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marylin monroe
Showing posts with label SFA. Show all posts
Showing posts with label SFA. Show all posts

On Short Notice: Nucleotide Supplementation Increases Performance & Fortifies Immune Response. Plus: Oleic Acid Increases, SFA Lowers E2, Testosterone & DHT Binding

Are nucleotides a useful supplements for intensity maniacs and can olive oil reduce your free testosterone levels?
If you have been visiting the SuppVersity for a while now, you were probably surprised to see that the "Short News" (aka "On Short Notice") are back. The reason, I changed my mind and reintroduced this assembly of short news items is that I realized that there is an intemediate category of news and infos between the very short Facebook news that (a) disappear in the oblivion of the SuppVersity Facebook Wall, (b) don't allow me to post graphics that would illustrate the study results and (c) still take some time to write and the detailed analysis in the "original" SuppVersity articles.

So, if you disagree and can give me a good reason why I should not post news compilations like the one at hand more regularly, speak now or forever hold your peace ;-)

Nucliotide supplementation counters immune suppressive effects of exercise

(Ostojic. 2013) - I think I mentioned a similar study a couple of weeks ago in the SuppVersity Facebook News, but since this most recent investigation into the ergogenic effects of the small organic nitrogen-based combinations of a five-carbon sugar and a phosphate group that
  • form the building blocks of nucleic acids, such as DNA and RNA, and 
  • participate in cellular signaling and metabolism
deals with in young, healthy, fit men and their response to the provision of a supplement that looks similar to something you are probably goint to see on the market pretty soon, I thought it may be interesting enough to make it into this "news" article-format.
Figure 1: Illustration of the molecular structure of nuleotides (Sadava. 2000)
The supplement we are talking about is a combination of different nucleotides, i.e. cytidine 5′-monophosphate, uridine 5′-monophosphate, guanosine 5′-mono-phosphate and adenosine 5′-mono-phosphate from partially purified (90%) germinated barley seeds extracted during sporulation and the reason it's worth knowing what was in it, because it was able to ...
  • Want a quick performance fix? Use sodium bicarbonate | learn more
    significantly increase time to exhaustion (+7%)
  • ramp up serum levels of immunoglobulin A and
  • elevate the NKC cytotoxic activity
in the blood of the 14 recreationally active participants (age 22; BMI 24kg/m²; body fat 11%) who participated in a standardized incremental exercise test on the treadmill ("Run till you drop") after taking 50mg/day of this product for 2 weeks.

Oleic Acid Increases E2, Testosterone & DHT Binding

Not from Greece, the land of olive oil and eve's cheese, but from Spain comes a study that links Oleic acid, the mono-unsaturated fat from Olive oil to increases in SHBG. The researchers from the Universitat Autònoma de Barcelona analyzed the lab reports and nutrition data of a total of 315 men and observed that
"SHBG serum levels were significantly higher in subjects using olive oil for cooking in comparison with subjects using sunflower oil. The SHBG levels correlated positively with MUFA (p < 0.001) and negatively with saturated fatty acids (p = 0.003)." (Sáez-López. 2013)
Based on multiple regression analysis of the data, the scientists calculated that the amount of MUFA in the subjects' diets accounted for 20.4% of SHBG variance. Despite the fact that this means that your MUFA intake determines "only" 20% your SHBG levels, the data in Figure 1 (left), clearly indicates that these 20% show pretty significant correlations with important health markers.
Figure 2: Correlation between SHBG levels and BMI, MUFA intake (in % total fat) and fasting blood glucose - left; correlation between phospholipid MUFA and SFA content and SHBG - right (Sáez-López. 2013)
In order to elucidate the underlying mechanisms, the scientists conduced an additional in-vitro study, in the course of which Sáez-López were able to confirm that oleoyl-CoA, a metabolite that's produced, when oleic acid is metabolized, downregulates PPAR-γ in the liver (HepG2 cells).

As a SuppVersity veteran, you'll know that any reduction in PPAR-gamma in the adipose tissue will result in a decreased propensity of fat storage (read up on it). In the liver, PPAR-gamma is  responsible for the production of SHBG, as well. In view of the fact that SHBG binds and deactivates* androgens and estrogens (*this is not essentially correct for all tissues!), your MUFA intake could thus be one of the set-screws that determine the level of unbound sex-steroids in your blood.
With 60-80% olive oil is one of the best sources of oleic acid and this is not a reason to stop consuming it - irrespective of T-binding (read more)
Bottom Line: Based on the currently available evidence it appears as if nucleotide supplements could have a future as immune and performance booster for intense training athletes.

Despite the fact that it is unlikely that there will be any side effects, (a) the increased immune activity, which could be a problem for people with auto-immune disease and (b) the non-existence of scientific evidence to support their long-time efficacy (and safety), I would wait and see how things develop before investing significant amounts of money in supplemental RNA / DNA precursor.

Something very similar is true for results of the Sáez-López study that investigated the "SHBG raising" effects of oleic acid. In view of the negative association between SHBG levels BMI and fasting blood glucose, which have, by the way, been observed in previous studies: Phillips & Gerald, for example, observed a significant negative correlation between SHBG and the waist / hip ratio in 55 obese men aged 21 to 70 (Philips. 1993). And while SHBG binds testosterone the small change will not render all your testosterone useless, so that you don't have to be afraid of sudden olive oil induced anti-virility effects ;-)

References:
  • Ostojic, Sergej M., Kemal Idrizovic, and Marko D. Stojanovic. "Sublingual Nucleotides Prolong Run Time to Exhaustion in Young Physically Active Men." Nutrients 5.11 (2013): 4776-4785.
  • Phillips, Gerald B. "Relationship between serum sex hormones and the glucose-insulin-lipid defect in men with obesity." Metabolism 42.1 (1993): 116-120.
  • Sadava, D. et al. Life: The Science of Biology, 9th ed. 2009
  • Sáez‐López, Cristina, et al. "Oleic acid increases hepatic sex hormone binding globulin production in men." Molecular nutrition & food research (2013).

PUFA Increases Postprandial Thermogenesis in Healthy Premenopausal Women & Beyond - 14% Increase Over MUFA & SFA Sounds Huge, But Does it Matter?

Is there something to the good vs. bad fat shenanigan, after all?
Only recently scientists from the Texas Tech University report that a PUFA-rich high-fat meal led to a greater diet-induced thermogenesis in normal-weight premenopausal women compared with SFA- or MUFA-rich high-fat meals.

Reason enough to take a closer look at this and previous studies investigating the diet-induced thermogenic effects of PUFA-, MUFA- and SFA-rich meals and to conduct a reality check wrt to the question whether these differences actually matter - I mean, will you get and stay lean by upping your PUFA intake? Let's take a look!
You can learn more about fat at the SuppVersity

Are Men Fat- & Women Sugar-Cravers?

Fat, not Fructose Cons. Increased in the US
Adding Fats to Carbs Does not Reduce Insulin

The Forgotten Pro-Insulinogenic Effects of SFAs

Margarine Not Butter Incr. EU Waists

Low Fat to Blame for Low Vitamin D Epidemic?
In the initially mentioned study, Hui C. Clevenger, Amanda L. Kozimor, Chad M. Paton and Jamie A. Cooper explored the effect of three HF meals enriched with different fatty acids (MUFAs, PUFAs or SFAs) on metabolism in premenopausal women of normal weight. In that, the metabolic parameters of interest included postprandial energy expenditure (EE), which is then used to calculate DIT, and substrate oxidation, which included respiratory exchange ratio (RER), fat oxidation and carbohydrate (CHO) oxidation.

Based on previous research in men of normal weight, the Texas Tech researchers hypothesized that the diet induced thermogenesis (DIT) and fat oxidation would be the highest after the PUFA- and MUFA-rich meals and lowest after the SFA-rich meal in premenopausal women - a result of which you already know that it was only partly confirmed.
Figure 1: Diet-induced thermogenesis and respiratory exchange rate (higher RER = lower fatty acid oxidation vs. higher CHO oxidation) in the 5h after the test meal (Clevenger. 2014)
The data in Figure 1 does after all tell you that the expected MUFA-induced increase in diet-induced thermogenesis did not occur. PUFAs, on the other hand did the job, Clevenger et al. expected them to do. They increased the DIT by an ostensibly whopping 14% over the DIT the scientists observed in response to the ingestion of the high MUFA and SFA liquid meals that had been prepared with the same base of 8 fl oz (237 ml) of chocolate Ensure(R) with soy lecithin and Nesquik (R, but contained different additional dietary fatty acids added depending on the treatment condition:
  • Table 1: Liquid meal nutrient composition
    breakdown (Clevenger. 2014).
    The PUFA-rich meal was ‘base’ plus sunflower oil and flaxseed oil, with 42% of total energy coming from PUFA.
     
  • The MUFA-rich meal was ‘base’ plus canola oil and extra virgin olive oil, with 42% of total energy coming from MUFA.

  • Finally, the SFA-rich meal was ‘base’ plus butter, coconut oil and palm oil, with 40% of total energy coming from SFA. 
As the data in Table 1 indicates, the nutrient profiles didn't differ much. The fatty acid composition, on the other hand did, with the SFA meal being the only one with measurable amounts of Butyric, Caprioc, Caprylic, Capric, Lauric, Myristic and Hepatedic acid. Fatty acids of which previous research indicate that they induces an obesity-linked proinflammatory gene expression profile in adipose tissue of subjects at risk of metabolic syndrome (van Dijk. 2009).

High MUFA diets, on the other hand, have been shown to potentiate the effects of weight loss in obese NIDDM patients (Low. 1996). They are the major group of fatty acids in the one oil, everyone appears to agree that it's health (Olive oil). And last but not least, even the allegedly unhealthy omega-6s have been shown in randomized controlled to reduce liver fat and modestly improve metabolic status, without weight loss, when compared to high saturated fat diets (Bjermo. 2012).

All of these effects / this evidence could potentially be more important than the increase postprandial thermogenesis in the study at hand - so the ultimate question is: Does DIT even matter?
Now, does this increase in DIT matter? Westerterpet et al. who found a negative correlation between body fat levels and the diet induced thermogenesis in their 2008 study (Westerterpet al. 2008), certainly believe it matters. If we look at the total extra diet-induced energy expenditure in 5h after the test-meal in the study at hand, on the other hand, I cannot but ask myself, whether those 1.4kcal can actually make a difference.

I am not sure what you think, but considering the fact that you can burn those 1.4 extra calories in less than one minute in the gym, it's hard to believe that the increased thermogenesis alone warrants the layman's conclusion that the study at hand would provide evidence for the superiority ot PUFAs over MUFAs and saturated fats ... what do you think?
References:
  • Bjermo, Helena, et al. "Effects of n− 6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial." The American journal of clinical nutrition 95.5 (2012): 1003-1012.
  • Clevenger, Hui C., et al. "Acute effect of dietary fatty acid composition on postprandial metabolism in women." Experimental physiology (2014): expphysiol-2013.
  • Westerterp, Klaas R., et al. "Dietary fat oxidation as a function of body fat." The American journal of clinical nutrition 87.1 (2008): 132-135.

The Female(?) Athlete Triad - Part III/III: Road to Recovery! Step #2 = Accept There is No Magic Macronutrient Ratio

No need to raid another tomb, Lara, the quest for the one and only ideal macronutrient composition that will yield optimal results for the rest of your life ends here (img courtesy of Paramount)!
I am not planning to bore you with a longish summary of the previous installment(s) of this series, here. Still, I don't want to head on to the 2nd step of the "Road to Recovery", which is going to deal with the quest for the "optimal" macronutrient ratio, without a brief reminder of the central role of nutrient availability in both the etiology, as well as the recovery from the athlete triad - or, as Dr. Zanker from the Carnegie Research Institute at the Leeds Metropolitan University in the United Kingdom puts it, the simple fact that the "exercise associated reproductive dysfunction in women is attributable to deficits of readily available energy" (Zanker. 2006)

In a couple of more general remarks some of you have recently (not without good reason, by the way) criticized my excessive and in parts random use of mark-ups like bold print or underlining. In the introductory paragraph to today's post the word "readily" is however so important that the underlining is obligatory.

Your hypothalamus does not like to wait, therefore "readily" is the keyword, here!

It is after all the lack of appropriate readily available energy, primarily in the form of circulating glucose, liver glycogen, and adipose tissue triacylglycerol that precedes the low plasma insulin concentration and reductions in total body fat content and corresponding disturbance of leptin secretion, ghrelin, cortisol, thyroid and of course luteinizing hormone (see data in figure 1; the absolute levels from the healthy group may also serve as a reference to compare your own labwork to; mind the units!).
Figure 1: Hormonal and glucose metabolism (* indicates 24h values) of women with functional hypothalamic amenorrhea (not necessarily exercise induced) expressed relative to values in eumenorrheic control; values above the bars indicate the total values of the respective markers in healthy controls and may provide you with some orientation, when you are looking at your own bloodwork (data based on Loughlin. 1998)
In order to avoid / counter the reproductive and associated problems and break out of the vicious circle of the athlete's triad, Zanker proposes the following three steps (based on Zanker. 2006; yet with a couple of additions from my side): 
  • Avoid abrupt and rapid weight loss and maintain an “adequate” body fat content, which may be individually specific, but coincides with regular reproductive function.
  • Consume adequate amounts of energy to fuel your increased metabolic demands; never go below your resting energy expenditure, regardless of whether you  want to or even have to lose weight.
  • Make sure you get an adequate amount of carbohydrates either on a continuous (low GI carbs with every meal) or in a cyclic manner as part of a low(er)* carbohydrate diet with a baseline intake of 90-120g/day and additional carbs after every workout.
    *compared to the RDA of ~60% carbs
"Carbohydrates? But aren't those just making you fat?" With this very question that's now probably on the mind of one or two (or three ;-) of you, we did eventually arrive at the topic of this episode of the Athlete's Triad Series:
Is there a ideal macronutrient ratio that will prevent the onset
and help you get rid of the athlete's triad?
To be honest, I don't know the answer to this question... and although I had almost typed the word "yet" win the place where you now see the "..." , I must admit that I am not even sure if there actually is a definitive answer to this question. What I do have to offer, though, is a couple of things to keep in mind, when it comes to the macronutrient make-up of your diet.
  1. There is no such thing as a "bad" nutrient. There are about as many good arguments to vilify the overconsumption of protein, as there are arguments against the usual scapegoats, carbohydrates and fats.
  2. Glucose and saturated fats can be essential, too. Just because your body can produce carbs and saturated fats on its own, this does not mean that you do not have to, let alone should not eat them.
  3. The optimal macronutrient ratio will change over time - just like and in response to the way your physique, conditioning, lifestyle, training and general stress levels  will be changing. This implies that diet X, which may have worked magically for you, when you got rid of slabs of body fat is now that you are finally in the "normal range", let alone already so lean that your body's alarm bells are constantly ringing, hampering your progress.
And even if the previous comments on the importance of readily available energy and glycogen repletion would suggest that carbohydrates should make up the lion's share of the diet of any athlete trying to recover from the triad (or not to fall victim to it), an extreme high carbohydrate alone is neither guaranteed to solve the problem nor is it a sustainable way of eating you could stick to once you've "carbed" yourself out of the dark hole you have been digging over the past months.

Readily available energy? Does that mean I have to eat sugar all day?

Figure 2: Cortisol (left) and testosterone (right) levels in healthy men after 10 days on high protein vs. high carbohydrate diets (based on Anderson. 1987). Tegelman et al. report similar results from Swedish elite male Ice Hockey players after a reduction of fat and an increase in carbs (Tegelman. 2007)
On the one hand, we've known for over two decades that a high carbohydrate diet based on bread, vegetables, fruit, juices, pastry, and candy having a protein / carb / fat ratio of 10% / 70% / 20% will result in lower cortisol and higher testosterone levels (in men) than a high protein diet with a protein / carb / fat ratio of 44% / 35% / 21% that's based on lots of meat, fish, poultry, egg whites, and a liquid dietary supplement protein supplement (Anderson. 1987; see figure 2). On the other hand, a closer analysis of the data I compiled based on the tabular overview of pertinent studies on amenorrheic from the review by Manore (see figure 3 in the last installment) suggests that real.world advantage of carbohydrates depends on the deepness of the whole you already dug (the deeper the more advantageous) and your willingness / ability to cover or even surpass your daily energy requirements (the more you eat on a daily basis and in at least three square meals spread equally across the day, the less you will depend on the readily available energy from carbs).

Against that background, the high carbohydrate intake (62% of total energy from carbohydrates; nutrient ratio in grams 16% protein, 71% carbs, 14% fats) was probably necessary for the women in the eumenorrheic group with an energy intake of slightly less than 30g/kg body weight (figure 3, R5).
Figure 3: Macronutrient compositions (in kcal!) of amenorrheic and eumenorrheic women from 15 different studies (based on an overview in Manore. 2002)
For the eumenorrheic female athletes who were at, or way above the average mean energy intake of 35g/kg body weight, the "high" carbohydrate intake of 265g/day probably wasn't detrimental. On the other hand, it appears questionable, whether an increase in protein intake from 1.2g protein per kg of body weight to 1.5-2.0g/kg and a corresponding protein to carbohydrate ratio of 25% / 62% would not have been more facilitative to their goals (specifically if those include strength training). The same goes for both, the replacement of yet another part of the carbohydrate ration with an isocaloric amount of fats and the overall role of fats in the etiology of and the recovery from the athlete's triad.

The fat-phobia still loomed large, when the majority of studies was conducted

Part of the problem of reconciling theoretical considerations, such as the "availability advantage" of carbohydrates and the scarce and almost exclusively observational data based on which I compiled the overview in figure 3 of this, as well as the last installment of this series, is that eating patterns of both the eumenorrheic, as well as the amennorheic athletes was geared towards the dietary paradigm of the day. With "the day" being the late 1980s and 1990s, i.e. those years in which the fat-phobia literally climaxed, it should be obvious that the baseline diet was low in fat and high in carbs.

Against that background it should also be clear that anyone trying to "cut calories" would reduce the amount of fats, the "bad energy dense heart killers" and keep the intake of carbohydrates constant (=high). This is probably also, the reason that the ostensible disproportionate lack of fats in the diets of the amenorrheic women vanished, once I weighted the data with the number of participants.
Figure 4: Total dietary intake of protein, carbohydrates and fats (in g; left) and differences between women with and without regular menses (right); data expressed either as simple group averages or weighed for the number of study participants (same sources as figure 3)
The picture that emerges after this adjustment has been done (figure 4, right, light bars) is clear and stands in line with my initial remarks on the primary of readily available energy in the form of circulating glucose, liver glycogen, and adipose tissue triacylglycerol, of which at least the former are way more readily derived from carbohydrates than fats.

And even the triacylglycers do, as the name implies, require a certain amount of glucose for the glycerol backbone (could be produced in the liver from amino acids and/or fats, though) and a minimal amount insulin to be stored in the fat cells (can be secreted in response to high amounts of protein and fat, as well, though).

So no fats? Just carbs and some protein?

Yet though carbohydrates have the availability bonus and proteins are necessary to maintain, better even build muscle mass, you would be ill-advised to steer clear of all dietary fats and, even more so the many good foods that contain them. Not so much because of the "essential" polyunsaturated fatty acid, though. According to a study by Tomten and Høstmark the dietary intake of PUFAs in 20 female runners with regular (n=10) and irregular (n=10) menses (LH levels of 7.6 vs. 2.9 IU/l!) was not statistically different. The intake saturated fats (-28%) and even more the intake of MUFAs (-38%), on the other hand was (Tomten. 2009) and the corresponding total fat-intake of 1.1g/kg body weight was obviously not sufficient to maintain optimal hormonal levels in the presence of a training volume of 7.5h per week.

What about vegetarianism? I know a few of you won't like this, but unless you are at least ovo-lacto vegetarian, i.e. a person who eats dairy and eggs, you are going to have a hard time fueling your athletic endeavors appropriately. After all, vegetarianism is associated with hormonal and menstrual abnormalities even in the non-athletic population, when they are dieting (Pirke. 1986). If you combine a mild energy deficit, as it is often seen in vegetarian, let alone vegan athletes, simply because it's harder for them to cover their energy and specifically protein and fat requirements without guzzling omega-6 oils and soy shakes all day (both not advisable, by the way), it is actually not surprising that Benson et al. mention vegetarianism right along low calorie intakes, nutritional inadequacies and low body fat stores as one of the main contributers to the (female) athlete triad (Benson. 1996).
Now you can certainly argue that all this comes down to the energy density and the correspondingly lower overall energy intake and could have been compensated for, if the women with menstrual irregularities had simply eaten more carbohydrates. In view of the fact that they didn't do so, I can hardly refute this argument. On the other hand, we have seen in the previous installment that an overexpression of GH and ghrelin is in as much part of the problem as too little insulin and a pathologically high insulin sensitivity. And some more fat in the diet (alongside carbs / not as the sole energy source!) couId in fact come handy to get that back in check.

Moreover, having a carb to fat ratio of ~2:1 (in energy equivalents) and a baseline fat intake in the range  of 80-100g (total) as the female runners with regular menses in the Tomton sudy had, has the beauty of never having to throw away the egg yolks, being able to get your share of fatty fish, full fat dairy, Kerrygold butter, virgin coconut and olive oil and beef or better calf liver as well as nuts once in a while. This in turn will allow you not just to stay sane and flexible with your diet, but also to satisfy your need for all those vital micronutrients you won't find in any of E-number laden fat-reduced garbage from the "low fat" shelves at the supermarket.

You see, in the end it all comes back eating simply more of the usual suspects, many people would probably file under "a paleo diet with lots of (safe) starches & fruit to fuel the energetic demands of a hard working athlete", these days.

If we think of the hypothetical daily energy requirement of 2000kcal/day which is often used as a reference for the nutrition information on those products of which you are going to buy less in the future (most real foods don't have nutritional information printed on them, you know ;-), the corresponding "numbers" could be anywhere on a continuum
  • from 110g protein / 190g carbs / 100g fats, for someone without an endurance component in his workouts*, 
  • to 100g protein / 240g carbs / 80g fats for someone who has a major endurance component and / or follows a high volume lifting routine*
    *pre- and post workout nutrition are not included, here!
This approach would ensure that you get enough protein, appropriate amounts of readily available energy, mainly in the form of safe starches and fruit, quasi unlimited amounts of vegetables and so much fat that you don't have to resort to the devastating "chicken breast, rice and broccoli diet", which will only worsen your situation.


References:
  • Anderson KE, Rosner W, Khan MS, New MI, Pang SY, Wissel PS, Kappas A. Diet-hormone interactions: protein/carbohydrate ratio alters reciprocally the plasma levels of testosterone and cortisol and their respective binding globulins in man. Life Sci. 1987 May 4;40(18):1761-8.
  • Benson JE, Engelbert-Fenton KA, Eisenman PA. Nutritional aspects of amenorrhea in the female athlete triad. Int J Sport Nutr. 1996 Jun;6(2):134-45.
  • Laughlin GA, Dominguez CE, Yen SS. Nutritional and endocrine-metabolic aberrations in women with functional hypothalamic amenorrhea. J Clin Endocrinol Metab. 1998 Jan;83(1):25-32.
  • Manore MM. Dietary recommendations and athletic menstrual dysfunction. Sports Med. 2002;32(14):887-901.
  • Pirke KM, Schweiger U, Laessle R, Dickhaut B, Schweiger M, Waechtler M. Dieting influences the menstrual cycle: vegetarian versus nonvegetarian diet. Fertil Steril. 1986 Dec;46(6):1083-8.
  • Tegelman R, Aberg T, Pousette A, Carlström K. Effects of a diet regimen on pituitary and steroid hormones in male ice hockey players. Int J Sports Med. 1992 Jul;13(5):424-30.
  • Tomten SE, Høstmark AT. Serum vitamin E concentration and osmotic fragility in female long-distance runners. J Sports Sci. 2009 Jan 1;27(1):69-76.
  • Zanker CL. Regulation of reproductive function in athletic women: an investigation of the roles of energy availability and body composition. Br J Sports Med. 2006 Jun;40(6):489-90; discussion 490.

Demonized N-6 Pufas Surprisingly Ergogenic: Safflower Oil More Than Doubles Swimming Endurance of Aging Mice.

Image 1: Unexpectedly ergogenic - Carthamus tinctorius L., better known as "safflower", a highly branched, herbaceous, thistle-like annual.
As a regular visitor of the SuppVersity and/or listener of SuperHumanRadio, you will be familiar with my skepticism towards fish oil supplementation as the "good for all" wonder-supplement in an athletic population. You will also be familiar with studies such as Filaire et al. (2010) which showed increased MDA (malondyaldehide) levels (and thus more, not less toxic waste) in athletes receiving 600mg of EPA and 400mg of DHA for 6 weeks. Thusly, it may not come as a total surprise that Guihua Zhang and his colleagues the National Food Research Institute and the National Institute of Vegetable and Tea Sciences in Japan found that 12 weeks on a diet containing 6% fish oil reduced endurance performance in aged mice by -20%. What may be more surprising, though, is that the vilified n6-pufas from safflower oil more than doubled the rodents' endurance performance.
Video 1: Not the swimming test performed in the study, but maybe an explanation why mouse-oil might be good for fish, but not vice versa - or have you ever seen a mouse eating a fish?
In view of the fact that the mice in the lard group suffered a similar loss in endurance performance, it should be said that the overall effect of fish oil, as well as lard, could in fact have been a null-effect. In other words, contrary to safflower oil, fish oil and lard had no beneficial effect on swimming endurance, so that an age-related decline in swimming endurance would have become obvious. After all, the average mouse-life is no longer than ~100-150 weeks, so that another 12 weeks are quite a time-span for 52 weeks old mice. On the other hand, previous studies such as Shimomura et al. (Shimomura. 1990) and Rustan (Rustan. 1993) would point toward an overall negative effect of high SFA+MUFA (lard) and high N3-PUFA (fish oil) on fatty acid oxidation in skeletal muscle and subsequently (endurance) exercise performance.
In the study, 40 male Crlj:CD-1 (ICR) mice had been randomly assigned to one out of three groups with the 6% of fatty acids of their experimental diet coming from either lard (n=13), safflower oil (n=13) or fish oil (n = 14) for 12 weeks.
Figure 1: Effect of 12 weeks on diets with 6% lard, fish oil and safflower oil on swimming endurance of aged mice (data calculated based on Zhang. 2011).
As the data in figure 1 goes to show, the fat content of the diet, i.e. low PUFA (lard), high N3-PUFA (fish oil) and high N6-PUFA (safflower oil) had a profound impact on the swimming performance of the animals. In view of the fact that we cannot completely rule out that the "negative effect" of lard and fish oil were simply due to an age-induced decline in swimming performance (cf. red box above), the most important finding of this study is however the +113% endurance increase in the safflower group, and not so much the -20% performance decreases in the other groups in swimming endurance [if you asked me, it's a pitty that there is no control group on a mixed diet]
Figure 2: Effect of 12 weeks on diets with 6% lard, fish oil and safflower oil on lactate levels pre and post endurance exercise in aged mice (data calculated based on Zhang. 2011).
As Zhang et al. point out, this increase in endurance performance cannot be explained based on increases in muscle or liver glycogen stores, because scientists measured "[s]imilar glycogen storage and plasma glucose levels in sedentary mice in the three diet groups suggest". A better explanation relates to the significant differences in the accumulation of plasma lactate following swimming (cf. figure 2), where lactate levels were "significantly lower" in the safflower oil group than in the lard (+57%) and non-significantly higher in the fish oil (+14%) group.
These results imply that the improved endurance associated with dietary safflower oil may be due, at least in part, to glycogen sparing. The working skeletal muscle is not only the major site of lactate production but is also important for utilization of lactate, which is mainly removed by oxidation. The decreased accumulation of lactate observed in aged mice fed safflower oil could be due to increased lactate oxidation and subsequent utilization as an additional energy source during swimming.
Yet the effect on accumulation or utilization of lactate was not the only difference that may have contributed to the increase in swimming performance that was observed in the safflower oil group. As the researchers point out,
the significant increase in muscle and liver CPT activities and decrease in plasma NEFA levels observed following exhaustive swimming in mice fed safflower oil implies an upregulation of fatty acid metabolism in these mice.
The absence of these effect in the lard or fish oil fed animals suggest that "the safflower oil group may have increased fatty acid utilization for energy than the other diet groups". In that, it is particularly noteworthy that we are talking about a localized increase in CPT activity and consequent fatty acid oxidation in muscle tissue. The increased liver CPT in the fish oil group, on the other hand could have contributed to an overall negative effect of fish oil consumption on endurance performance that would have been corroborated by the established suppressive effect of N3PUFAs on fatty acid synthesis (Kim. 1999; Nakatani. 2004)  and lipid oxidation (Rustan. 1993), against the backdrop of which less fatty acids became available for and subsequently oxidized in skeletal muscle.
Image 2: Biological activities of IL-6 (illustration by Prof. Dr. Heinrich)
Not directly relevant to the endurance aspect, but nevertheless interesting is another result of the study, which is the absence, respectively statistically insignificant elevation of elevations in the inflammatory maker IL-6 in the exercised (non-existent) and sedentary (non-significant) mice on the safflower oil diet. A result the anti-n6-faction in the diet-guru camp will probably find surprising and which goes against previous findings by Moon et al. (Moon. 2003) and Garcia-Escobar (Garcia-Escobar. 2010) - on the other hand, this also means that it was not the increase in IL6, which has in human studies been shown to selectively stimulate lipolysis in skeletal muscle (Wolsk. 2010), that facilitated the increase in endurance performance.
If and in what extent the reduction in plasma ferritin (fe) levels in the fish oil group (-13% sedentary; -24% exercised; both compared to lard, with slightly greater reductions compared to safflower oil) could have been an additional factor in a complex equation of substrate availability, usage and enzyme activity which could eventually explain the perfomance increases and decreases in the different groups is questionable. After all, the fe levels in the lard and safflower oil groups were virtually identical.

So, what would be the overall lesson, we can learn from the results of this study? Fish oil is poison, safflower oil liquid gold? Probably not. Yet, while it may still be questionable in how far the mouse metabolism is a good model for the human one, the inhibition of fatty acid synthesis and the increased fatty acid oxidation observed in mice as a consequence of fish oil feeding is present in humans, as well. Moreover, I assume you would agree that not everything that would be beneficial for the average sedentary borderline to morbidly obese inhabitant of the Western Hemisphere, is equally beneficial for performance-oriented athletes - or would you suggest 200 meter sprinters start swallowing statins and blood pressure medications? So, wouldn't it be remotely possible, then that a physical culturist (as I hope you would consider yourself to be one) would be much better off with a reasonable amount of those "nasty" n6-PUFAs in his/her diet to keep the fire in the mitochondrial furnace of his/her muscles in full blast? If you want to, ask your guru about it ;-)

On Short Notice: Worst Transfat Offenders Cookies & Co + Cinnamophilin For Joints + Tomato Powder Battles Cancer Like Aspirin + Creatine Protects Cell Walls + Carboholism Starts in the Womb, Intermittent Fasting Helps... + More!

Image 1 (lecker.de): They may look cute and harmless, but they are just one of the many incarnations of the worst transfatty acids offenders in the diets of the "average American" cake, cookie and pastry lovers. Believe it or not: Some of them manage to eat almost 100g of the proatherogenic fats per day (!)
Saturday and therefore time for a handful of "On Short Notice" news. We've got some ground to cover, today, so let's get started right away: We will start out by taking a look at the joint-healing / -protective effects of cinnamophilin, a compound from the roots of the cinnamomum trees. We will reconsider the importance of adiponectin for the non-obese physical culturist, switch from aspirin to tomato powder as our cancer prevention "drug" of choice and re-appreciate the newly discovered cell-protective value of a supplement 90% of you are probably already taking: creatine! Once we are done with that we revisit the potential connection between chronically low blood glucose, chronic catecholamine over-expression and the chronic fatigue syndrome. We will then take a look at how high carb diets and intermittent fasting of pregnant rats program the orexin A expression in the brains of their offspring and how that can predispose them to become obese.

During a brief water-break we will discard the idea of hyperhydration as idiotic and decide against carrying another kg of water weight around for the rest of this installment of "On Short Notice". Eventually we will reject pulses as a new staple diet food due to their potential to damage our gut mucosa and their strange gender-specific effects on insulin release and shake our heads over the average and not so average American's daily trans-fatty acid intake, which borders - in some cases - the 100g (!) ceiling of unhealthy absurdity.
  • Image 2: I must admit that I am not 100% sure if you would see similar benefits from regular cinnamon, not just because it is probably not from Cinnamomum philippinense, but also because the active ingredieant cinnamophilin has originally been extracted from the roots of the tree, not it's bark, which is what regular cinnamon is made from - it is obviously likely that some, yet probably lower amounts, would also be contained in the bark and a teaspoon of regular cinnamon probably won't hurt, anyway (cf. Wu. 1994 and Lu. 2012)
    Do your joints a favor and dig up some cinnamomum roots. While I am honestly not sure if cinnamophilin content of regular cinnamon (-bark) vs. Cinnamomum philippinense (nor whether this stuff is even in the bark, which is the raw material for "regular" cinnamon - a paper by Wu would suggest that it is extracted from the roots; cf. Wu. 1994), as it was used in a recently published study from College of Medicine, Taipei Medical University, will be sufficient, it is relatively certain that the anti-inflammatory effects of this highly lipophilic antioxidant and free radical-scavenging agent, which has also been shown to inhibit thromboxane synthase and the thromboxane A2 receptor (means it will reduce unwanted blood clots; Yu. 1994), to block Na+ and Ca2+ inward currents in rat cardiac cells (means it helps to protect the contractile function of your heart; Su. 1999), and to reduce brain infarction and protect against transient focal cerebral ischemia (rodent studies by Lee. 2005 & 2009), would silence any ongoing joint inflammation.
    And while Ju et al. can only speculate about the exact mechanism it appears to involve the modulation of NF-κB or ERK/p38 MAPK downregulation and/or suppresion of p-c-Jun pathways. Since both are involved in the etiology of other inflammatory, degenerative diseases, as well, it appears almost certain that there will soon be more exciting applications for yet another medicinal component from your kitchen cupboard.
  • Adipokines are not necessarily your friend - not even adpinonectin: Despite being the latest and (supposedly) greatest of the powerful cytokines that are released from your body fat, may keep you healthy when you are fat, it's negative correlation Pisto et al. observed in an epidemiological cross-sectional study involving 54 normotensive, non-smoking men with normal OGTT, clearly suggests that increasing adiponectin expression probably ain't the best way to get big and buffed (Pisto. 2012). Rather than that, you better diet and work out till you are big and buffed and wait for adiponectin (and leptin, which was by the way not significantly correlated with muscle size after adjustment for total adiposity) to fall in place.
  • Image 3: Tomato(powder)'s aspirin-like anti-cancer effects could be another reason for the health benefits of the so-called Mediterranean Diet
    Tomato powder mimics aspirins cancer protective effects At least in the gastrointestinal tract the COX-2 inhibition of tomato powder appears to exert similar protective effects against colorectal cancer (Tuzcu. 2012); and in view of the fact that the rodents in the Turkish study were fed a 5% enriched chow you would however not even have to consume tons of it - 90g or 1.14g/kg body weight would suffice ;-) If that's still more than you want or can stomach, just eat more tomatoes and/or (even better) tomato paste, which is quasi the water-containing version of the dry extract.
    And if you can't do tons of either, don't forget: Just like all the bad junk that may not be a problem if you ingested just junk A and maybe junk B, from time to time, becomes really nasty once C, D, E, etc. join the assault, it may be the pound of tomatoes you ate over the course of the last 2 weeks that helped you to avoid that the literal last straw that would otherwise not have broken the camel's but your back.
  • Figure 1 : Lipid vesicle permabilization after exposure to melittin + (1) NaCl , (2) 100 mM DMBG), (3) Creatine, or (4) PCr (Tokarska-Schlattne. 2012).
    (Phospho-)Creatine protects lipids in cell walls! In their latest paper a group of French and Swiss researchers report that they demonstrated for the first time that phosphocreatine (PCr), the explosive power, short-term energy substrate you are trying to increase, when you are taking creatine (monohydrate or whatever else), is more than just an energy source (Tokarska-Schlattne. 2012). As the data in the figure 1 shows, it has direct protective effects on the lipid fraction of your cells as well. And while this observation does not make creatine a bit more effective, it does provide another piece to the puzzle that explains why it is also useful in so many sports-unrelated areas such myopathies and a plethora of neurodegenerative diseases.
  • Constant subphysiological glycemia (= hypoglycemia without symptoms) could be the reason that you centrally fatigue, after all the constant elevation of epinephrine and glucagon, Ana María Arbeláez and her colleagues observed in a cleverly conducted study, where they limited the glucose levels in 8 healthy human volunteers to 65 mg/dL (3.6 mmol/L) for two hours showed a constant elevation of epinephrine and glucagon (Arbeláez. 2012). That the latter will only work for so long hardly suffice to keep you functioning normal (by no means optimal) should be clear... So how do you prevent that? Don't overtrain, don't undereat, don't eat only protein and don't be f***ing scared of eating as much carbs and fats, as you need to fuel an active lifestyle (Arbeláez. 2012).
  • Figure 2: Orexin A expression in the PvNP in the offstring of rat dams on different pregnancy diets
    You have the choice: Obese or normal kids? It all depends on the way you eat during pregnancy, at least that is the result of a soon-to-be-published study in Brain Research (, which found that compared to the normal pregnancy diet, a diet with an extra load of carbohydrates lead to a lower body weight at birth, but increased orexin A expression in the parvocellular part of the paraventricular nucleus (PvNP) which predisposed the rat pubs of the high carb dams to gain weight at a faster rate and catch-up and overtake the rodents from the control group after no more than 9 weeks.
    Another 10 weeks later, the rodents born to rats in the high carb group were already the heaviest of the four experimental groups and still as hungry as before.
    Now that alone would not necessarily make a SuppVersity news, if the scientists had not, without even noticing made a (imho) very relevant discovery. In addition to the group with free access to normal chow, they had another group which mimicked the time-restricted feeding pattern in the high fat and high carb groups, who received their chow only within a fixed 6h window, which would essentially equate to intermittent fasting; and while I doubt that the results reach statistical significance, it is still quite telling that the pubs born to the intermittently fastest (IF) rats on the regular diets, were normal weight at birth, had the lowest orexin A (hunger signal expressed in the brain) expression in the PvNP and were subsequently the lightest at the 19 week weight in...
    I still wouldn't suggest you start to fast intermittently, just because you notice you are pregnant, after all we don't know whether or how this translates to humans and if the pubs of the IF-dams were not simply undermuscled and therefore exhibited a lower body weight.
  • Image 4: As long as you got a couple of tables with water, sugary electrolyte bevarages, or even better salted coconut water along the roadside, you don't need to carry another 2lbs of water weight with you on your 1/2 marathon races.
    If you want to carry another kilo of useless weight around in the heat, go on and practice hyperhydration, otherwise you better stick to a bottle of water with some salt and sugar in it on your next 18km TT run in the heat (and cold). This is the actually not very surprising take home message of a recently conducted randomized cross-over trial from the University of Sherbrooke, in Canada, in the course of which Pierre-Yves Gigou and his colleagues investigated the effects of hyperhydration (=water loading) with 26 mL/kg bodyweight of a 130 mmol/L sodium solution before four successive 4.5 km blocks alternating between 2.5 km at 1% and 2 km at 6% gradient on a treadmill (Gigou. 2012).
    For the well-trained triathletes in the study, it did not make a difference whatsoever, as long as they could guzzle away their 500ml of gatorade during the 80-90min of running they were fine.
  • Are pulses superfoods, for women only or simply not suitable for daily consumption? It appears that similar to their nasty brethren, the soybeans, yellow peas, chickpeas, navy beans and lentils have the potential to become e hip diet food that could do more harm than good, especially to its male consumers. In a recently conducted study, a group of researchers from the University of Toronto found that pulses can help both men and women lose weight without prescribed caloric restriction (Mollar. 2012).
    Image 5: Pulsing of protein is something you are familiar with, but what about eating pulses.. yeah, we are talking about yellow peas, chickpeas, navy beans and lentils; that stuff your grandma maybe told your patents to eat from time to time. Are they the good twin of the evil soy bean?
    Contrary to the subjects in the calorically restricted "control" arm (-500kcal/day) of the study, the overweight or obese (mean BMI 32.8 kg/m²) adults in the pulse group, who were provided with a whopping dose of five cups of pulses per week (on average 896 g/week), had reduced their energy intake ad-libitum to about the same level as their peers "involuntarily" and accordingly seen similar reductions in body weight, waist circumference, systolic and diastolic blood pressure (statistical significance for intergroup differences were non-significant, i.e.  p >> 0.05, for all). At the end of the 8 week period there were however a couple of unwanted side-effects: While the minimal increase in HDL form the pulses would certainly count as a plus, increasing  C-peptide levels already suggest that there appears to be a problem with the glucose management in the pulse-eaters.
    And in fact, while the average female participants insulin AUC (the area under the insulin curve is a measure for the total amount of insulin the pancreas spills out in response to an oral glucose tolerance test, as it was performed in the study at hand) did go down by 13.9%, there was a profound increase (27.3 % in males) in the male pulse eaters.
    Figure 3 (radiancenutrition.com): Daily consumption of pulses appears appears to entail the risk of developing leaky gut.
    And even the women would have been better off (at least from a glucose tolerance perspective) without their yellow peas, chickpeas, navy beans and lentils - on the classic diet, they lost the same amount of weight and improved their insulin response by 24.2% and thus still 19.4% more than the men (the men had a reduction of -4.8 % in insulin AUC) and 10.3% more than with the pulse diet. I am therefore not convinced whether the scientists' euphoric conclusion that the "frequent consumption of pulses in an ad libitum diet reduced risk factors of the MetSyn [metabolic syndrome] and these effects were equivalent, and in some instances stronger, than counselling for dietary energy reduction" is not a little too optimistic - and that despite the fact that the HOMA-IR Mollar et al. reference as their indicator of improved insulin sensitivity suggests that they may be right...
    And before I forget it, the significant, but still meager improvements in LDL scientists from the University Saskatchevan report in another pulse diet study from the same supplement to the British Journal of Nutrition involving only elderly subjects would not convince me to eat 2x150g of beans, chickpeas, peas or lentils every day, either (Abeysekara. 2012) - why? Contrary to Whitlock et al. who are apparently not very concerned about the "abrasive" effect of pulses on the thickness of the mucosa in the gut (-25% in rodent experts; cf. Whitlock. 2012), I am not going to open up my "internal doors" to foreigners for a minuscule reduction in LDL, alleged improvements in glucose metabolism (see above) and some weightloss that comes about because you are so bloated that you become anorexic by twice let alone thrice daily pulse consumption.
  • Figure 5: Fat, TFA intake across age groups and sources (Kris-Etherton. 2012)
    Transfats (TFA): Cakes, cookies, pies and pastries are the worst offenders That's the unsurprising finding of the latest analysis of data from the National Health and Nutrition Examination Survey (NHANES; data from 1999-2002; Kris-Etherton. 2012). Among the 16,669 individuals (age ≥3 years) the median TFA intake was 2.3 % of calories (5 g/day) with 0.9–4.5 % of energy (1.5–13.1 g/day) over different quintiles of intake. The mean (that's the arithmetic mean vs. just the value right in the middle, which is the median) TFA intake was 2.5 % of energy (6.1 g/day).
    The overall range of TFA intakes in the highest quintile was almost crazily broad and ranged from already health compromising 8.8 up to 92.4 g/day. In view of the fact that the lions-share of this shit (sorry, but I just can't find a better name for it) came from cakes, cookies, pies, and pastries, the easiest solution to the problem and a major relief to the future public health insurance system in the US would be to ban this junk from the supermarkets or at least require the use of TFA-free and heat-stable fats in their production... but I think we all know that this is not going to happen, anytime soon.
"What? That's it, already?" If that's what you are just thinking I suggest you take a detour to the SuppVersity Facebook Wall and check out how Citrulline may protect your brain from aging, how your heart might protect itself by becoming insulin resistant and many other recent news from the realms of exercise, nutrition and health science!

References
  • Arbeláez AM, Rutlin JR, Hershey T, Powers WJ, Videen TO, Cryer PE. Thalamic Activation During Slightly Subphysiological Glycemia in Humans. Diabetes Care. 2012 Aug 13.
  • Abeysekara S, Chilibeck PD, Vatanparast H, Zello GA. A pulse-based diet is effective for reducing total and LDL-cholesterol in older adults. British Journal of Nutrition. 2012; 108:S103-S110.
  • Beck B, Richy S, Archer ZA, Mercer JB. Early and persistent up-regulation of hypothalamic orexigenic peptides in rat offspring born to dams fed a high-carbohydrate supplement during gestation. Brain Research. 17 August 2012.
  • Gigou PY, Dion T, Asselin A, Berrigan F, Goulet EDB. Pre-Exercise Hyperhydration-Induced Bodyweight Gain Does Not Alter Prolonged Treadmill Running Time-Trial Performance in Warm Ambient Conditions. Nutrients. 2012; 4(8):949-966.
  • Kris-Etherton PM, Lefevre M, Mensink RP, Petersen B, Fleming J, Flickinger BD. Trans Fatty Acid Intakes and Food Sources in the U.S. Population: NHANES 1999-2002. Lipids. 2012 Aug 18.
  • Lu YC, Hsiao G, Lin KH, Hsieh MS, Jayakumar T, Wu TS, Sheu JR. Cinnamophilin Isolated from Cinnamomum philippinense Protects against Collagen Degradation in Human Chondrocytes. Phytother Res. 2012 Aug 18.
  • Lee EJ, Chen HY, Lee MY, et al. Cinnamophilin reduces oxidative damage and protects against transient focal cerebral ischemia in mice. Free Radic Biol Med. 2005; 39: 495–510.
  • Lee EJ, Chen HY, Hung YC, et al. Therapeutic window for cinnamophilin following oxygen-glucose deprivation and transient focal cerebral ischemia. Exp Neurol. 2009; 217: 74–83.
  • Mollard RC, Luhovyy BL, Panahi S, Nunez M, Hanley A, Anderson GH. Regular consumption of pulses for 8 weeks reduces metabolic syndrome risk factors in overweight and obese adults. British Journal of Nutrition. 2012;108:S111-S122.
  • Pisto P, Santaniemi M, Turpeinen JP, Ukkola O, Kesäniemi YA. Adiponectin concentration in plasma is associated with muscle fiber size in healthy middle-aged men. Scand J Clin Lab Invest. 2012 Sep;72(5):395-402.
  • Su MJ, Chen WP, Lo TY, Wu TS. Ionic mechanisms for the antiarrhythmic action of cinnamophilin in rat heart. J Biomed Sci. 1999;6: 376–386.
  • Tokarska-Schlattner M, Epand RF, Meiler F, Zandomeneghi G, Neumann D, Widmer HR, Meier BH, Epand RM, Saks V, Wallimann T, Schlattner U. Phosphocreatine interacts with phospholipids, affects membrane properties and exerts membrane-protective effects. PLoS One. 2012;7(8):e43178. 
  • Tuzcu M, Aslan A, Tuzcu Z, Yabas M, Bahcecioglu IH, Ozercan IH, Kucuk O, Sahin K. Tomato powder impedes the development of azoxymethane-induced colorectal cancer in rats through suppression of COX-2 expression via NF-κB and regulating Nrf2/HO-1 pathway. Mol Nutr Food Res. 2012 Aug 1.
  • Whitlock KA, Kozicky L, Yee AJH, Ha C, Morris J, Field CJ, Bell RC, Ozga JA, Chan CB. Assessment of the mechanisms exerting glucose-lowering effects of dried peas in glucose-intolerant rats. British Journal of Nutrition. 2012;108:S91-S102. 
  • Wu TS, Leu YL, Chan YY, Yua SM, Tenga CM, Sua JD. Lignans and an aromatic acid from Cinnamomum philippinense. Phytochemistry. June 1994;36(3):785–788
  • Yu SM, Ko FN, Wu TS, Lee JY, Teng CM. Cinnamophilin, a novel thromboxane A2 receptor antagonist, isolated from Cinnamomum philippinense. Eur J Pharmacol. 1994; 256: 85–91.

Body Fat Modulation with Corn Oil & L-Carnitine: What You Can Learn From Your Schnitzel

Its quite remarkable that, primates aside, swine are among the best models of human metabolism. So, even if you do not feel piggy at all, the fact that pigs just as humans are omnivores, makes them a much better model for metabolic disease than rodents. It is thus not too unrealistic to assume that we can learn something about ourselves from the results of a very recent study published in the Journal of Animal Science (Apple. 2011).
Figure 1: American Pork Cuts; quality is determined by corn-oil and carnitine intake of the swine.
What lessons can you learn from our pink relatives?
Investigating the effects of l-carnitine supplementation on the quality characteristics of fresh pork bellies from pigs fed three levels of corn oil, J.K. Apple and his co-workers observed a linear trend towards decreased belly-firmness with increasing amounts of corn oil (0, 2 or 4%) in the diet. If you look at the average American, his/her high corn oil consumption and their respective (pot-)bellies, this should not surprise you. All aesthetic considerations aside, those feisty pot-bellies are nothing but the outward sign of metabolic derangements that - without appropriate lifestyle interventions - have their owners suffer from diabetes, high blood pressure, chronic inflammation, and all the other players in the (eventually) deadly "game" of metabolic syndrome.

[...] belly firmness decreased linearly (P < 0.001) with increasing dietary OIL, but there was no (P ≥ 0.137) effect of CARN on any belly firmness measure.
Now, did the touted fat-burner l-carnitine prevent these effects? No, it didn't. Yet, what it did do is it increased the amount of saturated (SFA) and mono-unsaturated (MUFA) fatty acids and decreased the amount of polyunsaturated fatty acids (PUFA) in the belly tissue:
Dietary CARN increased (P < 0.05) the proportion of total SFA in the intermuscular fat layer, increased (P < 0.05) the proportion of total MUFA in the primary and secondary lean layers, and decreased (P < 0.05) the proportion of total PUFA in the intermuscular fat and secondary lean layers of pork bellies.
In view of the finding that increasing the amount of corn oil in the diet tended to increase the PUFA content of the belly tissue, while depositing the highly oxidative polyunsaturated fatty acids preferentially in fat and not lean layers, one must acknowledge that L-carnitine, despite not being able to prevent the outwardly visible (and touchable) negative effects of a diet high in omega-6 rich corn oil, was yet able to modulate the effects of excess PUFAs on intra-tissue body fat composition.

Against the background of the recent changes in the scientifically accepted perspective on the previously vilified saturated fatty acids and possible beneficial effects on cell stability and inflammation the significance of these results goes beyond profane insights into the management of pork quality and solidify the foundation of my previous recommendation to avoid omega-6 instead of increasing the overall PUFA load by additional omega-3 supplementation. What's new, however, is the role l-carnitine supplementation may play in your efforts to get rid of overly high tissue levels of omega-6, since the reduced storage in fat tissue and the increased storage in muscle could be able to (a) decrease inflammation of the fat tissue and, at the same time, (b) increase oxidation of PUFAs in exercised muscle tissue. Yet, without appropriate dietary changes and the incorporation of regular exercise sessions into your  new, healthier lifestyle all carnitine in the world won't help you, if you insist on eating too many breaded and fried schnitzel with French fries and a boatload of mayonnaise and ketchup.

The Meaty Gritty on the Red Meat Debate: A Comprehensive Rebuttal of the Constant Assault On My Beloved Steaks

Image 1: Even if you find this disgusting, I would like to invite you at least read what the outspoken carnivor in me has to tell you.
It appears to be an endless debate: Can you eat meat? May you eat meat? And even should you eat meat? I already mentioned in my post on the "Chinese meat supplement" study from last week that many of the accepted "truths" about real, unprocesed red meat are about as "true" as the hilarious statement that "going to the hospital causes pre-mature death"... After reading my friend Carl Lanore's luckily very reasonable and not overtly "ranting" blogpost on "What to say to a Vegan", a few days ago, I decided to sum up some of the research to scrutinize, which of the objections against and arguments for eating meat are actually rooted in science (I mean, my life as a meat eater could depend on it, right? ;-).

Pork rules, but is that a good thing?

If we take a look at the actual meat consumption in what is usully called the "developed world" (this is us), we find that pork is the most widely consumed form of red meat (>50% in developed countries; FAO. 2009)  - what's more, pork is rarely consumed "intact", in the form of a whole cut of meat, but more often as processed meat like sausages etc. Overall, the average available amount of red meat (pork, beef and veal, sheep) people in the developed world consume on a daily basis is ~110g, which is well within the "save limit" of as defined by the dietary recommendations in the respective countries.
Figure 1: Relative contribution of beef (total and lean) to individual nutrient consumption in the American diet (adapted from Zanovec. 2010)
In fact, a 2010 dietary analysis by Zanovec et al. suggests that with an average beef intake of 49.3g/day US adults eat way less than the recommended 142-198g of meat per day (at least if we count beef alone; Zanovec. 2010). In this context it is also worth mentioning that:

"Lean beef contributes significant amount of key nutrients to the US diet"

This statement, by the way, is taken directly from the title of Zanovec's analysis of data from the National Health and Nutrition Examination Survey (NHANES. 1999-2004). The years of dietary recommendations asking the public to avoid red meats, because their high saturated fat content would clog their arteries have obviously made a profound impact on people's perception of meat as a "dietary treat" that is about as unhealthy, if not worse, than their beloved potato chips, twinkies and dingdongs and that despite increasing evidence that saturated fat is not associated with an increased risk of heart disease, but showed a statistically non-significant association with reduced risk of stroke (-19%, p = 0.11; Siri-Tarino. 2010).

The dietary advice people are given does "not reflect available scientific literature"

In a relatively recent "review of the reviews" the purported experts on respective dietary advisory boards conduct,  Robert Hoenselaar a researcher from the Department of Nutrition and Dietetics at the High School of Arnheim and Nijmegen in the Netherlands concludes that
[t]he results and conclusions about saturated fat intake in relation to CVD, from leading advisory committees, do not reflect the available scientific literature."
and criticizes the policymakers (if applicable to a certain organization, I will name the latter in brackets after each statement) for
  • advising people to replace saturated with polyunsaturated fats in their diets based on two non-randomized trials (EFSA)
  • mentioning the existing evidence that saturated fat intake increases HDL cholesterol, but ignoring the conclusive evidence that increased HDL levels are associated with a lower CVD risk (IOM, EFSA)
  • not taking into account data from existing prospective studies examining the direct relation between saturated fat intake and CVD (USDA, IOM, EFSA) and instead including their "own randomly selected data on this subject" in their reports
  • ignoring their own previous results (USDA), which suggest that replacing saturated fats by carbohydrates or monounsaturated fats decreases the CHD risk and the mere fact that in the studies Hoenselar analyzed, none of the authors concluded that "changes in saturated fat intake would change the risk of CVD, regardless of the study design and the endpoint"
  • not discussing other modifiable dietary risk factors, which often go hand in hand with an increased meat consumption such as higher intakes of industrial trans fatty acids, a overtly high salt intake or a carbohydrate-laden high GI diet.
Any probably inevitable selection biases aside, it is also interesting that papers such as the one by Li et al., which found no increase in cholesterol (in fact a reduction in LDL) or thrombotic risk factors from the consumption of lean red meat (grass- and grain-fed) in their 2005 review of 54 pertinent studies (Li. 2005), do not appear in the extensive lists of literature the members on respective advisory boards attach to their well-worded reviews.

RCTs confirm independent reviews of the literature and well-conducted epidemiological studies

Moreover, most recent randomized controlled trials, such as Roussell et al. support the notion that the inclusion of lean red meats (153g/day) in a "heart healthy" DASH-like diet does not diminish its favorable effects on markers of cardiovascular disease (Roussell. 2012), but...
[...] in conjunction with the beneficial effects on apolipoprotein CVD risk factors after consumption of the BOLD and BOLD+ [BOLD 133g; BOLD+ 153g/day of lean beef, cf. DASH <28g/day] diets, which were greater with the BOLD+ diet, provide support for including lean beef in a heart-healthy dietary pattern.
Eating a small steak every day is thusly - according to the results from the latest randomized controlled trials more beneficial for your heart (and probably overall health, e.g. "Heal Your Thyroid by Eating More Beef") than avoiding red meat like a plague.

Don't freak out over real meat, or your blood pressure will raise; yet not from the meat!

The list of studies showing no association to another often touted "meat-related" cardiovascular risk factor, high blood pressure (the "silent killer"), is extensive, and even the 2010 U.S. Dietary Guidelines Advisory Committee recently concluded that there is
[...] no clear association between intake of animal protein products and blood pressure in prospective cohort studies.

In randomized controlled trials, as those by Hodgson et al. and Nowson et al,. the addition of red meat to a diet that was "otherwise considered heart healthy" lead to modest reductions (not increases!) in blood pressure (Hodgson. 2006; Nowson. 2009). It is thusly no wonder that in a forerunner study to the aforementioned Roussell trial a sixfold increase in real red meat intake (from DASH to BOLD, cf. above) did not lead to any statistically significant elevations in blood pressure. What is quite interesting in this context is that, at least in the Nowson trial, the dietary restriction of sodium basically precluded the intake of "regular" processed "meats" (I personally would not call them such, but scientists and most people consider sausages & co "meat").

Meat does not make you fat! It can make you lean - not skinny, though...

Another commonly touted myth that is widely accepted - especially among female mainstream dieters - is that meat will make you fat (or if not fat, then at least "bulky"). That this is not the case and chicken and fish are not per se better protein sources when you are dieting for weight loss has been shown in randomized controlled trials (Leslie. 2002; Campbell. 2010) - particularly in women, by the way. This should also remind the "regulars" among you (i.e. all of you who follow my advice to get their daily dose of SuppVersity news in order to stay sane and prolong their lives ;-) of a previous blogpost of mine, in which I discussed the results of a study by Petzke et al. from September 2011, which found increases in lean mass in weight stable women who were advised to include additional lean pork (=red meat ;-) in their diets. I have written about similar results in an obviously tighter controlled rodent study, little less than a week or two, ago.

Image 2: If you put any faith in prospective studies, you should make sure that your grand parents do not follow this selfish advise.
A 14-year prospective follow-up study of older adults by Gilsing et al. did even identify the men in the highest quintile of beef consumption (>40g/day, which is hilarious and just goes to show you why old people get sick and fragile, by the way) as those with the lowest increase in BMI (Gilsing. 2012). However (and moreover), at the end of the 14 year follow up, ...
[...], a significantly higher increase in BMI was associated with higher intakes of pork in women (BMI change highest vs. lowest quintile: 0.47 kg/m²) and chicken in both sexes (BMI change highest vs. lowest category in both men and women: 0.36 kg/m²).
To stay away from unprocessed red meats, and beef, in particular, in order to lose weight or maintain a healthy body weight, is thusly not only unnecessary, but probably even counter-indicated. Also, because red meat is one of the richest sources of protein, iron, zinc, vitamin A and other vital nutrients, all of which could be scarce on voluntary (young dieters) or involuntary (loss of appetite in the elderly) calorie reduced diets.

"Fine, but you will die from cancer, when you eat too much meat"

When the CVD and obesity debate are settled, the meat opponents usually feel that it's now time to play what they believe is their ultimate trump: The red meat "causes" cancer argument - an argument on the validity of which McNeill et al. state (McNeill. 2012):
Disentangling the independent effects of individual foods, such as red meat, in cancer etiology is a substantial challenge (Magalhaes et al., 2012). Although many epidemiologic studies have observed positive associations between red/processed meat intake or associated dietary patterns and various cancers and thus concluded that these convincingly increase cancer risk, these associations have generally been weak in magnitude and/or the large majority of associations have not been statistically significant (Chan et al., 2011; Alexander et al., 2010; Alexander et al., 2010b; Alexander et al., 2009b).  Not surprisingly, analyses of data from large prospective studies have found little or no association between fresh red meat consumption and colorectal cancer risk.
Image 3: Linda van Horn is a chair on the 2010 US Dietary Guidelines Advisory Commitee that is going back on its previous advice against all things meat.
As in the case of increased blood pressure, the 2010 US Dietary Guidelines Advisory Committee (DGAC) is thusly backpedaling on previous statements and recommendations and ascertains that the existing scientific evidence shows "no consistent findings on type of meat or meat product and colorectal cancer" and even recommends that
Americans may choose animal products as part of their diet based on the body of evidence showing a general lack of relationship between animal protein consumption and selected health outcomes (DGAC, 2010).
In view of the fact that there are still epidemiological trials, which do suggest that increased consumption of red meat could pose an increased cancer risk, it will be all the more important to try and eliminate methodological shortcomings, such as
  • heterogeneous definitions of red and processed meat (is Pizza Salami really "red meat"?),
  • variable and unreliable measures of meat consumption, and
  • profound inter-study differences in the analytical evaluation of the data
as well as confounding factors such as physical activity, body mass index, body fat levels, alcohol intake, or adherence to screening recommendations, in order to pinpoint any allegedly meat-related increases in cancer risk in the future.

The non-health related ethical dilemma

By now, I have hopefully encouraged my fellow carnivores and maybe even convinced some skeptics (you know I love you ;-) that the allegedly conclusive data on the potential health hazards from an average, let alone increased consumption of real (unprocessed) red meats are at least not conclusive, and, from my naturally biased reading of the available evidence, non-justifiable and to a great extend the result of paradigmatic ignorance towards contradictory research.

Yet whatever your take on the health effects of red meat consumption may be, now that you have reached the end of this article, it is still up to you to decide if you want or don't want to eat formerly living creatures. I have made my decision and ask you to accept mine, just as I will accept yours - whatever it may be. Thank you!