Fat-Blocker Effect of Tea Catechins Confirmed (?) in Man - Sign. Abdominal Fat Loss (5-8%) in 12 Weeks W/Out Diet

Tea catechins (which can also be found in black and jasmin tea | see Figure 3) can help you keep particularly unhealthy abdominal fat (Després. 2012) at bay.

It is one thing to have in-vitro and rodent data that green tea can inhibit the digestion of dietary fat (reported previously in the SuppVersity Facebook News); it is another thing, however, to have a human study like the one Makoto Kobayashi and colleagues are about to publish in the peer-reviewed scientific journal Food & Function that shows that the "[i]ngestion of a green tea beverage enriched with catechins with a galloyl moiety (THEA-FLAN 90S) during a high-fat meal reduces body fat in moderately obese adults" (Kobayashi. 2015).

Ok, the abdominal fat loss does not, as the previous quote from the conclusion appears to suggest, occur instantly right after you've consumed your first tea w/ a single meal.

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Rather than that, 124 subjects (two of the initially 126 subjects 2 dropped out for personal reasons unrelated to the trial), 53 men, 71 women, who consumed similar, albeit non-standardized diets (see Figure 1 | note: physical activity was also identical) and began the study with body fat levels of ca. 31-35% had to consume the previously mentioned tea beverage that contained tea catechins (250 mL with 215.3 mg green tea catechins containing 211.0 mg green tea catechins with a galloyl moiety) twice or three times daily during mealtimes for 12 weeks, before the significant reduction in body fat became visible.

Figure 1: Macronutrient composition (in g an % of energy) of the non-energy reduced diets the subjects consumed; the values in the left pie chart represent a group average of all three intervention groups. Since the data is based on food records with photographs, it is probably more reliable than in your average diet study (Kobayashi. 2015).

Now, in view of the fact that this is not the first study to demonstrate weight loss effects in overweight subjects consuming green tea or, as in most other studies, green tea extracts, the word "during" and thus the fact that the green tea beverage was consumed with at least two of the three meals per day should be highlighted as a specific feature of the study at hand that is highly relevant to its interpretation.

Figure 2: Detailed analysis of the rel. change in fat area in the abdominal depot of the subjects (Kobayashi. 2015)

It is after all the requirement that the green tea beverage had to be consumed with a (preferable high fat) meal that allows the authors to conclude that the significant fat loss Kobayashi et al. measured by the means of computer tomography predominantly in the abdominal area are the result of an inhibition or slowing of the intestinal fat absorption and thus warrant the conclusion that "the ingestion of green tea beverages enriched with CGM together with high-fat meals may be an effective strategy for reducing body fat in moderately obese adults" (Kobayashi. 2015) - an observation of which I would like to add that the underlying mechanism is not 100% certain.

What about weight and, even more importantly, muscle loss? No, losing lean mass was not an issue in, because weight loss (-0.6 and -0.8% in the low and high dose group, respectively | measured by bio-electrical impedance vs. computer tomography as it was the case for the abdominal fat area) was actually not an issue, either. If you want to measure your success on the scale, green tea is thus not going to be the "diet tool of choice" (unless you use it alongside an energy-reduced diet)... however, if you take into account that the placebo group actually did what the average Westerner does, these days, i.e. gain weight and body fat over the 12-week study period, you may argue that you can still see the results on the scale which could finally stand still after years of displaying subtle, but eventually relevant increases in body weight.

The authors base their conclusion that it is "unlikely that absorbed green tea CGM leads to increased energy expenditure, followed by reduced abdominal body fat area" (Kobayashi. 2015) on two reasonable, but experimentally (in this study) not confirmed assumptions which are that little to no catechins actually made it into the bloodstream, because ...

1. the low caffeine content of the beverage limits the bioavailability of EGCG & co (caffeine enhances its bioavailability | Nakagawa. 2009) and
2. the ingestion of the beverage with a meal has been shown to significantly reduce the bioavailability of green tea catechins in comparison to the fasted state (Chow. 2005).

The assumption that its just a blockade of the digestion of fat becomes even more questionable, if you (re-)read my 2014 article on the carb blocking effects of tea... Well, eventually, though, you may argue that it does not matter if the reduction in abdominal fat was due to thermogenic effects, thermogenic and fat-blocking effects or, as the scientists believe, mediated exclusively an "inhibit[ion] or slowing [of the subjects'] intestinal fat absorption" (Kobayashi. 2015). And let's be honest, I guess you're right. What matters is that there were significant reduction ins abdominal fat (visceral, subcutaneous and total abdominal fat area). Reduction of which the data in Figure 2 tells you that ...

1. 

   Table 1: Catechin composition of the test beverages.

   the fat loss in the abdominal area was dose dependent - even if the differences between the low and high dose group did not reach statistical significance (for the exact catechin composition see Table 1 on the right) - and that 
2. roughly 50% of the benefits were lost within only 5 weeks when the subjects stopped consuming the green tea beverage, even though their diet didn't change at all (in fact, they consumed minimally less energy in the withdrawal phase from week 12-17).

Now, (b) is obviously good news for green tea lovers, but bad news for those who cannot imagine consuming green tea containing beverages "for the rest of their lives".

Green tea forever, it is then!? Well, as usual we have to consider what limits the generalizability of the results. Firstly, we are dealing with a group of people who have more than a few pounds of extra-weight on their hips. An abdominal fat loss of 8% in 12 weeks is thus not impossible, but not exactly likely to be seen in someone who starts at a body fat percentage of 15% or less (which is half what the subjects in the study at hand began with).

Figure 3: Catechin content (mg/10ml) of black, green and jasmine tea prepared from commercial tea w/ different infusion times (Bronner. 1998).

The second thing we have to keep in mind is the beverage itself. As you've previously read, it has been enhanced with catechins with a galloyl moiety (CGMs | EGCG, ECG, GCG, CG). Does this mean that you cannot achieve similar results if you simply drink green tea? Luckily, data from Bronner, et al. (1998) suggests otherwise. As you can see in Figure 3, it would take only 100 ml of commercially available freshly brewed (infusion time 3 min) green tea and even less black tea to achieve similar concentrations of EGCG and the other catechins with a galloyl moiety in your tea. Accordingly, the second obstacle to the gene- relizability of the study is actually irrelevant.

Third- and lastly, there's yet still the fast reversal of the effects which suggests that it is necessary to become a habitual tea drinker to see long-term / lasting benefits of green tea (or as the data in Figure 3 suggests even catechin containing tea in general) on your body weight and, more importantly, body fat you're carrying around | Comment on Facebook!

References:

• Bronner, W. E., and G. R. Beecher. "Method for determining the content of catechins in tea infusions by high-performance liquid chromatography." Journal of Chromatography A 805.1 (1998): 137-142.
• Chow, HH Sherry, et al. "Effects of dosing condition on the oral bioavailability of green tea catechins after single-dose administration of Polyphenon E in healthy individuals." Clinical Cancer Research 11.12 (2005): 4627-4633.
• Després, Jean-Pierre. "Body fat distribution and risk of cardiovascular disease an update." Circulation 126.10 (2012): 1301-1313.
• Kobayashi, Makoto, et al. "Green tea beverages enriched with catechins with a galloyl moiety reduce body fat in moderately obese adults: a randomized double-blind placebo-controlled trial." Food & Function (2016).
• Nakagawa, Kiyotaka, et al. "Effects of co-administration of tea epigallocatechin-3-gallate (EGCG) and caffeine on absorption and metabolism of EGCG in humans." Bioscience, biotechnology, and biochemistry 73.9 (2009): 2014-2017.

Supplemental Melatonin Protects Against Alzheimer's and Has The Highly Desirable "Side Effect" of Reducing Body Fat Percentages by More Than 50%!

Image 1: If you don't want your brain to shrivel up like that, I suppose you better get more than just an occasional night of good night's sleep and (not or) think about taking some supplemental melatonin.

Those of you who are also following me on facebook, will probably have seen the link to the study a group of Indian scientists conducted to assess the effect of melatonin supplementation in overiectomized (=model for human menopause) rats (Baxi. 2011). Much to my own surprise, the melatonin supplement did not only eradicate all the majority of overiectomy-induced metabolic changes, it was also more potent than the standard estrogen treatment that served as a control! And that in the absence of any of the side-effects of regular estrogen therapy. In that, the Baxi study is only one out of a handful of recently published paper, which suggest that melatonin is probably one of the most underrated supplements you can still (as soon as the FDA realizes what this stuff can do, they will probably ban it) buy without a script.

Don't let your brain shrivel away!

Published in the December issue of Neurobiology of Aging is a paper that investigated the effects of six months of high dose (10mg/kg) melatonin supplementation and/or exercise on six-month-old 3xTg-AD mice. Due to their specific genetic make-up, these mice are prone, or rather destined to develop Alzheimer's at a pretty young age. Based on previous research on the effects of exercise and the anti-oxidative properties of melatonin, the researchers speculated that if each of them could exert beneficial effects on the development of the Alzheimer's-inducing plaque in the brain of the mice, the combination of exercise + melatonin should be even more protective.

Figure 1: Amyloid- beta and phospho-tau in the cerebral cortex of nontransgenic mice (control) mice, 3xTg-AD (Tg) mice, and Tg mice treated with melatonin, physical exercise, and melatonin plus exercise (data adapted from Garcia-Mesa. 2011)

And in fact, if you take a closer look at the data on the formation of "plaque" (Ameloid-beta and Phospho-Tau) in the brains of the Alzheimer's mice (figure 1), it becomes quite obvious that the effects of exercise and melatonin may both be overall "ameliorative", a distinct reduction in both markers of Alzheimer's disease can only be seen in the melatonin group. In the exercise group (voluntary running on treadmill; ~20-25km/week), on the other hand, there was even a slight (and statistically non-significant increase) over the "sedentary" control Alzheimer's prone animals.

Figure 3: Effects of different treatments on cerebral cortical redox status of 3xTg-AD (Tg) mice; * p < 0.05, *** p < 0.001 compared with healthy control; # p < 0.05, ## p < 0.01, ### p < 0.001 compared with Alzheimer's prone control; & p < 0.05, && p < 0.01 compared with melatonin alone; $ p < 0.05 compared with exercise alone (data calculated based on Garcia-Mesa. 2011).

Similarly, both treatments ameliorated changes in the cerebral cortical redox status (figure 2) of the 3xTG-Ad mice. In that it is noteworthy that the different effects both treatments and their respective combination had on the measured redox parameters in the brain of the mice actually reflect in the overall outcome of the study:

Six-month chronic treatments began at a moderate pathology phase, when animals already present cognitive loss and brain pathology. Overall, both melatonin and exercise groups showed a remarkable amelioration of cognitive and brain redox states up to NTg mouse levels. Differential neuroprotection was obtained against other alterations. Namely, behavioral and psychological symptoms of dementia were protected by exercise and senescence parameters by melatonin. Interestingly, the combined treatment induced neuroprotective effects against brain mitochondria deterioration.

The last observation, that only the combination of both treatments could protect the mice against brain mitochondria deterioration is actually particularly interesting with regards to the concept of mitohormesis and the issue of "how much stress is too much stress", I have broached in a number of previous blogpost. If we took the results of the study at hand as a reference, the answer to this question would be as much exercise induced and thusly beneficial stress as your antioxidant system can handle ... and the capcity of the latter was obviously profoundly upregulated in response to the high dose melatonin supplement the mice received in their drinking water.

The treatment was yet not without (un-?)wanted side-effects

Now obviously almost no effective drug, or in this case a hormone, is without side-effects and you should thusly not be surprised that the 10mg/kg melatonin the mice consumed on a daily basis (this is a human equivalent of ~65g!) were not completely side-effect free.

Figure 3: Relative changes in body weight, white adipose tissue (%), brown adipose tissue (%) and thymus (%) vs. healthy control (data calculated based on Garcia-Mesa. 2011)

So, just to make sure how dangerous this hormone (all MDs please cry out loud, now ;-) actually is, I have compiled the data on the nasty side effects in figure 3 (remember: these are reduction vs. the normal not the Alzheimer's control!):

• - 61% reduction in white adipose tissue mass,
• -9% in brown adipose tissue mass, and
• 16% less reduction in thymus mass

If that sounds "scary", I suppose you are the CEO of one of the big pharma companies, because I guess neither of their drugs would be capable of similarly beneficial side-effects while still effectively battling the causes and symptoms of Alzheimer's.

Melatonin as an ergogenic weight loss adjuvant?

If you have been following my blogposts for quite some time now, you will already be aware that melatonin is far more than your bodies natural sleeping pill. On June, 4, 2011 I discussed the results of an amazing study, where a funky melatonin-loading-protocol effectively reduced the profound increase of inflammatory markers following an ultra-endurance race (cf. "More Than Restorative Sleep in a Pill"). In a more recent paper that is going to be published in the January edition of the Journal of Pineal Research, Germaine Escames et al. speculate about another exercise-melatonin interaction, the effects of which could be much more pronounced than the potential ergogenic effects in the aforementioned study: The exercise induced depletion of inodole, which is used to combat the oxidative stress, and the subsequent depletion of melatonin could in fact have negative impacts on the circadian system of which we are just beginning to realize that it has profound effects on how we look, feel and perform (Escames. 2012), so that strategic supplementation with melatonin could eventually turn out to be of particular importance for the overall health, not just the performance of athletes.

Figure 4: Body weight (left axis) and liver and intra-abdominal fat weight (right axes) after 4 weeks on control or high fructose diet without melatonin and after two additional weeks with daily injection of 1mg/kg or 10mg/kg melatonin (data adapted from Kitagawa. 2012)

And while I am still waiting for respective research on the optimal dosing scheme for athletic purposes, I can already tell you now that based on the results of Akira Kitagawa, Yoshiji Ohta and Koji Ohashi, the beneficial metabolic effects and subsequent reductions in body weight do occur at much lower doses than the ~60mg human equivalent from the Alhzeimer's study (cf. figure 4). Yet while both the low = 1mg/kg (human equivalent: 0.2mg/kg) and high = 10mg (human equivalent: 2.1mg/kg) reduced the intra-abdominal fat in both the rats on the normal, as well as on the high fructose diet,  "the higher serum insulin response curve in the oral glucose tolerance test and insulin resistance [after] 6-wk high fructose feeding" was reduced more effectively by the higher dose.

In view of these recent studies, I am pretty sure that we are soon going to see more research - including human data - on the subject. And I guess that I don't have to tell you that the SuppVersity is where you will find the detailed analyses of the results of those trials first, do I ;-) ?