The Science Behind the Teas

After losing 10 pounds on a diet of low-glycemic-index foods, Durk added the high-beta-glucan-containing barley to his food to further reduce glycemic index and to slow and reduce absorption of glucose and fats, and Sandy incorporated the erythritol and resistant starch into their food. Shortly afterward, he added a supplement of a selected combination of teas. The result was a further weight loss of 25 pounds, and that is how Durk reached a weight of about 35 pounds less than his weight at baseline.

In our research, we had learned of several weight-loss mechanisms reported in studies of various types of tea (Camellia sinensis), including green, oolong, black, and Pu-erh. Thus began Durk’s long search for the best combination of tea types and of the best varieties of the types of teas for weight loss. It involved trying literally dozens of different teas and tea combinations.

There are probably hundreds of different teas, which contain various combinations of bioactive ingredients, including: polyphenols; gallated and nongallated catechins; tannins; and monomers, oligomers, and polymers of tea catechins, to name a few. The biological effects of each tea depend on the different “cocktail” of these ingredients and, importantly, on the chemical interactions and synergies of the ingredients. Producing a partially (oolong) or fully (black or Pu-erh) fermented tea results in an even more complex stew of molecular ingredients. Pu-erh tea is produced by fermentation, like black tea, but in a different way, and it is preserved (aged) to improve the quality (like a fine wine). Whereas all other teas autooxidize and become weaker with storage, Pu-erh tea doesn’t. Pu-erh is a type unto itself; although often referred to in America as an oolong or black tea, it is neither. Some researchers have suggested (Chiang, 2006) that some active substances in Pu-erh tea may be formed during the preservation period; however, the literature describing the chemistry and biological properties of Pu-erh tea is scarce, and the production techniques are quite varied and highly proprietary.

We learned of many mechanisms (little discussed outside the scientific literature) that have been reported in various studies of different teas that may account for some of their effect in reducing weight, and we report them here. In the process of studying these mechanisms, we realized that these mechanisms did far more than promote weight loss, but included the promotion of better health and the exciting possibility of contributing directly to longer lifespan.

I. Reducing Fat Synthesis by Inhibiting Fatty Acid Synthase

A. Increasing malonyl-CoA, the substrate for fatty acid synthase

B. Increasing energy expenditure

C. Uregulating PGC-1alpha

Fatty acid synthase (FAS) is an enzyme that plays a central role in the conversion of dietary calories to stored body fat in mammals. Interestingly, it has been reported that various types of tea contain inhibitors of FAS that are hypothesized to contribute to their antiobesity effects (Chiang, 2006; Zhang, 2006; Yeh, 2003; Ikeda, 2005). For example, catechin gallate (Zhang, 2006) and epigallocatechin-3-gallate (Brusselmans, 2003) have been identified as potent FAS inhibitors found in tea.

One potential limitation on the inhibition of fatty acid synthase is that a “regular” Western diet, loaded with digestible carbohydrates, results in such a large oversupply of malonyl-CoA, the substrate for FAS that is formed in the fat-synthesizing pathway from glucose, that any potential inhibition of FAS is largely overpowered. Hence, we have found that going on a reduced-glycemic-index diet is absolutely necessary in order to benefit from tea’s FAS inhibitors. This may be a reason why, although the antiobesity and anticancer effects (many human cancers overexpress FAS) of FAS inhibitors have been known for several years (Loftus, 2000), there appear to have been no Phase I trials to date of such inhibitors by pharmaceutical companies. On a regular American diet, they wouldn’t work.

The inhibition of fatty acid synthase results in a pileup of the FAS substrate malonyl-CoA, which has now been identified as a key regulator of energy metabolism and food consumption (Cha, 2006; Hu, 2003; Wolf, 2006; Hu, 2005). Basically, when FAS is inhibited, the large supplies of malonyl-CoA that pile up are interpreted by your brain as being the result of your eating a huge meal and loading your FAS pathway with substrate, which results in your brain’s signaling the suppression of hunger and feeding behavior. It also results in the turning on of genes involved in energy expenditure and oxidative protection (Cha, Rodgers, 2006; Dulloo, 2000; St-Pierre, 2006), as well as turning on PGC-1alpha (peroxisome proliferator-activated receptor gamma coactivator-1alpha), which performs a number of extremely interesting fat-loss and age-reversing tricks, such as: increasing the creation of mitochondria in muscles (Cha, Rodgers, 2006; Finck and Kelly, 2006; Wu and Pulgserver, 1999), which increases energy expenditure by muscles (Walczak and Tontonoz, 2003); reducing the expression of atrophy genes in muscle during disuse or denervation (Sandri, 2006); increasing the production of the fatigue-resistant slow-twitch muscle fibers (Lin, 2002); suppressing reactive oxygen species and neurodegeneration (St-Pierre, 2006); and FAS inhibitors may possibly be a caloric restriction (CR) mimic for many of CR’s effects by reversing the age-dependent decrease in PGC-1alpha (Corton and Brown-Borg, 2005).

II. Increased Energy Expenditure

A. Upregulation of PGC-1alpha (thermogenesis, mitochondrial biogenesis, increased expression of UCP2 and UCP3, increased antioxidant defenses)

B. Upregulation of beta-adrenergic signaling to muscles

Increased energy expenditure results from inhibiting FAS because its substrate, malonyl-CoA, is not turned into fat and just piles up. This is a signal that you are full of energy and turns on energy-expenditure mechanisms such as thermogenesis (Rimpler, 2001; Wu, Pulgserver, 1999) via upregulation of PGC-1alpha and PGC-1beta in muscles (by beta-adrenergic signaling from the brain) that include increasing uncoupling proteins (that allow the “wasting” of calories by using their energy to create heat) (Walczak and Tontonoz, 2003; Finck and Kelly, 2006; Wu, Pulgserver, 1999) and increasing the creation of mitochondria in muscles (Finck and Kelly, 2006; Cha, Rodgers, 2006; Wu, Pulgserver, 1999). Loss of mitochondria is a very important aging process.

III. Alpha-Glucosidase Inhibitors

Another mechanism whereby various teas to one degree or another reduce the accumulation of fat is through the inhibition of alpha-glucosidase (an enzyme found in the small intestine that is required for digestive breakdown of carbohydrate polymers, such as starch, into glucose). Catechins and theaflavins found in teas (theaflavins are found only in fermented teas, while catechins are most plentiful in green tea) have been identified as inhibitors of alpha-glucosidase (Matsui, 2007).

IV. Lipase Inhibitors

Pancreatic lipases are enzymes important in the digestion of fats. Hence, one way to decrease fatty acid uptake from the gut is to inhibit these enzymes. A paper has reported on the inhibitory effects of oolong (partially fermented) tea polyphenols on pancreatic lipase (Nakai, 2005).

V. Other Possible Mechanisms

Curiously, one paper reports finding lovastatin, a cholesterol-lowering substance (it works by inhibiting the enzyme HMG-CoA reductase, which manufactures cholesterol) in some batches of Pu-erh tea (Hwang, 2003). The finding of statins is not unprecedented in foods: lovastatin has also been reported in red yeast rice. We make no claim for this, nor are we measuring lovastatin levels in our Pu-erh teas. The microbial fermentation process that converts green tea to Pu-erh is exceedingly complex and involves a whole ecosystem of microorganisms, unlike fermentation to make beer or wine, which uses only yeast.

In one study, black, green, and oolong teas (Pu-erh was not tested) were shown to enhance insulin activity, thereby improving insulin sensitivity, which keeps blood glucose down (Anderson and Polansky, 2002). The authors identified the predominant active ingredient as epigallocatechin gallate (EGCG), found in especially large amounts in green tea. Curiously, they reported that milk, nondairy creamers, and soy milk added to tea decreased the insulin-enhancing activity. We think this effect is due to the biologically (and chemically) reactive polyphenols binding to the proteins in these additives.

EGCG was also reported in another paper (Waltner-Law, 2002) to repress hepatic (liver) glucose production. This could be due to EGCG’s insulin-enhancing effects, as one of the functions of insulin is to suppress hepatic gluconeogenesis (creation of glucose).

A further paper (Tsuneki, 2004) reported that glucose tolerance in healthy human volunteers was improved significantly after drinking 1.5 grams of green tea powder in 150 ml of hot water, as compared to hot water alone.

VI. Conclusion

To sum up, we have developed another formulation for our own personal use, this one to help reduce body fat when used with a low-glycemic-index diet and also to improve muscle function and increase the creation of mitochondria. We certainly hope that more attention will be paid in future research to the “other” teas (i.e., those other than green tea, upon which most of the attention of researchers has so far been focused). Existing evidence indicates that fermentation of green tea creates a huge range of new compounds not found in green tea and that may be, as we report here, extremely useful.

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