ONLINE DRIVERS MEDIA

Eggs or Flakes? Not 30% vs. 25% protein! A brief reminder of the fact that the stuff you eat is still food.

I am not quite sure when or why this happened, but I know that more and more people are thinking in terms of "macros" instead of foods. What I do know, though, is that the recent publication of studies from the Pennington Biomedical Research Center at the Louisiana State University System (Bayham. 2014) and an ostensibly unrelated study that was conducted by researchers from the Alimentary Pharmabiotic Centre, Biosciences Institute in Cork and scientists working at the local university and the University of Pittsburgh School of Medicine (Patterson. 2014) confirms - once again (!) - how futile this ignorant approach to nutrition actually is.

Eggs vs. cereals - not the best example, but...

In that, I am well aware that the "battle" between an egg- and a cereal-based breakfast in the Patterson study is not exactly a good model of whats currently going on in the health and fitness community. With cereals being labeled as "the devil" (its always nice to be "anti", isnt it?), no one would after all consider having ...

• One-and-a-half cup of Special K® RTE cereal, 200 ml Silk® original soymilk, one slice of Natural Grain “Wheat n’ Fiber”® bread, 13 g of butter, and 10 g of sugar-free strawberry jam (CG)

... for breakfast. In view of the fact that the same can be said for the calorie- and mocronutrient matched "high quality protein" breakfast, i.e.

• Two scrambled eggs, 120 mL skim milk, two slices of Holsum® thin white  bread, 5 g of butter, and 18 g of Smuckers® strawberry jam

... I still believe that the consequences of "breaking the fast" (learn why I am calling breakfast thus in "Breakfast or Breaking the Fast" | read more) with eggs vs. Special K are still relevant to the previously introduced context. And if you know that the acetylated form of ghrelin and PYY are "satiety hormones", it does not take a rocket scientists to interpret the data in Figure 1.

Figure 1: Level(s) of "satiety hormones" after the different breakfasts (Bayham. 2014)

What is difficult to tell, though, is whether the increased satiety after the egg breakfast would actually lead to a reduced intake at the subsequent meal.

• On an individual basis, i.e. on just one of the two eating occasions, the higher levels of acetylated ghrelin and PYY did not suppress the 20 healthy overweight or obese subjects energy intake during the subsequent lunch
• For day 1 and day 7, together, on the other hand, the 64kcal the egg eaters consumed less than the cereal eaters did reach statistical significance.

If we throw overboard all the things we (believe) we know about the fallacy of calorie counting, this would translate into a ~448kcal difference for one week and a whopping difference of 23,360kcal for a year, which should shed ~3.3kg of body fat a year.
Whether or not similar concrete weight loss vs. gain effects can be achieved with different types of fat is nothing study #2 in todays science mash-up here at the SuppVersity could answer. What it can tell you though, is that protein and obviously carbohydrates, where even Mr. Average Joe thinks in terms of "low GI" = good and "high GI" = bad carbs, these days, is by no means the only food component, where unspecifically counting macros is not going to cut it (or get you cut, if thats what you want to achieve).

This is not just about fish oil

"Of course, the bad omega-6s" ... I know that this is what youre thinking right now, but lets be honest, isnt that a bit narrow-minded?  It sure is and still, the results Ellaine Petterson and her Irish and American colleagues present in their most recent paper demonstrate quite clearly that the ingestion of fish and flax seed oil has pretty unique effects that go beyond its ability to increase the tissue concentrations of DHA to levels way beyond what youd see in low fat or high fat diets with palm, olive or safflower oil powered high fat diets.
In addition it lead to an increase in the relative abundance of bifidobacteria, a gut tenant that has been linked to all sorts of beneficial health effects, but has recently been outshadowed by various strains of lactobacilli (0.95% vs. more than 2% in all other groups), which - and this is an important information - were the lowest in the rodents who were kept on diets with 45% of the energy from fish and flaxseed oils.

Whether or not, the negative effects of fish oil on the lactobacillacea count in the guts of the lab animals is also partly responsible for the more or less disappointing effects the fish and flax seed diet had on the body composition (Figure 2) of the wild-type C57BL/6J male mice (21 d old) in the study at hand is questionable.

Figure 2: Body composition analysis at the end of the study (Patterson. 2014)

Its not impossible, though. A brief glance at the insulin levels and leptin levels in Figure 3 reveals that neither of them looks anyway close to what someone whos religiously taking his fish oil caps on a daily basis would be expecting. In the end, it is thus not really that surprising that only the palm oil diet group ended up with an inferior lean-to-fat mass ratio of 1.17 (vs. 1.33 in the omega-3 group).

Figure 3: Changes (%) in relevant metabolic markers in response to the different diets (Patterson. 2014)

The results of the study at hand, i.e. the effects on body composition (Figure 2), as well as blood glucose and lipid metabolism (Figure 3) are thus clearly not in line with the ubiquitously placated message that "fish oil is good for you" - a message, the indoctrinated average supplement junkie will still discern from the abstract of the study:

"[...] Ingestion of the HF-flaxseed/fish oil diet for 16 weeks led to significantly increased tissue concentrations of EPA, docosapentaenoic acid and DHA compared with ingestion of all the other diets (P< 0·05); furthermore, the diet significantly increased the intestinal population of Bifidobacterium at the genus level compared with the LF-high-maize starch diet (P< 0·05). These data indicate that both the quantity and quality of fat have an impact on host physiology with further downstream alterations to the intestinal microbiota population, with a HF diet supplemented with flaxseed/fish oil positively shaping the host microbial ecosystem." (Petterson. 2014).

Neither the "loss" of lactobacilli, nor the - if anything - negative effects of the high omega-3 diet on the lean-to-fat-mass ratio and the amount of insulin thats floating around in the rodents blood are mentioned in said abstract.

Fat = Diabetes - A FAT Mistake?

If you go take a look at the actual study data, we are thus left with the question, whether the purported benefits of having high amounts of omega-3 fatty acids in our cells (see red info box a couple of paragraphs above) are real enough (or really enough - whatever you prefer) to discard the fact that the study at hand would actually suggest that olive and not fish + flaxseed oil should be your go-to source of dietary fat on a high fat diet.

Moreover, if we abandon any paradigmatic believes, we would even have to concede that - within the current context, i.e. a rodent study and a diet with protein contents of only 19.2% (low fat) and 23% (high fat), the low fat mix of 1.25% of palm, 1.25% olive, 1.25% safflower oil, 0.625% fish and 0.625% flaxseed oil the rodents in the starch and sucrose groups received is superior to any of the high fat variants.

You may say that this is "rodent shit" (and it is, because this is what the scientists analyzed to access the SFCA metabolism of the mice) and a mere coincidence, but wouldnt you agree that this oil mix looks a little too much like the mixture youd get on a low-to-moderate fat diet with olive oil as a staple for everything, where you add oils, palm and safflower oil from processed foods on your cheat days and fish oil / omega-3s from your once or twice a week serving of salmon... ?
References: 

• Bayham, Brooke E., et al. "A Randomized Trial to Manipulate the Quality Instead of Quantity of Dietary Proteins to Influence the Markers of Satiety." Journal of Diabetes and its Complications (2014).
• Filaire, Edith, et al. "Effect of 6 Weeks of n-3 fatty-acid supplementation on oxidative stress in Judo athletes." International journal of sport nutrition 20.6 (2010): 496.
• Danthiir, Vanessa, et al. "Cognitive Performance in Older Adults Is Inversely Associated with Fish Consumption but Not Erythrocyte Membrane n–3 Fatty Acids." The Journal of nutrition (2014): jn-113.
• Patterson, E., et al. "Impact of dietary fatty acids on metabolic activity and host intestinal microbiota composition in C57BL/6J mice." The British journal of nutrition (2014): 1-13.

Ever since the Vinson study showed that green coffee bean extracts can help overweight women lose weight, green coffee is sexier than roasted one.

Only weeks after Vinson et al. were able to show that "Green Coffee Bean Extract Helps Pre-Obese Men and Women Shed 16lbs in 22 Weeks" (read more), green coffee bean supplements began to swamp the market - a great financial success for the supplement producers, and that despite the fact that follow-up studies that would confirm the amazing effects Vinson et al. report are still lacking. Two recent studies, one from the Queen Margaret University in the UK (Revuelta-Iniesta. 2014), the other from the  Jiangxi Agricultural University in the Peoples Republic of China (Zheng. 2014) could now shed a little more light on the weight loss effects of green coffee beans and the combination of caffeine and cholorgenic acid (CGA), the allegedly most important active ingredient in unroasted, green coffee beans.
In their 24-week rodent study, Zhang et al. (2014) tried to elucidate the mechanism by which CGA and caffeine regulate lipid metabolism. To this ends, they randomized their forty hairy subjects to diets containing no CGA or caffeine, CGA, caffeine, or CGA + caffeine.

Figure 1: Rel. (vs. control) body weight changes and liver and intraperitoneal adipose tissue weight (Zhang. 2014)

Over the course of the 24-weeks study, the scientists recorded body weight, intraperitoneal adipose tissue (IPAT) weight, and serum biochemical parameters of the rodents, tracked the the activities and mRNA and protein expression of lipid metabolism-related enzymes and analyzed the effects of caffeine, CGA and the combination of the two. What they found was...

1. Figure 2: Effects of chlorogenic acid (CGA) and caffeine on the hepatic protein expression levels of AMP-activated protein kinase (AMPK), adipose TAG lipase (ATGL) and fatty acid synthase (FAS; Zhang. 2014)

   decreases in the body weight and IPAT weight of mice fed the CGA + caffeine diet,
2. significant decreases in the serum and hepatic concentrations of total cholesterol, TAG and leptin of mice fed the CGA + caffeine diet,
3. increases of the activity of carnitine acyltransferase (CAT) and acyl-CoA oxidase (ACO), 
4. decreased levels of fatty acid synthase (FAS) and the respective mRNA levels
5. significantly upregulated mRNA expression levels of AMP-activated protein kinase (AMPK), CAT and ACO
6. pronounced reductions of PPARg2

If we group these findings as follows 3 + 5 and 4+6, we could say that they triggered 1 + 2 by (a) increasing the oxidation of fatty acids (3+5) and (b) decreasing the synthesis and storage of fatty acids (4+6) - an observation that could certainly explain the benefits Vinson et al. observed in their human study which has been retracted in October 2014, though. On the other hand, the amount of CGA and caffeine in the rodent diets (0.2 % CGA + 0.03 % caffeine) was quite significant and previous rodent studies on other allegedly promising fat burners were not replicable in human beings either (example: CLA). Against that background its good to have study #2 by R. Revuelta-Iniesta and E. A. S. Al-Dujaili, who investigated the effects of green coffee (GC), rich in chlorogenic acid, and black coffee (BC) on cardiovascular markers.

New human data with surprising results

The researchers designed a randomised pilot crossover study with healthy subjects who consumed both coffees for 2 weeks.

• The green coffee (GC) used in this project was Ethiopian Harrar 4 (100% Arabica) and the black coffee (BC) was Sainsbury’s Original Blend Cafetitère Coffee.
• The BC was  a blend of Brazilian, Colombian, Mexican, Nicaraguan, Peruvian, and Rwandan beans.

The study participants were asked to have 40 g of GC and BC per day distributed throughout the day into four cups of coffee. Thus, the scientists tried to ensure that high plasma coffee antioxidant concentrations were maintained over a period of time, "allowing effects to take place and the body to develop tolerance to caffeine, which can take 2-3 days." (Revuelta-Iniesta. 2014).

Table 1: Concentration of total polyphenols and antioxidant capacity determined in GC and BC as compared by the three methods of  coffee preparation (Revuelta-Iniesta. 2014).

The GC beans were grounded to powder using an electric coffee grinder. Instructions on how to make the coffee were provided and the Italian cafetière, the French cafetière, or the filter coffee machine was used to prepare the coffee drink.

The researchers measured anthropometry, blood pressure, and arterial elasticity after each intervention and collected urine samples to monitor antioxidant capacity. The free cortisol and cortisone levels you see in Table 2 were obtained from urine and analysed by specific ELISA methods.

Table 2: Comparison of results obtained (mean±SEM) after 14 days of green coffee vs. black coffee intervention (2-week cross over study); F: cortisol; E: cortisone; orange = almost bordeline significant; green = statist. significant inter-group difference (Revuelta-Iniesta. 2014).

In view of the short duration of the study (remember 2 weeks on each coffee), its not really surprising that we didnt see changes in any of the anthropometric measures. On the other hand, the mere fact that the cortisol/cortisone ratio (indicating 11beta-HSD1 activity) was reduced after GC (from 3.5 +/- 1.9 to 1.7 +/- 1.04, P = 0.002) does not suggest that you will see beneficial effects on body composition in the absence of significant reductions in energy intake. A reduction in glucocorticoid activity can in fact hamper not accelerate weight loss (learn more) and the researchers hypothesis that "GC can play a role in reducing cardiovascular risk factors" (Revuelta-Iniesta. 2014) is a possible, but unconfirmed hypothesis.
References:

• Jaquet, Muriel, et al. "Impact of coffee consumption on the gut microbiota: a human volunteer study." International journal of food microbiology 130.2 (2009): 117-121.
• Revuelta-Iniesta, R., and E. A. S. Al-Dujaili. "Consumption of Green Coffee Reduces Blood Pressure and Body Composition by Influencing 11?-HSD1 Enzyme Activity in Healthy Individuals: A Pilot Crossover Study Using Green and Black Coffee." BioMed Research International 2014 (2014).
• Vinson, Joe A., Bryan R. Burnham, and Mysore V. Nagendran. "Randomized, double-blind, placebo-controlled, linear dose, crossover study to evaluate the efficacy and safety of a green coffee bean extract in overweight subjects." Diabetes, metabolic syndrome and obesity: targets and therapy 5 (2012): 21.
• Zheng, et al. "Chlorogenic acid and caffeine in combination inhibit fat accumulation by regulating hepatic lipid metabolism-related enzymes in mice." British Journal of Nutrition (2014). Ahead of Print.

Cortisol is not your enemy. In fact, cortisol is one of the few hormones you really need to survive.

Cortisol is a problem. However, just as it is the case with insulin, its not the fact that your body produces it thats problematic. Its the fact that it tends to so in copious amounts and chronically, simply at the wrong time or - believe it or not - not at all / enough. All that, i.e. changes / problems with the natural rhythm, the up and down, the spikes and troughs that get lost, when you are chronically stressed and/or inflamed - thats the actual problem and not the fact that your body produces a hormone without which you cant survive. Against that background, it may go against everything the supplement industry is trying to tell you, but still cannot be really surprising to hear that E. Allansson Kjölhede and colleagues from the Linköping and Ume a Universities present in their latest paper in Acta Pædiatrica results that show that obese children have low, not high cortisol levels (Kjölhede. 2014).

Using three salivary samples from 342 children aged 6–12 years the scientists had tried to reconcile previous, inconsistent findings and found that the

"average cortisol levels in early morning, late morning and evening were significantly lower in overweight and obese children than in their normal weight counterparts."

Whats particularly interesting is that the early morning spike, we have identified as critical component of a healthy biorhythm, previously (see "All About Cortisol"), was reduced by -33% (see Figure 1):

Figure 1: Morning (8:30 am), late morning (10:30 am) and evening (9:00pm or pre-bed, if earlier) salivary cortisol in 342 normal-weight, overweight and obese children (Kjölhede. 2014).

As Kjölheide et al. point out, these results should be followed up by more comprehensive studies that would allow us to better classify and understand the "relationship between stress and obesity in
children" - and I would like to add: Which of these comes first - being obese or having low morning cortisol and thus not being able to benefit from the "wake-up and get going" effects of cortisol.
Thats also interesting, because previous studies by Toledo-Corral et al. have shown that a dampened cortisol awakening response is not just associated with obesity, it is also a predictive factor of higher carotid artery intima-media thickness (CIMT) in overweight African American and Latino youth (Toledo-Corral. 2013), which in turn is a risk factor for myocardial infarction and stroke.

And Ursache et al. (just because its funny: "Ursache" means "cause" in German ;-) report that  dolescents with insulin resistance exhibited

• a blunted cortisol awakening response (CAR),
• smaller hippocampal volumes, and 
• greater frontal lobe atrophy 

compared to controls. Closer scrutiny of the data also revealed that "a smaller CAR was associated with higher BMI which was in turn associated with fasting insulin levels" (Ursache. 2012).

Despite the fact that it is virtually impossible to tell what exactly the "ursache" for the irrefutable correlation between low morning cortisol levels and high body fatness, artery intima-media thickness, myocardial infarction and stroke is, the cumulative evidence clearly speaks against the use of cortisol-reducing drugs and supplements - at least if their effects are not extremely short-lived and will thus not mess with the natural up-and-down thats lost not just in obese, but also in chronically fatigued patients.

Reference: 

• Champaneri, Shivam, et al. "Diurnal salivary cortisol is associated with body mass index and waist circumference: the Multiethnic Study of Atherosclerosis." Obesity 21.1 (2013): E56-E63.
• Toledo-Corral, Claudia M., et al. "Blunted nocturnal cortisol rise is associated with higher carotid artery intima-media thickness (CIMT) in overweight African American and Latino youth." Psychoneuroendocrinology 38.9 (2013): 1658-1667.
• Tominaga, Yuji, et al. "Licorice Flavonoid Oil Effects Body Weight Loss by Reduction of Body Fat Mass in Overweight." Journal of health science 52.6 (2006): 672-683.
• Tominaga, Yuji, et al. "Licorice flavonoid oil reduces total body fat and visceral fat in overweight subjects: A randomized, double-blind, placebo-controlled study." Obesity research & clinical practice 3.3 (2009): 169-178.
• Ursache, Alexandra, et al. "Preliminary evidence for obesity and elevations in fasting insulin mediating associations between cortisol awakening response and hippocampal volumes and frontal atrophy." Psychoneuroendocrinology 37.8 (2012): 1270-1276.
• Zenk, John L., et al. "The effect of 7-Keto Naturalean™ on weight loss: A randomized, double-blind, placebo-controlled trial." Current therapeutic research 63.4 (2002): 263-272.