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.

Post-Workout Chlorogenic Acid / Caffeine Supplementation - For Good or For Worse? Plus: Glycogen Synthesis & Why A Post-Workout May Be a Better Idea Than You'd Think

"Done,... where is my post-workout coffee?" - Post workout caffeine / chlorogenic acid - good or bad idea?

I know it's kind of late to post an article like this months after the ISSN conference, but I recently hit on an overview of the poster presentations and noticed that I did actually miss a couple of interesting studies. Don't worry, I won't be addressing a couple of them in the weeks to come in some detail.

Not all are really news-worthy, but aside from today's item on caffeine and chlorogenic acid, there were also posters on nutrient timing, different forms of protein, commercially available supplements and other stuff that's all classic "SuppVersity fodder"?

Chlorogenic acid? Isn't that Ozzy's green coffee bean stuff? You are correct, but could actually read about it here at the SuppVersityway before it was on Dr. Oz. Plus, I still believe that there is something wrong with the corresponding study and do still have to meet someone who has successfully lost weight by just adding some GCB to the diet, which is effectively what Ozzy and the study promised | learn more

Caffeine and chlorogenic acid? Right, that sounds like green coffee bean extract, but in the case of Jason R Beam et al.'s study, we are dealing with an artificial stack of

• 5mg/kg body weight of caffeine plus 75 g of dextrose (CAF), 
• 5 mg/kg body weight of chlorogenic acid plus 75 g of dextrose (CGA), or 
• 5 mg/body weight of dextrose plus 75 g dextrose (PLA)

the 10 moderately to highly trained study participants consumed after 30-minutes of  high intensity cycling at 60% of peak power output (~90% HR max).

Figure 1:

As you can see in Figure 1, we do see quite extra-ordinary effects of the administration of both caffeine and chlorogenic acid on post-workout glucose metabolism. The changes in the area under the cure (2h AUC) do yet overestimate the real-world difference between the glucose curves (not shown), which have a slightly higher spike immediately after the ingestion.

"Ok, no caffeine after a workout - right!?"

In the case of caffeine that was to be expected, it has after all been shown to decrease the insulin-induced glucose uptake (Graham. 2001). The fact that the glycemic response was - within the statistically probable margins - still identical, is simply the result that the stimulation of glucose uptake and hepatic, as well as muscular glucose storage is not really necessary as long at the glycogen stores are low. Accordingly, a 2004 study by Battram et al. was unable to show any effect of caffeine ingestion on proglycogen and macroglycogen resynthesis after a workout (Battram. 2004).

Figure 2: Skeletal muscle glycogen content (mmol/kg dw) immediately after exercise 0. 1, 4h after cycling to volitional fatigue (70% Vo2Peak) w/ or w/out coingestion of 8mg/kg BW (+ 1g/kg glucose) after the workout - left; corresponding levels of pCAMK and p-Akt (arbitrary units) 1h and 4h after the workout, right (Pederson. 2009).

As you can see in Figure 2 the net amount of glucose that ends up in the musculature after exhaustive (if you don't deplete the stores this effect won't be there) exercise was in fact favorably affected by the congestion of 8mg/kg caffeine and 1g/kg glucose in with caffeine in the 7 endurance-trained cyclists and triathletes in a study by Pedersen et al. from 2009. The exact underlying mechanisms of this beneficial effects, as well as dose response relationships do yet still have to be determined, but Pederson et al. speculate that it may a result of the increased activation of p-AKT:

You think you've heard about p-Akt before, but are not sure where? Well, chances are it was here at the SuppVersity, yet probably in a different context, i.e. as part of the Intermittent Thoughts on Building Muscle | read more

"The increase [in p-AKT] tended to be higher after the ingestion of caffeine with CHO after both 1 and4hof recovery, but failed to reach statistical significance. Akt seems to regulate glucose uptake by phosphorylating and inhibiting the Rab-GTPase-activating protein AS160. Thus it is tempting to speculate on the role of Akt in glucose transport given that the Akt substrate AS160 has been identified as an important regulator of GLUT4 traffic.

We have recently shown that AS160 is phosphorylated in human skeletal muscle after endurance exercise with concomitant phosphorylation of Akt (7), providing correlative evidence to suggest AS160 is an exercise-responsive protein with a role in glucose uptake." (Pederson. 2009)

If we discard potential negative effects of the caffeine-induced CNS activation on post-exercise nervous system recovery, and take into account that the elevated glucose + insulin AUC Beam observed in the experiments for his dissertation and ISSN conference poster are negligible, the preliminary bottom line for post-workout caffeine intake would be: "If glycogen resynthesis is what you are looking for, do it!"

"What about the effects of chlorogenic acid. Shouldn't the exact opposite happen?"

Now that we've searched for explanations of the effects of caffeine on post-workout glycemia we are still left with the astonishing increase in the two-hour glucose area under the curve, i.e. total glycemia, Beam observed in the glucose + chlorogenic arm of his study.

Figure 3: Insulin (AUC) for each subject during the placebo, caffeine, and chlorogenic acid trials (Beam. 2013)

If you take a closer look at the data to the right, you won't get a mechanistic explanation of the underyling reasons, but you will at least get an idea of what statistical significance means and why we are talking about it in almost every study analysis, even if it does not equate physiological significance.

In this particular case the 2 outliers, subject 1 and subject 6 do not simply "ruin" the statistical significance, they are actually the (almost) only reason that insulin response is not virtually identical to the placebo trial.

As far as potential negative consequences of the post-workout consumption of cholorgenic acid goes, you do thus not have to be worried, whether it is actually a good idea to use a supplement that's meant to increase the activity of AMPK in a phase, when the latter is already maximized, is however questionable. In the best case, the additional benefits will be minimal, in the worst case it  CGA will ruin the glucose repartitioning effects of the workout by increasing AMPK and thus glucose uptake in the fat cells (Alonso-Castro. 2008).

If you actually have problems with insulin resistance / glucose uptake (which is not the case for 90%+ of the people who buy corresponding supps), I suggest you check out this list of useful anti-diabetes agents.

Bottom line: I would assume that you will not have expected that, but based on the results of the study at hand and the review of previous literature the effects of caffeine and chlorogenic acid on post-workout glycemia are most likely negligible.

If you still insist on supplementing with one or the other immediately after a workout, though, there would be a rationale to use caffeine. The use of chlorogenic acid, green coffee bean extracts or any other highly advertised and for physical culturist 100% useless "nutrient repartitioning agents", would be at least non-sensical, in view of the potential negative effect on the true nutrient repartitioning effects, even potentially downright counterproductive.

References:

• Alonso-Castro, A. J., Miranda-Torres, A. C., González-Chávez, M. M., & Salazar-Olivo, L. A. (2008). Cecropia obtusifolia Bertol and its active compound, chlorogenic acid, stimulate 2-NBD glucose uptake in both insulin-sensitive and insulin-resistant 3T3 adipocytes. Journal of ethnopharmacology, 120(3), 458-464. 
• Beam, J. (2013). The effect of post-exercise caffeine and chlorogenic acid supplementation on blood glucose disposal and insulin sensitivity.
• Battram, D. S., Shearer, J., Robinson, D., & Graham, T. E. (2004). Caffeine ingestion does not impede the resynthesis of proglycogen and macroglycogen after prolonged exercise and carbohydrate supplementation in humans. Journal of Applied Physiology, 96(3), 943-950.
• Pedersen, D. J., Lessard, S. J., Coffey, V. G., Churchley, E. G., Wootton, A. M., Ng, T., ... & Hawley, J. A. (2008). High rates of muscle glycogen resynthesis after exhaustive exercise when carbohydrate is coingested with caffeine. Journal of Applied Physiology, 105(1), 7-13.

Caffeine & Cholorogenic Acid - Anti-Obesity Agents from Your Coffee Mug? Human Study Reveals Cortisol Lowering Effects, Mouse Study Confirms Anti-Obesity Effects

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 People's 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.

There is evidence of beneficial effects of GCA on your gut microbiome (Jaquet. 2009)

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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 it's 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), it's not really surprising that we didn't 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.

Yes, agents like glycerric acid from licorice increase cortisol levels. Contrary to common believe this will yet not trash your testosterone levels and/or induce weight loss - quite the contrary | learn more

Bottom line: While the rodent study by Zhang et al. appears to support the accuracy of the data Vinson et al. published two years ago, you as a SuppVersity reader should be aware of the fact that the reduction in cortisol / cortisone activity Revuelta-Iniesta and Al-Dujaili observed in their subjects is not necessarily going to facilitate weight loss. As discussed in the corresponding Science Round Up, a normal circadian cortisol rhythm with both spikes and troughs is a prerequisite of optimal fat loss, so that it's suppression by green coffee beans or other means is beneficial only for those of us who suffer from chronically elevated cortisol levels.

Overall, we are thus left with a single study the whole "green coffee bean for weight loss"-hype is based on. Well, who cares. For the majority of best-selling supplements we don't even have that ;-)

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 11β-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.

Double Your Workout Volume With 3,4-DA - Chlorogenic Acid Metabolite, Dihydroxycinnamic Acid, Makes Rats Run 60% Longer, 30% Faster 90% Further!

Image 1 (sodahead.com): Another reason to supersize your cup of coffee; no not the girl, or ... well ;-)

Those of you who can no longer be without their well-deserved daily dose of SuppVersity news will probably remember the amazing weight loss effects an extract from green coffee beans yielded in a 2012 trial by Vinson et al. (cf. "GCB Another Fatloss Acronym: Green Coffee Bean Extract Helps Pre-Obese Men and Women Shed 16lbs in 22 weeks"; Vinson. 2012) and while I am still not convinced that you would see similar results in non-obese individuals, another recently published study by Novaes et al. does suggest that even those of you who don't think that they have another lbs of body fat to spare, could largely benefit not just from the caffeine, but also from the 0.5-1.0g of chlorogenic acid and the subsequent conversion of the latter into 250-500mg of 3,4-Dihydroxycinnamic acid (3,4-DA) even 400ml of regular coffee do contain (Chung. 2004; Novaes. 2012).

3,4-DA is like legal gear from the brown brew

Compared to placebo and vitamin C (25mg/kg), the hydrolyzed chlorogenic acid molecule, of which the 8-week-old male Wistar rats in the Noves study received either 5mg or 25mg per kg body weight (HED for 80kg human being: 65mg or 324mg) had almost incredibly potent "ergogenic" effects:

Figure 1: Time to fatigue (TTF), speed, workload and total distance covered (secondary axis) during exhaustive treadmill running after oral supplementation with placebo (control), vitamin C or 4,5 DA at doses of 5mg/kg and 25m/kg (based on Novaes. 2012)

As you can see in figure 1 the rodents in the high dose group ran 60% longer, 30% faster, 90% further and performed overall twice as much work (42 vs. 21 kg*m) than the rodents who had received the human equivalent of ~325mg vitamin C before a forced running test on a motor-driven treadmill.

Less ROS = Increased efficacy?!

Interestingly, the lactate levels of the 3,4-DA rodents were significantly lower and the remaining liver glycogen levels were significantly higher than in the placebo and vitamin C group (see figure 2).

Figure 2: Serum triglyceride (group effects non-significant) and lactate levels, hepatic glycogen content and protein arbonyl and malondialdehyde levels after the exercise (based on Novaes. 2012)

As Novaes et al. point out this suggests that the effect is partly mediated by a higher metabolic efficiency. The latter is probably a direct result of the profound reduction in reactive oxygen specimen, which have been associated with impairments of the cellular metabolism and subsequently reduced aerobic energy production (Atalay. 2002) - a hypothesis that would be supported by the reduced levels of protein carbonyl and malondialdehyde in the liver of the 3,4-DA treated rodents.

But don't we need ROS?

Image 2: Don't worry those love handles will go away - rather with the antioxidant + caffeine power of coffee than without it!

These observations are also quite revealing as the offer an alternative explanation for the previously mentioned possibly negative effects of antioxidants on the exercise-induced improvements in glucose metabolism (cf. "Update on Antioxidants & Exercise - Neither Vitamin C Nor E Have ANY Effect on the Response to Intense Exercise"): If high doses of other anti-oxidants have the same beneficial effects on metabolic efficacy, it stands to reason that even weaker antioxidants than 3,4-DA would spare liver (and muscle) glycogen and thus reduce the exercise-induced expression of AMPK of which you may remember from posts like "AMPK II/III: Leucine, HMB and a Glimpse on Other AMPK Modulators" that it is expressed in response to intracellular glucose, or more specifically ATP depletion, and the subsequent increase in glucose (re-uptake).

A huge cup of coffee before your workout will therefore neither hamper the weight loss, nor the health effects of your workout, as long as you do actually make use of its ergogenic effect and train 60% longer, 30% faster, 90% further and perform overall twice as much work... just kiddin', if you train regularly you should be more concerned about keeping the amount of inflammation at bay - some is probably necessary, too much counter-productive, but that would the topic of another SuppVersity post. I for one am now going to get myself a nice cup of coffee...yummy!

Suggested reads on coffee:

• GCB Another Fatloss Acronym: Green Coffee Bean Extract Helps Pre-Obese Men and Women Shed 16lbs in 22 weeks.
• Warding Off Holiday Weight Gain 2.0: The Anti-Diabesity Effect of Coffee Goes Beyond its Caffeine Content.
• Only "Real", Not Decaffeinated Instant Coffee Increases Fatty Acid Oxidation. Revisited: Caffeine's Dose-Dependent Effects on Testosterone & Cortisol Response to Exercise
• Study Identifies Caffeic Acid Induced AMPK-α2 Activity Behind the Fat Burning, Insulin-Sensitizing & Life-Extending Effects of Coffee. Plus: Why Creatine & Coffee Don't Mix!

• all about coffee

References:

1. Atalay M, Laaksonen DE. Diabetes, oxidative stress and training. Journal of Sports Science and Medicine 2002 Jan; 1 - 14.
2. Chung TW, Moon SK, Chang YC, Ko JH, Lee YC, Cho G, Kim SH, Kim JG, Kim CH. Novel and therapeutic effect of caffeic acid and caffeic acid phenyl ester on hepatocarcinoma cells: complete regression of hepatoma growth and metastasis by dual mechanism. FASEB J. 2004 Nov;18(14):1670-81.
3. Novaes RD, Gonçalves RV, Peluzio Mdo C, Natali AJ, Maldonado IR. 3,4-dihydroxycinnamic Acid attenuates the fatigue and improves exercise tolerance in rats. Biosci Biotechnol Biochem. 2012 May 23;76(5):1025-7.
4. Vinson JA, Burnham BR, Nagendran MV. 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 Metab Syndr Obes. 2012;5:21-7. Epub 2012 Jan 18.

Can An OTC Supplement Quadruple Your Weight Loss Success? Recent Study Says: Yes It Can! But The Absolute Improvements in Body Composition Are Still Pathetic

I am sorry, but I have to tell you: Significant weight loss does not happen without effort. Even if you take a pill that comes with just this promise.

I guess you will not have heard about "IQP-GC-101", before - right? Well, me neither, but it is obviously a patented blend of a bunch of very familiar weight loss adjuvants, namely Garcinia cambogia, Camellia sinensis, unroasted Coffea arabica (aka green coffee bean extract), and Lagerstroemia speciosa. All of them were pressed into tablets, the scientists from InQpharm, the producer and patent owner handed to 92 German subjects who had volunteered to participate in a double-blinded randomized study in the course of which they had to (a) adhere to a -500kcal/day energy deficit and (b) consume three tablets of either IQP-GC-101 or an identically looking placebo twice a day - once 30min before breakfast and once 30 minutes before lunch.

The "lose fat effortlessly"-myth is not the only one, learn more about Myths & Truths 

Pasta "Al Dente" = Anti-Diabetic

Vinegar & Gums for Weight Loss

Teflon Pans Will Kill You!

You Can Drum Yourself Lean

You Can Wash Pesticides Away

Milk = Poisonous Hormone Cocktail

Now, it goes without saying that this is not the first sponsored weight loss study. So you may be asking yourselves rightly, why this one made it into the SuppVersity news while most of the other trash did not, right?  Well, there are actually a handful of reasons, of which I consider the following two to be most significant:

• The study design: Double-blinded, an impressive number of subjects (n=91; one subject was "lost to follow up after randomization"; Chong. 2014), all caucasian with a mean age of 42.8 ± 11.2 years (31.9% were male), and full details on the ingredients of the supplement - that's nothing you will see with the average "pimp my product" study

• The supplement ingredients: Garcinia cambogia aka HCA, camelia sinensis aka green tea, coffea arabica aka green coffee bean extract and lagerstroemia speciosa aka Banaba are all ingredients you will find in many of the currently available supplements.

I guess, I could add that interesting supplement news are slow, these days and that I am so freaking busy that I had to pick the next best study from my "could be something to write about in the future" folder, but I am not sure how relevant that would be ;-)

Apropos "relevant", what certainly is relevant is the ingredient profile each of the 6 tablets (2x3) the subjects consumed on a daily basis:

• 

  Table 1: Subjects' demographics at baseline - age (years), height (cm), body weight (kg; from Chong. 2014)

  G.cambogiaextract (650 mg) – standardized to at least 60% HCA; 
• C.sinensis extract (100 mg) – at least 15% epigallocatechin-3-gallate and 11% caffeine;
• unroasted C.arabica extract (75 mg) – at least 25% chlorogenic acid and 5% caffeine; and 
• L. speciosa extract (25 mg) – at least 5% corosolic acid in a standardized extract

The "at least..." indicates that the producer guarantees a certain level of active ingredients. That's the case for most of the reputable companies, but in view of the fact that there are more than enough snake oil vendors out there, I think it may be prudent to repeat my advice: Whenever you look at the ingredient level make sure the producer declares the level of active ingredients.

Do not buy non-standardized herbal / natural supplements! You could not only be wasting your money on products without active ingredients, you could - in the worst case - end up with a sloppily produced extract that contains all the bad stuff from the raw material (e.g. all the heavy metals from Chinese green tea | learn more) and not a single microgram of the of the active ingredient.

You don't want "green tea" in your fat burner, you want a green tea extract with a standardized amount of catechins in it and if the bottle doesn't say anything about "standardization" / "standardized for", etc. you can be sure that what you are buying is hardly different from the content of the contents of the cheapest tea bags from the supermarket next door - the only difference being: It did not have to pass the rigorous quality control of the supermarket chain!

But let's get back to the study at hand. The subjects consumed what I would call a pretty lame iteration of the SGD, the "standard German diet". It's not as "SAD" as the standard American one, but my fellow countrymen and -women have gained some ground in terms of eating unhealthy over the past two decades; and the fact that "[t]he diet plans were compiled by a dietician and ensured a balanced diet providing 30% of the ingested energy as fat," (Chong. 2014) does not increase my confidence in the overall quality of the foods the subjects consumed at one out of five distinct energy equivalents, i.e. 1500, 1800, 2000, 2200, and 2500 kcal per day - obviously calculated based on the theoretical energy requirements of the subjects.

The kcal-display lies to her!

SuppVersity Suggested Reads: "Predictive Value of Equations to Calculate Your Resting Metabolic Rate (RMR) Flawed: Results Can Be 14-29% Off" | read more - At this point I would like to invite you to take a look at the real-world validity and the corresponding "value" of calculated energy requirements. In the corresponding article, as well as in a more detailed follow up that includes 9 Tips to Optimize Fat Loss and successfully manage your weight, I outline a couple of commonly known but often overlooked principles that facilitate real and lasting fat, not weight loss.

If we rely on the messed up 3,500kcal per pound of fat calculation I've debunked years ago (read the corresponding article "Busting the 3,500kcal = 1lbs Weight Loss Myth!"),  the "diet" alone should have yielded a net reduction in body fat of ~1lbs per week and thus a total fat loss of 12weeks x 1lbs per week = 12lbs or ~6kg of pure fat!

I hope you are not surprised to see that this was exactly not what happened. In fact, after the first four weeks, when the subjects in both groups should have had lost roughly 2kg of body fat, the average study participants in the active and the placebo arm of the study had lost only ~1lbs of body fat and a total of ~1.5lbs of weight.

Figure 1: Absolute changes in body weight (kg) and body fat (kg) over the 12-week study period (Chong. 2014)

Now, in all fairness, it should be said that the 4-week margin was actually the 2-week margin for the active treatment. There was a 2-week run-in, after which 10 non-compliant subjects were removed and the rest of the subjects were randomized to receive either the placebo or active treatment. Against that background, it makes sense to isolate the body weight and body fat trajectory from week 2 to week 12 ... et voilá! The result does already look much more promising. Still, in spite of the fact that the subjects in the active arm lost almost 4x more body fat, the overall result, i.e. -1.21kg of fat over 12 weeks in overweight subjects, is still pretty pathetic.

Programming a 500kcal deficit based on calculated energy expenditure is stupid

Moreover, the fact that the subjects in the placebo arm gained almost 1lbs of body fat does not speak to either, the competence of the "registered dieticians" who compiled their diets, or the subjects' ability to stick to their alleged 500kcal deficit.

2x-3x higher than RDA protein help men and women lose fat, not weight, but there is a limit to wheer more is actually better | learn more

If you have not read it, already, this would be a good time to read my previous article on the "validity" *rofl* of the currently available equations to calculate your energy requirements (read more). And remember, while I personally don't believe that there is such a thing as diet induced "metabolic damage", it's a scientifically validated matter of fact that there are normal-, hyper- and hypometabolizers. And people with a mean BMI of 28+kg/m² (see Table 1) who belong to the sedentary average of the German society and are thus not just by definition "overweight" are probably more likely to be hypo- than normal- let alone hypermetabolizers.

This means, compared to the average for whom the equations the dietitians used to calculate their baseline intake may be more or less accurate, their real energy expenditure would be lower than what the equation says.

It's thus not impossible that their weight and fat gain (see Figure 1) was a simple result of the dieticians' stoic over-reliance on unreliable math and a minimal real-world calorie deficit (probably way below 500kcal) that was further reduced by non-adherence - especially in the placebo group.

Is garcinia or hydroxycitric acid aka HCA even safe? Ever since the FDA report about Hydroxycut(TM) (FDA. 2013). Most people think garcina was not safe. If you look at the evidence, it's yet not as "black" as the FDA has painted it in their warning against Hydroxicut(TM). If you look at some of the latest studies, you will even find conclusions such as the following statement from a well-referenced letter to the editor of the World Journal of Gastroenterology:

"In both animal and clinical literature, elevated intakes of HCA per se have not led to signs of inflammation or hepatotoxicity. The compound has been found to reduce markers of inflammation in brain, intestines, kidney and serum."(Clouatre. 2013) 

In the study at hand, the researchers did likewise not observe any liver problems or similar allegedly HCA-related side effects. In view of the rather mediocre results, the safety question may yet be more or less irrelevant, anyway.

 Bottom line: Specifically in view of the last remarks on dietary adherence, the significant inter-group differences speaks in favor of the the use of the patented weight loss formula in an average Joe's messed up diet scenario with a focus on food and macronutrient quantities, instead of qualities, a low protein intake (learn more about 2xRDA protein intakes, while you're dieting | here) and no exercise component, which would steer the total weight loss away from lean and towards fat mass.

On the other hand, the absolute amount of fat the subjects lost even when they were using the "fat burner" was pathetic. Any appetite suppressing or fat burning effects the formula may have are thus not pronounced enough to produce meaningful, or at least statistically significant weight, let alone fat loss. With standard deviations of 1.84 kg and thus 150% of the statistically mean in the active arm of the study, there were more than enough subjects who gained body fat in spite of the fact that they (supposedly) consumed less energy than they needed and were taking a patented weight loss adjuvant. A weight loss adjuvant with "proven" ingredients.... or should I say, with ingredients for which you can cherry pick evidence that they may increase fatty acid oxidation, inhibit lipid synthesis, decrease inflammation, increase insulin sensitivity and reduce food intake - in many cases even in human studies (see References). The fact that this does not necessarily mean that you will experience significant and visible fat loss effects, is thus probably the actual bottom line to the study at hand; and that's a bottom line that's valid irrespective of all declared conflicts of interest.

Reference:

• Acheson KJ, Zahorska-Markiewicz B, Pittet P, Anantharaman K, Jequier E. 1980. Caffeine and coffee: their influence on metabolic rate and substrate utilization in normal weight and obese individuals. Am J Clin Nutr33(5): 989–997. 
• Chong, P. W., Beah, Z. M., Grube, B., & Riede, L. (2014). IQP‐GC‐101 Reduces Body Weight and Body Fat Mass: A Randomized, Double‐Blind, Placebo‐Controlled Study. Phytotherapy Research. 
• Clouatre, Dallas L., and Harry G. Preuss. "Hydroxycitric acid does not promote inflammation or liver toxicity." World journal of gastroenterology: WJG 19.44 (2013): 8160.
• Deocaris CC, Aguinaldo RR, dela Ysla JL, Asencion AS, Mojica ERE. 2005. Hypoglycemic activity of irradiated Banaba (Lagerstroemia speciosaLinn.) leaves.J Appl Sci Res1(1): 95–98
• Dulloo AG, Duret C, Rohrer D,et al. 1999. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24-h energy expenditure and fat oxidation in humans.Am J Clin Nutr70(6): 1040–1045
• Hayamizu K, Ishii Y, Shigematsu N,et al. 2003. Safety ofGarcinia cambogiaextract in healthy men: high doses administration study I.J Oleo Sci52(9): 499–504
• Heymsfield SB, Allison DB, Vasselli JR, Pietrobelli A, Greenfield D, Nunez C. 1998.Garcinia cambogia(Hydroxycitric acid) as a potential antiobesity agent.JAMA280(18): 1596–1600.
• Hursel R, Viechtbauer W, Westerterp-Plantenga MS. 2009. The effects of green tea on weight loss and weight maintenance: a meta-analysis.Int J Obes (Lond) 33(9): 956–961.
• Jayaprakasha GK, Sakariah KK. 1998. Determination of organic acids inGarcinia cambogia(Desr.) by high-performance liquid chromatography.J Chromatogr A806(2): 337–339.
• Klein G, Kim J, Himmeldirk K, Cao Y, Chen X. 2007. Antidiabetes and anti-obesity activity ofLagerstroemia speciosa.Evid Base Compl Alternative Med4(4): 401–407.
• Liu S, Kim J, Li Y, Liu X, Li J, Chen X. 2001. An extract of Lagerstroemia speciosa L. has insulin-like glucose uptake– stimulatory and adipocyte differentiation–inhibitory activities in 3T3-L1 cells. J Nutr131(9): 2242–2247.
• Ohia SE, Opere CA, LeDay AM, Bagchi M, Bagchi D, Stohs SJ. 2002. Safety and mechanism of appetite suppression by a novel hydroxycitric acid extract (HCA-SX).Mol Cell Biochem 238 (1–2): 89–103.
• Onakpoya I, Terry R, Ernst E. 2011b. The use of green coffee extract as a weight loss supplement: a systematic review and meta-analysis of randomized clinical trials.Gastroenterol Res Pract. DOI: 10.1155/2011/382852.
• Satomi T, Seigo K, Masaki M, Haruki M. 2006. An inhibitory effect on the increase in the postprandial blood glucose by Banaba extract capsule enriched corosolic acid.J Integr Study Dietary Habits17(3): 255–259.
• Shimoda H, Seki E, Aitani M. 2006. Inhibitory effect of green coffee bean extract on fat accumulation and body weight gain in mice. BMC Complement Altern Med6:9.
• Stobs SJ, Miller H, Kaats GR. 2012. A review of the efficacy and safety of banaba (Lagerstroemia speciosaL.) and corosolic acid.Phytother Res26: 317–324.
• Sullivan AC, Triscari J, Hamilton JG, Miller ON, Wheatley VR. 1974. Effect of ( )-Hydroxycitrate upon the accumulation of lipid in the rat II: appetite. Lipids9(2): 129–134.
• Sullivan AC, Singh M, Srere PA, Glusker JP. 1977. Reactivity and inhibitor potential of hydroxycitrate isomers with citrate synthase, citrate lyase and ATP citrate lyase.J Biol Chem 252(21): 7583–7590.
• U.S. Food and Drug Administration. Warning on Hydroxycut prod ucts. http://www.fda.gov/forconsumers/consumerupdates/ ucm152152.htm [Accessed 20 August 2013].

GCB Another Fatloss Acronym: Green Coffee Bean Extract Helps Pre-Obese Men and Women Shed 16lbs in 22 weeks

Image 1: Coffee! Would you have recognized it?

HCG, GTE, GSE, DNP and obviously ECA! If you have ever done some research into pharmacological and non-pharmacological weight loss agents, you are probably familiar with this alphabet soup. But would you know right off your head what GCB stands for? No, ...? "G" as in "green", "C"  as in "coffee" and "B" as in "bean" - if you make it GCBE, with an "E" for "extract" it could make another item on your list of potential weight loss tools - moreover, one that has actual human data to back it up.

Green seems to be a good color for weight loss ;-)

In a recently published paper, a group of scientists from the University of Scranton, in the US, and the Health Sciences Clinic in Bangalore, India, report on the results of 22-week cross-over trial, in which the researchers tested the efficacy and safety of high (3x 350mg) and low (2x 350mg) doses of a commercial green coffee extract product (GCA by Applied Food Sciences; a 45.9% chlorogenic acid in an extract from unroasted = green coffee beans) in 16 overweight subjects (eight males and eight females; aged 22–46, mean age 33.19y; BMI 28.22km/m²). In each of the three arms of the studies, the subjects received the high and low dose supplement in a different order, so that the individual supplementation protocols looked like this:

• group 1: 6 weeks 3x 350mg / WA / 6 weeks 2x350mg / WA / 6 weeks placebo
• group 2: 6 weeks 2x350mg / WA / 6 weeks placebo / WA / 6 weeks 3x 350mg
• group 3: 6 weeks placebo / WA / 6 weeks 3x350mg / 6 weeks 2x 250mg
  * WA: 2-week wash-out period without supplementation

The results you see in figure 1, especially in the beginning of the study, are impressive, given the fact that the reduction in calorie intake (which is unfortunately not group-speficic) amounted to no more than -2% over the whole study period.

Figure 1: Mean weight over the whole 22-week study period and change in body fat percentage during the individual 6-week supplementation phases (data calculated based on Vinson. 2012).

It is yet somewhat suspicious that a) this phenomenon arose in both the high and the low-dose group (it was even more pronounced in the latter) and b) that the group which received the high dose in the beginning of the study experienced a profound "jojo-effect", when during the last 6-weeks, in which they received the placebo supplement.

Maybe helpful for the obese, but questionable for anyone who is already lean

Image 2: Coffee beans are not the only food (or raw material for a beverage) that loses some of its active and oftentimes healthy ingredients, when it is heated, or, as with coffee beans, roasted.

Moreover, the actual fat loss, which was measure only via one of those notoriously unreliable body impedance devices (SFB7 from Impedimed) is not exactly impressive and was statistically significant not only in the high and low dose, but also in the placebo phases of the trial (the 0.3% difference is laughable) left the subjects with still more than 23% body fat on their hips. So that, despite the existing evidence for the health and fat loss benefits of chlorogenic acid, I personally have my doubts that anyone with a dialed in nutrition and exercise regimen, would derive great fat-loss benefits from supplementing with two or three servings of this extract per day.

If you are yet still relatively chubby (the Peter Griffin type from the "Intermittent Thoughts") just interested in losing weight (an average of 16lbs or -10.5% in the study at hand) - and for the pre-obese individuals in the study at hand, this could actually be the case - GCB may really be an acronym to memorize, though.

Note: I stuck to the acronym GCB, also because it differs from the brand name of the patented "GCA" used in the study. After all, there is no reason to pay for the "A", when all you have to look for is a green coffee bean extract with a cholorogenic acid content of ~46% and a total chydroxycinnamic acid of ~57% (note: chlorogenic acid is in fact one of those chydroxycinnamic acids). And if you are not into popping pills, why don't you just make your own green coffee bean instant coffee - should work just as it is described in this guide on eHow for the regular, roasted variety... ah, and if you do, let me know how it tastes ;-)