"An Apple A Day" & More: Alex Leaf's Reviews Folk Wisdom and Scientific Evidence on a Forbiddenly Healthy Fruit Item

Forbidden fruit or not: You got to love your daily apples ;-)

Guestpost by Alex Leaf

An apple a day keeps the doctor away. I’m sure you’ve heard this before. And while there are many ways in which we could keep the doctor at bay with an apple (target practice anyone?), our wellbeing demands we eat the luscious fruit. Truthfully, the old adage could not be truer for a variety of reasons. So to keep things organized I am going to worm through the benefits of apples categorically. Also remember we are dealing with the apple fruit, not the apple fritter or apple flavored candy or the iPhone.

I suppose the best starting point is the apple’s nutritional worth. As you can see in the nutritional label to the right, a single medium apple is less than 100 Calories and provides over 10% of the RDA for fiber. Apples also contain every vitamin needed by the body with the exception of Vitamin B12, which is only found in animal products, and Vitamin D, which you can produce by eating your apple under the sun. The same applies to minerals, with apples providing a little of everything except selenium.

A hearty bite for a healthy heart

If you have ever looked at an apple you may have noticed it resembles the humble heart, and for good reason. A comprehensive review of nine human studies conducted by researchers at the British Nutrition Foundation in London examined the effects of apples on cardiovascular disease risk factors and found that apple polyphenols, a type of antioxidant, have a positive influence on blood lipids and blood pressure in human beings (Weichselbaum, Wyness and Stanner 2010). Furthermore, don’t think that apple juice has you covered, since these compounds are most concentrated in the peel of the apple (Wolfe, Wu and Liu 2003). In fact, whole apples have an average of 57 times more polyphenols than commercial apple juice (Hyson 2011; cf. Figure 1).

Figure 1: Phenols in whole apples vs. juices (Markowski. 2005)

Not for juicers (addendum by Adel)! I won't tire and repeat it once again. If you want to eat fruit, do so - EAT it, don't juice it, or buy juices from the supermarket. Why? Just take a  look at the phenol loss in juices in Figure 1 and you have your answer.

I know that some of you are juice-o-holoics, so in case you still insist on juicing, keep the pomace and throw away the juice, not the other way around ;-)

Okay, so heart health is from the antioxidants in apples and I can get those in any fruit or vegetable. Well, not quite. In one study of nonsmoking healthy middle-age adults who ate apples less than twice a month, simply eating one apple per day lowered blood levels of oxidized LDL – a substance linked to hardening of the arteries – by 40% (Ohio State University 2012). And it’s not just because of the polyphenols either, since a group in this study that took a polyphenol supplement instead of eating the apple had similar but not as pronounced effects. Even dried apples show promise, with a separate study concluding that daily dried apple consumption “can significantly lower atherogenic cholesterol levels” (Chai, et al. 2012). The only caveat is that you need to eat the equivalent of two apples per day if dried rather than fresh.

Apples can help with weight management and protect against cancer

In a very recent study, researchers from the University of Navarra in Spain sought to determine the mechanisms through which the beneficial effects of apple polyphenols act on diet-induced obesity (Boqué, et al. 2013). Overall, they found that apple polyphenols exerted potent anti-obesity and anti-diabetic effects through prevention of fat cell growth, decreased intestinal glucose uptake, and increased fat breakdown. These effects were observed at both the surface and genetic level. The researchers even conclude their study with the acknowledgement that apple polyphenols can act “as a promising functional food ingredient for the management of obesity and its metabolic complications”.

Figure 2: Vitamin & Mineral content of one large apple relative to RDA. Data based on USDA food database for 09003, Apples, raw, with skin (USDA. 2013) - left;  Nutritional label of one raw apple with skin - right (skipthepie.org. 2013)

A review summarizing the current knowledge on potential cancer preventive effects of apples conducted by a lone researcher at the German Cancer Research Center in Germany found that apples influence multiple mechanisms relevant for cancer prevention on the genetic level, and regular consumption of one (or more) apple per day has been shown to prevent skin, breast, and colon cancer (Gerhauser 2008). And it all comes back to the whole fruit, with some of the most potent anti-cancer compounds residing in the peel (Cornell University 2007).

Apples can do even more!

The antioxidants in apples have been shown to extend the average lifespan of fruit flies by 10% (American Chemical Society 2011). Granted the relevance to humans is debatable, but it’s interesting nonetheless. Apple polyphenols may even provide protection against some autoimmune diseases such as ulcerative colitis and Crohn’s disease (Federation of American Societies for Experimental Biology 2011). Another unique compound found in apple peels, ursolic acid, prevents muscle loss during illness and aging, and “animals given ursolic acid also became leaner and had lower blood levels of glucose, cholesterol and triglycerides” (Cell Press 2011).

And it doesn’t end there. In a review and analysis of apples and related compounds, Dianne Hyson (Hyson 2011) from the Department of Family and Consumer Sciences, California State University concluded that, There are current data suggesting that [apple polyphenols] might be linked to reduced risk of several forms of cancer, cardiovascular disease, and asthma. [Apple polyphenols] may also have beneficial effects on outcomes related to Alzheimer’s disease, cognitive decline of normal aging, diabetes, weight management, bone health, and gastrointestinal protection from drug injury.

Red Delicious is king, when it comes to its antioxidant power.

Talk about natural medicine! While everyone has their own apple preferences, some of us may want to know how to capitalize on this apple investment. If that’s the case, then I present the Red Delicious apple. Studying the antioxidant amounts of every apple variety would be difficult, but less broad comparisons have been done. One of these studies looked at eight popular apple varieties grown on the same farm under similar conditions and found that the Red Delicious had the most antioxidant activity (American Chemical Society 2005).

This makes sense when you think back to “eating the rainbow” in fruits and vegetables, since the above study also found the antioxidants to be five times higher in the skin than the flesh of the apples, and Red Delicious apples are renowned for their seductive red coating. It’s also better to go organic with this one as organic apples have on average higher antioxidant capacity than their conventional counterparts (Stracke, et al. 2009). So if you ever needed more reasoning for heading down to farmer Joe…

Oh, and before I forget. Apples are harvested in the fall, which makes local organic difficult to find during other times of the year. Usually, a bunch of apples will be picked and stored through the winter until the next harvest. Fret not, since “long-term storage, both at refrigerator temperature and under controlled atmosphere conditions, was found not to influence flavonoid concentration or antioxidant activity” (van der Sluis, et al. 2001) of the apple.

Emotional Eating

Have your head in the clouds from choosing to eat that apple with lunch? I’m not surprised, given that recent research has shown that eating fruit and vegetables may promote emotional wellbeing (White, Horwath and Conner 2013). More specifically, “on days when people ate more fruits and vegetables, they reported feeling calmer, happier and more energetic than they normally did" (IANS 2013). Even just eating apples in everyday life has been shown to reduce hunger and elevate mood (Macht and Dettmer 2006). Eating more apples isn’t challenging either. Actually, it’s as simple as buying a new fruit bowl. People are more likely to eat apples when they are visible and easily accessible (Privitera and Creary 2012). So keep your fruits close, and your apples closer. Especially during stressful times, as you may find yourself a little less anxious (Hyson 2011).

Promise me! Never throw away the pomace, if you insist on juicing your apples, then keep the pomace in whatever the result may be. This is where all the good stuff is and this is what made the difference between a 5% reduction in type II diabetes risk for apple eaters and a 8% increase in type II diabetes risk for apple (and other) juice drinkers in a recent analysis of three prospective longitudinal cohort studies by Muraki et al. (2013).

Bottom line (by Adel): If you are not convinced of the benefits of apples (not Apple!), yet, you may want to have a parting look at a study that made a direct comparison between statins and apples with respect to their cardio- and stroke-protective effects in otherwise healthy adults over 50 years.

The results of the model the scientists fed with data from previous studies are quite astonishing: With a assumed compliance of 70% compliance in the "an apple a day" arm of the study, the scientists except a reduction in vascular mortality of 12%. Now, allegedly that's based on the estimate that this would be the necessary consequence of the "apple-induced" reduction in low density lipoprotein... but alas, it's better than the hilarious and obviously 100% irrelevant witch-hunt on apples and other "high fructose fruit items" *rofl* - I mean, I find it "lustig" (German word for "funny") that people believe that someone would develop diabetes & NAFLD from eating whole apples.

References:

• American Chemical Society. Eating apples extends lifespan of test animals by 10 percent. March 8, 2011. http://www.sciencedaily.com/releases/2011/03/110302121702.htm (accessed May 13, 2013). 
• —. Red Delicious, Northern Spy Apples Have Most Antioxidants, Chemists Find. May 23, 2005. http://www.sciencedaily.com/releases/2005/05/050523234141.htm (accessed May 16, 2013). 
• Boqué, Noemi, et al. "Prevention of diet-induced obesity by apple polyphenols in Wistar rats through regulation of adipocyte gene expression and DNA methylation patterns." Molecular Nutrition & Food Research, 2013: [ePub ahead of print].
• Cell Press. Apple Ingredient Keeps Muscles Strong: Component of Apple Peels Found to Help Prevent Muscle Weakening in Mice. June 7, 2011. http://www.sciencedaily.com/releases/2011/06/110607131718.htm (accessed May 13, 2013).
• Chai, S C, S Hooshmand, R L Saadat, M E Payton, K Brummel-Smith, and B H Arjmandi. "Daily apple versus dried plum: impact on cardiovascular disease risk factors in postmenopausal women." J Acad Nutr Diet 112, no. 8 (2012): 1158-1168.
• Cornell University. An Apple Peel A Day Might Keep Cancer At Bay. June 3, 2007. http://www.sciencedaily.com/releases/2007/06/070601181005.htm (accessed May 13, 2013).
  Federation of American Societies for Experimental Biology. Scientists discover anti-inflammatory polyphenols in apple peels. December 15, 2011. http://www.sciencedaily.com/releases/2011/11/111130100455.htm (accessed May 13, 2013).
• Gerhauser, Clarissa. "Cancer Chemopreventive Potential of Apples, Apple Juice, and Apple Components." Planta Medica 74, no. 13 (2008): 1608-1624.
• Hyson, Dianne A. "A Comprehensive Review of Apples and Apple Components and Their Relationship to Human Health." Advances in Nutrition 2, no. 5 (2011): 408-420.
  IANS. Eating fruits, vegetables linked to emotional well being. January 30, 2013. http://cooks.ndtv.com/article/show/eating-fruits-vegetables-linked-to-emotional-well-being-321793 (accessed May 16, 2013).
• Macht, M, and D Dettmer. "Everyday mood and emotions after eating a chocolate bar or an apple." Appetite 46, no. 3 (2006): 332-336. 
• Markowski, J., W. Plocharski, and M. Mieszczakowska. "Effect of cultivar and processing on phenolics and antioxidant activity of apple products." I International Symposium on Human Health Effects of Fruits and Vegetables 744. 2005.
• Muraki, Isao, et al. "Fruit consumption and risk of type 2 diabetes: results from three prospective longitudinal cohort studies." BMJ: British Medical Journal 347 (2013).
• Nutritional Info: Raw Apple with skin. 2013. http://skipthepie.org/fruits-and-fruit-juices/apples-raw-with-skin/?weight=182 (accessed May 2, 2013). 
• Ohio State University. An apple a day lowers level of blood chemical linked to hardening of the arteries, research suggests. October 2, 2012. http://www.sciencedaily.com/releases/2012/10/121002143220.htm (accessed May 13, 2013).
• Privitera, G J, and H E Creary. "Proximity and Visibility of Fruits and Vegetables Influence Intake in a Kitchen Setting Among College Students." Environment and Behavior, 2012.
  Stracke, B A, C E Rüfer, F P Weibel, A Bub, and B Watzl. "Three-year comparison of the polyphenol contents and antioxidant capacities in organically and conventionally produced apples ( Malus domestica Bork. Cultivar 'Golden Delicious')." J Agric Food Chem 57, no. 11 (2009): 4598-4605.
• U.S. Department of Agriculture. "USDA National Nutrient Database for Standard Reference, Release 26." 2013.
• van der Sluis, A A, M Dekker, A de Jager, and W M Jongen. "Activity and concentration of polyphenolic antioxidants in apple: effect of cultivar, harvest year, and storage conditions." J Agric Food Chem 49, no. 8 (2001): 3606-3613. 
• Weichselbaum, E, L Wyness, and S Stanner. "Apple polyphenols and cardiovascular disease – a review of the evidence." Nutrition Bulletin 35, no. 2 (2010): 92-101.
• White, Bonnie A, Caroline C Horwath, and Tamlin S Conner. "Many apples a day keep the blues away – Daily experiences of negative and positive affect and food consumption in young adults." British Journal of Health Psychology, January 2013.
• Wolfe, Kelly, Xianzhong Wu, and Rui Hai Liu. "Antioxidant Activity of Apple Peels." J. Agric. Food Chem 51, no. 3 (2003): 609-614.

Complete Meals & GI (Non-)Sense, Glutamine & GLP-1, Low Thyroid & High Trigs, N-3 vs. N-6 Interactions, Optimal DHA Dosage in Kids W/ NAFLD, Selenium vs. Aluminum Toxicity

While this is not the exact combination of chicken breast, mashed potatoes and salad in the first one of today's news items, it's more than likely that the predicted GI (and thus probably what you would find if you looked it up in a table) overestimates the postprandial glucose response to this meal by ~50% and says absolutely nothing about the insulin response. It looks like complex meals and over-simplified theories, don't mix well, at all ;-)

78% that's the SuppVersity Figure of the Week and actually part of the additional information I provided on one of today's On Short Notice items. It's the increase in coronary heart disease risk women with subclinical hypothyroidism have compared to their peers with spot on TSH levels of 0.5-1.5mU/L (Asvold. 2012). In conjunction with other more or less recent studies, such as Mitchel's, Hsu's and Sahai's paper confirming the previously often talked about but not well-established 2-fold increase in congenital hypothyroidism from the early 1990s to the first years of the new millennium (Mitchel 2011), the predictive value of high TSH levels in the first trimester (early pregnancy hypothyroidism) for adverse pregnancy outcomes (Schneuer. 2012), the 30% risk increase in all-cause mortality in both women and men with subclinical hypothyroidism Tseng et al. reported in their paper earlier this year or the impairment of spatial working memory (Yin. 2012), Asvold's results only add to the evidence that the potential pitfalls of an increasingly prevalent metabolic dysfunction may have been ignored way too long.

• More GI lovin' - On the menu today: Mashed potaoes with chicken, rapeseed oil or both (Hätönen. 2011) - I thought a mini-follow-up on Friday's post on the GI would be nice, 'cause some of you have not without reason been complaining that not everyone would eat pure white bread, like my students do.
  
  

  

  Figure 1: The real (=measured) GI of a meal does differ significantly from the theoretical prediction. So, even if the concept was worth bothering, the GIs of complete meals simply wrong, if they are not measured (Hötönen. 2011).

  Moreover, the mere fact that the scientists from the Department of Lifestyles and Participation at the National Institute for Health and Welfare in Helsinki, Finland, found that the addition of chicken breast, rapeseed oil and a salad, individually and in combination, had the GI of a meal containing six mashed potatoes (this was the parameter that was held constant) induced more than twofold changes in GI, with the addition of chicken breast having the greatest deviation from the predicted value in this group of 11 (initially 12) healthy subjects, three men and nine women, aged 36.2 (SD 14.1) years with a BMI of 21.3 (SD 1.7) kg/m² and normal glucose tolerance (see figure 1).
  
  Now given the fact that most data on the GI of complete meals has never been measured, but is actually based on the same predictions the scientists used, it stands to reason that...
  

  [...] this highlights the problems encountered when predicting the GI values of mixed meals. The protein com-ponent of the mixed meal evoked the largest insulinaemic responses and markedly increased the II of the mixed meal containing protein. However, introducing fat into the meal decreased the effect of protein on the insulinaemic responses (Hätönen. 2011)

  So, this does not simply bust the idea that you could calculate the GI, it does likewise show you that people who are still overtly scared of insulin (which is hillarious as long as you are insulin sensitive) are doing he exact wrong thing, when they make food-choices based on GI: Whey protein would in that case be in as much a no-go as simply eating a chicken breast with your mashed potatoes would be, because other than what most people believe, it does increase the insulin spike and thus reduce the glycemic index by allowing your body to clear the glucose more efficiently from the circulation.
  
  Suggested reads: The red box in the "Whey is More Insulinogenic than White Bread" post on the partitioning effects of BCAAs and yesterday's Facebook post on the anti-Alzheimer's effects of insulin.

• 

  Suggested read: Amino Acids for Super Humans the purported ergogenic effects of l-glutamine

  30g of oral glutamine have similar effects on GLP-1 as 75g of glucose (Greenfield. 2008) - Still a follow up on the GI discussion, I think you may be interested in. If you are someone who follows the questionable practice of ingesting large boluses of glutamine in the futile believe that this would increase your gains or speed up recovery, you may be pleased to hear that only 30g of oral l-glutamine produced an increase in the "Fat Burning Satiety Hormone GLP-1" (read more on GLP-1) that's on a gram to gram basis more pronounced than in response to insulin (0.41pmol/L per gram glucose vs. 0.75pmol/L per gram of glutamine; in 8 healthy subjects).
  
  Before you go and buy tons of glutamine, you should however consider that GIP, the pro-insulinogenic peptide and glucagon (ramps up gluconeogenesis in the liver) were likewise increased by the ingestion of this bolus of glutamine. It is therefore no wonder that glutamine has never been shown to be a "fat burner". Nonetheless, a 1999 study by Bowtell et al. would suggest that it may come handy to replenish liver and muscle glycogen after a workout (8g alone did increase glucose storage after a workout to a similar degree as a 18.5% glucose polymer solution and additional 25% glucose storage mostly in the liver, when both were coingested; cf. Bowtell. 1999). And if you don't care about that - your gut integrity could also be a reason to consider supplementation in the vicinity of particular strenuous or length workouts (see "Shedding Some Light on the Leaky Gut <> Exercise Connection") 

• Practical relevance? Based on data from a 12-year longitudinal study, even women with subclinical hypothyroidism have 76% risk for coronary heart disease (p = 0.005), than women with spot on TSH levels of 0.5-1.5mU/L (Asvold. 2012). And even women well within in the "normal range" (TSH of 1.5-2.4mU/l) have a 41% higher risk of heart disease, although this is only borderline significant (p = 0.08). For men the TSH level alone had not predictive value. Spec. w/ regards to T3, there are also reports of increased incidence of ventricular disfuntion (Cassetti. 2009), increased cardiac death in CVD patients (Iervasi. 2003) and impaired recovery after a stroke (Alevizaki. 2007). We do yet have to be cautious, here as "low T3" syndrome could as well be the consequence of overall inflammation and the association does not tell us anything about what's the chicken and the egg.
  Low thyroid, high triglyceride (Hashimoto. 2012) -- If you are wondering why on earth your trigs won't come down, it may well be that it's the absence of sufficient amounts of thyroid hormone. I a soon-to-be-published paper in Endocrinology scientists from the Gunma University in Maebashi, Gunma, Japan, report that thyroid hormone regulates the expression of a Stearoyl-CoA desaturase-1 (SCD-1) which controls the production of trigs from carbohydrates.
  
  Surprisingly the 75% increase due to hypothyroidism and the 75% decrease in SCD-1 mRNA expression (both compared to a euthyroid state) the scientists observed in rodents in response to the administration of T3 were not mediated by receptor binding, but simply as a down-stream effect of direct modifications of the SCD-1 gene promoter between -124 and -92 bp by T3.
  
  On a related side note: It is actually the last mentioned mechanism which is the major new finding in the study at hand and not the fact that T3 can reduce the conversion of carbohydrates to triglicerides that is the actual news here. After all, the latter is something scientist should know, but obviously like to forget about ever since the late 1999s (Waters. 1997)

• Omega-6 intake and not low omega-3 intake is the problem (Liou. 2007) -- Another older study, but one I am posting in response to a discussion some of you are having about omega-3 (ALA) intake in the post about safflower oil and DHT, because I simply feel that it's necessary to shed some light  on the erroneous assumption that by simply upping your intake of omega-3s or fish oil intake you could get away without decreasing your omega-6 intake, which in and out of itself will already increase the amount of anti-inflammatory omega-3 fatty acids (supplementation of DHA can still be advisable, specifically if you are a vegetarian).
  
  

  

  Figure 2: Effect of 4 weeks of high (red) vs. 4 weeks of low (green) linoleic acid (n-6) intake on short and long-chain omega-3 plasma phospholipid content in healthy men (Liou. 2007)

  In 2007, already Liu et al. conducted a very interesting experiment in the course of which they fed healthy men diets with identical amounts of omega-3 fatty acids (1% of the total energy intake), but two different amounts of linoleic acid (omega-6) and found that the high omega-6 intake (10.1% vs. 3.8% of the total energy intake) alone decreased the total amount of EPA among the plasma phospholipids (the major long-chain omega-3 fatty acid in fish oil), not just the ratio of omega-3 to omega-6, in the blood of their 29-45 year-old subjects by more than 25% (see figure 2). The paradoxical effect on DHA, on the other hand, would warrant further investigation, and underlines how reliant we are - if anything on the intake of pure DHA, which dropped in consequence to the test diet, which was devoid of fatty fish, while the original diet of the non-vegetarian subjects had fish in it.
  
  In this context, I would also like to point out that DHA is exactly where real fish is far superior to fish oil caps, because it has a way more favorable EPA:DHA ratio than fish oil caps. Salmon fillets for example have - depending on the fatty acid source in the diet 8.5g : 13.8g, 4.4g : 7.8g and 1.5g : 2.9g (all values per 100g) when the feed contains fish oil, fish and rapeseed and fish + rapeseed and rapeseed, only.
  
  And while the ratios are similar regardless of the chow, the data from the Seierstad et al. clearly shows that the fatty acid content of the diets can induce almost 5-fold differences in terms of the total DHA content and the omega-3 to omega 6 ratio (fish oil diet: 6.5, fish oil + rapeseed: 1.7, rapeseed: 0.6) of salmon fillets (Seierstad. 2003). 

• It does not take much: 500mg DHA not more effective than 250mg  (Nobili. 2012) -- At least if it comes to its beneficial effects against liver steatosis in children  (mean age 11 years; BMI 26.6kg/m² and 24.4kg/m², in the low and high dose groups respectively with with NAFLD, the amount of DHA does not appear to be so important. According to the results of their 2-year registered controlled trial, both 250mg and 500mg of Docosahexaenoic acid lead to identical and profound reductions in the odds ratio of developing more severe steatosis during the study period.
  
  

  

  Figure 3: Odds ratio (comparing DHA supplement vs. placebo) of more severe vs. less severe liver steatosis determined every 6 months during the 24-month study period (Nobili. 2012)

  If you take a closer look at the data in figure 3, you will even have to concede that the lower dosage did a better job - while the mean odds ratios were only marginally lower in the 250mg DHA group, the extremely high standard deviations in the 500mg DHA would suggest that the 250mg dose appears to be more reliable. In this regard it may be interesting that the increase in serum DHA did mirror the dosages. With a 0.65% and 1.15% increase in DHA those were about 2x higher in the 20 boys and girls in the high dose group compared to the 20 kids in the control group who received a 290 mg linoleic acid germ oil supplement "placebo" (by the way, a monosaturated fatty acid placebo would have been more of a placebo than 290mg of omega-6)
  
  In view of the fact that the changes in triglycerides, ALT, HOMA-IR and BMI (which was not even different from the placebo group) were likewise identical, it does not appear as if anything that goes beyond the amount you will find in 2x cheap fish oil caps, or 10g even of the cheapest salmon fillet (see last paragraph of previous item) would be necessary to ellicit the anti-steatosis effect of fish oil - since those kids weight on average 55kg, an adult may want to add in another fish oil cap to get up to 360mg DHA per day or simply eat his fatty fish once or twice a week.

• Selenium ameliorates aluminum toxicity (Viezeliene. 2012) -- With the whole upheaval about the potential negative side effects of the aluminum in vaccines, the formerly overlooked yet well-known neurotoxic (Exley. 1992; Gupta. 2005), hepatotoxic (Abubakar. 2003; Perez. 2005) and nephrotoxic metal (Geyikoglu. 2012) has all of a sudden returned to the center of public interest.
  
  Therefore I thought that you will be interested in the results of a study that's going to be published in the next issue of the Journal of Trace Elements in Medicine and Biology - irrespective of whether you believe, like Tomljenovic and Shaw that
  

  "the possibility that vaccine benefits may have been overrated and the risk of potential adverse effects underestimated, has not been rigorously evaluated in the medical and scientific community"(Tomljenovic. 2011)

  After all, vaccines are not the only potential source of aluminum in our environment, so that the ameliorative effects (all values remained normal in the aluminum exposed group, while there were 30%, 55% and 42% increases in GSH in the animals who received only the selenium injection) the co-administration of supplemental selenium had on the GSH reductions in liver, kidney and brain of Balb/c mice weighing 20–25g who were exposed (by i.p. injection)to AlCl3 (25 mg Al(3+)/kg body mass) for 16h could be important, regardless of whether you do or don't intend to get vaccinated.
  
  

  

  There is more about selenium at the SuppVersity, for example on its pro-fertility effects, and its anti-corrosive effects in the brain.

  That said, the dosage requirements necessary to maintain healthy GSH levels are probably much lower than the hillarious (for a healthy individual) in the study at hand 1,250µg/kg body weight of sodium selenite (Na2SeO3). Considering the elemental selenium content in Na2SeO3, the latter would equal to ~3,650µg - unquestionably WAY too much (remember this was a one-time dosage that was specifically co-administered w/ the aluminum). Even the 'no observed adverse effect' level for a 70kg man of intake which is ~1000µg/d (Whanger. 1999) appears unnecessarily high, so that the consumption of a handful of brazil nuts once or twice a week and/or other high selenium foods such as tuna, cod, oysters, shrimp, but also eggs, meats, poultry, mushroom and onions on a regular should suffice to get what you need, to fortify yourself against the constant assault of heavy metals.
  
  What would be interesting, though, is a study into the effects of adding selenium to the "safe" aluminum in vaccines. I mean, you cannot seriously tell me that we could not afford doing that and if it reduced any toxicity issues, why not?

That's about it for today, I did not post all too many new facebook news as of yet (I mean, come on, it's Saturday ;-), but if you are into medicinal horror-stories, you will certainly like the story about the flesh eating killer fungus. If you prefer microbes over fungi, you are probably better off with the latest insights into the associations of certain gutbacteria with the incidence of stroke. And if you are more into other aspects of the digestive tract you may be interested in the effects of gastric emptying time on postprandial gylcemia and insulin release.

If none of those news is to your liking, I suggest you either wait for me to post something else (could be happening within the next hours at www.facebook.com/SuppVersity), or simply enjoy the weekend and come back tomorrow when you are rested for another (hopefully) enlightening SuppVersity post.

References:

• Abubakar  MG,  Taylor  A,  Ferns  GA.  Aluminium  administration  is  associated  with enhanced  hepatic  oxidant  stress  that  may  be  offset  by  dietary  vitamin  E  in  the rat. Int J Exp Pathol 2003;84:49–54.
• Asvold BO, Bjøro T, Platou C, Vatten LJ. Thyroid function and the risk of coronary heart disease: 12-year follow-up of the HUNT Study in Norway. Clin Endocrinol (Oxf). 2012 Dec;77(6):911-7.
• Bowtell JL, Gelly K, Jackman ML, Patel A, Simeoni M, Rennie MJ. Effect of oral glutamine on whole body carbohydrate storage during recovery from exhaustive exercise. J Appl Physiol. 1999 Jun;86(6):1770-7.
• Cassetti G, Pinelli M, Bindi M, Bianchi M, Castiglioni M. [Low T3 syndrome and left ventricular diastolic function]. G Ital Cardiol (Rome). 2009 Aug;10(8):553-7. 
• Exley  C,  Birchall  JD.  The  cellular  toxicity  of  aluminium.  J  Theor  Biol 1992;159:83–98.
• Geyikoglu  F,  Turkez  H,  Ozhan  Bakir  T,  Cicek  M.  The  genotoxic,  hepa- totoxic,  nephrotoxic,  haematotoxic  and  histopathological  effects  in  rats after aluminium chronic intoxication. Toxicol Ind Health 2012;15.
• Greenfield JR, Farooqi IS, Keogh JM, Henning E, Habib AM, Blackwood A, Reimann F, Holst JJ, Gribble FM. Oral glutamine increases circulating glucagon-like peptide 1, glucagon, and insulin concentrations in lean, obese, and type 2 diabetic subjects. Am J Clin Nutr. 2009 Jan;89(1):106-13.
• Gupta  VB,  Anitha  S,  Hegde  ML,  Zecca  L,  Garruto  RM,  Ravid  R,  et  al.  Alu- minium  in  Alzheimer’s  disease:  are  we  still  at  a  crossroad?  Cell  Mol  Life  Sci 2005;62:143–58.
• Hashimoto K, Ishida E, Miura A, Ozawa A, Shibusawa N, Satoh T, Okada S, Yamada M, Mori M. Human Stearoyl-CoA Desaturase 1 (SCD-1) Gene Expression Is Negatively Regulated by Thyroid Hormone without Direct Binding of Thyroid Hormone Receptor to the Gene Promoter. Endocrinology. 2012 Dec 7.
• Hätönen KA, Virtamo J, Eriksson JG, Sinkko HK, Sundvall JE, Valsta LM. Protein and fat modify the glycaemic and insulinaemic responses to a mashed potato-based meal. Br J Nutr. 2011 Jul;106(2):248-53. 
• Iervasi G, Pingitore A, Landi P, Raciti M, Ripoli A, Scarlattini M, L'Abbate A, Donato L. Low-T3 syndrome: a strong prognostic predictor of death in patients with heart disease. Circulation. 2003 Feb 11;107(5):708-13.
• Liou YA, King DJ, Zibrik D, Innis SM. Decreasing linoleic acid with constant alpha-linolenic acid in dietary fats increases (n-3) eicosapentaenoic acid in plasma phospholipids in healthy men. J Nutr. 2007 Apr;137(4):945-52. 
• Mitchell ML, Hsu HW, Sahai I; Massachusetts Pediatric Endocrine Work Group. The increased incidence of congenital hypothyroidism: fact or fancy? Clin Endocrinol (Oxf). 2011 Dec;75(6):806-10.
• Perez  G,  Pregi  N,  Vittori  D,  Di  Risio  C,  Garbossa  G,  Nesse  A.  Aluminium  expo- sure  affects  transferrin-dependent  and  -independent  iron  uptake  by  K562  cells. Biochim  Biophys  Acta  2005;1745:124–30. 
• Schneuer FJ, Nassar N, Tasevski V, Morris JM, Roberts CL. Association and predictive accuracy of high TSH serum levels in first trimester and adverse pregnancy outcomes. J Clin Endocrinol Metab. 2012 Sep;97(9):3115-22.
• Seierstad SL, Seljeflot I, Johansen O, Hansen R, Haugen M, Rosenlund G, Frøyland L, Arnesen H. Dietary intake of differently fed salmon; the influence on markers of human atherosclerosis. Eur J Clin Invest. 2005 Jan;35(1):52-9.
• Waters KM, Miller CW, Ntambi JM. Localization of a negative thyroid hormone-response region in hepatic stearoyl-CoA desaturase gene 1. Biochem Biophys Res Commun. 1997 Apr 28;233(3):838-43. 
• Whanger P, Vendeland S, Park Y-C & Xia Y. Metabolism of sub-toxic levels of selenium in animals and humans. Annals of Clinical Laboratory Science. 1996;26, 99-113.

Vitamin C & CVD Mortality Maximal Reduction W/ Medium High Serum Levels | Restaurant Eaters Eat More Salt, Fat, Sugar & Co in Fast Food & Full-Service Restaurants

Does eating out put us at risk of too much unhealthy stuff, even if we avoid McDonald's, Burger King & Co? Recent study says: Yes it does!

When I woke up today, I thought it would be nice to do some short news and get rid of a handful of studies in my "to be written about in the future" folder. What about the U-shaped dose-response curve for the cardio-protective effects of vitamin C, for example?

In their latest paper in the Proceedings of the Nutrition Society scientists from the Queen’s University Belfast and the MONICA Institutes in Belgium and France report that there is a U-shaped dose-response relationship between vitamin C intakes and cardiovascular disease (CVD) and mortality risk in the ~10,000 50–59 year-old Irish, Belgian and French men who participated in the PRIME study from 1991–1993 (Lyner. 2014).

Learn more about hormesis and potential neg. effects of antioxidants at the SuppVersity

Is Vitamin E Good for the Sedentary Slob, Only?

NAC Impairs Anabolic Effects of Exercise

Vitamin C + E Hamper Gains in the Elderly

C+E Useless or Detrimental for Healthy People

Vitamin C and Glucose Management?

Antiox. & Health Benefits Don't Correlate

Said study had originally been designed to examine the substantial differences in cardiovascular incidence and mortality between Northern Ireland and France.

The data is based on blood samples that were taken from participants at baseline, stabilised and frozen at −150°C and complemented by additional follow ups every year. Over the total study duration of 10 years, the scientists lost only 5% of their subjects due to non-compliance.

Figure 1: Changes in overall mortality risk and CVD risk in the 2nd to 4th quartile of serum vitamin C levels; only the risk reductions in the third quartile were statistically significant (Lyner. 2014)

The relevant data, the graph in Figure 1 is based on stems from those 6.2% (n= 654) who died, and the 5.2% (n= 546) who had a CVD event that was validated by a medical committee.

What do previous studies say? Randomized controlled trials did not show significant reductions in mortality risk with vitamin C supplementation (Bjelakovic. 2007). A subsequently published Cochraine Review even found slight reductions in all-cause mortality in healthy individuals who use vitamin C supplements (+2%; Bjelakovic. 2012). Higher total vitamin C intakes from food have yet been linked to 35% and 10% reductions in all-cause mortality risk in US men and women, respectively (Enstrom. 1992).

As you can see, the vitamin C levels in the blood, which were measured on a BMG FLUOstar Optima plate reader predict the risk of overall mortality and CVD incidence the risk at both high and low levels. In that, it should be obvious that you're far worse off with "no" vitamin C in your blood than you'd be with very high levels. And still, the fact that the happy (high) medium, i.e. vitamin C levels in the 3rd quartile, was associated with the most significant risk reduction, provides additional evidence that having as much as possible of a good thing is not necessarily optimal.

I'd love to see data on supplementation and / or nutrition practices, but unfortunately (or luckily? due to accuracy) the study at hand is based on serum measures, only. Overall, the data still speak in favor of the scientists' hypothesis that "increasing vitamin C status [and I would add 'by eating high vitamin C foods, like fruits and vegetables'] in the population could contribute to reduced rates of mortality" (Lyner. 2014).

Speaking of fruits and vegetables! Those are obviously not available at US restaurants.

I bet that the subjects in the "restaurant eater" group in a recent study from the American Cancer Society and the University of Illinois at Chicago did not consume exactly much of these healthy food items (fruits and vegetables). What they ate, on the other hand, were significantly more salt, saturated fat and total kcal.

More energy, less nutrients: Previous studies based on datasets from 1994–1996 indicate that  adults who reported eating fast food had higher intakes of energy, total fat, saturated fat, Na and carbonated soft drinks, and lower intakes of vitamin A, vitamin C, calcium, iron, fibre, milk, fruits and vegetables than those who did not report eating out - fast food or not (Paeratakul. 2003; Bowman. 2004, Lachat. 2012).

If you look at the comparison of fast food and full-service restaurants, you may be surprised to see that the former are comparably harmless, when it comes to salt (remember: it's probably not an issue for most of us). I guess that is a result of the implementation of "salt reduction practices" in response to public pressure.

Figure 2: Relative increase in energy, sugar, saturated fat, and salt intake in full-service / fast food restaurants vs. at home (Nguyen. 2014).

What's almost shocking and offers a look ahead into Americas future is the fact that the negative effects of eating out are significantly more pronounced in young adults (aka future diabetics). Similar negative trends are obvious for black (296kcal / 277kcal in fast food and full-service restaurants) vs. white & hispanic Americans (~180kcal) and people with middle & low (~230kcal extra) vs. high income (~160kcal extra).

In the discussion of their results, Nguyen and Powell point out that their research also suggests that restaurant food consumption as a snack was associated with particularly high additional energy intake, i.e. 260.99 kcal for fast-food and 234.20 kcal for full-service restaurants. It is thus only logical that they advise "that adults do not sufficiently reduce non-restaurant intake to compensate for additional energy intake on days consuming at restaurants." (Nguyen. 2014).

Vitamin C + E supplements block the adaptational response to exercise, but appear to boost fat loss, recent study shows - seems like you just cannot have it all | learn more.

Bottom line: Personally, I find none of the the previously presented study results surprising. Well, maybe the fact that full-service restaurants have people overeat even more than fast food restaurants.

The fact that very high vitamin C levels were associated with lower reductions in all-cause mortality and cardiovascular incidence risk, on the other hand, is something that shouldn't surprise you in view of the evidence from experimental trials on the non-existing benefits of vitamin C supplementation and the fact that the study participants in the "very high" vitamin C level quartile four of the study by Lyner et al. probably didn't get there due to their exuberant fruit and vegetable consumption  | Comment on Facebook!

References:

• Bjelakovic, Goran, et al. "Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis." Jama 297.8 (2007): 842-857.
• Bjelakovic, Goran, et al. "Antioxidant supplements for prevention of mortality in healthy participants and patients with various diseases." Cochrane Database Syst Rev 3.3 (2012).
• Bowman, Shanthy A., and Bryan T. Vinyard. "Fast food consumption of US adults: impact on energy and nutrient intakes and overweight status." Journal of the American College of Nutrition 23.2 (2004): 163-168.
• Enstrom, James E., Linda E. Kanim, and Morton A. Klein. "Vitamin C intake and mortality among a sample of the United States population." Epidemiology 3.3 (1992): 194-202.
• Lachat, Carl, et al. "Eating out of home and its association with dietary intake: a systematic review of the evidence." Obesity Reviews 13.4 (2012): 329-346.
• Paeratakul, Sahasporn, et al. "Fast-food consumption among US adults and children: dietary and nutrient intake profile." Journal of the American Dietetic Association 103.10 (2003): 1332-1338.

Dairy - The Good, the Bad or The Ugly? Latest Studies On Heart Disease, Diabetes, Cancer, Obesity and Co. Plus: What Dairy Peptides Do For Your Heart, Gut, Brain, etc.

Do you take Liz Hurley's word and set all warnings about the "non-paleo-ness" of dairy in general and milk in particular at naught? Or do you put faith into the "got milk?" campaign? Personally, I'd suggest not to do one or the other. I'd rather suggest you join me and take a look at a selection of recent studies.

If you've been following the SuppVersity Facebook News and / or have read previous SuppVersity articles on milk and dairy, you will be aware that I am not exactly convinced that the mere existence of allergic reactions and the "fact" that "our ancestors did not drink milk before ..." *put your favorite guesstimate here* allows for the conclusion that we are "not meant" to consume cow's milk. I am nevertheless open to scientific arguments that would convince me that dairy is bad for me - it's just that I don't see this evidence outside of "western diet + dairy makes you fat and that makes you sick" contexts.

What I do see, though, are papers such as the one Sandra Abreu or the recent review by Flávia Galvão Cândido et al. - studies that tell us that the intake of milk is negatively associated with the clustering of cardiometabolic risk factors in adolescents (Abreu. 2013), and reviews which conclude that "the consumption of low-fat dairy products may be an important strategy to prevent and control T2DM [type 2 diabetes]" (Cândido. 2013).

The evidence that dairy is bad for us all is simply not there

But hey, ... let's tackle the evidence one by one. I mean, there is plenty of news-worthy material here and we don't want the fun to be over prematurely, do we? So, let's start with a brief sketch of what Sandra Abreu and her colleagues from the University of Porto base their assessment that the intake of milk, but not total dairy, yogurt, or cheese, is negatively associated with the clustering of cardiometabolic risk factors in Spanish adolescents - shall we?

No! Full-fat dairy is not bad for you: While most of the epidemiological studies with their hilariously unreliable food questionnaires appear to suggest that only low fat dairy was good for your heart, a recent study from the Harvard School of Public Health found a clever way to test the association more objectively. Instead of questioning their subjects, 2837 US adults aged 45 to 84 years, they tested the amount of certain phospholipids in their blood and found that "plasma phospholipid 15:0, a biomarker of dairy fat, was inversely associated with incident CVD [-19%] and CHD [-26%]." (de Oliveira Otto. 2013) The fact that other dairy related phospholipids were not associated (neither positive nor negative) with cardiovascular and coronary heart disease risk does yet, as the scientists rightly point out, warrant further investigation.

"To test th[e] hypothesis [that a higher dairy product intake is associated with lower cardiometabolic risk factor clustering in adolescents], a cross-sectional study was conducted with 494 adolescents aged 15 to 18 years from the Azorean Archipelago, Portugal. We measured fasting glucose, insulin, total cholesterol, high-density lipoprotein cholesterol, triglycerides, systolic blood pressure, body fat, and cardiorespiratory fitness. We also calculated homeostatic model assessment and total cholesterol/high-density lipoprotein cholesterol ratio. For each one of these variables, a z score was computed using age and sex. A cardiometabolic risk score (CMRS) was constructed by summing up the z scores of all individual risk factors. High risk was considered to exist when an individual had at least 1 SD from this score. Diet was evaluated using a food frequency questionnaire, and the intake of total dairy (included milk, yogurt, and cheese), milk, yogurt, and cheese was categorized as low (equal to or below the median of the total sample) or “appropriate” (above the median of the total sample). The association between dairy product intake and CMRS was evaluated using separate logistic regression, and the results were adjusted for confounders." (Abreu. 2013)

I know that sounds really sophisticated, but in the end, it's just standard procedure for cross-sectional studies like this - studies with one unfortunate downside: It's impossible to detect causal relationships. 

Figure 1: Dietary intake in the low and "adequate" dairy-, milk-, yogurt-intake groups (Abreu. 2013)

Keep that in mind, when you take a closer look at the data in Figure 2 which indicates that the average adolescent milk connoisseur of whom you can see in Figure 1 that he / she consumes significantly more energy on a daily basis has a significantly reduced cardiometabolic risk (predicted by cardiometabolic risk score; CMRS):

Figure 2: Cardiometabolic risk in "adequate" vs. low dairy, milk, yogurt and cheese consuming adolescents; adjusted for parental education , pubertal stage, low-energy reporter, energy intake, total fat , protein , and dietary fiber intake.

I personally was surprised to see a statistically significant protective effect only with milk - it's not that I had expected to see that for all forms of dairy, but based on previous studies I would have expected the fermented yogurt products to outperform conventional milk.

The negative effects of cheese on the other hand are by no means surprising. Food logs do after all include all types of "cheese" including the fake yellow vegetable oil based cheese analogues the kids shovel down with their pizzas, burgers and the rest of the fast food dirt. A high cheese intake has thus (unfortunately) become an indicator of low diet quality and the results of the study at hand hardly a credible marker that cheese is bad for you.

If 95% of your "dairy intake" comes from pizza, you are unlikely to see...

... any of the following benefits of dairy peptides, Blanca Hernández-Ledesma, María José García-Nebot, Samuel Fernández-Tomé, Lourdes Amigo, and Isidra Recio summarized in a soon-to-be-published review in the peer-reviewed scientific journal International Dairy Science:

• 

  Figure 3: Reduction of systolic blood pressure in mmHg per mg/kg of the said peptide you consume - mind the logarithmic scale(!); data calculated based on rodent studies summarized in Hernández-Ledesma (2014)

  Cardiovascular health effects due to the antihypertensive, anti-inflammatory, general antioxidant and hypocholesterolaemic properties of various dairy peptides
• Intestinal health effects due to the ability of dairy peptides to modulate and regenerate the gut mucosa, increase mineral absorption, exert local anti-inflammatory effects at the gastrointestinal level
• Antidiabesity effects that are related to both direct pro-insulinogenic effects of dairy peptides ant their ability to increase satiety. 
• Central nervous system relaxant and antinociceptive (pain-killing) effects
• Immune health which is promoted by antimicrobial and immunomodulatory peptides that are either already present in dairy or arise during the digestion process
• Anticancer effects that are mediated by the overall anti-inflammatory properties of certain dairy peptides, as well as direct anti-proliferative effects of dairy

Now, it goes without saying that you won't see the same effect from eating some goat kefir as Miguel et al. (2010) observed it, when they administered fraction 58-68 of goat casein to their lab rodents, but the data in Figure 3 can explain the well-established blood pressure lowering effects of dairy in general and the whey and casein induced BP reduction Figueroa et al. observed only recently in a study with obese women (Figueroa. 2013; see SuppVersity Facebook News).

Bottom line: You can't expect dairy to fully protect you against diabesity, cancer and a leaky, you can't expect it to lean you out in days, and you can't expect it to build muscle overnight, but you can expect general health benefits not detriments from incorporating a variety of fermented and unfermented dairy products into your diet - as long as you ain't lactose intolerant.

"Are Camels the Better Cows? Cancer, CVD, Allergies,Infections & More - Camel Milk Prevents or Fixes All These Ailments" | more

One thing you should keep in mind, though, is the unfortunate fact that the amount of "non-dairy" cheese, cream and other products is increasing by the day. Especially the former, the fake yellow vegetable oil based cheese analogues is something you want to avoid. The same goes for many of low fat products. While much of the "magic" is in the peptides, most of the commercially available "diet" products contain tons of sugar and all sorts of questionable additive to make up for the loss of color, taste and texture that's brought about by the removal of the fat. And lastly all products that extend the shelf-life to "eternity" by adding questionable preservatives.

References

• Abreu, S., Moreira, P., Moreira, C., Mota, J., Moreira-Silva, I., Santos, P. C., & Santos, R. (2013). Intake of milk, but not total dairy, yogurt, or cheese, is negatively associated with the clustering of cardiometabolic risk factors in adolescents. Nutrition Research.
• Cândido, F.G., Ton, T. S., & Alfenas, R. D. C. G. (2013). Dairy products consumption versus type 2 diabetes prevention and treatment; a review of recent findings from human studies. Nutr Hosp, 28(5), 1384-1395.
• de Oliveira Otto, M. C., Nettleton, J. A., Lemaitre, R. N., Steffen, L. M., Kromhout, D., Rich, S. S., ... & Mozaffarian, D. (2013). Biomarkers of dairy fatty acids and risk of cardiovascular disease in the multi‐ethnic study of atherosclerosis. Journal of the American Heart Association, 2(4), e000092.
• Figueroa, A., Wong, A., Kinsey, A., Kalfon, R., Eddy, W., & Ormsbee, M. J. (2013). Effects of Milk Proteins and Combined Exercise Training on Aortic Hemodynamics and Arterial Stiffness in Young Obese Women With High Blood Pressure. American Journal of Hypertension, hpt224. 
• Freedman, B. J. (1980). Sulphur dioxide in foods and beverages: its use as a preservative and its effect on asthma. British Journal of Diseases of the Chest, 74, 128-134.
• Hernández-Ledesma, B., García-Nebot, M.J., Fernández-Tomé, S., Amigo, L.,
  Recio, I., Dairy protein hydrolysates: Peptides for health benefits, International Dairy Journal(2014), ahead of print
• Iammarino, M., Di Taranto, A., Palermo, C., & Muscarella, M. (2011). Survey of benzoic acid in cheeses: contribution to the estimation of an admissible maximum limit. Food Additives and Contaminants: Part B, 4(4), 231-237.

100-200ml Red Wine Per Day Improve HDL and the LDL/HDL Ratio With & Without Mediterranean Diet & Exercise

Good for him, good for her, good for everyone? Is it really possible that red wine can help even those who don't want to the necessary lifestyle changes?

You all know about the limitations of epidemiological studies and the fallacy of the over-generalization of associations between health parameters and red wine consumption in the mainstream media. For me this *bs* is so annoying that I usually don't even take a look at "red wine studies". Luckily, a recent paper by Dirk W. Dorste and his colleagues did still catch my attention: It's about to be published in the December issue of Nutrition Journal and is not based on epidemiological data.

The Luxembourgian scientists gathered their data in the course of a randomized unblinded 2-year trial that involved 108 patients with carotid atherosclerosis and >30% reduced blood flow (65% of the patients were on statin therapy).

122 patients, 4 intervention groups, red wine and/or lifestyle changes

While half of the patients did nothing to improve their health and fitness, the other half of the patients, the lifestyle change group, had to follow a modified Mediterranean diet and perform moderate physical exercise during 30 min/day for 20 weeks. In both of these groups half of the patients were randomized either to no alcohol or red wine groups (100ml/day for women, 200ml/day for men). The end results of this process was a 2 x 2 design that looked like this:

• Med. diet + exercise only
• Med. diet + exercise + red wine

• regular diet + laziness only
• regular diet + laziness + red wine

While the subjects in the groups in the left "regular diet + laziness" column did not receive any dietary advice and were not encouraged to work out, the participants in the "Med. diet + exercise groups" had five 30 min sessions with a registered dietitian "giving advice on healthy eating based on a modified Mediterranean diet and physical exercise" - the cornerstones of this advice were:

• 

  Not into red wine? Learn about "The Ergogenic Effect of Nonalcoholic Beer Front- & Back Loading" | more

  eat 5 portions of fruit/vegetables per day, 
• consume a diet low in absolute fat, 
• prefer vegetable oil (olive or canola oil), 
• eat whole grain products, poultry, low fat dairy products, 
• consume a fat and a lean fish meal per week,
• reduce your consumption of red meat, 
• avoid pork and ready made-meals,
• stay away from sugar and excessive amounts of salt,
• drink 1.5-2 l plain water every day,
• eat the occasional 25g of dark (70%) chocolate,
• include tomatoes and walnuts in your diet,
• get at least 30 min of moderate daily physical activity

Yes, I know, not all of these points are exactly in line with what you (and even I) believe to be cornerstones of a healthy diet, but I do not write about this study, because it was an awesome example for highly beneficial lifestyle changes - quite the contrary: I picked it because the booze worked even without lifestyle changes:

Figure 1: Relative changes (in %) in total cholesterol, LDL, HDL, LDL/HDL and triglycerides after 4 and 20 weeks on one of the four "interventions" (Droste. 2013)

If you compare the red wine only and lifestyle only data from the end of week 20, it is not easy to tell the difference between the two - the greater improvements in HDL cholesterol, and higher reductions in LDL actually give the impression that simply guzzling red wine would be more effective than reinventing your diet and exercise habits

If we take a closer look at the data we do yet (luckily) have to acknowledge that the the subjects who did reinvent their lives were the only ones with lasting beneficial effects on total cholesterol, HDL, the LDL/HDL ratio and the total amount of triglycerides after 20 weeks - and that irrespective of the missing dietary and exercise / training control and despite the disputable dietary advice they received!

"Hard Liquor Increases Post Workout Testosterone by Almost 100% " | more

Bottom Line: This is not the experiment to confirm the hilarious mainstream media hype about the health benefits of red wine, but the results of this prospective study are still intriguing. They do after all support the hypothesis that the literal glass of wine can actually be a crutch that helps you to take a first baby step towards a healthier life. It does not hamper, but improve the beneficial effects of lifestyle interventions on CVD-relevant plasma markers and it's stand-alone effect on the HDL/LDL ratio is - I have to admit that - downright surprising.

Reference:

• Droste, Dirk W., et al. "A daily glass of red wine associated with lifestyle changes independently improves blood lipids in patients with carotid arteriosclerosis: results from a randomized controlled trial." Nutrition journal 12.1 (2013): 147.

Pimp My Olive Oil! When Virgin is not Phenol-Rich Enough: The Pharmacokinetics of Phenol-Enriched Virgin Olive Oil.

Image 1:  "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 health-remedy nature has provided for us. In the past this approach was not particularly healthy, though... is phenol-enriched olive oil going to be the exception to the rule?

Being the health-conscious person you obviously are (why else would you visit the SuppVersity ;-), chances are that olive oil, or, to be specific, extra virgin olive oil is one if not primary source of of mono- and polyunsaturated fats in your diet. But do you actually know why? I mean why olive oil? And why extra virgin? What? "Mediterranean diet", "high MUFA content", "lower incidence of coronary heart disease and cancer"? All right, you have done your homework on olive oil, but what about the "extra virgin"? The polyphenols, right. The phenolic content is in fact what distinguishes a "good" olive oil. The phenolic alcohols, the secoiridoid derivatives, the phenolic acids, the lignans and the flavonoids in concert have been reported to have anti-oxidant, anti-inflammatory, anti-atherogenic and anti-carcineogenic properties and are probably as, if not more important for the beneficial health effects of the Mediterranean gold than its fatty acid profile (Covas. 2007; Covas. 2008).

So, if those polyphenols are the "active ingredients" in olive oil, wouldn't it be nice if we had an oil that had even more of these beneficial healthy secondary plant metabolits in our oils, right?

Now we have tons of polyphenols, but does that make a difference?

The thought, that a souped up version of the already phenol-rich virgin olive oil would be an even more potent health promoter must have occurred to a group of researcher from Spain, as well. Back in 2010 already, Manual Suárez and his coworkers published a paper in the Journal of Argiculture and Food Chemistry in which they describe the development of a "phenol-enriched olive oil with phenolic compounds from olive cake" (Suárez. 2010). In essence, the scientists just put back some of the pulp (an extract to be precise) that is produced when the oil is squeezed from the olives into the end-product. In a more recent study the scientists did now try to evaluate how much of these (additional) health promoters in 30ml of regular virgin olive oil (VO) and the enhanced virgin olive oil (EVOO) actually make it into the blood of 16 (8 men, 8 women) healthy subjects in a randomized, controlled, cross-over trial (Suárez. 2011).

Figure 1: Compositional differences (phenol-enriched vs. standard virgin olive oil) in polyphenol content (data calculated based on Suárez. 2011)

If you take a look at the compositional differences between the regular and the "phenol-enriched" virgin olive oil, it is quite obvious that, from a mere quantitative point of view, Suárez' product with on average 3.3x more secondary plant metabolits should be the more potent health promoter. After all, numerous previous studies have shown that those olive oils with (naturally!) particularly high phenol-content exhibit the most pronounced beneficial health effects (Samanego Sanchéz. 2007). This would yet require adequate absorption of the respective compounds from a now obviously more dense solution, which, according to the results of this study, does not seem to be the case for all compounds - and more importantly, all subjects:

The in vivo study showed that the concentration of fourteen of twenty-four compounds detected was higher in the plasma samples from the EVOO than after ingestion of VOO. Among these, two of them, hydroxytyrosol sulphate and vanil-lin sulphate, were statistically significant in attending their pharmacokinetic parameters, demonstrating the suitability of enrichment. In general, a displacement of the time to reach the maximum concentration is observed in the samples, which indicates that more time is needed to absorb the higher phenolic content. However, inter-individual variabilityin the concentration of the plasma phenol metabolites shows that it is difficult to show statistically significant differences between the VOO and the EVOO.

The scientists thusly conclude that the "metabolism of phenols is affected first by the individual". So until we actually know which influence these are, the label "phenol-enriched" on olive oils and other products has little meaning for you as an individual. And even if you belong to the "lucky" high-absorbers, only two, namely vanillin sulphate and hydroxytyrosol sulphate will reach what the scientists call "pharmocokinetic" levels, if you ingest two tablespoons of the super-potent "phenol-enriched" virgin (and still relatively natural) olive oil.

Figure 2: Changes in total antioxidant activity (TAA) of experimental oils subsequent to heat treatment (from Pellegrini. 2001)

Note: Common Internet wisdom would suggest that you have to be particularly cautious with those "phenol-enriched virgin olive oils", when respective products hit the market (and I bet this won't take long). After all, you will all have heard how heating those oils damages the healthy polyphenols - and while that may to some extend be the case, a 2001 study by Nicoletta Pellegrini et al. found that the total antioxidant value of olive oil does not only increase with increased polyphenol content, but that those polyphenols are also "stabilizers of R-tocopherol during olive oil heating, thus contributing to the nutritional value of cooked foods" and "the prevention of antioxidant activity decay in olive oil during realistic heating conditions" (Pellegrini. 2001), which ranged from 30min at 160°C to 120min at 190°C. The latter happens to be at the upper end of the regular deep-frying temperature and would thus suggest that the commonly heard recommendation not to use extra virgin olive oil for frying is not valid, at least when we focus exclusively on its total antioxidant capacity as measured by Trolox essays (cf. figure 2). In that it should be mentioned that, with its relatively high content of highly oxidizable omega-6 fats, olive oil still isn't the "ideal" frying oil - notwithstanding that frying does not constitute the healthiest way of preparing your food anyways ;-)

And though a recent study has shown that the latter conjugates with LDL and thusly protects it from oxidative damage (González-Santiago. 2010), it remains to be verified whether the consumer variety of the olive oil in this study will actually provide any health benefits. And this is particularly true in view of the fact that the food giants will, as they already do it in the case of "normal" virgin olive oil, minuscule amounts this probably expensive ingredient into their otherwise unhealthy convenient products, just to be able to put the highly marketable "contains phenol-enriched virgin olive oil" on the label... but, hey! I guess, this is just the never-ending story of complete nutritional idiocy ;-)

Chicken, Rice, Veggies & Oil and How Their Effects on Your Insulin & Glucose Levels Are 50% Off Those You'd Expect Based on the Calculated Glycemic Index of This Meal

The power of GI calculations is limited and even with meals as simple as the one in the picture, the calculated glycemic index can be ~50% off!

As a SuppVersity reader you've repeatedly read about macronutrient interactions, such as the insulin boosting effects of whey protein or dietary fat, studies that investigate the effects of the individual ingredients of a complete meal on the glycemic response healthy men and women, however, are scarce. Against that background the results of a recent study from the Clinical Nutrition Research Centre at the Singapore Institute for Clinical Sciences are of particular interest. After all, the Lijun Sun et al. (2014) determined the effect of co-ingesting a high-protein food (breast chicken), a fat (ground nut oil), a leafy vegetable or all three on the glycaemic and insulinaemic responses of white rice in healthy adults and did thus produce results that could be practically relevant for all of us - more relevant than inaccurately calculated GIs.

Use sugar alternatives if you want to improve your blood glucose!

Unsatiating Truth About Sweeteners?

Will Artificial Sweeteners Spike Insulin?

Sweeteners & the Gut Microbiome Each is Diff.

Sweeter Than Your Tongue Allows!

Stevia, Much More Than Sweet?

Artif. Sweetened Foods Good, Not Bad for Fat Loss.

Before we get to the study results, though, let's briefly recap what the researchers actually did: Sun et al. recruited twelve healthy participants (six female and six male) by means of advertisements, flyers and personal communications.

"Before inclusion into the study, potential participants were briefed on all aspects of the experiment and were given the opportunity to ask questions. Following the securing of consent, a health assessment was performed which included anthropometric measurements and a health questionnaire (giving details of food allergies/intolerance, metabolic diseases, special dietary needs and smoking habits). Those who fulfilled all the inclusion criteria [body mass index 18.5–24.99 kg/m2; blood pressure (BP)—systolic BP between 110 and 120 mmHg and diastolic BP between 75 and 85 mmHg; age 21–50 years; fasting blood glucose, 4–6 mmol/L; not on prescription medication, non-smoking; no genetic or metabolic diseases) were enrolled into the study." (Sun. 2014)

In addition, the amount of regular physical activity was quantified and subjects who were partaking in competitive sports and endurance events were excluded. Eventually, the scientists ended up with a group of normal-weight men and women at the age of 21–34 years.

Table 1: Composition of the test meals, ACHO = available carbohydrates.
Nutritional data were obtained from the manufacturers (Sun. 2014).

The subjects visited the laboratory 5 times (plus a baseline testing with a glucose solution). On each of these testing sessions, which were separated by at least one week, the subjects arrived at the laboratory between 7:30 and 8:30 after an overnight fast and received one of the five test meals from Table 1, which contained 194 g white of plain white rice,  254 g of white rice with fat, 294 g of plain white rice with chicken breast, 314g of white rice with vegetable and 474g of white rice with fat, chicken and vegetable, respectively.

Ground nut oil? I guess most of you will know the oil that was used in the study at hand as "peanut oil" and it is - as you will probably know, as well - not exactly high in "holy" omega-3 fatty acids. Rather than that, peanut oil contains oleic acid (46.8% as olein), linoleic acid (33.4% as linolein), and palmitic acid (10.0% as palmitin), as well as small amounts of stearic acid, arachidic acid, arachidonic acid, behenic acid, lignoceric acid, but not a singly milligram of omega-3s.
The test or reference food was then given to consume within 15 min. Further blood samples for glucose and insulin analysis were taken for the subsequent 180 min (every 15 min in the first hour and every 30 min for the subsequent hours) - a procedure that yielded the following results.

Figure 1: Glucose levels expressed relative to the ingestion of 250g of glucose (Sun. 2014)

The values in Figure 1 are expressed relative to the glucose response to 250g of pure glucose, of which a brief glimpse at the data tells you that they produce higher peak and incremental area under the curve (iAUC, a measure for the glycemia over the whole testing period) levels than any of the meals. Statistical significant differences were yet observed only for rice with chicken breast, rice with vegetable, and rice with fat, chicken and vegetable - yet not for the plain rice and the rice + fat meal (the latter was to be expected based on the discussion in my previously referenced article "True or False? Adding Fat to A Carby Meal Lowers Insulin Response" | read more).

Significant differences for the insulin response were observed for the white rice + chicken meal, where the insulin response was significantly higher compared to the white rice only (+22%), as well as the rice with + vegetable meal, where the insulin response was significantly lower compared to the white rice only condition (-16%).

The combination of foods determines the GI of the meal

Based on the classic equation that's usually used to determine the glycemic index of a meal (Hätönen. 2011), Sun et al. calculated the predicted glycemic of the five test meals and compared it to the actual glycemic index (GI) that was calculated based on the measured glucose and insulin response of the subjects.

Figure 2: Predicted and measured glycemic index as well as measured insulinemic index of the meals (Sun. 2014)

As you can see in Figure 2, the comparison yields an unsurprising result. As it's usually the case, when simple equations are used to predict physiological effects, the real GI values were significantly different from the calculated ones and  - significantly lower, that is. Accordingly, the meal with the least impact on postprandial glycemia and a comparatively low insulinemic effect is the one containing rice, fat, chicken and veggies - in other words, the complete meal. 

Suggested Read: "Get Your Protein, Veggies & Fruits and Get Them Regularly: High(er) Meal Frequency (6 à Day) + High(er) Protein Diet Support Weight & Fat Loss on a Diet." | read more

Bottom line: While the importance of the glycemic index (GI) has long been totally overrated, there is accumulating evidence that high postprandial glucose levels are a significant contributor to increases in cardiovascular disease risk even in healthy individuals (Einarson. 2011; Mah. 2011). Against that background the results of this recent trial support my previous recommendation to consume balanced meals containing protein, fat and carbohydrates, instead of no-fat or no-carb meals.

In contrast to what the "paleo hypothesis" and the notion that our ancestors would not have collected some berries or boiled some rice to have it alongside the chicken they just caught would say, the contemporary scientific evidence indicates that we are well equipped to handle complex meals, as long as they don't contain exorbitant amounts of fat and carbohydrates.

One thing we should not forget, though, is that the 50% discrepancy between the calculated and real glycemic index of the "complex" test meal (four ingredients is not exactly "complex", actually) suggests that one of the reasons that many of the previous studies failed to detect a meaningful association between the (obviously calculated) GI of an individuals diet and his / her cardiovascular or diabetes risk may be that the data the scientists used was similarly inaccurate as the predicted glycemic indices of the test meal in the study at hand | Comment on Facebook!

References:

• Hätönen, Katja A., et al. "Protein and fat modify the glycaemic and insulinaemic responses to a mashed potato-based meal." British Journal of Nutrition 106.02 (2011): 248-253.
• Mah, Eunice, et al. "Postprandial hyperglycemia impairs vascular endothelial function in healthy men by inducing lipid peroxidation and increasing asymmetric dimethylarginine: arginine." The Journal of nutrition 141.11 (2011): 1961-1968. 
• Sun, Lijuan, et al. "Effect of chicken, fat and vegetable on glycaemia and insulinaemia to a white rice-based meal in healthy adults." European journal of nutrition (2014): 1-8.
• Wolever, T. M. S. "Is glycaemic index (GI) a valid measure of carbohydrate quality&quest." European journal of clinical nutrition 67.5 (2013): 522-531.