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If you want to know how to get of pubertal acne, you got to ask professional pubescents ;-)

The study at hand is not only the first experimental verification of the efficacy of omega-3 + gamma linoleic acid supplementation in acne treatment, its also "paleo approved", because it cites a study by no one else but Loraine Cordaine himself ;-) Dont worry, I am just kiddin around. In spite of the fact that Cordains study "Acne vulgaris: a disease of Western civilization" (Cordain. 2002) is in fact the #1 on the reference list, the scientists from the Seoul National University College of Medicine refrain from (paleolithic) dairy bashing in their evaluation of "the clinical efficacy and safety of omega-3 fatty acids and of GLA for the treatment of mild to moderate facial acne." (Jung. 2014)

If you google "natural acne treatment" it will usually not take long until you find a reference to fish oil and gamma linoleic acid (as in borage or starflower oil). Against that background it is surprising that the Korean scientist are obviously the first to scrutinize the efficacy of 2,000 mg of eicosapentaenoic acid and docosahexaenoic acid and 400 mg ?-linoleic acid (from borage oil) in a parallel design dietary intervention study.

Long-standing "natural acne cure" now scientifically proven

The 45 participants with mild to moderate acne, were allocated to either of the intervention groups for 10 weeks, after which the effect on their skin was evaluated visually and via heamatoxylin, eosin and immunohistochemical staining of the lesions.
And what the scientists observed was ... positive, at least in the omega-3 group, the mean inflammatory acne lesion count was significantly reduced (from 10.1 ± 3.2 in week 0 to 5.8 ± 3.4 in week 10; p < 0.05).

Figure 1: Changes in inflammatory acne lesion counts with time (left, top), noninflammatory acne lesion counts with time (left, bottom), and changes in patients subjective assessment (VAS) with time (right; Jung. 2014)

As you can see in Figure 1, a similar change was observed in the GLA (9.8 ± 5.2 before vs. 8.0 ± 4.6 after 5 weeks vs. 6.6 ± 3.7 after 10 weeks, p < 0.05), but not in the control group (9.9 ± 4.3 before to 10.2 ± 6.2 after 10 weeks).

Figure 2: Before (top) and after (bottom) photos (Jung. 2014)

"Mean non-inflammatory acne lesion counts were also reduced by omega-3 and GLA supplementation (23.5 ± 9.2 to 18.9 ± 8.3, p < 0.05, and 22.8 ± 8.4 to 19.2 ± 7.2, p < 0.05, respectively) at final visits, whereas mean lesion count in the control group was unchanged (from 21.8 ± 9.7 to 22.0 ± 8.6). Significant differences were evident between the treatment groups and the control group after 10 weeks (p < 0.05)." (Jung. 2014)

In the end, there was no no significant difference between the two treatments for any of the measured parameters, so that it is probably up to you, whether you try to control the "fire within your skin" with GLA or DHA + EPA supplements.
References:

• Cordain, Loren, et al. "Acne vulgaris: a disease of Western civilization." Archives of Dermatology 138.12 (2002): 1584-1590.
• Jung, Jae Yoon, et al. "Effect of Dietary Supplementation with Omega-3 Fatty Acid and gamma-linolenic Acid on Acne Vulgaris: A Randomised, Double-blind, Controlled Trial." (2014).
• Wolf, Ronni, Hagit Matz, and Edith Orion. "Acne and diet." Clinics in dermatology 22.5 (2004): 387-393.

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)
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.
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.
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 ?-carotene cocktail enhances basal neutrophil antioxidant enzymes in athletes." Pflügers Archiv 443.5-6 (2002): 791-797.

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

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

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

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

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

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

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

New human data with surprising results

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

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

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

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

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

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

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

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

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

Blueberries and other foods w/ tons of polyphenols are GSH boosters (Moskaug. 2005) and make supplements obsolete.

If you have been interested in dietary supplements for some time, I am pretty sure that you will have heard about oral glutathione ob(GSH) supplements in one of the "snake oil warnings" on various websites. The "master antioxidant" as it is called is after all believed by many to be not bioavailable - at least not orally. Studies in animal models, however, have already shown that oral GSH, administered either in the diet or by gavage, has the ability to increase plasma and tissue GSH levels ( Loven. 1986; Aw. 1991; Favilli. 1997; Kariya. 2007). It would thus be more appropriate to say that the efficacy of oral glutathione in humans has not yet been tested in peer-reviewed studies.
Now, the absence of human studies should definitely ring an alarm bell in the head of every healthily skeptic supplement user, what it should not do, though is mislead you to believe that GSH supplements dont work in human beings.

Now this is where John P. Richie Jr. and his colleagues from the Penn State Cancer Institute, the Department of Microbiology and Immunology at the Penn State University College of Medicine and the Orentreich Foundation for the Advancement of Science, come into play. As the scientist state, their "objective was to determine the long-term effectiveness of oral GSH supplementation on body stores of GSH in healthy adults." (Richie. 2014)
To this end, they conducted a 6-month randomized, double-blinded,placebo-controlled trial in the course of which the subjects, 41 women and 13 men (6 dropouts not included) with a normal BMI and no known health issues, consumed either ...

• an oral GSH supplement dosed at 250mg/day,
• an oral GSH supplement dosed at 1,000mg/day, or
• an identically looking placebo.

The main study outcomes were obviously analyses of the GSH levels in (a) blood, (b) erythrocytes, (c) plasma, (d) lymphocytes and (e) exfoliated buccal mucosal cells (the effects on a battery of immune markers was tested only in a handful of subjects).

Figure 1: Effects of 6 months GSH supplementation on ratio of oxidized to reduced GSH and natural killer cell cytotoxicity in healthy men and women aged 28-72y (Richie. 2014)

As the data in Figure 1 already suggests, there was a dose-dependent increase in GSH levels. With the high dose (1,000mg/day) producing GSH increases of 30–35 % in erythrocytes, plasma and lymphocytes and 260 % in buccal cells (P<0.05) and increases of 17 and 29 % in blood and erythrocytes, respectively, in the low-dose group (P<0.05 - data not shown in Figure 1).

These improvements had beneficial downstream effects on the overall status of the subjects antioxidant defense system. A fact you can conclude based on the decreased ratio of oxidized (used) to reduced (fresh) glutathione in whole blood the scientists observed in their subjects after 6 months. These benefits came hand in hand with an increase in natural killer cytotoxicity (+100%), another potentially highly desirable health benefit.

References:

• Aw, Tak Yee, Grazyna Wierzbicka, and Dean P. Jones. "Oral glutathione increases tissue glutathione in vivo." Chemico-biological interactions 80.1 (1991): 89-97.
• Favilli, Fabio, et al. "Effect of orally administered glutathione on glutathione levels in some organs of rats: role of specific transporters." British journal of nutrition 78.02 (1997): 293-300.
• Kariya, Chirag, et al. "A role for CFTR in the elevation of glutathione levels in the lung by oral glutathione administration." American Journal of Physiology-Lung Cellular and Molecular Physiology 37.6 (2007): L1590.
• Loven, Dean, et al. "Effect of insulin and oral glutathione on glutathione levels and superoxide dismutase activities in organs of rats with streptozocin-induced diabetes." Diabetes 35.5 (1986): 503-507.
• Moskaug, Jan Ø., et al. "Polyphenols and glutathione synthesis regulation." The American journal of clinical nutrition 81.1 (2005): 277S-283S.
• Richie Jr, John P., et al. "Randomized controlled trial of oral glutathione supplementation on body stores of glutathione." European journal of nutrition (2014): 1-13.