Tag Archives: fat

Cardio Makes You Fat and Apples Will Rise

 

By Jose Antonio PhD FNSCA FISSN 

Key Points To Memorize for the ‘Cardio Makes You Fat’ Crowdsm_cardio-fat-banner

  • Longitudinal training studies of fat kids shows that aerobic training results in a loss of body fat.
  • Longitudinal training studies of fat adults shows that aerobic training results in a loss of body fat.
  • Those who do the most cardio over a 15- to 20-year period exhibit the lowest levels of body fat.
  • Athletes that are engaged in highly aerobic exercise have single digit body fat percentages.
  • Triathletes with a higher training volume have a lower % fat than those with a lower training volume.
  • Cardio does not make you fat.
  • Eating too much makes you fat.
  • Sitting on your ass all day makes you fat.
  • Your brain is comprised mainly of fat.  (This has nothing to do with the article but it is a fun fact).

After seeing another headline of “Does Cardio Make You Fat?” with the answer that ‘of course it does,’ I felt an urge to get off my couch, hit the pause button on “The Blacklist,” (awesome show BTW), and remind people that there is something called “science” that can actually answer that question. “I’m not sure why cardio has become the carb of the exercise world” says Rutgers professor Shawn Arent PhD.  And Dr. Arent hates cardio like rats hate cats, cats hate dogs, and dogs hate Michael Vick.

Pauline loves lifting heavy things, doing cardio and drinking coffee. She'll kick your ass too. Ok maybe not.

Pauline loves lifting heavy things, doing cardio and eating Swedish meatballs. Ok. I made the meatball part up.

What the heck happened to folks actually reading the scientific literature? You know. Those studies in which scientists actually measure body fat. Instead folks fall hook, line and sinker for this pettifogging bullshit of how cardio affects your appetite, cortisol etc. If the claim is that ‘cardio makes you fat,’ the ONLY measure that matters is whether it makes you fat. Guess what? You need to measure body fat. It reminds me of these acute feeding studies that use whey, casein, amino acids etc. that try to extrapolate how much muscle you’d gain in the long run by looking at acute changes in muscle protein synthesis. I have a better idea. Why don’t you actually measure muscle or lean body mass after a treatment period that matters (ex. 8-12 weeks)? Getting back to my original point, imagine how boring the world would be without carbs or cardio?  You couldn’t eat donuts, take walks on the beach, or do both at the same time.

When did doing cardio suddenly become bad for fat loss?  The boneheads who write these articles should at least make a feeble attempt to read the literature. A simple search on Pubmed cross-referencing ‘aerobic’ with ‘body composition’ shows 517 publications.  There are umpteen other searches of key words you can perform. I’m certain there’s at least one study that’s looked at whether cardio turns you from a lean mean kale-eating machine to a fat slob who dreads the day that buffets are outlawed by Congress.

So what gives? Why has the ‘cardio makes you fat camp’ become so entrenched among a few vocal gurus in the fitness industry? Answer: I haven’t an f’in clue.

Anyhow, let’s harken back to when Ronald Reagan was the President of the USA; that’s the 1980s for those who flunked US History.  Twelve weeks of doing aerobic dance training (3 days per week for 45 min) resulted in “…significant increases in lean body mass and body density, together with decreases in percentage body fat and the sum of four skinfold thicknesses…”[1] Holy smokes did you read that?  They lost weight and fat doing aerobic dance no less. Hmmm.

Bill-Clinton-Jogging-for-Weight-Loss

President Clinton should have done more cardio and less McDonalds.

Let’s fast forward to when Bill Clinton was America’s Commander-in-Chief. In this particular study, 60 Japanese women (~51 years of age) participated in a 3-month weight-loss program consisting of two groups: aerobic dance group and jogging and/or cycling group. Guess what, whether you dance, jogged or cycled, you lost body weight and body fat.  The study’s authors stated “low impact aerobic dance is as useful as jogging or cycling in improving body composition and aerobic power for mildly obese middle-aged women.”  Whoa Nellie.  Isn’t cardio supposed to make you fat?[2]

What happens to fat kids who are put on an aerobic exercise program? Inquiring minds want to know. Scientists put 28 obese children (16 boys, 12 girls; aged 12-14 years) into an exercise group or control group. The exercise group participated in 16-week aerobic exercise program (four 60-min sessions per week at 70-85% of HRmax), in addition to the school’s physical education. So did the fat kids get fatter? Uh no. The kids who did aerobic exercise not only demonstrated a smaller waistline (time to buy new belts), but they also showed a significant drop in fat mass.[3]

Now let’s get a bunch of fat adults and see what happens? In this study, science nerds determined the effect of aerobic exercise, without energy restriction, on weight loss in sedentary overweight and obese men and women. The key words being ‘without energy restriction.’ Thus if cardio truly makes you a porky pig, then it would happen in this study.

Participants were randomized into a 400 calorie/session, a 600 calorie/session or to a non-exercise control. Exercise was supervised, 5 days/week, for 10 months.  Now if we use the sterling logic of the ‘cardio makes you fat’ crowd, then one would predict that the 600-calorie/session group would be the fattest at the end of the study, correct?  Well, good thing we have science to answer this question and not some voodoo-witch doctor-fitness guru bullshit.  What happened? “Significant changes in percent body fat over 10 months were observed in both the 400 (-2.9%) and 600 (-4.4%) kcal/session groups. Percent fat was unchanged in the control group (-0.6%). The reductions in body weight observed in both exercise groups were a result of decreased fat mass and preservation or increase in fat-free mass.”[4] Wait did I read that right? The group that did more aerobic exercise actually lost body weight and fat?  What’s going on here?  Why aren’t these cardio kings and queens getting fat?  Because exercising (no matter what type) doesn’t make you fat. And if you believe otherwise, then you may as well get into the business of unicorn breeding.guys-unicorns-mating_design

Are you bored yet? Does science have a way of beating the crap out of dogma? Anyone who claims that ‘cardio makes you fat’ has more hot air than the Hindenburg.

Here are a few more bite-sized bullets for you to remember:

  • A 10-week aerobic exercise program results in a small decrease in energy intake and an associated decrease in percentage of body fat in obese adolescents.[5]
  • Twelve weeks of regular aerobic exercise led to significant reductions in body weight, body fat percentage, and body mass index in the obese.[6]
  • Aerobic exercise training can reduce % body fat and enhance vascular compliance in obese male adolescents.[7]
  • “Aerobic training is the optimal mode of exercise for reducing fat mass and body mass, while a program including resistance training is needed for increasing lean mass in middle-aged, overweight/obese individuals.”[8]
  • In obese adolescent boys, both aerobic and weight-training exercises for a 3-month period resulted in a loss of total and visceral fat.[9]

What happens to athletes who train for years? This is where the story gets interesting. It should be as clear as the majestic blue water of the Caribbean that in untrained, fat, and/or average individuals, doing consistent aerobic exercise leads to a drop in body fat. The fact that I’m typing that sentence shows how silly the fitness industry has become. Perhaps in my next article, I’ll attempt to convince you that water is wet. But apparently some need convincing. Anyhow, there are several very cool studies on athletes. Do they get fat with all that aerobic exercise?

Check out my friend Arlene Semeco (left) with Dara Torres. All that cardio (swimming) sure is making them fat, huh?

Check out my friend Arlene Semeco (left) with Dara Torres. All that swimming sure is making them fat, huh?

Steve Fleck PhD did a descriptive study back in 1983 showing the physical characteristics of elite American athletes.[10] (See Table 1) If cardio truly made you fat, then for chrissakes why are marathon runners so lean? I know I know. Genetics. Are they lean because they run?  Or do they run because they are lean? Or both? You might look at swimmers and say ‘hey, their body fat percentage tends to be higher than other elite athletes.’ And you’re correct. It has to do in part with thermoregulation (water is colder than ambient air temp), the buoyancy of fat (it floats), etc.  But to say ‘swimming makes you fat’ would make about as much sense as telling an Irishman to lay off the pint, feckin eh.’ You’ll notice that sports that are very anaerobic as well as highly aerobic in nature have athletes that demonstrate single digit body fat levels. Sports in which your body weight is supported tend to have higher body fat levels. So if your tutorial on science was from internet experts and the ‘science for dummies’ book, then you might conclude that having your body weight supported makes you fat. Watch. Some dipshit will post that as an internet meme.

Table 1. Body Composition of the Elite American Athletes[10]

Sport % Fat Male % Fat Female
Average College 15 25
Canoe/Kayak 13.0 22.2
Swimming 12.4 19.5
Boxing 6.9 n/a
Wrestling 7.9 n/a
Sprinters (100, 200, 400 m) 6.5 13.7
Marathon (26.2 miles) 6.4 n/a

A 1997 study from former QB Tim Tebow’s alma mater did a 20-year follow-up of track and field athletes.[11]  Six of these athletes ran the 800m, 17 did the 1500m distance or longer, and two were race walkers.  Athletes were divided into the follow three groups: high (remained elite), moderate (still performed frequent moderate to rigorous endurance training) and last but not least, low (greatly reduced training). So using the ‘cardio makes you fat’ logic, would not those who trained the most (i.e. high) exhibit the highest levels of fat?  See the answer in Table 2.

Table 2. 20-Year Follow Up of Track and Field Athletes

Athletic Level Baseline % Fat 20-years Later – % Fat
Low 15.7 21.8
Moderate 13.2 17.7
High 10.2 15.3

As you can see (and if you can’t, you need eyeglasses), those who train the most, have the lowest amount of fat.  This applies even as they age.  If anything, it should be clear that getting old results in higher body fat levels.  Yes.  In the battle of aging versus you doing everything right (i.e. exercise regularly and eating well), aging ALWAYS wins.

Distance Runners versus Bobsledders – In a classic comparison of endurance versus power athletes, Marti and Howald investigated the alterations in their physical characteristics over a 15-year period from 1973 to 1988.[12]  First let’s do a direct comparison of runners and bobsledders. (Table 3)Bob sledders

Table 3. 15-Year Follow-Up of Runners and Bobsledders

Group

 % Fat in 1973 % Fat in 1988

Runners

 8.0 12.5

Bobsledders

 20.1 22.1

You’ll notice that runners are leaner than bobsledders at all time points. Wait a sec. I thought cardio makes you fat? Interestingly, bobsledders are quintessential power athletes. Shouldn’t they be leaner than distance runners? Now let’s just look at the distance runners and divide them into highly active (ran >90 km/wk), active (30-65 km/wk) and former runners (less than 30 km/wk).  (Table 4)

Table 4. 15-Year Follow-Up of Distance Runners Grouped By Distance Run/Week

Group

 % Fat in 1973 % Fat in 1988
Highly Active 9.0 5.1
Active 6.5 8.6
Former 10.3 21.2
suzy_favor_hamilton4-getty_1356117573_540x540

Suzy Favor could run! We wrote a book about training and nutrition for distance running many moons ago. Check it out. It’s called “Fast Track.”

Well whaddya know.  Distance running (in general) keeps you pretty lean. Those who kept running (and did the most mileage per week) were the leanest. Those who did the least amount of that dreaded cardio, got fatter.[12]  In fact, triathletes that perform more aerobic training actually have lower % body fat levels than those who do less.[13] Why that is surprising to anyone baffles me. It’s like being surprised that kangaroos jump, eagles fly and Venezuela runs out of toilet paper.

Cardio and Muscle Mass – On the flip side, too much cardio may promote a loss of lean body mass.  But that’s NOT the same as saying ‘cardio makes you fat.’ Sometimes I feel like folks who post dopey stuff on social media need a class in ‘how to ask the right question.’  One particular study showed that in young women, doing aerobic exercise for 12 weeks promoted a loss of body weight, % body fat and BMI. But it also resulted in a loss of lean body mass.[14] On the other hand, aerobic exercise attenuated the loss of muscle mass during calorie restriction in adults with fat bellies.  Folks that dieted only lost fat and lean body mass.[15] So if you want to argue that aerobic training might result in a loss of muscle mass, you’ll have scientific support.  But it certainly isn’t universal.  Some might lose lean body mass, others not so.  Heck, some might actually gain lean body mass if they are initially very untrained.

Side Bar – Fasted versus Fed Cardio – In an elegant study by Shoenfeld et al., they investigated changes in fat mass and fat-free mass following four weeks of volume-equated fasted versus fed aerobic exercise in young women on a lower calorie diet. Training consisted of 1 hour of steady-state aerobic exercise performed 3 days per week. Holy smokes!  Dr. Brad is going to make these girls fat.  How did he ever get this through the IRB and Human Subjects Review? What did they discover? Both groups showed a significant loss of weight and fat mass from baseline; however, there were no significant between-group differences. All that cardio made them fat said no scientist ever.

The moral of the story:

Pooks running

My pet dachshund “Pooks” hates cardio; she loves to sprint. But not as much as she loves to eat ground beef.

  • First of all, anyone who tells you that exercise x, y, and z (you fill in the blank) makes you fat, has about as much science training as my pet Dachshund.
  • We have a plethora longitudinal training studies as well as cross-sectional data which clearly show that performing cardio helps you lose body fat.
  • The preponderance of scientific evidence clearly demonstrates that aerobic or ‘cardio’ training results in a loss of fat.
  • If you prefer anecdotes as your ‘evidence,’ then I’d suggest you get your training/nutrition advice from Jenny McCarthy or the Food Babe.
  • If your goal is to lose body fat and look purrrty, why on god’s earth would you eliminate one form of exercise (i.e. aerobic exercise or ‘cardio’) entirely?
  • If your goal is to compete in an endurance event, then clearly you must do cardio.
  • If you’re a strength-power athlete (e.g. discus, shot put, Olympic weight lifter, powerlifter, high jump etc), you shouldn’t do any cardio.
  • If you like doing cardio, do it.
  • If you hate doing cardio, don’t do it.
  • But don’t be a fool and repeat the ‘cardio makes you fat’ mantra.
  • Getting fat is affected more by your kitchen habits than what you do in the gym/outdoors.
  • Goals determine strategies. Know your goal.

Take home message: Apples won’t rise, Pigs won’t fly, and Aerobic exercise won’t make you fat.applenewton1

Read This All You Cardio Haters

1.            Williams, L.D. and A.R. Morton, Changes in selected cardiorespiratory responses to exercise and in body composition following a 12-week aerobic dance programme. J Sports Sci, 1986. 4(3): p. 189-99.

2.            Shimamoto, H., et al., Low impact aerobic dance as a useful exercise mode for reducing body mass in mildly obese middle-aged women. Appl Human Sci, 1998. 17(3): p. 109-14.

3.            Regaieg, S., et al., The effects of an exercise training program on body composition and aerobic capacity parameters in Tunisian obese children. Indian J Endocrinol Metab, 2013. 17(6): p. 1040-5.

4.            Donnelly, J.E., et al., Aerobic exercise alone results in clinically significant weight loss for men and women: midwest exercise trial 2. Obesity (Silver Spring), 2013. 21(3): p. E219-28.

5.            Thivel, D., et al., Is energy intake altered by a 10-week aerobic exercise intervention in obese adolescents? Physiol Behav, 2014. 135: p. 130-4.

6.            Lee, S.S., et al., The Effects of 12 Weeks Regular Aerobic Exercise on Brain-derived Neurotrophic Factor and Inflammatory Factors in Juvenile Obesity and Type 2 Diabetes Mellitus. J Phys Ther Sci, 2014. 26(8): p. 1199-204.

7.            Song, J.K., et al., Effects of 12 weeks of aerobic exercise on body composition and vascular compliance in obese boys. J Sports Med Phys Fitness, 2012. 52(5): p. 522-9.

8.            Willis, L.H., et al., Effects of aerobic and/or resistance training on body mass and fat mass in overweight or obese adults. J Appl Physiol (1985), 2012. 113(12): p. 1831-7.

9.            Lee, S., et al., Effects of aerobic versus resistance exercise without caloric restriction on abdominal fat, intrahepatic lipid, and insulin sensitivity in obese adolescent boys: a randomized, controlled trial. Diabetes, 2012. 61(11): p. 2787-95.

10.          Fleck, S.J., Body composition of elite American athletes. Am J Sports Med, 1983. 11(6): p. 398-403.

11.          Pollock, M.L., et al., Twenty-year follow-up of aerobic power and body composition of older track athletes. J Appl Physiol (1985), 1997. 82(5): p. 1508-16.

12.          Marti, B. and H. Howald, Long-term effects of physical training on aerobic capacity: controlled study of former elite athletes. J Appl Physiol (1985), 1990. 69(4): p. 1451-9.

13.          Knechtle, B., et al., A comparison of anthropometric and training characteristics of Ironman triathletes and Triple Iron ultra-triathletes. J Sports Sci, 2011. 29(13): p. 1373-80.

14.          Kostrzewa-Nowak, D., et al., Effect of 12-week-long aerobic training programme on body composition, aerobic capacity, complete blood count and blood lipid profile among young women. Biochem Med (Zagreb), 2015. 25(1): p. 103-13.

15.          Yoshimura, E., et al., Aerobic exercise attenuates the loss of skeletal muscle during energy restriction in adults with visceral adiposity. Obes Facts, 2014. 7(1): p. 26-35.

BIO – Jose Antonio PhD wishes he could run but he’s slower than a sloth on Xanax. He wishes he could swim but he looks like a drunk bulldog flappin’ in the water. Instead he Paddling race SUP Clermont March 2015paddles. The beach, sunshine, and a good sweat – you can’t beat that. :-)  If you want to buy me a beer or donate money to support my sushi habit, meet me in Austin Texas June 11-13, 2015 at the ISSN Conference and Expo.

Why Not Fat?

Jordan M. Joy CISSN.  What do we think of when we think of “bad” food? No, not the tastes bad Fear Factor type foods, but the naughty foods we’re discouraged from eating. Desserts, potato chips, hot dogs, deep fried mayonnaise balls, and the list goes on. Generally speaking, we classify fats as “bad,” and we classify sugars as “bad.” I can get behind sugar as bad for the most part (it is beneficial in some situations), but fat as bad? That’s a notion I can’t support.

Why do we, as a society, criminalize dietary fat? Well its NAME is FAT! If we were to just call healthy_high_fat_foods_draft_2them lipids from the get go, they would probably be more accepted. Nomenclature aside, the United States used to support an “eat more” diet, as nutrient deficiencies were highly prevalent in the early 1900’s. However, the progression into our current, overweight society became a concern around the 1960’s, and a globally conducted study associated fat with death rates, while complex carbohydrates were negatively associated. Thus, we now have the recommendation that ~50% of daily calories should come from carbohydrates. Unfortunately, the “complex” portion of carbohydrates has been lost for most individuals, and if trends mean anything, we’re likely worse off than before.

Interestingly, 150g had, at least at one time, been determined to be the minimum amount of carbohydrate necessary for maintenance of health. However, carbohydrates are not an essential nutrient soooo… uhh what? You don’t need them! Your body can actually produce up to 200g of its own carbohydrate per day. Moreover, that global study from I mentioned doesn’t translate to the good ol’ US of A, and the replacement of saturated fat with carbohydrate does NOT lower risk for CHD whereas the replacement of saturated fat with polyunsaturated fat does lower risk for CHD. In addition, there is overwhelming support for a very low carbohydrate, ketogenic diet for improving symptoms of metabolic syndrome. Of course while following a ketogenic diet, dietary fat is much higher than recommended. Fat is not bad on its own. However, fat in combination with sugar reduces fatty acid oxidation. So for the desserts or the potato chips or the hot dogs, is it any one of the nutrients or is it the combination? More evidence is necessary to fully clarify, but so far it seems that it is the combination. So really, why not fat as a primary fuel source?

For most of you or someone you know, the answer is energy systems, and most athletes tend to care about their performance during the ~10-120 second range. Outside the population of competitive athletes, fats are perfectly suitable for composing the primary energy source, and they’re likely beneficial. Thinking of the roles between the two, carbohydrates supply energy and not very much of anything else, while fats have a role in hormone synthesis, vitamin absorption, neural function, and so on. All of these things are critical for athletic performance. The thing about carbohydrates are they’re only needed for high intensity exercise. For the casual 5k runner, they’re not all that important (evidence demonstrates low intensity exercise is not altered by a ketogenic diet), but a soccer player absolutely would benefit. Still, how useful is your mouth guard from pee wee football? Not very because you only need it when you need it. Sugars are the same way; have them during periods of activity and “load” other carbohydrates prior to competition. Have your fat separate from carbohydrates when possible, but certainly don’t fear it.

In short, dietary fat is not to be feared. In all actuality, it seems that sugar exacerbates health problems more so than fat, and it may possibly make fat bad, so just like picking your friends nose, you can have your bacon, and you can have your bagel (whole grain, of course), but you might not want to put your bacon on your bagel.

BIO – Jordan Joy is currently a Research Coordinator at MusclePharm Sports Science Institute. He is a CISSN certified sport nutritionist and CSCS certified strength coach. He has his BS in Exercise Science from the University of Tampa and is pursuing his MS in Applied Nutrition with Northeastern University.

References

  • Masironi, R. (1970). Dietary factors and coronary heart disease. Bulletin of the World Health Organization, 42(1), 103
  • Nestle, M. (2013). Food politics: How the food industry influences nutrition and health (Vol. 3). Univ of California Press
  • Westman, E. C. (2002). Is dietary carbohydrate essential for human nutrition? The American journal of clinical nutrition, 75(5), 951-953.
  • Astrup, A., Dyerberg, J., Elwood, P., Hermansen, K., Hu, F. B., Jakobsen, M. U. & Willett, W. C. (2011). The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010 The American journal of clinical nutrition, 93(4), 684-688.
  • Volek, J. S., & Feinman, R. D. (2005). Carbohydrate restriction improves the features of Metabolic Syndrome. Metabolic Syndrome may be defined by the response to carbohydrate restriction. Nutr Metab (Lond), 2(1), 31.
  • Phinney, S. D. (2004). Ketogenic diets and physical performance. Nutr Metab (Lond), 1(1), 2.

Fish Oil For Fat Loss

Fish oil is most known for its beneficial cardiovascular and cardiac health effects, and continues to top the list of health promoting supplements. In 2004 FDA approved a prescription fish oil preparation for treatment of high blood triglycerides (hypertriglyceridemia) (1). Recently several studies have shown that fish oil also has other beneficial effects, which might appeal more to the younger crowd, and especially to fitness and bodybuilding enthusiasts. One of these effects is fat loss.

Fish Oil Induced Fat Loss

In the 80s early 90s, several animal studies showed that fish oil reduces body fat (2-5) and weight gain (6-9), and limits adipose tissue expansion (10-12). These effects have been seen during both a decreased (3, 7), constant (5) or even increased energy intakes (6). This indicates that the fatty acids in fish oil, notably EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid), have an effect on the partitioning of fat between oxidation (fat burning) and storage in the body.

Mechanism – how does it work?

In search for the mechanisms behind fish oil induced fat loss, it has been found that fish oil exerts favorable metabolic effects by modulating gene expression (which is the process by which the information encoded in a gene is converted into protein)(2, 13-26). While we inherit our genes (or blueprints) from our parents, what determines the way in which our blueprints are interpreted is largely dictated by a collection of environmental factors. The nutrients we consume are among the most influential of these environmental factors (27, 28). One dietary constituent that has a strong influence on our genetic makeup is dietary fat (2, 13, 14, 16-19, 21-23, 25, 29). Fatty acids from dietary fat not only influences hormonal signaling events, but also have a very strong direct influence on the molecular events that govern gene expression.

More specifically, it has been shown that the fatty acids EPA and DHA from fish oil (by affecting gene expression) inhibit the activities of fat synthesizing (lipogenic) enzymes (30-37), while at the same time stimulating the activities of key enzymes that govern fat oxidation (fat burning) (2, 38-46).

Fish oil also has been shown to increase levels of adiponectin and decrease levels of cortisol (47, 48). Adiponectin is a novel adipose tissue-specific protein that circulates in human plasma at high levels (49). It is one of the physiologically active polypeptides secreted by adipose tissue, whose multiple functions have started to be understood in the last few years. Some of its beneficial effects are enhanced insulin sensitivity, and lowered plasma glucose (blood sugar) and triglyceride levels (49, 50). A reduction in adiponectin expression is associated with insulin resistance (49), and adiponectin levels are inversely related to the degree of adiposity (50). The activity of adiponectin has also been associated with steroid and thyroid hormones, glucocorticoids, and nitric oxide, and has anti-atherogenic and anti-inflammatory properties (50). Thus, it is plausible that fish oil induces some of its effect by affecting adiponectin levels.

While the functions of adiponectin are just starting to emerge, it is likely to become a target for therapeutic applications in the future.

It is interesting that fish oil lowers cortisol. While the exact role of cortisol in obesity isn’t fully elucidated (51, 52), it is known that excessive cortisol levels result in substantial fat mass gain (53, 54). Thus, the reduction in cortisol levels after fish oil supplementation could contribute at least partly to the fat loss observed with fish oil supplementation. In another article I’m covering the anti-catabolic/muscle growth effects of fish oil in more detail.

Fish Oil for Muscle Growth

Does it work in humans – what’s in it for me?

At this point you might be thinking “ok, that all sounds nice, but I’m not a rat. Does it work in humans”?

Yes! Read on…

Non-dieting

Recently several studies have shown that fish oil also can help people to get in shape. In a landmark study in healthy young non-obese males, 6 g of fat from butter, olive oil, sunflower oil and peanut oil was replaced with 6 g fish oil (corresponding to 1,100 mg EPA and 700 mg DHA) per day (55). After 3 weeks the researchers noted a significantly increased resting fat burning (fat oxidation) and a 1.94 lb (0.88 kg) decrease in body fat (measured by the golden standard method DEXA). There was no change in body weight. This fat loss was seen despite that subjects were told not to change their usual exercise and food habits.

Other studies have confirmed the fat loss effects of fish oil when added to people’s usual lifestyle habits.

One study gave healthy men and women (mean age 33 yrs), who were told to maintain their current food and exercise practices 4 g fish oil, providing 1,600 mg EPA and 800 mg DHA (48). After 6 weeks, the placebo group, which was given 4 g of safflower oil, showed a tendency towards fat gain. In contrast, the fish oil group experienced a significant reduction in fat mass of 1.1 lb (0.5 kg) and increase in fat-free mass of 1.1 lb (0.5 kg) (measured by air displacement plethysmography), with no change in body weight.

A 1.1 lb reduction in fat mass combined with a 1.1 lb increase in fat-free mass, without changes in subject’s typical food and exercise habits is pretty remarkable body composition improvement. It also underscores the importance of investigating fat mass and lean mass separately, since just measuring body weight will not tell anything about potential body composition changes, which after all is what is interesting from both a health, esthetic and physical performance viewpoint. For more into on the anti-catabolic and lean mass gaining effects of fish oil, see Fish Oil for Muscle Growth

Another study, also against a background of constant food and exercise routines, gave obese type 2 diabetic female subjects 1,080 mg EPA and 720 mg DHA for 2 months, or placebo paraffin oil (56). Even though there was no change in body weight, the fish oil group demonstrated a significant reduction in fat mass by 3.6 lb (1,614 kg). This fat mass reduction was mainly due to a decrease in trunk (belly) fat. In addition, fish oil group experienced a reduction in fat cell size by 6.3 % (56).

It has also been found that supplementing with fish oil for 3 weeks (1,100 g EPA and 700 g DHA daily) significantly decreases insulin levels and increases fat burning after consumption of carbohydrate rich meals (57). Supplementation with fish oil providing 2,400 mg EPA and 1,600 mg DHA for 3 weeks also boosts fat burning during jogging exercise (58).

Combined with exercise

Fish oil seems to be even more effective when combined with exercise. In obese men and women, the effects of the addition of 6 g of fish oil daily (providing 360 mg EPA and 1,560 mg DHA) in combination with regular aerobic activity (walking 45 min three times per week at an intensity of 75% of age-predicted maximal heart rate) for 12 weeks, was investigated (59). The results showed that the combination of fish oil and regular aerobic activity not only improved several risk factors for cardiovascular disease, but also significantly reduced body fat mass with 4.4 lb (2 kg) (59). The finding that

body weight and body fat percentage didn’t change in the placebo group (which was put on the same exercise program but received 6 g sunflower oil instead of the fish oil)  underscores the efficacy of fish oil for fat loss.

It is interesting that the fat loss seen in the fish oil – exercise group occurred even though the subjects did not change their usual food habits; they just added the fish oil supplement and exercise program to their regimen. This indicates the great potential benefits of fish oil combined with regular physical activity for improving body composition and cardiovascular health.

In this study, no fat loss was seen in fish oil only group (which didn’t exercise). This is probably due to the very low dose of EPA. Most studies showing that fish oil increases fat loss have use fish oil products that provide 1.5-2 times more EPA than DHA, like Lean Lipid Complex does.

Combined with a calorie restricted diet

Fish oil supplementation can boost calorie restricted diets as well. This was found in a study that investigated the effect of including fish oil as part of an energy-restricted diet, on weight loss (60). Young obese adults were put on a calorie restricted diet (30 % less calories than their usual intake, about 600 calorie deficit), supplemented with 6 g fish oil providing 1,500 mg EPA + DHA, or placebo (sunflower oil capsules). It was found that the fish oil enriched diet resulted in 2.2 lb (1 kg) more weight loss and greater reductions in waist circumference after only 4 weeks, than the same diet without fish oil (60).

Combined with a calorie restricted diet and exercise program

In a study that tested the effect of adding 2,800 mg/day fish oil (EPA:DHA ratio 2:1) to a low-calorie diet combined with an exercise program, severely obese women (61). After 3 weeks the fish oil group lost 3.3 lb (1.5 kg) more weight and slashed almost 1 inch (2.3 cm) more fat from their hips, than the non-supplemented group.

While body fat changes were not reported, the researchers did find a greater increase in blood beta-hydroxybutyrate (a ketone body) in the fish oil supplemented group compared with control group, and interpreted this as providing evidence of greater fat oxidation in the fish oil group (61). These findings indicate that the addition of fish oil to a relatively short (3 week) weight loss program comprising severe caloric restriction and exercise, may increase fat oxidation and lead to greater improvement in body composition.

Perspective on fish oil and fat loss

In contrast to the positive studies, there are a few that didn’t show any fat loss with fish oil supplementation (62-65). This could be due to differences in subject characteristics (age, initial body fat mass, baseline physical activity), methodological differences, and differences in fish oil preparations.

As outlined above, several high quality studies have shown that fish oil supplementation has a significant fat loss effect in addition to all its other health promoting effects. The majority of evidence thus supports fish oil’s ability to shift fat metabolism away from storage towards burning of body fat, even in humans.

It’s getting better – fat loss combined with lean mass (muscle) gain

In one of the most recent studies on fish oil’s fat loss effect, men and women (mean age 33 yrs) where given 4 g of fish oil corresponding to 1600 mg EPA and 800 mg DHA (48). After 6 weeks, the placebo group, which was given 4 g of safflower oil, showed a tendency towards fat gain. The fish oil group instead had lost 0.5 kg of fat mass and gained 0.5 kg of lean mass, with no change in body weight.

This is a very beneficial body composition effect and underscores the importance of investigating fat mass and lean mass separately, since just measuring body weight will not tell anything about changes in body composition. After all, it’s not weight loss per see, but fat loss and muscle gain that’s interesting from both a health, esthetic and physical performance viewpoint. I cover the muscle growth stimulating and anti-catabolic effect of fish oil in another article

Fish Oil for Muscle Growth

Bottom Line

Whether you are on a diet or not, adding a fish oil supplement to your regimen can effectively help you get in shape. The additional calories from the fish oil will not get stored (66); quite to the contrary, fish oil will help you get rid of calories you already have stored in your body fat. What’s interesting is that fish oil supplementation seems to reduce body fat and waist circumference despite unchanged exercise and/or other dietary practices.

Aim for a daily fish oil intake that provides you with at least 1600 mg EPA and 800 mg DHA, but a higher dose, 2400 mg EPA and 1600 mg DHA (a total of 4 g EPA and DHA total), might result in a larger fat loss. To achieve this high intake of EPA and DHA it is advisable to take a fish oil concentrate. In an upcoming article I will go into more detail about fish oil concentrates, different ratios of EPA to DHA in fish oil preparations, their relative effectiveness, safety aspects of high dose fish oil supplementation, and sort through the myriad of fish oil supplements currently available on the market, to help you find a good fish oil supplement that will give you the best bang and effectiveness for your buck.

References:

1.           Mason CM, Long J, Conroy C 2011 Prescription Omega-3s: An Overview for Nurse Practitioners. The Journal of cardiovascular nursing 26:290-297

2.           Baillie RA, Takada R, Nakamura M, Clarke SD 1999 Coordinate induction of peroxisomal acyl-CoA oxidase and UCP-3 by dietary fish oil: a mechanism for decreased body fat deposition. Prostaglandins, leukotrienes, and essential fatty acids 60:351-356

3.           Hill JO, Peters JC, Lin D, Yakubu F, Greene H, Swift L 1993 Lipid accumulation and body fat distribution is influenced by type of dietary fat fed to rats. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 17:223-236

4.           Ikemoto S, Takahashi M, Tsunoda N, Maruyama K, Itakura H, Ezaki O 1996 High-fat diet-induced hyperglycemia and obesity in mice: differential effects of dietary oils. Metabolism: clinical and experimental 45:1539-1546

5.           Su W, Jones PJ 1993 Dietary fatty acid composition influences energy accretion in rats. The Journal of nutrition 123:2109-2114

6.           Cunnane SC, McAdoo KR, Horrobin DF 1986 n-3 Essential fatty acids decrease weight gain in genetically obese mice. The British journal of nutrition 56:87-95

7.           LeBoeuf RC, Veldee MS 1993 Genetically determined body weight loss in mice fed diets containing salmon oil. The Journal of nutrition 123:547-558

8.           Mori T, Kondo H, Hase T, Tokimitsu I, Murase T 2007 Dietary fish oil upregulates intestinal lipid metabolism and reduces body weight gain in C57BL/6J mice. The Journal of nutrition 137:2629-2634

9.           Pan DA, Storlien LH 1993 Dietary lipid profile is a determinant of tissue phospholipid fatty acid composition and rate of weight gain in rats. The Journal of nutrition 123:512-519

10.         Belzung F, Raclot T, Groscolas R 1993 Fish oil n-3 fatty acids selectively limit the hypertrophy of abdominal fat depots in growing rats fed high-fat diets. The American journal of physiology 264:R1111-1118

11.         Parrish CC, Pathy DA, Angel A 1990 Dietary fish oils limit adipose tissue hypertrophy in rats. Metabolism: clinical and experimental 39:217-219

12.         Ruzickova J, Rossmeisl M, Prazak T, Flachs P, Sponarova J, Veck M, Tvrzicka E, Bryhn M, Kopecky J 2004 Omega-3 PUFA of marine origin limit diet-induced obesity in mice by reducing cellularity of adipose tissue. Lipids 39:1177-1185

13.         Clarke SD 2000 Polyunsaturated fatty acid regulation of gene transcription: a mechanism to improve energy balance and insulin resistance. The British journal of nutrition 83 Suppl 1:S59-66

14.         Clarke SD 2001 Polyunsaturated fatty acid regulation of gene transcription: a molecular mechanism to improve the metabolic syndrome. The Journal of nutrition 131:1129-1132

15.         Clarke SD 2004 The multi-dimensional regulation of gene expression by fatty acids: polyunsaturated fats as nutrient sensors. Current opinion in lipidology 15:13-18

16.         Clarke SD, Baillie R, Jump DB, Nakamura MT 1997 Fatty acid regulation of gene expression. Its role in fuel partitioning and insulin resistance. Annals of the New York Academy of Sciences 827:178-187

17.         Clarke SD, Gasperikova D, Nelson C, Lapillonne A, Heird WC 2002 Fatty acid regulation of gene expression: a genomic explanation for the benefits of the mediterranean diet. Annals of the New York Academy of Sciences 967:283-298

18.         Clarke SD, Jump DB 1994 Dietary polyunsaturated fatty acid regulation of gene transcription. Annual review of nutrition 14:83-98

19.         Clarke SD, Thuillier P, Baillie RA, Sha X 1999 Peroxisome proliferator-activated receptors: a family of lipid-activated transcription factors. The American journal of clinical nutrition 70:566-571

20.         Davidson MH 2006 Mechanisms for the hypotriglyceridemic effect of marine omega-3 fatty acids. The American journal of cardiology 98:27i-33i

21.         Jump DB, Clarke SD, Thelen A, Liimatta M, Ren B, Badin M 1996 Dietary polyunsaturated fatty acid regulation of gene transcription. Progress in lipid research 35:227-241

22.         Jump DB, Clarke SD, Thelen A, Liimatta M, Ren B, Badin MV 1997 Dietary fat, genes, and human health. Advances in experimental medicine and biology 422:167-176

23.         Nakamura MT, Cho HP, Xu J, Tang Z, Clarke SD 2001 Metabolism and functions of highly unsaturated fatty acids: an update. Lipids 36:961-964

24.         Ntambi JM, Bene H 2001 Polyunsaturated fatty acid regulation of gene expression. Journal of molecular neuroscience : MN 16:273-278; discussion 279-284

25.         Price PT, Nelson CM, Clarke SD 2000 Omega-3 polyunsaturated fatty acid regulation of gene expression. Current opinion in lipidology 11:3-7

26.         Raclot T, Oudart H 1999 Selectivity of fatty acids on lipid metabolism and gene expression. The Proceedings of the Nutrition Society 58:633-646

27.         Moustaid-Moussa N, Berdanier CD 2001 Nutrient-Gene Interactions in Health and Disease. 2nd ed ed: CRC Press

28.         Berdanier CD, Moustaid-Moussa N 2004 Genomics and Proteomics in Nutrition. 1st ed ed: CRC Press

29.         Lapillonne A, Clarke SD, Heird WC 2004 Polyunsaturated fatty acids and gene expression. Current opinion in clinical nutrition and metabolic care 7:151-156

30.         Hannah VC, Ou J, Luong A, Goldstein JL, Brown MS 2001 Unsaturated fatty acids down-regulate srebp isoforms 1a and 1c by two mechanisms in HEK-293 cells. The Journal of biological chemistry 276:4365-4372

31.         Kim HJ, Takahashi M, Ezaki O 1999 Fish oil feeding decreases mature sterol regulatory element-binding protein 1 (SREBP-1) by down-regulation of SREBP-1c mRNA in mouse liver. A possible mechanism for down-regulation of lipogenic enzyme mRNAs. The Journal of biological chemistry 274:25892-25898

32.         Mater MK, Thelen AP, Pan DA, Jump DB 1999 Sterol response element-binding protein 1c (SREBP1c) is involved in the polyunsaturated fatty acid suppression of hepatic S14 gene transcription. The Journal of biological chemistry 274:32725-32732

33.         Nakatani T, Kim HJ, Kaburagi Y, Yasuda K, Ezaki O 2003 A low fish oil inhibits SREBP-1 proteolytic cascade, while a high-fish-oil feeding decreases SREBP-1 mRNA in mice liver: relationship to anti-obesity. Journal of lipid research 44:369-379

34.         Shimano H, Yahagi N, Amemiya-Kudo M, Hasty AH, Osuga J, Tamura Y, Shionoiri F, Iizuka Y, Ohashi K, Harada K, Gotoda T, Ishibashi S, Yamada N 1999 Sterol regulatory element-binding protein-1 as a key transcription factor for nutritional induction of lipogenic enzyme genes. The Journal of biological chemistry 274:35832-35839

35.         Worgall TS, Sturley SL, Seo T, Osborne TF, Deckelbaum RJ 1998 Polyunsaturated fatty acids decrease expression of promoters with sterol regulatory elements by decreasing levels of mature sterol regulatory element-binding protein. The Journal of biological chemistry 273:25537-25540

36.         Xu J, Nakamura MT, Cho HP, Clarke SD 1999 Sterol regulatory element binding protein-1 expression is suppressed by dietary polyunsaturated fatty acids. A mechanism for the coordinate suppression of lipogenic genes by polyunsaturated fats. The Journal of biological chemistry 274:23577-23583

37.         Yahagi N, Shimano H, Hasty AH, Amemiya-Kudo M, Okazaki H, Tamura Y, Iizuka Y, Shionoiri F, Ohashi K, Osuga J, Harada K, Gotoda T, Nagai R, Ishibashi S, Yamada N 1999 A crucial role of sterol regulatory element-binding protein-1 in the regulation of lipogenic gene expression by polyunsaturated fatty acids. The Journal of biological chemistry 274:35840-35844

38.         Desvergne B, Wahli W 1999 Peroxisome proliferator-activated receptors: nuclear control of metabolism. Endocrine reviews 20:649-688

39.         Kersten S, Desvergne B, Wahli W 2000 Roles of PPARs in health and disease. Nature 405:421-424

40.         Latruffe N, Vamecq J 1997 Peroxisome proliferators and peroxisome proliferator activated receptors (PPARs) as regulators of lipid metabolism. Biochimie 79:81-94

41.         Minnich A, Tian N, Byan L, Bilder G 2001 A potent PPARalpha agonist stimulates mitochondrial fatty acid beta-oxidation in liver and skeletal muscle. American journal of physiology Endocrinology and metabolism 280:E270-279

42.         Nakatani T, Tsuboyama-Kasaoka N, Takahashi M, Miura S, Ezaki O 2002 Mechanism for peroxisome proliferator-activated receptor-alpha activator-induced up-regulation of UCP2 mRNA in rodent hepatocytes. The Journal of biological chemistry 277:9562-9569

43.         Power GW, Newsholme EA 1997 Dietary fatty acids influence the activity and metabolic control of mitochondrial carnitine palmitoyltransferase I in rat heart and skeletal muscle. The Journal of nutrition 127:2142-2150

44.         Schoonjans K, Staels B, Auwerx J 1996 The peroxisome proliferator activated receptors (PPARS) and their effects on lipid metabolism and adipocyte differentiation. Biochimica et biophysica acta 1302:93-109

45.         Krey G, Braissant O, L’Horset F, Kalkhoven E, Perroud M, Parker MG, Wahli W 1997 Fatty acids, eicosanoids, and hypolipidemic agents identified as ligands of peroxisome proliferator-activated receptors by coactivator-dependent receptor ligand assay. Mol Endocrinol 11:779-791

46.         Reddy JK, Mannaerts GP 1994 Peroxisomal lipid metabolism. Annual review of nutrition 14:343-370

47.         Delarue J, Matzinger O, Binnert C, Schneiter P, Chiolero R, Tappy L 2003 Fish oil prevents the adrenal activation elicited by mental stress in healthy men. Diabetes & metabolism 29:289-295

48.         Noreen EE, Sass MJ, Crowe ML, Pabon VA, Brandauer J, Averill LK 2010 Effects of supplemental fish oil on resting metabolic rate, body composition, and salivary cortisol in healthy adults. Journal of the International Society of Sports Nutrition 7:31

49.         Diez JJ, Iglesias P 2003 The role of the novel adipocyte-derived hormone adiponectin in human disease. European journal of endocrinology / European Federation of Endocrine Societies 148:293-300

50.         Nedvidkova J, Smitka K, Kopsky V, Hainer V 2005 Adiponectin, an adipocyte-derived protein. Physiological research / Academia Scientiarum Bohemoslovaca 54:133-140

51.         Walker BR 2001 Activation of the hypothalamic-pituitary-adrenal axis in obesity: cause or consequence? Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society 11 Suppl A:S91-95

52.         Salehi M, Ferenczi A, Zumoff B 2005 Obesity and cortisol status. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 37:193-197

53.         Bjorntorp P, Rosmond R 2000 Obesity and cortisol. Nutrition 16:924-936

54.         Pasquali R, Vicennati V, Cacciari M, Pagotto U 2006 The hypothalamic-pituitary-adrenal axis activity in obesity and the metabolic syndrome. Annals of the New York Academy of Sciences 1083:111-128

55.         Couet C, Delarue J, Ritz P, Antoine JM, Lamisse F 1997 Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 21:637-643

56.         Kabir M, Skurnik G, Naour N, Pechtner V, Meugnier E, Rome S, Quignard-Boulange A, Vidal H, Slama G, Clement K, Guerre-Millo M, Rizkalla SW 2007 Treatment for 2 mo with n 3 polyunsaturated fatty acids reduces adiposity and some atherogenic factors but does not improve insulin sensitivity in women with type 2 diabetes: a randomized controlled study. The American journal of clinical nutrition 86:1670-1679

57.         Delarue J, Couet C, Cohen R, Brechot JF, Antoine JM, Lamisse F 1996 Effects of fish oil on metabolic responses to oral fructose and glucose loads in healthy humans. The American journal of physiology 270:E353-362

58.         Huffman DM, Michaelson JL, Thomas T, R. 2004 Chronic supplementation with fish oil increases fat oxidation during exercise in young men. . JEPonline 7:48-56

59.         Hill AM, Buckley JD, Murphy KJ, Howe PR 2007 Combining fish-oil supplements with regular aerobic exercise improves body composition and cardiovascular disease risk factors. The American journal of clinical nutrition 85:1267-1274

60.         Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, Bandarra NM, Schaafsma G, Martinez JA 2007 Randomized trial of weight-loss-diets for young adults varying in fish and fish oil content. Int J Obes (Lond) 31:1560-1566

61.         Kunesova M, Braunerova R, Hlavaty P, Tvrzicka E, Stankova B, Skrha J, Hilgertova J, Hill M, Kopecky J, Wagenknecht M, Hainer V, Matoulek M, Parizkova J, Zak A, Svacina S 2006 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. Physiological research / Academia Scientiarum Bohemoslovaca 55:63-72

62.         Brilla LR, Landerholm TE 1990 Effect of fish oil supplementation and exercise on serum lipids and aerobic fitness. The Journal of sports medicine and physical fitness 30:173-180

63.         Warner JG, Jr., Ullrich IH, Albrink MJ, Yeater RA 1989 Combined effects of aerobic exercise and omega-3 fatty acids in hyperlipidemic persons. Medicine and science in sports and exercise 21:498-505

64.         Krebs JD, Browning LM, McLean NK, Rothwell JL, Mishra GD, Moore CS, Jebb SA 2006 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) 30:1535-1544

65.         DeFina LF, Marcoux LG, Devers SM, Cleaver JP, Willis BL 2011 Effects of omega-3 supplementation in combination with diet and exercise on weight loss and body composition. The American journal of clinical nutrition 93:455-462

66.         Bays HE, Maki KC, Doyle RT, Stein E 2009 The effect of prescription omega-3 fatty acids on body weight after 8 to 16 weeks of treatment for very high triglyceride levels. Postgraduate medicine 121:145-150

About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor and Master degree in Nutrition from the University of Stockholm / Karolinska Institue, Sweden. She has also done PhD level course work at renowned Baylor University, TX. Today Monica works as diet/health counselor, medical writer, health journalist, and website developer. She is also a fitness model.

As a young athlete, Monica realized the importance of nutrition for maximal performance, and went for a major in Nutrition at the University of Stockholm. During her years at the University she was a regular contributor to Swedish fitness and bodybuilding magazines. She has written a book (in Swedish) for health professionals, “Functional Foods for Health and Energy Control” with over 700 scientific research citations, and authored several book chapters in Swedish popular press publications.

After having earned her Bachelor and Master degree in Nutrition, she completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, Department of Health Human Performance and Recreation.

Having lost her father in a lifestyle induced heart attack at an age of 49, she is specializing in cardiovascular health, and primordial/primary prevention. She is a strong advocate of early intervention in adolescence and young adulthood, and the importance of lifestyle habits for health promotion at all ages.

Today, Monica is sharing her solid academic knowledge, real-life hands on experience and passion by offering diet/nutrition/exercise/health consultation services, and working as a health journalist and medical writer, specializing in fitness, health promotion and anti-aging.

 

Saturated Fat – Not Guilty!

By Scott Robinson.   There’s some serious confusion about saturated fat, and whether it is bad for the heart and is associated with diseases such as diabetes, stroke, and cancers.

The demonization of saturated fat began about 100 years ago, when a researcher fed a rabbit a high cholesterol carnivore diet and observed that its arteries became blocked with plaque.  However, this really took shape in the Fifties with the Seven Countries study by Ancel Keys(1), who reported that a higher saturated fat High_Fat_Foodsintake was associated with a higher cholesterol level and a higher rate of heart disease. The basic premise on which this condemnation lies is that saturated fat (found in foods such as meat, eggs, dairy products, coconut and palm oil) raises cholesterol which in turn, increases the risk of clogged arteries (atherosclerosis). Subsequently, the emergence of low-fat diets and ‘fat-free’ foods has spread with whipping speed and sweep with millions of people deciding to put low fat items into their shopping trolley in the belief that it is doing them good. But is fat, specifically saturated fat, the real criminal here or have we been somewhat misguided by company-funded research, fat-phobic conventional medical wisdom and the advertising prowess of a concept that now encompasses a multi-million dollar industry?

Saturated Fat is Essential for a Healthy Life

Fatty acids play several key roles in the body; they are essential components of all cell membranes, they are responsible for the absorption of the fat-soluble vitamins A, D, E and K, and include the essential n-3 and n-6 poly-unsaturated fatty-acids (PUFA).

The evidence that saturated fat is bad is limited. In fact, contemporary research states quite the opposite. A recent meta-analysis of prospective cohort studies(2) showed that the intake of saturated fat is not associated _73638186_fried_sausages-spl-1with an increased risk of coronary heart disease, stroke or those two combined (i.e. cardiovascular disease, CVD) before(2) or after(3) adjustment for serum total cholesterol. What’s more, an eloquent study published in the journal Nutrition(4), where researchers looked at the average intake of saturated fat in 41 European countries in 1998 (the latest available data) and the age-adjusted risk of mortality from heart disease, revealed something quite remarkable:

More saturated fat, less heart disease; less saturated fat, more heart disease!

That is, as percentages of saturated fat increased, rates of death from heart disease fell. For example, France who consumed the most saturated fat (15.5% of diet) had the lowest rate of heart disease in all of Europe, whereas Bosnia and Herzegovina who consumed very little saturated fat (<4% of diet) had the highest incidence of heart disease. It is worth baring in mind that ecological data such as this doesn’t necessarily prove that saturated fat can protect against heart disease, but it can more or less disprove a theory as let’s face it, it’s difficult to believe that saturated fat is a major contributor to heart disease when Europeans who are consuming it in abundance are so much healthier, without exception.

So, who is the Culprit?

A comprehensive review of studies on saturated fat, carbohydrates and cardiovascular disease by Kuipers et al. in 2011(5) purported that it is the accumulation of saturated fat in body lipids which should concern us and not the damaging effects of dietary saturated fat per se. Take for instance a study published in Lipids(6) which found that when subjects with the metabolic syndrome were fed either a low-CHO/high fat diet with high saturated fat content or a high-CHO/low-fat diet with low saturated fat content, the low-CHO/high-saturated fat diet resulted in lower saturated fat levels in plasma lipids compared with the high-CHO/low-saturated fat diet. What’s more, an analysis of studies found that replacing saturated fat by CHO with a high glycemic index was associated with a whopping 33% increased risk of myocardial infarction(7). Such findings suggest that replacing saturated fat with carbohydrate in the diet, particularly those with a high glycemic index, may increase risk of heart disease.

N-6 vs. N-3 PUFA

Epidemiological and clinical studies show that PUFA plays a key role in the protection against CVD which has led to the suggestion that replacing saturated fat with PUFA is beneficial to cardiovascular health. A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction found that replacing 5 en%  saturated fat by 5 en% PUFA reduces the risk of coronary heart disease by 9.1% (8). Interestingly, Kuipers et al. (5) reported that the replacement of SAFA with n-6 PUFA (notably linoleic acid) shows no health benefit and may actually signal towards increased CVD risk which tells us that the protective role of PUFA in the diet lies with n-3 PUFA!

Take-Home Message:

Going ‘low-fat’ isn’t a particularly good option for weight loss nor health and well-being. Fat forms an essential component of the diet and there is increasing evidence to suggest that increasing saturated fat to ~15% total daily intake isn’t hazardous to heart health and may indeed provide a protective effect against heart disease. It is worth noting that many fat-free or low-fat foods are crammed with artificial sugars and sweeteners and therefore many of us who do go ‘low-fat’ often replace fat with carbohydrates; the consequences of which appear to be an increased risk of heart disease as well as other uncommunicable diseases such as diabetes and cancers. It goes without saying that we must not over-indulge ourselves with saturated fat, but eating less dietary carbohydrate (particularly those with a high-glycemic index), trans-fatty acids and linoleic acid, while increasing the consumption of fish, red meat, vegetables and fruit may be an attractive means of keeping our heart healthy.

‘Our genes should be well adapted to eating ~15% saturated fat – 2 x that recommended as maximum by USDA, yet as much as the healthiest populations in Europe’ Coincidence?

References:

Keys A. B. (1980). Seven countries: a multivariate analysis of death and coronary heart disease. London, England: Harvard University Press, Cambridge Massachusetts.

Siri-Tarino, P. W., Sun, Q., Hu F. B., et al. (2010). Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. American Journal of Clinical Nutrition, 91, 535-46.

Scarborough, P., Rayner, M., van Dis I., et al. (2010). Meta-analysis of effect of saturated fat intake on cardiovascular disease: over-adjustment obscures true associations. American Journal of Clinical Nutrition, 92, 458-464.

European cardiovascular disease statistics (2008 edition). British Heart Foundation Health Promotion Research Group Department of Public Health, University of Oxford and Health Economics Research Centre, Department of Public Health, University of Oxford.

Kuipers, R. S., de Graaf, D. J., Luxwolda, M. F., Muskiet, M. H. A., Dijck-Brouwer, D. A. J, & Muskiet, F. A. J. (2011). Saturated fat, carbohydrates and cardiovascular disease. Netherlands, The Journal of Medicine, 69, 372-378.

Volek J. S., Phinney, S. D., Forsythe, C. E, et al. (2009). Carbohydrate restriction has a more favourable impact on the metabolic syndrome than a low fat diet. Lipids, 44, 297-309.

Jakobsen, M. U., Dethlefsen, C., Joensen, A. M., et al. (2010). Intake of carbohydrates compared with intake of saturated fatty acids and risk of myocardial infarction: importance of the glycemic index. American Journal of Clinical Nutrition, 91, 1764-8.

Stampfer, M. J., Sacks, F. M., Salvini, S., et al. (1991). A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction. New England Journal of Medicine, 325, 373-81.

Bio: Scott is a Doctoral Researcher in Exercise Metabolism at the University of Birmingham, UK. He holds a First Class Honours degree in Sports Science and a Masters with Distinction in Sports Physiology. He currently works as a Nutrition advisor for Myprotein UK who are the UK’s number one online sports nutrition company. For regular updates on the latest in exercise metabolism and nutrition, follow Scott on Twitter @scottrobinson8 or if you have any questions please feel free to email him slr247@bham.ac.uk  

Why Mainstream Media Got it Wrong About Fat

by Brad Dieter, MS, CISSN, CSCS.

This post started out to be a brief overview of fats and then my nerdy side kicked in and I wanted to address a wide range of questions; therefore, I decided to start a small series of fat related topics.  So, the first post in quest to explain fat is to address why they have been vilified, and why the early research was not correct.

Fat gives you love handles, clogs your arteries, causes disease, and should be avoided at all costs. The government says so, your low-fat Wheat Thins says so, and your very well intentioned marathon running uncle says so.  Therefore, fat is bad, AND you shouldn’t eat fat. I mean that sounds like solid logic right? Well unfortunately your well intentioned uncle is wrong, your Wheat Thins aren’t helping your six pack, and the government is lying to you.

In fact, fat is essential, your body requires it and you can’t live without it. Dietary fat is not the main culprit behind your love handles, your “clogged” arteries, or your diabetes, and should be consumed in healthily large quantities. Now, there is a caveat to that in regards to what kinds of fat you should consume and how much is too much and I will dive into that later.  First let’s take a look at what exactly fat is and what it is involved in.

Fat is the collective name given to a wide variety of water-insoluble (cannot be dissolved in water) including all fats and oils in our diet and in our bodies1.  Their chemical structure is similar to carbohydrates (CHO) in the fact that they are made up entirely of carbon (C), hydrogen (H), and oxygen (O); however in fats, the ratio of O to C and H is lower, which makes it a more concentrated source of energy. Aside from its role as an energy provider, fat serves a wide variety of functions in the human body.

FAT NOMENCLATURE

  1. Lipid: A class of compounds consisting of phospholipids, sterols, and triaglycerols1.
  2. Triglyceride: A glycerol molecule with three fatty acids attached.
  3. Glycerol: A three carbon sugar that serves as a backbone for triglycerides.
  4. Fatty Acids: Chains of carbon atoms of varying lengths that attach to a glycerol molecule to form a triaglycerol.
  5. Saturated Fat (SFA): All carbon molecules in the chain are fully bonded with either carbon or hydrogen and contain no double bonds.
  6. Monounsaturated Fat (MUFA): A chain with one double bond.
  7. Polyunsaturated Fat (PUFA): A chain with more than one double bond. The essential N-3 and N-6 (The Omega’s) are examples of PUFAs

Role Fat Plays in The Body

  1. Phospholipids (specific types of fat) make up a large portion of our cell membranes.
  2. They are responsible for transporting fat soluble vitamins (A, D, K, and E) along with other crucial molecules through the body including cholesterol (a special fat we will get to in a minute)
  3. Essential for transmission of nerve signals.
  4. Provide satiety
  5. Produce hormones (specifically leptin) that control homeostasis in terms of your body fat set point (this is known as the adipostat)2
  6. Insulate from thermal stress.
  7. Are essential in the production of corticosteroid hormones3

The definitions and role fats play have been laid out, so now we can dive into the nerdy details! Get excited because this is interesting stuff and will change the way you think about fat!

It is quite apparent that fat is crucial in maintaining a healthy, properly function, metabolic system.  So why have fats been “vilified” by mainstream media? I have a few beliefs on why this happened.

FAT IS MORE CALORIE DENSE

The first idea is that when the beginning of the obesity trend coincided with an increase in caloric intake and as fat has the energy equivalent of 9kcal/gram compared to protein and CHO which have 4kcal/gram, researchers jumped to the conclusion excess calories due to excess fat are responsible for gaining weight. Those researchers also made the assumption that it is strictly an energy balance (calories in vs. calories out) that is responsible for weight gain.

While some small piece of that may be true, it is wildly presumptuous to insinuate that fat is wholly responsible, inherently bad, and should be radically decreased or eliminated.  In fact, as previously stated, fat promotes satiety, which in turns may actually help you you limit overall caloric intake. Also, the researcher’s assumption that “energy balance” is the sole culprit responsible for weight gain and obesity has been proven false in a wide range of literature.  In the light of recent research, it appears that the body has a built in mechanism designed to maintain a set body fat (the adipostat), despite minor, and in some cases major, changes in daily caloric intake. An increase in calories due to fat does not wholly explain the massive increase in obesity.

I would love to dive into this topic even further but that is quite a deep rabbit hole and I want to stay on topic. There are some great studies to read and I have provided a review to read if you are interested2. I really respect Dr. Guyenet’s work and think his ideas bring to light a big issue in why our obesity rates have skyrocketed, and I will come back to this at a future date.

NOT ALL FATS ARE CREATED EQUAL

The second is that not all fats are created equal, and many of the studies that linked fat intake to weight gain did not control for the type of fat, or used extremely poor quality fats (i.e. corn oil). The type of fat you consume can and does dictate how your body handles them. I think Dr. Michael and Mary Eades put it best when they stated in the book The Protein Power Lifeplan, “You are the fat you eat”. The different types of fats and their metabolic effects and biochemical interactions could be and entire Ph.D, but I am going to give you a brief crash course so you can understand why those studies aren’t a great source to hang your hat on. Buckle up and get ready for a read, but I promise at the end of it, I’ll tie it all together.

As all fats are considered acids, and are composed of C,H, and O, the way they are put together drastically alters how they act. First off, fats come in different sizes and length is determined by how many carbons they have, from few, to some, to many, and are referred to as short chain, medium chain, and long chain fatty acids respectively. Carbon attaches to other molecules via “bonds” and has the potential to form four bonds. In fats, carbons are attached to another C or an H. When all of the C atoms are full of hydrogen, the fat is considered to be “saturated”.  When a fat is missing one or H’s and the empty spot is considered “weak” and forms a double bond with the neighboring C, a less stable bond that when it was “saturated”. MUFA’s have one of these bonds while PUFA’s have more than one.

Therefore, saturated fats are the most stable, while PUFA’s are considered the least stable.  Does this make you curious as to why saturated fats have been vilified and considered a killer in terms of CVD? Let me assure you that the current state of the evidence indicates this is not the case, and I will attack this issue in full force in a later post will full data to back it up, but for now just trust me on this one (and eat some steak and coconut oil in the meantime)!

Saturated fats are solid at room temperature and are found in butter, coconut oil, and lard. MUFA’s are relatively stable (meaning they do not “break apart” easily, or in a chemical sense become oxidized), and are found in olive oil, nuts, lard, and avocados. PUFA’s are the most unstable, are liquid at room temperature and are prone to oxidation.  It appears as though PUFA’s would be the most dangerous, in terms of oxidation, and that is accurate; however, there are PUFA’s that are essential, i.e. we must consume them, and are vital to our health (In walks the Omega’s).  The two fatty acids that are essential are linoleic acid (18:2 n-6) and α-linolenic acid (18:3 n-3).  From these two acids we can derive the other essential fatty acids, namely γ-linolenic acid (18:3 n-6), arachadonic acids (20:4 n-6), eicosapentaenoic acid (EPA) (20:5 n-3), and docosahexaenoic acid (DHA) (22:6 n-3). All those numbers are more geek speak and indicate how long the FA is, how many double bonds there are, and precisely where the first double bonds occur. For example, EPA (20:5 n-3) is 20 C’s long, has 5 double bonds, and the first one occurs at the third C. Here is a nice little picture of these EFA’s.

Now that you have the big names of the essential fatty acids (EFA’s), let’s talk about what they do exactly. The EFA’s are unique in that they are the only FA that can be converted into something called eicosanoids.  Eicosanoids are part of the immune response of the body and are mediators in the inflammatory response and are either pro-inflammatory or anti-inflammatory.  Without getting into too much detail, in general the Omega-6 (n-6)fat derived eicosanoids are pro-inflammatory, while the Omega-3 (n-3) eicosanoids are anti-inflammatory.

Now that you have “the skinny on fats”, how does this apply to why fats were vilified for a long time? Lets start with why researchers believed fats were bad for your health, and caused heart disease.

We previously discussed how Omega-6 (n-6) fat derived eicosanoids are pro-inflammatory, while the Omega-3 (n-3) eicosanoids are anti-inflammatory. Well, our body functions best when these two processes are in balance, which means that we should attempt to consume Omega-6 EFA’s and Omega-3 EFA’s in equal quantities. Unfortunately, that is not the case with our standard American diet. Omega-6 EFA’s are found in industrial oils such as corn, safflower, soybean, cotton seed, sunflower, and peanut oil, and small amounts in animal fat. Omega-3 EFA’s are found predominantly in fish, algae, shellfish, and leafy vegetables. Our current diets have n-6:n-3 ratios of anywhere between 12:1 and 16:1. . . can you see an issue here? I do, our current trend of fat intake is highly inflammatory in nature. In the studies that related fat to weight gain they were utilizing fats that had extremely high O6:O3 ratios, no wonder there were some health issues observed in their outcomes.

Placing this concept in the “evolutionary based nutrition” sphere definitely gives the argument for a more ancestral based some decent purchase.  In a paper by Eaton et al. in 19985 it is suggested that our intake of O6:O3 were around as 1:1 and a study by Weber in 19896 suggests the ratio may have even been as low as .79:1.

The hypothesis of increased n-6 intake as a cause of the deleterious health affects of fat has solid theory behind its mechanism, however there is little research to fully substantiate that claim.  The one solid study I was able to track down was the Lyon Heart Study (a quick Google search will bring up the full text).  In this randomized secondary prevention study, the researchers found that diets in which n-3 consumption was higher, thus balancing out the n-6:n-3 ratio, adjusted risk ratio for overall mortality was .30 (p=.02).  Essentially, lowering the n-6:n-3 ratio cut their risk of overall mortality to 1/3 that of the control population.

The next PUFA on the list deserves its own paragraph. This FA is a chimera, an abomination that should never have been created, and deserves to be sent back to the laboratory it came from. Usher in the “Trans Fat”.  Now, in the name of honest science, I have to say that trans fats do exist in nature (i.e. in very small amounts in milk fats). But, that being said, the amounts in which they exist in commercially created foods gives them the deleterious health effects I will explain in a minute.

Trans fats are a product of chemically altering PUFA’s by hydrogenating them. The process involves changing a “cis” bond into a “trans” bond.  Don’t worry about the geek speak there, basically this process makes them solid at room temperature and more “plastic” for easier spreading (think about your margarine spread you put on your toast).  The introduction of trans fats was a product of mass food commercialization and increasing the palatability and reward factor of food. Once again, commercialized food is after your wallets, not your heart (in the context of heart health).  In a diet high in trans fats, we observe a decrease in HDL, increase in LDL, and may increase risk of myocardial infarction and death due to CHD6,7.  The long and short of trans fat is, if it comes in a box, a bag, or a wrapper, don’t eat it, and swap your margarine for real butter.

TRENDS IN FAT INTAKE vs. TRENDS IN OBESITY

The notion of fat intake as a correlate for bad for health and causing disease can greatly be explained by the fact that in our modern “Western” diet, n-6:n-3 ratios are extremely imbalanced and our intake of those evil “trans-fats” has increased.

In terms of the weight gain, we have to look at poor research methods, and a trend of researchers jumping on the low-fat bandwagon. In fact, it is extremely difficult to even find those studies that came out in the early 90’s as they have been buried under a pile of current research that shows healthy dietary fat is not an independent predictor in weight gain. I would like to go into detail on those studies, but for the sake of being concise I will show you a few charts and quotes that convey my message rather clearly (and loudly if I may be so bold).

“Reduced fat and calorie intake and frequent use of low-calorie food products have been associated with a paradoxical increase in the prevalence of obesity”.8

“The emphasis on total fat reduction has been a serious distraction in efforts to control obesity and improve health in general”.9

U.S. Department of Agriculture, 1965 and 1977-78 Nationwide Food Consumption Surveys, and 1989-91 and 1994-95 Continuing Survey of Food Intakes by Individuals.

Guyenet, S. J. More Thoughts on Macronutrient Trends, Friday, September 14, 2012. http://wholehealthsource.blogspot.com/2012/09/more-thoughts-on-macronutrient-trends.html#more

CDC/NCHS, Health, United States, 2008, Figure 7. Data from the National Health and Nutrition Examination Survey.

As you can see, the drastic increase in obesity rates since 1970 are not coinciding with a marked increase in dietary fat. If any conclusion could be drawn from this data is that our increased carbohydrate intake has a greater impact on obesity rates than fat does.  The data are rather inconclusive and the obesity epidemic is much more multifactorial than just macronutrient content, yet another topic I want to address in a future post.

Hopefully by now I have convinced you of a few things:

1) Fats are essential to your body and your health, you have to eat them to survive.

2) Not all fats are equal, some are amazingly healthy, some can be downright dangerous.

3) Saturated fat is not evil, it is solely (maybe not even partially) responsible for heart disease, and I promise I will fully explain that in detail in an upcoming post.

4) The balance of n-6:n-3 actually does mean something and our modern diet is not well balanced.

5) The early research and the notion of “ dietary fat makes you fat” is wrong, there are some subtle nuances that may make that statement partially true but as a blanket statement, it could not be further from the truth.

6) Fats are awesome, go grab some coconut oil toss it on some veggies to go along side a nice porterhouse steak (grass fed if you can muster one up!)

References

  1. Antonio, J., Kalman, D., Stout, J. R., Greenwood, M., Willoughby, D. S., & Haff, G. G. (2008). Essentials of Sports Nutrition and Supplements. Humana Press.
  2. Guyenet, S. J., Schwartz, M. W.,  Clinical review: Regulation of food intake, energy balance, and body fat mass: implications for the pathogenesis and treatment of obesity.  Journal of Clinical Endocrinology and Metabolism, 2012, 97(3), 745-755.
  3. Gropper, S. S., Smith, J. L., & Groff, J. L. (2005). Advanced Nutrition and Human Metabolism.Belmont, CA: Thomson Wadsworth.
  4. Eaton, S. B., Eaton III, S. B., Sinclair, A. J., Cordain, L., & Mann, N. J. (1998). Dietary intake of long-chain polyunsaturated fatty acids during the Paleolithic. World Review of Nutrition & Dietetics , 83, 12-23.
  5. Weber, P. C. (1989). Are we what we eat? Fatty acids in nutrition and in cell membranes: cell functions and disorders induced by dietary conditions. Svanoy Foundations, Svanoybukt.
  6. Ascherio, A., & Willett, W. (1997). Health effects of trans fatty acids. American Journal of Clinical Nutrition , 66, 1006-1010.
  7. Mensink, R. P., & Katan, M. B. (1990). Effect of dietary trans fatty acids on high density and low density lipoprotein cholestrol levels in healthy subjects. New England Journal of Medicine , 323, 439-445.
  8. Heini, A. F., & Weinser, R. L. (1997). Divergent trends in obesity and fat intake patterns: The American paradox. The American Journal of Medicine , 102, 259-264.
  9. Willet, W. C. (2002). Dietary fat plays a major role in obesity: no. Obesity Review , 3 (2), 59-68.

Brad is a Ph.D. student at the University of Idaho in Exercise Science. He received his M.S. degree in biomechanics from the University of Idaho and is a Certified Sports Nutritionist (CISSN) and a Certified Strength and Conditioning Specialist (CSCS). He has experience as a nutrition and fitness consultant, a collegiate strength coach, and a trauma representative in the orthopedic industry. Outside of school research, his research interests are in developing a better understanding of the nutrition, health, and performance axis and real world application of that knowledge.

Essential Fats – No, They’re Not All Equal

by Brad Dieter, MS, CISSN, CSCS.

Protein and fat are the two obligatory substrates people have to consume in order to sustain life, while carbohydrates are not.   In layman’s terms, you have to eat fat and protein to live, while carbohydrates are just extra, you really do not need them to survive. If fat is entirely excluded from the diet of humans, a condition develops that is characterized by retarded growth, dermatitis, kidney lesions, and early death1.

Research has shown that these conditions are reverse when subjects consumed certain unsaturated fatty acids, namely the Omega-3 and Omega-6 PUFA’s.  These specific PUFA’s cannot be synthesized in the human body and must be acquired in our diet, thus, these are the essential fatty acids (EFA’s). The names of these PUFA’s are linoleic acid (LA), an Omega-6, and alpha linolenic acid (ALA), an Omega-3. From these two PUFA’s our body can manufacture the subsequent compounds necessary for our bodies to properly function. . . . at least that is what science says, but we will see in a later post why LA and ALA may not be the effective way to obtain the “essential” fats that we need to include in our diet.

What Exactly Do These “Essential Fats” Do?

The main role EFA’s play in the body are for formation of cell membranes and are precursors to a group compounds known as Eicosanoids.  The Eicosanoids are long (20 carbons in length), highly unsaturated fatty acids and form prostaglandins (PG’s), thromboxanes (TBX’s), and leukotrienes (LK’s).  Ok, sorry for the big scientific terms and I will try and limit using them, but these are big time players in maintaing your body. The PG’s, TBX’s and LK’s are involved in some important physiological processes, including: 1) lowering blood pressure, 2) blood platelet aggregation (clotting), 3) immune response and regulation, 4) smooth muscle contraction (i.e. the muscles involved in breathing, blood vessels, and your digestive system), and 5) they act as signals all over the body. 

I know what you are thinking, Holy Smokes, I did not know fats did all those things for you.  Now compare the roles the many different roles that fats play in the human body when you compare it to the myopic role of carbohydrates. That is absolutely amazing if you ask me, but then again I am a huge nerd and love this stuff.

It’s pretty apparent that Omega-3 and Omega-6 EFA’s are pretty darn important… but are they equal? Well, lets find out.

Omega-3 Vs. Omega-6

Omega-3 EFA’s differ from Omega-6 EFA’s in that their first double carbon bond occurs at the location of the 3rd carbon from the methyl end of the chain where in the Omega-6 , EFA’s, that first bond occurs at the 6th carbon.  Big nerd terms aside, this just means that they play quite different roles in the body.

How different you ask? Well to answer that as simply as possible, the end products of Omega-3 EFA’s are generally considered anti-inflammatory and are reported to have hypolipidemic (lowering lipids/fat) and antithrombotic (preventing excess clotting) effects, while Omega-6 EFA’s are considered pro-inflammatory in nature.  Here is a great diagram that shows you the end products of the Omega-6′s and the Omega’s.

Clearly, the EFA’s are not equal, they play complementary roles to each other. Just like everything else in the world, too much of one, and not enough of the other has some serious consequences. . . In the case of the EFA’s, too much Omega-6 increases inflammation.

INFLAMMATION

Ok, so you eat too much Omega-6 EFAs and have a little more inflammation than you should… Who cares is probably what you are thinking. Well, I care, and I care a lot. The whole reason I write this blog, went to grad school, and spend my free time learning about the human body is because I care about all of you and your health!

That being said, what is the big deal? Inflammation is a normal physiological response that is crucial to maintaining health; however excess inflammation, or uncontrolled inflammation leads to impaired function, and disease2. Inflammation is a critical component in the development of cardiovascular disease, THE NUMBER ONE KILLER IN THE WORLD.

Why is cardiovascular disease so rampant? Well I believe a large part of it has to do with the inflammatory nature of the standard western diet, and both epidemiological studies and clinical studies can substantiate this belief.  This is where we can really push the “paleo”/ evolutionary view on nutrition.

Quick recap, Omega-6 EFA’s are generally pro-inflammatory while Omega-3 EFA’s are generally anti-inflammatory in nature.  The standard Western Diet has a Omega-6:Omega-3 ratio of anywhere from 10:1 to upwards of 25:1, where our Paleolithic ancestors had a diet that was closer to 1:1. . . . Do you see the stark differences?

The average American consumes a diet that promotes an inflammatory state 10-25 times great than an anti-inflammatory state. Holy COW, no wonder we all drop dead of diseases linked to inflammation. Why is the Omega-6: Omega-3 ratio so out of control?  Here is a list of foods high in Omega 6 and Omega 3 and you can see what we eat a lot of and what we eat a little of.

Omega 6 Omega 3

Corn   oil

 

Safflower   Oil

Soybean   Oil

Almonds

Cashews

Sunflower   Seeds

 

Marine   Algae

Salmon

Mackerel

Sardines

Grass-fed   meat

Flax   Seed

Are you beginning to see why the whole “Fish Oil” movement has taken hold in the past decade? Fish oil supplements are high in Omega-3 and virtually void of any omega-6, which helps us balance out the Omega-3:Omega 6 ratio. I am not generally a big supplementation person, but in light of these facts and the state of the western diet, I definitely suggest people take fish oil supplements high in DHA and EPA. In fact, there have been a number of clinical trials assessing the benefits of dietary supplementation with fish oils in several inflammatory and autoimmune diseases in humans, including rheumatoid arthritis3.

Think about how much you just learned in about 10 minutes of dedicated reading!  Thanks for tuning in this week, I am excited about the next post where we tackle another amazing fat, CHOLESTEROL!  I am also going to come back to the EFA’s and explain why EPA and DHA are so essential and why just eating ALA (remember the basic precursor to EPA and DHA) doesn’t quite cut it.

References

1) Gropper, S. S., Smith, J. L., & Groff, J. L. (2005). Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth.

2. Chiang, Y., Haddad, E., Rajaram, S., Shavlik, D., & Sabate, J. (2012). The effect of dietary walnuts compared to fatty fish on eicosanoids, cytokines, soluble endothelial adhesion molecules and lymphocyte subsets: a randomized, controlled crossover trial. Prostaglandins, Leukotrienes and Essential Fatty Acids , 87, 111-117.

3) Simopoulos, A. (2002). Omega-3 fatty acids in inflammation and autoimmune diseases. Journal of the American College of Nutrition , 21 (6), 495-505.

BIO – Brad is a Ph.D. student at the University of Idaho in Exercise Science. He received his M.S. degree in biomechanics from the University of Idaho and is a Certified Sports Nutritionist (CISSN) and a Certified Strength and Conditioning Specialist (CSCS). He has experience as a nutrition and fitness consultant, a collegiate strength coach, and a trauma representative in the orthopedic industry. Outside of school research, his research interests are in developing a better understanding of the nutrition, health, and performance axis and real world application of that knowledge.

 

Interview – Omega-3 Fatty Acid Expert Doug Bibus PhD

SNI:  Folks talk constantly about having the proper ratio between omega-6 and omega-3 fatty acids. What is the ‘ideal’ ratio (if it exists) and why?omega3-vs-omega6

Dr. Bibus: This is a common but very good question. With the excessive consumption of omega 6 largely as soybean oil in the standard American diet, current dietary ratios of omega 6 to omega 3 are from 10 to 20:1.  Large amounts of omega 6 in the face of smaller amounts of omega 3, reduce our bodies own metabolism omega 3, facilitating omega 3 deficiency.  See attached figure from Holman circa 1964 (Slide #3 in PPT).  Ideally if we can reduce our dietary ratio to 1:1 by limiting intake of omega 6 and/or increasing omega 3 we can get significant conversion of omega 3.  I typically state the ‘ideal’ dietary omega 6 to omega 3 ratio to be less than 5 to 1.  Below a 5 to 1 ratio we begin to see decent conversion of omega 3 and our blood levels of omega 3 increase to more healthy levels. Dr Bill Lands has made food selection simple for determining your omega 3 balance.  You can find his Omega 3-6 Balance Score program at www.FastLearner.org.

SNI: Of the omega 3 fats, what are the similarities and differences vis a vis their benefits between EPA and DHA?  Also, what’s the scoop on DPA?

Dr. Bibus: All long chain omega 3 like EPA, DPA and DHA have anti-inflammatory characteristics.  EPA however tends to be touted more as the anti-inflammatory omega 3 as it is converted into series 3 eicosanoids or hormone like compounds that have much lower inflammatory potentials than those derived from omega 6.  DHA is typically found in membranes or the bags that surround our cells.  DHA is thought to be a major player in how our cells communicate through membrane interactions of expression of genes or our DNA.  DHA is also important for glucose uptake in muscle as insulin sentivity of muscle is predicted by muscle content of DHA.  Our eyes, brain and liver have fairly high levels of DHA.  DHA makes up the majority of the fatty acids in he retina and about 20% in brain.  DPA is the exciting ‘new’ omega 3 fatty acid.  DPA has always been ‘around’ but research is increasingly recognizing its significance.  It is structural similar to DHA with just 1 less double bond.  We tend to store twice the amount of DPA in our blood than EPA and about half as much DPA as DHA.  While DPA is found only in small amounts in our diet, unless you are eating Menhaden or taking sources of menhaden oil, its significant presence in the blood comments on it potential for health.  Several studies have reported blood levels of DPA to be as predictive or more predictive of cardiovascular risk than EPA and DHA yet this nutrient is often ignored when we talk about omega 3.  DPA is in fact often referred to as “other” omega 3 on supplement labels.  There is an increasing awareness around DPA and its health benefits so look for new products touting DPA in your nutrition stores soon.

SNI: I have an acquaintance who takes 10 grams of fish oil daily.  Can you take ‘too much?’  And if so, what are the side effects?  What is the  ‘ideal’ dose of fish oil per day?

Dr. Bibus: I often take 10 grams per day which represents about 10% of my normal daily fat intake.  Can you take too much…from a practical standpoint no.  Arctic populations living on marine based diets consume on average 100-200 grams of marine based fat per day from fish, seal and whale blubber.  These populations have very low levels of heart disease but do have a tendency to bleed longer.  Bleeding is NOT a problem for people taking fish oil supplements. The FDA conservatively states that up to 3g or 3000mg of EPA and DHA are safe to consume each day.  For standard fish oil this is about 10grams per day.  There are no real side effects to fish oil consumption.  If you are taking medications to prevent clotting or have a clotting disorder you should talk to your physician about fish oil before you start taking it.  There is no federal recommendation for how much long chain omega 3 (EPA, DPA and DHA) should be in our daily diet.  I advocate consuming 2000mg or 2g of EPA, DPA and DHA combined per day.  This is about 7 – 1gram capsules of standard fish oil or 2-3 grams of concentrated fish oil.  Why 2000mg?  This is the amount required to raise our blood values of omega 3 to around 50% omega 3 in HUFA (highly unsaturated fatty acids) which is correlated with a 50% reduction in the incidence of death.

SNI:  Many middle-aged men take both aspirin and fish oil.  Inasmuch as both increase clotting time, should these two be taken concurrently?

Dr. Bibus:  Taking aspirin and fish oil both reduce clotting time which is a GOOD thing.  In America, our high omega 6 diet causes us to clot too much.  Salicylates or aspirin has many health benefits outside of reducing clotting.  Regular aspirin consumption has been also reported to reduce cancer risk.  If you have a clotting disorder you should consult with your doctor before starting any fish oil regimen.

SNI: Why do some fish oil products taste so ‘fishy’ and smell like a wharf in San Francisco while others seem to be less stinky?pier-39-in-san-francisco

Dr. Bibus:  The fishy smell from fish comes from certain nitrogen containing compounds (tertiary amines) and also from oxidized omega 3.  There are many different types of oxidized fatty acids often called aldehydes.  One type in particular can be smelled by our nose at relative small concentrations, helping our noses determine good from bad fish oils. That fishy smell comes from break down or degradation products of fish oil.  Good clean fish oil will have a very slight to no fishy aroma.  Fish oil processing helps clean up fish oil and proper storage and handling if fish oil, once made, are critical for keeping an oil healthy and oxidtaively stable.  A general rule of thumb is that if an oil smells bad it is bad and should be avoided.  Oxidized fatty acids are not healthy for u to consume.  Happily most oil producers today do a good job at produce stable oils.  There are still a few bad actors but luckily your nose can show you the way!

SNI: What new projects do you have on the horizon?  Tell the SNI audience please.

Dr. Bibus:  I am really excited to see a number of new products focused on athletic performance in the omega 3 area.  Also a number of DPA enriched omega 3 products will soon be entering the market place.  A company called Omega Protein has learned how to enrich DPA and are now selling omega 3 oils with up to 10% DPA.  There are also a host of omega 3 delivery systems that are out there now.  Emulsions are particularly interesting to me as they offer omega 3 in a form that is readily absorbed.  A number of fish oils are now concentrated which helps reduce the overall pill count to achieve 2-3 g per day intakes of long chain omega 3.

About Dr. Bibus – Dr. Doug Bibus received his BS from Mankato State University and earned his MS in nutrition and Ph.D in nutritional biochemistry from the University of Minnesota. Dr. Bibus is a community faculty member at the University of Minnesota’s Center for Spirituality and Healing and a researcher in the area of fatty acid biochemistry and nutrition. Dr. Bibus is considered as one of the top omega 3 experts in the world, a distinction that stems from his work at the academic lab (Professor Ralph T. Holman) that invented the omega 3 terminology as well as discovered the metabolism and definitive essentiality of omega 3. Dr Bibus’s research interests include the role of essential fatty acids in human and animal nutrition, the role of omega 3 fatty acids in attenuating the inflammatory response, the application of fatty acids in the treatment of disease and the impact of oxidative stress on performance animals and humans. Dr. Bibus is a member of The American Oil Chemists’ Society, The American Chemical Society, The Society for Critical Care Medicine and The International Society for the Study of Fatty Acids and Lipids. He has been a two-time winner of the American Chemical Society’s Award in Analytical Chemistry. Dr. Bibus is a foundation board member for AOCS and chairman of the health and nutrition division and award committee.

 

Coconut or Coco-No? Is Coconut Oil the Next Big Thing?

By Brooke Kugler, MS, CISSN.CoconutOil

Coconut oil has been acclaimed to be associated with a wide array of health benefits such as: hair/skin care, weight loss, stress relief, increased immunity, relief from kidney problems, HIV and cancer, bone strength, maintenance of cholesterol levels and much more. But, only limited research has been done on this particular oil.  Although many of the components (lipids/fatty acids) that make up this fruit’s oil have been known to fulfill such claims, the BIG question is…. does the oil itself prove to do the same?

Let’s see What Makes Coconut Oil Special?

Coconut oil composition— The benefits of coconut oil can be attributed to its unique combination of essential components. Coconut oil is 92% saturated fat, but unlike other saturated fats, such as from animal and dairy products, coconut oil is composed of a majority of medium chain triglycerides (MCT). The main MCT’s in coconut oil are: lauric acid (44-52%), palmitic acid (8-11%), and myristic acid (13-19%). The liver metabolizes these MCT’s very fast, similar to how the liver metabolizes carbohydrates just without the insulin spike, and MCT’s raise LDL-, HDL- and total-cholesterol. This is even why MCT’s are used in infant formulas and used to nourish hospital patients. In addition, other organic acids that are present in coconut oil, such as capric acid and caprylic acid, support health and overall quality of life through their antimicrobial, antioxidant, antifungal, antibacterial and soothing properties. The interesting thing about coconut oil is that you can receive certain benefits through consumption (dietary) and topical application.

Should you eat it? Or, should you apply it to your skin? (Dietary Vs. Topical)

Let’s go over the Dietary Benefits/Claims:

Boosts Immunity—The antimicrobial lipids (lauric acid, capric acid and caprylic acid) have antifungal, antibacterial and antiviral properties. Registered dietitian and sports dietitian Kristy Richardson explains that the body converts lauric acid to monolaurin, which is thought to be an anti-viral and anti-bacterial and can help boost immunity. Monolaurin is claimed to help in dealing with viruses and bacteria causing diseases such as herpes, influenza, cytomegalovirus and HIV. A study done on coconut oil in health and disease and specifically its potential as a cure for HIV/AIDS (Dayrit, 2000) shows how coconut oil plays an instrumental role in reducing viral susceptibility of HIV and cancer patients, and this preliminary research has shown the effect of coconut oil on reducing the viral load of HIV patients. In addition, according to the Coconut Research Center, coconut oil kills viruses that cause the above diseases as well as measles, hepatitis and SARS also killing bacterial that cause ulcers, throat infections, urinary tract infection and pneumonia.

Cholesterol Levels—Research on Pacific Island and Asian populations whose diets are naturally very high in coconut oil has shown unexpectedly low rates of heart disease. But, these populations also eat a mostly plant-based diet (opposed to a Western Diet) and are far more active than the average American, making a direct cause and effect comparison rather bias if the two populations were to be compared.cholesterol1

One study, in the Journal of Lipids found that women with too much abdominal fat (waist size >35”) paired with consumption of coconut oil while following a low-calorie diet and walking almost an hour a day raised HDL and lowered belly fat more than a diet using soybean oil. Another larger study of Filipino women showed association between coconut oil intake and higher levels of HDL and no significant association with “bad” LDL-cholesterol. These findings reveal that there could be a link between coconut oil consumption and increase of HDL along with a decrease in fat mass. However, studies to date are limited and inconsistent. Much more research must be done to land on a solid conclusion to determine the accurate and true relationship between coconut oil and weight loss paired with cholesterol levels/ratios.

Weight loss & Digestion—Coconut oil contains short and medium chain fatty acids that aid in improving weight loss and digestion. It supports healthy functioning of the thyroid and enzyme systems while reducing stress on the pancreas by increasing body metabolism. Most vegetable or seed oils are comprised of long-chain fatty acids (LCT’s), and these molecules are difficult to break down, thus they are predominantly stored as fat.

Coconut oil has also been found to help in the prevention of various stomach and digestion related problems including chronic fatigue syndrome, IBS, and Crohn’s disease. However, there is insufficient evidence (limited number of studies) to rate its true effectiveness.

Cooking: Put on the Heat!—Coconut oil, with a smoke point of up to 450°F, is high in vitamin E and stable enough to resist heat-induced damage while cooking. Other vegetable oils, such as olive oil, have a lower smoke point up to 405°F, and if the range is higher than an oil’s smoke point, the fatty acids can be damaged. This is why coconut oil is great for cooking—it’s a heat-stable oil. It is also solid at room temperature as it is composed of mostly saturated fats; therefore, its lack of polyunsaturated fatty acids (PUFA’s) actually allows it to be stored for a longer duration, increasing its shelf life, due to a slower rancidification rate.

Let’s go over the Topical Benefits/Claims:

Skin and Hair Care—Want silky, smooth, shiny hair? Well, coconut oil can help you in this department! Regular massage of the head with coconut oil moisturizes your scalp with its oils. It is used extensively in the Indian sub-continent for hair care. It can act as an excellent conditioner and aid in re-growth of damaged hair by providing essential proteins for nourishing damaged hair. This is why it is used in the manufacturing of various conditioners, and dandruff relief creams.

Coconut oil has also been found to be an effective moisturizer on all types of skins (especially drier skin types) and is comparable to that of mineral oil. But, unlike mineral oil there is zero chance of adverse side effects when applying coconut oil to your skin. Furthermore, there are claims that it delays wrinkles from aging, which can be due to its oil composition as well as its antioxidant properties.

Physiologist and biochemist Ray Peat, Ph.D. considers coconut oil to be an antioxidant due to its stability and resistance to oxidation and free radical formation. In addition, coconut oil has been used in the treatment of various skin problems including psoriasis, dermatitis, eczema, and other skin infections. It also forms a major ingredient in many body care products—soaps, lotions, and creams.

Stress Relief – Due to its soothing effects, coconut oil has been found to help relieve and tame stress. Apply coconut oil to the head followed with gentle massage, and this could help in removing mental fatigue and anxiety.

What’s it looking like– Coconut? Or, Coco-No?

There is much controversy over this unique oil. As we all know, coconut oil is very high in saturated fat, and this shadows its potential health and therapeutic benefits on the body.

For those trying to determine if coconut oil is everything it’s been “mocked” up to be, Kristy Richardson gives her recommendation, “Continue to follow the Academy of Nutrition and Dietetics recommendations to limit saturated fat intake to less than 10% of total calories from fat. For vegans or people who prefer the taste and flavor, coconut oil adds to dishes and baked goods so it can be a good replacement for butter or Crisco.” The Academy of Nutrition and Dietetics recommends limiting intake of saturated fats, trans fats and cholesterol, and to replace saturated fat with mono- or polyunsaturated fats as much as possible while increasing intake of omega-3 fatty acids.

Richardson further explains that small amounts of coconut oil in the diet are probably not harmful, however, “research is so limited and there is no concrete scientific evidence to support all of the coconut health benefit claims.” When asked if she recommends coconut oil to her clients she said, “Coconut oil can be a good replacement for less healthy saturated and trans fats, but the key is replacement and substitution, not addition.”

Topical Vs. Dietary Overall Conclusions:  The Skinny on this Type of Fat

The benefits (skin and hair care) that come of topical application of coconut oil seem to be safe and effective if used on a regular basis. This can also be a far less expensive treatment when compared to most other hair and skin care treatments.

The rule of thumb– “Be careful consuming, when assuming.” Consuming a product can have many consequences, side effects and repercussions when health claims are made without substantial evidence to back them up. This is why we need to be cautious and avoid being too quick to believe everything and anything we see, read and hear.

In the realm of coconut oil, research is very limited, thus far. “There is simply not enough evidence to substantiate any sweeping claims for coconut oil,” says Evelyn Tribole, a dietitian and author of The Ultimate Omega-3 Diet. As Tribole explains, “We can’t just look at classes of fat, we have to look at the individual type of fat.” She further explains that she wouldn’t go out of her way to add it to her diet, but in small amounts this oil is a great way to add flavor to foods you make at home.

Inadequate exploration of coconut oil leaves us hanging without definite answers. But, there are reasons why this oil is sparking up new questions, which calls on research to do its job best. Until we can bring merit to all of its health benefits, the Academy of Nutrition and Dietetics (AND) and registered dietitians say, “We should substitute other oils and saturated/trans fats with coconut oil rather than make it an addition to our diets.” So, all-in-all, coco-yes or coco-no? Certainty will come with time.

About Brooke R. Kugler, M.S., CISSN

Brooke has devoted her life to research and the practical application of dietetics and sports nutrition. She has been involved in competitive sports throughout her entire life, including 14 years of professional figure skating. But, it wasn’t until she began competing in figure and fitness competitions where she realized her true passion for the field of sports nutrition, and that was the spark that set the stage for the rest of her life! She believes that there’s nothing better than helping someone achieve a successful and positive physical and mental—full-body–transformation. She will soon be a registered dietitian and plans on focusing her efforts on bridging the gap between sports nutrition research and sport nutrition practice.

References

Academy of Nutrition and Dietetics (2012). Retrieved May 27, 2012, from http://www.eatright.org/

Dayrit, CS. (2000). Coconut oil in health and disease: Its and monolaurin’s potential     as cure for HIV/AIDS. Retrieved from     http://www.apccsec.org/document/Dayrit.PDF.

Peat, R. Why is coconut oil for skin so beneficial? Retrieved from http://www.be-healthy-with-coconuts.com/coconut-oil-for-skin.html.

Richardson, K. MS, MPH, CSSD, CHES. Personal Interview. May 28, 2012.

CLA Supplementation For Weight Management

By Ross Edgley, BSc Sports Science

Daily supplementation of Conjugated Linoleic Acid (CLA) may reduce body fat and favorably change body composition researchers at I-Shou University in China reveal.   The study led by Chih-Kun Huang, MD took 63 subjects and randomly assigned them to receive daily supplements of CLA (3.4 grams) or a placebo (salad oil) in a milk product for 12 weeks. Results showed that after 12 weeks of supplementation participants in the CLA group displayed average decreases in bodyweight of 0.7kg, BMI of 0.31 kg/m2, body fat mass of 0.58kg and fat percentage of 0.6%. Chih-Kun Huang said ‘to our knowledge this is the first randomized, double-blinded, placebo-controlled clinical trial to evaluate the effect of CLA on body fat composition and the results seem promising.’ Concluding ‘the consumption of milk supplemented with CLA (3.4 grams per day) significantly decreased the body weight, BMI, body fat mass, fat percentage, subcutaneous fat mass and the waist-to-hip ratio in subjects over just 12 weeks.’

But what exactly is conjugated linoleic acid and what are the benefits for athletes, bodybuilders or gym goers? Well it’s a naturally occurring fatty acid found mainly in cheese and beef however it’s only found in these foods in very low doses (no way near the 3.4 grams used in the study at I-Shou University previously mentioned). Furthermore similar promising results were found at Uppsala University in Sweden where they found supplementing 4.2 grams of CLA a day in healthy, young subjects resulted in a 3.8% decrease in body fat compared with individuals not taking the supplement.

Whilst it’s clear studies support the use of CLA to lower your body fat, experts still aren’t entirely clear as to the mechanism by which it works. It’s been theorized that it reduces your body fat in 3 ways: firstly research conducted at the University of País Vasco found that conjugated linoleic acid interferes with a substance in your body called lipoprotein lipase, which aside from various other roles in the body is mainly responsible for storing fat in the body. Furthermore Simón. E et al 2005 of the same study found that CLA actually helped the body use its existing fat for energy. Therefore studies show CLA not only inhibits the storing of fat it also enhances the burning of fat.

Thirdly, and perhaps most important for athletes, bodybuilders or those training for aesthetics, it was found CLA supplementation actually increased muscle mass as well as lowering body fat. This in turn increases your basal metabolic rate and the amount of calories you burn at rest. Scientists concluded therefore that CLA doesn’t actually make you lose weight (like thermogenics do) but rather it favorably changes your body composition (i.e. body fat to muscle ratio). This notion is further supported by the 1 year human study published in the American Journal of Clinical Nutrition that found CLA supplementation produced a 9% reduction in body fat and 2% increase in muscle mass.

So in summation, CLA supplementation may prove effective for athletes wanting to change their body composition (such as American Football players wanting to get rid of unwanted fat and develop a more powerful and ‘functional’ physique) but perhaps not so effective for athletes wanting to lower their weight such as boxers, martial artists or anyone athletes needing to make a weight cut. Regarding dosage, there seems to be different amounts that have proved effective in various studies ranging from 1.4 grams to 6.5 grams. The most common dosage seems to be 3 grams per day, so it may be advisable to start with this dosage and increase or decrease depending on how your body responds.

 

About the Author: Ross Edgley is a Sports Scientist with a BSc Degree in Sports Science from Loughborough University. Ross Edgley was a Strength and Conditioning Coach at The English Institute of Sport working alongside Britain’s Olympic Physicians, Nutritionists and S&C coaches and is currently fitness and nutrition advisor to a range of athletes and the UK’s biggest online sports nutrition company Myprotein.com.

 

References:

Mougios V, Matsakas A, Petridou A, Ring S, Sagredos A, Melissopoulou A,Tsigilis N, Nikolaidis M. Effect of supplementation with conjugated linoleic acid on human serum lipids and body fat. J NutrBiochem 2001;12:585-94

Blankson H, Stakkestad JA, Fagertun H,Thom E, Wadstein J, Gudmundsen O.Conjugated linoleic acid reduces body fat mass in overweight and obese humans. J.Nutr. 130:2943-2948 (2000).

Roche HM, Noone E, Nugent A, Gibney MJ. Conjugated linoleic acid: a novel therapeutic nutrient? Nutr. Res. Rev. 187 (2001).

Smedman A,Vessby B.Conjugated linoleic acid supplementation in humans – Metabolic effects. Lipids 36:773-781 (2001).

Lowery L.M., Appicelli P.A. and Lemon P.W.R. (1998). Conjugated linoleic acid enhances muscle size and strength gains in novice bodybuilders. Medicine and Science in Sports and Exercise, 30.182.

Kreider RB, Ferreira MP,Greenwood M, Wilson M, Almada AL. Effects of conjugated linoleic acid supplementation during resistance-training on body composition. Bone density, strength, and selected hematological markers. J Strength Cond Res 2002; 3:325-34.

Berven G, Bye A, Hals O, Blankson H, Fagertun H, Thom E,Wadstein J, Gudmundsen O. Safety of conjugated linoleic acid (CLA) in overweight or obese human volunteers. European J. Lipid Sci.Technol. 102:455;462 (2000).

Thom E,Wadstein J, Gudmundson O. Conjugated linoleic acid reduces body fat in healthy exercising humans. J Int Med Res 2001;29:392-6.

Kamphuis MMJW, Lejeune MPGM, Saris WHM, Westerterp-Plantinga MS. The effect of conjugated linoleic acid supplementation after weight loss on body weight regain, body composition, and resting metabolic rate in overweight subjects. Int J Obesity 2003; 27: 840-847.

Gaullier Jm, Hasle J,Hoye K., Kristiansen K., Berven G., Blankson H and Gudmonson O. Effects of CLA in moderate overweights during one year supplementation. 94th AOCS annual meeting and Expo, Kansas,May 2003

A. Zabala et al (2006) ‘Trans-10,cis-12 Conjugated linoleic acid inhibits lipoprotein lipase but increases the activity of lipogenic enzymes in adipose tissue from hamsters fed an atherogenic diet.’ Br J Nutr. 2006 Jun;95(6):1112-9.

 

 

 

 

Should You “Spike” This Hormone?

By Brian St. Pierre, CSCS, CISSN.

Well Everybody Knows – Everybody knows that the first rule of a post-training shake is that it has to be fast. You must drink it as soon as you are done or you won’t get lean. You must drink the fastest protein on earth with only the fastest carbs, no fiber or fat allowed! This usually entails people drinking whey protein, either in the form of isolates or hydrolysates, because concentrates are just too darn slow. The carbs are usually from maltodextrin or dextrose, and maybe even that fancy defense-against-the-backlash-on-protein-powders_anew waxy maize starch. Anything with fiber , fat or fructose is terrible and will decrease absorption time. Right? We know all of this because that is what we have always been told. No one denies that this is effective, as it has worked for millions of people, but does effective equal optimal? What are we actually trying to accomplish with this shake?  I do want to preface all this with the fact that there isn’t one perfect pre-and-post-training feeding for everyone. It is always context specific. The protein/carbohydrate/fat/fluid/micronutrition requirements for a 155lb endurance athlete in the midst of marathon training vs. a 225lb bodybuilder recovering from a heavy resistance-training session are quite different. Times of training year will also dictate different needs in the post-exercise recovery period. That same bodybuilder will need a different approach when they start to diet in preparation for a show. In reality proper pre-training nutrition also alters the needs of the post-training period. Having said all that, these recommendations are appropriate for the average gym-goer, looking to gain (or retain) some lean mass while trying to stay relatively lean and healthy. Your actual needs may vary.

Hierarchy of Needs – There is a distinct hierarchy of needs for pre-and-post-training recovery. The goal of pre-training nutrition is to fuel the upcoming training session, maintain hydration, boost training performance, increase muscle protein synthesis, decrease muscle protein breakdown, and spare muscle and liver glycogen. The goal of post-training nutrition is not at all dissimilar: recover from the completed training session, maintain hydration, increase muscle protein synthesis, decrease muscle protein breakdown, and replenish muscle and liver glycogen. Does 40g of whey hydrolysate with 80g grams of maltodextrin and/or dextrose optimally achieve the desired result? Let’s dig a little deeper and find out.

Do We Really Need to “Spike” Insulin? – Contrary to popular belief it is not necessary to use refined carbohydrates and sugars to “spike” insulin levels and restore muscle and liver glycogen as rapidly as possible. In fact research has shown that unrefined carbohydrates and fructose (preferably from fruit, to protect and restore liver glycogen), is every bit the equal of those high-GI carbs. This combination restores glycogen as effectively over a 24 hour time period as the high-GI carbs, and might (I emphasize might) actually lead to better next-day performance. While it is clear that unrefined carbs are just as effective as refined high-GI carbs at enhancing recovery and restoring glycogen levels over a 24 hour period, there are certainly times when a simple high-GI shake is warranted. In particular when endurance athletes have two glycogen depleting sessions within eight hours of each other, as the speed of glycogen replenishment is imperative in this scenario. In addition to that there are times when convenience and portability are deciding factors, and pre-made high-GI powders still allow people to get in some quality nutrition before and/or after they train.

In that same vein, research has also shown that muscle protein breakdown is maximally inhibited when insulin is only 2-3 times above fasting levels. This is easily accomplished by a mixed meal or shake an hour or two before training. In reality, proper pre-training nutrition is at the very least equal, if not superior to post-training nutrition for maximal results. It sets the stage for recovery and provides fuel for the session, allowing for potentially better training; without this you are definitely not getting the most out of your sessions.

This high quality mixed meal or shake has been shown to elevate insulin levels well above those needed for maximal anabolic and anti-catabolic effects for at least 5 hours, and it remains elevated even after a training session. This tells us that worrying about spiking our insulin immediately after training with tremendous amounts of high-GI carbs is not necessary, as our insulin is already above the threshold for exerting its maximal benefit. This isn’t to say that you shouldn’t have carbs after training, you should, but you should worry more about the quality of the source, rather than exact timing or the speed of its digestion.

Protein – The Good, The Bad and The Ugly – Well what about protein you ask? There has been a lot of recent hype over whey and casein hydrolysate, and their alleged ability to drastically improve your results. However, research has shown that large doses of whey hydrolysate are actually too fast. It is in and out of the blood stream too rapidly to maximally stimulate protein synthesis and inhibit protein breakdown. In addition to failure of whey hydrolysate to showcase its superiority, casein hydrolysate has failed to live up to its billing. It has been found to be preferentially taken up by the splanchnic bed, so unless your goal is to get jacked organs it probably isn’t the way to go either. A blend of low-temperature processed whey proteins, especially pre-training where it can get into your bloodstream rapidly, is superior to either whey or casein hydrolysates, as it also contains the ever-important biologically active fractions.

The Glory of Fat – On top of protein and carbohydrates, it is often recommended that fat and fiber be restricted from the pre or post training period, again because of the idea that it would limit speed of absorption and decrease results. Research has found that consuming as much as 55 grams of fat post-training and in two subsequent meals did not inhibit glycogen replenishment. As well it has been found that whole milk was superior to skim milk post-training, even when skim milk was calorically matched. The skim milk actually contained more protein (14g to 8g) and yet the whole milk, with 8g of fat to skim’s 0g, was more anabolic. While this is just one study, clearly fat does not inhibit maximal results, even if it does decrease speed of absorption. In reality post-training fat consumption may potentially improve results!

The Finish – The best pre-and-post-training meals will contain a combination of high quality proteins, high quality carbohydrates, healthy fats and some fruit and/or vegetables. These whole foods provide a plethora of nutrients: protein, carbohydrates, fats, fiber, vitamins, minerals, antioxidants, anti-inflammatory compounds and phytonutrients that supply energy, decrease inflammation, boost recovery, maximally stimulate protein synthesis and maximally inhibit protein breakdown. However as noted above, if you have two glycogen depleting sessions within 8 hours of each other, or are a time-crunched individual who requires highly portable and convenient pre and/or post-training nutrition, a pre-made high-GI powder will work best for you.

These meals can come in the form of solid food or shakes, and the amounts of each macronutrient can vary depending on your needs as well as personal preferences and tolerances. I have personally found that liquid meals pre-training seem to be ideal because they supply rapid uptake while minimizing the volume of food in your stomach. This will make it easier to consume closer to training so that the substrates are available to your body as you train and after, rather than having to consume a solid food meal several hours before training. Post-training I have found a solid meal to be top-notch, but this can also depend on personal preference and tolerance. Many trainees do not have an appetite post-training, or are seeking to pack in as many calories as possible, and liquid meals are more feasible in these situations.

References

Erith S, et al. The effect of high carbohydrate meals with different glycemic indices on recovery of performance during prolonged intermittent high-intensity shuttle running. Int J Sport Nutr Exerc Metab. 2006 Aug;16(4):393-404.

Stevenson E. Improved recovery from prolonged exercise following the consumption of low glycemic index carbohydrate meals. Int J Sport Nutr Exerc Metab. 2005 Aug;15(4):333-49.

Jentjens RL, Jeukendrup AE. High rates of exogenous carbohydrate oxidation from a mixture of glucose and fructose ingested during prolonged cycling exercise. Br J Nutr. 2005 Apr;93(4):485-92.

Jentjens RL, et al. Oxidation of exogenous glucose, sucrose and maltose during prolonged cycling exercise. J Apply Physiol. 2004 Apr;96(4):1285-91.

Jentjens RL, et al. Oxidation of combined ingestion of glucose and fructose during exercise. J Apply Physiol. 2004 Apr;96(4):1277-84.

Jentjens RL, Jeukendrup AE. Determinants of postexercise glycogen synthesis during short-term recovery. Sports Med. 2003;33(2):117-44.

Bloom PC, et al. Effect of different post-exercise sugar diets on the rate of muscle glycogen synthesis. Med Sci Sports Exerc. 1987 Oct;19(5):491-6.

Burke LM, et al. Effect of coingestion of fat and protein with carbohydrate feedings on muscle glycogen storage. J Appl Physiol. 1995 Jun;78(6):2187-92.

Rennie MJ, et al. Branched-chain amino acids as fuels and anabolic signals in human muscle. J Nutr. 2006 Jan;136(1 Suppl):264S-8S.

Tipton KD, et al. Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol Endocrinol Metab. 2001 Aug;281(2):E197-206.

Tipton KD, et al. Stimulation of net muscle protein synthesis by whey protein ingestion before and after exercise. Am J Physiol Endocrinol Metab. 2007 Jan;292(1):E71-6.

Farnfield MM, et al. Plasma amino acid response after ingestion of different whey protein fractions. Int J Food Sci Nutr. 2008 May 8:1-11.

LaCroix M, et al. Compared with casein or total milk protein, digestion of milk soluble proteins is too rapid to sustain the anabolic postprandial amino acid requirement. Am J Clin Nutr. 2006 Nov;84(5):1070-9.

Deglaire A, et al. Hydrolyzed dietary casein as compared with the intact protein reduces postprandial peripheral, but not whole-body, uptake of nitrogen in humans. Am J Clin Nutr. 2009 Oct;90(4):1011-22.

Elliot TA, et al. Milk ingestion stimulates net muscle protein synthesis following resistance exercise. Med Sci Sports Exerc. 2006 Apr;38(4):667-74.

Fox AK, et al. Adding fat calories to meals after exercise does not alter glucose tolerance. J Appl Physiol. 2004 Jul;97(1):11-6.

Keizer HA, et al. Influence of liquid and solid meals on muscle glycogen resynthesis, plasma fuel hormone response, and maximal physical working capacity. Int J Sports Med. 1987 Apr;8(2):99-104.

Reed MJ, et al. Muscle glycogen storage postexercise: effect of mode of carbohydrate administration. J Appl Physiol. 1989 Feb;66(2):99-104.

 

The Ultimate Butter Meltdown

iStock_000006937653SmallBy Ana Castilla CISSN.

Warning! This statement has not been evaluated by the food and drug administration.This product is not intended to diagnose, treat, cure, or prevent any disease.  Good.  Because that should keep me out of trouble right? Because the Rx today is BUTTER.  I personally can’t believe it’s not butter as I stroll through the fat-free-infested dairy isle at my local Publix®. For my peace of mind, and for those in the vicinity, I tend to reach for my beloved grass-feed (yes extremely fatty) Kerrygold butter as fast as my phosphocreatine stores will allow me, before I overhear one more chat about how smart balance buttery spread can lower cholesterol.

See, keeping trans and saturated fats at bay is part of any sound “heart healthy” nutrition plan  (1).Yep. I do pay attention in class! However If you’re one to follow this dogma, I will excuse myself in advance because I actually will appear quite unsound, maybe it’s all that butter melting in my mouth you know, must have messed with my head (Hallelujah for that one). The heretic of low fat living might just be a superfood in disguise.

Sure Ana…go ahead and clog up your arteries; just have us on speed dial so that we can take your overweight behind to the ER! Hummm, not at all the case.  In fact let’s considers a couple of thoughts on why the fat in butter is indeed your smartest mouthful.

Starting with the biggest evil of them all: trans fats. Trans fatty acids are what happens when man decides shoot up hydrocarbon chains with hydrogen bullets; well for the most part. These buggers are very unreactive little ones and can be found say in your regular Mc-fried-thing (1) . That said, I don’t want you to hyperventilate when you discover trans fats on your grass-fed T-bone, because these are the kind that occur naturally in many dairy and meat products. It’s called CLA.

Conjugated linoleic acid might have at one point caught your eye, all bottled up, promising you that beach body over at GNC®. Well CLA is the trans fat -insert fat-phobic shiver here- found abundantly in meat and butterfat of happy-grass-grazing -cows (2)(3). CLA has shown promising positive shifts in body composition and weight loss in animal studies (4).  I know I know.  Animals are not humans; but it’s certainly a nudge in the right direction. And in case you also care about silly little things like cancer prevention, CLA appears to play a role in that as well (5)(6)(7).

To make matters worse, butter is also high in the other fat we give the cold shoulder to: Saturated fat! Now as you can see I am not using trans and saturated fat interchangeably as you have grown accustomed to.  Ok brace yourself; this might require a smidge more brain cells.

Saturated fatty acids are naturally occurring hydrocarbons, of varying length, that are naturally “saturated” with hydrogens and yes they are extremely inert or stable. Ooh no! That sounds bad just like trans fat!  Not quite. Take a jar of coconut oil for example (well butter too but I like the jar analogy, not as messy) and leave it opened in the sun for a couple of days. It is very unlikely that it will become rancid or oxidized, due exactly to its stability. Oxidized fats in our bloodstream are a bad thing (8). For starters we want the fats we consume to be metabolized efficiently and not left to be rancid in the blood, but given our modern lifestyle that becomes tricky sometimes. Saturated fats are also ideal for cooking because, unless you are constantly deep frying your chicken, you will dramatically reduce the risk of consuming oxidized oils.

Additionally, speaking of coconuty things, let’s not forget about this particular kind of saturated fat, MCTs or medium chain triglycerides, their benefits (9) and also their presence in butter.

La RotondeAlright on to more controversy.  Ever heard of the French paradox? Yep, frenchies have one of the highest consumptions of saturated fats and cholesterol (we WILL get to my favorite sterol, don’t you worry) in their diets yet low incidences of heart disease and mortality (10). They are having a jolly good time, why can’t we? Maybe we have hunted down the wrong guy.

It looks like low carbohydrate diets, that are rich in saturated fat, actually improve the risk factors for diabetes and cardiovascular disease (11). The saturated fat,  Palmitic acid, 16C, found abundantly in butter, fails to raise the so called “bad cholesterol” LDL(12). But how about raising the “good cholesterol” HDL? Well replacing carbohydrate with any kind of fat will do the trick, but the most benefit will come from substitution with saturated fat. TAKE THAT OLIVE OIL! (13).

I’m going to blow your mind here and give you one more paradox, the American paradox.  Saturated fat can not only be harmless but -the outrage- actually beneficial (14).  In this study the researchers examined the reduction in the progression of coronary atherosclerosis when saturated fat was introduced into a low fat diet. Wait a minute.  Is that butter I smell? Looks like saturated fat also helps you breath better! (15)

And guys.  If you were looking to have testosterone levels higher than those of a 13 year old girl, you might want to consider what a high saturated fat diet can offer (16) (17). No need to reach for the TEST cream quite yet.

Oh I almost forgot.  Since many of us already know the benefits of reducing carbs in the diet(11) (one caveat here before I get jumped, I am not talking about those superhero-olympic-triathletes and crossfitters among us)  I believe it is worth pointing out that saturated fat can also help you lose some pounds in a non-omg-I-am-starving-way (18)(19) and also keep it off ( 20) (21) just in case you were on the edge there.

In the interest of keeping this discussion nice and fatty onto my PUFAs. Polyunsaturated fatty acids are the celebrities of the healthy fat propaganda these days.  Fish oil anyone? Butter provides a balanced amount of omega-3 and omega-6s.No need to ramble about the benefits of these fats (22) when we observe a ratio closer to 1:1 in the body. Although if you’re curious take a look at this article(http://sportsnutritioninsider.insidefitnessmag.com/3588/fish-oil-the-real-deal-fat-fighter) on fish oil or this one (http://sportsnutritioninsider.insidefitnessmag.com/3559/pufas-essential-or-toxic) on PUFAS.

Moving on to chunkier topics…..Cholesterol!

Little Johnny: So mom how are babies made?

Momma bear: you see Johny, the stork brings new mommy’s their babies.

Little Johny: wow that makes so much sense! Every time I see a stork fly…I also see babies. Storks deliver babies!

Listen up little Johnny, sometimes it just ain’t that simple.  Correlation is NOT causation. Momma bear’s version of why cholesterol will kill you goes a like this: Arteries are like pipes and all that nasty trans and saturated fat, as well as cholesterol, are the gunk that clogs the pipes up. Yep, just what you were thinking right? It certainly looks like a big fat solid piece of gunk of course it clogs up our arteries  –  even thou its about 30 degrees steamier in there  – and of course it’s the causative factor for all global problems from cardiovascular disease and obesity to starving African kids and dying polar bears.

Right?  So spare me the details.  Should it go down the pie hole? As far as I am concerned, definitely! If you’re not in the business lowering peoples IQ you make sure they have their cholesterol. Your brain is the fattest kid on the block and therefore cholesterol ts essential for brain development (23) where it mostly helps with nerve cell signaling aka THINKING (24)! Want to digest your food properly? Cholesterol is needed to produce those bile salts. Want to be all macho-macho and conserve your virility? Ladies any concerns about fertility? Well cholesterol makes sex hormones too – amazing!

I say skip the Goji berries and melt me some butter! Cholesterol an anti-oxidant?

I knew all along she was nuts!

Actually, this super-sterol comes to our rescue when it’s time to fight of those harmful free radicals that occur in our bodies when we eat rancid fats in margarine and highly processed vegetable oils (25). In the ultimate margarine vs butter battle, men that consumed real butter were half as likely to develop heart disease (26). Real Men eat real BUTTER! And lovely ladies do so too! In fact carbohydrate intake is better associated with a greater progression of plaque formation in the arteries of postmenopausal women (27).

Now if you will excuse me there is a lonely stick of butter in my fridge calling my name and I do hope, by now, it its calling yours too.

It is time to stop being slow, weak and frail.  Discover THE BUTTER MELTDOWN! Available now at a retail near you!

About the Author:  Ana Castilla CISSN is a Biology major at Nova Southeastern University who is a certified sports nutritionist from the International Society of Sport Nutrition. She gives Paleo Diet nutrition lectures at Crossfit affiliates such as 911 Crossfit and City.

References

  1.  American Heart Association .Policy Position Statement on Regulatory and Legislative Efforts to Improve Cardiovascular Health by Decreasing Consumption of Industrially Produced Trans Fats.www.heart.org/idc/groups/heart-public/@wcm/…/ucm_301697.pdf.
  2. French P, et al. Fatty acid composition, including conjugated linoleic acid, of intramuscular fat from steers offered grazed grass, grass silage, or concentrate-based diets. Journal of Animal Science, 2000 Nov;78(11):2849-55. http://www.ncbi.nlm.nih.gov/pubmed/11063308.
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