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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.

Nutritional Counseling and Free Speech Update

By Rick Collins, JD, FISSN

Does nutritional advice raise an issue of Free Speech? A recent Fourth Circuit case from North Carolina should be of interest to the nutrition community as it moves forward through the court system [Cooksey v. Futrell, et al, http://www.ij.org/images/pdf_folder/first_amendment/paleo/paleo-4th-opinion.pdf]. The relevant facts and Court’s holding follow.

In 2009, Steve Cooksey was rushed to the hospital in a diabetic coma. Diagnosed with Type II diabetes, he was advised by licensed dietitians to eat a diet high in carbohydrates and low in fat. Instead, he adopted a “Paleolithic diet” high in fat and low in carbohydrates. On this regimen, he purportedly dropped 78 pounds, ceased need for medications, and regained his health. The following year, he launched a website now called “Diabetes Warrior.” The site contained a disclaimer that Cooksey was not a licensed medical professional and did not have any formal medical education or special dietary qualifications. The site promoted the high fat/low carbohydrate diet and Paleo lifestyle to combat obesity and diabetes.

Cooksey’s website had three relevant components: (1) a free advice column of visitor questions and his answers; (2) a free “Personal Dietary Mentoring” section, in which visitors would post questions or share stories and he would respond; and (3) a fee-based diabetes coaching service, in which Cooksey provided individualized advice on the Paleo diet.

Cooksey came to the attention of the North Carolina Board of Dietetics/Nutrition when he attended a nutritional seminar on diabetes and expressed dissenting opinions during the question-and-answer segment of the seminar. Someone present at the seminar reported Cooksey to the Board, which is charged with administering North Carolina’s Dietetics/Nutrition Practice Act, claiming that Cooksey was engaging in the unlicensed practice of dietetics – a Class 1 misdemeanor. The Executive Director of the Board called Cooksey and told him that “he and his website were under investigation.” He was told to take down the fee-based portion of his website and make other changes. Cooksey reluctantly complied “because he feared civil and criminal action against him . . . .” The State Board subsequently sent Cooksey documents with a red-pen review of his site, noting areas of “concern” with large red “X’s.” He was told not to address “specific questions” or give specific advice (e.g., suggesting to a site visitor to introduce “whipping cream” into her diet). He was told that having a meal plan on the site was permissible, but that “recommending it directly to people you speak to or who write you” requires a license. Cooksey did not contact the Board further, but instead altered his website and “ceased expressing opinions in the form of personal dietary advice based on his fear of civil and criminal action against him by the State of North Carolina.”

Cooksey thereafter filed suit in the Western District of North Carolina, alleging the Board violated his First Amendment rights. He claimed that restricting his speech in the advice column, personal dietary mentoring, and the fee-based coaching sections of his site was an unconstitutional restriction and “chilling” of free speech. The American Civil Liberties Union of North Carolina filed a friend-of-the-court brief in Cooksey’s support. The Board filed a motion to dismiss for lack of standing and ripeness, and for failure to state a First Amendment claim. Essentially, they argued that because they had issued no formal decision and Cooksey had voluntarily taken down the relevant sections of his site, Cooksey had suffered no actual injury – that he had no standing to raise a First Amendment claim and that such claim was premature. The district court agreed and dismissed the complaint.

However, the three-judge appellate panel, which included retired Supreme Court Justice Sandra O’Connor, held that the district court erred in not analyzing Cooksey’s claims under the First Amendment standing framework. The appellate court held that Cooksey had sufficiently satisfied the First Amendment injury requirement by showing that the State Board’s actions had an “objectively reasonable chilling effect on the advice and commentary he posted on his website.” Thus, the district court’s order dismissing Cooksey’s complaint was vacated and the case was sent back to be considered on the merits.

What happens from here forward could have big implications not only for the nutritional community but for millions of other people who give free or paid advice over the Internet, as the court will now need to decide the case on First Amendment grounds. How far can a licensing board or other government authority go in regulating or censoring speech? And what is the proper balance between protecting the public and ensuring protected free speech? Stay tuned for further proceedings in Cooksey’s case…

[© Rick Collins, 2013. All rights reserved. For informational purposes only, not to be construed as legal or medical advice. Rick Collins is Legal Counsel to the ISSN; visit Rick at www.rickcollins.com.]

BIO – Rick Collins, Esq., FISSN is a popular personality in the bodybuilding, health, fitness and nutrition communities. A successful lawyer, author, lecturer and magazine columnist, he is a partner in the law firm of Collins, McDonald & Gann, PC, in Mineola, New York. He was formerly a criminal prosecutor, personal trainer and film actor. As an attorney, he has been awarded the highest accolades for legal abilities and ethical standards (AV-rating) from the prestigious Martindale-Hubbell directory of lawyers, and he is listed in the Bar Register of Preeminent Lawyers. Rick serves on the Advisory Board of the ISSN, www.theissn.org.

Out-Muscling Neurological Disorders with Creatine

By Chantal Isabela Charo, Ph.D. Creatine is one of the most popular ergogenic aids in sports nutrition, used by athletes, bodybuilders, the military or anyone participating in a physical activity involving short bursts of high intensity exercise. One of the mechanisms in which creatine improves exercise capacity is via an increase in the stored phosphagens (e.g. ATP and PCr). In the human body, creatine exists in both the free and phosphorylated form (phosphocreatine or PCr) and more than 95% is contained within skeletal muscle. Creatine is mostly known as a performance enhancer in sports nutrition; however, it has become more evident that creatine plays a role in in the central nervous system which will be reviewed in this article. Several studies have shown a similar pattern of impaired creatine metabolism in psychiatric patients with neurological diseases such as Huntington and Parkinson’s which lead scientists and clinicians to question the therapeutic role of creatine in treating and/or preventing mental illnesses. Although many of the molecular mechanisms are not well understood, exogenous creatine supplementation has been proposed and/or proven to improve the outcome of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, ALS, and Huntington’s. Although the detailed mechanisms of the creatine-induced neuroprotection for each disease is different, the basic overall hypothesis is that creatine supplementation is improves the overall bioenergetics and/or mitochondrial deficits associated with each particular neurodegenerative disease. A study done by Watanabe’s group in 2002, showed that creatine supplementation improved mental concentration, memory and learning in normal healthy subjects and early stage Alzheimer’s Disease patients. Another group, conducted a study on Lou Gehring patients (another neurological disease caused by the degeneration of neurons in the central nervous system), showed that buffering cellular energy with exogenous creatine might have a neuroprotective effect (Hervias etal, 2006). Strong support for exogenous creatine supplementation to be an effective neuroprotective agent comes from studies done on Huntington Disease (characterized by abnormal “dance like” body movements and lack of muscular coordination) which may ultimately improve and/or extend the quality of life for individuals afflicted with HD. Studies showed improved motor performance, extended survival, attenuated the loss in body weight and brain weight, reduced neuron atrophy, upon creatine supplementation (Ferrante et al. 2000; Andreassen et al. 2001; Dedeoglu et al. 2003). Additionally, some studies have found an association between creatine metabolism and cognitive function in schizophrenia, generating much interest in the role creatine plays in the pathogenesis of the disorder. In addition to its neuroprotective roles, research suggests that creatine might not only enhance physical performance. there has been a significant amount of research done on creatine supplementation as an enhancer of cognitive performance and brain function. Another study by Watanabe’s group showed that creatine supplementation reduced mental fatigue (Watanabe et al.,2002). Interestingly, recent emphasis has been on the role of creatine supplementation and depression in women. Studies from the University of Utah, brain institute, have shown that patients who combine creatine with an antidepressant respond to their medications faster and better than patients who take antidepressants alone. The eight-week study included 52 women with depression taking the antidepressant Lexapro. Researchers observed dramatic improvements in women’s brain chemistry after combining only 5 grams of creatine with their daily doses of antidepressant medications.

For those who don’t respond well to antidepressants, creatine could become an inexpensive way to improve treatment outcomes. Furthermore, exogenous creatine was shown to improve working memory and intelligence scores in human subjects with diminished phosphocreatine levels due to limited meat intake (Rae et al., 2003).
Creatine supplementation has been generally regarded as safe and has been used for extended periods of times by athletes with few reported side effects. Creatine is a constituent of a normal diet of protein-based foods, such as milk, meat, and nuts. It is not considered an essential nutrient because the kidneys, liver, pancreas, and possibly brain cells are able to synthesize about half of the body’s requirements of creatine from the amino acids arginine, glycine, and methionine (Andres et al., 2008; Béard and Braissant, 2010; Wyss and Kaddurah-Daouk, 2000).

Bottom line – Creatine is not only good for your muscles, but it’s pretty darn good for the brain.

BIO – Dr. Chantal Charo is an Asst. Professor of Physiology, a Sports Nutritionist and a Medical Writer from Miami, FL. Her research particularly focuses on undestanding hormonal imbalances and sugar metabolism in pancreatic diseases. Dr. Charo is also involved in numerous clinical trial in her field and has most recently completed a trial on NSAIDs and pancreatic diseases. Chantal earned her Ph.Ds. in Biomedical Sciences and Cancer Biology from the prestigious University of Texas Houston and the UT MD Anderson Cancer Center. As a sports nutritionist Dr. Charo collaborated with leading supplement companies across the United States by researching ways to target insulin resistance and hormonal imbalance in women, as well as the Euthyroid Sick syndrome and the female athlete using functional nutrition and biomedicine. Chantal hosts a medical segment on a local daily talk show which aims at promoting awareness to women and combating health illiteracy. In support of her research, Chantal has received fellowships from National Cancer Institute, the National Institute of Health and more. She is a Fellow of the American Association of Cancer Researchers, the American Pancreatic Association and the American Breast Cancer Association, and was the recipient for many outstanding scientist awards. The link to Dr. Charo’s Sports and Functional Nutrition Clinic is www.facebook.com/sportsnutritionclinic

Manipulating Night-Time Anabolic/Catabolic Cycles

For years we sports nutritionist missed the boat when it came to maximizing muscle mass because we ignored the night time decrease in muscle growth caused by post-absorptive muscle catabolism. We now know that the body is primed for growth and repair during sleep. What we must do is give the body the necessary materials it needs to do its job. Dr. Mauro Di Pasquale, M.D.

When you review the comments above by the renowned sports nutritional physiologist Dr. Mauro Di Pasquale, they imply that for some time researchers may have considered night-time catabolism’s impact on growth to be negligible and didn’t warrant attention. Those comments also imply that this reasoning may have stemmed from the fact that the problems with the body’s ability to absorb and utilize nutrients during sleep couldn’t be altered or minimized as the body simply breaks down existing muscle tissue to supply the energy needed to keep its metabolic activities going. Despite this innate back-up process, it is a process that occurs for an 8 to 9 hour time frame. The fact is that every night becomes a catabolic night of biblical proportions the minute you lay down to sleep. Catabolic processes begin there assault with a pre-programmed set of muscle destroying instructions. So precise and destructive is this catabolic activity that it naturally occurs via cyclical up-regulation of various catabolic compounds or hormones during normal sleep cycles, hence its reference to as the post absorptive muscle catabolic syndrome.

When It Rains It Pours

As a point of reference here a syndrome is defined as a set of general symptoms all occurring at the same time that collectively indicate or characterize being in a morbid (unhealthy) state. Scientifically, this internal network or place were all this muscle breakdown occurs and is converted to energy is referred to as the ubiquitin-proteasome or UPP pathway. It is here where cortisol the stress and muscle wasting hormone production is increased and accelerated as a direct result of exercise induced stress. Contrary to popular belief, the sleep cycle isn’t just a rest, repair and detoxification phase. In practical terms here, sleep becomes a survival and catabolic period to the body because of a lack of nutrients it has to work with. However, researchers now know that by the time you switch this catabolic switch off, that you have lost substantial amounts of lean muscle tissue. The other part of this axiom is the fact that you are consistently playing catch-up to promote growth. The question then becomes how can the nutrients the body needs be proved or maintained over the course of a normal sleep cycle to combat this impending catabolic syndrome before bedtime?

Understanding Post-Absorptive Physiology

Based on Dr. Pasquale’s comments above, the body is primed for growth and repair during sleep and that there are ways to counter-balance this catabolic cycle. The fact is the body has some built in mechanisms to protect itself via the release of certain hormones to minimize the impending catabolism. This could be somewhat compared to bears getting set for hibernation, when no new nutrients will be coming in for a period of time. For example, testosterone, growth hormone, and IGF-1(insulin growth factor) and insulin tend to remain elevated during sleep. These hormones guard against muscle wasting by reducing the production of cortisol and other catabolic hormones to help maintain protein synthesis. Other compounds the body calls upon include circulating glucose, fatty acids, liver and muscle glycogen (stored glucose), branch chained amino acids, glutamine and other amino acids. These sources can supply up to 1200 needed calories to slow down catabolic activity for about 12 hours. The bottom line here, maintaining your scheduled intake of nutrients throughout the day can impact night-time catabolism, especially your amino acid intake. Additionally, your carbohydrate intake replenishes lost glycogen that is stored within the liver and muscle tissue that serve as backup fuel when blood glucose levels fall. Conversely, the body uses part of your internal amino acid pool to fuel metabolic activity during sleep. If that pool is low, the body will breakdown your existing muscle tissue to support its nutritional needs.

Please Note: as a point of clarification here, to replenish glycogen stores lost during the day, they are replenished via carb intake, not protein. To replenish diminished glycogen researchers recommend a daily intake of 3 to 5 grams of carbohydrate for every pound of your body weight across the day, divided evenly with your feedings. Additionally, if you are taking a few individual amino acids like glutamine and arginine I strongly suggest that you also take a full pre-digested amino acid formula following a workout and right before bedtime.

Know Your Anabolic Hormones

As stated there are a number of hormones the body secretes to counter-act night-time muscle loss. Make no mistake about it, how adept you are at sustaining the balance and symmetry between the repeated cascade of your anabolic and catabolic hormones has a direct impact on your ability to preserve muscle tissue during sleep. Having a working knowledge of the anabolic / catabolic aspects of these hormones is just prudent. For example, you have the ability to help the body accelerate the secretion of growth hormone during sleep via the intake of various amino acids (arginine, glutamine, ornithine) and other supplements. The following synopsis outlines a few of these anabolic hormones that focus on minimizing night-time muscle catabolism, as well as its acceleration.

The Anabolic Hormones

Androgens – this class of hormones are considered male dominate hormones with testosterone being the most well-known. Androgens have a dramatic impact on muscle development. They are drawn to tiny receptors found in muscle tissue that appear to signal muscle cells to accelerate protein synthesis via a process known as androgen receptor complex binding. This process appears to turn on muscle cell DNA while also inhibiting the up-regulation of glucocorticoids like cortisol that cause muscle wasting. Androgens like testosterone also help stimulate the production of other anabolic hormones like insulin growth factor ( IGF) and growth hormone. Resistance training itself causes natural spikes in testosterone, however, lack of sleep, overtraining, stress, and sugary drinks and snacks can inhibit testosterone secretion at night. In fact data indicates that a small glucose drink can reduce testosterone production by 25%. Additionally, deficiencies of vitamin D definitively lower testosterone levels. As cited by Lee Meyer, author of Low Testosterone: By The Numbers vitamin D biologically acts more like a hormone than a vitamin, despite being referred to as the muscle vitamin. Studies have shown that when muscle receptor cells levels of vitamin D fall, decreased muscle strength and performance follow, as a direct result of its positive impact on testosterone production. Conversely, intense physical and mental stress lowers testosterone as a direct result of its down-regulation of the enzyme 11BHSD-1 located in the Leydig cells of the testes.

Stress: An Androgens Worst Nightmare

It is important to remember your body is a network of multiple deeply interconnected systems, all of which get impacted to various degrees by heavy training. Recovering from this ordeal is about more than just not lifting. It’s about giving your muscles and joints the space to heal and super-compensate, letting your nervous system calm down, and getting adequate rest. In general terms here, some researchers, especially Russian physiologist, recommend the use of adaptogens before bed and or following workout to restore order to these interconnected systems. This in essence primes the body for growth as cited above by Dr. Pasquale.Some well- known anti-stress supplements you may want to consider here include, vitamin B- complex, DHEA (dehydroepiandrosterone) , siberian ginseng and rhodiola rosea. Rhodiola has been used extensively by Russian power lifters. Research shows that this herb actually primes the system to deal with the heavier aftershocks of stress that disrupt normal metabolic processes when exercised induced stress begins to sound the alarm to internal body systems. When this occurs to help the body secretes more cortisol, which accelerates muscle tissue breakdown. It is here where rhodiola steps in to neutralize this mishap, and restore order, much like paratroopers dropped into a war zone, hence it tag as a adaptogen ( a substance that restores balance).

Please Note: to help your body maintain the anabolic potential testosterone affords, some of the most widely used supplements that stimulate testosterone production in the bodybuilding industry are: arginine, aromataste inhibitors( substances which block estrogen production) like chrysin, DHEA, long jack root. maca root, muira puama, tribulus and ZMA( zinc maganesium aspartate).

Growth Hormone (GH) – this hormone is composed of many different amino acids linked together known as peptides. Growth hormone improves the efficiency of muscle cells to take in amino acids, thus enhancing protein synthesis, muscle growth and repair. GH also regulates carbohydrate and fat metabolism, encouraging increased fat burning while preserving carbohydrates. This can have a positive impact on replenishment and maintenance of glycogen (stored glucose). Growth hormone secretions occur during exercise, however larger spikes occur during sleep, which can be improved via intake of amino acid combinations like arginine/ornithine/ lysine as well as single doses of Gaba and glutamine, about ½ hr before bedtime. Also many amino acids like arginine inhibit the actions of the catabolic hormone somatostatin which inhibits the release of glycogen, growth hormone and insulin.

Insulin Growth Factor (IGF)- IGF is a peptide hormone and helps prevent protein breakdown and plays a major role with the body’s fat-burning activities. Researchers attribute the increase in new muscle tissue you have been working hard to build to IGF, because it speeds up the activity of cells in the muscle known as satellite cells. Satellite cells appear to down-regulate the activity of the myostatin gene which is known to inhibit muscle growth. Satellite cell promote hyperplasia (the growth of new muscle tissue).

Protein and the Post Sleep Catabolic Phase

Dr. Deepak Chopra the renowned mind-body researcher reminds us that the world’s greatest chemistry set is the human body. He maintains that the vast array of botanicals studied are done so to mimic the actions of natural chemicals produced by the human body. Based on the examples thus far of the things the body calls upon to protective itself from sleep cycles of catabolism, some protein sources appear to be better suited to help and sustain anabolic activities during sleep. Casein protein and egg protein appear to better suit than whey protein to help nourish the muscles during both the pre-primed and post sleep absorptive phase of protective growth and repair. These proteins tend to break down slowly over the course of a 6 to 8 hour time frame. Whey takes about 20 minutes to reach the veins and within forty minutes your system is flooded with amino acids. Within the hour whey protein has either gone through various metabolic processes and has been synthesized (individual cells constructing various proteins). Simply put, whey can’t help sustain anabolic process during the post-sleep absorptive phase. Studies also indicate that as a direct result of increased oxidation that appears to follow the synthesis of whey protein, this limits its ability to sustain growth and repair for a substantial amount of time.

Please Note: While some oxidation is beneficial this process accelerates muscle protein breakdown during the day and night. Because of the above it may be a good idea to take a regimen of anti-oxidants (vitamins A, E, C, CoQ10, etc.) to offset this negative aspect of whey protein.

Casein and Egg Proteins Absorptive Physiology

While whey protein may afford more benefits during the course of the day, casein protein is the better choice later in the evening and at night. This due to the fact that casein, a milk protein, curdles in the stomach as it unites with various enzymes. It generally takes 3 to 4 hours before amino acids hit your blood stream to start the repair of muscle tissue. In fact in a recent study conducted by researchers in France at the University of Clermont Auvergne comparing whey to casein protein, subjects were given 30 grams of either whey or casein . After 7 hours researchers found that with casein there was a marked decrease in protein synthesis by 31%. However, there was 27% less oxidation (degradation) of casein protein vs. whey resulting in a more sustained period of nitrogen retention. The final and most critical aspect of these numbers was a 34% decrease in muscle protein breakdown. Bottom line here, this study and countless others confirm why casein should be your protein of choice before bedtime. It helps to create and up-regulate the body’s innate post sleep anti-catabolic environment by enhancing your muscle tissues ability to neutralize the mixture of catabolic chemicals building up a head of steam toward muscle destruction, as you approach the REM stage of sleep. As a point of reference REM stands for rapid eye movement. This stage of sleep is characterized by rapid twitching of the eyes and low-voltage brain wave activity. What is important here is the fact that it is during this time most of the body’s repair cycles occur.

Please Note: Like whey, casein protein is derived from milk. When you purchase casein protein, make sure it isn’t listed as caseinate or calcium caseinate. These forms have been extracted before the curdling process and are actually a much lower grade of casein protein.

Egg Protein: A Medium Timed Releasing Protein

Although egg protein has taken a back seat since whey’s introduction to the market place, it is still considered one of nature’s perfect foods. Egg protein contains all of the essential amino acids in the exact proportions needed to promote the growth and maintenance of lean muscle tissue. Egg protein also has a BV of 100 ( biological value) meaning its ability to help muscles maintain nitrogen is excellent. Nitrogen is the amine portion of the amino acid NH2 intimately involved with the growth of lean muscle tissue. Egg protein also has a digestibility ratio of 97% meaning that 97% of it is absorbed as amino acids, major players in the repair process. Current data indicates that egg protein exponentially increases total muscle protein synthesis following a workout. Because of this egg serves as an key pre-priming sleep post-absorptive nutrient. Another key aspect of egg protein’s post absorptive anabolic ability is its high leucine (the key anabolic signaling amino acid) content, its impact on testosterone production and inhibition of myostatin activity ( a muscle growth inhibiting compound). For these reasons egg protein is considered a very good post sleep absorptive nutrient that will assist in maintaining your pool of amino acids, thus inhibiting night-time catabolism.

Please Note: Based on the findings presented in this report the suggestion that whey may not be all its hyped up to be, this assumption if made should be quickly down-regulated to inconsequential. Its ability to quickly flood the system with amino acids will quickly initiate muscle repair as you awake from the post sleep catabolic phase. The other aspect here surrounds whey intake before a morning workout and right afterwards. Current data indicates that as little as 10 grams of whey can jumpstart protein synthesis, as well as cited earlier flood your system with needed amino acids within 45 minutes.

Conclusions

It is important to remember that the majority of your growth occurs when you aren’t working out. The biggest mistake you could make in reaching your full anabolic growth potential is not to prepare for natural night time muscle catabolism. Helping to support the body’s attempts to maintain some semblance of its anabolic potential during sleep is the real key to sustaining growth for the long hall.

References

Andersen, L.L., Tufekovic, G., et. al., The effect of resistance training combined with timed ingestion of protein on muscle fiber size and muscle strength, Metabolism, 2005 Feb.; 54(2): 151-156.

Boirie, Y., Dangin, M., et. al., Slow and fast dietary proteins differently modulate postprandial protein accretion, Proceedings of the National Academy of Sciences (USA), 1992; 94: 14930-14935.

Chopra , D. Creating Health. Houghton Mifflin: New York. 1991.

Chromiak, J.A., Antonio, J. Use of amino acids as growth hormone- releasing agents by athletes. Nutrition. 2002 Jul; 187 (7-8): 657-661.

Dangin, M., Bione, Y., et.al., The digestion rate of protein is an independent regulating factor of postprandial protein retention, American Journal of Physiology, Endocrinology, and Metabolism, 2001; 280: E340-E348.

Goto, K., Ishii, N. et.al. The impact of metabolic stress on hormonal responses and muscular adaptations. Medical Science and Sports Exercise. 2005 Jun; 37960; 955-963.

Hackney, A.J., Bruenger, J.T., et.al., Timing protein intake increases energy expenditure 24 h after resistance training. Medicine and Science in Sports and Exercise. 2010 May; 42 95):998-1003.

Kanaley, J.A. growth hormone, arginine, and exercise, Current Opinion in Clinical Nutrition Metabolism and Care. 2008 Jan; 11 (1):50-54.

Kreider, R., et.al., Effects of whey protein supplementation with casein or bcaa and glutamine on training adaptations 1: Body composition. Medical Science and Sports Exercise. 2003; 2205: 35-5.

Miller, S.L., Tipton, K.K., et. al., Independent and combined effects of amino acids and glucose after resistance exercise, Medicine, Science, Sports and Exercise, 2003; 35(3): 449-455.

Mosoni, L., Mirand, P.P. Type and timing of protein feeding to optimize anabolism, Current Opinions in Clinical Nutrition and Metabolic Care, 2003; 6(3): 301-306.

Myer, L., Low Testosterone : By The Numbers, Amazon Digital Services: Aug. 2011.

Tang, J.E., Manolakos, J. J., et.al., Minimal whey protein with carbohydrate stimulates muscle protein synthesis following resistance exercise in trained young men. Medicine and Science in Sports and Exercise. 2007Dec.;32(60:1132-1138.

Tipton, K. D., Wolfe, R. R., Exercise, protein metabolism and muscle growth. International Journal of Sport Nutrition and Exercise Metabolism. 2001 Mar.;11(1):109-132.

Volek, J.K., Kraemer, W.J., et.al. Testosterone and cortisol in relationship to dietary nutrient and resistance exercise. Journal of Applied Physiology, 1997 Jan; 82(1); 49-54.

Wiegant, F.A., Surinova, S., et.al. Plant adaptogens increase lifespan and stress resistance in C. elegans, Biogerontology. 2009 Feb; 10 (1);27-42.

BIO

George L. Redmon PhD has been associated with the vitamin and health industry for over 25years, having served as The National Product and Education Director for one of the countries largest retailers of nutritional supplements. He has been widely published in many major bodybuilding, fitness and alternative medicine publications. He is the author of Natural Born Fat Burners, Energy for Life and is a member of The National Academy of Sports Medicine and The International Society of Sports Nutrition.

Arachidonic Acid 101

Editor’s Note: A GREAT resource for sports nutrition and supplement information is Examine.com (Thanks to Kurtis Frank and Sol Orwell [not to be confused with George Orwell).

You’ll find easy to follow and concise summaries of many of the major categories. It’s perfect if you’re a lazy a@@ and don’t feel like doing searches on pubmed. jk

Here’s an update on one of our favorite fatty acids Enjoy!

Arachidonic Acid 101

What is it / how does it work?

Arachidonic acid is the most physiologically relevant omega-6 fatty acid. Produced at the end of linoleic-acid metabolism, arachidonic acid is a polyunsaturated fat that is deposited in the membrane of cells. Upon stimulation of the cell by stressors (physical stress, oxidative stress, inflammatory cytokines), arachidonic acid is released by various phospholipase enzymes.

The released arachidonic acid can produce a variety of eicosanoids, which are potent intracellular signaling molecules, including the subclasses of thromboxanes, prostaglandins, and leukotrienes. These eicosanoids have their own receptors to act on, and those receptors mediate the effects of arachidonic acid.

Arachidonic acid is in a unique and odd position. First, it is very well studied by virtue of being an essential fatty acid. In the past, however, epidemiological research suggested that arachidonic acid may be a contributing factor in the association between meat products and health conditions (although more recent evidence for the association is inconclusive), and the popularity that fish oil has achieved has also painted arachidonic acid in a negative light since they are antagonistic to one another in many respects (where the omega 3:6 ratio matters).

Despite the large body of evidence on what arachidonic acid is and does, there is very little evidence regarding oral supplementation of arachidonic acid in humans. This position means that although there isn’t enough evidence to claim anything about arachidonic acid with certainty, there is a plethora of educated guesses we can make.

What does it do and what is it used for?

Arachidonic acid has become more popular lately due to its supposed muscle-building potential. One of the eicosanoids known as prostaglandin 2 F alpha (PGF2a) is able to induce muscle protein synthesis by acting on the PGF2a receptor, and injections of this prostaglandin are sometimes (illegally) used in the form of Dinoprost to promote muscle growth.

It is thought that with more arachidonic acid in the cell membrane, when the muscle cell is stressed (which occurs with the stretch reflex of skeletal muscle) a greater percentage of arachidonic acid is released and subsequently more PGF2a is produced.

Another prostaglandin, called PGE2, also promotes muscle growth, but works via different receptors and appears to be a tad weaker; it goes by the name Dinoprostone.

○ What does it actually do?

There is currently not enough evidence to say what supplementation of arachidonic acid actually does, but due to the large body of evidence on fish oil (and correlating benefits to the omega 3:6 ratio) and studies manipulating both the arachidonic acid content of the diets and the ratio of omega 3:6, we can make a few very reasonable guesses.

Arachidonic acid appears to be more immunosupportive/pro-inflammatory than fish oil. This can be beneficial from a muscle-building perspective (as the inflammatory signaling cascade after a workout plays a role in muscle protein synthesis) but may also aggravate inflammatory conditions; particularly those that respond well to fish-oil supplementation.

The eicosanoids produced from omega-6 also appear to be more prone to inducing muscle protein synthesis than do eicosanoids from fish oil.

○ Anything it may theoretically help with?

There appears to be a role for arachidonic acid in elderly persons, as it seems that conversion of linoleic acid to arachidonic acid is suppressed in the aging process. There is also very preliminary evidence for using arachidonic acid in older persons to support cognition. However, the dose used in the aforementioned studies is quite low and food may be sufficient to support cognition.

How do I take it?

○ Who would benefit from supplementing?

Assuming the science starts to take a positive turn in the next few years, then arachidonic acid would likely be useful for young athletes who want to build muscle mass and do not mind additional muscle soreness. Furthermore, a lack of inflammatory disorders or joint pain might be required prior to supplementing to minimize theoretical side effects.

○ How much

Currently, 1,000 mg of arachidonic acid has been used daily in humans. There is no evidence to suggest whether this is the optimal dosage, and given how supplementation involves an omega-6 fatty acid and the cell membrane the optimal dose is likely related to the overall dietary ratios of omega-3 to omega-6.

○ When

There currently is not enough evidence to suggest when the best time of day to supplement this compound is. If the benefits rely on the omega 3:6 ratio, it is not likely to be dependent on timing.

○ What condition (aka fasting)

Although there is not enough evidence to suggest when to take this compound, it might be prudent to take it with a meal. It is unlikely that this is an absolute requirement (it is fat-soluble, but since it is also a dietary fat itself it can be absorbed via chylomicron formation) but pharmacokinetic studies have not yet been conducted.

What can I eat to get it?

Arachidonic acid appears to be present in animal products, including skeletal muscle (both the meat and the gristle, including in fish) and in egg yolks. Although not as good a source, there is also some in milk (including human breast milk).

The amount of arachidonic acid found in meat products and egg yolks is fairly significant. Although it would be difficult to get a full gram of arachidonic acid via food products (that would require at minimum a half kilogram of salmon or eggs, or a kilogram of other meat products) it is still possible to get a decent dose.

Is it particularly good/bad with other supplements?

Arachidonic acid can potentially have its benefits hindered by supplemental fish oil, as the fish oil fatty acids (EPA and DHA) will compete with arachidonic acid for placement in the cellular membrane.

Anything I should know about?

○ Cautions

Based on studies using high and low arachidonic acid diets, it is plausible that supplemental arachidonic acid can worsen symptoms of both osteo- and rheumatoid arthritis. Supplemental arachidonic acid may also attenuate the benefits of fish oil on these arthritic conditions (and in these instances, dietary deprivation of arachidonic acid augments the benefits of fish-oil supplementation).

Because arachidonic acid is known to be more pro-inflammatory than fish oil, inflammatory conditions that see benefit with fish-oil supplementation (ulcerative colitis, asthma, joint pain and muscle soreness in general, etc.) can potentially be aggravated with arachidonic acid supplementation. This is theoretically plausible but currently unexplored, and a current tentative rule of thumb could be “if the subject would benefit greatly from fish oil supplementation and the issue is related to the omega 3:6 ratio, then supplementation of arachidonic acid is potentially adverse.”

Is Dieting and Being Bikini Ready Year Around Safe?

By Chris and Eric Martinez, CISSN. We’ve always thought it was funny when women would tell us that they can stay in bikini shape year-around and still make gains in their physiques. We would sit there and ask them, “So how exactly do you plan on doing this?” They would always reply with, “Oh just be strict on my diet and ‘eat clean,’ low calories, low carb it, lots of cardio, and stick to my high rep training to stay toned.”

We kid you not, every answer was something along those lines and we wouldn’t critique their responses because we knew that these were A) The type that got their info from Gwyneth Paltrow out of a magazine and B) The type of women that would not listen to a word that came out of our mouths and would just nod their pretty little faces and go on about their business in their Lululemon yoga pants.

We decided to do some research on this, ask some fellow experts in the field, use our real world practice, experience, and results from our female clients, and write this article. We want to inform you if being in bikini shape year-round is safe, smart, realistic, healthy, and then some. You ready to find out if you can stay in bikini shape year-around and still make progress in your body?

Crashing Your Metabolism

Let’s start this off with crashing your metabolism or a more appropriate word would be ‘Metabolic Adaptation’ through excessive calorie restriction and excessive aerobic training volumes. What’s metabolic adaptation you ask? The way we define this is your metabolism is permitted from losing body fat unless you starve yourself. It’s a lack of weight loss disproportionate to your calorie intake.

A common example of this would be a bikini or figure competitor. They would be on an extremely low calorie diet, anywhere form 600-1,000 calories and doing a high volume of low intensity aerobic exercise, anywhere from 2-3 hours a day and up to 5-6 times a week, and eventually they would end up not being able to drop body fat.

“The reason they can’t drop body fat is because their body adapts to the low calorie intake and the high calorie output so much to where they don’t get any caloric burn from exercise. They also have very little thermogenic effect from foods and low basal metabolic rates. Their metabolism is blunted, so they don’t have any type of metabolic cushion to work with and thus they can’t lose adipose tissue.” says Layne Norton.

(Note: For more info on Metabolic Adaptation click here)

When you’re in a severe caloric restriction and doing high volumes of aerobic training, which 99% of the time means trying to attain low body fat levels so you can fit in that poke a dot bikini, you have to understand that maintaining this shape is very difficult, unhealthy, and most of the times unrealistic.

Is it Possible to be in Bikini Shape Year-Round?

In our opinions, there are four ways that you can realistically stay in bikini shape and still improve your physique, more on that in a moment. We went ahead and asked expert Alan Aragon what ways he thought someone could stay bikini ready year-around:

“Whether or not it’s realistic to stay in bikini shape all year-round depends on just how ‘in-shape’ we’re talking about. While hard work and dedication is obviously involved, the look of women on fitness magazine covers is largely based on genetics. In many cases, it’s a matter of having won the genetic lottery, plus getting some extra help from drugs.”

We agree with some of Alan’s points; however we feel there are some other ways that you can realistically stay in bikini shape and still improve your physique:

You are genetically gifted and have all the right things going for you
Having an ectomorphic body type with a greyhound type (very fast) metabolism
Extra help from drugs
Implement Reverse dieting

Since we all aren’t genetic freaks, don’t have sky rocketing metabolisms, and last time we checked drugs were illegal, let’s focus on the last one, implementing reverse dieting.

Enter Reverse Dieting

When you implement reverse dieting you want to focus on improving your metabolic capacity so that you can handle a higher level of calories for gaining muscle mass, without putting on excessive body fat. When you can fully maximize your metabolic capacity, this will play a key role in dropping body fat when you’re in a caloric restriction aka dieting for that bikini.

For example, who’s going to have an easier time losing fat?

Subject A) Person who maintains their body weight on 3000 calories or

Subject B) Person who maintains their body weight on 1500 calories

It’s subject ‘A’ because they have a higher metabolic capacity. Subject ‘A’ has more caloric cushion to work with when it comes to dropping calories over the course of time.

Reverse dieting will also help with re-storing your metabolism to a more suitable rate to your body. In order to do this you must slowly, deliberately, and in a controlled fashion add in calories to your diet.

Reverse dieting could also possibly help lose body fat because your metabolism becomes stimulated. If you want to drop fat, you have to have the metabolic capacity to do so and if you’re constantly maintaining your weight in bikini shape around 1,000 calories then you aren’t going to have the metabolic cushion to lose fat nor will you have the caloric intake to gain muscle mass and make improvements in your physique.

Is It Safe To Be In Bikini Shape Year-Round?

Prolonged dieting and severe calorie restriction isn’t a very smart thing to do and if you want us to be frank, it’s pretty damn stupid just to sit there and attempt this just to say you can fit into a sexy leopard bikini all year around or hop on a red eye to Vegas any time of the year.

We know this is a big deal for some of you ladies, some others it’s not, but there are serious psychological and physiological health implications from doing this. Allow us:

The high volume of training, low energy intake (calories), and stress hormones produced by psychological stress, may lead to a physiological alteration in the endocrinological control of the menstrual cycle (loss of periods).
Low energy levels over a period of time can cause higher concentrations of growth hormone, cortisol, and lower concentrations of leptin, insulin, and triiodothyronine. These are all hormones related to metabolism, and thus to nutritional and metabolic status.
Some female athletes have a classic eating disorder, potentially driven by a need to maintain a low body mass for performance (i.e., bikini body).
You could potentially develop osteoporosis (thin and weak bones) from malnutrition and low energy intake.
Your mental health state can become a real issue when it comes to relationships, social events, work, etc.

That sexy leopard bikini and Vegas trip with the girls can wait until summer.

Plumping Up That Booty

Now, we know you don’t want to have a flat booty in your sexy bikini year after year right? So how do you expect to get your booty to improve if you’re constantly low calorie dieting with tons of cardio? The answer is you can’t. You will have a flat behind in your sexy bikini year-around, year after year, unless you do some of the things we discussed in the earlier part of this article. You also have to target your glutes directly when you train and use movements such as: Barbell hip thrusts, barbell glute bridges, single leg hip thrusts, etc.

(For more info on direct glute training click here).

You just can’t make improvements to your physique if you’re low calorie dieting all year around. You simply won’t have the calories or energy to build muscle or even train hard. On the contrary, if you have more calories in your diet, then you’ll have more energy, more strength, increased glycogen in the muscle, you’ll train harder, you’ll recover better, and thus you’ll make more gains in your physique, especially the booty.

Wrap Up

As you can see, it was very hard to sit there and critique these pretty ladies responses to staying bikini ready all year-around in a quick conversation. Hopefully we’ve informed you on why it’s just not safe and smart to try and stay bikini ready all-year around. Some take home points are:

Don’t eat extreme low calorie diets and do excessive amounts of low intensity aerobic exercise, this is a recipe for Metabolic Adaptation.
Metabolic Adaptation does occur, although there’s not much data on this yet, the anecdotal evidence is very clear and should not be taken lightly.
Implement reverse dieting to build your caloric and metabolic capacity.
Understand that maintaining this type of shape is very difficult, unhealthy, and most of the times unrealistic.
If you want to improve your physique, you should reverse diet and slowly add in calories over time along with a proper training protocol.

It may look cute and feel good to stay bikini ready year-around, but the cons out weigh the pros and we personally would never want to be complacent and look the same year after year. So, unless you’re one of the rare and gifted ones out there, don’t think you can just stay in bikini shape year-around and still make improvements in your physique. Put in the work senoritas.

Special Thanks To:

Layne Norton and Alan Aragon for their thoughts and comments on this subject.

References

Johannsen et al. Metabolic Slowing with Massive Weight Loss Despite Preservation of Fat-Free Mass. J Clin Endocrinol Metab. 2012
Wong et al. Caloric Restriction Induces Changes in Insulin and Body Weight Measurements That Are Inversely Associated with Subsequent Weight regain. PLoS one. 2012
Sports and Women Athletes: The Female Triad Athlete. Am Fam Physician. 2004. http://www.aafp.org/afp/2004/0401/p1734.html
Karen Birch. Female Triad Athlete. BMJ. 2005. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC546077/
Layne Norton. Metabolic Damage. 2012 Dec. http://youtu.be/QHHzie6XRGk

About The Authors:

Chris and Eric Martinez, CISSN, CPT, BA, also known as the “Dynamic Duo” operate a world class personal training and online training business “Dynamic Duo Training,” They’re also fitness and nutrition writers, fitness models, and coaches that love helping people reach their goals. Their philosophy is “No excuses, only solutions.”

Visit them at:

Gain Weight the Right Way

by Jenna Stranzl RD CISSN. This article was originally posted at http://jennastranzl.com

Pizza. Burgers. Candy bars. Cheesesteaks. Whole milk. Have you ever tried any of these strategies to gain weight? Some of you may want to throw darts at this post because you would do anything to have this problem – gaining weight. For many athletes or even those with simply a furnace metabolism, this can truly be an aggravating experience.

Thing is, gaining weight can be done two ways – by either eating every thing in sight, or by training smart and eating higher calorie *smart* foods that have better nutrient profiles than a, let’s say, pork roll sandwich. When people just eat to gain weight, they often select fatty foods and those that lack any nutritional value. This makes an individual more likely to have increased risk for things such as heart disease, hypertension, disturbed sleep, lack of concentration, and especially with athletics – a decrease in performance.

Just like losing weight, the same applies to weight gain – patience and a healthy way of life. Eating lean proteins, healthy fats, complex carbohydrates, and limiting added fats, sugar, and sodium. Remember, to gain one pound per week, one must eat an additional 500 calories per day. This could be as simple as 2 tablespoons of peanut butter, banana, and honey on your AM breakfast toast, an extra drizzle of olive oil on your salad, and a large glass of low-fat or skim milk before bed.

Easy calorie boost to toast — PB, banana, & drizzle honey

Need some additional ideas? Look no further. Here are 25 suggestions to help put on the pounds.

Add calcium-rich cheese when making mashed potatoes (keep the skin in the mash to add a boost of fiber)
Opt for light dressings – fat free dressings add minimal calories, but non-creamy dressings like balsamic, Italian, or oil and vinegar add healthy fats. The healthy fats in the dressing actually help absorb the fat-soluable vitamins in the salad’s nutrients
Use hearty complex carbohydrates like bulgar and wheatberry when making a pasta salad – great amount of calories in a small portion and packed with good for you nutrients
Opt for quinoa over white rice. Quinoa is a complete protein – who knew? Use it with some tomatoes, garlic, and toss in some lean chicken or shrimp for a nice balanced dish
Simply use thicker 100% whole-wheat bread slices versus thin sliced. Many bakeries can cut the bread to a thicker slice, so speak up when at the counter.

Just a handful of almonds can add 100+ calories and heart-healthy fats

Don’t go too long without eating! Solution? Carry around 100-calorie packs of foods. Stock them in your car, duffle bag, locker, desk drawer, purse – wherever you can sneak a bag. Even almonds come in 100-calorie packs (thank you Emeralds!!)
High calorie snack? Munch on trail mix! Heart healthy nuts, fiber-rich dried fruits, and even toss in some pumpkin or sunflower seeds. Limit the dried banana chips though, as they tend to be fried before packaging.
Opt for a hefty bagel with cream cheese versus a bagel. When you pick a whole-wheat bagel, you’re getting a better dose of the right type of carbohydrate, minimal fats. They pretty much have the same amount of calories, but the bagel offers a better nutrient profile. Or, add an egg to the bagel for a dose of protein.
Pesto sauce! Pesto sauce is heavy on the olive oil and heart healthy pine nuts so you can eat small amounts and gain calories quickly. Toss into your pasta with a side of hearty bread and a salad drizzled with some olive oil and your calories are adding up!
Pizza? Opt for thick crust or Sicilian versus thin crust pizza. Thick crust has more carbohydrate (our bodies prime source of fuel as athletes!) and calories. You can also opt to add some lean proteins like shrimp and crabmeat or roasted turkey or chicken breast.
Only use mustard on your sandwich? Spread on some hummus! Hummus boosts healthy fats, protein, and some fiber (chickpeas, lemon, and olive oil) and can create a fun alternative. Just 2 tablespoons can boost the sandwich with an additional 50-100 calories.
Avoid diet foods that might be in the house. Steer away from mom’s Special K bars and Crystal Light. Stick to heartier granola bars like Nature Valley and Cliff Bars.
Toss the sodas as a means of added calories. The sub? Make your own! Use 2 liters of seltzer water or club soda PLUS one tub of 100% fruit juice concentrate. Mix and drink!

Why go skim? Skim milk lacks the artery clogging saturated fats whole milk provides but contains the same protein content.

Drink 2% milk versus whole milk. Whole milk just has additional saturated fats (a thumbs down for the heart). Get your calories elsewhere from healthy calorie boosters like peanut butter, olive oils, dried fruits, etc. The protein content of all milks (skim, low-fat, whole) are the exact same.
Protein shakes are fine – just stick to those that are NSF approved. Meaning, they are approved for sport. If you take a drug test, you are knowing you are taking a protein supplement that has been tested and safe for use. A lot of products out there may create a positive drug test, simply because there are components that fall into it during production or you do not know about. EAS Myoplex and Muscle Milk Collegiate are GREAT options.
Snack on dried fruits! Dried fruits come in many types: peach rinds, apple slices, raisins, prunes (LOVE THEM!), cranberries, etc. While there is sugar added during the drying process, they still contain a fiber boost and added calories. Toss in your cereal, oatmeal, yogurt, ice cream, trail mix, and salads. Prunes for example are high in antioxidants, which reduce free radical damage. This can ultimately reduce muscle soreness after a workout.
Skip creamy alfredo. Why? High in saturated fats and low in nutrients. A simple substitution with a matching calorie content? Penne pasta with grilled chicken, sautéed vegetables (in olive oil), and marinara sauce. See, it is about the meal composition – selecting healthier options, with similar caloric content.
Chocolate? Dark chocolate! It packs a punch in terms of antioxidants. Make sure to select dark chocolates that offer over 65% cacao – meaning, the higher the percentage, the better the antioxidant level in the chocolate.
Chomp on olives. Heart healthy and can add calories without feeling like you ate a ton.

Fatty fish like salmon, mackarel, or trout provide anti-inflammatory properties that are helpful for an athletes training regime and recovery.

Opt for lean meats or healthy fatty meats. What is a healthy fatty meat? Salmon, for example. Salmon boosts more calories per ounce than tuna, but why? Simply because of its oils and we know that fish oil does wonders for athletes. Tuna is also a great choice though – because it boosts quality protein. Select white meats versus dark to lower fat content (turkey and chicken). Pork tenderloin is another great low-fat, hearty protein option.

Making eggs? Boost calories by wrapping those eggs into a whole-wheat tortilla! Then add some cheese, peppers, onions, and mushrooms for an added veggie and calcium boost!
Soups on! Avoid creamy soups and select hearty bean soups like turkey chili, vegetarian chili, or lentil soups. These soups have a high fiber, high protein profile with a similar amount of calories.
Re-create your bland salad. A salad can add healthy calories quickly. How? Add some of the following: sunflower seeds, dried cranberries, pecans or walnuts, feta cheese, soybeans, and lean proteins like turkey, fish, or chicken.
Munch on nuts! A small dose packs a heavy calorie punch (20 almonds or 12-13 walnuts is a serving). Snack on these throughout the day to add up your numbers.
Save room for your appetite. Don’t always fill up on liquids – instead, focus on foods with a hearty nutrient profile. Beef up your oatmeal or cereals by adding nuts, honey, fruits (dried or fresh), and a dash of granola

Most importantly, learn that weight gain is not an easy process and takes time. Keep positive and understand that in order to gain, you must acknowledge that you may need to try foods you may not have thought to. Step outside of the box and eventually, you will see these foods can make you become better, stronger, and healthier.

BIO

Jenna is a registered dietitian (RD) and sports nutritionist (CISSN). She currently serves as the consulting sports nutritionist for The PGA Tour 2012, the Philadelphia Flyers (NHL), Trenton Titans (ECHL), Velocity Sports Peformance – Cherry Hill and Allentown/Lehigh Valley. Jenna has experience with athletes of all ages including recreational, elite, and professional athletes. She has worked for IMG Academies as a sports nutritionist to high-school and professional athletes in Bradenton, FL – including the US Men’s Soccer U17 National Team, the Penn State Sports Nutrition Clinic, and development of dietary supplements and pediatric nutrition research for Wyeth Nutrition/Pharmaceuticals. Additional experience includes a professional development at Athletes’ Performance, contributions for MLB’s RBI Program (Reviving Baseball in Inner Cities), Major League Strength, the Taylor Hooton Foundation, STACK Media, and ShowcaseU. Additional clients include athletes’ within professional and collegiate baseball, basketball, gymnastic, football, horse racing, and track & field. Jenna is also currently the Program Coordinator of Nutrition at Drexel University, in conjuction with the Eat.Right.Now Program for the city of Philadelphia. As an avid runner, Jenna has participated in several marathons; therefore, ensuring sports nutrition is a part of her daily training and lifestyle. If you really love this article, check out the rest at http://jennastranzl.com/about/

Delicious Protein – a GIANT Hit Indeed!

Seems Giant Sports Products has a bona fide “hit” with their Delicious Protein. The Company is a little over a year old and their products are already available on 5 continents while getting rave reviews in print and on-line (www.stack3d.com/2013/05/delicious-protein-is-in-fact-delicious.html). Available in GNC, Vitamin Shoppe, BB.com, Popeye’s, Amazon.com, & distributed by Europa Sports this brand has taken the industry by storm in a short time. Started by long time industry veterans Joe Babick & Bruce Kneller (along with their partner, Peter Jungsberger), they also have an innovative weight loss product called Dexamine and plan to launch two more products by the end of 2013. For more information e-mail contact@giantsportsproducts.com

Sprint on the Beach for HIIT Cardio!

Calling all athletes, what kind of surfaces are you sprinting on these days? We truly hope you are not sprinting on concrete surfaces, unless you are sprinting away from your girlfriend because you forgot it was her birthday. Otherwise sprinting on concrete is a big no no and could cause a potential injury and are tough on your joints overall.

We remember when we were kids and we used to have sprint competitions against our friends on concrete surfaces, boy those were fun until one of us took a hard spill. After thinking about that hard spill, we think other surfaces would be more optimal to sprint on. All kidding aside, one of the best surfaces to do some all out sprints or HIIT cardio is on sand. Yes, sand, as in beaches, beautiful weather, and hot babes all around. Now, we know everyone doesn’t have access to sand surfaces, but for those that do it’s time to try doing your sprints on them.

Sand surfaces are harder to walk and run on than other surfaces because the feet slip and sink, which requires the leg muscles to stabilize the feet during the application of force. We promise you will not be disappointed with how grueling and tough sprinting on sand surfaces are. Oh and your joints will thank you in the long run, along with the rest of your body.

Where’s the proof in all this mumbo jumbo sprinting in sand talk, you ask? Before we discuss the study, we would like to give researcher Chris Beardsley a round of applause for discovering this study. A 2012 study conducted in the Journal of Science and Medicine in Sport, tested the biomechanics and predicted energetics of sprinting on sand surfaces. Previous researchers have observed that the energy cost of walking on sand is 1.8 – 2.7 times that of walking on from ground, while the energy cost of running on sand is 1.2– 1.6 times that of running on from ground. If you think about it, that is a pretty significant difference and could really be beneficial in everyone’s favor, especially athletes training in pre-season or possibly for rehabilitation purposes.

So what did the researcher’s do?

The researchers wanted to compare short sprints with or without changes in direction on sand, grass, and artificial turf. So they recruited 29 male professional soccer players

(7 defenders, 15 mid- fielders and 7 forwards). After a standardized 12-minute warm up, the researchers asked the athletes to perform a 12m maximum speed sprint and a 24m maximum speed shuttle sprint (with a 180 degree change of direction). The athletes performed both of these sprints on sand, grass, and artificial turf. Not concrete surfaces as we mentioned earlier, could be disadvantageous.

So what happened?

Measurement decreases on sand: The researchers observed significant decreases in average speed, maximum speed, average acceleration, maximum acceleration, average stride length, flight time, mechanical power, and stiffness on sand than on grass or artificial turf.

Measurement increases on sand: The researchers also noted that average energy cost, average metabolic power, and contact time were highest during sprinting on sand.

Changes in efficiency in sand: The researchers found that efficiency values (i.e., the ratio between mechanical power and metabolic power) of the sprints were 0.17 on natural grass and artificial turf, while the ratio was only 0.12 for sand.

Similarity in stride frequency across all surfaces: The researchers were surprised by the lack of variation in stride frequency between the various surfaces.

So what did the researchers conclude in all of this?

This can’t be a study if there’s no conclusion right? Well, the researchers concluded that running on sand could be a useful tool for the following: training, injury prevention, and recovery. Pretty darn good benefits if you ask us. The main reasons they came to this conclusion was due to the stiffness values and how maximal speeds become lower on sand surfaces. Not to mention as we said earlier, this could serve your body well over time from possible joint issues or even the famous “shin splints” which can be pretty painful. The researchers also noted that “it is possible to carry out maximal intensity sprints on sand without reaching maximum speed, with lower stiffness, while also maintaining the same stride frequency but by reducing stride length, which represent less injury risk.” At the end of the day we are pretty sure everyone wants to stay injury free in order to maximize their full potential.

Wrapping this up

So we have some pretty cool data here to support the notion that sand is indeed a great and beneficial surface to do sprints on. Now, we are not saying that sprinting on grass, turf, or tracks are bad. We sprint on those surfaces all the time and have no pain what so ever. We are simply saying that sprinting on sand has its valid benefits and are very tough due to how your feet slip and sink in the sand to create the leg muscles to stabilize the feet during the application of force. Oh yes, not to mention if you have access to a beach then why the hell not take advantage of some awesome weather and do some sprints while flexing your guns and glutes. Overall you can’t go wrong with sprinting on sand, it’s great on your body, great for rehabilitation, great scenery, and whether you’re an athlete or not, just get out there and do some damn sprints!

References:

(1)Gaudino, Gaudino, Albertia, and Minetti, Biomechanics and predicted energetic of sprinting on sand, Journal of science and medicine in sport, 2012.

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Exercise in a Pill: Not so Fast

By Brad Dieter, MS, CSCS, CISSN. I just returned from the American College of Sports Medicine conference in which the theme was “Exercise is Medicine”. I would argue that exercise is indeed medicine and that diet and exercise are the most powerful “medicines” to combat the current epidemic of modern chronic diseases such as obesity, type 2 diabetes, and heart disease. In fact, Robert H. Butler stated, “If exercise could be purchased in a pill, it would be the single most widely prescribed and beneficial medicine in the nation”. The advances of modern science have reached a point where they can mimic the effects of exercise through pharmacological agents at a cellular level. The purpose of this article is to review some of these pharmacological agents and provide a comparison of them to actual real exercise in regards to obesity, type 2 diabetes, and heart disease. Unfortunately, in order to fully grasp the concept of “exercise in a pill” I have to explain some rather technical concepts.

Obesity, Type 2 Diabetes, and Heart Disease

It is quite clear that obesity, type 2 diabetes, and heart disease are the biggest health issues in America. While this is an oversimplification, I believe these three diseases are connected and are related to metabolic dysfunction. Additionally, I argue that this metabolic dysfunction can be attributed to lipid accumulation and mitochondrial dysfunction for when we examine the data regarding of these three diseases, we observe both lipid accumulation and mitochondrial dysfunction.

Exercise and Muscle Adaptation

Exercise induces physiological changes in every system of our body with our muscle tissue undergoing the most dramatic and metabolically significant changes. The adaptations in muscle that arise from exercise are both acute and chronic, with each type impacting metabolic processes and function. The most salient adaptations to this discussion include non-insulin dependent glucose transport, increased intramuscular fatty-acid oxidation, increased insulin sensitivity, and enhanced mitochondrial function. Furthermore, each of these adaptations aid in attenuating and reversing lipid accumulation and mitochondrial dysfunction. There are currently several hypotheses on the pathogenesis of these diseased states with lipid accumulation and mitochondrial dysfunction serving as a uniting factor in each of them. Taken together, this suggests the cellular adaptations to muscle tissue that arise from exercise are beneficial to obesity, type 2 diabetes, and heart disease. Therefore, inducing these adaptations or activating the same signaling pathways through pharmacological interventions may produce benefits similar to exercise. Two main signaling processes involved in exercise that are currently being targeted with pharmacological agents are AMPK and the PGC1/PPAR co-activator/transcription factor.

AMPK

One of the best understood metabolic enzymes is AMP-activated protein kinase (AMPK), a master regulator of cellular and organism metabolism whose function is conserved in all eukaryotes (1). AMPK is involved in glucose homeostasis and is direct impacted through exercise. Briefly, AMPK is activated in response to an increase in the AMP/ATP ratio which increases during exercise with ATP is utilized for fuel (See Figure 1). This indicates that during exercise, AMPK signals GLUT4 translocation and non-insulin dependent glucose disposal.

A brilliant paper by Fryer et al. (2002) demonstrated all of the necessary components to indicate the critical role AMPK plays in the beneficial adaptations of exercise in glucose homeostasis and how pharmacological therapy can mimic cellular conditions present during exercise (2). In the paper, the authors successfully demonstrated that AMPK does indeed stimulate glucose uptake into cells. More importantly, they demonstrated that pharmacological agents can mimic the effect of exercise by “activating” AMPK. In their study they demonstrated that AICAR, a synthetic analogue of AMP, effectively increased AMPK signaling and glucose transport in skeletal muscle tissue. These results are not unique, another study in 2002 demonstrated that AICAR increased glucose transport (3). Put simply, AICAR mimics muscle contraction and AMPK activation by increasing the AMP/ATP ratio (Figure 2). Furthermore, it has been shown that the anti-diabetic drugs Rosiglitazone and Metformin improve glucose control through the AMPK pathway (4). Taken together, this indicates that AICAR, and other pharmacological agents, can mimic the acute effects exercise has on glucose disposal through activating AMPK and GLUT4 translocation.

PPAR- γ and PGC-1 Agonists

Exercise can induce adaptations in genetic expression in muscle tissue which result in the manufacturing of certain proteins that alter muscle cell function. Many of these adaptations occur via Peroxisome proliferator-activated receptors (PPAR) and its co-activator PGC-1. Briefly, PPAR is a nuclear receptor that regulates glucose and fatty acid metabolism and PGC-1 effects biologic responses that equip the cell to meet the energy demands of a changing environment, including augmentation of mitochondrial biogenesis, cellular respiration rates, and energy substrate uptake and utilization (5). While we can discuss PGC-1 and PPAR-γ separate from AMPK, they can also be discussed together as AMPK influences PGC-1 and PPAR (6, 7). This discussion is interesting but is outside the scope of this article. A brief explanation is depicted in figure 3, and while there are additional AMPK independent pathways (i.e. p38 MAPK) I feel this figure shows the concept easily enough.

Put simply, type 2 diabetes is a metabolic disease in which we observe dysfunction in the metabolism of both carbohydrate and fat. As metabolism is initially controlled at a cellular level we observed differences in gene expression and nuclear receptor activation between type 2 diabetics and normal, healthy individuals. One key difference is a lower expression of PGC1-α in type 2 diabetics (8). This down of PGC1-α is concurrent with decreased oxidative phosphorylation, indicating mitochondrial dysfunction (9). Exercise has been shown to upregulate transcription of PGC-1. This upregulation leads to enhanced lipid metabolism, improved mitochondrial function, and mitochondrial biogenesis (10, 11). Taken together, this indicates that exercise improves lipid accumulation and mitochondrial function through PGC-1α

PGC-1 agonist drugs have been shown to mimic the cellular adaptations of exercise through PGC-1 and that the adaptations are functional as enhance exercise endurance in rats (12)

While it is clear that PGC-1 is a key player in exercise-induced skeletal muscle adaptations, specifically mitochondrial biogenesis, it is not the only player. Researchers have demonstrated that there are other mechanisms that contribute to this exercise induced adaptations with PGC-1α knockout mice (13). This appears to indicate that while PGC-1 agonists can have a beneficial effect on skeletal muscle, there are other mechanisms through which exercise induces beneficial adaptions. Taken together, I would conclude that while these drug therapies may be beneficial, the specific targets of these drugs (PGC-1 agonists) do not mimic the full extent of exercise as I will touch on next.

Both PPAR-γ and its co-activator, PGC-1, have been targets for pharmacological therapy to treat type 2 diabetes, specifically thiazolidinediones (TZD’s) (14). These agents have shown to be efficacious for glucose control in diabetes even though the mechanisms were not fully explained at the time. Additionally, PPAR-γ agonists do not specifically target the muscle cells, they also interact with adipocytes and promote lipid storage (Figure 4). Taken together, it appears these pharmacological agents may mimic exercise and are effective in improving lipid metabolism (PPAR-γ) and improving mitochondrial function and biogenesis (PGC-1) in muscle cells; however, they are not muscle cell specific, indicating they may also increase body fat which has negative consequences on inflammation and metabolism.

In Summary

As evidenced in this article, pharmacological therapy can mimic many of the effects of exercise at a cellular level and may indeed have a place in treating obesity. These therapies may be powerful tools in the initial treatment to help “kick start” an exercise regimen and begin to shift our metabolic engine in a better direction. That being said, I do not believe we have truly replaced exercise. As witnessed with these drugs, many of their positive effects at the muscle tissue may be counteracted in the adipose tissue (i.e. TZDs). Furthermore, they do not confer the same benefits in regards to psychological health or skeletal health. As with all drugs they ought to be a tool to augment the role of a healthy lifestyle that includes proper diet and exercise.

BIO – Brad is a Ph.D. student at the University of Idaho. He is in a joint program studying exercise physiology and ethics. He received his M.S. degree in biomechanics and has a passion for evolutionary nutrition and the potential it has to combat the current declining state of health. Brad has a background as an athlete, basketball coach, and strength and conditioning coach. He loves learning about the human body, how it functions, and how we can optimally nourish it. He is focusing his doctoral work on how diet and exercise influence metabolism and health in relation to chronic, lifestyle diseases such as diabetes and heart disease.

Unscrambling the Hard Boiled Truth

by Anamaria Cretu. With about 70 calories, five grams of fat, six grams of protein, vitamins and minerals galore, and a whopping 185 milligrams of cholesterol inside its shell, the egg really packs a punch [1]! So, what’s the “shell” with eggs? With the ‘incredible egg’ is actually the best way to start the day providing high nutrient contents and overall bodily benefits [1]. However, the word out of every quack’s mouth encourages you to limit egg consumption in your diet to reduce the chances of cardiovascular disease [2, 25, 26, 27]. Let’s break open the shell and let the eggcellent truth spill out for all to realize that eggs are healthy and have little effect on cardiovascular risk [2]. Hear the truth, become a fan and follow Sam because I do like green eggs and ham, and you should like them like Sam I am [20].

Although it’s been deemed that an egg a day won’t keep the doctor away since many docs rave about eggs being the cause for cardiovascular disease (CVD) and even heart failure [6]. Yet, eggs are like the shield of armor for a knight, which can fight off the ‘bad’ cholesterol and actually prevent CVD [7]. Much of the claims that eggs in the diet actually increase LDL greater than the high-density lipoprotein (HDL) are really a misrepresentation of the ‘incredible egg’ [19]. When consuming the cracked contents of eggs, it has been shown to elevate this anti-inflammatory and anti-artherogenic agent that may be the reason for fighting off CVD [7]. No doubt, the egg is one mighty superhero for the body.

Are my eyes really seeing the truth that eggs increase HDL and lower LDL cholesterol [7]? Although, doc has told us that eggs are terribly bad for the body, the eye popping nutrients inside the eggs are truly the fountain of youth for the eyes in keeping them healthy [8]. So your mom may not have told you, but eggs are a good source of carotenoids, which are the same things in those vegetables that you avoid eating [8]. The blind side of eggs is within the yolk which contains these carotenoid factors known as lutein and zeaxanthin to basically enhance eye pigmentation for adequate vision [8]. Forget the vegetables and crack open a couple of eggs; they’ll surely do your eyes and body a favor.

When you worry less about cholesterol causing CVD and losing your eye vision, then you’ll love your scale more than ever. Eating eggs truly is the icing on the cake, but without the extra meaningless calories; the great news is that consuming higher cholesterol during a low energy diet promotes a constant weight management [9]. Up till now, docs have been preaching about a diet low in saturated fat and cholesterol by limiting egg consumption [11, 18], but you’re wrong doc because the egg is what it’s cracked up to be. The ‘incredible egg’ can provide the essential amino acids which are those good’ole proteins that make your body big and strong and even make you fit in those skinny jeans[11]. There’s a reason to scramble ourselves some eggs in the morning rather than eating that cardboard cereal that we always indulge in.

Aren’t we literally the bread consumers of the world? Referring to the actual grains, we have become copy cats believing that having a higher fat diet will result in heart failure [10]. Eggs are loaded with fats [11], however, these aren’t the same fats you get from doughnuts. Folks, there is such a thing as healthy fats. These are known as your omega 3 fatty acids. They are anti-inflammatory agents and may even prevent certain types of cancer and coronary heart disease [12, 13, 23]. This may shock you but eating a couple of eggs a day doesn’t contribute to negative effects on blood lipid results [13, 26]. However, the goodness of fats is nothing like the muscle enhancer of protein inside the shell of the eggs.

Those docs love to drive you to eat all the whole grain carbohydrates because it seems to them to be the way to lower heart failure; however, fellow egg lovers know that those high carbohydrate diets may not be the best way to lose that stubborn fat since our bodies suck up carbohydrates like vacuums [10, 16]. Being satiated from protein seems to be the way to decrease the chances you’d pull up to the drive-thru window at McDonald’s [16]. You may want to join the latest fad of consuming more protein over carbohydrates since it will be the first class ticket for you to get your next Schwarzenegger looking like body and for your young one to grow and be brain smart [14, 15, 16, 22].

All the focus on egg sensitivity and allergies make eggs seem just as bad for your infants and children, right [14]? Wrong, mothers-to- be you need to listen up here; breast milk has shown a failure in providing the adequate amount of iron needed for the infant, so the super egg is here to fix it all [14]. The yolk is really no joke because it contains the needed sources for iron to prevent early onset of deficiencies in infants [14]. Want to hear more? The nutrient rich fats in eggs are considered to also be a sufficient source for infants’ brains for memory and sleep especially in the first months of life [14, 22]. In reality, the effects of eggs on infants and children is virtually irrelevant to adults even though the consumption has been shown to maintain the HDL and LDL levels of cholesterol [14, 15]. We know that eggs are so good for you, so what’s the buzz about eggs causing cancer?

With all eyes on the cancers of the world, it isn’t surprising that eggs have captured the attention as an agent causing ovarian cancer in women [17]. If it was that simple for cells to become cancerous after eating the fats and protein of eggs, then we’d all be walking cancers [24]. The eggciting news about eggs is that they have the same association to cancer as does a piece of red meat [17]. What about the diet and the environment as a factor for the hormone distribution in the body to associate with cancer; everyone loves to blame eggs for everything even though they do more good than bad [17, 24]. Never fear though, super egg is here:-)

The egg really is what it’s cracked up to be! Eggs are truly an ideal source for improving not only overall health but potential risk factors for disease and cancer too [2, 3, 8, 9, 11, 13, 14, 16, 17 ]. Watch out for the super egg because it’s flying in for a landing on your morning plate to provide its goodness for both you and your young one’s body and mind.

About the Author: Anamaria Cretu is an undergraduate student at Nova Southeastern University. Her field of study is Exercise Science.

References

1. Incredible Edible Egg. (2012). Retrieved Oct. 20, 2012. http://www.incredibleegg.org/health-and-nutrition/egg-nutrients/nutrient-label

2. Scrafford, C., Tran, N., Barraj, L., & Mink, P. (2011). Egg consumption and CHD and stroke mortality: a prospective study of US adults. Public Health Nutrition. 14, 261-270 doi:10.1017/S1368980010001874.

3. Nakamura, Y., Iso, H., Kita, Y., Ueshima, H., Okada, K., Konishi, M., . . . Tsugane, S. (2006). Egg consumption, serum total cholesterol concentrations and coronary heart disease incidence: Japan Public Health Center based prospective study. British Journal of Nutrition. 96, 921-928 doi:10.1017/BJN20061937.

4. Djousse, L., Gaziano, M. (2008). Egg Consumption and Cardiovascular Disease and Mortality The Physicians’ Health Study. Am J Clin Nutr, 87(4): 964–969.

5. Houston, D., Ding, J., Lee, J., Garcia, M., Kanaya, A., Tylavsky, F., . . . Kritchevsky, K. (2011). Dietary Fat and Cholesterol and Risk of Cardiovascular Disease in Older Adults: the Health ABC Study. Nutr Metab Cardiovasc Dis. 21(6), 430–437. doi:10.1016/j.numecd.2009.11.007.

6. Djousse, L., Gaziano, M. (2008). Egg Consumption and Risk of Heart Failure in the Physicians’ Health Study. Circulation. 117(4): 512–516. doi:10.1161/CIRCULATIONAHA.107.734210.

7. Klangjareonchai, T., Putadechakum, S., Sritara, P., & Roongpisuthipong, C. (2012). The Effect of Egg Consumption in Hyperlipidemic Subjects during Treatment with Lipid-Lowering Drugs. Journal of Lipids. 1-4. doi:10.1155/2012/672720.

8. Moeller, S., Jacques, P., & Blumberg, J. (2000). The Potential Role of Dietary Xanthophylls in Cataract and Age-Related Macular Degeneration. Journal of the American College of Nutrition. 19(5), 522S–527S.

9. Lacombe, C., Corraze, G., Nibbelink, M., Boulze, D., Douste-Blazy, P., & Camare, R. (1986). Effects of a low energy diet associated with egg supplementation on plasma cholesterol and lipoprotein levels in normal subjects: results of a crossover study. British Journal of Nutrition. 56, 561-575. doi:10.1079/BJN19860137.

10. Nettleton, J., Steffen, L., Loehr, L., Rosamond, W., Folsom, A. (2008). Incident Heart Failure Is Associated with Lower Whole-Grain Intake and Greater High-Fat Dairy and Egg Intake in the Atherosclerosis Risk in Communities (ARIC) Study. J Am Diet Assoc. 108(11), 1881–1887. doi:10.1016/j.jada.2008.08.015.

11. Kummerow, F., Kim, Y., Hull., Pollard, J., Ilinov, P., Dorossiev, D., Valek, J. (1977). The influence of egg consumption on the serum cholesterol level in human subjects. Am J Clin Nutr. 30, 664-673.

12. Endevelt, R., & Shahar, D. (2004). Omega 3: the Vanishing Nutrient beyond Cardiovascular Prevention and Treatment. IMAJ. 6, 235-239.

13. Lewis, N., Seburg, S., & Flanagan, N. (2000). Enriched Eggs as a Source of N-3 Polyunsaturated Fatty Acids for Humans. Poultry Science. 79, 971–974.

14. Makarides, M., Hawkes, J., Neumann, M., & Gibson, R. (2002). Nutritional effect of including egg yolk in the weaning diet of breast-fed and formula-fed infants: a randomized controlled trial. Am J Clin Nutr. 75, 1084-1092.

15. Ballesteros, M., Cabrera, R., Saucedo, M., & Fernandez, M. (2004). Dietary cholesterol does not increase biomarkers for chronic disease in a pediatric population from northern Mexico. Am J Clin Nutr. 80, 855-861.

16. Weigle, D., Breen, P., Matthys, C., Callahan, H., Meeuws, K., Burden, V., & Purnell, J. (2005). A high-protein diet induces sustained reductions in appetite, adlibitum caloric intake, and body weight despite compensatory changes in diurnal plasma leptin and ghrelin concentrations. Am J Clin Nutr. 82, 41– 48.

17. Larsson, S. & Wolk, A. (2005). No Association of Meat, Fish, and Egg Consumption with Ovarian Cancer Risk. Cancer Epidemiol Biomarkers Prev. 14, 1024-1025.

18. Dawber, T., Nickerson, R., Brand, F., & Pool, J. (1982). Eggs, serum cholesterol, and coronary heart disease. Am J Clin Nutr. 36, 617-625.

19. Roberts, S., McMurray, M., & Connor, W. (1981). Does egg feeding (i.e., dietary cholesterol) affect plasma cholesterol levels in humans? The results of a double-blind study. Am J Clin Nutr. 34, 2092-2099.

20. Geisel, T. (1960). Green Eggs and Ham. Retrieved from http://www.mfwi.edu/MFWI/Recordings/Green%20Eggs%20and%20Ham.pdf

21. Spence, J., Jenkins, D., & Davignon, J. (2010). Dietary cholesterol and egg yolks: Not for patients at risk of vascular disease. Can J Cardiol. 26(9), e336-e339.

22. Mitchell, E., Slettenaar, M., Quadt, F., Giesbrecht, T., Kloek, J., Gerhardt, C.,Wiseman, S. (2011). Effect of hydrolysed egg protein on brain tryptophan availability. British Journal of Nutrition. 105, 611-617. doi:10.1017/S0007114510004150.

23. Bautista, L., Herran, O., & Serrano, C. (2001). Effects of palm oil and dietary cholesterol on plasma lipoproteins:results from a dietary crossover trial in free-living subjects. European Journal of Clinical Nutrition. 55, 748-754.

24. Bertone, E., Rosner, B., Hunter, D., Stampfer, M., Speizer, F., Colditz, G.,Hankinson, S. (2002). Dietary Fat Intake and Ovarian Cancer in a Cohort of US Women. American Journal of Epidemiology. 156(1), 22-31. doi: 10.1093/aje/kwf008.

25. Nakamura, Y., Okamura, T., Tamaki, S., Kadowaki, T., Hayakawa, T., Kita, Y., . . . Ueshima, H. (2004). Egg consumption, serum cholesterol, and cause-specific and all-cause mortality: the National Integrated Project for Prospective Observation of Non-communicable Disease and Its Trends in the Aged, 1980. Am J Clin Nutr. 80, 58-63.

26. Njike, V., Faridi, Z., Dutta, S., Gonzalez-Simon, A., & Katz, D. (2010). Daily egg consumption in hyperlipidemic adults -Effects on endothelial function and cardiovascular risk. Nutrition Journal. 9(28), 1-9.

27. Weggemans, R., Zock, P., & Katan, M. (2001). Dietary cholesterol from eggs increases the ratio of total cholesterol to high-density lipoprotein cholesterol in humans: a meta-analysis. Am J Clin Nutr. 73, 885-891.

Omega-3s in Athletes

Wanna lose weight? Take some Omega-3, Have joint pain? Take Omega-3s, Depressed? Omega-3!! Overweight, underweight, building muscle, slimming down… Omega-3s seem to be the answer to anything and everything. Even though Omega-3 fatty acids have been making headlines, you might not understand why you need them. Are these fats really that amazing? Here’s a rundown of the essential Omega-3 facts every athlete should know. There are three primary types of omega-3 fatty acids that come from foods. These are ALAs, or alpha-linolenic acids, EPAs, eicosapentaenoic acids, or DHAs, or docosahexaenoic acids. Once consumed, the body converts ALA to EPA and DHA, the two kinds of omega-3 fatty acids that can be more readily harnessed and used by the body. Epidemiological studies show that people in Western Countries consume a diet rich in Omega-6, therefore resulting in a disruption of the bodies’ Omega-6/Omega-3 balance. On average, American diets are up to 25 times higher in omega-6s than omega-3s. Scientists attribute an unbalanced diet of Omega-3 and Omega-6 to an increase in chronic inflammation and even cancer. Omega-3s, mostly DHA and EPA, share strong anti-inflammatory properties that function by blocking various signaling pathways in the cell. Omega-3s may enhance cardiovascular health, lower triglycerides, glucose metabolism and regulate immune cells. Researchers demonstrate that Omega-3s have catabolic and anabolic effects.

Omega-3s and fat loss

Supplementing the athlete’s diet with Omega-3s result in an increase rate of fat loss compared to controls who did not take Omega-3s. A bit confusing. How can you eat fat to lose fat? Physiologically, there are several possible mechanisms by which addition of Omega-3s to the athlete’s diet can result in fat loss. Studies show that Omega-3s can act as appetite suppressants by reducing insulin resistance and affecting the body’s tolerance to glucose. Remember, reducing your insulin levels also means that your body’s preferred fuel becomes fat. Further biochemical studies published a correlation between increased Omega-3s consumption and fat oxidation, or fat loss. Another research group reported that Omega-3s have an effect on hemodynamics. Results from that study illustrate increased blood flow to muscles during exercise with increased Omega-3 consumption which also again increases fat loss.

Omega-3s and muscle hypertrophy

Loss of muscle is a problem athletes and older individuals face. As previously mentioned, dietary Omega-3s have anabolic properties and can contribute to muscle hypertrophy. The anabolic effects of Omega-3s are noted particularly when ingested in combination with high-protein meals by athletes following a fasting regimen (Intermittent fasting, for example)/post hypoinsulinemia. Omega-3s stimulate muscle protein synthesis (MPS), which may be useful not only for athletes, but also for the prevention and treatment of sarcopenia, or muscle loss associated with aging. Reports of increased anabolic biomarkers expression in response to Omega-3 supplementations, confirm the importance of Omega-3s in muscle hypertrophy. Interestingly, the anabolic biomarkers that were affected by Omega-3s supplementation were the same biomarkers stimulated in response to weight training (Rheb/vps34 expression). A study measuring Leucine resistance (marker of muscle loss/related to aging) shows a decrease in Leucine resistance in response to Omega-3 consumption, therefore suggesting an increase in protein synthesis. Interestingly, muscle protein synthesis rate was increased by ~50%-120% post omega-3 supplementation. That same group reported an increase in the total anabolic signaling pathway (mTOR) in response to Omega-3 consumption post-fasting.

Where can you get Omega-3s from?

Omega-3 fatty acids can be commonly found in fatty fish (salmon, halibut, tuna, sardines, and herring), flaxseeds, pumpkin seeds, and walnuts.

How much Omega-3s do Athletes need?

The needs are tailored individually but range from 1.5g to 3g of Omega-3s/day. Make sure the omega-3 supplement you purchase has about 120mg of EPA and 180mg DHA on the label, a total of 300 mg/capsule. In that case, you will be needing 2 capsules with each meal or about 10 a day. Seems a lot? If you eat a diet rich in fatty fish such as salmon, you would not need to increase your omega-3s intake.

References

Omega-3 Fatty Acids EPA and DHA: Health Benefits Throughout Life. Adv Nutr.2012
Omega-3 polyunsaturated fatty acids augment the muscle protein anabolic response to hyperinsulinaemia–hyperaminoacidaemia in healthy young and middle-aged men and women. Clinical Science. 2011
Fish oil prevents insulin resistance induced by high-fat feeding in rats. Science. 1987
Long-chain omega-3 fatty acids regulate bovine whole-body protein metabolism by promoting muscle insulin signalling to the Akt-mTOR-S6K1 pathway and insulin sensitivity. J. Physiol. 2007 1
Dietary omega-3 fatty acid supplementation increases the rate of muscle protein synthesis in older adults: a randomized controlled trial. Am J Clin Nutr. 2011

BIO

Chantal Charo is an Assistant Professor of Physiology, a Sports Nutritionist and a Medical Writer from Miami, FL. Her interdisciplinary biomedical research particularly focuses on gastrointestinal diseases, such as diabetes, pancreatic cancer and the role of insulin resistance in pathophysiology. Dr. Charo is also involved in numerous clinical trial in her field and has most recently completed a trial on NSAIDs and pancreatic diseases. Chantal earned her Ph.Ds. in Biomedical Sciences and Cancer Biology from the prestigious University of Texas Houston and the UT MD Anderson Cancer Center. As sports nutritionist Dr. Charo has trained with leading supplement companies across the United States by researching ways to target insulin resistance and hormonal balance in women, as well as the Euthyroid Sick syndrome and the female athlete. Chantal hosts a medical segment on a local daily talk show which aims at promoting awareness to women and combating health illiteracy. In support of her research, Chantal has received fellowships from National Cancer Institute, the National Institute of Health and more. She is a Fellow of the American Association of Cancer Researchers, the American Pancreatic Association and the American Breast Cancer Association, and was the recipient for many outstanding scientist awards. The link to Dr. Charo’s sports nutrition clinic is www.facebook.com/sportsnutritionclinic