3g Taurine Improve Post-Workout Glycogen Resynthesis, Protect the Testes of Doping Sinners & Battles Alzheimer's

Taurine - A useful supplement for chemical, natural athletes and even sedentary slobs who are afraid of diabetes.

Taurine, or 2-aminoethanesulfonic acid, as Wikipedia says, is an organic acid widely distributed in animal tissues. It is a major constituent of bile and can be found in the large intestine, and accounts for up to 0.1% of total human body weight. That does not sound like much, but taurine has many fundamental biological roles, such as conjugation of bile acids, antioxidation, osmoregulation, membrane stabilization, and modulation of calcium signaling. It is essential for cardiovascular function, and development and function of skeletal muscle, the retina, and the central nervous system and you were thus probably not too surprised, when you've recently read on the SuppVersity Facebook Page that taurine may help with Alzheimer's disease.

You can learn more about taurine & other amino acids at the SuppVersity

Taurine Pumps Up Strength & Recovery?

Taurine Improves Insulin + Glucose Metabolism

Taurine ➲ 180% Testosterone Increase

Taurine + BCAA Work Hand in Hand

43% Reduced Performance W/ BCAAs

BCAA Neurotransmitter Depletion

In the corresponding paper that was published only recently in the ScientificReports on Nature.com Kim et al. report that orally administered taurine via drinking water rescued the cognitive deficits in a standard rodent model of Alzheimer's (APP/PS1 mice) and brought them back up to age-matching wild-type mice.

Figure 1: Improvement in spatial and hippocampal learning behaviours in taurine-treated transgenic mice. 7-month old wild-type (Wt) and agematched APP/PS1 transgenic (Tg) male mice were orally administered water or taurine (1,000 mg/kg/day) for 6 weeks (n 5 8–10 per group). After 6 weeks, behavioural tests were administered to the 8.5-month old mice. (Left) Y-maze. Average alternation (%) of each group of mice was calculated. (Right) Passive avoidance. Average latency time in seconds for each group of mice was measured (Kim. 2014).

That's unquestionably impressive, but what's more impressive is that this is by far not the first study to report that taurine exhibits a plethora of physiological functions in the central nervous system.

But taurine gives me diarrhea! If it does try taking it with a meal that will greatly reduce the risk of having to rush to the toilette and should not reduce the physiological benefits significantly. At least for the muscular effects its unlikely that it will matter at all. For the beneficial effects on the brain, it may be necessary to achieve higher serum peak levels. In view of the fact that the rodents in the aforementioned study by Menzie et al. received the taurine in the drinking water, even this is yet unlikely. If the taurine "goes right through", though, it's certainly not going to help you ;-)

In a recent review in the scientific journal Amino Acids review, Janet Menzie et al. describe the mode of action of taurine and its clinical application in the neurological diseases: Alzheimer’s disease, Parkinson’s disease and Huntington’s disease and conclude that taurine...

"[...] functions through multiple neuroprotective mechanisms: regulation of cellular osmolarity , anti-oxidant, neuromodulator of GABAergic transmission, maintenance of calcium homeostasis, inhibition of glutamate excitotoxicity, attenuation of endoplasmic reticulum stress, modulation of mitochondrial pore permeability, downregulation of a range of proapoptotic proteins while upregulating anti-apoptotic proteins and downregulation of inflammatory mediators." (Menzie. 2014)

Moroever, Menzie et al. believe that there is "strong evidence" of the existence of a specific taurine receptor, which is activated exclusively by taurine, but not by structurally similar amino acids such as glutamate, GABA and glycine and could be responsible for many of the beneficial effects taurine exerts in the context of central nervous system disorders. More specifically existing evidence clearly suggests protective effects in Alzheimer’s, Parkinson and Huntington diseases. Three pathologies that share a number of broad mechanisms: Oxidative stress, mitochondrial dysfunction, excitotoxicity, calcium imbalance, inflammatory changes apoptosis - and *tadaa* a reduced level of (Arai. 1985; Alom. 1991; Molina. 1997).

Enough of the health stuff, what about the post-workout goodness?

I know, as long as we are healthy we don't really care about debilitating central nervous system disorders... well, ok. I will spare you my moral pointing finger and get straight to the similarly unsurprising results of a recent study from the University of Tokyo. A study which clearly indicates that the provision of taurine after workouts can lead to a significant enhancement of the already elevated glycogen synthesis after your workouts.

Figure 2: Muscle and liver glycogen and serum free fatty acids (FFA) before and after the workout (Takahashi. 2014).

In two rodent studies, the Japanese researchers tested whether the oral administered of taurine  at a dosage of 0.5 g/kg body weight (for human beings that's 0.04g/kg or approximately 3g total | the SuppVersity suggested dose from previous articles, by the way) immediately after treadmill running at 25 m/ min for 90 min would alter the metabolic response and glycogen synthesis after workouts when it was (A) administered alone or (B) as part of a glucose solution containing taurine and glucose at a ratio of 1:2 - in this case 0.5g/kg taurine and 1.0g/kg glucose.

Figure 3: AUC for glucose after for 60min and 120min after the ingestion of the taurine + glucose solution. As the data indicates taurine helped to "clear" the sugar from the blood stream (Takahashi. 2014).

As the scientists point out, their "results show that post-exercise taurine administration enhances glycogen repletion in skeletal muscle" (Takahashi. 2014). The underling cause, however, is still speculative. Takahashi et al. believe that it is triggered by

1. 

   Figure 4: Changes in general oxidative damage (TBARs), protein damage and exercise performance in response to taurine vs. placebo vs. bet alanine supplementation; expressed relative to untrained control (Dawson. 2002).

   an acceleration of glucose uptake, and
2. an increase in fat oxidation

of which the latter will have a carbohydrate sparing effect and will thus leave a higher amount of carbs for glycogen repletion. In conjunction with previously established benefits of taurine, such as

• the attenuation of exercise-induced DNA damage during workouts (young men | Zhang. 2004),
• the amelioration of cytotoxic (cell damaging) effects of exercise (rodents | Dawson. 2002),
• an increase in exercise performance (specifically endurance ex. | Dawson. 2002; Miyazaki. 2004),
• additional effects on the benefits of BCAA intake for the delayed-onset muscle soreness and muscle damage induced by high-intensity eccentric exercise (Ra. 2013),
• an improvement in osmoregulation (water balance) of the muscle (Cuisinier. 2002), and
• decreases in oxidative stress during eccentric exercises (Silva. 2011)

The optimal dosing for performance increments, by the way, is between 1.2-6.0g for 2 weeks (other timing has not been tested, so it's possible that one week will suffice, too). That's at least what the only hitherto published study that investigated the effects of different doses of taurine as a means to improve the endurance performance (Miyazaki. 2004). If you want the nutrient partitioning effects, though, you would have to consume CHO + taurine after the workout - 3g of taurine should suffice. Judged by the hitherto published studies this should automatically help you to increase your workout performance after 2 weeks (the beneficial effects will, just as it is the case for creatine, accumulate until the levels are saturated).

And there are more benefits - health benefits, for juicers and non-juicers

The former, i.e. the juicers will probably be happy to hear that taurine does not just have liver protective effects (Miyazaki. 2005), but will also reverse the nandrolone decanoate induced perturbations in sperm characteristics, normalize the serum testosterone level, and restore the activities of the key steroidogenic enzymes in rodents that are treated with nandrolone and taurine (at a dosage equivalent to only 1.3g/day | Ahmed. 2014).

In spite of the fact that the administration of taurine did also prevent the nandrolone decanoate-induced testicular toxicity and DNA damage by virtue of its antioxidant, anti-inflammatory, and anti-apoptotic effects, I would like to point out that this article is not intended as an incentive for nandrolone doping.

While taurine is not made from the sperm of Belgian Blues it may still boost your testosterone levels - whether that's going to be by 140% as in this study is questionable, though.

From performance to health doping: If you are not into "natural performance enhances" and don't care about the direct performance increases, reduced oxidative damage and increases in glycogen repletion during workouts. I would recommend you reread the previous SuppVersity article about the testosterone boosting effects of taurine, it's ability to improve your strength and recovery during and after resistance training sessions, as well as it's ability to improve your glucose metabolism (Franconi. 2006; Carneiro. 2009), to increase your glucose sensitivity (Han. 2004; Nakaya. 2000), to prevent insulin resistance in hyperglycemic states (Haber. 2003), to prevent the development of hypertension as a result of fructose overfeeding (Rahman. 2011), to prevent the cardiac damage due to iron overload (Oudit. 2004), to protect you from the kidney damaging assault of chemotherapy (Saad. 2010), and god knows which benefits I have simply forgotten in the aforementioned list | Comment of Facebook!

References:

• Ahmed, Maha AE. "Amelioration of Nandrolone Decanoate-Induced Testicular and Sperm Toxicity in Rats by Taurine: Effects on Steroidogenesis, Redox and Inflammatory Cascades, and Intrinsic Apoptotic Pathway." Toxicology and Applied Pharmacology (2014).
• Alom, J., et al. "Cerebrospinal fluid taurine in Alzheimer's disease." Annals of neurology 30.5 (1991): 735-735.
• Arai, Heii, et al. "A preliminary study of free amino acids in the postmorten temporal cortex from Alzheimer-type dementia patients." Neurobiology of aging 5.4 (1985): 319-321. 
• Carneiro, Everardo M., et al. "Taurine supplementation modulates glucose homeostasis and islet function." The Journal of nutritional biochemistry 20.7 (2009): 503-511.
• Cuisinier, Claire, et al. "Role of taurine in osmoregulation during endurance exercise." European journal of applied physiology 87.6 (2002): 489-495.
• Dawson Jr, R., et al. "The cytoprotective role of taurine in exercise-induced muscle injury." Amino acids 22.4 (2002): 309-324. 
• Franconi, Flavia, et al. "Taurine supplementation and diabetes mellitus." Current Opinion in Clinical Nutrition & Metabolic Care 9.1 (2006): 32-36.
• Haber, C. Andrew, et al. "N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress." American Journal of Physiology-Endocrinology and Metabolism 285.4 (2003): E744-E753.
• Han, Jin, et al. "Taurine increases glucose sensitivity of UCP2-overexpressing β-cells by ameliorating mitochondrial metabolism." American Journal of Physiology-Endocrinology and Metabolism 287.5 (2004): E1008-E1018. 
• Kim, Hye Yun, et al. "Taurine in drinking water recovers learning and memory in the adult APP/PS1 mouse model of Alzheimer's disease." Scientific Reports 4 (2014).
• Menzie, Janet, et al. "Taurine and central nervous system disorders." Amino acids 46.1 (2014): 31-46.
• Miyazaki, T., et al. "Optimal and effective oral dose of taurine to prolong exercise performance in rat." Amino Acids 27.3-4 (2004): 291-298.
• Miyazaki, Teruo, et al. "Taurine inhibits oxidative damage and prevents fibrosis in carbon tetrachloride-induced hepatic fibrosis." Journal of hepatology 43.1 (2005): 117-125.
• Molina, José A., et al. "Decreased cerebrospinal fluid levels of neutral and basic amino acids in patients with Parkinson's disease." Journal of the neurological sciences 150.2 (1997): 123-127.
• Nakaya, Yutaka, et al. "Taurine improves insulin sensitivity in the Otsuka Long-Evans Tokushima Fatty rat, a model of spontaneous type 2 diabetes." The American journal of clinical nutrition 71.1 (2000): 54-58.
• Oudit, Gavin Y., et al. "Taurine supplementation reduces oxidative stress and improves cardiovascular function in an iron-overload murine model." Circulation 109.15 (2004): 1877-1885.
• Rahman, Mizanur M., et al. "Taurine prevents hypertension and increases exercise capacity in rats with fructose-induced hypertension." American journal of hypertension 24.5 (2011): 574-581.
• Saad, Sherif Y., and Ammar C. Al-Rikabi. "Protection effects of taurine supplementation against cisplatin-induced nephrotoxicity in rats." Chemotherapy 48.1 (2010): 42-48.
• Silva, Luciano A., et al. "Taurine supplementation decreases oxidative stress in skeletal muscle after eccentric exercise." Cell biochemistry and function 29.1 (2011): 43-49. 
• Takahashi, Yumiko, et al. "Post-exercise taurine administration enhances glycogen repletion in tibialis anterior muscle." The Journal of Physical Fitness and Sports Medicine 3.5 (2014): 531-537.
• Zhang, M., et al. "Role of taurine supplementation to prevent exercise-induced oxidative stress in healthy young men." Amino acids 26.2 (2004): 203-207.

True or False: Mycotoxins in Coffee Are a Serious Threat to Our Health and the Only Way to Avoid Them is Abstinence

As we are about to see coffee is by far not the worst aflotoxin offender in the human diet. Still, that does not mean that the coffee related exposure to this form of mold that can befall all sorts of grains, nuts and seeds is harmless.

You will probably remember that I casually touched on the possibility of being exposed to aflotoxins and more importantly ochratoxins as a result of the consumption of mold-infected coffee in previous coffee articles. When the issue of the « coffee ➲ aflotoxin / ochratoxin exposure ➲ serious health » triage resurfaced in a brief facebook conversation, recently, I realized that I was not 100% sure if these mycotoxins that are produced by Aspergillus flavus, Aspergillus ochraceus, Aspergillus niger, and Aspergillus carbonarius do or don't pose a serious health risk.

Well, you know how much I hate unanswered questions, so I kept digging until I'd found what I consider to be a half-way satisfying answer to this life-or-death question ;-)

You can learn more about coffee at the SuppVersity

Remember: With Coffee More Won't Help More

Coffee - The Good, Bad & Interesting

Three Cups of Coffee Keep Insulin At Bay

Caffeine's Effect on Testosterone, Estrogen & SHBG

Coffee + Cacao for Breast Cancer Prevention

"Decaf" Won't Help With Weight, ... Ahh, Fat Loss

"The amount of aflotoxin in the average cup of coffee is a serious threat to our health!"

In 90% of the cases the above statement is FALSE! Despite the fact that it is difficult to tell how much mycotoxins you've been flushing down with your morning coffee today, the exact amount of the more common aflotoxins and their similarly kidney-toxic, pro-carcinogenic and coffee-loving cousins, the ochratoxin, in the average cup of (roasted) coffee is probably way too low to be worried about.

Figure 1: Mycotoxin exposure from coffee; calculated based on data from Europe (Vd Stegen. 1997)

Based on the studies I have reviewed for this article, it appears almost certain to say that the relatively low amount of coffee beans per cup (4-8g) reduces your average mycotoxin exposure from 1-4 cups of coffee per day to levels that are almost certainly within one of the various (multi-)national reference ranges (Van Egmond. 2007):

• Europe: 5µg/kg
• Africa: 10µg/kg

• North America: 20µg/kg

• Asia: 15µg/kg
• Latin America: 20µg/kg

Using a selection of commercially available regular and soluble coffee brands, van der Stegen et al. have actually calculated the average daily mycotoxin intake of Europeans with an average coffee consumption of 1-4  to be in the nanogram range - 19ng and 10ng, specifically, for regular and instant coffee drinkers, respectively.

Please remember: We don't know if / what happens or doesn't happen if you stay within or break the arbitrary intake limits. If you take a look at the available evidence from rodent studies, the results Epstein et al. presented in their 1969 paper (see Table 1) later in this article, would suggest that a sensible intake limit would have to be below the 1µg range if we assume a similar toxicity for the average mycotoxin mixture as for the aflotoxin B Epstein et al. used. This assumption is obviously not realistic, but it should remind you of the arbitrariness of the "intake limits".

Just to make sure, we understand each other, here: That's 1000x less than you'd get from only 20g of some of the Brazilian peanuts Freitas and Brigido analyzed in a 1998 study for their mean and maximal mycotoxin content. With 1099µg/kg the worst offenders in this study would easily have you breach the already lax American (North & Latin America) max. tolerable intake limit of 20µg/kg per day - and that despite the fact that this limit is more than 1000x higher than the amount of mycotoxins you'll have in your average cup of coffee.

Green vs. roasted coffee: Do we have to chose between anti-oxidants and mycotoxins?

It goes without saying that the mere fact that the dangers of being exposed to high amounts of mycotoxins from adequately processed and stored coffee appears negligible, does not warrant ignoring the problem completely. The effects of processing and storage are and will thus always be an important issue.

Given the fact that humid and cool (but not cold) is what mold needs to thrive, you will probably already have suspected that the hot and arid environment of a coffee roastery is not exactly the favorite growth environment for the Aspergillus family.

Figure 2: Ochratoxin content (µg/kg) in green, roasted & soluble coffee, left; total antioxidant activity in TROLOX essay of green (=unroasted), lightly, medium and dark roast coffee (Blanc. 1998; del Castillo. 2002)

A lower mycotoxin content is yet not the only beneficial effect of roasting. Contrary to what 99% of the people will tell you, when you ask them, the roasting process increases not decreases the total antioxidant capacity of coffee (TAC).

What does the latest review say about regular coffee consumption and cancer? "The epidemiological evidence consis-tently indicates that coffee protects against liver cancer, and also point toward protective effects for risk of colorectal cancers (with relative risks of 0.50 (95% CI: 0.42–0.59) and 0.83 (95% CI: 0.75–0.92), respectively, in the most recent meta-analyses)" (Bøhn. 2013). The evidence for protective effects against breast and prostate cancer on the other hand is inconclusive - irrespective of the established chemo-preventive effects of coffee phytochemicals Bøhn et al. list in their soon to be published paper in Molecular Nutrition & Food Research early in 2014.

Due to the formation of a whole host of new antioxidant molecules during the roasting process, light or mildly roasted coffee beans have a higher total antioxidant capacity than green ones - irrespective of the reduced chlorogenic acid content, for which the green beans are currently (over-)hyped. If you look at the data in Figure 2 you will see that even the heavily roasted, tar-black coffee beans still have a minimally higher anti-oxidant activity than the "natural" green coffee beans (del Castillo. 2002) - an observation that has been made both in the Petri dish, as well as ex vivo rodent studies (Daglia. 2002).

You've been drinking tons green coffee, lately?

Don't worry! Your past green coffee consumption probably isn't a real problem either. It does after all look as if those beans were yet another example for the infamous "nature kows best" principle. I mean, can it really be "coincidence" that the beans come with "anti-mycotoxin agents" in form of cafestol and kahweol. These coffee-specific diterpenes have been shown to ameliorate the aflotoxin B induced genotoxicity (Cavin. 1998) and the subsequent pro-carcinogenic effects (Cavin. 2001) and can be expected to exert protective effects against ochratoxin toxicity, as well.

In view of the fact that similar evidence exists for chlorogenic acids (CGA), dodecyl chlorogenates (DCGA) and a high(er) coffee consumption, in general (Suárez‐Quiroz. 2013; Ferk. 2013), it is actually not surprising that studies like Shank et al. (1972)  or Bulatoa-Jaym et al. (1982) found links between aflotoxin contaminated corn, grains, potato, peanuts & co., but could not identify an increased risk in liver cancer for coffee aficionados. Consequently, it's (imho) relatively unlikely that your health has already taken a beating - irrespective of the amount of the number of cups of green coffee you've been consuming over the past weeks.

Coffee is not the worst mycotoxin offender in the human diet: In a case-control dietary study of primary liver cancer in humans Bulatoa-Jaym et al. found that 51.2% of their subjects daily aflotoxin exposure came from cassava, 20.3% from corn, 6.8% frompeanuts and 5.8% from sweet potato (Bulatao-Jaim. 1982). On the other hand, many scientists argue that the ochratoxin content of coffee is the real danger, anyway (Bayman. 2006)

I would still like to remind you that even the sum of the previous remarks must not be misunderstood as an incentive to willy nilly forget all previously harbored concerns about "moldy coffee beans"... and I say this in spite of the existing epidemiological evidence that a high coffee consumption decreases the risk of developing and dying from liver cancer (Kurozawa. 2005; El–Serag. 2007). The liver is after all not the only organ that may be affected by the pro-carcinogenic toxins. The kidneys are at least as susceptible to the toxic assault from the mycotoxin filtrate that passes through them.

The liver is not the only organ that's taking a beating

It may thus be hypothetical, but not impossible that a 2x / 2.6x increased risk to develop renal cell carcinoma Mimi et al. report in a 1986 paper on the associations between coffee consumption and kidney cancer may at least be partially related to the higher mycotoxin exposure in those 61 study participants who consumed 1-4 cups of coffee per day (Mimi. 1986).

That mycotoxins can promote the development of kindey cancer had been demonstrated 17 years before the publication of Mimi's paper by Epstein, Bartus & Farber (1969) whose Wistar rats developed renal epithelial neoplasms after being exposed to food-borne aflatoxin B1.

Table 1: Incidence of renal epithelial and malignant hepatic tumors in male Wistar rats ingesting aflatoxin B1 for 147 days; the indces a, b, c provide irrelevant (in this context) extra information (Epstein. 1969)

In that, it's quite remarkable that even the lowest aflotoxin dosage the researchers used in their study (0.25µg/kg chow; HED  ~1.2ng/kg body weight, ; see Table 1) lead to significant rates of cancerous growth in both kidney (28%, if we count both developing and full-blown renal neoplasms) and liver  within the 21 week study period.

There is just one no-go: Storing unroasted beans for years in your humid basement

In view of the large regional difference in aflotoxin infection rates, the different susceptibility of the various coffee cultivars and the influences of weather, storage conditions, blending, processing, and all the other factors that increase or decrease the amount of mold and mycotoxins on coffee (see Figure 3), I would still be hesitant to exclude the possibility that stocking up on highly aflotoxin contaminated unroasted coffee you possibly even stock in a very humid basement of yours to consume the coffee over the course of months if not years could have negative effects on the health of your organs, in general, and the function of your kidney and liver, in particular.

Figure 3: Percent infection of coffee cherries and beans byAspergillusspecies potentially capable of producing ochratoxin A in four Brazilian coffee growing regions from the 1999 and 2000 harvests (Taniwaki. 2003)

I mean, look at the data in Figure 3. It's probably no coincidence that the otherwise virtually uninfected beans of coffee from the 1999 and 2000 harvests in the Cerrado Miniero exhibits a 4% infection rate after being stored intermediately before it is either roasted, shredded or both or simply forwarded "raw" to the mailbox of an "unroasted coffee enthusiast". Similar effects can be expected when the huge coffee manufacturers mix harvests from various regions. If only one is infected, all it takes to have Aspergillus flavus literally "all over the place" is enough time in one of the huge storage silos or the hold of one of the container ships that transport coffee from the "New" back into the "Old World".

Figure 4: The amino acid make up of coffee changes upon roasting (data from Cirilo. 2003).

Life kills, anyway! Let's be honest. In the end, living is a pretty deadly undertaking, anyway. Against that background the uncertainty with respect to the tolerable intake of mycotoxins should not bother you so much to ignore the existing evidence of the beneficial effects of regular coffee consumption (see "Coffee - The Good, the Bad & The Interesting" | read more).

One thing you may keep in mind, though, is that this evidence is based on data from average coffee drinkers, people who drink coffee that's made of roasted beans. Beans that are virtually mycotoxin-free (see Figure 2, left) and have a higher, not lower antioxidant capacity than green coffee beans.

What roasted beans lack, though, are chlorogenic acid and trace amounts of amino acids (see Figure 4), including serotonin. If you are looking for one of these molecules specifically, you are yet probably better of with a hopefully aflotoxin and mycotoxin free green coffee extract and a bottle of pills with the serotonin precursor 5-HTP, anyways.

References:

• Bayman, P., & Baker, J. L. (2006). Ochratoxins: a global perspective. Mycopathologia, 162(3), 215-223. 
• Blanc, M., Pittet, A., Muñoz-Box, R., & Viani, R. (1998). Behavior of ochratoxin A during green coffee roasting and soluble coffee manufacture. Journal of agricultural and food chemistry, 46(2), 673-675.
• Bøhn et al. (2013) Coffee and cancer risk, epidemiological evidence, and molecular mechanisms. Molecular Nutrition & Food Research [early view article]
• Bulatoa-Jaym J, et al. (1982). A Case-Control Dietary Study of Primary Liver Cancer Risk from Aflatoxin Exposure*. International journal of epidemiology, 11(2), 112-119.
• Cavin, C., Holzhäuser, D., Constable, A., Huggett, A. C., & Schilter, B. (1998). The coffee-specific diterpenes cafestol and kahweol protect against aflatoxin B1-induced genotoxicity through a dual mechanism. Carcinogenesis, 19(8), 1369-1375.
• Cavin, C., Mace, K., Offord, E. A., & Schilter, B. (2001). Protective effects of coffee diterpenes against aflatoxin B< sub> 1</sub>-induced genotoxicity: mechanisms in rat and human cells. Food and Chemical toxicology, 39(6), 549-556.
• del Castillo, M. D., Ames, J. M., & Gordon, M. H. (2002). Effect of roasting on the antioxidant activity of coffee brews. Journal of Agricultural and Food Chemistry, 50(13), 3698-3703. 
• Cirilo, M. P., Coelho, A. F. S., Araújo, C. M., Gonçalves, F. R., Nogueira, F. D., & Glória, M. B. A. (2003). Profile and levels of bioactive amines in green and roasted coffee. Food Chemistry, 82(3), 397-402.
• Daglia, M., Papetti, A., Gregotti, C., Bertè, F., & Gazzani, G. (2000). In vitro antioxidant and ex vivo protective activities of green and roasted coffee. Journal of Agricultural and Food Chemistry, 48(5), 1449-1454.
• Epstein, S. M., Bartus, B., & Farber, E. (1969). Renal epithelial neoplasms induced in male Wistar rats by oral aflatoxin B1. Cancer Research, 29(5), 1045-1050.
• El–Serag, H. B., & Rudolph, K. L. (2007). Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. Gastroenterology, 132(7), 2557-2576. 
• Ferk, F., Huber, W. W., Grasl‐Kraupp, B., Speer, K., Buchmann, S., Bohacek, R., ... & Knasmüller, S. (2013). Protective effects of coffee against induction of DNA damage and pre‐neoplastic foci by aflatoxin B1. Molecular nutrition & food research. 
• Freitas, V. P., & Brigido, B. M. (1998). Occurrence of aflatoxins B1, B2, G1, and G2 in peanuts and their products marketed in the region of Campinas, Brazil in 1995 and 1996. Food Additives & Contaminants, 15(7), 807-811.
• Kurozawa, Y., Ogimoto, I., Shibata, A., Nose, T., Yoshimura, T., Suzuki, H., ... & Tamakoshi, A. (2005). Coffee and risk of death from hepatocellular carcinoma in a large cohort study in Japan. British journal of cancer, 93(5), 607-610. 
• Mimi, C. Y., Mack, T. M., Hanisch, R., Cicioni, C., & Henderson, B. E. (1986). Cigarette smoking, obesity, diuretic use, and coffee consumption as risk factors for renal cell carcinoma. Journal of the National Cancer Institute, 77(2), 351-356.
• Shank, R. C., Wogan, G. N., & Gibson, J. B. (1972). Dietary aflatoxins and human liver cancer. I. Toxigenic moulds in foods and foodstuffs of tropical South-East Asia. Food and Cosmetics Toxicology, 10(1), 51-60.
• Taniwaki, M. H., Pitt, J. I., Teixeira, A. A., & Iamanaka, B. T. (2003). The source of ochratoxin A in Brazilian coffee and its formation in relation to processing methods. International Journal of Food Microbiology, 82(2), 173-179. 
• Van Egmond, H. P., Schothorst, R. C., & Jonker, M. A. (2007). Regulations relating to mycotoxins in food. Analytical and bioanalytical chemistry, 389(1), 147-157. 
• Vd Stegen, G., Jörissen, U., Pittet, A., Saccon, M., Steiner, W., Vincenzi, M., ... & Schlatter, C. (1997). Screening of European coffee final products for occurrence of ochratoxin A (OTA). Food Additives & Contaminants, 14(3), 211-216. 
• Yamato, T., Yamasaki, S., Misumi, Y., Kino, M., Obata, T., & Aomine, M. (2002). Modulation of the stress response by coffee: an in vivo microdialysis study of hippocampal serotonin and dopamine levels in rat. Neuroscience letters, 332(2), 87-90.

First Human Study to Confirm That Repleting Low Vitamin C Levels W/ 1g Vitamin C Boosts Aerobic Performance

The study at hand used plain ascorbic acid, no quack supplements with "advanced vitamin C".

While people tend to believe that vitamin C is good for anything, the evidence that it actually does anything good is relatively scarce. Against that background I am happy to tell you that a group of Greek researchers from the School of Physical Education and Sport Science, the European University Cyprus and theAristotle University of Thessaloniki have now finally confirmed what many of you probably thought was a long-established fact: "[L]ow vitamin C concentration is linked with decreased physical performance and increased oxidative stress and that vitamin C supplementation decreases oxidative stress and might increase exercise performance only in those with low initial concentration of vitamin C." (Paschalis. 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

When they came up with the study design, Paschalis et al. simply assumed that the mythical ergogenic effect of vitamin C actually existed. To test this hypothesis, they screened 100 males for vitamin C baseline values in blood, picked the 10 individuals with the lowest and the 10 with the highest vitamin C values from their baseline sample and assigned them to two groups.

Figure 1: Overview of the study design (Paschalis. 2014)

Using a placebo-controlled crossover design, the 20 selected subjects performed aerobic exercise to exhaustion (oxidant stimulus) before and after vitamin C supplementation for 30 days.

An overview of the study design is shown in Fig. 1. All measurements were performed between 08:00 and 11:00 h after overnight fasting. Initially, to examine whether rest ing blood vitamin C concentration affects aerobic perfor mance, VO2max was assessed (using incremental cycling test to volitional exhaustion) and was compared in both the low and the high vitamin C groups (Monark, Vansbro, Swe den). More specifially, the protocol started with a 50 W load at 50 rpm and increased by 10 W every 2 min until volitional fatigue. The test was terminated when three of the following four criteria VO2max were met: (1) volitional fatigue, (2) a lower than 2 mL/kg/min increase in VO2 despite an increase in workload, (3) a respiratory exchange ratio greater than or equal to 1.10, and (4) heart rate within 10 bpm of the predicted maximal heart rate (220–age). Res piratory gas variables were measured using a metabolic cart (Quark b2, Cosmed, Italy), which was calibrated before each test using standard gases of known concentration. The VO 2max assessment was used as a reference value to cal culate the workload at the relative intensity of each subject and ensured that all subjects would cycle at similar relative intensity during the following aerobic exercise sessions.

After the baseline testing had been done, the subjects within both the low and the high vitamin C groups received either placebo (3x333mg of lactose) or vitamin C supplementation (3x333mg of vitamin C), in a double-blind randomized crossover fashion (see Figure 1).

Figure 2: Changes in VO2max (left) and redox status (right) in subjects according to initial vitamin C status before and after vitamin C supplementation for 30 days (Paschalis. 2014).

As you can see in Figure 2 there were measurable differences in the response to the acute exhaustive exercise protocol (an oxidant stimulus), the subjects in both groups performed before and after vitamin C or placebo supplementation for 30 days. The data in Figure 2 does yet also show that the subjects who had been randomly assigned to the vitamin C supplement group had lower baseline VO2max levels. A fact that raises the question whether this is the result of a lower vitamin C intake or whether the vitamin C intake correlates with an unhealthier lifestyle that left the subjects unfit and with low vitamin C levels.

Illustration of the relationship between radicals and antioxidants in the determination of redox balance. An increase in radicals or antioxidants results in a disturbance in redox balance (Powers. 2004).

So what, to supplement with antioxidants or not? I have voiced my opinion often enough and still people ask me time and again whether it "may not be a good idea to..." Against that background I will not repeat myself, but quote someone else, Scott K. Powers and Kurt J. Sollanek who wrote an extensive review of the literature for one of the latest issue of the Sports Science Exchange: "Exercise promotes radical production in the working muscles and prolonged/intense exercise can produce an imbalance between radical production and muscle antioxidants altering the “redox balance” and resulting in oxidative stress. To protect against radical mediated damage, muscle cells contain endogenous antioxidants to scavenge radicals.

Moreover, exogenous antioxidants obtained in the diet cooperate with endogenous antioxidants to form a supportive network of cellular protection against radical-mediated oxidative stress. In regard to exogenous antioxidants, a varied diet of fruits and vegetables is a sensible means of obtaining a balance of exogenous antioxidants. In contrast, because of the risk of negative consequences, consuming megadoses of antioxidants via supplements is not recommended" (Powers. 2014 | my emphases).

Unfortunately, this question is hard to answer based on the available research on vitamin C. While we have conflicting results with respect to its ability to impair the adaptational response to exercise (Close. 2014), there is very little evidence that it will actually have beneficial effects on any meaningful performance parameters. In fact, a study by Huck et al. that was published in the scientific journal Nutrition in 2013 is probably what comes closest to the results of the study at hand.

Figure 3: Effects of 500mg vitamin C per day on selected parameters in a 4 week chronic exercise + diet supplementation in obese men and women (Huck. 2013)

In said study Huck et al. observed that the provision of 500mg of vitamin C as an adjunct to exercise and diet in obese individuals lead to significant reductions in heart rate and the ratings of perceived exertion during exercise. The data in in Figure 3 does yet also tell you that there were no beneficial effects on VO2max, which best reflects the adaptational response to exercise.

This results of stands in contrast to the study at hand, but in line with previous results of studies in athletes, where only more or less irrelevant reductions of the acute inflammatory response to exercise were observed (Nieman. 2000; Peters. 2001; Tauler. 2002). A response of which you as a SuppVersity reader know that it is an essential part of the signalling cascade that triggers the adaptational response to. If we eventually get back to the Paschalis study, it would thus appear that athletes who are usually consuming more than enough vitamin C in their diets and are not at particular risk of developing low serum vitamin C levels would see similar results as the "high vitamin C" subjects in the Paschalis study, i.e. none - even worse, in view of the potential negative effects on the training induced adaptations that could not become visible in the study at hand, because there was no exercise protocol involved, it could even harm their progress.

Bottom line: Just like the researchers had expected, they found higher resting levels of oxidative stress and decreased exercise performance in the individuals with low baseline values of vitamin C compared to those with high vitamin C values.

Figure 3: Rel. changes in PGC-1α in cytosolfractions in the vitamin C and E group and the placebo group of a randomized controlled antioxidant + exercise study by Paulsen et al. (2014) - find out what boosts PGC-1α | here.

Since the provision of 1g of vitamin C oxidative stress, it is thus not surprising that there was a concomitant increase in exercise performance. What is "surprising", though, is that the latter was "marginally" and clearly "non-signifiant." Furthermore, it was observed only in those individuals with a poor initial vitamin C status. In that, it is a novel finding that you do not need to suffer from hypovitaminosis C  (<23µmol/L) or vitamin C deficiency to be derive acute benefit from vitamin C supplementation as regards to redox status and physical performance. Previous studies which combined the provision if vitamin C with chronic exercise training, however, indicate that the ingestion of anti-oxidants can blunt the intra-cellular adaptive responses to exercise (Paulsen. 2014) - an effect that obviously couldn't be confirmed or negated in the study at hand, because it lacks a chronic exercise component | Comment on Facebook!

References:

• Close, G. L., and M. J. Jackson. "Antioxidants and exercise: a tale of the complexities of relating signalling processes to physiological function?." The Journal of physiology 592.8 (2014): 1721-1722.
• Huck, Corey J., et al. "Vitamin C status and perception of effort during exercise in obese adults adhering to a calorie-reduced diet." Nutrition 29.1 (2013): 42-45.
• Nieman, David C., et al. "Influence of vitamin C supplementation on cytokine changes following an ultramarathon." Journal of Interferon & Cytokine Research 20.11 (2000): 1029-1035.
• Paschilis, V. et al. "Low vitamin C values are linked with decreased physical performance and increased oxidative stress: reversal by vitamin C supplementation." Eur J Nutr (2014). Ahead of print.
• Paulsen, Gøran, et al. "Vitamin C and E supplementation hampers cellular adaptation to endurance training in humans: a double‐blind, randomised, controlled trial." The Journal of physiology 592.8 (2014): 1887-1901.
• Peters, E. M., et al. "Vitamin C supplementation attenuates the increases in circulating cortisol, adrenaline and anti-inflammatory polypeptides following ultramarathon running." International journal of sports medicine 22.7 (2001): 537-543.
• Picklo, Matthew. "Supplementation with vitamin E and vitamin C inversely alters mitochondrial copy number and mitochondrial protein in obese, exercising rats (1030.5)." The FASEB Journal 28.1 Supplement (2014): 1030-5. 
• Powers, Scott K., et al. "Dietary antioxidants and exercise." Journal of sports sciences 22.1 (2004): 81-94.
• Powers, Scott K., And Kurt J. Sollanek. "Endurance Exercise And Antioxidant Supplementation: Sense Or Nonsense?-Part." Sports Science 27.137 (2014): 1-4.
• Tauler, P., et al. "Diet supplementation with vitamin E, vitamin C and β-carotene cocktail enhances basal neutrophil antioxidant enzymes in athletes." Pflügers Archiv 443.5-6 (2002): 791-797.

CLnA, the "Omega-3 Variety" of CLA from Pomegranate & Co, Has Potent Anti-Obesity Effects and the Potential to Become More Than Just Another Anti-Diabetes Drug.

Image 1: Pomegranate - I loved to eat them even before I realized that their seeds are the #1 dietary source (83%) of punic acid.

While more and more people are beginning to grasp the notion that with (naturally occurring) fats - as with everything else in life - there is no simple "good" and "bad", no clearcut "black" and "white" and no definite "beneficial" and "detrimental". The number of different fatty acids and their respective effects on the human metabolism is so vast that it is pretty hard to keep track of all those varieties of saturated and unsaturated carboxylic acids. I would thusly not be surprised if you simply assumed that the "n" in the headline of this blogpost was a type that had slipped in because poor Dr.Andro is chronically stressed from Christmas shopping... well, while the latter is actually correct, the former is not: CLnA is actually the omega-3 variety of the famous conjugated linoic acid (CLA), which in and out of itself is not a single but a group of 28 different trans- and cis-isomers that occur in our diet mainly in the shape of high and full-fat meat and dairy products.

CLnA - Conjugated Linolenic Acid is not a typo ;-)

Within the last couple of years even the medical establishment has come to realize that the chronic omega-6 (n6: linolic acid) overload in our diet is killing us. The "heart-healthy" PUFAs have now become the more and less heart-healthy PUFAs with the totally healthy *rofl* omega-3s and the not just as healthy omega-6s - both, of course, still totally "essential" and WAY better than saturated fats,... (attention: the afore statements are full or irony! Saturated fats are of course NOT the bad guys. Sorry, David if that lead to confusion)... but I am getting derailed, here. So let's get to the point. What every reasonable person appears to agree on, these days, is that we have to lower the ratio of n6:n3 fatty acids in our diets. Now, I am asking you: Has it ever occured to you that CLA essentially is an omega-6 fatty acid? I mean its conjugated linoleic acid - "linoleic" as in omega 6 = linoleic acid! Probably not, right? The reason for that is yet (hopefully ;-) not that you are dump, but simply that the existence of an omega-3 "variety of CLA", namely conjugated linolenic acid, or short, CLnA, is something about which you will only hear, when you read blogs (such as the SuppVersity ;-), which do not stick to copying, pasting and commenting the stuff the authors have read on one of the major news-portals.

Table 1: CLnA isomer content in natural sources (data adapted from Hennesey. 2011)

From a molecular perspective,  CLnA isomers combine the conjugated double bond system of the classic conjugated linolic acid, you know, with the octadecatrienoic fatty acid (C18:3) structure of omega-3s, i.e. linolenic acid. Interestingly, this make-up confers these fatty acids with a high bio-active potential. Now, while this may sound like one of the frankenfood test-tube results of the gene-technology laboratories of Monsanto, we know at least 10 CLnA isomers which occur naturally in foodstuff or as byproduct of fermention processes (cf. table 1).

Adiposity, hyperlipidemia, cancer - CLnAs could help with all!

Image 2: Even if CLnAs would just prevent obesity, this illustration I borrowed from multiplemyelomalifeexpectancy.tk, shows that not being / getting obese alone would prevent a plethora of related maladies. Such as kidney failure, arthritis, gallbladder disease, infertility, asthma, fatty liver disease, sleep apnoea, depression, heart disease, hyperlipidemia, diabetes,... basically every major ailment the increasingly obese convenience society of the Western hemisphere is suffering from.

Due to their anti-adipogenic (meaning preventing the accumulation of body fat) effects CLnA fatty acids have been investigated as potential candidates for the treatment of the obesity epidemic for quite some time, now (Hennesey. 2011). In a 2002 article that was published in the Journal of Applied Biochemistry and Biotechnology, Nishimura et al. report that CLnA isomers exert apoptotic effects on mouse preadipocyte 3T3-L1 cell - or, in plain English, incubation with CLnA did not only hinder the "pubertal" fat cells from becoming mature adipocytes, it actually killed them. In vivo studies with rodents, such as Arao et al. (2004), where the administration of a diet that was enriched with 1% pomegrenate seed oil lead to a 27% reductin in omental white adipose tissue, were able to confirm the "rodent-real world signficance" of these test-tube results.

Other studies showed a normalization of hyperlipidemia in rodent models of the metabolic syndrome and a hand full of studies have explored the usage of CLnA isomers as cytotoxins in the treatment of cancer. In their concise review of the literature, Hennesey, et al. thusly rightly conclude that with their "potent inflammatory and immune modulating properties", their ability to "reduce the risk of obesity, improve cardiovascular health, and mediate strong anti-carcinogenic activity", the use of CLnA isomers or dietary enrichments could offer treatment strategies for pathologies, which "represent some of the greatest mortality risks to humans in the Western world and have been inextricably linked with diet" (Hennesey. 2011).

Adding diabetes to the list of potential targets for CLnA

For today, we are however going to focus on the most recent result from the research front: The effects of CLnAs on diabetes, or, to be precise, the increases in blood glucose, and decreases in anti-oxidant capacity that go hand in hand with the latter. In a recently published study (Saha. 2011), Siddhartha S. Saha and Mahua Ghosh from the Department of Chemical Technology at the University College of Science and Technology of the University of Calcutta (I don't have to tell you that this is in India, do I?) injected male albino lab rats with 60mg/kg streptozotocin (STZ) - this is a common and well-established method to induce a metabolic state that serves as a model of type II diabetes - and fed them diets that contained either no, or 0.5% of the total fat in the form of alpha-eleostearic acid (from bitter gourd, cf. table 1) or punic acid (which was in this case taken from snake gourd oil, but could as well have been extracted from the eponymous pomegrenate, cf. table 1).

Figure 1: Relative blood glucose levels vs. non-STZ injected control in streptozotocin injected rats over the course of the dietary intervention (data calculated based on Saha. 2011)

As you can see in figure 1, this 100% natural "food additive" had a more than pronounced effect on the +300% (vs. non STZ-injected control) elevated blood glucose levels of the "type-2 diabetic" rodents.

Figure 2: Relative level of lipid peroxidation (left) and total antioxidant capacity (right) levels vs. non-STZ injected control in streptozotocin injected rats after the 28-day dietary intervention (data calculated based on Saha. 2011)

And while the glucose levels were still 150% above those of the healthy control levels, the streptozotocin-induced lipid peroxidation in plasma, pancreas and erythrocytes of the lab animals was ameliorated by the snake gourd oil treatment (remember that is the stuff from pomegranate) and even reversed by the bitter gourd diet. Judged by the standardized FRAP assay, the "diabetic animals" that were fed a diet that contained 0.1% alpha-eleostearic acid (of the total diet, which had 20% fat) even exhibited a 10% greater total antioxidant capacity than the totally healthy control!

Figure 3: Relative expression of inflammatory cytokines, TNF-alpha and interleukin 6 in plasma capacity (right) levels vs. non-STZ injected control in streptozotocin injected rats after the 28-day dietary intervention (data calculated based on Saha. 2011)

Snake gourd oil, on the other hand, exhibited more profound effects on the elevated TNF-alpha, interleukin-6 and NF-kappaB levels of the STZ-treated rodents (cf. figure 2) and thus, at least this is my humble opinion, render punic acid the overall more promising agent with respect to the treatment of all sorts of inflammatory (or related diseases). After all, disturbances in the regulation of the nuclear factor kappa-light-chain-enhancer of activated B cells  (NF-kappaB) and the downstream over-expression of TNF-alpha and IL-6 are hallmark features of allmost all the aforementioned ailments of the increasingly obese western convenience society. This is also why I am quite certain that we are going to hear much more about the CLnAs in the month to come... and I guess, I don't have to tell you that right here, at the SuppVersity, is where you will read about respective studies first!

"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.