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marylin monroe
Showing posts with label heart disease. Show all posts
Showing posts with label heart disease. Show all posts

Leaky Gut & Gluten Belly: Bacterial Firebugs Translocate from Your Gut to Your Ever-Growing Visceral Fat Depots

Image 1: Gluttony or a victim of bacterial translocation from an unrecognized gluten-sensitive leaky gut (img from COPD Lighthouse)
"Leaky gut", for decades one of those concepts, the belief in which divided self-proclaimed "real scientists" from their "hippie" counterparts, has eventually found its way to mainstream science. What began with a few tentative studies into the role of a pathologically increased gut permeability in Crohn's disease and co., is about to become a recognized research area with about 150 related publications within the first 9 month of 2011, alone. Out of these 150 publications, a study by Professor Pierre Desreumaux, and his colleagues from the Universitè Lille Nord de France (Desreumaux. 2011) is unquestionably among those, which could have a major impact on the established image of the gut and its biota as an isolated system that sustains the rest of the body with nutrients and has - due to the insulating epithelial layer - little or no direct impact on all the ailments and illnesses by which the Western civilization has been befallen in the course of its quest for highly palatable, optically pleasant, economic and convenient (franken-)food.

The study comprised 22 patients with Chron's disease, 17 patients with ulcerative colitis and 21 controls, who were normal weight, had no history of diabetes mellitus and were not being treated with speci fic medications known to modulate visceral fat. All patients had been scheduled for operations, during which - with their consent - the required subcutaneous/mesenteric fat specimens were taken and the ileal and colonic transparietal biopsies were performed.
Figure 1: CRP mRNA expression [arbitrary units] in mesenteric and subcutaneous fat pads of control, Crohn's disease (CD), and ulcerative colitis (UC) patients (data adapted from Desreumaux. 2011)
While the result that the mRNA expression of c-reactive protein (CRP) in the Crohn's disease group was 83x higher than in the patients with ulcerative colitis (UC) and 3000x higher than in the control group, alone would probably have been worth the whole procedure, a way more interesting result is that the 83x increase over the UC group is fat-depot specific. This means, only the mesenteric fat that is situated right next to the organs of the intestinal tract produces this 83x exaggerated amount of the acute phase protein CRP that is released in response to acute profound inflammation and has been implicated as a marker for peripheral vascular disease (Abdellaui. 2007), liver inflammation (Rodrigez-Leal. 2006), and other unwanted metabolic consequences of the rampant obesity-pandemic (Oda. 2008). This novel observation led the scientists to believe that CRP expression may be enhanced by inflammatory and bacterial stimuli related / subsequent to the pathologically increased gut permeability in Chron's patients.
Image 6: Could Glutamine be
the cheap colostrum?
Can you take measures to decrease your gut permeability and spare your visceral fat e.coli and other bacterial infections? Yes you can! And if you are a diligent student of the SuppVersity, who does not miss a single "course" (i.e. blogpost), you already know that
have been shown to increase gut integrity and to reverse the negative effects of strenuous exercise (such as heavy weight lifting and marathon running ;-) on intestinal permeability.
And in fact, Desreumaux et al. were able to show that in Crohn's disease patients, bacterial translocation, which is usually defined as the migration of bacteria from the gastrointestinal tract to mesenteric lymph nodes and then to peripheral organs such as the liver and spleen, can also affect the mesentric fat pads and increases during experimental ileitis (i.e. inflammation of the ilium, of which a permanently increased mucosal permeability is a characteristic feature; Kroesen. 2008):
Bacterial translocation to mesenteric adipose tissue occurred in 80% of indomethacin-treated rats [model for inflammatory bowel diseases] compared with 11% of control rats. Higher rates of bacterial translocation to mesenteric lymph nodes were also noted in rats following intraperitoneal administration of indomethacin when compared to control animals (67% vs 22%, p < 0.089). The rates of bacterial trans-location were broadly similar in mesenteric adipose tissue and mesenteric lymph nodes (80% vs 67%) in indomethacin-treated rats, as well as in control animals (11% vs 22%).
With 27% the rate in the Crohn's patients was lower, yet still more than two 2x higher than in the "healthy" controls (13%). Basically, this means that a healthy gut keeps >87% of the bacteria from wreaking havoc on your visceral fat depots (and other organs) a "leaky" one, on the other hand, may allow up to 80% of these tiny firebugs to make themselves at home in the fat tissue next to your digestive organs. Now, that would not be a problem, if the local "fire" your new subtenant are sparking within those fat pads would not results in chronic and systemic inflammation (the scientists were able to show a linear relation between visceral CRP and systemic CRP levels) and thus predispose you to obesity, diabetes, heart disease, Alzheimer's, cancer and all the other plagues of the 21st century.

"Eggs" - 4-Letter Food Improves Both Cholesterol Particle & Phospholipid Profile + HDL-Driven Lipid Reverse-Transport

In addition to the previously reported improvements in cholesterol particle profile, the regular consumption of whole eggs increases HDL's ability to carry lipids out of the macrophages. If these accumulate, they will turn the macrophage into pro-atherogenic foam cells (cf. Eckardstein. 2001).
You will probably remember the long-boycotted(*) 2012 study by Blesso et al. which showed quite conclusively that daily whole egg consumption has a  beneficial impact on the HDL-C levels and the particle size profile of overweight and obese patients following a diet with a moderate amount of carbohydrates (read all about the study in the SuppVersity article from October 2012)

(*) I obviously have no evidence that the publication of the Blesso study was mischievously delayed, but it is unquestionably conspicuous that a paper with 100% convincing data that the witch hunt on eggs of the medical establishment is totally unwarranted was postponed from September 2012 (date of the online publication) to March 2013, isn't it?

Be that as it may, let's now after devoting our precious time to the always popular conspiracy theories, take a look at the actual news - news, which come right from the labs of the same laboratory, but this time with a slight twist:
"We recently demonstrated that daily whole egg consumption during moderate carbohydrate restriction leads to greater increases in plasma HDL-cholesterol (HDL-C) and improvements in HDL profiles in metabolic syndrome (MetS) when compared to intake of a yolk-free egg substitute. We further investigated the effects of this intervention on HDL composition and function, hypothesizing that the phospholipid species present in egg yolk modulate HDL lipid composition to increase the cholesterol-accepting capacity of subject serum." (Anderson. 2013)
As you gather from the above citation the dataset, or I should say the blood samples the scientists from the University of Connecticut analyzed to gather their data, were the same as in the previous study accordingly, there is little I could tell you about the 37 subjects (25 women; 12 men) classified with MetS who were recruited to participate in the previously described 12-week parallel, randomized, single-blind diet intervention.
Figure 1: Phospholipid composition of whole egg and egg substitute products; data displayed in mg/serving x 10,  y-axis logarithmically scaled (Anderson. 2013)
"During the 12-week study, subjects were instructed to follow an ad libitum moderate carbohydrate-restricted diet (25–30%) of energy from carbohydrates) in addition to consuming either three whole eggs (EGG group) or the equivalent amount of egg yolk-free egg substitute (SUB group) each day. The egg substitute product consisted of egg whites (99 %), 1 % xanthan and guar gums, beta-carotene for color, and provided 0 mg of cholesterol, whereas the daily serving of whole egg contained 534 mg of cholesterol." (Andersen. 2013)
In the course of the intervention the HDL-cholesteryl ester content in the blood of all subjects increased (relative to other forms of HDL). This increase was, as the data in figure 2 goes to show you, more pronounced in the SUB [=no egg yolks] group. The HDL triacylglycerol content, on the other hand, was reduced in the subjects receiving the whole eggs, only (EGG group). Consequently, the egg intervention resulted in an increases in HDL-CE/TAG ratios in both groups. More importantly, though, ...
Figure 2: Effects of egg feeding on HDL-phospholipid class distribution during moderate carbohydrate restriction  (Andersen. 2013)
"[...p]hospholipid analysis [ (PtdCho phosphatidyl-choline, PtdEtn phosphatidyl-ethanolamine, CerPCho sphingomyelin, LysoPtdCho lysophosphatidyl-choline, PtdIns phosphatidyl-inositol; cf. figure 2] by mass spectrometry revealed that HDL became enriched in phosphatidylethanolamine in the EGG group, and that EGG group HDL better reflected sphingomyelin species present in the whole egg product at week 12 compared to baseline." (Andersen. 2013)
In addition, and in line with previous results suggesting that greater enrichment of HDL in phospholipids—such as PtdCho and CerPCho—are associated with a greater lipid-accepting capacity
of HDL and/or human serum (Fournier. 1996 & 1997), the macrophage cholesterol efflux of the subject in the EGG group increased from baseline to week 12 (+2.4% from baseline). This physiologically highly relevant effect which correspond to the previously reported improvements in HDL particle profiles (see post from October, 2012) is the actual news this re-analysis of the blood samples has to offer, as it goes to show us that the beneficial effects of daily consumption of the "4-letter" food "eggs" does not only promotes favorable shifts in the particle size distribution of the lipoproteins in a patient group with a high baseline risk for cardiovascular diseases. No, the "bad" eggs also improve the HDL lipid composition (lowering the triglyceride content) and the function of the HDL molecules.



Bottom line: If you have been following the SuppVersity Facebook News over the past couple of weeks, you will now probably be thinking: "Wait a minute.. wasn't there..."? And yes, there was. Scientists from the IMIM-Research Institut Hospital del Mar in Barcelona, Spain (Farràs. 2013), have observed very similar effect in a rodent study in response to the consumption of the phenols from a highly praised "8-letter food": Olive Oil!
 
  "If we have not somehow pimped it, it can never be good enough!" appears to be one of the credos with which mankind approaches almost every natural health-remedy. In the past this approach was not particularly healthy, though... is phenol-enriched olive oil going to be the exception to the rule? (learn more)
I know that parts of the medical establishment are not going to like it, but a  short and concise bottom line of the study at hand could thus well be:  

Eggs and olive oil belong to the same category of health foods whose beneficial effects on lipid metabolism go well beyond promoting a more favorable lipoprotein profile. They will also boost the ability of the "good" cholesterol to do it's job and clear the otherwise plaque forming cholesterol from the cells... 

whether this message will ever make it into the headlines of the "science" colums of mainstream media is unfortunately highly questionable.

References:
  • Andersen CJ, Blesso CN, Lee J, Barona J, Shah D, Thomas MJ, Fernandez ML. Egg Consumption Modulates HDL Lipid Composition and Increases the Cholesterol-Accepting Capacity of Serum in Metabolic Syndrome. Lipids. 2013 Jun;48(6):557-67.
  • Blesso CN, Andersen CJ, Barona J, Volek JS, Fernandez ML. Whole egg consumption improves lipoprotein profiles and insulin sensitivity to a greater extent than yolk-free egg substitute in individuals with metabolic syndrome. Metabolism. 2012 Sep 26.
  • von Eckardstein A, Nofer JR, Assmann G. High density lipoproteins and arteriosclerosis. Role of cholesterol efflux and reverse cholesterol transport. Arterioscler Thromb Vasc Biol. 2001 Jan;21(1):13-27. 
  • Farràs M, Valls RM, Fernández-Castillejo S, Giralt M, Solà R, Subirana I, Motilva MJ, Konstantinidou V, Covas MI, Fitó M. Olive oil polyphenols enhance the expression of cholesterol efflux related genes in vivo in humans. A randomized controlled trial. J Nutr Biochem. 2013 Jan 17.
  • Fournier N, de la Llera Moya M, Burkey BF, Swaney JB, Paterniti J Jr, Moatti N, Atger V, Rothblat GH. Role of HDL phospholipid in efflux of cell cholesterol to whole serum: studies with human apoA-I transgenic rats. J Lipid Res. 1996 Aug;37(8):1704-11. 
  • Fournier N, Paul JL, Atger V, Cogny A, Soni T, de la Llera-Moya M, Rothblat G, Moatti N. HDL phospholipid content and composition as a major factor determining cholesterol efflux capacity from Fu5AH cells to human serum. Arterioscler Thromb Vasc Biol. 1997 Nov;17(11):2685-91.

Heart Disease: Insufficient Sleep ✔ Diet ✔✔ Inactivity ✔✔✔ - Inactivity is the #1 Risk Factor for Heart Disease Across Adult Lifespan. Plus: Top 10 Reasons For Global Disease

You don't have to do kettlebell handstands. Just be active, girls!
We are often talking about the importance of sleep, and in fact, people who don't sleep enough have an increased risk of developing heart disease (+45%) and the fact that sleeping "too much" 9h+ is associated with a similar increase in (+38%) risk of heart disease in women (Ayas. 2003; similar data is available for men), alone, would not justify discarding the important contribution of short sleep durations to the ever-increasing number of patients with heart disease.

Similarly, a hypercaloric high fat + high sugar Western / Standard American style convenience + fast food based diet and its unwanted consequences, i.e. obesity, diabetes, etc. are unquestionably among the cornerstones of the heart disease epidemic.
One way to maximize your activity is HIIT - learn more at the SuppVersity

Never Train To Burn Calories!

Tabata = 14.2kcal /min ≠ Fat Loss

30s Intervals + 2:1 Work/Rec.

Making HIIT a Hit Part I/II

Making HIIT a Hit Part II/II

Triple Your Energy Exp.
And still, according to a recent study from the Centre for Research on Exercise, Physical Activity and Health at the School of Human Movement Studies of the University of Queensland  in St Lucia, Queensland, Australia, says: "From about age 30, the population risk of heart disease attributable to inactivity outweighs that of other risk factors, including high BMI" (Brown. 2014)

Now, we cannot tell, whether the same is true for men, as well, but even if it wasn't, the data from Table 1 would obviously be both, remarkable and memorable.
Table 1: Age-specific relative risks for ischaemic heart disease (IHD) for four risk factors in women (Brown. 2014)
If you look at the "population attributable risk (%)"-graph from the original paper (Figure 1), it becomes even more obvious: physical activity is the key to heart health - actually even more so for young vs. old women (187% increased risk in 20-24-year-olds vs. 95% risk increase in 53-58-year-olds; see Table 1).
 Figure 1: Population attributable risk (%) for four risk factors for IHD in women across the adult lifespan (Brown. 2014)
Even smoking is not match for inactivity, when it comes to the downstream effects on heart health. It is thus not surprising that scientists from the Albert Einstein College of Medicine report in a recent paper that for otherwise healthy middle-aged women who are overweight or obese, physical activity may be their best option for avoiding heart disease.

According to a study that followed nearly 900 women for seven years. These findings were reported in a paper led by authors at Albert Einstein College of Medicine of Yeshiva University and Montefiore Medical Center, the University Hospital for Einstein, and published today in the Journal of Clinical Endocrinology & Metabolism.
Inactivity is a major factor, but there are other heart disease triggers: As previously stated, inactivity is one factor out of many, the study by Wang et al. identified the following additional triggers of heart diseases, namely, elevated bloog glucose = 3x higher risk, hypertension = 3 higher risk, weight gain = 16% higher risk.
Throughout the seven-year study, the women were tested annually for heart disease risk factors. They also completed an annual survey describing their physical activity for the prior 12 months, which ranged from active living, caregiving and doing household chores to exercise and sports.

METs, i.e. metabolic equivalents are a way to measure the intensity of physical activity (occupational data based on Church. 2011)
During the seven years, 373 of the participants—43 percent of the total—had progressed from having at most a single risk factor for heart disease (i.e., metabolically benign overweight/obese) to at-risk overweight/obese, meaning they had developed two or more of the following five heart-disease risk factors: hypertension; low blood level of HDL ("good") cholesterol; elevated blood levels of triglycerides, elevated fasting glucose level (indicating pre-diabetes or diabetes); and elevated levels of C-reactive protein ( indicating inflammation).

And contrary to what you may have expected in view of the constant upheaval about "eating healthy", low-to-moderate physical activity—at the start of the study and during it—was the only lifestyle factor found to protect overweight/obese women from becoming at-risk for heart disease - to be specific, their heart disease risk was reduced by 16%.
Top 10 risk factors ranked by attributa- ble burden of disease globally and in Australasia (Australia, New Zealand, New Guinea (Brown. 2014)
Make no mistake about it: While being inactive is the major risk factor, it's usually so intricately linked to being obese, which is usually promoted by an unhealthy diet and a lack of regular sleep that we cannot fully discard any of the other factors. If you look at the data in the table to the right, you will also see that "globally", i.e. across all ailings and age groups, other factors are the major determinants of health & disease and ultimately, life or death!

Accordingly, health is always about the whole package, a package that includes an exercise (related Facebook News), a diet and an anti-stress + sleep component. And you don't want to miss one of them, your health depends on them!
Reference: 
  • Ayas, Najib T., et al. "A prospective study of sleep duration and coronary heart disease in women." Archives of Internal Medicine 163.2 (2003): 205-209.
  • Brown, Wendy J., Toby Pavey, and Adrian E. Bauman. "Comparing population attributable risks for heart disease across the adult lifespan in women." British journal of sports medicine (2014): bjsports-2013.
  • Church, Timothy S., et al. "Trends over 5 decades in US occupation-related physical activity and their associations with obesity." PloS one 6.5 (2011): e19657.
  • Wang, D, et al. "Progression from Metabolically Benign to At-risk Obesity in Perimenopausal Women: A Longitudinal Analysis of Study of Women Across the Nation (SWAN)." JCEM (2014).

Detrimental Effects of Aerobic & High Oxygen Packaging on Meat Quality: 2x Higher Lipid & Cholesterol Oxidation, Less Tender, More Drip Loss, Less Juicy... but More Convenient!

Rosy, but rusty: "Fresh" meat packaged with 70% oxygen.
I don't know about the US, but most of the "fresh" meat, you buy at the Supermarket here in Germany is packaged in what the label calls a "Schutzatmosphäre". Literally translated this means nothing but a "protective atmosphere" and it refers to the supposedly bacteria-free high oxygen air that's pumped into the airtight packaging in which the chicken breasts and beef steaks, the pork and lamb and all the other appetizingly looking meats are stored for up to a week in the fridges of the meat counter.

Good to now it's protected! Right?

If you ever bought a product like that you will have realized that you can easily store it for the whole 7day+ period in you fridge and - as long as the airtight plastic container is not broken - it will look and smell almost as it did on day one, when you rip the container open and take a closer look, whether the meat you are about to prepare is still good to eat; Looking good!

What you cannot see though, is that the "protective atmosphere" protects, may have protected the looks of the meat, but not its nutritional quality. 

I mean think about it: What happens when you put metal into a wet high oxygen environment? Right! It starts to oxidize. Now guess what has happened to your appetizing piece of chicken, beef, pork or lamb while it was (highly conveniently, obviously) waiting for you in your fridge. Right it began to rust.
Figure 1: Content of cholesterol oxidation products (COPs) in non-irradiated raw chicken/turkey leg and raw beef with packaging, and storage time; data expressed relative to baseline (Nam. 2001)
As the data in figure 1 goes to show aerobic packaging (this is not yet a high oxygen environment) accelerates the rate of lipid and protein oxidation, so that the content of potentially hazardous cholesterol oxidation products (COPs) in your turkey legs, raw beef on day 7 is anywhere between 20-100% higher than on day one.
"Although the packaging conditions of meat during storage were critical for the oxidation of cholesterol in raw meat, irradiation synergistically increased it." (Nam. 2001)
And as Nam et al. point out this effect is even more pronounced if the meat has been irridated before packaging. The vacuum packaging, most producers and vendors are reluctant to use, because the meat does not look anywhere as fresh as the one that's packaged with highly oxygenated air (in fact it's the oxidized oxyhaemoglobin MbO2 that's responsible for the rosy color, cf. Rennere. 1999), on the other hand, "was enough to protect cholesterol and fatty acids from oxidation regardless of irradiation dose." (Nam. 2001)

Red deception in the "fresh" food corner

Figure 2: T-bar levels (a marker of lipid oxidation) in air, high oxygen and vacuum packaged pork during refrigeration for 0-20 days (Cayuela. 2004)
Now, with normal air, the nice red color will at some time give way to a brownish one, with extra high oxygen air that's used in high oxygen packaging, it will prevail, but at the same time,
"[t]he use of modified atmospheres with a high oxygen concentration (70%) act[s] as a pro-oxidation factor both for fatty acids and for cholesterol (an increase of 86.4% on the initial COPS content)." (Cayuela. 2004)
And that's a plus of almost 90% on top of what you would see with "regular" air packaging, as it was used in the Nam study.

Ah, and did I mention that this "meat" will also be less tender, less juicy and will have a 4-6x higher drip loss than "regular" packaged meat, when it's stored at 4°C for several days (Lund. 2004).



Vacuum + Irridation = Plastimeat 2.0 According to a 2012 paper the phtalate DEHP content of vacuumed meats increases "dramatically" by 2.55, 2.75, 2.18 and 2.16 times in comparison to that in control samples having a fat content of 10%, 20%, 30% and 40%, respectively, when it is exposed to 20 h of UV irradiation at an intensity 900µW/cm² (Zhang. 2012).
Bottom line: As inconvenient as it may sound, the lipid and cholesterol oxidation meat undergoes, when it is packaged surrounded by a "protective atmosphere" of highly oxygenated air is just another example of how our urge for "convenience" and immediate 365 x 24/7 availability of whatever we want to eat can contribute to the overall burden of dietary-related diseases.

Don't get me wrong, you certainly won't die when you eat meat from the supermarket and still - the oxidized fats and cholesterol from the gas packaged meats from the supermarket are another on its own probably negligible piece to the puzzle that holds the answer to the complex question why we are fat and sick. One thing appears to be relatively certain, though, the terms "convenience" and "revenue" relate to almost every item on the never ending list of causative and confounding factors of the obesity epidemic in one or the other way.

References:
  • Cayuela JM, Gil MD, Bañón S, Garrido MD. Effect of vacuum and modified atmosphere packaging on the quality of pork loin. European Food Research and Technology. 2004; 219(4), 316-320.
  • Lund MN, Lametsch R, Hviid MS, Jensen ON, Skibsted LH. High-oxygen packaging atmosphere influences protein oxidation and tenderness of porcine longissimus dorsi during chill storage. Meat Sci. 2007 Nov;77(3):295-303. 
  • Nam KC, Du M, Jo C, Ahn DU. Cholesterol oxidation products in irradiated raw meat with different packaging and storage time. Meat Sci. 2001 Aug;58(4):431-5.
  • Rennere, M. Factors involved in the discoloration of beef meat. International Journal of Food Science & Technology. 1990; 25: 613–630.
  • Zhang SL. Effect of UV Irradiation on the Migration of DEHP from Food-Grade PVC Film into Packaged Ground Meat . Advanced Materials Research. 2012; 601(94).

Fish Oil Compromises, Fish Improves Adiponectin Levels in "Overweight, But Healthy" Individuals. Neither Promotes Weight or Fat Loss Within a 4-Week Study Period

Fish are smart, they tell you about the good things "omega-3" fatty acids will do, without pointing you to the fact that eating them will yield a more favorable DHA:EPA ratio than popping pills that are made from the same remnants of their deceased relatives the fishery industry has dumbed for decades.
With the vitamin D news the other day (go back), you are now probably thinking "hell, no Adel's other favorite topic to rant about"... an yes! You are right: I just like to rant against mainstream stupidity and one-size-fits-it all approaches everybody loves because they are so "easy"! Take your fish oil! And everything is going to be all right. Much easier and so much more compelling, than my advice to eat fatty fish at least once, better twice or thrice a week to promote, not magically achieve metabolic health.

And while you've heard about the anabolic and blood pressure lowering benefits of fish protein in previous articles, here at the SuppVersity, it is more than unlikely that you've already gotten wind of the latest study from the Smart Foods Centre, School of Health Sciences (you got to love that name!) at the University of Wollongong, New South Wales, Australia (Neale. 2013)... and that despite the fact that it took - just as with the egg study, showing only beneficial effects on blood lipids (learn more) - suspiciously long for the study to make it from an "accepted manuscript" into a print article in the scientific journal Metabolism.

Scaled fish or capped oils - is that even a question?

In what is by no means the first, and certainly not going to be the last paper comparing the metabolic effects of fish oil caps to the food item, the oil is supposed to be delivered with (the fish ;-), Elizabeth P. Neale and her colleagues recruited 18–65 year old volunteers, who were willing to consume fish, but had a low- or moderate habitual fish intake to begin with (<3x per week). The subjects had to have a BMI somwhere in-between 25 and 37 kg/m² and a chubby midline with awaist circumference of >94 cm for men, >80 cm for women. Exclusion criteria were pregnancy, diabetes mellitus, impaired renal function, smoking, not weight stable for the past six months, food allergies or habits inhibiting compliance with the study design, illiteracy and inadequate conversational English; plus, they were excluded if they were currently taking medications including thiazolidinediones, valproic acid, ACE in-hibitors, and glucocorticoids.This left the researchers with N=30 subjects who were randomized to consume either
  • fish providing 1.86 g of LC n-3 PUFA (812mg EPA +1044 mg DHA)per day -- three serves of 135 g salmon (Birds Eye Atlantic Salmon Fillets, Simplot Australia), two serves of 66 g sardines (adjusted for percentage fish in total canned product; John West Sardines in Tomato Sauce, Simplot Australia) and one serve of 55.1 g tuna (adjusted for percentage fish; John West Tuna Tempters Lemon and Cracked Pepper, Simplot Australia) per week, or
  • supplemental fish oil (Blackmores Omega Daily) containing the same amount of LC n-3 PUFAs, yet - and this is a consequence of the low DHA/EPA ratio in fish oil vs. real fish - 1055.1 mg EPA and only 744.9 mg DHA
for 4 weeks, on a daily basis. And while the participants in the supplement group were "not expressly told to avoid fish", they were not "encouraged to consume it in preference to other protein sources", either (Neale. 2013).

What did the scientists want to measure?

The primary outcome parameter of the study were the differential effects of fish and fish oil on the plasma total and high molecular weight adiponectin levels in overweight humans and, secondary, to identify the genetic variations in participant's ADIPOQand FTO genes that may influence that response.
Figure 1: Relative changes in weight, BMI, waist, body fat (%), glucose, insulin and EPA + DHA levels in serum from t = -2 weeks (i.e. before the 2-week run in in which the diets and activity levels were standardized to 25% protein, 45% carbohydrate, and 30% fat) to t = 4 weeks (Neale. 2013)
As the data in figure 1 goes to show you this did not stop the scientists from evaluation the effects the intervention had on anthropometric parameters (waist, body fat, etc.) of their subjects, as well. Neither of these, nor the effects on blood glucose and insulin showed any significant inter-group difference. If we discard the identical changes in the EPA and DHA levels of the subjects, the dietary / supplement intervention had absolutely zero effects on any of these "extra-parameters" - no weight loss, no visible improvement in glucose metabolism.

No reduction in body fat or waist circumference in with fish or fish oil

Reason enough to ask yourself, whether we should not go back to baseline and ask "is fish / fish oil even good for you"? Certainly not - or I should say, only if you put faith in the hilarious promises of "instant weight loss, improvements in glucose metabolism" and what not, if you finally jump aboard and take your "essential fish oil supplements" that are plastered all over the Internet. If you discard these advertisment claims or simply apply some critical thinking skills, it should be obvious that you got to content yourself with changes in your potential to shed fat / improve glucose metabolism by simultaneously committing to lifestyle that's juxtaposed to the way of living that has gotten you into all the trouble to begin with.
Figure 2: Total and high molecular weight adiponectin levels expressed relative to the levels after the 2-weeks run-in (left) and the ratio of the absolute values after 4 weeks (right; Neale. 2013)
The changes in adiponectin expression in figure 2 are such an indicator of a change in the potential of getting rid of the blubber, the high blood glucose - and it is obvious to see that fish oil is inferior to fish, when it comes to inducing these changes.
"The results of this study suggest that short-termconsumption of fish and fish oil supplements does not have the same effect on HMW adiponectin levels in overweight humans. [...] This was due to a small increase in HMW adiponectin in the ‘fish’ group, whilst the ‘supplement’ group exhibited a significant decrease in HMW adiponectin concentrations. A similar pattern was seen for total adiponectin; however this did not reach statistical significance." (Neale. 2013)
As mentioned in the previous paragraph, these changes were not associated with differential effects on body weight, insulin levels and body fat mass, all of which "remained relatively constant" (Neale. 2013)



Fatty acid content in g/100g of wild and farmed salmon (left) and respective omega-3 to omega-6 ratios; learn more about making the "right fish choices", here
Unfortunately(?), the underlying mechanisms behind the differential effects on HMW adiponectin are as of now not known. Neale et al. do yet also subscribe to the "synergy hypothesis" I alluded to earlier in the first paragraphs of this article. The proven benefits of fish protein on insulin sensitivity and chronic inflammation (Soucy. 1999; Ouellet. 2007; Pilon. 2011), as well as the "other components present in fish such as selenium and vitamin D [, which] have also been associated with a range of health benefits in humans" [Rayman. 2000; Garland. 2006)...

...Oh, no! I know what you are thinking now. "I got all those in my multi! And I guess whey will do just as well as fish protein..." - come on, are you serious? Synergy is about ratios, about competition, about ups and downs, about co-factors and adjuvants. It's not about a kitchen sink supplementation approaches that try to reunite what has been ripped apart in a helpless effort to "make things easier" for the lazy consumer who does not like his fish and does not want to spend some of his daily screen time on buying fresh foods and preparing them... sorry, now I am really ranting ;-)

Handpicked suggested reads:
  • Study on Krill Powder Suggests: There is More to Seafood Than Fat - Can Krill Give You What Fish Oil Can't? Plus: Krill Protein's EAA Content More Than an Able Match to Whey (read more)
  • Phospholipid or Triglyceride? What's in Your Fish Oil Caps? Only Phospholipid Based DHA+EPA Reduces Fat Cell Growth & Elevated Insulin Levels Despite Obesogenic Diet (read more)


References:
  • Moroi M, Akter S, Nakazato R, Kunimasa T, Masai H, Furuhashi T, Fukuda H, Koda E, Sugi K, Jesmin S. Lower ratio of high-molecular-weight adiponectin level to total may be associated with coronary high-risk plaque. BMC Res Notes. 2013 Mar 6;6:83. 
  • Neale EP, Muhlhausler B, Probst YC, Batterham MJ, Fernandez F, Tapsell LC. Short-term effects of fish and fish oil consumption on total and high molecular weight adiponectin levels in overweight and obese adults. Metabolism. 2013 May;62(5):651-60.
  • Ouellet V, Marois J, Weisnagel S, et al. Dietary cod protein improves insulin sensitivity in insulin-resistant men and women: a randomized controlled trial. Diabetes Care 2007;30(11):2816.
  • Pilon G, Ruzzin J, Rioux L-E, et al. Differential effects of various fish proteins in altering bodyweight, adiposity, inflammatory status, and insulin sensitivity in high-fat–fed rats. Metabolism 2011;60(8):1122–30. 
  • Rayman MP. The importance of selenium to human health. Lancet 2000;356(9225):233–41.
  • Soucy J, LeBlanc J. The effects of a beef and fish meal on plasma amino acids, insulin and glucagon levels. Nutr Res 1999;19(1):17–24.

Choline Deficiency, Its Consequences and How You Fix It | Part 2 of the "Common Nutrient Deficiencies, Their Health Consequences and How You Can Fix Them" Series

Don't you tell me there was no fancy cooking with the choline source #1, i.e. egg yolk! What about egg yolk on ricotta cauliflower ravioli filling, for example | get the recipe @ tastespotting.com
If you've read the last installment of this series, you can hardly be surprised that today, we are about to talk or rather I am about to write about choline. Choline is, as Wikipedia informs us, a water-soluble essential nutrient. Why choline is not officially called a "vitamin" is beyond me. "Experts" will still group it within the B-complex vitamins, anyway.

In my analyses in the series on nutrients other than cabohydrates that influence glucose control, you've read that the former, the "other", "real" B-vitamins are - in my humble opinion - totally overrated. Choline, which can come in various forms of quaternary ammonium salts all of which contain the caracteristic N,N,N-trimethylethanolammonium cation, on the other hand, it probably the most underrated micronutrient - not only for glucose control, by the way.
You can learn more about choline at the SuppVersity

Huge GH Spikes from GPC!?

Choline & Classic Bodybuilding

Improved Lipid Profile W/ Eggs

Caffeine, Choline, L-Car = Fat Loss

Choline Maximizes Carnitine Storage

Choline as a Nootropic?
One of the reasons choline has been depreciated is probably that it occurs in all the good foods of which scientists have been (falsely) telling you that you must not eat them for decades.

Figure 1: Eggs, or rather their fatty yolks, are a very good source of choline. One too few people appreciate for its nutritional density and too many people fear for its allegedly bad cholesterol content | learn why this is bullocks
Voilà, exhibit A (see Figure 1), an egg. The "bad" yolk of a single egg contains enough choline to "get you through the day" - whether that's also enough choline for optimal health is a question we are about to tackle later in today's installment of the Common Nutrient Deficiencies, Their Health Consequences and How You Can Fix Them" Series (you can browse through past and previous issues, here, if you have an RSS compatible web-browser).

The fact that generations of bodybuilders have been throwing away the yolks only to supplement with even more choline than they'd have gotten from their eggs does yet certainly tell you something about the importance of this nutrient.

But I am digressing, here. What we actually wanted to talk about is after all "normal" people, not bodybuilders. Normal people like the participants of the 2005 National Health and Nutrition Examination Survey (NHANES) among which only 2% of postmenopausal women consumed the recommended amount of for choline, and in general "mean choline intakes for older children, men, women and pregnant women are far below the Adequate Intake established by the IOM" (Zeisel. 1991).

When people don't get enough choline in their diets, and the amount of choline in their system declines, will eventually lose their ability to methylate homocysteine to methionine. The result, their plasma levels of homocysteine increase and heart disease, dementia and even cancer are lurking right around the corner.
Why is high plasma homocysteine bad? In spite of the fact that it is still questionable, whether homocysteine is causally involved in the etiology of heart disease (Brattström. 2000), the present evidence leaves little doubt that high homocysteine levels are a marker of increased risks for several chronic diseases and conditions including cardiovascular disease, cancer, cognitive decline and bone fractures (HSC. 2002; Wu. 2002; Seshadri. 2002; van Meurs. 2004).
Even in the absence of vitamin B6, and B12, of which everybody is talking these days, choline and its cousin betaine have the ability to lower homocysteine levels (Chiuve. 2007). In this context you should also keep in mind that (a) homocysteine levels and the development of the triage we call "metabolic syndrom" (obesity, diabetes, high cholesterol) and that (b) choline is "lost" (oxidized) during the methylation process -- the choline requirements of the average, meanwhile at least chubby US citizen are thus naturally higher than the RDA scientists have determined in a day and age, when a BMI of >30 was still the exception.
Figure 2: The maintenance of healthy homocysteine levels is only one of choline's many important effects.
Aside from being involved in the clearance of homocysteine, choline is also, and maybe even more importantly, used in the synthesis of the constructional components of your body's cell membranes and much more (see Figure 2, as well):
  • Choline figures in cell signaling, where the choline-containing phospholipids, phosphatidylcholine and sphingomyelin, are precursors for the intracellular messenger molecules, diacylglycerol and ceramide. And with the platelet activating factor (PAF, an activator and mediator of many leukocyte functions, including platelet aggregation and degranulation, inflammation, and anaphylaxis) and sphingophosphorylcholine (regulate trafficing around / across the cell membrane; Ramstedt. 2002), there are two additional choline metabolites with important systemic functions.
  • The transmission of never impulses is another, certainly one of the most important functions of choline or rather acetylcholine, an important neurotransmitter involved in muscle control, memory, and many other functions. No wonder that low choline levels have been associated with the progression of Alzheimer's and non-Alzheimer's dementia (Babic. 1999; Seshadri. 2002)
Apropos beyond methylation - choline can make up for a lack of folate! The often decried lack of folate intake (just as a reminder the folate fortfication program in the US made no one healthier - with one exception, maybe: The recommendations to increase folate intake for pregnant women/women of childbearing age has been relatively successful for preventing neural tube defects in infants) would be much less of an issue in the diabesity problem, if the average American consumed 2,200mg of choline per day. The same amount of choline that is which preserved the markers of cellular methylation and attenuated folate deficiency related DNA damage in a genetic subgroup of folate-compromised men in a 2010 study by Shin et al.
  • The effects on lipid (fat) transport and metabolism are probably still totally underrated by both the public and certain parts of the medical establishment. The fat and cholesterol that's consumed in the diet is after all transported to the liver by lipoproteins (chylomicrons) which are built from phosphatidylcholine. If there is not enough choline to build these 'cholesterol shuttles' the fat and cholesterol will begin to accumulate in you liver. No wonder scientists have long discovered an intricate relationship between choline intakes, on the one hand, and the development of non-alcoholic fatty liver disease, on the other hand - in fact, more recent evidence suggests that millions of US citizens have been able to escape a non-alcoholic fatty liver only due to "good genes" that allow them to budget their insufficient choline intake better than others (Spencer. 2011).
In spite of the fact that a full-blown choline deficiency will impair your exercise performance, the provision of supplemental choline has not been shown to consistently produce meaningful increases in exercise performance (Penry. 2008). As a physical culturist, you should still keep in mind that intense exercise will increase your basal choline requirements of which the wise USDA says based on data of which the researchers say that its quality "varies widely across studies", with the most significant sources of potential sources being over- or underreporting of portion sizes and frequency of intake, omission of foods, and inaccuracies related to the use of food composition tables. Accordingly Yates et al. add for consideration:
Table 1: High choline foods for omnivores and vegetarians; choline content in milligrams / 100g | data adapted from nutritiondata.com
"Therefore, the values reported by nationwide surveys or studies that rely on self-report may be somewhat inaccurate and possibly biased. Food composition databases that are used to calculate nutrient intake from self-reported and observed intake data introduce errors due to random variability, genetic variation in the nutrient content, analytical errors, and missing or imputed data.

In general, when nutrient intakes for groups are estimated, the effect of errors in the composition data is probably considerably smaller than the effect of errors in the self-reported intake data (NRC, 1986). However, it is not known to what extent this is true for folate, biotin, pantothenic acid, or choline." (Yates. 1998)
That's bad, because the first signs of liver damage in humans (beginning NAFLD if you will) occur after only 3 weeks on a choline deficient diet (Zeisel. 1991). In view of the fact that doses of safe therapeutic doses go into the 8-10 gram range and considering the fact that the total amount of choline in foods is not exactly exorbitantly high, it would appear prudent to follow the "more is better principle", when it comes to choline-rich foods (see Table 1 and bottom line for suggestions | Didn't find the food you were looking for? Try the official USDA Overview).
Don't go overboard on supplements! When it comes to supplementation, on the other hand, you better be careful not do overdo it. While choline is generally relatively benign, it can produce side effects that range from increased potassium and magnesium requirements over depressive like symptoms (a general sluggishness) to vomiting and, in some people, acne-like skin rashes. Dosages in the below 3g per day range do yet generally appear to be tolerated very well. In the long term the phospholipid bound forms of choline can yet produce quite nasty depressive-like side-effects - another reason to prefer the cheap and effective citrates and tartrates if you are just "supplementing" your diet or looking for the metabolic effects, primarily.
Unless you are following a no fat diet, the use of dietary supplements to cover your baseline requirements of 500-600mg (I am deliberaterly not using the ostensibly "accurate" RDA, here) shouldn't  be necessary - at least if you eat your healthy eggs every day ;-)

Choline as a "metabolic activator" and diet aid!?

If you mimic the old-school body- builders and have your choline supps with meat, this will increase the retention & effects of carnitine.
If you remember my previous article on the relatively unknown "CCC-Stack" which consists of caffeine, carnitine, and... you guessed it, choline you will yet remember that doubling your intake with 500mg of choline tartrate or citrate had quite remarkable effects on the metabolism (learn more | for metabolic purposes I would prefer the citrate and tartrate forms over the expensive phospholipid bound version of choline, which may have its advantages, though, when it comes to brain-related effects).

Moroever, a recent study from the Zagazig and the Mansura University in Egypt suggests that choline alone, will produce quite impressive weight loss effects - even in the absence of the "fat liberator" caffeine and the "fat transporter" carnitine, i.e. the other "C"s in the CCC stack.

The study, Elsawy, Abdelrahman and Hamza conduted investigated the effects of choline supplementation on body mass reduction and leptin levels among female taekwondo and judo athletes in the pre-competition phase (Elsawy. 2014).
Figure 3: Relative changes in lipid oxidation, body fat (%), body mass and strength parameters in female athletes during contest prep with (choline) and without (control) 2x2g of supplemental choline in their meals (Elsawy. 2014)
Twenty-two female athletes (15 taekwondo and 7 judo athletes) were selected from different weight
categories and divided into two groups, according to weight. The players in the experimental group consumed their choline supplements (2x2.0g of choline bitartrate) daily with meals for one week.

I guess the results actually speak for themselves. As expected, the experiment revealed significant differences between pre- and post-competition measurements of free plasma choline, and urine choline levels. The significantly higher fat loss, on the other hand, is something even the researchers did not necessary expect to see. In view of the reduction in malondyaldehyde (MDA = lipid oxidation) and the increase in carnitine retention and effects you've read about in a previous SuppVersity article ("Choline Maximizes Carnitine Retention + Effects" | read more) it is yet eventually not surprising that the choline group lost more body fat without suffering significant reductions in strength and lean mass.
Eat three of these or combine two of them: One whole eggs, 4oz of shrimp, or 5oz scallop, 5oz chicken, 5oz turkey
Eat four of these or combine four of them: 4oz cod, 1.5 cups of collard greens, 1.75 cups of Brussel sprouts, 1.75cups of broccoli, 5oz tuna, 5oz salmon, 6oz beef, 6 oz saridines
Eat five of these or combine one of each 2cups of swiss chard, 2cups of cauliflower, 2cups of asparagus, 2.25cups of spinach, 2cups green peas, 2.5 cups cabbage, 2 cups of Shiitake mushrooms
Other foods with choline, of which you'd yet probably have to eat too much to get to your SRI (SuppVersity recommended intake for adults) of 500-600mg are green beans and bok choy (5% of SRI per cup), summer squash, miso and tomatoes (1-2% of SRI per cup)
Bottom line: I am well aware that the fat loss effects, I deliberately mentioned last are probably the "sexiest" benefits choline has to offer. Compared to the conservation of liver, brain and heart hearth for which you "just" have to make sure that you consume enough of the foods in the list to the left, the ability of supplemental choline to promote fat loss and conserve lean mass and strength in "average Janes" (read more) and competitive athletes (Figure 3) is actually quite pathetic.

Speaking of "pathetic" the notion that eggs would be bad for you, because they contain cholesterol is probably even more pathetic than the notion that being ripped was more attractive than being healthy. In view of the fact that the amount of highly bioavailable choline in a single egg can cover 20%-35% (depending on its size) of your daily choline demands, having an egg for breakfast is nothing you should consider, but rather something you should simply do! The increase in choline intake, the beneficial effects on your cholesterol particle and phospholipid profile and the increase in HDL-driven lipid reverse-transport are after all something you don't want to sacrifice on the altar or unwarranted prejudices and in blind obedience to dietary guidelines of which more and more researchers say that they "are not benefiting the public as a whole and may actually have negative nutritional implications." (Herron. 2004)
References:
  • Babic, T. "The cholinergic hypothesis of Alzheimer’s disease: a review of progress." Journal of Neurology, Neurosurgery & Psychiatry 67.4 (1999): 558-558.
  • Brattström, Lars, and David EL Wilcken. "Homocysteine and cardiovascular disease: cause or effect?." The American journal of clinical nutrition 72.2 (2000): 315-323.
  • Elsawy, Gehan, Osama Abdelrahman, and Amr Hamza. "Effect of Choline Supplementation on Rapid Weight Loss and Biochemical Variables Among Female Taekwondo and Judo Athletes." Journal of Human Kinetics 40.1 (2014): 77-82.
  • Herron, Kristin L., and Maria Luz Fernandez. "Are the current dietary guidelines regarding egg consumption appropriate?." The Journal of nutrition 134.1 (2004): 187-190.
  • HSC: Homocysteine Studies Collaboration. "Homocysteine and risk of ischemic heart disease and stroke: a meta-analysis." Jama 288.16 (2002): 2015-2022. 
  • Penry, Jason T., and Melinda M. Manore. "Choline: an important micronutrient for maximal endurance-exercise performance?." International journal of sport nutrition and exercise metabolism 18.2 (2008): 191.
  • Ramstedt, Bodil, and J. Peter Slotte. "Membrane properties of sphingomyelins." FEBS letters 531.1 (2002): 33-37.
  • Seshadri, Sudha, et al. "Plasma homocysteine as a risk factor for dementia and Alzheimer's disease." New England Journal of Medicine 346.7 (2002): 476-483. 
  • Shin, William, et al. "Choline intake exceeding current dietary recommendations preserves markers of cellular methylation in a genetic subgroup of folate-compromised men." The Journal of nutrition 140.5 (2010): 975-980.
  • Spencer, Melanie D., et al. "Association between composition of the human gastrointestinal microbiome and development of fatty liver with choline deficiency." Gastroenterology 140.3 (2011): 976-986.
  • van Meurs, Joyce BJ, et al. "Homocysteine levels and the risk of osteoporotic fracture." New England Journal of Medicine 350.20 (2004): 2033-2041.
  • Wu, Lily L., and James T. Wu. "Hyperhomocysteinemia is a risk factor for cancer and a new potential tumor marker." Clinica Chimica Acta 322.1 (2002): 21-28.
  • Yates, Allison A., Sandra A. Schlicker, and Carol W. Suitor. "Dietary reference intakes: the new basis for recommendations for calcium and related nutrients, B vitamins, and choline." Journal of the American Dietetic Association 98.6 (1998): 699-706. 
  • Zeisel, STEVEN H., et al. "Choline, an essential nutrient for humans." The FASEB journal 5.7 (1991): 2093-2098.

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!