Tag Archives: fish fat

Fish Oil and Athletic Performance

Athletes are always looking for a competitive edge to improve athletic performance. Whether the end result is a 5- to 10-lb. increase in muscle mass, less muscle soreness, or a reduction in body fat, athletes will go the extra mile to find that edge. Gaining an advantage over the opponent could mean winning a gold medal, making the final shot, or having the energy to outlast a competitor on the mat or in the ring. In addition to a balanced diet, athletes are turning to dietary supplements to gain that advantage. Popular supplements such as creatine, branched chain amino acids (BCAA’s), HMB, beta-alanine, and caffeine have been widely used throughout the athletic community. One supplement that has gained the attention of athletes is fish oil.

The growth of fish oil use among consumers has been quite impressive, as sales have risen from $425 million in 2007 to $1 billion dollars in 2012. Widely touted for its beneficial effects for cardiovascular health, fish oil has not been considered an essential piece in an athlete’s supplement regimen. In this article, I will discuss why fish oil is a critical piece to help athletes gain that competitive edge and stay in the game.

Healthy Joints, Range of Motion – Whether you’re participating in a year-round strength and conditioning program, playing multiple sports, or training at a high intensity, your muscles, joints, and tissues will experience inflammation (i.e. swelling, soreness, and redness). Inflammation is not necessarily a bad thing as this is a critical component of the recovery process. At the same time, acute and chronic inflammation may augment muscle soreness which can limit range of motion and potentially impair athletic performance. In addition, the American diet is saturated with omega-6 rich foods (fried foods, vegetable and soybean oils, salad dressings, potato chips, etc.) that promote inflammation. A diet rich in omega-3 essential fatty acids from fish (salmon, mackerel, halibut, anchovies) and/or from fish oil supplementation, can balance the effects of a diet high in omega-6 fatty acids. A study by Bloomer et al. demonstrated 4 grams of omega-3 fatty acids (2224 mg EPA + 2208 mg DHA) reduces markers of inflammation (i.e. CRP and TNF-alpha) after an intense exercise session (i.e. 60 min treadmill climb with weighted backpack). (1)

Improve Body Composition – Most people don’t expect to read about consuming fat and losing body fat in the same sentence. The essential fatty acids in fish oil (EPA and DHA) were studied in numerous animal models throughout the 80s and 90s and demonstrated a reduction in body fat (2,3) and a prevention of adipose tissue growth (4-6). Does fish oil have the same effect in humans? A study was conducted in which young, non-obese males were given 6 grams of fish oil (1100 mg EPA and 700 mg DHA) in place of 6 grams of butter, olive oil, peanut oil, or sunflower oil. After three weeks, subjects experienced a significant increase in fat oxidation and a 1.94 lb decrease in body fat (7). In a more recent study, young men and women were give 4 grams of fish oil per day (1600 mg EPA and 800 mg DHA) for six weeks vs. 4 grams of safflower oil in the placebo group. The fish oil group lost 0.5 kg of fat mass and gained 0.5 g of lean mass whereas the safflower oil group showed a tendency to gain fat mass. (8). The mechanism of action between fish oil and fat loss seems to be related to its ability to improve insulin sensitivity which improves fat burning and inhibits fat storage (9,10). Furthermore, studies have also shown fish oil supplementation can reduce the stress hormone cortisol (11), which when elevated, can result in a significant increase in fat mass (12).

Muscle Growth – Creatine, beta-alanine, HMB, and the amino acid leucine have held the title as the most popular supplements used by athletes to improve muscle strength, size, and endurance. It’s time to include omega-3 fish oil supplementation in that discussion as new science has emerged examining its anabolic potential. A recent study demonstrated 4 grams of fish oil supplementation (1.86 g EPA and 1.5 g DHA) increased protein synthesis, mTOR signaling pathway (key for muscle growth), and the muscle/protein DNA ratio (i.e. muscle cell size) (13). A similar protocol was used by the same research team to see if these effects were the same in adults over 65. Remarkably, 4 grams of fish oil supplementation increased the muscle protein synthesis response in elderly adults. (14).

How Much to Take? – The levels of omega-3 fats in your body will vary depending on the amount of omega-3 rich fish you eat or the amount of fish oil you take as a supplement. Based on the scientific evidence reported in this article, it seems 3-4 grams per day (1.5 to 2 grams of EPA and 1.5 to 2 grams of DHA) is the ideal dosage to improve joint mobility, improve body composition, and augment muscle growth.

To optimize your omega-3 levels in your blood, while also focusing on improving markers of athletic performance, take 2 grams of fish oil before and after an intense training session. For athletes participating at the collegiate, professional, or Olympic level, to reduce your risk of testing positive for a banned substance, you want a fish oil that has been tested for Sport by NSF (www.nsfsport.com), such as Nordic Naturals Ultimate Omega-D3 Sport®.

BIO: One of the leading sports nutritionist in the industry, Tavis Piattoly is the Sports Dietitian for Tulane Athletics and the NFLPA Brain and Body Trust Program. He served as the Nutritionist for the New Orleans Saints from 2006 to 2013. He works with athletes at all levels, designing nutrition programs for peak performance. An expert on sports supplements, Tavis speaks on supplement safety for young athletes. www.mysportsdconnect.com

References

Bloomer RJ, Larson DE, Fisher-Wellmann KH, Galpin AJ, Schilling BK, Effect of eicosapentaenoic and docosahexaenoic acid on resting and exercise-induced inflammatory and oxidative stress biomarkers: a randomized, placebo controlled, cross-over study. Lipids Health Disease 2009; 19:8:36.
Hill JO, Peters JC, Lin D, Yakubu F, Greene H, Swift L, Lipid accumulation and body fat distribution is influenced by type to dietary fat fed to rats. International Journal of Obesity and Related Metabolic Disorders 1993; 17:223-236.
Ikemoto S, Takahashi M, Tsunoda N, Maruyama K, Itakura H, Ezaki O, High Fat Diet induced hyperglycemia and obesity in mice: differential effects of dietary oils. Metabolism 1996; 45: 1539-1546.
Belzung F, Raclot T, Groscolas R, 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 1993; 264: R1111-1118.
Parish CC, Pathy DA, Angel A, Dietary Fish Oils limit adipose tissue hypertrophy in rats. Metabolism: Clinical and Experimental 1990; 39: 217-219.
Ruzickova J, Rossmeisl M, Prazak T, Flachs P, Sponarova J, Veck M, Tvrzicka E, Bryhn M, Kopecky J, Omega-3 PUFA of marine origin limit diet induced obesity in mice by reducing cellularity of adipose tissue. Lipids 2004; 39:1177-1185.
Couet C, Delarue J, Ritz P, Antoine JM, Lamisse F, Effect of dietary fish oil on body mass and basal fat oxidation in healthy adults. International Journal of Obesity and Related Metabolic Disorders 1997; 21:637-643.
Noreen EE, Sass MJ, Crowe ML, Pabon VA, Brandauer J, Averill LK, 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 2010; 7:31.
Kim HJ, Takahashi M, Ezaki O, 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 1999; 274: 25892-25898.
Natatani T, Kim HJ, Kaburagi Y, Yasuda K, Ezaki O, 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 2003; 44: 369-379.
Delarue J, Matzinger O, Binnert C, Schneiter P, Chiolero R, Tappy L, Fish Oil prevents the adrenal activation elicited by mental stress in healthy men. Diabetes and Metabolism 2003; 29:289-295.
Bjorntorp P, Rosmond R, Obesity and Cortisol 2000; 16: 924-936.
Smith GI, Atherton P, Reeds DN, Mohammed BS, Rankin D, Rennie MJ, Omega-3 polyunsaturated fatty acids augment the muscle protein anabolic response to hyperoinsulinemia-hyperaminoacidaemia in healthy young and middle-aged men and women. Clinical Science (London) 2011; 121 (6): 267-78.
Smith GI, Atherton P, Reeds DN, Mohammed BS, Rankin D, Rennie MJ, Dietary omega-3 fatty acid supplementation increases the rate of muscle protein synthesis in older adults: a randomized controlled trial. American Journal of Clinical Nutrition 2011; 93 (2): 402-12.

Long-Chain Omega-3 Fatty Acids: Friend or Foe to Prostate?

Long-Chain Omega-3 Fatty Acids: Friend or Foe to Prostate?

There’s more than meets the eye regarding the recent controversy over omega-3 levels and prostate cancer risk — Lets take a closer look. Hector Lopez, MD, CSCS, FAAPMR. A large-scale prospective case-cohort study evaluating plasma fatty acid levels and prostate cancer risk, published in JNCI (Journal of the National Cancer Institute) online ahead of print on July 10^th, 2013 has created quite the stir amongst media, health care professionals, nutrition researchers, and the dietary supplement industry…Again! To quote the great Yogi Berra, “It’s like déjà vu, all over again.”

This recent study was led by Drs. Alan Kristal from the Fred Hutchinson Cancer Research Center, and Theodore Brasky of The Ohio State University Comprehensive Cancer Center in the USA as a follow up to their 2011 study. This new study analyzed data and blood plasma phospholipid status from men who participated in the SELECT (Selenium and Vitamin E Cancer Prevention Trial) trial from 427 participating sites across Europe, USA, Canada and Puerto Rico. Blood was analyzed for 834 “cases” diagnosed with prostate cancer (156 of which were high-grade), and an age-matched subcohort, comparison group of 1,393 all of which were selected from the 35,533 participants.

Without going into an in-depth review of the study (beyond the scope or goal of this post), the men with the highest blood plasma levels of the long-chain omega-3 PUFAs (EPA, DPA, and DHA) were associated with increased risk for low-grade, high-grade and total prostate cancer (44%, 71% and 43% increased risk, respectively). Intriguingly, a higher omega-6 level (Linoleic acid) was associated with reduced risk of low-grade and total prostate cancer, but there was no dose response relationship.

A few salient points to consider here:

1) Within the prostate cancer cases, their plasma phospholipid fatty acid profile was divided into quartiles. The lowest risk group had < 3.68% tissue levels (plasma phospholipids) VS. highest prostate CA risk group being at > 5.3%. This is quite a narrow range of plasma phospholipid fatty acid concentration to draw conclusions from. Moreover, the mean EPA + DPA + DPA fatty acid % in plasma phospholipids was only 4.48% in controls (non-cancer group), and 4.66% in the total cancer case group. Again, an even narrower range–caution must be taken before drawing sweeping or extreme conclusions and interpretation of this data. So, what does that mean for individuals who are supplementing actively with fish oil and simultaneously keeping vegetable oil LA (omega-6) intake down that typically walk around at 7-15% (who incidentally have lowest sudden cardiac death risk and lowest 25-year mortality rates)?

It is possible, that some biochemical scenario plays out where, with respect to prostate CA, you are better off either being real low (at which point your risk for cardiovascular morbidity & mortality goes up), or at the higher goal range of >8%? There is some interesting preclinical, mechanistic data showing that high levels of DHA increases expression of SDC-1 (a transmembrane proteoglycan) in prostate tissue. SDC-1 may help with mediating apoptosis (programmed cell death) of prostate cancer cells, by suppressing proto-oncogene (a normal gene that when mutated can cause cancer by deranging cell growth and differentiation mechanisms) signaling.

2) This is NOT a (RDBCT)…it isn’t even an open label “intervention-based” trial. Simply an epidemiologic, nested case-cohort based association. The SELECT study was not designed specifically to look at omega-3 fatty acid associations, a priori (from earlier knowledge). That simply means the original SELECT randomized, placebo-cotrolled clinical trial was not originally set up to answer the question of whether “Increased intake of long-chain omega-3 polyunsaturated fatty acids lead to increased rates of prostate cancer development.” Hence, that limits the “robustness” and “strength of causality assessment” of the data. Further, there was no mention in the study of dietary fish intake or fish oil supplementation. Is it possible that the sicker individuals began taking fish oil or increasing their fish intake in an attempt to improve their health? Again, it does not allow us to discern whether the “association” exists with fish oil supplementation vs. fish from food sources vs. particular type of fish [Salmon vs. Mackerel vs. Sardine vs. Cooked (Grilled, Baked or Fried) or Raw as in Sushi]. Could there be some xenobiotic or persistent organic pollutants acting as a carcinogen in one of these sources? After all, it is well established that certain heavy metals (e.g., cadmium, mercury), dioxins and PCBs are mutagenic and carcinogenic.

A few things stand out about the methods used to evaluate fatty acid status. First, the plasma phospholipid fatty acid assay is considered to be more representative of ACUTE and dynamic biomarker of omega-3 fatty acid intake by many experts in the biochemical analysis of fatty acids. Short-term factors such as a single meal or supplemental fish oil dose can increase plasma phospholipid omega-3 levels by over 2-fold within 6-10 hours. That is because this assay includes lipids found in the lipoprotein fraction of blood (such as chylomicrons, LDL subtypes, VLDL, etc.), not just in cell plasma membranes such as the omega-3 index (% of omega-3 fatty acids in RBC membrane). Erythrocyte (or Red Blood Cell) membrane fatty acid analysis is a more reliable biomarker of SUBACUTE omega-3 fatty acid intake, with stable values reflecting dietary intake over a 2-3 month period.

Let’s admit that this study utilized data mined from a very large, prospective study, with a large number of prostate cancer cases—this is a strength. The SELECT trial that this study was based on had a very good follow up and small amount of attrition. This minimizes the potential for a phenomenon we observe in research known as attrition bias (a kind of selection bias, where the subjects who dropout are discounted, effectively changing the characteristics of one comparison group vs. another that may lead to drawing inappropriate conclusions from the data/results).

3) Then, we do need to consider the question of whether there is “fire at the heart of this smoke” that could be attributable to some as yet undetermined mechanism? After all, there are at least 3 more large studies that support the findings of this study. However, there are also at least 3 other studies that conflicts with the current study showing an inverse relationship between long-chain n-3 PUFA tissue levels and prostate cancer risk. Keep in mind that cancer biology is incredibly complex with, not only many factors that contribute to risk, progression, etc., but also many of these very factors interact to create even more layers of complexity.

Having said that, I have a few theories, including:

** In the case of prostate biology, immune “surveillance” of cellular oncoproteins play a much larger role in identifying and creating cytotoxicity and apoptosis (programmed cell death pathways) to keep these precancerous cells at bay.

** At certain levels of tissue n-3 concentration, there may be a physiologic/molecular environment whereby mitogenic/ oncogenic and cellular proliferative pathways are driven forward and, while tumor suppressive and differentiation pathways are inhibited. This scenario could promote tumorigenesis/ carcinogensis, especially in a scenario where there is just enough immune suppression to allow for this cellular activity to spiral out of control, without the typical safety mechanism and breaks that would limit DNA mutagenesis & damage.

** Lipid peroxides generated at the local prostatic tissue level may, in certain individuals, overwhelm their capacity to neutralize this oxidative stress. This scenario could theoretically lead to increased DNA damage, that increases potential to outpace DNA repair mechanisms and transform cells to loose cell growth/proliferation regulation.

** Could there be certain genotypes (nutrigenetic & epigenetic mechanisms) that increase susceptibility to the above theories? Given what we have learned from genome wide association studies (GWAS) in the last decade, this is certainly a possibility.

4) Interestingly, this association appears to be tissue specific. As opposite association (inverse relationships) exist for omega-3 status and other cancers, e.g., breast, colon, and possibly pancreatic.

5) There is interesting data that demonstrates what I would refer to as a “metabolic dissonance” in energy metabolism of prostate cancer cells. In stark contrast to cancers of other tissues, where metabolism becomes more heavily glycolytic (strong preference to using glucose for fuel during energy metabolism), prostate adenocarcinoma cells appear to switch toward greater beta-oxidation of fatty acids to drive its bioenergetic needs! This “metabolic dissonance” with respect to the unique physiology of prostate cancer could very well be a major factor leading to the observed association between long-chain omega-3 PUFA and prostate tumorigenesis in Brasky et al study.

6) Prostate cancer detection has increased dramatically over the last 10-15 years, not only due to the prevalence of PSA screening, but also lower threshold to biopsy has lead to increased diagnosis. This is particularly the case with detection of microfoci of prostate malignant cells in smaller (lower volume) prostates…Hence, there is a greater probability of sampling malignant microfoci in smaller prostates. This is an aspect that was not controlled for (Hazard ratios in the study were not adjusted for this variable) in the Brasky et al study.

7) There is also robust evidence that contradicts and opposes the conclusions and interpretation of the Brasky et al data. For example, the work of Chua et al. (2013), Sorongon-Legaspi et al. (2013), Torfadottir et al. (2013), Chavarro et al (2008), Terry et al. (2001), Harvei et al (1997), and others show a protective effect of higher levels of tissue omega-3 fatty acid status, with lower prostate cancer risk and prostate cancer mortality.

8) It is also imperative to try adding context and maintaining perspective whenever faced with new information that may change behavior; or in this case, information that may change clinical management and dietary advice. Lets keep the following numbers in mind to add some more perspective, color and light to this data from a public health, and risk assessment standpoint. (from National Cancer Institute-Surveillance Epidemiology and End Results, and National Heart, Blood and Lung Institute-NIH):

Prostate Cancer- U.S. :

Age-adjusted incidence rates (for all races) from 2006-2010: ~152/ per 100,000 men
Age-adjusted death rates (for all races) from 2006-2010: ~23/ per 100,000 men
Prevalence of prostate cancer diagnosis: ~2.6 million men on January 1, 2010
Direct cost burden from prostate cancer in U.S. in 2010: ~$14 Billion

Cardiovascular Disease- U.S.

Age-adjusted death rates (for all races) from in 2008: ~244/ per 100,000 population (both men and women)
Prevalence of cardiovascular disease diagnosis: ~82.6 million men in 2006
Direct cost burden from CVD in U.S. in 2008: ~$218 Billion

9) Although the jury is still not out with respect to the relationship long-chain omega-3 PUFAs found in fatty fish and fish oil and prostate cancer risk, progression or severity, I believe the sheer numbers tell us what the lowest hanging fruit is relative to public health focus and resources. I do agree with the authors that prostate health history should be taken at least be taken into consideration, when weighing potential risk to benefit ratio of increasing long-chain n-3 PUFA intake.

10) As with so much in science, medicine, health and nutrition, the more data we have access to, the more questions arise. One burning question this study raises that is of interest to consumers, industry and health care providers—How would these findings change when evaluating specific dietary sources of long-chain n-3 PUFA (e.g., concentrated fish oil supplements vs. Sushi vs. Baked, Grilled or Fried fish)?

Overall, the benefits of increasing omega-3 status (and decreasing omega-6 overabudnance) for most people FAR outweigh potential risks. Stay tuned…but as always keep a cool head and try to avoid being drawn into dramatic, emotionally-charged and sensational headlines. These observational, case-control cohort studies may be useful for generating hypotheses to test in well-controlled prospective clinical trials, but far from establishing causality. So, what am I doing with this information you ask? Well…I’m still taking my fish oil, eating a variety of fish while we await for stronger evidence (which I seriously doubt we’ll ever see :)). Oh, and by the way, NO…I am not going to intentionally increase my omega-6 vegetable oil intake—despite the fact that this study revealed that elevated plasma omega-6 fatty acid levels were associated with decreased risk of low-grade and total prostate cancer. Remember to take your fish oil and call me in the morning! J

BIO – Hector Lopez, MD, CSCS, FAAPMR

Dr. Lopez is a board-certified specialist in physical medicine and rehabilitation, with a concentration in spine, sports and musculoskeletal medicine. He also has post-graduate training in nutritional biochemistry. An active researcher, speaker, author, and clinician, he is recognized for uniquely integrating the best available methods in the fields of musculoskeletal medicine, endocrinology and metabolism, regenerative medicine, exercise and nutritional science. Dr. Lopez has been a founding partner and director of several integrative orthopedic, spine, and sports medicine facilities, and he is a principal and chief medical officer of the Center for Applied Health Sciences (CAHS), a leading multidisciplinary clinical research institute. Dr. Lopez is also co-founder of Supplement Safety Solutions (SSS), a Nutravigilance^TM, quality assurance, medical monitoring, and regulatory consulting company. In addition, he is a consultant to professional athletes and to the nutritional supplement industry as product developer, research advocate, and safety and regulatory expert.

References

Brasky T, Darke A, Song X, Tangen C, Goodman P, Thompson I, Meyskens F, Goodman G, Minasian L, Parnes H, Klein E, Kristal AR. Plasma Phospholipid Fatty Acids and Prostate Cancer Risk in the SELECT Trial. J Natl Cancer Inst. 2013 Jul 10 [Epub ahead of print].

Chua ME, Sio MC, Sorongon MC, Morales ML Jr. The relevance of serum levels of long chain omega-3 polyunsaturated fatty acids and prostate cancer risk: A meta-analysis. Can Urol Assoc J. 2013 May;7(5-6):E333-43.

Harris WS, Pottala JV, Varvel SA, Borowski JJ, Ward JN, McConnell JP. Erythrocyte omega-3 fatty acids increase and linoleic acid decreases with age: observations from 160,000 patients. Prostaglandins Leukot Essent Fatty Acids. 2013 Apr;88(4):257-63.

Harris WS, Thomas RM. Biological variability of blood omega-3 biomarkers. Clin Biochem. 2010 Feb;43(3):338-40.

Harvei S, Bjerve KS, Tretli S, et al. Prediagnostic level of fatty acids in serum phospholipids: omega-3 and omega-6 fatty acids and the risk of prostate cancer. Int J Cancer. 1997;71(4):545–551.

Howlader N, Noone AM, Krapcho M, Garshell J, Neyman N, Altekruse SF, Kosary CL, Yu M, Ruhl J, Tatalovich Z, Cho H, Mariotto A, Lewis DR, Chen HS, Feuer EJ, Cronin KA (eds). SEER Cancer Statistics Review, 1975-2010, National Cancer Institute. Bethesda, MD, http://seer.cancer.gov/csr/1975_2010/, based on November 2012 SEER data submission, posted to the SEER web site, 2013.

Hu Y, Sun H, Owens RT, Gu Z, Wu J, Chen YQ, O’Flaherty JT, Edwards IJ. Syndecan-1-dependent suppression of PDK1/Akt/bad signaling by docosahexaenoic acid induces apoptosis in prostate cancer. Neoplasia. 2010 Oct;12(10):826-36.

Liu Y. Fatty acid oxidation is a dominant bioenergetic pathway in prostate cancer. Prostate Cancer Prostatic Dis. 2006;9(3):230-4.

National Heart, Lung, and Blood Institute. Unpublished Tabulations of the National Health Interview Survey, 2010. Available at: http://www.cdc.gov/nchs/nhis/nhis_2010_data_release.htm.

O’Flaherty JT, Hu Y, Wooten RE, Horita DA, Samuel MP, Thomas MJ, Sun H, Edwards IJ. 15-lipoxygenase metabolites of docosahexaenoic acid inhibit prostate cancer cell proliferation and survival. PLoS One. 2012;7(9):e45480.

Sorongon-Legaspi MK, Chua M, Sio MC, Morales M Jr. Blood level omega-3 Fatty acids as risk determinant molecular biomarker for prostate cancer. Prostate Cancer. 2013;2013:875615.

Terry P, Lichtenstein P, Feychting M, Ahlbom A, Wolk A. Fatty fish consumption and risk of prostate cancer. Lancet. 2001 Jun 2;357(9270):1764-6.

Torfadottir JE, Valdimarsdottir UA, Mucci LA, Kasperzyk JL, Fall K,Tryggvadottir L, Aspelund T, Olafsson O, Harris TB, Jonsson E, Tulinius H, Gudnason V, Adami HO, Stampfer M, Steingrimsdottir L. Consumption of fish products across the lifespan and prostate cancer risk. PLoS One. 2013 Apr 17;8(4):e59799.

Zha S, Ferdinandusse S, Hicks JL, Denis S, Dunn TA, Wanders RJ, Luo J, De Marzo AM, Isaacs WB. Peroxisomal branched chain fatty acid beta-oxidation pathway is upregulated in prostate cancer. Prostate. 2005 Jun 1;63(4):316-23.

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

Lipid: A class of compounds consisting of phospholipids, sterols, and triaglycerols¹.
Triglyceride: A glycerol molecule with three fatty acids attached.
Glycerol: A three carbon sugar that serves as a backbone for triglycerides.
Fatty Acids: Chains of carbon atoms of varying lengths that attach to a glycerol molecule to form a triaglycerol.
Saturated Fat (SFA): All carbon molecules in the chain are fully bonded with either carbon or hydrogen and contain no double bonds.
Monounsaturated Fat (MUFA): A chain with one double bond.
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

Phospholipids (specific types of fat) make up a large portion of our cell membranes.
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)
Essential for transmission of nerve signals.
Provide satiety
Produce hormones (specifically leptin) that control homeostasis in terms of your body fat set point (this is known as the adipostat)²
Insulate from thermal stress.
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 CHD^6,7. 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

Antonio, J., Kalman, D., Stout, J. R., Greenwood, M., Willoughby, D. S., & Haff, G. G. (2008). Essentials of Sports Nutrition and Supplements. Humana Press.
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.
Gropper, S. S., Smith, J. L., & Groff, J. L. (2005). Advanced Nutrition and Human Metabolism.Belmont, CA: Thomson Wadsworth.
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.
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.
Ascherio, A., & Willett, W. (1997). Health effects of trans fatty acids. American Journal of Clinical Nutrition , 66, 1006-1010.
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.
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.
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.

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?

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?

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.

Fish Oil – The Real Deal Fat Fighter

by Monica Mollica MSc. (Editor’s note: Take at least ~1600 mg EPA and ~800 mg DHA daily! Fish oil should be in the top 3 of everyone’s daily supplement).

Fish oil is well known for its beneficial cardiovascular and cardiac health effects. In 2004 FDA approved a prescription fish oil preparation for treatment of high blood triglycerides (hypertriglyceridemia) ¹. However, recently several studies have shown that fish oil also has other beneficial effects, which might appeal more to the younger population, 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 of 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 to the fat loss effect of fish oil. In another upcoming article I will cover the anti-catabolic effects of fish oil in more detail.

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…In a landmark study, healthy male participants were given a diet where 6 g of fat from butter, olive oil, sunflower oil and peanut oil was replaced with 6 g fish oil (corresponding to 1.1 g EPA and 0.7 g DHA) per day ⁵⁵. After 3 weeks the researchers noted a significant increase in resting fat oxidation (fat burning) and a 1.94 lb (0.88 kg) decrease in body fat (measured by DEXA), in the face of a constant energy intake. Since there was no change in body weight, this implies that the fish oil supplement increased lean body mass (more on that in an upcoming article). This effect was seen despite the fact that the subjects were told not to change their usual exercise and diet habits.

Another study confirmed the ability of fish oil supplementation to increase fat oxidation (fat burning) during exercise ⁵⁶. In this study, recreationally active men were given a daily fish oil supplement corresponding to 2400 mg EPA and 1600 mg DHA for 3 weeks. At the end of the study subjects performed a 60 min jogging exercise bout at 60% of VO2max, during which fat metabolism was measured. It was shown that the fish oil supplementation significantly increased the oxidation of fat for energy (e.g. fat burning) during the exercise session ⁵⁶. It has also been shown that supplementing with fish oil for 3 weeks (1.1 g EPA and 0.7 g DHA daily) significantly decreases insulin levels and increases fat oxidation (fat burning) by 35% (!) after consumption of carbohydrate rich meals ⁵⁷.

Recently, more studies have been published on the topic. In overweight men and women, the effects of the addition of 6 g of fish oil daily (corresponding to 360 mg EPA and 1560 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 ⁵⁸. 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 the amount of body fat ⁵⁸. It is interesting that these effects were noted even though the subjects did not change their usual food habits other than adding the fish oil supplement. 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 (that didn’t exercise). This could be due to the older age of the subjects (47-51 yrs) in this study compared to the previous studies, and the relatively low dose of EPA. Fish oil supplementation has also been shown to result in a 2.22 lb (1 kg) greater weight loss after 4 weeks of dieting (reduced caloric intake) ⁵⁹.

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 ^60-63. 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 (see below). However, 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. Overall, fish oil seems to have the ability to shift fat metabolism away from storage toward burning of body fat.

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 potential compositional changes, which after all is what is interesting from both a health, esthetic and physical performance viewpoint. I will cover the anti-catabolic and potential lean mass gaining effects of fish oil in another upcoming article.

Wrap up

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 ⁶⁴; 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. Prescription Omega-3s: An Overview for Nurse Practitioners. The Journal of cardiovascular nursing 2011;26(4):290-97.

2. Baillie RA, Takada R, Nakamura M, Clarke SD. 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 1999;60(5-6):351-6.

3. Hill JO, Peters JC, Lin D, Yakubu F, Greene H, Swift L. 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 1993;17(4):223-36.

4. Ikemoto S, Takahashi M, Tsunoda N, Maruyama K, Itakura H, Ezaki O. High-fat diet-induced hyperglycemia and obesity in mice: differential effects of dietary oils. Metabolism: clinical and experimental 1996;45(12):1539-46.

5. Su W, Jones PJ. Dietary fatty acid composition influences energy accretion in rats. The Journal of nutrition 1993;123(12):2109-14.

6. Cunnane SC, McAdoo KR, Horrobin DF. n-3 Essential fatty acids decrease weight gain in genetically obese mice. The British journal of nutrition 1986;56(1):87-95.

7. LeBoeuf RC, Veldee MS. Genetically determined body weight loss in mice fed diets containing salmon oil. The Journal of nutrition 1993;123(3):547-58.

8. Mori T, Kondo H, Hase T, Tokimitsu I, Murase T. Dietary fish oil upregulates intestinal lipid metabolism and reduces body weight gain in C57BL/6J mice. The Journal of nutrition 2007;137(12):2629-34.

9. Pan DA, Storlien LH. Dietary lipid profile is a determinant of tissue phospholipid fatty acid composition and rate of weight gain in rats. The Journal of nutrition 1993;123(3):512-9.

10. Belzung F, Raclot T, Groscolas R. 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 1993;264(6 Pt 2):R1111-8.

11. Parrish CC, Pathy DA, Angel A. Dietary fish oils limit adipose tissue hypertrophy in rats. Metabolism: clinical and experimental 1990;39(3):217-9.

12. Ruzickova J, Rossmeisl M, Prazak T, Flachs P, Sponarova J, Veck M, et al. Omega-3 PUFA of marine origin limit diet-induced obesity in mice by reducing cellularity of adipose tissue. Lipids 2004;39(12):1177-85.

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

14. Clarke SD. Polyunsaturated fatty acid regulation of gene transcription: a molecular mechanism to improve the metabolic syndrome. The Journal of nutrition 2001;131(4):1129-32.

15. Clarke SD. The multi-dimensional regulation of gene expression by fatty acids: polyunsaturated fats as nutrient sensors. Current opinion in lipidology 2004;15(1):13-8.

16. Clarke SD, Baillie R, Jump DB, Nakamura MT. Fatty acid regulation of gene expression. Its role in fuel partitioning and insulin resistance. Annals of the New York Academy of Sciences 1997;827:178-87.

17. Clarke SD, Gasperikova D, Nelson C, Lapillonne A, Heird WC. Fatty acid regulation of gene expression: a genomic explanation for the benefits of the mediterranean diet. Annals of the New York Academy of Sciences 2002;967:283-98.

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

19. Clarke SD, Thuillier P, Baillie RA, Sha X. Peroxisome proliferator-activated receptors: a family of lipid-activated transcription factors. The American journal of clinical nutrition 1999;70(4):566-71.

20. Davidson MH. Mechanisms for the hypotriglyceridemic effect of marine omega-3 fatty acids. The American journal of cardiology 2006;98(4A):27i-33i.

21. Jump DB, Clarke SD, Thelen A, Liimatta M, Ren B, Badin M. Dietary polyunsaturated fatty acid regulation of gene transcription. Progress in lipid research 1996;35(3):227-41.

22. Jump DB, Clarke SD, Thelen A, Liimatta M, Ren B, Badin MV. Dietary fat, genes, and human health. Advances in experimental medicine and biology 1997;422:167-76.

23. Nakamura MT, Cho HP, Xu J, Tang Z, Clarke SD. Metabolism and functions of highly unsaturated fatty acids: an update. Lipids 2001;36(9):961-4.

24. Ntambi JM, Bene H. Polyunsaturated fatty acid regulation of gene expression. Journal of molecular neuroscience : MN 2001;16(2-3):273-8; discussion 79-84.

25. Price PT, Nelson CM, Clarke SD. Omega-3 polyunsaturated fatty acid regulation of gene expression. Current opinion in lipidology 2000;11(1):3-7.

26. Raclot T, Oudart H. Selectivity of fatty acids on lipid metabolism and gene expression. The Proceedings of the Nutrition Society 1999;58(3):633-46.

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

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

29. Lapillonne A, Clarke SD, Heird WC. Polyunsaturated fatty acids and gene expression. Current opinion in clinical nutrition and metabolic care 2004;7(2):151-6.

30. Hannah VC, Ou J, Luong A, Goldstein JL, Brown MS. Unsaturated fatty acids down-regulate srebp isoforms 1a and 1c by two mechanisms in HEK-293 cells. The Journal of biological chemistry 2001;276(6):4365-72.

31. Kim HJ, Takahashi M, Ezaki O. 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 1999;274(36):25892-8.

32. Mater MK, Thelen AP, Pan DA, Jump DB. 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 1999;274(46):32725-32.

33. Nakatani T, Kim HJ, Kaburagi Y, Yasuda K, Ezaki O. 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 2003;44(2):369-79.

34. Shimano H, Yahagi N, Amemiya-Kudo M, Hasty AH, Osuga J, Tamura Y, et al. Sterol regulatory element-binding protein-1 as a key transcription factor for nutritional induction of lipogenic enzyme genes. The Journal of biological chemistry 1999;274(50):35832-9.

35. Worgall TS, Sturley SL, Seo T, Osborne TF, Deckelbaum RJ. 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 1998;273(40):25537-40.

36. Xu J, Nakamura MT, Cho HP, Clarke SD. 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 1999;274(33):23577-83.

37. Yahagi N, Shimano H, Hasty AH, Amemiya-Kudo M, Okazaki H, Tamura Y, et al. 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 1999;274(50):35840-4.

38. Desvergne B, Wahli W. Peroxisome proliferator-activated receptors: nuclear control of metabolism. Endocrine reviews 1999;20(5):649-88.

39. Kersten S, Desvergne B, Wahli W. Roles of PPARs in health and disease. Nature 2000;405(6785):421-4.

40. Latruffe N, Vamecq J. Peroxisome proliferators and peroxisome proliferator activated receptors (PPARs) as regulators of lipid metabolism. Biochimie 1997;79(2-3):81-94.

41. Minnich A, Tian N, Byan L, Bilder G. A potent PPARalpha agonist stimulates mitochondrial fatty acid beta-oxidation in liver and skeletal muscle. American journal of physiology. Endocrinology and metabolism 2001;280(2):E270-9.

42. Nakatani T, Tsuboyama-Kasaoka N, Takahashi M, Miura S, Ezaki O. Mechanism for peroxisome proliferator-activated receptor-alpha activator-induced up-regulation of UCP2 mRNA in rodent hepatocytes. The Journal of biological chemistry 2002;277(11):9562-9.

43. Power GW, Newsholme EA. Dietary fatty acids influence the activity and metabolic control of mitochondrial carnitine palmitoyltransferase I in rat heart and skeletal muscle. The Journal of nutrition 1997;127(11):2142-50.

44. Schoonjans K, Staels B, Auwerx J. The peroxisome proliferator activated receptors (PPARS) and their effects on lipid metabolism and adipocyte differentiation. Biochimica et biophysica acta 1996;1302(2):93-109.

45. Krey G, Braissant O, L’Horset F, Kalkhoven E, Perroud M, Parker MG, et al. Fatty acids, eicosanoids, and hypolipidemic agents identified as ligands of peroxisome proliferator-activated receptors by coactivator-dependent receptor ligand assay. Mol Endocrinol 1997;11(6):779-91.

46. Reddy JK, Mannaerts GP. Peroxisomal lipid metabolism. Annual review of nutrition 1994;14:343-70.

47. Delarue J, Matzinger O, Binnert C, Schneiter P, Chiolero R, Tappy L. Fish oil prevents the adrenal activation elicited by mental stress in healthy men. Diabetes & metabolism 2003;29(3):289-95.

48. Noreen EE, Sass MJ, Crowe ML, Pabon VA, Brandauer J, Averill LK. 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 2010;7:31.

49. Diez JJ, Iglesias P. The role of the novel adipocyte-derived hormone adiponectin in human disease. European journal of endocrinology / European Federation of Endocrine Societies 2003;148(3):293-300.

50. Nedvidkova J, Smitka K, Kopsky V, Hainer V. Adiponectin, an adipocyte-derived protein. Physiological research / Academia Scientiarum Bohemoslovaca 2005;54(2):133-40.

51. Walker BR. 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 2001;11 Suppl A:S91-5.

52. Salehi M, Ferenczi A, Zumoff B. Obesity and cortisol status. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme 2005;37(4):193-7.

53. Bjorntorp P, Rosmond R. Obesity and cortisol. Nutrition 2000;16(10):924-36.

54. Pasquali R, Vicennati V, Cacciari M, Pagotto U. The hypothalamic-pituitary-adrenal axis activity in obesity and the metabolic syndrome. Annals of the New York Academy of Sciences 2006;1083:111-28.

55. Couet C, Delarue J, Ritz P, Antoine JM, Lamisse F. 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 1997;21(8):637-43.

56. Huffman DM, Michaelson JL, Thomas T, R. . Chronic supplementation with fish oil increases fat oxidation during exercise in young men. . JEPonline 2004;7(1):48-56.

57. Delarue J, Couet C, Cohen R, Brechot JF, Antoine JM, Lamisse F. Effects of fish oil on metabolic responses to oral fructose and glucose loads in healthy humans. The American journal of physiology 1996;270(2 Pt 1):E353-62.

58. Hill AM, Buckley JD, Murphy KJ, Howe PR. Combining fish-oil supplements with regular aerobic exercise improves body composition and cardiovascular disease risk factors. The American journal of clinical nutrition 2007;85(5):1267-74.

59. Thorsdottir I, Tomasson H, Gunnarsdottir I, Gisladottir E, Kiely M, Parra MD, et al. Randomized trial of weight-loss-diets for young adults varying in fish and fish oil content. Int J Obes (Lond) 2007;31(10):1560-6.

60. Brilla LR, Landerholm TE. Effect of fish oil supplementation and exercise on serum lipids and aerobic fitness. The Journal of sports medicine and physical fitness 1990;30(2):173-80.

61. Warner JG, Jr., Ullrich IH, Albrink MJ, Yeater RA. Combined effects of aerobic exercise and omega-3 fatty acids in hyperlipidemic persons. Medicine and science in sports and exercise 1989;21(5):498-505.

62. Krebs JD, Browning LM, McLean NK, Rothwell JL, Mishra GD, Moore CS, et al. Additive benefits of long-chain n-3 polyunsaturated fatty acids and weight-loss in the management of cardiovascular disease risk in overweight hyperinsulinaemic women. Int J Obes (Lond) 2006;30(10):1535-44.

63. DeFina LF, Marcoux LG, Devers SM, Cleaver JP, Willis BL. Effects of omega-3 supplementation in combination with diet and exercise on weight loss and body composition. The American journal of clinical nutrition 2011;93(2):455-62.

64. Bays HE, Maki KC, Doyle RT, Stein E. 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 2009;121(5):145-50.

About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer; Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an early teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a major in Nutrition at the University. During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications. It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to bodybuilding, fitness, health and anti-aging.