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marylin monroe
Showing posts with label whole foods. Show all posts
Showing posts with label whole foods. Show all posts

Warding Off Holiday Weight Gain 2.0: The Anti-Diabesity Effect of Coffee Goes Beyond its Caffeine Content.

Image 1: If they are not laden with pesticides and anti-fungals, the small brown beans from the coffee pant can easily compete with green, black oolong and pu-erh teas, when it comes to countering the unwanted side-effects of the "holiday diet"
Back in the days, both, tea and coffee were luxury goods and people felt privileged if they could have any of them. Today, they have become another of the endless commodities of our convenience society, where coffee, the former drink of the kings (and popes), has gotten a bad rep lately as being the underlying cause of the "adrenal burnout" that has befallen 90% of the visitors of pertinent Internet bulletin boards. I was thusly not surprised that SuppVersity student Fat Free commented yesterday's blogpost on the anti-obesity effects of tea rather sheepishly. As if his wish for "a coffee" on the list of the anti-holiday-weight-gain items was some atrocious act in the sense that "a coffee" could never be as healthy as a hip green tea. I mean wasn't it bad enough that the "holy" green tea was outperformed by its primitive black brother?

Well, guess what, dear green tea connoisseurs, it may well be that (organic) coffee beans are in no way inferior to the unquestionably healthy, yet recently slightly over-hyped unoxidized camellia sinensis leaves. At least this is what a soon to be published study by Yuji Matsuda and his colleagues from the Nagoja University in Japan would suggest (Matsuda. 2011).

Tea or coffee during the holiday season - only a matter taste?

Matsuda et al. put a group of 8-week old mice on a pro-diabetic high-fat diet (this is the type of "high fat diet" that is high both in fat and in carbs and thusly is a perfect image of what 75% of the people are "eating" in the holiday season ;-). In the course of the 17-week study period the mice received either regular drinking water, or 2.5x diluted coffee, or water that was laced with 200mg of caffeine per liter (with a water intake of 13-14g/100g BW this would translate to a daily dose of 2.8mg/100mg and a human equivalent of 2.3mg/kg, or 182mg of caffeine per day for an 80kg human being). The intention was to investigate whether the results of epidemiological studies by van Dam (2002; 2005), Huxley (2009) and Goto (2011), which suggest that regular coffee consumption is associated with a profoundly reduced risk of developing metabolic syndrome or type II diabetes, could be replicated in a laboratory setting.
Figure 1: Body weight at the beginning and end of the study period in the control group and the mice receiving 2.5x dilluted coffee or 200mg/L caffeine in their drinking water; food intake in g per 100g of  body weight (data adapted from Matsuda. 2011).
If you look at the weight changes of the animals in figure 1, it becomes evident that despite a (non significantly) greater food intake esp. in the "real coffee" group, the mice on the coffee or caffeine supplemented high-fat diets gained approx. 8% less body weight than their water guzzling peers.
Figure 2: Fat weight in mice after 17 weeks on high fat diet with either water, 2.5x diluted coffee or water + 200mg caffeine per L (data adapted from Matsuda. 2011).
Now while the intrinsically flawed concept of a "body mass index" that is still propagated by mainstream media would suggest that there is something like an "ideal body weight", the numbers on your scale, alone, have no predictive value in terms of future health risk. The reductions in visceral (epididymal fat) and subcatenous fat accumulation in the mice of the coffee and caffeine arm is thusly a considerably more important finding of this study than the slightly reduced weight gain. After all, the amount of visceral (=inter-organ) fat you are carrying around is one of the few relatively reliable indicators of whether you are going to see your grand-children graduate, or not.

Time and again: Whole foods, or drinks, outperform extracts

If you take a closer look you will notice that despite a general tendency towards lower body fat levels in the coffee and caffeine group, the "whole food", or I should say, "whole beverage" has a much more pronounced effect on the "bad" visceral (epididymal) fat depots. So, just in case you still like your pills, caps and powders: This is only the latest in a long line of foods (this is the stuff that is not sold in caps or powder form) with verified health benefits, where one isolated compound, of which we believe that it is the "active ingredient" turns less potent than the whole food - so, could it possibly be that Nature knows best?
Figure 3: Reductions in inflammatory cytokine (MCP-1, TNF-alpha, IL-6) and adipokine expression in the epididymal fat pads of mice receiving 2.5x diluted coffee or water laced with 200mg/L caffeine in addition to their high fat diet (data calculated based on Matsuda. 2011).
The "whole foods" vs. "extract" difference is also evident in the differential effects coffee and caffeine had the expression of the inflammatory cytokines MCP-1, TNF-Alpha and IL-6 and the adipokines adiponectin and leptin. With a more pronounced expression of the latter (leptin) and an almost identical expression of the former (adiponectin) indicating an improved visceral fat metabolism in the epididymal fat pads of the "coffee-drinking" mice.
Figure 4: Insulin response (area under the curve in mg * min / dl) during glucose tolerance at different time-points during the 17-week study period (data calculated based on Matsuda. 2011).
As the areas under the insulin response curve in the glucose tolerance test go to show. Coffee (=whole food!) consumption does also reduce the transient caffeine induced decrease in insulin sensitivity that has been touted as one of the reasons why coffee would be "bad" for you. As the data from the study goes to show, this effect is only temporary, even for plain caffeine and should not be an issue for the habitual coffee drinker. Moreover, the long term benefits totally outweigh any short term increases in fasting blood glucose (approx. +8% in the first weeks of the study) - or, getting back to the initial research hypothesis: Coffee consumption is a possible way to reduce the risk of developing type II diabetes (at least  for mice ;-)

Coffee or tea? The choice is up to thee!

Since a direct comparison of the data from yesterday's tea study on teas would not be valid, anyways, and because I do not want to disturb the pre-Chrismas harmony and provoke a war between coffee and tea drinkers in the comment area of this blogpost, I would just advice everyone to just decline the soda your relatives may be offering you over the holidays and stick to either tea or coffee... whatever you like better - and by the way, dehydration is neither an issue for the habitual tea nor the habitual coffee drinker (Grandjean. 2000)!

Glucose vs. Fructose and Their Effects on Glucose, Insulin & Fat Oxidation in Men on Both Ends of the BMI Spectrum

"Fructose handles"? "Glucose handles"? "Saturated fat handles"? No, just the net result of a trashy diet.
I don't have to tell you that I don't buy into the "fructose is the devil" hysteria that's rampant in the blogosphere and certain parts of the scientific community. It's a matter of quantity and quality that determines the toxicity of a poison and in most of the "convincing" evidence on the detrimental effects fructose. I mean let's be honest, you don't have to be a rocket scientists to figure out that 5+ cans of Coke a day cannot be good for you (cf. "Fat Content Per Energy Drink 0g, Body Fat Gain Per Energy Drink 18g!"; read more) "194 Bananas in Three Weeks", on the other hand, are nothing to be afraid of (learn why).Have we been fooled again or is it just a high fructose corn syrup producer conspiracy?

Enough of the rants, let's get to the facts!

I guess that's enough for the "ranty" introduction. Let's now have a look at what a group of researchers from the School of Medicine in Portland has in stock for us: It's a paper titled "Change in postprandial substrate oxidation after a highfructose meal is related to body mass index in healthy men" that's about to be published in one of the future installments of Nutrition Research. As you will by now probably have figured out, the Anne C. Smeraglio and her colleagues had two things in mind, when they came up with the protocol that involved
  • What did the subjects eat? Participants were fed an egg omelet, bagel with cream cheese, and sweetened beverage breakfast consisting of one-third of their estimated daily caloric. The meal consisted of 30% fat, 15% protein, and 55% CHO (as % of energy). The CHO energy was further divided into complex and simple CHOs; 25% of the total calories were from complex CHOs and 30% of the calories were from either glucose or fructose added to the beverage.
    12 healthy men without diabetes, with a mean age of 25 (23-31) years and a BMI less than 30 kg/m²,
  • 2 visits at their labs that were separated by at least 1 week, but less than 1 month,
  • two meals that were high in glucose or fructose which were served in random order as a breakfast after an overnight fast, and
  • fasting for 7h after the ingestion of the standardized breakfast (sitting around watching TV or performing other, non-exciting quiet activities without the propensity to produce a catecholamine response)
During the experiment, the oxygen consumption and CO2 production were measured by indirect calorimetry to calculate resting energy expenditure and respiratory quotient (RQ; high RQ = burning predominantly glucose, low burning predominantly fat). The scientists also took blood samples at pre-defined intervals and collected the urine of their participants.
Figure 1: Insulin and glucose levels, as well as non protein respiratory quotient (high = carb oxidation; low = fat oxidation) 0-7h after the fructose and glucose breakfasts (Smeraglio. 2013)
The data in figure 1 is a summary of the the most "significant" results. In that the "quotation marks" enclosing the word "significant" is in my humble opinion the most significant information here - one that's encoded with irony, because after all, the only statistically significant effect the scientists observed were the ~2.5x higher insulin levels in the glucose group 60min after the ingestion of the test meal... yep, that's in the glucose group.

"There must be a mistake here!? Fructose is bad for you!"

The scientists have really done their homework as they did even take into account whether or not the amount of protein in the meals would have been responsible for differences in the respiratory quotient. The latter was not the case, the "baseline RQs between the fructose and glucose study visits were equivalent (0.82 ± 0.08 and 0.81 ± 0.10, respectively) and the p-value, indicating that there was a difference even rose from 0.72 to 0.75, when "when protein use was accounted for by evaluating NPRQ [non-protein respiratory quotient]" (Smeraglio. 2013)
Surprised? Well, I guess over all the lustig (=German for "funny") and unwarranted hoopla about how bad even small amounts of fructose are, you must have forgotten why scientists believed not too long ago that fructose could be the solution to, not the cause of the diabesity epidemic. After all, the paradigm of the mid to late 20th century was: Fructose does not spike glucose, so it should be the ideal sweetener for diabetics, because it is not necessary that your pancreas produces insulin to get rid of it.

I will not have to tell you, though that this assumption and the corresponding notion that totally replacing glucose with fructose would be a great idea is about as unwarranted, as the current fear of the "toxicity" of the small amounts fructose contained you'll be exposed to from a couple of pieces of fruit. I mean, let's take a peek at the data again.

Compared to the same amount of glucose, the consumption of the fructose equivalent of 5-6 medium sized (185g) apples (50-70g fructose, which is the amount of fructose the subjects in the study consumed) produces lower insulin levels and does not change either the leptin, triglyceride or glucose concentration in the blood or the ratio of glucose to fatty acid oxidation in healthy non-obese volunteers...

...apropos, non-obese, there was another thing to the headline wasn't there?

You are absolutely right, the research question involved (a) finding out what happens if you ingest a realistic breakfast where the carbohydrate content comes from (i) glucose or (ii) fructose and (b) determining whether the reaction would depend on the body weight / height² (BMI) ratio of the participants. So what about that, then? Let's see...
Did you know that there is a catalytic dose of ~40g of fructose per day (=6 normal size bananas) that will improve your glucose metabolism? (learn more)
"Although the absolute values for fat and CHO oxidation were not different between the fructose and glucose study visits, we did find a correlation between BMI and change in fat oxidation as a result of consuming the high-fructose meal compared with the high-glucose meal. The difference in fat oxidation (fat oxidation after the fructose meal minus fat oxidation after the glucose meal) was negatively correlated with BMI at the 4- and 7-hour time-points (Fig. 3; r =−0.59 [P= .04] andr=−0.59 [P= .04] for 4- and 7-hour time points, respectively) but not the 1-hour time point (Fig. 3; r=−0.52, P< .09). Nonprotein RQ displayed these same trends but did not reach significance." (Smeraglio. 2013)
As the scientists rightly point out, this suggests that the postprandial fat oxidation after the fructose meal was less than the fat oxidation after the glucose meal only among subjects with a higher BMI, and that the correlation with body weight, but not the difference itself was statistical significant.

Figure 2: Correlation of BMI with change in fat oxidation pearson correlation with linear regression trend lines between BMI and change in fat oxidation (fat oxidation after the fructose study visit minus fat oxidation after the glucose study visit; Smeraglio. 2013)
What's more, if you take a peek at the linear regression in the graph on the right hand side (figure 2) you will realize that that this does also mean that the fatty acid oxidation in lean individuals is actually increased after the ingestion of fructose. If I intended to drive my message "fructose from real foods is not your problem, folks!" home at all costs (which is what the "fructose is the devil" advocates like to do), I could seize on this observation and tell you: "Look folks, as long as you are already lean fructose will help, not impair your effort to get ridiculously shredded." I would yet hope that you are clever enough to see through this tactics and realize that neither the effect on the left hand side (=more fatty acid oxidation in the leaner folks with fructose vs. glucose), nor the one on the right hand side of figure 2 is physiologically relevant.

And that's not just because it's simply too small, but also because the ratio of glucose to fatty acid oxidation, i.e. the respiratory quotient (RQ) is not determining whether you store or lose body fat - if it were, you'd better be training in the "fat burning zone" for the rest of your (in that case) miserable lives.



Figure 3: Adding 7.5g of fructose ( to a 75g glucose load will improve not detoriate the glucose metabolism and that without increasing the amount of insulin that's released in response to the glucose load (Moore. 2000)
Bottom line: I am confident that that even without resorting to extreme interpretations of cherry picked data, the main message of today's article is clear. The comparatively small amounts of fructose you'll get right with the appropriate polyphenols & other cofactors from fruit and other fructose containing whole foods in your diet is not your enemy (Other items? Yeah, you know that even onions have 2g fructose, right?).

On a related note, you are aware that small amounts of fructose, like the 7.5g of fructose scientists added to the 75 g of glucose their 11 healthy subjects ingested during an oral glucose tolerance test had an up to 31% lower glucose response (these were the values for the 6 subjects with the highest level on the regular test) in the absence of concomitant increases in insulin response (see figure 3; Moore. 2000)!? You did not know that? Well, I guess it was about time to take a mental note, then ;-)

References:
  • Moore MC, Cherrington AD, Mann SL, Davis SN. Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults. J Clin Endocrinol Metab. 2000 Dec;85(12):4515-9. 
  • Smeraglio AC, et al. Change in postprandial substrate oxidation after a high-fructose meal is related to body mass index in healthy men. Nutr Res.2013 [epub ahead of print]

Eat Whole Eggs All Day and Throw Your Statins Away? 375x Increased Dietary Cholesterol Intake From Eggs Reduces Visceral Fat & Promotes Healthy Cholesterol Metabolism

Image 1: You better make sure you don't miss out on these delicious heart- and brain-healthy cholesterol bombs.
Most of you will probably be familiar with the good old saying "An apple a day, keeps the doctor away!", right? And if you are an otherwise healthy individual the micronutrients from the apple will probably really help you maintain this status. But what if the doctor was already there to put you on the healthy low fat diet, the negative health consequences of which I have addressed in yesterday's blogpost? In that case, whole eggs probably provide a more promising escape route from that low-fat, high-carb trap - at least this is what the the results of a soon to be published study from the Huazhong Agricultural University in Wuhan, China would suggest (Yang. 2012).

Surprising(?) -9% belly-fat reduction on whole egg diet

In their 60 to 90 day experiment, the Chinese researchers put a group of 8-week old Sprague-Dawley rats (n=18 for each group) on dietary regimen which differed in either cholesterol content (control vs. experimental groups) or the source of dietary cholesterol, i.e. 17.5% lard + synthetic cholesterol, 31.25% freeze dried egg yolk or 55.56% whole egg powder.
Figure 1: Composition of the control and the three experimental diets (adapted from Yang. 2012)
If you take a closer look at the exact composition of the diets in figure 1 the you will probably notice that macronutrient-wise the three standard-chow + lard/yolk/whole egg "high cholesterol" diets are miles-apart from what the average "low carber" would consider a healthy high fat diet. Still, the idea of choosing whole eggs as a major constituent (>55%) of one's diet should ring a bell for everyone who is familiar with the practical realization of the so-called "induction phase" of the purportedly (from the perspective of the same people who recommend the purportedly "heart-healthy low-fat diet") artery-clogging Atkins diet.
Figure 2: Body weight gain, food intake, food efficiency (food intake / weight gain) and relative visceral fat weight (per body weight) in Sprague Dawley rats after 60 and 90 days on experimental diets; data expressed relative to control group on standard rodent chow (data calculated based on Yang. 2012)
Interestingly, the data in figure 2 shows that even this version of "Atkins gone wrong", with a 40% carbohydrate content in the whole egg group (cf. figure 1) lead to significant reductions in weight gain and food efficiency (weight gain per gram of chow) and, more importantly, produced statistically significant reductions in the visceral fat / total body weight ratio at the end of the 90day study period (at 60 days there were no statistical significant inter-group differences).

55.56% whole egg diet kickstarts healthy cholesterol metabolism

In view of the fact that it has never been the notion that eggs would make you fat, but rather their purported negative effect on cholesterol levels due to which eggs, in general, and yolks, in particular, have gotten a bad rep over the last years, I guess that the visceral fat argument, alone, won't suffice to convince the egg-white consumer that they are missing out on the best part of the egg. After all, it was and unfortunately still is their purported negative effect on cholesterol that is literally at the heart of the egg(yolk)-scare.
Figure 3: Triglyceride, total, low density (LDL) and high desnity (HDL) cholesterol in Sprague Dawley rats after 60 and 90 days on experimental diets; data expressed relative to control group on standard rodent chow (data calculated based on Yang. 2012)
If you do yet take a look at the actual effects the natural cholesterol from the egg-containing diets had on the blood lipids of the rodents (cf figure 3), you will notice that those were statistically non-existent. In other words, only the lard + synthetic cholesterol diet had a statistically significant negative impact on the plasma lipids of the rats.
Figure 4: mRNA expression of hydroxymethylglutaryl CoA reductase (HMG-CoA R), LDL receptor (LDL-r), cholesterol 7a -hydroxylase (CYP71A), acyl-CoA:cholesterol acyltransferase (ACAT) lecithin cholesterol acyltransferase (LCAT) expressed relative to control (data adapted from Yang. 2012)
The 375x higher dietary cholesterol intake in the egg-groups, on the other hand, did not only shut down the endogenous cholesterol synthesis, as evidenced by the reduction in hydroxymethylglutaryl CoA reductase expression (HMG-CoA R, cf. figure 4) and increase its metabolization into bile acid via cholesterol 7a -hydroxylase (CYP71A), it also increased the LDL receptor expression in the liver (lack of LDL-r expression in the brain is associated with increased plaque formation in Alzheimer's, cf. Katsouri. 2011), lowered the formation and storage of cholesterol esterified cholesterol in the tissue by reducing acyl-CoA:cholesterol acyltransferase (ACAT) and increased the maturation of HDL and peripheral tissue cholesterol efflux via increased lecithin cholesterol acyltransferase (LCAT) expression.
In case you doubt that this rodent data has any significance for human beings, I just want to remind you that a 2008 study by Mayurasakorn et al., which found that "[i]n the majority of healthy adults" the addition of one egg per day to a "normal fat diet" lead to increases in HDL-c and decreases of the total cholesterol to HDL ratio (Mayurasakorn. 2008). Their conclusion that "egg consumption might benefit blood cholesterol" was however similarly ignored as the absence of scientific data to support the "eggs = increased risk of heart disease"-myth.
It is thusly not surprising that the Chinese scientists conclude that contrary to the "conventional approach to weight reduction", of which the scientists state that it is "a high-carbohydrate, low-fat, energy-deficient diet" that "has not proven to be very effective for many obese and over-weight individuals [I am not making that up, it is the exact wording from the study ;-]", an "egg diet", which "theoretically [...] would be more likely to cause obesity", could not only help those individuals finally shed unhealthy visceral fat, it could also lead to significant improvements in their lipid metabolism. If it were not for the statement that
[...] the mechanisms by which an egg diet lowers plasma cholesterol need to be further characterized and the special functional factors in egg need to be identified
one could be led to believe that Yang et al. had finally grasped the notion that just eating the right (whole) foods could solve the problem... the term "functional factors" does yet tell me that they are probably just trying to developing an "egg in a pill" that will soon be patented and sold as an adjunct to the standard statin therapy,