In order to answer this questions appropriately, it is necessary to look at both the quantitative and qualitative aspects of dieting, and the physiological and psychological responses they each elicit.

Dieting – what are we really talking about?

The dictionary definition of “diet” and “dieting” is “to eat and drink sparingly or according to prescribed rules” or “a controlled intake of foods, as for medical reasons or cosmetic weight loss”.

However, these definitions do not tell us anything about the two different aspects of dieting; the quantitative and qualitative parts, and their respective consequences.  In everyday parlance, dieting usually implies both eating less calories (quantitative aspect) than usual and eating “specific” foods (qualitative aspect).

Nevertheless, when considering the consequences of “cheating” (more formally known as dieting consistency / inconsistency) and trying to answer the question whether it is a good or bad practice, it is important to distinguish these aspects of dieting. Let’s take a quick look at each:

Calorie restriction

Calorie restriction (also known as dietary restriction). When reducing calories our bodies respond by lowering basal metabolic rate, and there also is reduction is spontaneous physical activity. If the calorie restriction is severe enough, our bodies go into starvation mode, which will counteract any fat loss efforts ^1,2.

Specific food restriction

A diet usually has an explicit (or implicit) list of foods that it recommends. Eating specific foods has a more psychological impact than calorie restriction per see, especially if you don’t like the foods that are part of your diet plan.

The different types of “cheating”

Now back to the issue of cheating. Looking at calorie restriction and specific food restriction separately, you see that that you can cheat in three different ways:

- eating more calories from the same “dieting foods” = quantitative cheating

- eating non-dieting “forbidden” foods, but still within your daily calorie allotment  = quantitative cheating

- eating non-dieting “forbidden” foods, and exceeding your daily calorie allotment  = double whammy cheating!!

Dieting consistency/inconsistency is not yo-yo dieting!

Before we continue I want to make clear that this discussion on diet cheating (dieting consistency) should not be confused with yo-yo dieting (also called weight cycling; when one is repeatedly losing and regaining weight). Yo-yo dieting definitely has detrimental effects, especially psychologically ^3,4.

Dieting consistency in this context is about maintaining the same diet regimen on weekends as on weekdays. For many people, diet and activity patterns differ substantially on weekends as compared to weekdays, with potential consequences on long term body fat weight that could promote the development or maintenance of excess fat storage and obesity if the pattern is repeated throughout the year.

Possible benefits and risk with cheating on a diet?

Allowing some diet flexibility on weekends, holidays, and vacations might reduce boredom, which is a known contributor to dieting lapses ⁵, and be more realistic from a long-term perspective. However, flexibility might also increase exposure to high-risk situations, a the chance for loss of control. This is especially true among people with addictive personalities ⁶.

What does the research say?

While it is well documented that holidays are associated with fat gain ^7-9 it wasn’t until recently that studies started to investigate the influence of weekend eating patterns on short- and long-term body fat weight. The first study on weekend eating patterns was done on National Weight Control Registry subjects, who had successfully maintained a weight loss of at least 13.6 kg for 8 years ¹⁰. The purpose of the study was to examine whether maintaining the same diet regimen across the week and year promotes weight control or if dieting more strictly on weekdays and/or non-holidays is more conducive to long-term maintenance. Participants who reported greater dieting consistency were more likely to maintain their weight within 2.3 kg during the subsequent year, whereas participants with lower dieting consistency scores were more likely to regain weight during the subsequent year ¹⁰. A more recent study, where subjects consumed on average 236 calories more on weekend days, confirmed that weekend dietary indulgences contribute to weight gain or cessation of weight loss ¹¹.

It has also been documented that as the duration of a diet increases, a shift in the balance between the effort and pleasure of weight maintenance may occur, which makes it easier to stick to the diet and thereby increases the likelihood of continued maintenance ¹². This is supported by findings showing that repeated exposure trains flavor preference ¹³. In other words, a strong correlation exists between a person’s customary intake of a flavor and his preference for that flavor.

Bottom Line

Whether cheating on a diet (that is, a low diet consistency) will cause you any harm or good depends on your personal inclinations, and the reasons for the cheating.

From a biological perspective, I believe quantitative cheating, when you eat more calories from the same “dieting foods”, can be a good thing, since it can prevent lowering your resting metabolic rate and drops in spontaneous physical activity.

When it comes to the other types of  cheating, the consequences are more of a psychological origin. If you have an addictive personality, do not even think about cheating. Remember, the best cure for any addiction is complete abstinence.

If you don’t have an addictive personality, but have a lot of fat to loose, it is ok for you to engage in quantitative or qualitative cheating on weekends, when you eat non-dieting “forbidden” foods, but still within your daily calorie allotment. But only do this if you feel that it helps you stay on track with your diet during the week days.

If you don’t have much fat to loose, and are just dieting to get in a little better shape, you can indulge  in double whammy cheating, when you eat non-dieting “forbidden” foods AND exceed your daily calorie allotment. Just don’t go too much overboard; your body and mind will still take note of what you’re doing.

In any case, the reason for you to cheat on a diet should be that it helps you to stick to in the long run. Not because other people coerce you into it or are trying to make you believe that you “have to” cheat on your diet to get results. That’s nonsense you often hear from folks who don’t have the willpower and discipline themselves. It has actually been shown that friends have an even larger impact on a person’s risk of obesity than genes do ¹⁴. So don’t fall for the peer-pressure and never engage in risky behaviors because your friends do!

My advice to you is to be your own scientist and lab rat; try and see how you feel. If you lose control you know cheating on a diet is not for you, and you better put your foot down and stick to your guns. However, a slip doesn’t have to mean failure; turn the experience you gain from it into good data to guide your for future dietary decisions and long-term success!

About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer.

Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an young teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a BSc and MSc with a major in Nutrition at the University.

During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications.

It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to health, fitness, bodybuilding, anti-aging and longevity.

References:

1. Maclean PS, Bergouignan A, Cornier MA, Jackman MR. Biology’s response to dieting: the impetus for weight regain. American journal of physiology. Regulatory, integrative and comparative physiology. Sep 2011;301(3):R581-600.

2. Goran MI, Calles-Escandon J, Poehlman ET, O’Connell M, Danforth E, Jr. Effects of increased energy intake and/or physical activity on energy expenditure in young healthy men. J Appl Physiol. Jul 1994;77(1):366-372.

3. Osborn RL, Forys KL, Psota TL, Sbrocco T. Yo-yo dieting in African American women: weight cycling and health. Ethnicity & disease. Summer 2011;21(3):274-280.

4. Amigo I, Fernandez C. Effects of diets and their role in weight control. Psychology, health & medicine. May 2007;12(3):321-327.

5. Smith CF, Burke LE, Wing RR. Vegetarian and weight-loss diets among young adults. Obesity research. Mar 2000;8(2):123-129.

6. Avena NM, Rada P, Hoebel BG. Sugar and fat bingeing have notable differences in addictive-like behavior. The Journal of nutrition. Mar 2009;139(3):623-628.

7. Hull HR, Radley D, Dinger MK, Fields DA. The effect of the Thanksgiving holiday on weight gain. Nutrition journal. 2006;5:29.

8. Klesges RC, Klem ML, Bene CR. Effects of dietary restraint, obesity, and gender on holiday eating behavior and weight gain. Journal of abnormal psychology. Nov 1989;98(4):499-503.

9. Yanovski JA, Yanovski SZ, Sovik KN, Nguyen TT, O’Neil PM, Sebring NG. A prospective study of holiday weight gain. The New England journal of medicine. Mar 23 2000;342(12):861-867.

10. Gorin AA, Phelan S, Wing RR, Hill JO. Promoting long-term weight control: does dieting consistency matter? International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity. Feb 2004;28(2):278-281.

11. Racette SB, Weiss EP, Schechtman KB, et al. Influence of weekend lifestyle patterns on body weight. Obesity (Silver Spring). Aug 2008;16(8):1826-1830.

12. Klem ML, Wing RR, Lang W, McGuire MT, Hill JO. Does weight loss maintenance become easier over time? Obesity research. Sep 2000;8(6):438-444.

13. Liem DG, de Graaf C. Sweet and sour preferences in young children and adults: role of repeated exposure. Physiology & behavior. Dec 15 2004;83(3):421-429.

14. Christakis NA & Fowler JH (2007). The spread of obesity in a large social network over 32 years. N Engl J Med 357, 370–379.

Cheating on a diet – good or bad? is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

But seriously, this is a very important study,  I have said something similar for decades. For example, if you read my  article Brink’s Unified Theory Of Nutrition you will see I essentially concluded what this recent study found: Not all calories are created equal, macro nutrient ratios matter, and there’s profound effects from simple changes in those macro nutrient ratios on body comp, and tracking changes in fat vs. weight is what actually matters… I don’t know if this study will get the attention it deserves in the media, or by the main stream nutrition/med community, but it’s a seminal study. The fact is, older studies that simply track weight loss/gain need to be scrapped as they are essentially of no value in my view. Modern studies such as this, that actually look at end points that matter, are what will finally answer age old questions on nutrition.

Below is write up of the study for non-science types, and a link to the full study follows for those who wish to read that too.

Calories Raise Body Fat When People Overeat, Not Protein
Medical News Today

In a study published in the January 4 issue of JAMA, researchers assessed 25 healthy individuals who were randomized to different levels of overconsumption on protein diets whilst living in a controlled setting. They found that those who consumed the low-protein diet gained less weight compared with those eating normal and high protein diets. Furthermore, they established that calories alone and not protein seemed to contribute to increases in body fat and that protein did contribute to changes in energy expenditure and lean body mass.

According to background information in the article, “Obesity has become a major public health concern with more than 60 percent of adults in the United States categorized as overweight and more than 30 percent as obese.” However, which role the composition of a diet plays in response to overeating and energy dissipation remains unclear.

George A. Bray, M.D. and team decided to establish whether the level of dietary protein differentially affected body composition, weight gain, or energy expenditure under tightly controlled conditions. They conducted a randomized controlled trial in 25 healthy, weight-stable American male and female volunteers who were aged between 18 to 35 years with a body mass index between 19 and 30 at an inpatient metabolic unit. The first volunteer was admitted in June 2005 with the last one joining in October 2007.

Following a weight-stabilizing diet, the researchers randomized the participants to receive a diet containing 5% of energy from low protein, 15% from normal protein or 25% on a high protein diet. During the last 8 weeks of their 10- to 12-week stay at the inpatient metabolic unit, the researchers overfed the volunteers. The protein diets provided a raised energy intake of about 40 % translating to 954 calories per day in comparison to the energy intake the volunteers received during their weight stabilization period.

The researchers observed an increase in weight in all participants, irrespective of sex. They established that those in the low protein diet group gained considerably less weight compared with the other two groups, i.e. 6.97 lbs. (3.16 kg) compared with 13.3 lbs (6.05 kg) in volunteers of the normal protein diet group and 14.4 lbs or 6.51 kg in participants in the high protein diet group.

According to the researchers:

“Body fat increased similarly in all 3 protein diet groups and represented 50 percent to more than 90 percent of the excess stored calories. Resting energy expenditure, total energy expenditure, and body protein did not increase during overfeeding with the low protein diet.”

The findings showed that the lean body mass (body protein) in the low protein group was lowered by 0.70 kg (1.5 lbs) during the overeating period compared with a gain of 2.87 kg (6.3 lbs) in the normal protein diet group and 3.18 kg (7 lbs) in volunteers in the high protein diet group. In addition, the researchers noted that the resting energy expenditure of 160 calories per day in a normal protein diet and 227 calories per day in a high protein diet increased substantially in the normal and high protein diet groups.

The researchers conclude:

“In summary, weight gain when eating a low protein diet (5 percent of energy from protein) was blunted compared with weight gain when eating a normal protein diet (15 percent of energy from protein) with the same number of extra calories. Calories alone, however, contributed to the increase in body fat. In contrast, protein contributed to the changes in energy expenditure and lean body mass, but not to the increase in body fat. The key finding of this study is that calories are more important than protein while consuming excess amounts of energy with respect to increases in body fat.”

Editorial: Overeating and Overweight – Extra Calories Increase Fat Mass While Protein Increases Lean Mass

Drs. Zhaoping Li, and David Heber, of the University of California in Los Angeles comment in an accompanying editorial, that the results of this study:

“Inform primary care physicians and policy makers about the benefits of protein in weight management. The results suggest that overeating low protein diets may increase fat deposition leading to loss of lean body mass despite lesser increases in body weight.

Policy makers and primary care physicians need to understand the role of the Western diet in promoting overweight and obesity.

Because this diet increases the risks of over nutrition through fat deposition beyond that detected by body mass index, the method used to assess the current obesity epidemic and the magnitude of the obesity epidemic may have been underestimated. Clinicians should consider assessing a patient’s overall fatness rather than simply measuring body weight or body mass index and concentrate on the potential complications of excess fat accumulation. The goals for obesity treatment should involve fat reduction rather than simply weight loss, along with a better understanding of nutrition science.”

Full study: Effect of Dietary Protein Content on Weight Gain, Energy Expenditure, and Body Composition During Overeating, January 4, 2012, Bray et al. 307 (1): 47 ? JAMA

Calories, Not Protein, Leads To Increases In Body Fat When Eating Excess Calories! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

This is a long article, so here are some jump-to links:

Exercise Mimetics

PQQ

Quercetin

Resveratrol

Nootkatone

Naringin

Downsides…

Conclusion

To navigate back up, just hit ctrl+home. Oki, roll up your sleeves and off we go….

Age related mitochondrial changes and implications

Brain, heart, and skeletal muscle mitochondria are especially susceptible to age-induced declines in the capacity to produce energy (ATP), and ability to respond to increased energy demands ^2-6. It is well documented that mitochondrial number, mass and function declines with aging ^2-5, and that this decline plays an important role in the etiology of many disorders, including cardiovascular diseases, obesity, diabetes, neurodegenerative diseases, and cancer ^7-15. Physical inactivity and poor exercise capacity is a risk factor not only for the development of these diseases ^{8 16-18}, but also causes frailty, age-related physiologic functional declines ^19-22, and accelerates secondary aging (i.e., aging caused by diseases and environmental factors) ¹⁵.

The importance of exercise for mitochondrial function and prevention of age-related declines

We all know that exercise training increases muscle mitochondria number, mass and function ^23-26. Regular exercise counteracts the age-related decline in muscle mitochondrial expression and function ^27-32 and protects against development of age-related metabolic diseases like the metabolic syndrome, obesity, and diabetes ^{9 28 29 33-36}. Thus, regular exercise increases healthy life expectancy and prolongs life span through beneficial effects, in large part, at the level of the mitochondria ²⁸.

Muscle is the tissue with the largest capacity to increase caloric expenditure and energy production, and possesses the unique ability to increase metabolic rate nearly 100-fold during the transition from a basal resting state to maximal contractile activity ³⁷. Being such a metabolic prowess, the importance of mitochondria in muscle tissue is obvious. However, exercise training also has beneficial effects on mitochondria in other tissues, especially the heart ^{38 39}, and brain ⁴⁰. In the resting state, these tissues actually consume more calories on a per gram basis than does muscle tissue ^{41 42}. Several of the beneficial cardioprotective effects of exercise training can be traced to improved cardiac mitochondrial function ³⁸, and regular exercise also increases brain mitochondrial biogenesis ⁴⁰. This may have important implications, not only with regard to fatigue, but also with respect to various central nervous system diseases and age-related dementia that are often characterized by mitochondrial dysfunction ⁴⁰.

Recent advances in molecular biology have shed light on the mechanisms that regulate mitochondrial biogenesis (production of new mitochondria), and how exercise stimulates mitochondrial biogenesis. This is interesting not only from a physiological standpoint, but also from practical standpoint since it has allowed discovery of dietary substances (and potentially drugs) that could help us combat the age related mitochondrial decline. More on this in a bit. First, let’s take a quick look at what happens to our mitochondria when we exercise.

Mitochondria at the molecular level – exercise induced signaling targets

Energy stress from exercise triggers a host of signaling pathways in muscle cells ^43-47. One of the identified exercise-induced signals is AMPK (AMP-activated protein kinase) ^48-50. AMPK functions as a metabolic “fuel sensor” in muscle cells because it becomes activated in response to decreased energy levels (like for ex. during muscle contractions), and in turn activates catabolic processes that generate and restore ATP levels ^{48 51 52}.

Another energy sensor is SIRT1 (Sirtuin-1) ^{51 53 54}. There are actually seven sirtuins ⁵⁵;  they have generated a lot of scientific interest after the discovery that sitruins partly mediate the increase in longevity with calorie restriction that has been seen in lower organism and animals ^56-60. But sirtuins regulate a wide range of important biological processes ⁶¹. One of them is muscle precursor cell (MPC) proliferation. The finding that SIRT1 increases muscle precursor cell proliferation is very interesting since MPC proliferation has important implications in regulating muscle growth, maintenance, repair, and the aging-related loss of skeletal muscle mass ⁶².

Adult muscle stem cells, also called satellite cells or muscle precursor cells (MPCs), play an important role in the remarkable ability of muscle fibers to grow in size, repair and regenerate ^{63 64}. A hallmark of aging is diminished regenerative ability of muscle tissues, which is in large part due to age-related changes in tissue-specific stem cells ⁶⁵. Muscle precursor cells are important not only for regeneration after tissue damage, but also for maintenance. Age-related muscle loss (sarcopenia) is caused in large part by atrophy of type II muscle fibers ⁶⁶, which is associated with a fiber type-specific decline in muscle precursor cell content ⁶⁶. Thus, SIRT1 is an attractive target for dietary/exercise interventions to prevent the loss of muscle mass and function with aging ⁶⁶.

SIRT1 also works jointly with AMPK in regulating cellular fuel metabolism, inflammation, and mitochondrial function ⁵¹. In addition, SIRT1 activates and increases the activity of PGC-1 (peroxisome proliferator-activated receptor-γ coactivator,  a transcriptional coactivator), which finally activates transcription factors that turn on genes in our DNA that produce new mitochondria ^{23-25 54 67}. One such transcription factor is PPAR-gamma, which also contributes to mitochondrial biogenesis ⁶⁸.

Of the mentioned “control points” (AMPK, SIRT1, PPAR-gamma and PGC-1), PGC-1 is considered the “master regulator” of mitochondrial biogenesis ^69-71. It also increases oxidative phosphorylation and ATP (energy) production ⁷¹. As a result, increased expression of PGC-1 has been shown to increase peak oxygen uptake and delay fatigue during prolonged exercise ⁶⁹. In addition to its stimulatory effect on mitochondrial biogenesis and function, PGC-1 also regulates muscle fueling stores by increasing muscle glucose uptake, augmenting muscle glycogen storage, and preventing muscle glycogen depletion during exercise ⁷².

Ok, now you know enough molecular biology to understand the rationale behind exercise mimetics, which we will focus on next.

Exercise Mimetics

Elucidation of the molecular mechanisms behind mitochondrial biogenesis and function, coupled with the identification of dietary substances that seem to increase the expression of PGC-1, SIRT1, AMPK etc. and/or their regulators, has led to great interest in developing drugs and dietary supplements to target the SIRT1-PGC-1 complex and related signaling pathways ^{47 50 73-75}.

Because these supplements and drugs activate some of the signaling pathways that are activated by exercise, they have been labeled as “exercise mimetics” ^{47 74}. Here’s a rundown of some dietary bioactive substances that are currently in the scientific spotlight for their potential exercise mimetic effects.

PQQ

PQQ (short for Pyrroloquinoline Quinone, and also called methoxatin) is a less well known dietary compound that was discovered 1979 ^76-78. PQQ is present in tissues and body fluids, including human milk ^79-81 and in foods. The richest dietary sources are ⁸²:

Natto (fermented soybeans)         61 ng PQQ/g

Parsley                                               34 ng PQQ/g

Green tea                                          30 ng PQQ/g

Green pepper                                   28 ng PQQ/g

Kiwi                                                     27 ng PQQ/g

Papaya                                               27 ng PQQ/g

Tofu (soybean curd)                        24 ng PQQ/g

Spinach                                              22 ng PQQ/g

Carrot                                                17 ng PQQ/g

When you read supplement labels, remember that 1 milligram (mg) = 1,000,000 nanogram (ng)

PQQ acts as an antioxidant ⁸³, enzyme cofactor ^84-91, nero-protectant ^92-95, cardio-protectant ^96-98, and may have an important role in cell signaling ^{92 99-101}. In this context, the most interesting function of PQQ is that it affects the expression of genes involved in mithochondrial functions and biogenesis (most notably, PGC-1) ^{99 102}.

The nutritional importance of PQQ has been demonstrated by feeding rats and mice a diet that is devoid of PQQ; the animals show growth retardation, reproductive failure, compromised immune responses, skeletal deformities aortic aneurysms, and fragile skin ^{91 103 104}. This strongly suggests that PQQ is necessary for normal body functions and health. It is actually being debated whether PQQ might become the “next vitamin” ^{78 88}.

What’s more interesting is that varying the amount of PQQ in diets causes modulation in mitochondrial content, alters lipid metabolism, and reverses inhibition elicited by classical mitochondrial function inhibitors ^{97 104-106}. PQQ deficiency decreases both mitochondrial function and number ¹⁰⁶. The most recent study on PQQ fed rats a nutritionally complete diet either with or without PQQ ¹⁰⁵. The rats that got the PQQ diet not only exhibited lower blood triglycerides but also showed increased energy expenditure, hepatic (liver) mitochondrial content. In contrast, the rats that were fed the PQQ deficient diet instead exhibited deterioration in mitochondrial function, a lowered energy expenditure and reduced capacity to oxidize fat for energy (that is, reduced fat burning) ¹⁰⁵. However, at the time of this writing, no human study has investigated the effect(s) of PQQ on metabolic, muscular and mitochondrial parameters. PQQ can already be found on the supplement market, but for now we will have to be our own lab rats.

Quercetin

A natural polyphenolic flavonoid, quercetin is present in a wide variety of food plants, including red onions, apples, and berries ^{107 108}. Known for its multiple health benefits ^109-118, it has recently been shown that quercetin also beneficially affects mitochondrial energetics ^{119 120} and stimulates mitochondrial biogenesis (by increasing expression of PGC-1alpha and SIRT1) ¹²¹. The quercetin-induced increase in mitochondrial biogenesis was accompanied ¹²¹ with both maximal endurance capacity and voluntary wheel-running activity in mice ¹²¹.

However, findings from the few research studies on the ergogenic (i.e. performance enhancing) effects of quercetin supplementation in humans are equivocal ^122-127. A small preliminary study showed that when given in combination with other antioxidants for 6 weeks, quercetin improved endurance time-trial performance on a bicycle ergometer in humans ¹²⁶. Another study, conducted by the same research team that showed performance enhancing effects in mice, gave healthy but untrained participants 500 mg of quercetin twice daily. After 7 days it was shown that the quercetin supplementation resulted in a modest increase in VO2max along with a substantial (13.2%) increase in ride time to fatigue ¹²⁵. It was concluded that quercetin supplementation can increase endurance without previous exercise training in untrained participants ¹²⁵. In contrast, another controlled study conducted by another research team, which gave young healthy recreationally active men 1 g/day of quercetin in a sports hydration for 16 days failed to show any benefits over placebo; the quercetin supplementation did not improve neither muscle oxidative capacity or performance in a 10 min maximal-effort cycling test ¹²⁴. Also, supplementing with 1 g/day of quercetin for 3 weeks in trained cyclists failed to show a performance benefits ¹²⁷.

A recently published meta-analysis of human studies on quercetin and performance concluded that quercetin supplementation significantly endurance performance, but that the effect is very small ¹²⁸. The computed effect size for the performance enhancement was 3-5% over placebo ¹²⁸. This can be compared to the effect size for the performance enhancement with caffeine, which is in the range of 12% over placebo ¹²⁹. If at all, people with low fitness levels will probably most likely experience a performance benefit of quercetin supplementation, since highly fit individuals already have an elevated mitochondrial density and function.

There is a possibility that a longer supplementation duration is necessary for quercetin to exert a performance enhancing effect, and/or that it could be ergogenic in elderly. Hopefully, future studies will address that. Thus, while quercetin is a prudent supplement to take for its beneficial health effect, if you’re looking for a boost in mitochondrial function and/or performance, don’t expect too much.

Resveratrol

Resveratrol is the most well known SIRT1 activator ^130-132. A  natural compound present in grapes (especially grape skin) ^{133 134}, resveratrol has been in the spotlight since it was found to be one major factor explaining the French paradox and conferring the cardioprotective effect of red wine ^135-140. Fresh grape skin contains about 0.05-0.1 mg resveratrol per gram, while red wine is a concentrated source of resveratrol providing up to 14 mg per liter. Resveratrol also protects against cancer ¹³⁵, and induces several signaling pathways that are also seen with calorie restriction (I will cover this more in an upcoming article on calorie restriction mimetics).

More recently, it has been shown that resveratrol also might improve mitochondrial function and stimulate mothochondrial biogenesis ^{131 141}. In mice, intake of resveratrol together with habitual exercise, suppresses the aging-related decline in physical performance ¹⁴¹. This effect was attributable, at least in part, to improved muscle mitochondrial function ¹⁴¹. Another mice study showed that resveratrol increases aerobic capacity, as evidenced by an increased running time to exhaustion ¹³¹. On a molecular level, this effect was paralleled by an induction of genes for oxidative phosphorylation, increase in PGC-1alpha activity and enhanced mitochondrial biogenesis ¹³¹. Resveratrol also seems to be able to counteract muscle atrophy during periods of physical inactivity (mechanical unloading) in rats ¹⁴².

However, while there is ample of human data on the health promoting effects of resveratrol, at the time of this writing there are no human studies on its potential mitochondrial, metabolic and/or performance enhancing effects.

Nootkatone

A new kid on the block, nootkatone is another bioactive naturally occurring dietary compound that is found primarily in grapefruit (a whole grapefruit contains about 100 mg of nootkatone, mainly in the rind)¹⁴³.

It was recently shown in mice that nootkatone potently activates the AMPK signaling pathway in both muscle and liver, increases energy expenditure, endurance performance, and also suppresses diet-induced development of obesity, abdominal fat accumulation, and insulin resistance ¹⁴³. Body weight in nootkatone-fed mice was significantly decreased despite no significant decrease in energy intake ¹⁴³. It was concluded that activation of AMPK and subsequent induction of PGC-1α, with a possibly enhanced oxidative energy metabolism and stimulation of energy expenditure, is an underlying mechanism of the antiobesity effects of nootkatone ¹⁴³. This study supports the idea that AMPK activators could be useful as exercise mimetics or exercise-supporting supplements in preventing/treating obesity and/or metabolic syndrome, and for improving physical performance.

Nootkatone has a pleasant, citrusy grapefruit aroma, and is GRAS approved ¹⁴⁴ for use as a food flavoring agent, and as a fragrance in perfumes and essential oils ¹⁴⁵. You can even use it as a non-toxic effective repellent/insecticide against mosquitos and other insects ¹⁴⁶. Being this multi-functional, we will most likely hear more about nootkatone, in one way or the other, it in the near future. It is interesting to speculate whether the nootkatone-induced AMPK activation is part of the mechanism underlying the weight loss and increased insulin sensitivity that has been reported after grapefruit supplementation ¹⁴⁷. Even though nootkatone is currently not available as a dietary supplement in isolated form, you can always add some grapefruit to your regimen (remember that whole fruits are better than juice). However, if you are taking any medications, talk to your doctor first because grapefruit interferes with the enzymes that metabolize medications, and can cause a lethal buildup of medication in the body ^148-151.

Naringin

Another potential mitochondrial booster is naringin, which like nootkatone, is a flavonoid present in grapefruit, and also in other citrus fruits ¹⁷⁰ 171. Upon ingestion, the colonic microflora converts naringin to naringenin, which is the active form in the body ¹⁷².  In contrast the other bioactive compounds mentioned in this article, naringin primarily targets the liver, where it activates both PPAR-gamma and PPAR-alpha with a concomitant increase in hepatic fat oxidation (fat burning) and inhibition of fat and cholesterol synthesis ¹⁷³. An interesting recent finding is that naringin also seems to induce PGC-1 transcription, and thereby possibly could stimulate mitochondrial biogenesis in the liver as well. Since the liver is the metabolic hub in the body, this could have beneficial systemic (whole-body) effects. Naringin has already been shown in humans to have several beneficial health effects by preventing cardiovascular disease, protecting against cancer and being anti-inflammatory ^{171 174-177}, so if you try this supplement it won’t hurt you even though the evidence for its potential effect on mitochondrial biogenesis is still in its infancy.

Downsides…

The potential of exercise mimetics certainly appeals to the huge mass of lazy folks who cannot get their butts off the couch, and the pharmaceutical and supplement industry that sees the tremendous market potential. So we’ll most certainly be hearing a lot about these “exercise pills” in the near future. However, I want to emphasize that an “exercise pill” will never ever be a substitute for actual exercise training. Why? For several reasons:

Firstly, mimicking activation of exercise signaling pathways could result in a chronic catabolic state. For example, activation of AMPK could inhibit protein synthesis ¹⁵² and stimulate autophagy (cell cannibalism, that is, degradation of a cell’s own components through the lysosomal machinery) ¹⁵³. Also, while augmenting oxidative capacity in mice, overproduction of PGC-1α in muscle has been shown to result in severe muscle atrophy as mice aged ¹⁵⁴. These effects would clearly be detrimental, especially for aging people. This underscores the importance of striking an optimum balance between continuous compared with transient activation of exercise signaling pathways.

Secondly, intense exercise bouts induce significant temporary stress on various organ systems. With an over 15-fold increase in whole body oxygen consumption when transitioning from complete rest to intense exercise, it is no surprise that a complex myriad of signaling pathways are activated in multiple tissues, of which we only know a few. Even though science is making progress in elucidating the exercise response on a molecular level, we are still barely just scraping the tip of the iceberg.

Thirdly, exercise training has multiple health benefits that do not, at least directly or entirely, relate to the muscle-specific adaptations. For example, cardiovascular adaptations like blood pressure reduction and improved blood lipid profile are not completely (albeit partly) due to muscle-specific adaptations ^{155 156}. This is further underscored by the finding that beneficial effects of regular exercise are even seen in arteries of non-exercise-trained limbs ^157-160. Additionally, regular exercise results in a host of other health benefits; it prevents or reduces the severity of dementia and other neurological disorders, osteoarthritis, osteoporosis, fall-related injuries, depression, certain cancers and cardiovascular diseases ^{16 18 161-165}. Exercise also improves cardiac function and enhances stroke volume, increases VO2max (the maximal oxygen uptake, or aerobic capacity, which is the maximum capacity of the body to transport and use oxygen during exercise), increases nitric oxide levels in vascular endothelial cells, increases bone mass and strength, enhances the immune system, lowers TNF-α and other inflammatory markers, improves insulin sensitivity and blood lipid profiles, and increases muscle capillarization, muscle size and muscle strength ^{161 166}. Obviously, no single pharmaceutical or dietary agent could mimic this multifaceted response.

Fourthly, in order for an “exercise mimetic” to mimic the effect of exercise on obesity, it would have to result in an increase in energy expenditure to the same degree as exercise. Even though PQQ increases energy expenditure in rats (see above), this increase is nowhere near the increase that is seen with exercise. An increase in muscle mitochondria enhances exercise capacity and endurance, making it possible to expend more total energy, or the same amount of energy in a shorter time. So, an increase in mitochondria enhances the capacity to expend calories by means of exercise, and thereby could make exercise more effective in preventing and/or treating obesity. However, an increase in mitochondria per se has no major independent effect (in the absence of exercise) on energy expenditure.

Finally, regular exercise has psychological effects on constructs like self-mastery ¹⁶⁷, self-esteem ¹⁶⁷, self-perception ¹⁶⁷, self-efficacy ¹⁶⁸ self-regulation ¹⁶⁸ and also social engagement ¹⁶⁷, which no “magic” mimetic pill ever will be able to reproduce. The psychological effects of exercise might actually be at least as important as the physiological effects in the achievement of fat loss ¹⁵⁴.  This is an areas that I think deserves more attention.

A poly-pill containing a number of agents aimed at selected targets could theoretically address the second and third objection. However, as indicated in objection one, it is likely to be associated with multiple unwanted effects, and to be of questionable long-term efficacy. Thus, with the discovery and development of tissue-specific targets, only limited aspects of the exercise response can be mimicked. The term ‘exercise mimetic’ is therefore misleading, and could lull a false sense of security and give lazy folk another excuse not to exercise “I took this exercise pill so I don’t have to go to the gym”…. These days, unfortunately the general tendency is to look for a pill to solve our problems anytime we face obstacles. This fact is aptly highlighted by a comment from one of the most prominent researchers on the health benefits of regular physical activity “When will we treat physical activity as a legitimate medical therapy…even though it does not come in a pill?” ¹⁶⁹.

Conclusion

Exercise mimetics work by stimulating some of the molecular pathways that are also activated by actual exercise. Pharmacological stimulation of AMPK and PGC-1 in sedentary mice has been shown to induce metabolic genes and enhanced running endurance even without exercise ⁵⁰. Similarly, SIRT1 activation could protect against metabolic disorders by stimulating fat burning (oxidation). Also, the question remains as to what extent data from cell culture and rodent studies can be extrapolated to humans.

However, the terms “exercise mimetic”, and its synonym “exercise pill”, are very misleading. I prefer the term “mitochondrial booster”, since it doesn’t erroneously imply that these types of pills can substitute for the real thing. A mitochondrial booster (or exercise mimetic, if you wish) supplement could be a great adjunct to exercise, but never ever a substitute.

Bearing all the caveats in mind, since actual exercise and exercise mimetics at least partly target the same molecular pathways at potentially complementary control points, it is extremely interesting to speculate on the possible synergistic effects between exercise and exercise mimetics on muscle, mitochondrial function, performance, and in preventing the age-related declines in muscular function…indeed, there are preliminary data pointing towards promising synergistic effects ⁵⁰. Rest assured I will be keeping you posted here on BrinkZone.com.

However, exercise is and always will be necessary. Sorry folks, there are no magic bullets. There’s simply no way around it. Amen!!!

So here’s the take-home message:

If you are a regular exerciser; an exercise mimetic/mitochondrial booster could give you a little extra “push” and possibly enhance your long-term training response.

If you are a couch potato; no pill in the word will ever make up for your lazy ass!

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Exercise Mimetics & Mitochondrial Boosters is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

We all know about the cardiovascular health benefits of fish oil, and in a previous article I covered the fat loss effect of fish oil. Now let’s take a look at the potential application of fish oil for those of us who are interested in muscle growth…

Anti-catabolic effects of fish oil

Muscle protein undergoes a continuous process of synthesis (anabolism) and degradation (catabolism). In a healthy state, the anabolic and catabolic processes are balanced to maintain stability of or even increase muscle mass (as is observed with resistance training combined with proper nutrition).

Catabolism of muscle tissue is common in both clinical states (for example diabetes, renal failure, trauma and cancer) and during diet-induced weight loss and other stress conditions ^1-6. During these catabolic states, muscle protein degradation exceeds muscle protein synthesis, which results in muscle loss and weakness.

Muscle protein catabolism is primarily caused by the ubiquitin-proteasome system ^{3 6-11}. It is here fish oil enters the picture, since its fatty acid EPA significantly decreases the activity of the muscle protein catabolic (ubiquitin-proteasome) system ^{2 4 5 12-16}.

Another mechanism by which fish oil exerts its anti-catabolic effect is by reducing cortisol levels ^{17 18}. As we all know, cortisol breaks down muscle tissue ¹⁹ and has a host of other detrimental effects when present at chronically elevated levels (which is a topic in its own right), so this is a beneficial effect of fish oil beyond anti-catabolism.

Anabolic effects of fish oil

What makes fish oil especially interesting is that it seems to promote muscle growth by not only inhibiting muscle catabolism, but also by stimulating muscle anabolism. Recent studies showed that supplementing for 8 weeks with 4 g per day of fish oil concentrate providing a daily dose of 1.86 g EPA and 1.5 g DHA, significantly increases the anabolic response of muscle protein synthesis to amino acids and insulin ²⁰. The augmented anabolic response to amino acids and insulin was shown to be due to an increased activation of the mTOR/p70S6K signalling pathway, which is considered an integral control point for muscle protein anabolism ²¹ and muscle cell growth ^22-25.

Other mechanisms probably contribute as well. The same study showed that the fish oil supplementation in  25-45 year old healthy subjects doubled the proportion of EPA, DPA (another less talked about omega-3 fatty acid) and DHA in muscle cell membranes, at the expense of omega-6 fatty acids and mono-unsaturated fatty acids, with no change in saturated fatty acid) concentrations ²⁰. Thus, it is also possible that fish oil supplementation influences anabolic signalling cascades by affecting membrane lipid composition and/or fluidity ^26-29.

Are you older than 45 yr? Don’t fret, you will still benefit from the muscle anabolic effects of fish oil. The same research team conducted another study, using an identical research protocol (1.86 g EPA and 1.5 g DHA for 8 weeks), in healthy elderly subjects over 65 years (mean age 71 years). The results were the same as in the younger subjects; the fish oil supplementation significantly increased the muscle protein synthetic response to amino acids and insulin ³⁰. Thus, fish oil seems to attenuate the anabolic resistance associated with old age ^31-33. The researchers were so impressed with the response that they concluded fish oil can be useful for both prevention and treatment of sarcopenia ³⁰.

In both of these studies, muscle mass was not measured because the interventions only lasted for 8 weeks. However, taking into consideration that changes in muscle protein metabolism precede corresponding changes in muscle mass ^34-36, these results are promising. It is going to be interesting to see longer term studies that measure actual fish oil induced gains in muscle mass, and also how the anabolic response to fish oil interacts with resistance training.

Wrap up

Whether you’re looking to build muscle or prevent loss of muscle during a diet, evidence supports the addition of fish oil to your supplement regimen. Fish oil, and especially EPA, not only counteracts the detrimental loss of muscle mass that we see in stressful and catabolic states, but also boosts the anabolic response to nutritional stimuli in healthy muscle from both young, middle-age and older adults. Thus, it beneficially affects both the catabolic and anabolic sides of the muscle protein balance equation.

The studies to date used a fish oil dose corresponding to 1.86 g EPA and 1.5 g DHA (which can be considered to be a medium high dose). We don’t know yet if a higher or lower dose would have a greater/smaller effect, but this dose a good guideline to start with.

In my next article I will cover the safety aspects of high dose omega-3 supplementation regimens, and discuss the different supplemental sources of omega-3. For now, I can say that the dosages used to achieve the muscle anabolic and fat loss effects (see my other article “Fish Oil for Fat Loss“) are safe for healthy folks who are not taking any prescription medications. Stay tuned!

References:

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4. Whitehouse AS, Smith HJ, Drake JL, Tisdale MJ. Mechanism of attenuation of skeletal muscle protein catabolism in cancer cachexia by eicosapentaenoic acid. Cancer Res“2001;61(9):3604-9.

5. Whitehouse AS, Tisdale MJ. Downregulation of ubiquitin-dependent proteolysis by eicosapentaenoic acid in acute starvation. Biochemical and biophysical research communications 2001;285(3):598-602.

6. Wing SS, Goldberg AL. Glucocorticoids activate the ATP-ubiquitin-dependent proteolytic system in skeletal muscle during fasting. The American journal of physiology 1993;264(4 Pt 1):E668-76.

7. Attaix D, Aurousseau E, Combaret L, Kee A, Larbaud D, Ralliere C, et al. Ubiquitin-proteasome-dependent proteolysis in skeletal muscle. Reprod Nutr Dev 1998;38(2):153-65.

8. Attaix D, Ventadour S, Codran A, Bechet D, Taillandier D, Combaret L. The ubiquitin-proteasome system and skeletal muscle wasting. Essays Biochem 2005;41:173-86.

9. Jagoe RT, Goldberg AL. What do we really know about the ubiquitin-proteasome pathway in muscle atrophy? Current opinion in clinical nutrition and metabolic care 2001;4(3):183-90.

10. Mitch WE, Goldberg AL. Mechanisms of muscle wasting. The role of the ubiquitin-proteasome pathway. The New England journal of medicine 1996;335(25):1897-905.

11. Tisdale MJ. The ubiquitin-proteasome pathway as a therapeutic target for muscle wasting. J Support Oncol 2005;3(3):209-17.

12. Fearon KC, Von Meyenfeldt MF, Moses AG, Van Geenen R, Roy A, Gouma DJ, et al. Effect of a protein and energy dense N-3 fatty acid enriched oral supplement on loss of weight and lean tissue in cancer cachexia: a randomised double blind trial. Gut 2003;52(10):1479-86.

13. Smith HJ, Greenberg NA, Tisdale MJ. Effect of eicosapentaenoic acid, protein and amino acids on protein synthesis and degradation in skeletal muscle of cachectic mice. British journal of cancer 2004;91(2):408-12.

14. Smith HJ, Khal J, Tisdale MJ. Downregulation of ubiquitin-dependent protein degradation in murine myotubes during hyperthermia by eicosapentaenoic acid. Biochemical and biophysical research communications 2005;332(1):83-8.

15. Smith HJ, Lorite MJ, Tisdale MJ. Effect of a cancer cachectic factor on protein synthesis/degradation in murine C2C12 myoblasts: modulation by eicosapentaenoic acid. Cancer Res 1999;59(21):5507-13.

16. Smith HJ, Tisdale MJ. Induction of apoptosis by a cachectic-factor in murine myotubes and inhibition by eicosapentaenoic acid. Apoptosis 2003;8(2):161-9.

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

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

19. Rooyackers OE, Nair KS. Hormonal regulation of human muscle protein metabolism. Annual review of nutrition 1997;17:457-85.

20. Smith GI, Atherton P, Reeds DN, Mohammed BS, Rankin D, Rennie MJ, et al. Omega-3 polyunsaturated fatty acids augment the muscle protein anabolic response to hyperinsulinaemia-hyperaminoacidaemia in healthy young and middle-aged men and women. Clin Sci (Lond) 2011;121(6):267-78.

21. Drummond MJ, Fry CS, Glynn EL, Dreyer HC, Dhanani S, Timmerman KL, et al. Rapamycin administration in humans blocks the contraction-induced increase in skeletal muscle protein synthesis. The Journal of physiology 2009;587(Pt 7):1535-46.

22. Bodine SC, Stitt TN, Gonzalez M, Kline WO, Stover GL, Bauerlein R, et al. Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo. Nature cell biology 2001;3(11):1014-9.

23. Rommel C, Bodine SC, Clarke BA, Rossman R, Nunez L, Stitt TN, et al. Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways. Nature cell biology 2001;3(11):1009-13.

24. Baar K, Esser K. Phosphorylation of p70(S6k) correlates with increased skeletal muscle mass following resistance exercise. The American journal of physiology 1999;276(1 Pt 1):C120-7.

25. O’Neil TK, Duffy LR, Frey JW, Hornberger TA. The role of phosphoinositide 3-kinase and phosphatidic acid in the regulation of mammalian target of rapamycin following eccentric contractions. The Journal of physiology 2009;587(Pt 14):3691-701.

26. Mansilla MC, Banchio CE, de Mendoza D. Signalling pathways controlling fatty acid desaturation. Sub-cellular biochemistry 2008;49:71-99.

27. Stillwell W, Wassall SR. Docosahexaenoic acid: membrane properties of a unique fatty acid. Chemistry and physics of lipids 2003;126(1):1-27.

28. Armstrong VT, Brzustowicz MR, Wassall SR, Jenski LJ, Stillwell W. Rapid flip-flop in polyunsaturated (docosahexaenoate) phospholipid membranes. Archives of biochemistry and biophysics 2003;414(1):74-82.

29. Stillwell W, Shaikh SR, Zerouga M, Siddiqui R, Wassall SR. Docosahexaenoic acid affects cell signaling by altering lipid rafts. Reprod Nutr Dev 2005;45(5):559-79.

30. Smith GI, Atherton P, Reeds DN, Mohammed BS, Rankin D, Rennie MJ, et al. Dietary omega-3 fatty acid supplementation increases the rate of muscle protein synthesis in older adults: a randomized controlled trial. The American journal of clinical nutrition 2011;93(2):402-12.

31. Cuthbertson D, Smith K, Babraj J, Leese G, Waddell T, Atherton P, et al. Anabolic signaling deficits underlie amino acid resistance of wasting, aging muscle. The FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2005;19(3):422-4.

32. Guillet C, Prod’homme M, Balage M, Gachon P, Giraudet C, Morin L, et al. Impaired anabolic response of muscle protein synthesis is associated with S6K1 dysregulation in elderly humans. The FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2004;18(13):1586-7.

33. Rasmussen BB, Fujita S, Wolfe RR, Mittendorfer B, Roy M, Rowe VL, et al. Insulin resistance of muscle protein metabolism in aging. The FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2006;20(6):768-9.

34. Hawley JA, Tipton KD, Millard-Stafford ML. Promoting training adaptations through nutritional interventions. Journal of sports sciences 2006;24(7):709-21.

35. Hawley JA, Burke LM, Phillips SM, Spriet LL. Nutritional modulation of training-induced skeletal muscle adaptations. J Appl Physiol 2011;110(3):834-45.

36. Rennie MJ, Wackerhage H, Spangenburg EE, Booth FW. Control of the size of the human muscle mass. Annual review of physiology 2004;66:799-828.

About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer.

Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an early teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a major in Nutrition at the University.

During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications.

It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to bodybuilding, fitness, health and anti-aging.

Fish Oil for Muscle Growth is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

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

Fish Oil Induced Fat Loss

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

Mechanism – how does it work?

In search for the mechanisms behind fish oil induced fat loss, it has been found that fish oil exerts favorable metabolic effects by modulating gene expression (which is the process by which the information encoded in a gene is converted into protein)^{2 13-26}. While we inherit our genes (or blueprints) from our parents, what determines the way in which our blueprints are interpreted is largely dictated by a collection of environmental factors. The nutrients we consume are among the most influential of these environmental factors ^{27 28}. One dietary constituent that has a strong influence on our genetic makeup is dietary fat ^{2 13 14 16-19 21-23 25 29}. Fatty acids of dietary fat not only influences hormonal signaling events, but also have a very strong direct influence on the molecular events that govern gene expression. More specifically, it has been shown that the fatty acids EPA and DHA from fish oil (by affecting gene expression) inhibit the activities of fat synthesizing (lipogenic) enzymes ^30-37, while at the same time stimulating the activities of key enzymes that govern fat oxidation (fat burning) ^{2 38-46}.

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

It is also interesting that fish oil lowers cortisol. While the exact role of cortisol in obesity isn’t fully elucidated ^{51 52}, it is known that excessive cortisol levels result in substantial fat mass gain ^{53 54}. Thus, the reduction in cortisol levels after fish oil supplementation could contribute to the fat loss effect of fish oil.

What’s in it for me?

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

Yes! Read on…

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

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

Recently, more studies have been published on the topic. In overweight men and women, the effects of the addition of 6 g of fish oil daily (corresponding to 360 mg EPA and 1560 mg DHA) in combination with regular aerobic activity (walking 45 min three times per week at an intensity of 75% of age-predicted maximal heart rate) for 12 weeks, was investigated ⁵⁸.

The results showed that the combination of fish oil and regular aerobic activity not only improved several risk factors for cardiovascular disease, but also significantly reduced the amount of body fat ⁵⁸. It is interesting that these effects were noted even though the subjects did not change their usual food habits other than adding the fish oil supplement. This indicates the great potential benefits of fish oil combined with regular physical activity for improving body composition and cardiovascular health. In this study, no fat loss was seen in fish oil only group (that didn’t exercise). This could be due to the older age of the subjects (47-51 yrs) in this study compared to the previous studies, and the relatively low dose of EPA. Fish oil supplementation has also been shown to result in a 2.22 lb (1 kg) greater weight loss after 4 weeks of dieting (reduced caloric intake) ⁵⁹.

Perspective on fish oil and fat loss

In contrast to the positive studies, there are a few that didn’t show any fat loss with fish oil supplementation ^60-63. This could be due to differences in subject characteristics (age, initial body fat mass, baseline physical activity), methodological differences, and differences in fish oil preparations (see below). However, several high quality studies have shown that fish oil supplementation has a significant fat loss effect in addition to all its other health promoting effects. Overall, fish oil seems to have the ability to shift fat metabolism away from storage toward burning of body fat.

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

In one of the most recent studies on fish oil’s fat loss effect, men and women (mean age 33 yrs) where given 4 g of fish oil corresponding to 1600 mg EPA and 800 mg DHA ⁴⁸. After for 6 weeks, the placebo group, which was given 4 g of safflower oil, showed a tendency towards fat gain.

The fish oil group instead had lost 0.5 kg of fat mass and gained 0.5 kg of lean mass, with no change in body weight. This is a very beneficial body composition effect and underscores the importance of investigating fat mass and lean mass separately, since just measuring body weight will not tell anything about potential compositional changes, which after all is what is interesting from both a health, esthetic and physical performance viewpoint. I will cover the anti-catabolic and potential lean mass gaining effects of fish oil in more detail in an upcoming article.

Wrap up

Whether you are on a diet or not, adding a fish oil supplement to your regimen can effectively help you get in shape. The additional calories from the fish oil will not get stored ⁶⁴; quite to the contrary, fish oil will help you get rid of calories you already have stored in your body fat. What’s interesting is that fish oil supplementation seems to reduce body fat and waist circumference despite unchanged exercise and/or other dietary practices.

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

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

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

31. Kim HJ, Takahashi M, Ezaki O. Fish oil feeding decreases mature sterol regulatory element-binding protein 1 (SREBP-1) by down-regulation of SREBP-1c mRNA in mouse liver. A possible mechanism for down-regulation of lipogenic enzyme mRNAs. The Journal of biological chemistry 1999;274(36):25892-8.

32. Mater MK, Thelen AP, Pan DA, Jump DB. Sterol response element-binding protein 1c (SREBP1c) is involved in the polyunsaturated fatty acid suppression of hepatic S14 gene transcription. The Journal of biological chemistry 1999;274(46):32725-32.

33. Nakatani T, Kim HJ, Kaburagi Y, Yasuda K, Ezaki O. A low fish oil inhibits SREBP-1 proteolytic cascade, while a high-fish-oil feeding decreases SREBP-1 mRNA in mice liver: relationship to anti-obesity. Journal of lipid research 2003;44(2):369-79.

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

35. Worgall TS, Sturley SL, Seo T, Osborne TF, Deckelbaum RJ. Polyunsaturated fatty acids decrease expression of promoters with sterol regulatory elements by decreasing levels of mature sterol regulatory element-binding protein. The Journal of biological chemistry 1998;273(40):25537-40.

36. Xu J, Nakamura MT, Cho HP, Clarke SD. Sterol regulatory element binding protein-1 expression is suppressed by dietary polyunsaturated fatty acids. A mechanism for the coordinate suppression of lipogenic genes by polyunsaturated fats. The Journal of biological chemistry 1999;274(33):23577-83.

37. Yahagi N, Shimano H, Hasty AH, Amemiya-Kudo M, Okazaki H, Tamura Y, et al. A crucial role of sterol regulatory element-binding protein-1 in the regulation of lipogenic gene expression by polyunsaturated fatty acids. The Journal of biological chemistry 1999;274(50):35840-4.

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

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

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

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

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

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

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

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

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

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

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

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

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

51. Walker BR. Activation of the hypothalamic-pituitary-adrenal axis in obesity: cause or consequence? Growth hormone & IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society 2001;11 Suppl A:S91-5.

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

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

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

55. Couet C, Delarue J, Ritz P, Antoine JM, Lamisse F. Effect of dietary fish oil on body fat mass and basal fat oxidation in healthy adults. International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity 1997;21(8):637-43.

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

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

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

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

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

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

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

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

64. Bays HE, Maki KC, Doyle RT, Stein E. The effect of prescription omega-3 fatty acids on body weight after 8 to 16 weeks of treatment for very high triglyceride levels. Postgraduate medicine 2009;121(5):145-50.

About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer.

Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an early teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a major in Nutrition at the University.

During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications.

It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to bodybuilding, fitness, health and anti-aging.

Fish Oil for Fat Loss is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Vegetarian Eating For Athletes: The Facts! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Everybody wants to stay young and vital throughout life. But aging is topic surrounded by many questions and myths; here we’ll get to the bottom of it.

Different types of Aging – Chronological Aging and Physiological Aging

Before we get started, I want to make a distinction of two types of aging; chronological and physiological (or biological).

Chronological age is based on time and is the same for everyone who is born on the same date. It refers to age in number of years.

Physiological age, also called biological age, is the result of many factors, many of which are under your control, and varies from person to person (even if they were born on the same date). It refers to age in terms of physical capacity.

Chronological aging refers to how long you have been alive, and is determined by a mathematical formula that is the same for everybody: current date minus date of birth. It is a function of time and cannot be slowed, stopped or accelerated (a side note: according to Einstein’s Theory of Relativity, chronological can be modified, since as one approaches the speed of light, time slows down, and thus so does chronological age. But this isn’t relevant for us earthbound folks).

Physiological aging, on the other hand, describes the state of your body. What’s interesting with physiological aging is that many of the factors that impact it are under your full control (e.g. exercise, nutrition, sleep etc). While chronological and physiological aging are related, the years of your life doesn’t necessarily have much to do with the years of your body. Many people don’t like to tell their (chronological) age; however, if you have taken care of yourself you should be proud of it!

Thus, chronological age and physiologic age do not always coincide, and physical appearance and health status often do not always correspond to what is typical at a particular chronological age. When talking about aging and anti-aging, it is the physiological age we’re referring to. Ok, now that we got that cleared out, let’s move on.

Primary and Secondary Aging

Aging can also be conceptualized as the result of two interactive and overlapping processes, known as primary and secondary aging ¹. However, this theory is not universally accepted because it is hard to completely separate each factor.

Primary aging, or “intrinsic senescence,” is the progressive deterioration in physical structure and biological function that occurs with advancing age alone, independent of other factors. For example, changes in body composition (ie, decreased bone mineral density, decreased muscle mass, and abdominal fat accumulation) ^2-4 and progressive decline of cardiac, pulmonary, renal, and immune function occur normally with increasing age ^5-7.

Secondary aging is the accelerated deterioration in organ structure and function that is mediated by diseases, such as diabetes and hypertension, or by harmful environmental and lifestyle factors, such as tobacco smoking or excessive sun exposure ^8-10.

Definition of Aging

All humans and animals (and other living organisms as well for that matter) undergo changes with time. As a multidimensional reality of life, aging is difficult to define simply. The National Institute on Aging states that “in its broadest sense, aging merely refers to changes that occur during the lifespan”. The World Health Organization (WHO) defines aging as a “process of progressive change in the biological, psychological and social structure of individuals’. Yet another definition is “the lifelong process of growing older at cellular, organ, and whole-body level throughout the life span” ¹¹.

From a biological standpoint, aging is often used synonymously with the term senescence, defined as “a biological process of dysfunctional change by which organisms become less capable of maintaining physiological function and homeostasis ¹².

Thus, aging can be viewed as a decline, change or development. A decline in body and mental functions has a negative connotation. A change in body and mental functions is neutral in meaning. However, not all aspects of aging decline with age. Our ability to love and be loved does not diminish; at the beach we might pick up grand-kids instead of sweethearts, but our capacity for joy is undiminished. As we will see below, a third view of aging is that of further development. Like age itself, experience, knowledge and wisdom can only increase with time.

One of the reasons for the lack of a singular definition of aging is that it can be considered in so many different ways, according to social, behavioral, physiological, morphological, cellular and molecular changes and norms. Research has led to a number of theories being proposed that may explain the aging process.

Theories of Aging

I want to make it clear right from the start that the ultimate causes of aging remain unknown. The aging process is complex and multifactorial. However, intense research over the past decades has culminated in several theories of aging ^{13 14}. These theories of aging can be categorized into different levels: evolutionary, molecular, cellular and systemic (whole body). The table below summarizes these theories and gives a brief description of each.

Classification and brief description of main theories of aging

Don’t worry if you don’t understand all the terms in the table; I put it here just as a demonstration and summary of the different aging/anti-aging research domains.

The major theories of aging are all specific of a particular cause of aging, providing useful and important insights for the understanding of physiological changes occurring with aging. While proponents of any specific theory might state that their theory is the “one and only”, it should be noted that there is a lot of overlap between them. Alterations of molecular events with aging may lead to cellular alterations, and these, in turn, contribute to organ and systemic failure with evolutionary implications for reproduction and survival.

Thus, the search for a single cause of aging (such as a single gene or the decline of a single body system) has recently been replaced by the view of aging as an extremely complex, multifactorial process ¹⁵. In fact, it is very likely that several processes simultaneously interact and operate at different levels of the functional organization ¹⁶. In complex, multicellular organisms like humans and animals, the study of interactions among intrinsic (genetic), extrinsic (environmental), and stochastic (random damage to vital molecules) causes provides a more fruitful global approach conducive to a comprehensive and realistic understanding of the aging process. Therefore, different theories of aging should not be considered as mutually exclusive, but may be complementary of others to explain some or all the features of the normal aging process.

As the different theories of aging show, a great deal of the aging process is understood. In several animal species (rodents, monkeys), experimental interventions show that it is possible to delay the onset of functional decline and pathology, and to prolong the life span by manipulating molecular (e.g., free radical reduction), cellular (e.g., mitochondrial protection), and systemic (e.g., endocrine shifts) mechanisms ¹⁷. And recent progress in anti-aging research shows exciting promising applications for therapeutic human interventions ^18-22. I will cover this in detail in part two of this article.

Usual “Normal” Aging and Successful Aging

Many people see aging as a time of cognitive and physical decline. For the past three decades, the general public and most scientists and have accepted this negative age-stereotype as the norm ^{23 24}. The elderly have been viewed and labeled as, ‘ill and/or disabled’, impotent’, ‘ugly’, ‘mentally declining’, ‘mentally ill’, ‘useless’, ‘isolated’, ‘poor’ and ‘depressed’. This negative stereotyping of and discrimination against people because they are old is known as “ageism” ²³.

Studies of human aging in the 1960s to 1980s focused on average “normal” age-related functional losses with aging in organs and systems of the body ²⁵. While it is true that bodily functions degrade as we get old, we have all seen people who look younger and are more capable than their peers. This has even been scientifically documented ^{26 27}. The traditional aging research totally neglected this, despite evidence that there are substantial functional differences of older person within the same age groups. Differences in functionality within age groups were simply attributed to genetic endowment. Although genetic factors contribute to the way we age, and is a field of research on its own ²⁸, our genes still only account for a minor part of how gracefully we age. Twin studies that examined the influence of genes on aging have shown that heritability explains about 20-30% of differences in lifespan, and 22% of differences in functioning ²⁹. Both longevity and functioning appear less heritable than cognitive ability ³⁰. Thus, most of the differences between how gracefully we age stem from non-heritable influences of peoples environment and lifestyle, which are not part of the aging process.

Thankfully, in the 1980s and 1990s the view of aging started to shift and challenged the inevitability of functional impairment and of disease in the elderly ^{31 32}. This new view of aging groups the aging processes into three possible paths ^{31 32}:

1. Aging, with disease and disability.
2. Usual aging, with the absence of overt pathology, but with the presence of some declines in function.
3. Successful (or healthy) aging, with little or no pathology and little or no functional loss.

Such a grouping of aging processes de-emphasizes the view that aging is exclusively characterized by declines in functional competence and health, and re-focuses on the substantial heterogeneity among old persons. It also underscores the existence of positive outcomes (i.e. without disability, disease, or major physiological decline), and highlights the possible avoidance of many, if not all, the diseases and disabilities usually associated with old age.

According to the new perspective on aging, mechanisms of successful aging consist of:

1. Persistence of normal function.
2. Compensatory responses induced by exercise, good nutrition, and education to restore function.
3. Interventions to replace deficient function (as represented by replacement therapies).
4. Changing of health outcome by modifying risk profiles.
5. Prevention of disease.
6. Strengthening of social interactions.

With this new aging perspective, the traditional meaning of life span has been replaced by health span.

Successful Aging – what’s in a name?

While the concept of successful aging is popular among both scientists and the general population, there is no one single agreed upon definition for it. There’s even no agreement on the term to be used, with descriptors ranging from successful aging to healthy aging, productive aging, active life expectancy, healthy years, and aging well ^{31 33-37}.

According to the classic definition ^{31 32 38}, successful aging can be characterized as involving three components:

1. Freedom of disease and disability.
2. High physical and cognitive functioning
3. Social and productive engagement.

Later refinements to the definition have added psychosocial aspects to the definition, such as self-acceptance, positive relations with others, autonomy, environmental control, purpose in life, and personal growth ³⁹. It has also been suggested that successful aging is a developmental process that can be achieved at any stage in the life span ³⁹.

Regardless what criteria and what terms we use, we all want to have the capacity to thrive and prosper for as long as we live.

Lifespan, healthy life expectancy and longevity

Let’s take a look at some aging trends and projections.

The average lifespan of humans has increased over the past century, mainly a result of a significant improvement in sanitary conditions, public health reforms and improved personal hygiene, advances in medical knowledge and practices, and living standards ⁴⁰. The average life expectancy at birth is now approximately 75 years in males, and 80 years in females in the USA (World Health Organization 2003). This can be compared to 48 years at the beginning of the 1900s ⁴⁰.

In the United States, the population aged 65 and older was 3.1 million (4% of the total population) in 1900, in 1950, this number had increased to 12.2 million (8.1% of the total population), and in 2000 it grew to 35 million (12.4% of the total population) ⁴¹.  In 2008, 39 million people age 65 and over lived in the United States, accounting for 13 percent of the total population.

The older population grew from 3 million in 1900 to 39 million in 2008. The oldest-old population (those age 85 and over) grew from just over 100,000 in 1900 to 5.7 million in 2008. The baby boomers (those born between 1946 and 1964) will start turning 65 in 2011, and the number of older people will increase dramatically during the 2010–2030 period. The older population in 2030 is projected to be twice as large as their counterparts in 2000, growing from 35 million to 72 million and representing nearly 20 percent of the total U.S. population ⁴¹.  The oldest-old population is projected to grow rapidly after 2030, when the baby boomers move into this age group. The U.S. Census Bureau projects that the population age 85 and over could grow from 5.7 million in 2008 to 19 million by 2050. Some researchers predict that death rates at older ages will decline more rapidly than is reflected in the U.S. Census Bureau’s projections, which could lead to an even faster growth of this population ^42-44.

In 2000, the World Health Organization recognized that quality of life in old age is as important as increased longevity, and introduced the concept of healthy life expectancy (also called HALE), defined as the “average number of years that a person can expect to live in ‘full health’ by taking into account years lived in less than full health due to disease and/or injury” (World Health Organization 2000). A simpler way of saying this is that the healthy life expectancy is the number of years an individual is expected to live without any major debilitating diseases (World Health Organization 2000). The healthy life expectancy is about 67 years for males and 71 years for females (World Health Organization 2000).

The maximum observed lifespan represents the longest-lived member(s) of the population ⁴⁵. In humans, the oldest individual ever recorded was a woman, who died in 1997 in France at the age of 122 years ⁴⁶. The oldest recorded man  died in 1998 at the age of 115 ⁴⁷. By contrast, the average lifespan (or life expectancy at birth) refers to how long people live on average in a given population ⁴⁰. The theoretical maximum lifespan, or potential maximum lifespan,  is the theoretical highest attainable age ⁴⁵. Today, we don’t know what age this is, but it has been speculated to be around 125 years ⁴⁸.

Do we have an immutable life span limit?

A fundamental question in aging research is whether humans possess an immutable life span limit. However, whether the maximum observed lifespan can and has increased is still controversial. According to some scientists, it has remained constant ^{49 50}. In contrast, others have shown that the maximum age at death has been rising over the past century in industrialized countries ⁵¹. For ex. statistical analysis of the longest available series of reliable information on the upper limits of achieved human life span, has shown that from 1969 to 1999 maximum life span increased by 1.1 years every decade. The table below shows more specifically the progressive changes in the average and maximum life spans ⁴⁰.

Average change (in Years Per Decade) in average and maximum life spans in Sweden ⁵¹.

Thus, even though the average life span has increased more than the maximum observed life span, the data clearly shows that the maximum observed life span is not immutable, and that our life span limit is steadily increasing as well.

Predictors of Successful Aging – valuable lessons from our current centenarians

Let’s take a look at what our current successful elders are doing to age successfully, and what physiological characteristics they display. Centenarians, those who are 100 years old or older, represent an intriguing model for ageing studies, since they demonstrate extreme longevity, and at the same time a proportion of them have aged successfully and have less diseases than the younger elderly ^{52 53}.

It has been shown that autonomous centenarians partake in regular exercise (in proportion to their physical capabilities), have more frequent intakes of protein and regular sleep patterns, and no history of drinking ⁵⁴.  Other consistent predictors of healthy aging are low blood pressure, low serum glucose, not smoking cigarettes, and not being obese ⁵⁵. Typical of autonomous centenarians are better visual acuity, preserved masticatory ability and living at home ⁵⁴. They have been relatively healthy and independent for most of their lives and don’t experience a significant functional decline until the very end of their lives ⁵⁶.

Other factors that have been documented in centenarians are a higher resting metabolic rate and lower waist-to-hip ratio ^{57 58}, higher IGF-1 levels ⁵⁹, and preserved thyroid function ⁶⁰, immunity ⁶¹ insulin sensitivity and glucose action ⁶². Centenarians also have been shown to have a less atherogenic plasma lipid profile (lower LDL and higher HDL, and larger LDL and HDL particle sizes) than aged subjects ^{63 64}. Also, while the prevalence of dementia increases with age, it is not inevitable in centenarians ^65-67, and cognition actually seems to be important for longevity ⁶⁸.

The rise of Generation C

According to watchers of consumer trends, a new generation – Generation C – will emerge in the course of the next 10 years. Born after 1990, they are referred to as “digital natives”. Now beginning to attend university and enter the workforce, they are expected to transform the world as we know it ⁶⁹. The “C” stands for “connected,” “communicating,” “content-centric,” “creative,” and “change”; however, it may just as well stand for “centenarian” as for the first time in history many of this birth cohort will live 100 years or more.

Centenarians, once considered rare, are now starting to become commonplace. Indeed, they are the fastest growing demographic group of the world’s population, their numbers having roughly doubled every decade since 1950, and they are globally projected to more than quintuple between 2005 and 2030 ⁷⁰.

Allostatic load – small insults add up over lifetime

Beyond the biological effects of aging, much of the illness and disability in the elderly is related to risk factors present at younger ages ⁵⁵. If you are in your 30s and think “I start to worry about that when I hit 50” you’re wrong. The sooner you start to take care of your health by exercising regularly and eating healthy, the better off you will be when you get older. Even early age nutrition and exercise habits in kids and teenagers have an impact the aging process ⁷¹. It has been shown that healthy lifestyle choices encompassing diet, physical activity, body fat (weight) reduction and stress control can add at least ten years to healthy, good quality, life expectancy ⁷².

Related to successful aging and the risk for diseases and functional declines is allostatic load, which is the cumulative physiologic toll “wear and tear” exacted on the body over time by efforts to adapt to life experiences and demands ^{73 74}. Allostatic load is measured through a composite index of indicators of cumulative strain on several organs and tissues, but especially on the cardiovascular system, and reflects the damaging consequences of the body’s response to chronic stress ^{75 76}.

Higher allostatic load scores have been associated with increased mortality ⁷³ and poorer cognitive and physical functioning ⁷⁴, and predict larger decrements in cognitive and physical functioning in older men and women  ⁷⁴. In addition to being an index of wear and tear on the body, elevations in allostatic load predict an increased risk for the incidence of cardiovascular disease, independent of sociodemographic and other health risk factors ⁷⁴. Allostatic load is also an independent predictor of functional decline in elderly men and women ⁷⁷.

Thus, even if you’re in your 20s or 30s, it is smart to think about the health implications of your current habits and lifestyle.

It is never too late

If you think after having read the previous paragraph “Shoot, it’s too late for me now, the damage is already done”, you’re wrong! Several studies have shown that improving health related habits and reducing risk factors even at older ages confer substantial benefits.

For example, a study followed middle-aged men (45-68 years) who were free of morbidity and functional impairments at baseline, over to 40 years (1965-2005). The purpose was to assess overall and exceptional survival. Exceptional survival was defined as survival to 75, 80, 85, or 90 years without incidence of 6 major chronic diseases and without physical and cognitive impairment. Of the participants, 42% survived to age 85 years and 11% met the criteria for exceptional survival to age 85 years. High grip strength and avoidance of overweight, hyperglycemia, hypertension, smoking, and excessive alcohol consumption were associated with both overall and exceptional survival. In addition, high education and avoidance of hypertriglyceridemia were associated with exceptional survival, and lack of a marital partner was associated with mortality before age 85 years. A statistical risk factor models indicated that the probability of survival to oldest age is as high as 69% with no risk factors and as low as 22% with 6 or more risk factors. The probability of exceptional survival to age 85 years was 55% with no risk factors but decreased to 9% with 6 or more risk factors. Thus, if you have any of the common risk factors that face most middle-age individuals, and make lifestyle changes to correct them, you will increase your probability of a long and healthy life ⁷⁸.

In another study that evaluated the relationship between changes in physical fitness and risk of mortality in men, it was found that going from being unfit to fit leased to a reduction in mortality risk of 44% relative to those who remained unfit 5 years later, even after adjusting for other risk factors. For each minute increase in maximal treadmill time, there was a corresponding 8% decrease in risk of mortality. This is quite impressive, and should encourage unfit folks to improve their fitness by starting a physical activity program even if they are in the middle-age ⁷⁹.

In a study of the impact of middle-age physical activity on physical function in early old age, individuals aged 39 to 63 years at baseline, were followed to 9 years. It was found that relatively fit and healthy middle-aged men and women who were physically active at recommended levels, were more likely to report high physical function at follow-up, compared to their sedentary counterparts. The association between initial level of physical activity and high physical function at follow-up remained after adjustment for baseline level of physical function and the presence of long-standing illness. Thus, participation in a physically active lifestyle during mid-life appears to be critical to the maintenance of high physical function in old age ⁸⁰.

Benefits of risk factor prevention in Americans aged 51 years and older was shown in a study that assessed the potential health and economic impact of reducing common risk factors in older Americans. The gain in life span from successful treatment of obesity, hypertension (high blood pressure) and diabetes was estimated to be up to 4 years. Despite living longer, those successfully treated for any of these risk factors would have lower lifetime medical spending, which indicates that the extra years added to life are healthy disease free years ⁸¹.

Even at old age we have a notable capacity to adapt to regular exercise. Aerobic exercise results in improvements in functional capacity and reduced risk of developing type II diabetes in the elderly. High-intensity resistance training (above 60% of the 1 repetition maximum) has been demonstrated to cause large increases in strength in the elderly. In addition, resistance training results in significant increases in muscle size in elderly men and women, and has a positive effect on multiple risk factors for osteoporotic fractures in previously sedentary post-menopausal women. Thus, old age does not decrease the capacity to adapt to a progressive resistance training program, and exercise may minimize or reverse the syndrome of physical frailty which is so prevalent among the oldest old ⁸². Even in very elderly 87 year old people resistance exercise training is a feasible and effective means of counteracting muscle weakness and physical frailty ⁸³.

A very interesting study sought to characterize the muscle weakness of the very old and its reversibility through strength training ⁸⁴. Ten frail, institutionalized volunteers aged 90-96 years undertook 8 weeks of high-intensity resistance training. Strength gains averaged 174% and midthigh muscle area increased 9.0%, while gait speed improved 48% after training. It was concluded that high-resistance weight training leads to significant gains in muscle strength, size, and functional mobility among frail residents of nursing homes up to 96 years of age ⁸⁴. Thus, with exercise training of sufficient frequency, intensity and duration, it is quite possible to increase muscle mass, strength and endurance at any age, and prevent sarcopenia, obesity, type II diabetes, coronary artery disease, hypertension, and osteoporosis. There is no pharmacological intervention that holds a greater promise of improving health and promoting independence in the elderly than does exercise ⁸⁵.

These studies clearly prove that it is never too late to start living healthier and benefit from those changes. While it’s certainly better to start healthy habits at a young age and keep them for a lifetime, for those who have strayed (that is, most people!) nature is remarkably forgiving. Not only can we recover much lost function and decrease risk, but we can actually increase function and health beyond our prior level.

The three steps toward extending your life and health span

One way to look at our path to longevity and health span is to regard it as a journey over three sequential steps. Step 1 is based on therapies that exist today, like exercise, nutrition and dietary supplementation. Step 1 will take us to step 2, which consists of biotechnology therapies. Step 2 will then take us to step 3, the nanotechnology/artificial intelligence revolution, which will lead to life spans that are currently incomprehensible, but which will soon be commonplace, measuring in the hundreds of years ^{86 87}.

The step 2 and step 3 anti-aging technologies, which have potential to extend our health span more than we ever dreamed was possible, are controversial topics and surrounded by ethical and political issues. Since BrinkZone is a site about nutrition and exercise, I will not cover these topics here.

Wrap up

There’s no excuse to treat the aging process itself as a reason for disability and disease at older age. A wealth of studies are showing over and over again that many, if not most, of the aging related functional declines and disabilities and can be prevented with non-aging related lifestyle factors like exercise and nutrition. A successful old age lies not so much in out stars and genes, as in ourselves. Step up, take control, and start adding both years to your life, and life to your years!

In part two of this article I will cover nutrition and dietary supplements that are currently being researched for their potential anti-aging effects, and that you can expect to see popping up on the supplement shelves in the near future. Stay tuned!

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About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer.

Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an early teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a major in Nutrition at the University.

During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications.

It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to bodybuilding, fitness, health and anti-aging.

Successful Aging – it’s your choice! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Role of muscle in the body’s metabolism

Skeletal muscle is the most abundant tissue in the human body, and the maintenance of its mass is essential to ensure basic function as locomotion, strength and respiration (1). In order for us to survive, certain tissues and organs, like the brain, heart, liver and skin, need to maintain their protein content. These essential tissues and organs rely on a steady supply of amino acids via the blood to serve as precursors for the synthesis of new proteins to balance the persistent rate of protein breakdown that occurs in all tissues.

In the absence of nutrient intake (for example in between meals and during sleep) muscle protein serves as the principal reservoir to replace blood amino acid taken up by other tissues (2-4). In the fasting state, blood amino acids serve not only as precursors for the synthesis of proteins but also as precursors for hepatic gluconeogenesis (5). Consequently, the protein mass of essential tissues and organs, as well as the necessary plasma glucose concentration, can be maintained relatively constant despite the absence of nutritional intake, provided muscle mass is adequate to supply the required amino acids.

The primary fate of ingested amino acids is incorporation into muscle protein to replete the reserves of amino acids lost in the fasting state. Under normal conditions, gains in muscle protein mass in the fed state balance the loss of muscle protein mass in the fasted state. The ability of muscle protein breakdown to maintain plasma amino acid concentrations is remarkable, provided adequate muscle mass is available.

Role of muscle in chronic disease

Chronic diseases related to poor lifestyle behaviors account for more than two-thirds of deaths in the United States (6), and alterations in muscle and loss of muscle mass (muscle wasting) play an important role in the most common diseases and conditions (7). Heart disease and cancer are the major chronic diseases suffered in the Western world (6), and both cardiac failure and cancer are often associated with rapid and extensive loss of muscle mass, strength, and metabolic function (cachexia) (1, 8, 9). With cardiac and cancer cachexia, the loss of muscle mass is an important determinant of survival. In these conditions these are notable alterations in muscle metabolism (1), among all an increased expression of muscle catabolic pathways and myostatin (which inhibits muscle growth) (10).

Another chronic condition that is caused by muscle loss is sarcopenia, which is a progressive loss of muscle mass and function that occurs with aging and causes frailty (11-14). Sarcopenia is a widespread syndrome that has a devastating effect on quality of life, activities of daily living and ultimately survival (11-14). Muscle loss isn’t just negative for the elderly, is also occurs in younger people, and is then called myopenia (15).

Exercise training has been proven to be beneficial in chronic diseases and conditions that cause, or are caused by, muscle wasting (1, 8, 9, 11, 13, 14). Another chronic disease where muscle mass (and exercise) is of importance is osteoporosis.

Mechanical force on bone is essential for increasing and maintaining bone strength and mass (16). Whereas body weight and weight-bearing exercises provide a direct mechanical force on bones, the largest  loads on bone are proposed to come from muscle contractions (16). Correlations between grip strength and bone area, bone mineral content, and bone mineral density in both healthy athletes (17) and stroke patients (18) support the notion that muscle contractions play a significant role in bone strength and mass. Even the correlation between body weight and bone mass can be explained on the basis of the force exerted on bone by muscle contractions, in that it takes more force per unit area to move heavier bodies.

Furthermore, changes in bone mass and muscle strength move in the same direction over the life span (16). Although it is debatable whether it is muscle strength or simply muscle mass that is important in determining bone strength and mass, is has been shown that muscle mass correlates positively with bone mineral content and bone mineral density (19). Thus, maintenance of adequate bone strength and density with aging is highly dependent on the maintenance of adequate muscle mass and function.

Role of muscle in the prevention of obesity

Whereas the role of muscle is central and obvious in syndromes such as sarcopenia and cachexia, which are defined—at least in part—by loss of muscle mass and strength, the potential role of muscle in the prevention of obesity is less well appreciated.

The development of obesity results from an energy imbalance over a prolonged time, which means that energy intake exceeds energy expenditure.

An effect on energy balance can therefore be achieved by altering either energy intake or energy expenditure. In our diet focused society, the energy intake side of the energy balance equation gets almost all the attention. This is unfortunate since variations in our energy expenditure are at least as important. After all, it is called “energy balance” which means that both sides need to be balanced at a healthy level. Just cutting back on our caloric intake will not put our energy balance at a healthy level. Instead it will just cause deprivation and frustration.

Total energy expenditure is the sum of resting energy expenditure (REE), the thermic effect of food, and the activity energy expenditure related. Our muscle mass, and the energy expenditure related to muscle metabolism, affects both resting and activity energy expenditure. The energy expenditure caused by physical activity is obvious; the more muscle we have, the higher workloads we can move, and the more calories we’ll expend. However, the energy expenditure caused by our resting metabolism can be quite significant too if we have an enlarged muscle mass. Let’s take a look at a simple calculation to illustrate this:

The mass and protein turnover rates of the body’s organs and tissues is pretty constant (4). In contrast, large variations in muscle mass are possible, and the rate of muscle protein turnover (ie, muscle protein synthesis and breakdown) may vary as well. The synthesis and breakdown of muscle protein are principally responsible for the energy expenditure of resting muscle.

The average muscle mass of young, healthy males to range from 35 to 50 kg (20). In contrast, an elderly woman may have less than 13 kg muscle. While the exact energetic of muscle protein turnover aren’t known, a conservative estimate can be done on the basis of muscle protein synthesis. For our male and old woman, the energy expenditure per day as a result of muscle protein synthesis may range from 485 kcal/d to 120 kcal/d (21-24). This is a quite large difference, and doesn’t even consider any increase in protein turnover caused by physical activity. Note that in this example the male is not a bodybuilder. Extremes in muscle mass, for example male body builders to frail elderly, would cause even greater differences in resting energy expenditure.

In terms of whole-body energy balance, a difference in resting energy expenditure of 365 kcal/d, stemming from a difference in muscle protein turnover, would lead to a gain or loss of 47 g fat mass/day, because 1 kg (2.2 lb) of fat stores 7700 kcal (25). If activity and diet remained constant, this would mean a gain or loss of 1.4 kg (3.1 lb) fat mass/month. This effect on energy balance is particularly striking when it is realized that the estimate given above for the energy expenditure associated with muscle protein turnover is likely an underestimate, because protein breakdown also requires energy. It is evident from these estimations that, when a long-term perspective is considered, even relatively small differences (eg, 10 kg = 22lb) in muscle mass could have a significant effect on energy balance. Every 10-kg difference in lean mass translates to a difference in energy expenditure of ≈100 kcal/day, assuming a constant rate of protein turnover. In considering the magnitude of energy imbalances leading to obesity, it is reasonable to view the situation over long periods of time, because obesity often develops over months and even years. A difference in energy expenditure of 100 kcal/day translates to ≈4.7 kg (10.3 lb) fat mass/year. Thus, the maintenance of a large muscle mass and consequent muscle protein turnover can contribute to the prevention of obesity.

The expanded muscle mass can be capitalized on to facilitate fat loss. It is evident from the calculations presented above that a stimulation of muscle protein turnover in the setting of increased muscle mass could have a significant effect on resting energy expenditure and thereby energy balance. This can be accomplished through nutrition, because increasing amino acid availability, through and increased protein intake, increases muscle protein turnover (26).

What’s interesting is that the calories used to provide energy  for muscle protein turnover is largely derived from stored fat, because this is the preferred energy source of resting muscle (27). This has been confirmed in studies of testosterone injection in hypogonadal elderly men, in which increases in muscle protein synthesis and lean body mass over time was accompanied by a decrease in fat mass (28).

Bottom Line

Now you have some good and scientifically supported arguments to present when your friends and family members start complaining about your high protein intake and passion for training and growing muscle! And hopefully this information will also convince those women who are afraid to even touch a dumbbell, to start incorporate some resistance training into their routines.

I will leave the related topic of “how much muscle is adequate muscle” for another article and discussion. Hopefully studies will start to pop up in the near future on the relation of the fat free mass index (FFMA) and obesity and chronic diseases, and its importance for health and well being. For a low down of the fat free mass index and everything you ever wanted to know about body composition, see my looooong article over at www.trainergize.com

References:

1 Lenk K, Schuler G, Adams V. Skeletal muscle wasting in cachexia and sarcopenia: molecular pathophysiology and impact of exercise training. Journal of cachexia, sarcopenia and muscle. 2010 Sep;1(1):9-21.

2 Biolo G, Zhang XJ, Wolfe RR. Role of membrane transport in interorgan amino acid flow between muscle and small intestine. Metabolism: clinical and experimental. 1995 Jun;44(6):719-24.

3 Felig P, Owen OE, Wahren J, Cahill GF, Jr. Amino acid metabolism during prolonged starvation. The Journal of clinical investigation. 1969 Mar;48(3):584-94.

4 Matthews DE. Proteins and Amino Acids. In: Shils ME, Shike M, Ross AC, al e, editors. Modern Nutrition in Health and Disease. 10th ed; 2006.

5 Felig P. The glucose-alanine cycle. Metabolism: clinical and experimental. 1973 Feb;22(2):179-207.

6 Anderson RN, Smith BL. Deaths: leading causes for 2002. National Vital Statistics reports. : National Center for Health Statistics, 2005. (No. 17.); 2005.

7 Zamora E, Galan A, Simo R. [Role of myostatin in wasting syndrome associated with chronic diseases]. Medicina clinica. 2008 Nov 1;131(15):585-90.

8 Kung T, Szabo T, Springer J, Doehner W, Anker SD, von Haehling S. Cachexia in heart disease: highlights from the ESC 2010. Journal of cachexia, sarcopenia and muscle. 2011 Mar;2(1):63-9.

9 Lenk K, Erbs S, Hollriege R, et al. Exercise training leads to a reduction of elevated myostatin levels in patients with chronic heart failure. European journal of cardiovascular prevention and rehabilitation : official journal of the European Society of Cardiology, Working Groups on Epidemiology & Prevention and Cardiac Rehabilitation and Exercise Physiology. 2011 Mar 14.

10 Bamman MM. Regulation of muscle size in humans: role of myostatin? Journal of musculoskeletal & neuronal interactions. 2008 Oct-Dec;8(4):342-3.

11 Burton LA, Sumukadas D. Optimal management of sarcopenia. Clinical interventions in aging. 2010;5:217-28.

12 Evans WJ. What is sarcopenia? The journals of gerontology Series A, Biological sciences and medical sciences. 1995 Nov;50 Spec No:5-8.

13 Rolland Y, Dupuy C, Abellan van Kan G, Gillette S, Vellas B. Treatment strategies for sarcopenia and frailty. The Medical clinics of North America. 2011 May;95(3):427-38, ix.

14 Waters DL, Baumgartner RN, Garry PJ, Vellas B. Advantages of dietary, exercise-related, and therapeutic interventions to prevent and treat sarcopenia in adult patients: an update. Clinical interventions in aging. 2010;5:259-70.

15 Fearon K, Evans WJ, Anker SD. Myopenia-a new universal term for muscle wasting. Journal of cachexia, sarcopenia and muscle. 2011 Mar;2(1):1-3.

16 Frost HM. On our age-related bone loss: insights from a new paradigm. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. 1997 Oct;12(10):1539-46.

17 Ducher G, Jaffre C, Arlettaz A, Benhamou CL, Courteix D. Effects of long-term tennis playing on the muscle-bone relationship in the dominant and nondominant forearms. Canadian journal of applied physiology = Revue canadienne de physiologie appliquee. 2005 Feb;30(1):3-17.

18 Pang MY, Eng JJ. Muscle strength is a determinant of bone mineral content in the hemiparetic upper extremity: implications for stroke rehabilitation. Bone. 2005 Jul;37(1):103-11.

19 Szulc P, Beck TJ, Marchand F, Delmas PD. Low skeletal muscle mass is associated with poor structural parameters of bone and impaired balance in elderly men–the MINOS study. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research. 2005 May;20(5):721-9.

20 Tipton KD, Borsheim E, Wolf SE, Sanford AP, Wolfe RR. Acute response of net muscle protein balance reflects 24-h balance after exercise and amino acid ingestion. American journal of physiology Endocrinology and metabolism. 2003 Jan;284(1):E76-89.

21 Newsholme EA. Substrate cycles: their metabolic, energetic and thermic consequences in man. Biochemical Society symposium. 1978(43):183-205.

22 Waterlow JC. Emerging aspects of amino acid metabolism. Where do we go from here? The Journal of nutrition. 1994 Aug;124(8 Suppl):1524S-8S.

23 Waterlow JC. Whole-body protein turnover in humans–past, present, and future. Annual review of nutrition. 1995;15:57-92.

24 Waterlow JC. Protein Turnover. 1st ed: CABI; 2006.

25 MaArdle WD, Katch FI, Katch VL. Sports and Exercise Nutrition: Lippincott Williams & Wilkins; 2008.

26 Paddon-Jones D, Sheffield-Moore M, Aarsland A, Wolfe RR, Ferrando AA. Exogenous amino acids stimulate human muscle anabolism without interfering with the response to mixed meal ingestion. American journal of physiology Endocrinology and metabolism. 2005 Apr;288(4):E761-7.

27 Rasmussen BB, Wolfe RR. Regulation of fatty acid oxidation in skeletal muscle. Annual review of nutrition. 1999;19:463-84.

28 Ferrando AA, Sheffield-Moore M, Yeckel CW, et al. Testosterone administration to older men improves muscle function: molecular and physiological mechanisms. American journal of physiology Endocrinology and metabolism. 2002 Mar;282(3):E601-7.

About Monica Mollica > www.trainergize.com

Monica Mollica has a Bachelor’s and Master’s degree in Nutrition from the University of Stockholm, Sweden, and is an ISSA Certified Personal Trainer. She works a dietary consultant, health journalist and writer for www.BrinkZone.com, and is also a web designer and videographer.

Monica has admired and been fascinated by muscular and sculptured strong athletic bodies since childhood, and discovered bodybuilding as an early teenager. Realizing the importance of nutrition for maximal results in the gym, she went for a major in Nutrition at the University.

During her years at the University she was a regular contributor to the Swedish bodybuilding magazine BODY, and she has published the book (in Swedish) “Functional Foods for Health and Energy Balance”, and authored several book chapters in Swedish publications.

It was her insatiable thirst for knowledge and scientific research in the area of bodybuilding and health that brought her to the US. She has completed one semester at the PhD-program “Exercise, Nutrition and Preventive Health” at Baylor University Texas, at the department of Health Human Performance and Recreation, and worked as an ISSA certified personal trainer. Today, Monica is sharing her solid experience by doing dietary consultations and writing about topics related to bodybuilding, fitness, health and anti-aging.

Muscles – not just for bodybuilders! is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

Caffeine – a compound in the methylxanthine family – has its effects through various mechanisms on the central nervous system, and to be honest, I doubt those mechanisms are of great interest to most readers, so I won’t bother with an extensive discussion on it here. Suffice to say, caffeine positively impacts memory, performance, endurance, coordination and increases arousal, vigilance, while reducing fatigue, to name a few effects. Anyone who has used straight caffeine knows the stuff works, which is why the military, for example, adds it to gum as well as other things like bars and such. We all know the “energy drink/shot” category is all the rage these days even outside the gym setting. Although caffeine is not for everyone to be sure, it’s amazingly non-toxic. OK, so users of caffeine either know all this, or have at least experienced it, and don’t need much convincing it’s effective stuff for its intended uses. Let’s move into the more interesting info of this article, shall we?

Coffee Vs. Caffeine

Here’s where things get interesting, at least to science nerds like me. Most people think of coffee and caffeine as essentially interchangeable terms with the same effects. However, caffeine and coffee have very different effects and when we discuss the various positive effects of caffeine on performance or mental acuity, we are in fact talking about straight caffeine vs. coffee. That reality often comes as a surprise to many, but it’s true. Caffeine and coffee have different effects and it’s straight caffeine that has the pronounced effects on performance, mental acuity, and others briefly outlined above.

Studies have been carried out that used coffee matched for caffeine content vs. pure caffeine, and find it’s the straight caffeine that has the major impact on what we all generally associate with caffeine. Probably the most extensive study that compares coffee to caffeine was entitled Metabolic and exercise endurance effects of coffee and caffeine ingestion (1). This study found in a nutshell:

“…This study was designed to compare the metabolic and exercise endurance responses to the ingestion of the same amounts of caffeine as a coffee beverage and as pure caffeine with water. The caffeine was consumed in the same volume of coffee or water in the same period of time. It resulted in very similar plasma concentrations of plasma methylxanthines [meaning the caffeine appeared to be absorbed equally from the different sources], but only when it was consumed independent of coffee was there an enhancement of endurance. In addition, in this trial the initial impact on circulating epinephrine [adrenaline] concentration was greatest. Thus it appears that some component(s) in coffee interferes with the normal ergogenic response of caffeine.”

So for the non-science readers, what does the above mean? Essentially, coffee matched for caffeine content to caffeine capsules failed to have the same effects on adrenaline response (feeling “jacked up”) and endurance as straight caffeine. “Why is that, Will?!” is the obvious thought you have! No, I’m not a mind reader, just the obvious question.
Coffee is a complex biological substance with literally hundreds of compounds that are dissolved along with caffeine during the brewing process, all of which ends up in your coffee mug. Some of these compounds have effects completely separate from caffeine, and more important to this article, effects that appear to counteract the effects of caffeine. Besides the more obvious stuff found in coffee (e.g., lipids, carbohydrates, and proteins) you find compounds of potential metabolic importance, such as nicotinic acid, opiate-receptor antagonists, and cholinomimetics (agents that exert an effect “opposite” to adrenaline). Interestingly one group of researchers isolated a cholinomimetic compound from both regular and decaffeinated coffees that, when injected  into rats, resulted in decreases in heart rate and blood pressure. Thus, a compound that has direct counter regulatory effects to that of caffeine (and adrenaline).

Additional support for that is the fact these researchers also added pure caffeine to decaf coffee matched for dose to straight caffeine, and the effects were still inferior to caffeine alone on performance as well as other effects one usually associates to coffee vs. caffeine. According to the researchers from the above paper, “One possibility to account for this difference is that one or more of the multitude of compounds in coffee beverages antagonize the actions of caffeine, resulting in a reduced response.”
We know what the caffeine antagonist is in tea (from Camellia sinensis—the leaves that make white, green, oolong, and black teas). It is called L-theanine and you can buy it as a stand alone dietary supplement, and it’s also in some “relaxing” drinks and supplements. L-theanine combined with caffeine reduces both the blood pressure elevation and the alertness boosting effects of caffeine alone (2).

Caffeine Content of Coffee

As the previous section outlines, if you want to enjoy your cup of coffee because it tastes good, and gives you a coffee buzz – that’s likely due to a variety of naturally occurring compounds in the coffee in addition to the caffeine – go for it. I won’t be giving up my mug of strong morning coffee either. However, if you are looking specifically to get the known effects of caffeine on performance, increased alertness, etc., use straight caffeine.
Even if you are attempting to drink coffee for its caffeine content, that’s a hit or miss strategy. Researchers visited a variety of specialty coffee store for 6 consecutive days and tested a wide range of coffees and found the caffeine content varied considerably (3). According to these researchers:

“There was a wide range in caffeine content present in caffeinated coffees ranging from 58 to 259 mg/dose. The mean (SD) caffeine content of the brewed specialty coffees was 188 (36) mg for a 16-oz cup. Another notable find is the wide range of caffeine concentrations (259-564 mg/dose) in the same coffee beverage obtained from the same outlet on six consecutive days.”

So the same cup of coffee purchased from the same vendor (Starbucks) over six consecutive days ranged from 259 to 564 mg of caffeine!!! That’s like power gulping 3.2 to just over 7 small cans of Red Bull®—over 15-30 minutes (see below). If you want to try and experiment to confirm what the earlier mentioned study found regarding the different effects coffee has from straight caffeine, try 600mg of pure caffeine some time. Your head may explode, but you will never doubt again what an equal amount of caffeine feels like that can be found in a really strong cup of coffee.

So What About the Energy Drinks?

The “energy drink” category is all the rage these days, and cans of Red Bull and others of the ilk fly off the shelves. This has proven to be a very profitable market segment for sellers of these products. There’s nothing inherently problematic with them, but to get your 80mg of caffeine (the dose listed for Red Bull for example) you have to ingest additional stuff you may not want, be it sugar, various synthetic sweeteners, etc. and you are paying an exorbitant amount per serving compared to what you get from them.  Bang for the buck, these products are generally a poor deal in my view.

The same researchers who measured the caffeine content in coffees did a separate study and examined the caffeine content of a variety of sodas and energy drinks. Sodas such as Coke Classic had similar caffeine content to those energy drinks at the lower end of their caffeine content, such as KMX, which had 33.3mg of caffeine to Coke Classic’s 29.5mg but the caffeine content could vary. Interestingly, they found just 67mg of caffeine in a small can of Red Bull, a drop from the 80mg that is claimed to be inside (4) They summarize their findings:

“The caffeine content of 10 energy drinks, 19 carbonated sodas, and 7 other beverages was determined. In addition, the variability of the caffeine content of Coca-Cola fountain soda was evaluated…The caffeine concentration of the caffeinated energy drinks ranged from none detected to 141.1 mg/serving. The caffeine content of the carbonated sodas ranged from none detected to 48.2 mg/serving, and the content of the other beverages ranged from < 2.7 to 105.7 mg/serving.”

Take home is, I don’t have any beef per se with the energy drink/shot category of products, but I also don’t see them as a value for the money spent considering what you get, and I don’t like the taste of most of them (which admittedly is a subjective experience) and for me, they don’t make sense to spend money on.

Cost effective Caffeine

OK, so coffee is great stuff, but does not deliver the true caffeine experience, and energy drinks are, in my view, an overly expensive and unneeded method of getting caffeine. What next? A product called Fein came on my radar a few months back while at a show. I asked for some samples, tried it, and liked it It’s simplicity at its best: an inexpensive, essentially tasteless, easy to use way of getting pure caffeine when I want it—and it has zero calories and no artificial ingredients. It comes in a tiny packet of powder which can be used when and where I need it. At less then .50 cents per serving for a 75mg dose of caffeine that I can put into whatever I want, it’s a winner in my view.

Personally, I like to make my own energy drink before I go to the gym by mixing a packet of Fein and a packet of Crystal Light added to my water bottle, and I’m good to go. One can simply add Fein to water and have caffeine water. Hell, add it to oatmeal or a protein shake in the morning if you want.

As caffeine, usually via coffee and or energy drinks, is used by virtually all segments of society, I would say there are few who would not find this product both cost effective and effective for added energy, alertness, improved endurance, and other known benefits of caffeine.

Effective doses of caffeine varies widely with people, so some experimentation is needed. One study showed that a dose of pure caffeine as low as 12.5mg—in regular caffeine users—improved mental function. Generally speaking, for those who have been exposed to caffeine before – which is most human beings on the planet – 75 to 100mg is a good starting dose in my experience. Those particularly sensitive to stimulants, might try 25-50mg to start.

Obviously caffeine is a stimulant and, as with all stimulants, has its possible drawbacks, like insomnia if you take it too late in the day. Although caffeine has been shown to be exceedingly non-toxic, general warnings apply (like check with your doc before you take it if you have high blood pressure, are taking psychiatric drugs, or are pregnant), so make sure caffeine is right for you before proceeding.

Conclusion

That’s my report on my favorite type of product: effective, cheap, and well researched. Caffeine – particularly in the form of Fein – fits that bill for me. If you all give it a try, let me know your feedback to see if it jibes with my own experiences. People interested in Fein can get more info at their web site: www.GetFein.com

See you in the gym!

Cites:

(1)    Graham TE, et al. Metabolic and exercise endurance effects of coffee and caffeine ingestion. J Appl Physiol 1998;85:883-9.
(2)    Rogers PJ, et al. Time for tea: mood, blood pressure and cognitive performance effects of caffeine and theanine administered alone and together. Psychopharmacology 2008;195:569–77.
(3)    McCusker RR, et al. Caffeine content of specialty coffees. J Anal Toxicol 2003;27:520-2.
(4)    McCusker RR, et al. Caffeine content of energy drinks, carbonated sodas, and other beverages. J Anal Toxicol 2006;30:112-4.
(5)    Smit HJ and Rogers PJ. Effects of low doses of caffeine on cognitive performance, mood and thirst in low and higher caffeine consumers. Psychopharmacology 2000;152:167–73.

What You Need To Know About Caffeine is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness

The report outlines key nutritional interventions that may be of value to TBI. Below is the summery with link to download summery report as PDF file. What I found particularly interesting was the identification of creatine (among others) as a possible nutrient of benefit. I have written about creatine as a possible  Neurological Protection to brain injury and other insults:

A growing number of studies have found that creatine can protect the brain from neurotoxic agents, certain forms of injury and other insults.

Several in vitro studies found that neurons exposed to either glutamate or beta-amyloid (both highly toxic to neurons and involved in various neurological diseases) were protected when exposed to creatine.3 The researchers hypothesized that,

“… cells supplemented with the precursor creatine make more phosphocreatine (PCr) and create larger energy reserves with consequent neuroprotection against stressors.”

More recent studies, in vitro and in vivo in animals, have found creatine to be highly neuroprotective against other neurotoxic agents such as N-methyl-D-aspartate (NMDA) and malonate.4

Another study found that feeding rats creatine helped protect them against tetrahydropyridine (MPTP), which produces parkinsonism in animals through impaired energy production. The results were impressive enough for these researchers to conclude,

“These results further implicate metabolic dysfunction in MPTP neurotoxicity and suggest a novel therapeutic approach, which may have applicability in Parkinson’s disease.”5

Other studies have found creatine protected neurons from ischemic (low oxygen) damage as is often seen after strokes or injuries.6

Yet more studies have found creatine may play a therapeutic and or protective role in Huntington’s disease7, 8 as well as ALS (amyotrophic lateral sclerosis).9 This study found that

“… oral administration of creatine produced a dose-dependent improvement in motor performance and extended survival in G93A transgenic mice, and it protected mice from loss of both motor neurons and substantia nigra neurons at 120 days of age. Creatine administration protected G93A transgenic mice from increases in biochemical indices of oxidative damage. Therefore, creatine administration may be a new therapeutic strategy for ALS.”

This is only the tip of the iceberg showing creatine may have therapeutic uses for a wide range of neurological disease as well as injuries to the brain

The above is also dated and there’s been additional research since I wrote the above. If anyone wants the cites from the above, as well as a ton of additional info, you can download my report on creatine from “freebie” page HERE

Some topics covered where creatine may be of benefit:

* Sarcopenia
* Improve in brain function of healthy and damaged brains
* Modulate inflammation.
* Diseases effecting the neuro muscular system, such as muscular dystrophy (MD)
* Wasting syndromes/muscle atrophy
* Fatigue
* Gyrate atrophy
* Parkinson’s disease
* Huntington’s disease and other mitochondrial cytopathies
* Neuropathic disorders
* Various dystrophies
* Myopathies
* Various brain pathologies.
* May increasing growth hormone (GH) levels, to those seen with exercise
* Reduce homocysteine levels
* Possibly improving the symptoms of Chronic fatigue Syndrome
* Improve cardiac function in those with congestive heart failure

As well as the obvious athletic uses most associate with creatine

IOM Report Summery:

Nutrition and Traumatic Brain Injury: Improving Acute and Subacute Health Outcomes in Military Personnel

Released:
April 20, 2011
Type:
Consensus Report
Topics:
Food and Nutrition, Veterans Health
Activity:
Nutrition, Trauma, and the Brain
Board:
Food and Nutrition Board

Military personnel, especially those in combat zones, face a distinct risk of traumatic brain injury (TBI). The injuries can range from mild to severe, and their effects can appear within minutes or hours—or sometimes weeks or even years later. Although estimates of incidence and prevalence are elusive, some estimates suggest that TBI has accounted for up to one-third of combat-related injuries. TBI also is a major problem among civilians, especially those who engage in certain sports, with an estimated 1.6 to 3.8 million sports-related TBIs occurring annually. Despite such health tolls, the mechanisms and damaging effects of TBI on the brain are not fully understood. While some research has explained these mechanisms of injury, new information suggests that nutritional interventions could help in treating or even providing resilience against TBI.

In this light, the Department of Defense (DoD) asked the IOM to review the potential role of nutrition in the treatment of and resilience against TBI. Given the complexity of TBI and the current gaps in scientific knowledge, the IOM could identify only one action that can immediately improve treatment efforts: early feeding to patients with severe TBI. Research has shown that feeding the severely injured soon after an injury is known to help in decreasing mortality. In addition, new information suggests that nutritional interventions could help in treating or even providing resilience against TBI. The IOM identified a number of other possible benefits for specific nutritional interventions and recommends that the DoD and other collaborates conduct more research.

Creatine and Traumatic Brain Injury is a post from: The Final Frontier In Bodybuilding , Fat Loss, Health & Fitness