [7-10]. Therefore, despite whey being a refined/processed food, it has multiple benefits and minimal downsides.

The next commonly proposed qualifier for a food to be considered clean is its nutrient density. A little-known fact is that there is no scientific consensus on what nutrient density actually means. To quote Miller and colleagues [11],

“There is currently no science-based definition for either nutrient density or nutrient-dense foods. Without a definition that has been developed using an objective, scientific approach, the concept of what is a “nutritious” food is subjective and, therefore, inconsistent.”

The existence of multiple methods of measuring diet quality illustrates the point expressed in the quote above. Nutrient profiling systems include the Healthy Eating Index (HEI), Diet Quality Index, and Alternative HEI. The most recent profiling method is the Nutrient Rich Foods Index (NRFI). The NRFI attempts to consolidate principles from previous methods to establish a more comprehensive definition of nutrient density. It judges individual foods based on the presence of selected important nutrients and absence of problematic ones [12]. Still, the NRFI has its bugs and biases, particularly against saturated fat (& fat in general).

nitrean_frvanilla copy

Nitrean Natural’s combination of 3 whey fractions, casein, and egg proteins affords multiple proven benefits despite being a highly processed foodstuff product.

 

Attempts at Objectively Defining Clean

A simplistic learning tool called the “Go, Slow, and Whoa” (GSW) food classification system was designed to help children and families make better food choices [13]. GSW was recently compared with the more sophisticated NRFI, and despite some differences, both methods closely corresponded with each other in terms of distinguishing energy-dense and nutrient-rich foods [14]. Although the two methods aligned fairly well, they also share similar out-dated ideologies. For example, sports drinks have a “Slow” designation, and whole milk is nailed as a “Whoa” food – brilliant, huh? Tuna canned in water is in the most favorable “Go” column, while fatty fish like salmon is not even listed. A final example is the listing of egg whites in the “Go” column, and whole eggs in the “Slow” column. Unsurprisingly, the government-issued guidelines are still stuck in the fat-phobic era.

Perils of Judging the Parts & Not the Whole

In the process of classifying foods based on nutrient density, the context of the foods within the diet as a whole is often lost. Attempts at defining nutrient density of foods on an individual basis, for the most part, have failed. Much of the classifications are out-dated at best, and counterproductive at worst. It would seem to be a simple matter of labeling foods with a high ratio of micronutrients to calories as nutrient-dense, and foods with a high ratio of calories to micronutrients as energy-dense. However, this simply is not the case. An energy-dense food can still contain more essential macronutrition and/or bioavailable micronutrition than a nutrient-dense, energy-sparse food. Another thing that tends to get ignored is that athletes with high endurance demands or high overall training volume would compromise their performance if energy density was neglected. Ultimately, it’s impossible to judge a food in isolation from the rest of the diet. Furthermore, it’s impossible to judge a diet without considering the training protocol, goals, preferences, and tolerances of the individual.

Dirty Fat Loss

Clean diets are commonly touted to produce more favorable body composition changes than unclean diets. In fact, some even claim that dirty dieting will not allow fat loss to occur. For weight or fat loss, concerns of a dirty diet used to be centered on fat intake. That’s no longer the case; carbohydrate has been receiving the brunt of the contempt lately. In light of the current sugar-phobic climate with an emphasis on fructose, the following studies deserve special attention.

First up, Surwit and colleagues compared the 6-week effects of 2 hypocaloric diets – one with 43% of the total calories as sucrose (table sugar), and one with 4% of the total calories as sucrose [15]. No significant differences were seen in the loss of bodyweight or bodyfat between the high and low-sucrose groups. Strengthening these results was the use of dual X-ray absorptiometry (DXA) to measure body composition. Furthermore, no differences in blood lipids or metabolism were seen between the groups. It looks like a more sugary intake still cannot override a calorie deficit.

Janeil hands on hips

Janeil knows a thing or two about eating right.

 

Next up is a recent study by Madero and colleagues, comparing the 6-week effects of a low-fructose diet (less than 20 g/day) or a moderate-fructose diet (50-70 g/day) mostly from whole fruit [16]. The moderate-fructose group lost significantly more weight than the low-fructose group (4.19 kg versus 2.83 kg, respectively). Notably, the moderate-fructose group lost slightly more fat, but not to a statistically significant degree. Unfortunately, body composition was measured with bioelectrical impedance analysis (BIA) instead of something more reliable like DXA. Nevertheless, bodybuilders afraid of fruit would have to admit that the dirtier diet prevailed in this case.

Trans fatty acids (TFA) have earned a lot of bad press for their adverse effects on biomarkers of cardiovascular health [17,18]. However, some research indicates that not all TFA are harmful. A distinction should be made between industrially produced TFA via hydrogenation of vegetable oils, and naturally occurring TFA in dairy and meat [19]. Vaccenic acid, the main form of TFA in ruminant fats, might actually lower the risk for coronary heart disease [20]. Currently, there’s no controlled human research specifically comparing the effects of TFA with other types of fats on body composition. In any case, the fitness-conscious population has nothing to worry about unless they start indiscriminately gorging on fast food, cooking with vegetable shortening, and pounding loads of processed/packaged pastries and desserts.

All-or-Nothing Dieting & Eating Disorder Risk

In 1997, a general physician named Steven Bratman coined the term orthorexia nervosa [21], which he defines as, “an unhealthy obsession with eating healthy food.” It reminds me of the counterproductive dietary perfectionism I’ve seen among many athletes, trainers, and coaches. One of the fundamental pitfalls of dichotomizing foods as good or bad, or clean or dirty, is that it can form a destructive relationship with food. This isn’t just an empty claim; it’s been seen in research. Smith and colleagues found that flexible dieting was associated with the absence of overeating, lower bodyweight, and the absence of depression and anxiety [22]. They also found that a strict all-or-nothing approach to dieting was associated with overeating and increased bodyweight. Similarly, Stewart and colleagues found that rigid dieting was associated with symptoms of an eating disorder, mood disturbances, and anxiety [23]. Flexible dieting was not highly correlated with these qualities. Although these are observational study designs with self-reported data, anyone who spends enough time among fitness buffs knows that these findings are not off the mark.

Applying Moderation: The 10-20% Guideline

For those hoping that I’ll tell you to have fun eating whatever you want, you’re in luck. But, like everything in life, you’ll have to moderate your indulgence, and the 10-20% guideline is the best way I’ve found to do this. There currently is no compelling evidence suggesting that a diet whose calories are 80-90% from whole & minimally processed foods is not prudent enough for maximizing health, longevity, body composition, or training performance. As a matter of fact, research I just discussed points to the possibility that it’s more psychologically sound to allow a certain amount of flexibility for indulgences rather than none at all. And just to reiterate, processed does not always mean devoid of nutritional value. Whey and whey/casein blends are prime examples of nutritional powerhouses that happen to be removed from their original food matrix.

The 10-20% guideline isn’t only something I’ve used successfully with clients; it’s also within the bounds of research. Aside from field observations, there are three lines of evidence that happen to concur with this guideline. I’ll start with the most liberal one and work my way down. The current Dietary Reference Intakes report by Food & Nutrition Board of the Institute of Medicine lists the upper limit of added sugars as 25% of total calories [24]. Similarly, an exhaustive literature review by Gibson and colleagues found that 20% of total calories from added sugars is roughly the maximum amount that won’t adversely dilute the diet’s concentration of essential micronutrition [25]. Keep in mind that both of these figures are in reference to refined, extrinsic sugars, not naturally occurring sugars within whole foods like fruit or milk. Finally, the USDA has attempted to teach moderation with their concept of the discretionary calorie allotment, defined as follows [26]:

“…the difference between total energy requirements and the energy consumed to meet recommended nutrient intakes.”

Basically, discretionary calories comprise the margin of leftover calories that can be used flexibly once essential nutrient needs are met. Coincidentally, the USDA’s discretionary calorie allotment averages at approximately 10-20% of total calories [27]. Take note that discretionary calories are not just confined to added sugars. Any food or beverage is fair game. The USDA’s system is still far from perfect, since it includes naturally-occurring fats in certain foods as part of the discretionary calorie allotment. This is an obvious holdover from the fat-phobic era that the USDA clings to, despite substantial evidence to the contrary [28].

It’s important to keep in mind that protein and fat intake should not be compromised for the sake of fitting discretionary foods into the diet. In other words, make sure discretionary intake doesn’t consistently displace essential micro- & macronutrient needs, and this includes minimum daily protein and fat targets, which vary individually. This may be tough to accept, but alcohol is not an essential nutrient. Its risks can swiftly trump its benefits if it’s consumed in excess, so it falls into the discretionary category.

10% Versus 20%

Another legitimate question is why I’ve listed the discretionary range as 10-20% rather than just listing it as a maximum of 20%. This is because energy balance matters. In bulking scenarios, maintaining a 20% limit could potentially pose health risks that are already elevated by the process of weight gain, which in some cases involves a certain amount of fat gain. Conversely, weight loss tends to be an inherently cardioprotective process, independent of diet composition [29]. So, the 20% limit is more appropriate for those either losing or maintaining weight. Those who are gaining weight but want to play it safe should hover towards the lower & middle of the range (10-15%). Another factor that can influence the upper safe threshold is physical activity level. I’ll quote Johnson & Murray in a recent review [30]:

“Obesity and metabolic syndrome are rare among athletes, even though dietary fructose intake is often high, underscoring the robust protective role of regular exercise.”

 

In the above quote, you can substitute any controversial food or nutrient in place of the word fructose, and the same principle would apply. A greater range of dietary flexibility is one of the luxuries of regular training. Sedentary individuals do not have the same level of safeguarding from the potentially adverse effects of a higher proportion of indulgence foods. And just in case it wasn’t made clear enough, 10-20% indicates the maximum, not minimum discretionary allotment. If someone strives to consume 0% of calories from any food that’s been processed or refined from its original state, then that’s perfectly fine – as long as this is the person’s genuine preference, and not a painful battle of will. I’d also like to make it clear that there is still plenty of grey area in the study of dietary effects on health. As such, the nature and extent of the miscellaneous or rule-free food allotment is a delicate judgment call. In this case, it’s wise to keep scientific research at the head of the judging panel, but don’t ignore personal experience & individual feedback.

Final Note: Linear Versus Nonlinear Distribution

A legitimate question is, what’s the best way to distribute discretionary calories? Should they be confined to a daily limit, or can it be a weekly limit? The best answer is to let personal preference decide. If we use a 2000 kcal diet as an example, a flat/linear approach would mean that 200-400 kcal per day can come from whatever you want, while meeting essential needs otherwise in the diet. Weekly, this translates to 1400-2800 kcal, depending on the factors I previously discussed. One nonlinear option would be to break the weekly allotment in half, where 2 days per week you indulge in 700-1400 kcal of whatever you want, keeping the remaining 5 days relatively Spartan. Again, there is no universally superior method of distributing the discretionary allotment. The same principle applies to the choice of foods to fulfill it. Honoring personal preference is one of the most powerful yet underrated tactics for achieving optimal health and body composition. And that’s the nitty-gritty as I see it.

About the Author:

Alan Aragon has over 20 years of success in the fitness field, and is recognized as one of the most influential figures in the modern movement towards evidence-based information. He is a continuing education provider for the Commission on Dietetic Registration, National Academy of Sports Medicine, and National Strength & Conditioning Association. Alan lectures at universities and scientific conferences around the world, and writes a monthly research review focused on providing cutting-edge theoretical and practical information to health and fitness professionals. His research has been published in the popular media as well as the peer-reviewed scientific literature, including the number-one most viewed article in the history of the Journal of the International Society of Sports Nutrition. Alan maintains a private practice designing programs for recreational, Olympic, and professional athletes. His mission is to raise the standards of the fitness industry through a combination of scientific investigation and relentless pursuit of teaching excellence.

References

1. Kleiner SM, et al. Metabolic profiles, diet, and health practices of championship male and female bodybuilders. J Am Diet Assoc. 1990 Jul;90(7):962-7.
2. Kleiner SM, et al. Nutritional status of nationally ranked elite bodybuilders. Int J Sport Nutr. 1994 Mar;4(1):54-69.
3. Keith RE, et al. Nutritional status and lipid profiles of trained steroid-using bodybuilders. Int J Sport Nutr. 1996 Sep;6(3):247-54.Hoffman JR, Falvo MJ. Protein-which is best? J Sport Sci Med 2004; 3: 118-30.
4. Bamman MM, et al. Changes in body composition, diet, and strength of bodybuilders during the 12 weeks prior to competition. J Sports Med Phys Fitness. 1993 Dec;33(4):383-91.
5. Hoffman JR, Falvo MJ. Protein-which is best? J Sport Sci Med 2004; 3: 118-30.
6. Hulmi JJ, et al. Effect of protein/essential amino acids and resistance training on skeletal muscle hypertrophy: A case for whey protein. Nutr Metab (Lond). 2010 Jun 17;7:51.
7. Xu R. Effect of whey protein on the proliferation and differentiation of osteoblasts. J Dairy Sci. 2009 Jul;92(7):3014-8.
8. Krissansen GW. Emerging health properties of whey proteins and their clinical implications. J Am Coll Nutr. 2007 Dec;26(6):713S-23S.
9. Parodi PW. A role for milk proteins and their peptides in cancer prevention. Curr Pharm Des. 2007;13(8):813-28.
10. Marshall K. Therapeutic applications of whey protein. Altern Med Rev. 2004 Jun;9(2):136-56.
11. Miller GD, et al. It is time for a positive approach to dietary guidance using nutrient density as a basic principle. J Nutr. 2009 Jun;139(6):1198-202.
12. Fulgoni VL 3rd, et al. Development and validation of the nutrient-rich foods index: a tool to measure nutritional quality of foods. J Nutr. 2009 Aug;139(8):1549-54.
13. US Department of Health and Human Services, National Heart Lung and Blood Institute. We can! Go, Slow and Whoa foods. http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/downloads/gswtips.pdf
14. Drewnowski A, Fulgoni V 3rd. Comparing the nutrient rich foods index with “Go,” “Slow,” and “Whoa,” foods. J Am Diet Assoc. 2011 Feb;111(2):280-4.
15. Surwit RS, et al. Metabolic and behavioral effects of a high-sucrose diet during weight loss. Am J Clin Nutr. 1997 Apr;65(4):908-15.
16. Madero M, et al. The effect of two energy-restricted diets, a low-fructose diet versus a moderate natural fructose diet, on weight loss and metabolic syndrome parameters: a randomized controlled trial. Metabolism. 2011 May 27. [Epub ahead of print] 17. Mozaffarian D, Clarke R. Quantitative effects on cardiovascular risk factors and coronary heart disease risk of replacing partially hydrogenated vegetable oils with other fats and oils. Eur J Clin Nutr. 2009 May;63 Suppl 2:S22-33.
18. Wallace SK, Mozaffarian D. Trans-fatty acids and nonlipid risk factors. Curr Atheroscler Rep. 2009 Nov;11(6):423-33.
19. Chardingny JM, et al. Do trans fatty acids from industrially produced sources and from natural sources have the same effect on cardiovascular disease risk factors in healthy subjects? Results of the trans Fatty Acids Collaboration (TRANSFACT) study. Am J Clin Nutr. 2008 Mar;87(3):558-66.
20. Field CJ, et al. Human health benefits of vaccenic acid. Appl Physiol Nutr Metab. 2009 Oct;34(5):979-91.
21. Bratman S. What is orthorexia? Accessed August 2011. http://www.orthorexia.com/index.php?page=katef
22. Smith CF, et al. Flexible vs. Rigid dieting strategies: relationship with adverse behavioral outcomes. Appetite. 1999 Jun;32(3):295-305.
23. Stewart TM, et al. Rigid vs. flexible dieting: association with eating disorder symptoms in nonobese women. Appetite. 2002 Feb;38(1):39-44.
24. Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Energy, Carbohydrate, Fiber, Fat, Fatty Acids, Cholesterol, Protein, and Amino Acids. 2005.
25. Gibson SA. Dietary sugars intake and micronutrient adequacy: a systematic review of the evidence. Nutr Res Rev. 2007 Dec;20(2):121-31.
26. DGAC Advisory Committee, USDA. Part D, Section 3: Discretionary Calories. The Report of the Dietary Guidelines Advisory Committee on Dietary Guidelines for Americans, 2005.
27. Center for Nutrition Policy & Promotion. My Pyramid: Food intake patterns, 2005. http://www.choosemyplate.gov/downloads/MyPyramid_Food_Intake_Patterns.pdf
28. Hession M, et al. Systematic review of randomized controlled trials of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity and its comorbidities. Obes Rev. 2009 Jan;10(1):36-50.
29. Leenen R, et al. Relative effects of weight loss and dietary fat modification on serum lipid levels in the dietary treatment of obesity. J Lipid Res. 1993 Dec;34(12):2183-91.
30. Johnson RJ, Murray R. Fructose, exercise, and health. Curr Sports Med Rep. 2010 Jul-Aug;9(4):253-8.

Is there a limit to how much protein the body can use in a single meal?

Introduction

A longstanding belief in fitness circles is that the body can only use a certain amount of protein per meal, and the excess is either oxidized or excreted. The ballpark range thrown around is 20-30 grams, with 30 grams being perhaps the most common figure.

This guideline has led many trainees to go through the pains of consuming multiple doses of protein throughout the day, banking that it will maximize muscle anabolism or muscle retention.

Well, true or not, this concept fits in nicely with another longstanding fitness “rule” that you have to eat at least six times per day in order to keep the body’s metabolism revving high. Since the meal frequency and metabolism dogma has been thoroughly debunked [1-5], it’s time to dig into the topic of whether there’s a limit to effective protein dosing, and if so, what that limit might be. 

Looking at simple logic first

Let’s imagine an experiment involving two relatively lean 200 lb individuals. For the purposes of this illustration, I’ll assign a daily amount of protein known to adequately support the needs of the athletic population. We’ll give Person A 150 g protein spread over five meals at 30 g each. We’ll give Person B the same amount of protein, but in a single meal. Let’s say that this meal consists of a 16 oz steak, chased with a shake containing two scoops of protein powder.
 
If we really believed that only 30 g protein can be handled by the body in a single meal, then Person B would eventually run into protein deficiency symptoms because he supposedly is only absorbing a total of 30 g out of the 150 g we’re giving him. At 30 g/day, he’s only getting 0.33 g/kg of bodyweight, which isn’t even half of the already-low RDA of 0.8 g/kg. If the body worked this way, the human species would have quickly become extinct. The human body is more efficient and effective than we give it credit for.
 
The body will take all the sweet time it needs to effectively digest and absorb just about whatever dose you give it. Person A will have shorter digestion periods per meal in order to effectively absorb and utilize the small meals. Person B will have a longer digestion period in order to effectively absorb and utilize the large meal. While the truth in this logic seems self-evident, the important question is whether or not it’s supported by scientific research. Let’s look at the evidence, starting with immediate-effect (acute) studies, then move on to the longer-term trials.

Research examining speed of absorption

A thorough literature review by Bilsborough and Mann compiled data from studies by various investigators who measured the absorption rates of various protein sources [6]. Oddly, an amino acid mixture designed to mimic the composition of pork tenderloin made the top spot, at 10 g/hour, while whey took a close second at 8-10 g/hour. Other proteins fell in their respective spots below the top two, with little rhyme or reason behind the outcomes. As a matter of trivia, raw egg protein was the most slowly absorbed of them all at 1.3 g/hour.

It’s important to note that these data have some serious limitations. A major one is the variance of the methods used to determine the absorption rates (i.e., intravenous infusion, oral ingestion, ileal ingestion). Most of the methods are just too crude or far-fetched for serious consideration. Another limitation is that these figures could be skewed depending upon their concentration in solution, which can affect their rate of gastric evacuation. Another factor to consider is the timing of ingestion relative to exercise and how that might differentially affect absorption rates. Finally, short-term data leaves a lot open to question.

Short-term research supporting the magic limit

I’ve heard many folks parrot that the maximal anabolic effect of a single protein dose is limited to 20 grams, citing recent work by Moore and colleagues [7]. In this study’s 4-hour post-exercise test period, 40 g protein did not elicit a greater anabolic response than 20 g. I’d interpret these outcomes with caution. Fundamentally speaking, protein utilization can differ according to muscle mass. The requirements of a 140-lb person will differ markedly from someone who’s a lean 200. Additionally, a relatively low amount of total volume was used (12 sets total). Typical training bouts usually involve more than one muscle group and are commonly at least double that volume, which can potentially increase the demand for nutrient uptake. Finally, the conclusion of the authors is questionable. They state explicitly,

“…we speculate that no more than 5-6 times daily could one ingest this amount (~20 g) of protein and expect muscle protein synthesis to be maximally stimulated.”

So, they’re implying that 100-120 grams of protein per day is maximal for promoting muscle growth. Wait a minute, what? Based on both the bulk of the research evidence and numerous field observations, this is simply false [8,9]
 
In another recent study, Symons and colleagues compared the 5-hour response of a moderate serving of lean beef containing 30 g protein with a large serving containing 90 g protein [10]. The smaller serving increased protein synthesis by approximately 50%, and the larger serving caused no further increase in protein synthesis, despite being triple the dose. The researchers concluded that the ingestion of more than 30 g protein in a single meal does not further enhance muscle protein synthesis. While their conclusion indeed supports the outcomes of their short-term study, it’s pretty easy to predict the outcomes in muscle size and strength if we compared a total daily protein dose of 90 g with 30 g over a longer trial period, let alone one involving a structured exercise protocol. This brings me to the crucial point that acute outcomes merely provide grounds for hypothesis. It’s not completely meaningless, but it’s far from conclusive without examining the long-term effects.

Longer-term research challenging the magic limit

If we were to believe the premise that a 20-30 g dose of protein yields a maximal anabolic effect, then it follows that any excess beyond this dose would be wasted. On the contrary, the body is smarter than that. In a 14-day trial, Arnal and colleagues found no difference in fat-free mass or nitrogen retention between consuming 79% of the day’s protein needs (roughly 54 g) in one meal, versus the same amount spread across four meals [11].

Notably, this study was done on young female adults whose fat-free mass averaged 40.8 kg (89.8 lb). Considering that most non-sedentary males have considerably more lean mass than the female subjects used in the aforementioned trial, it’s plausible that much more than 54 g protein in a single meal can be efficiently processed for anabolic and/or anti-catabolic purposes. If we extrapolated the protein dose used in this study (79% of 1.67g/kg) to the average adult male, it would be roughly 85-95 g or even more, depending on just how close someone is to the end of the upper limits of muscular size.

When Arnal and colleagues applied the same protocol to the elderly population, the single-dose treatment actually caused better muscle protein retention than the multiple-dose treatment [12].  This raises the possibility that as we age, larger protein feedings might be necessary to achieve the same effect on protein retention as lesser amounts in our youth.

IF research nailing the coffin shut?

Perhaps the strongest case against the idea of a dosing limit beyond which anabolism or muscle retention can occur is the recent intermittent fasting (IF) research, particularly the trials with a control group on a conventional diet. For example, Soeters and colleagues compared two weeks of IF involving 20-hour fasting cycles with a conventional diet [13].  Despite the IF group’s consumption of an average of 101 g protein in a 4-hour window, there was no difference in preservation of lean mass and muscle protein between groups.

In another example, Stote and colleagues actually reported an improvement in body composition (including an increase in lean mass) after 8 weeks in the IF group consuming one meal per day, where roughly 86 g protein was ingested in a 4-hour window [14]. Interestingly, the conventional group consuming three meals spread throughout the day showed no significant body composition improvements.

Keep in mind that bioelectrical impedance (BIA) was used to determine body composition, so these outcomes should be viewed with caution. I’ve been highly critical of this study in the past, and I still am. Nevertheless, it cannot be completely written off and must be factored into the body of evidence against the idea of a magic protein dose limit.

Conclusion & application

Based on the available evidence, it’s false to assume that the body can only use a certain amount of protein per meal. Studies examining short-term effects have provided hints towards what might be an optimal protein dose for maximizing anabolism, but trials drawn out over longer periods haven’t supported this idea. So, is there a limit to how much protein per meal can be effectively used? Yes there is, but this limit is likely similar to the amount that’s maximally effective in an entire day. What’s the most protein that the body can effectively use in an entire day? The short answer is, a lot more than 20-30 g. The long answer is, it depends on several factors. In most cases it’s not too far from a gram per pound in drug-free trainees, given that adequate total calories are provided [8,9]

In terms of application, I’ve consistently observed the effectiveness of having approximately a quarter of your target bodyweight in both the pre- and post-exercise meal. Note: target bodyweight is a surrogate index of lean mass, and I use that to avoid making skewed calculations in cases where individuals are markedly over- or underweight. This dose surpasses the amounts seen to cause a maximal anabolic response but doesn’t impinge upon the rest of the day’s protein allotment, which can be distributed as desired. On days off from training, combine or split up your total protein allotment according to your personal preference and digestive tolerance. I realize that freedom and flexibility are uncommon terms in physique culture, but maybe it’s time for a paradigm shift.

In sum, view all information – especially gym folklore and short-term research – with caution. Don’t buy into the myth that protein won’t get used efficiently unless it’s dosed sparingly throughout the day. Hopefully, future research will definitively answer how different dosing schemes with various protein types affect relevant endpoints such as size and strength. In the mean time, feel free to eat the whole steak and drink the whole shake, and if you want to get the best bang for your buck, go for a quality protein blend such as Nitrean! 😉

Written By Alan Aragon

Discuss, comment or ask a question

If you have a comment, question or would like to discuss anything raised in this article, please do so in the following discussion thread on the Wannabebig Forums – Is there a limit to how much protein the body can use in a single meal discussion thread.

About Alan Aragon

Alan Aragon has over 15 years of success in the fitness field. He earned his Bachelor and Master of Science in Nutrition with top honors. Alan is a continuing education provider for the Commission on Dietetic Registration, National Academy of Sports Medicine, American Council on Exercise, and National Strength & Conditioning Association. Alan recently lectured to clinicians at the FDA and the annual conference of the Los Angeles Dietetic Association.

He maintains a private practice designing programs for recreational, Olympic, and professional athletes, including the Los Angeles Lakers, Los Angeles Kings, and Anaheim Mighty Ducks. Alan is a contributing editor and Weight Loss Coach of Men’s Health magazine.

His book Girth Control is considered one of the most in-depth manuals for physique improvement and understanding nutrition for fitness & sports. Last but not least, Alan writes a monthly research review providing of the latest science on nutrition, training, and supplementation. Visit Alan’s blog to keep up with his latest shenanigans.

References

1. Smeets AJ, Westerterp-Plantenga MS. Acute effects on metabolism and appetite profile of one meal difference in the lower range of meal frequency. Br J Nutr. 2008 Jun;99(6):1316-21.

2. Taylor MA, Garrow JS. Compared with nibbling, neither gorging nor a morning fast affect short-term energy balance in obese patients in a chamber calorimeter. Int J Obes Relat Metab Disord. 2001 Apr;25(4):519-28.

3. Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. Br J Nutr. 1997 Apr;77 Suppl 1:S57-70.

4. Verboeket-van de Venne WP, Westerterp KR. Frequency of feeding, weight reduction and energy metabolism. Int J Obes Relat Metab Disord. 1993 Jan;17(1):31-6.

5. Verboeket-van de Venne WP, Westerterp KR. Influence of the feeding frequency on nutrient utilization in man: consequences for energy metabolism. Eur J Clin Nutr. 1991 Mar;45(3):161-9.

6. Bilsborough S, Mann N. A review of issues of dietary protein intake in humans. Int J Sport Nutr Exerc Metab. 2006 Apr;16(2):129-52.

7. Moore DR, et al. Ingested protein dose response of muscle and albumin protein synthesis after resistance exercise in young men. Am J Clin Nutr. 2009 Jan;89(1):161-8.

8. Campbell B, et al. International Society of Sports Nutrition position stand: protein and exercise. J Int Soc Sports Nutr. 2007 Sep 26;4:8.

9. Tipton KD, Wolfe RR. Protein and amino acids for athletes. J Sports Sci. 2004 Jan;22(1):65-79.

10. Symons TB, et al. A moderate serving of high-quality protein maximally stimulates skeletal muscle protein synthesis in young and elderly subjects. J Am Diet Assoc. 2009 Sep;109(9):1582-6.

11. Arnal MA, et al. Protein feeding pattern does not affect protein retention in young women. J Nutr. 2000 Jul;130(7):1700-4.

12. Arnal MA, et al. Protein pulse feeding improves protein retention in elderly women. Am J Clin Nutr. 1999 Jun;69(6):1202-8.

13. Soeters MR, et al. Intermittent fasting does not affect whole-body glucose, lipid, or protein metabolism. Am J Clin Nutr. 2009 Nov;90(5):1244-51.

14. Stote KS, et al. A controlled trial of reduced meal frequency without caloric restriction in healthy, normal-weight, middle-aged adults. Am J Clin Nutr. 2007 Apr;85(4):981-8.

Fish Oil – Just The Facts

The Dawn of Fat Phobia

If you have a few years of training under your belt, you can probably remember what I call the “Fat-Free 80’s.” Think back to a time when dietary fat was the enemy. Ah, yes, a time when fat-free products lined the shelves of the supermarket. A time when it was not a bad thing to get a box of Entemann’s cinnamon rolls, as long as they were the FAT-FREE cinnamon rolls. Health Valley made some positively disgusting fat-free cookies, along with a host of other fat-free products that tasted like sugary cardboard. And we can’t forget the weight gainer products, those were priceless. 1,000, 2000, 4,000 calories per serving, and all you had to do was mix about a cup of powder into your favourite drink.

No worries, though, these gainers were virtually fat-free! What we were led to believe was that fat-free products equated to fat-free physiques. Unfortunately, that was far from the truth.

During the 1980’s national obesity rates started to drastically climb. Large behavioral trend studies such as the National Health and Nutrition Examination Study (NHANES II & III), the Behavioral Risk Factor Surveillance System (BRFSS), and the Calorie Control Council Report (CCCR) collectively showed a 31% increase in overweight prevalence from 1976-1991. What is the punch line? This increase in weight was accompanied by an 11% decrease in percentage of calories from fat (from 41.0% to 36.6%). The most recent report by the BRFSS shows a further decrease in fat intake to 33%, accompanied by an increase in obesity from 11.6% to 22.1%. This is a 90.5% increase in US obesity from 1990-2002[1]. It’s obvious that dietary fat is not the evil culprit in the expansion of the population’s waistline.

A Brief Evolution of Our Knowledge of Fats

As indicated by the fat-free product boom a couple of decades back, there indeed was the widespread belief that ALL fats were a substance to be minimized or avoided altogether. But with the forward march of research, we came to understand that different fats had different effects on health. Since it is human nature to think in black and white terms, the great divide initially fell between saturated (SFA) and mono- or polyunsaturated fatty acids (MUFA & PUFA). SFA were thought to be the root of all evil, conjuring images of arterial plaque and eventual heart failure, while unsaturated fat was regarded as a universally angelic substance. This turned out to be a gross oversimplification of reality.

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The intricacies and widely varying sources and subtypes of SFA is another article altogether, but suffice it to say that it’s not that simple to pigeonhole them as unhealthy. SFA are not created equal. They have markedly variable physiological effects from the detrimental all the way to the beneficial. Given this, it depends on which ones you want throw onto the theoretical chopping block. Stearic acid, an SFA abundant in meat & milk fat, has been consistently observed to actually reduce blood platelet aggregation [2]. This is a good thing. In contrast, trans fats (found in high concentrations in commercially baked goods as well as processed & fried foods) have been observed to negatively impact blood lipids by not only lowering HDL, but increasing LDL as well [3]. 

Ironically, experimental research exists on healthy humans showing the least fat was oxidized on the MUFA fat dietary treatment, and the most fat oxidized on a trans fat diet [4]. This result echoes what has been seen in rats as well. It appears that the tighter the control of the study, the less “superior” unsaturated fats turn out to be for any presumed effect on body composition compared to SFA. Throw in the fact that a reducing SFA intake and increasing the degree of unsaturation of fatty acids in the diet reduces testosterone levels [5], and then you have yet another wrinkle in the mix.

Then you have medium-chain triacylglycerols (MCT), which are SFAs that exhibit physiological behavior that is closer to carbohydrate than fat. MCT has been hyped to death by those who sell it. But the point is that they are a type of SFA that may potentially have minor benefits on body composition. I personally wouldn’t spend a dime on them, but they nevertheless illustrate the fact that SFAs are a complex and highly varied group of compounds in terms of physiological effect. As always, the effects of each type of fat undoubtedly vary with the population in question, as well as individual response.

Finally, with the black and white fallacy of saturated versus unsaturated fats out of the way, we can now shift the focus on fish oils, which happen to be a rich source of a particular class of fatty acids under intense study, the omega 3’s. 

Enter the Omega-3 Fatty Acids

Omega-3 fatty acids are 20-carbon compounds essential for normal growth and development, and are noted specifically for their powerful influence over multiple physiological processes. Alpha-linolenic acid (ALA), one of the two essential fatty acids (EFA) that the body cannot biosynthesize and must get from the diet, is an omega-3. Here’s a structure for those of you who miss your days in the classroom:

EFA are precursors to a class of biologically significant compounds called eicosanoids, which include prostaglandins, leukotrienes, and thromboxanes. Eicosapentanoic acid (EPA) and docosahexanoic acid (DHA) can be derived from fish oil, and to a lesser degree, flaxseed oil. Consumption of EPA and DHA has an appreciable number of positive health effects, including decreases in blood platelet aggregation, lowered blood pressure, enhancement of smooth muscle function, decreased inflammation, alleviation of dyslipidema, and treatment of mood disorders [6-9]. There is also emerging evidence pointing to the benefits of omega-3 fatty acids on bone health [10].

Archaeological research postulates that humans were biologically designed to thrive on a diet whose ratio of omega-6 to omega-3 fatty acids was approximately 1:1, and unlikely greater than 4:1. Today, consumption of n-6 to n-3 fatty acids is estimated at roughly 25:1 [11]. This is due in part to a predominance of omega-6 oils available commercially in our food supply (corn oil, sunflower oil, safflower oil, refined packaged grain products & pastries) and a relative minority of omega-3 sources (fatty marine fish such as salmon, mackerel, herring, and flaxseed oil, walnuts, & small amounts in canola oil). Industrial production of omega-6-rich animal feeds has also resulted in animal tissues (livestock, eggs, and cultured fish) rich in omega-6 and poor in omega-3 fatty acids. This disproportionately high intake of omega 6’s biases our physiology towards thrombosis, hyperlipidemia, and vasoconstriction. The reverse of those effects occurs simply by increasing the proportion of omega-3 fats.

Is Fish Oil a Fat Loss Supplement?

So far, the resume of fish oil’s health effects is very extensive. But can it add fat loss to the list as well? The buzz in the supplement industry would certainly want consumers to believe so. But as always, the answer can only begin to reveal itself in the research. Human studies examining the effect of fish oil supplementation on body composition are scarce, but that makes it easy to pick them apart.

A decade ago, Couet and colleagues investigated the effect of replacing 6g of visible dietary fat with 6g of fish oil in healthy adults over a 3-week period, done 12 weeks after a 3-week control diet period [12]. Bodyfat mass and respiratory quotient decreased in the fish oil phase. It’s important to note that the flaws in this study’s design are grave enough to almost completely invalidate it. Extremely small sample size (6 subjects total), short trial period (3 weeks), and a complete absence of randomization or treatment balance (opening the distinct possibility for seasonal variation, among other errors) are the main fatal knocks that render this data nearly useless.

In contrast, 2 more recent studies conducted within the past 3 years looking at weight-loss diets supplemented with omega-3’s have not observed any significant effects on body composition beyond what was caused by dietary restriction alone [13,14]. But it’s never that simple, since things may differ according to the population and protocol. In contrast to the previous two trials, Kunesova’s team examined the effects of omega-3 supplementation on severely obese female inpatients undergoing a 3-week very low calorie (525 kcal) in-patient weight reduction treatment [15]. Calories were controlled to accommodate the supplemental omega-3, which was 2.8g/day. Result? The omega-3 supplemented group lost 1.5 kg bodyweight and 2.2 cm more off the waist than the control group.

How about more relevant populations? As of this writing, there are only three trials in existence examining the effect of omega-3 supplementation combined with a structured aerobic exercise program on body composition. Let’s dig in.

In 1989, Warner and colleagues looked at the effect of walking or jogging 3 days/week for 45–50 minutes at 75-80% maximal heart rate in hyperlipidemic subjects randomly assigned to 1 of 4 groups: fish oil + exercise, fish oil alone, corn oil, or control [16]. Body fat was reduced only in the fish oil + exercise group. These data are severely limited by the absence of an exercise-only control group, leaving a huge question mark open regarding the relative contribution of exercise to the bottom line result. A year later, Brilla and Landerholm conducted a well-designed study on healthy, previously sedentary men [17]. This trial did contain an exercise-only control group, and no effect of fish oil on body fat was observed.

In the most recent fish oil + exercise study to date, Hill’s team examined the effect of fish oil supplementation (6g) on overweight hypertensive/hyperlipidemic subjects (24 men and 41 women) over a 12 week period [18]. Exercise was 3 days/week walking at 75% predicted maximal heart rate for 45 minutes. Body composition was assessed by dual energy X-ray absorptiometry (DEXA). Predictably, fish oil supplementation improved blood lipids and arterial vasodilation. As for body composition, fish oil by itself didn’t cause any bodyfat reduction from baseline levels, whereas the sunflower oil control gained body fat, but to an insignificant degree. However, fish oil + exercise caused a 1.1% greater bodyfat reduction compared to the sunflower oil + exercise control (1.2% reduction versus a 0.1% reduction in the sunflower oil group). If you re-read those body composition results, they’re nothing to get too excited over, especially considering small amount of fat lost in the 12 week duration.

The Dark Side of Over-doing Fish Oil Supplementation

Yes, Luke, there is always a dark side. In the world of unchecked marketing hype, fish oil has definitely gotten the “more is better” stamp. The problem is EPA and DHA have a well-documented ability to suppress the body’s immune response. Although not as consistent as the immune effects, data also exist on the ability of EPA and DHA to increase bleeding time and oxidation. Let’s take a look at a couple of the published peer-reviewed research that no one in the fitness industry talks about.

Thies and colleagues examined the 12-week effect of various fatty acid supplement mixes on healthy subjects [19]. Various blends of placebo oil and oils rich in ALA, GLA, AA, DHA, or EPA (720mg) + DHA (280mg) were compared. Total fat intake from the 9-capsule dose was 4 g/d. The EPA/DHA treatment was the only one that had a negative effect on immunity, significantly decreasing natural killer cell activity by 48%. This effect was reversed after 4 weeks of ceasing intake of the supplement.

Rees and colleagues investigated the effects of various amounts of EPA on immune markers in young and older men [20]. In a 12-week study, EPA was incorporated into plasma and mononuclear cell phospholipids. Supplemental EPA in amounts of 1.35, 2.7, and 4.05g/day caused a dose-dependent decrease in neutrophil respiratory burst, indicating the suppression of a cellular defense against immunity threats. This effect was seen in the older, but not the younger men. Based on these and the previous data, if you’re not a spring chicken, and immunity is an issue, you might not want to go hog-wild on the fish oil dosing.

Suggested Use & Take-Home Tips

The cardio-protective benefits of increasing the dietary proportion of omega-3 fatty acids is seen consistently in trials involving various populations and protocols. Fish oil is one of the few supplements that actually have a substantial body of scientific evidence backing it up. However, it’s easy to think in terms of pills instead of food. Those who love fish (and have the time or resources to prepare or order it) can simply increase or maintain their intake of fatty fish such as salmon, mackerel, lake trout, herring, albacore tuna, and sardines.

The American Heart Association (AHA) recommends at least two servings of fish per week for the general population. Think of a palm-sized piece as a serving. For those with high triacylglycerol levels, a supplemental 2-4g of combined EPA/DHA is their suggested therapeutic dose. However, note that the AHA cautions against supplementing more than 3g outside of a physician’s care [21]. I recommend maxing out your whole food options first before going the supplemental route. There’s always more complete and synergistic nutrition contained within whole foods. For those who can’t or won’t eat fish, there’s always fish oil capsules, which thankfully are inexpensive, and more convenient than getting your omega-3’s through fish.

The amount of EPA/DHA per capsule may vary with the brand. Capsules can contain anywhere from 250-500mg. Most healthy folks don’t need more than 3-6 capsules per day to meet or exceed the amounts that show benefits. There are no definitive conclusions about optimal proportion of EPA:DHA, so to error on the side of safety, I recommend finding roughly an even mix. It’s common and perfectly acceptable for products to contain slightly more EPA than DHA. If at all possible, make sure your supplement is verified by the USP (United States Pharmacopoeia) for the peace of mind that you’re getting what the label is claiming. I would also error on the side of safety and keep them refrigerated. As a side note, there’s a widespread belief that ALA from flaxseed is worthless for increasing EPA/DHA since the conversion is inefficient. However, Harper’s team recently observed 3g ALA/day (from 5.2g flaxseed oil) raise plasma EPA levels by 60% at the end of a 12-week trial [22].

Looking at the body of evidence as a whole, fish oil (or increased fish consumption) has great potential for improving cardiovascular health. But for reducing body fat, the effects are minor to nonexistent. Let’s not forget that fish oil isn’t some magical negative-calorie food. It still contains 9 calories per gram, and no matter how much of those calories are used in its processing within the body, it’s still a net gain in calories after consumption. To sum everything up, fish oil has health benefits, as well as potential risks. It’s certainly not a matter of more-is-better. It might have minor fat loss effects in the obese and overweight population, but their fat loss effect in general is far from conclusively established. Get a variety of fats in your diet, and get them from whole foods whenever possible. Fish oil is merely one of many agents that can contribute to optimal health within the context of well-balanced nutrition. Keep it in perspective, and keep your eye on the facts.

Written by Alan Aragon

Discuss, comment or ask a question

If you have a comment, question or would like to discuss anything raised in this article, please do so in the following discussion thread on the Wannabebig Forums – Fish Oil – Just The Facts discussion thread.

References

1. Centers for Disease Control: Behavioral Risk Factor Surveillance System. 1990-2002 trends data, nationwide.

2. Thijssen MA, et al. Stearic, oleic, and linoleic acids have comparable effects on markers of thrombotic tendency in healthy human subjects. J Nutr. 2005 Dec;135(12):2805-11.

3. Mozaffarian, et al. Trans fatty acids and cardiovascular disease. N. Engl. J. Med. 2006;354: 1601-1613.

4. Lovejoy JC, et al. Effects of diets enriched in saturated (palmitic), monounsaturated (oleic), or trans (elaidic) fatty acids on insulin sensitivity and substrate oxidation in healthy adults. Diabetes Care. 2002 Aug;25(8):1283-8.

5. Haalaininen E, et al. Diet and serum sex hormones in healthy men.
J Steroid Biochem. 1984 Jan;20(1):459-64.

6. Schwalfenberg G. Omega-3 fatty acids: their beneficial role in cardiovascular health.
Can Fam Physician. 2006 Jun;52:734-40.

7. Psota TL, et al. Dietary omega-3 fatty acid intake and cardiovascular risk.
Am J Cardiol. 2006 Aug 21;98(4A):3i-18i.

8. Ismail HM. The role of omega-3 fatty acids in cardiac protection: an overview.
Front Biosci. 2005 May 1;10:1079-88.

9. Parker G, et al. Omega-3 fatty acids and mood disorders.
Am J Psychiatry. 2006 Jun;163(6):969-78. Review. Erratum in: Am J Psychiatry. 2006 Oct;163(10):1842.

10. Griel AE, et al. An increase in dietary n-3 fatty acids decreases a marker of bone resorption in humans. Nutr J. 2007 Jan 16;6:2.

11. Simopolous AP. Omega-3 fatty acids in inflammation and autoimmune diseases. J Am Coll Nutr. 2002 Dec;21(6):495-505.

12. Couet C, et al. Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults. Int J Obes Relat Metab Disord. 1997 Aug;21(8):637-43.

13. Fontani G, Corradeschi F, Felici A, et al. Blood profiles, body fat and mood state in healthy subjects on different diets supplemented with omega-3 polyunsaturated fatty acids. Eur J Clin Invest 2005;35:499–507.

14. Krebs JD, et al. Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women. Int J Obes (Lond). 2006 Oct;30(10):1535-44.

15. Kunesova , et al. The influence of n-3 polyunsaturated fatty acids and very low calorie diet during a short-term weight reducing regimen on weight loss and serum fatty acid composition in severely obese women. Physiol Res. 2006;55(1):63-72

16. Warner JG, et al. Combined effects of aerobic exercise and omega-3 fatty acids in hyperlipidemic persons. Med Sci Sports Exerc 1989;21:498–505.

17. Brilla LR, Landerholm TE. Effect of fish oil supplementation and exercise on serum lipids and aerobic fitness. J Sports Med Phys Fitness 1990;30:173–80.

18. Hill AM, et al. Combining fish-oil supplements with regular aerobic exercise improves body composition and cardiovascular disease risk factors.
Am J Clin Nutr. 2007 May;85(5):1267-74.

19. Thies F, et al. Dietary supplementation with eicosapentaenoic acid, but not with other longchain n-3 or n-6 polyunsaturated fatty acids, decreases natural killer cell activity in healthy subjects aged >55 y. Am J Clin Nutr. 2001 Mar;73(3):539-48.

20. Rees D, et al. Dose-related effects of eicosapentaenoic acid on innate immune function in healthy humans: a comparison of young and older men. Am J Clin Nutr. 2006 Feb;83(2):187-8.

21. American Heart Association. New guidelines focus on fish, fish oil, omega-3 fatty acids. 2002.

22. Harper CR, et al. Flaxseed oil increases the plasma concentrations of cardioprotective (n-3) fatty acids in humans. J Nutr. 2006 Jan;136(1):83-7.