Q. I heard that Bitter Orange is just another name for ephedrine, is it dangerous?

A. Ephedrine is a fairly potent indirect-acting sympathicomimetic agent, found for example in the Chinese herb Ma huang, and is chemically and physiologically different from any of the alkaloids in Bitter Orange (Zhi shi). Bitter Orange is certainly not dangerous, it has been used in China for many hundreds of years, and also has major food uses (such as in marmelade). The doses used in traditional Chinese medicine, calculated on an alkaloid basis, are much higher than those used in our products, usually 3 – 15 grams of the natural herb at a time, but sometimes up to 45 grams! Since the herb contains about 0.8% of mixed alkaloids, with synephrine predominating (the natural form of the alkaloid is l-synephrine), so the normal dose of 3 - 15 grams would provide 24 - 120 mg of Citrus alkaloids per dose, with an intake of as much as 360 mg not being unusual. There are no reports of side effects at these dosage levels. In addition to administering the herb itself as a decoction, extracts are also administered by the intravenous route in the treatment of shock, in doses equivalent to 10 - 40 grams (80 - 320 mg alkaloids). The following instructions come from Ou Ming (1989):

Similar instructions for use are found in other Chinese reference works.

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Q. Is it true that Bitter Orange can interfere with absorption of prescription drugs?

A. There is no evidence that Bitter Orange either facilitates or reduces absorption of drugs. It has been variously speculated that Bitter Orange may either facilitate absorption of drugs (as has been shown for grapefruit), or conversely induce the Cytochrome P-450 enzyme system and increase the metabolism of drugs. There is no evidence to support either of these speculations. The well-publicized effect of grapefruit appears to be the result of a significant inhibition of gut wall cytochrome P-450 3A4 (CYP3A4) isoenzymes and P-glycoprotein (P-gp), which reduces the first-pass metabolic effect on drug absorption. This is due to substances called furanocoumarins, which have been demonstrated to inhibit the first-pass metabolism of certain drugs that are metabolized by CYP3A4. These compounds are found predominantly in the grapefruit flesh, followed by the sac, peel, and seed. They are not found in other Citrus varieties (Buslig, B. and Manthey, J.A., 2005). Furthermore, the extract of Bitter Orange used in our products consists of the alkaloids and small amounts of other water-soluble substances that have been stripped of other components during extraction.

The extract of Bitter Orange used also does not contain any substances known to induce the cytochrome P-450 system, and therefore is also not capable of increasing the rate of metabolism of concomitantly administered drugs.

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Q. I used Bitter Orange, and though my waist measurements fell nicely, I did not see any change in my body weight, why is that?

A. One aspect of thermogenesis and lipolysis that relates to use of Bitter Orange is the effect on body composition. The alkaloids of the immature Bitter Orange are thermogenic and lipolytic. This means that they firstly can increase the Resting Metabolic Rate (RMR), by stimulating physiological systems already present in the body, thus increasing energy expenditure. This is acknowledged as a very important way of helping weight loss; if energy intake remains the same, but expenditure is increased, the body has to draw on stored fat to make up the difference, and a loss of body fat, usually seen as a loss of weight, has to occur. Even when no loss of weight occurs, a loss of fat can be measured, and is generally to see in a reduction of waist line. Since the main medical objective of weight loss is the reduction of body fat content, this mechanism, which is unique among weight loss agents, is very suitable.

Without a diet, all users of products containing Bitter Orange will lose fat, but some will initially not see this as a simultaneous loss of body weight. This is because a subsidiary action of the Bitter Orange alkaloids is to increase muscle mass, particularly when an exercise programme is followed. The energy value of fat is 9 kilocalories per gram, whereas that of protein is only 4 kilocalories per gram. So when the body is converting fat to protein, it is easy to see that 1 gram of fat could give up to 2.25 grams of protein. Theoretically, weight could even increase, but it would be healthy weight. In practice, this does not occur, and what generally happens with those who initially lose fat but no weight is that as the proportion of lean body mass increases, they start to lose weight too. This is because thermogenesis (the increase in RMR) occurs mainly in muscles, and thus the body responds better as the composition of the body changes from fat to lean!

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Q. Is Ginkgo safe, I heard that it may increase the effects of "blood thinners"?

A. Mild stomach or intestinal complaints, headache, and allergic skin reactions have rarely been reported with normal doses of Ginkgo, which are several times higher than those used in our products. There have been rare mentions of internal bleeding when Ginkgo was combined with other "blood thinners" such as aspirin or coumadin (and even ibuprofen). Ginkgo has anti-platelet activity and hence could prolong the time it takes to form a blood clot at the site of damaged tissues, but it does not seem to affect the coagulation system. In fact, recent studies have indicated that Ginkgo biloba does not influence the clinical effect of Warfarin (Bal Dit Sollier et al., 2003). Additional studies also failed to show any effect of Ginkgo on platelet function or coagulation time (Engelsen et al., 2003; Jiang et al., 2005). It has been speculated that Ginkgo may interact with mono-amine oxidase inhibitors (MAOIs), but since MAOIs are absolutely contraindicated when using Bitter Orange-based products, this is of theoretical interest only. At the level used in our products, there are no safety concerns.

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Q. Does Bitter Orange interact with prescription drugs?

A. Effects could be potentiated, and in particular could give rise to increases in blood pressure, when Bitter orange is used together with mono-amine oxidase inhibitors, or sympathicomimetic agents such as decongestants, appetite suppressants, amphetamines and psychostimulants of the amphetamine type.

Since furazolidine and yohimbine may cause mono-amine oxidase inhibition, patients using either of these agents, or those using Dietary Supplements containing Pausinystalia johimbe (yohimbe), should not use products containing Bitter Orange.

Effects of certain antihypertensive drugs could be reduced or abolished by Bitter Orange; this applies particularly to bretylium, bethanidine, guanethidine, debrisoquine, methyldopa and adrenergic blocking agents (β and/or α). In many cases, use of these drugs would also reduce the thermogenic action of Bitter Orange.

Since the Bitter Orange alkaloids increase the availability of noradrenaline (norepinephrine) in peripheral synaptic gaps, they could theoretically potentiate the peripheral actions of noradrenaline re-uptake inhibitors currently used as anti-depressives. Such interactions have not been reported, but examples of such drugs are the mixed mechanism serotonin and noradrenaline re-uptake inhibitors (SNRIs) such as venlafaxine hydrochloride and duloxatine hydrochloride, and the more selective noradrenaline reuptake inhibitors (NRIs) such as bupropion, which inhibits re-uptake of both noradrenaline and dopamine, and reboxetine which inhibits only re-uptake of noradrenaline. Atomoxetine hydrochloride, used mainly for the treatment of attention deficit disorder in children, is also a selective inhibitor of noradrenaline re-uptake. These drugs are intended to potentiate serotonergic and/or noradrenergic activity in the central nervous system by inhibiting re-uptake of serotonin and/or noradrenaline. While they have been designed to exert their actions specifically in the central nervous system, they may also result in some degree of noradrenaline re-uptake inhibition in peripheral tissues, resulting in a further increase in the availability of noradrenaline and the possibility of unwanted reactions.

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Q. I heard that St. John's Wort could decrease the effects of some prescription drugs?

A. Quite true, though the effect may not be very significant with low doses of St. John's Wort. The effect was first reported for indinavir, an anti-AIDS drug, but it has been shown (Markowitz et al., 2003) that 900 mg of St. John's Wort extract per day just about doubled the metabolism of other drugs which are substrates for the CYP 3A4 enzyme system (a system in the body that deals with "foreign" substances), which meant that this daily dose of St. John's Wort had induced the enzyme (increased its activity by causing more to be formed). There have also been reports that use of St. John's Wort at this dose level may reduce the efficacy of oral contraceptives. The dose of St. John's Wort that was used in these studies is many times higher than that used in our Somatherm™, but depending on the prescription drug being used, even small reductions in efficacy could be important, so the physician prescribing the drug should be consulted.

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Q. When taking Somatherm™, my urine becomes bright yellow. Is this a problem?

A. No, some of the active substances in St. John's Wort are yellow and they discolour the urine when they are excreted. It is quite harmless.

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Q. Does St. John's Wort cause photosensitivity?

A. It has never been reported in humans. It does occasionally occur in sheep which are grazing on pastures where St. John's Wort grows.

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Q. Why do some people using starch-blockers suffer from bloating and flatulence during the first few days?

A. Because the alpha-amylase inhibitor prevents starch from being broken down and absorbed in the small intestine, the starch behaves like dietary fiber and passes into the large intestine where it is fermented by micro-organisms, in fact, just as dietary fiber is fermented. Initially, the micro-organisms present produce a lot of gas (hydrogen, methane, a little carbon dioxide), but as the large intestine adapts to the presence of the starch, there is what we call an overgrowth of organisms that are better adapted to fermenting the starch, and these organisms tend to convert the starch to volatile fatty acids with less gas. So the initial discomfort disappears.

In other words, exactly what happens when you first go onto a high-fiber diet! The microbial flora of the large intestine adapts to whatever nutrients are being offered.

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Q. What is Chitosan and why is it called a fat-blocker?

A. Chitosan is made by deacetylation of chitin , which is the structural element in the exoskeleton of crustaceans (crabs, shrimp, etc.). The degree of deacetylation (%DA) can be determined by NMR spectroscopy, and the %DA in commercial chitosans is in the range 60-100 %. In the human body, it actually behaves like a dietary fiber, since it is not absorbed and digested as such but passes into the large intestine where it can be fermented in much the same way as dietary fibers of plant origin.

The reason it is called a fat-blocker is that it tends to prevent the digestion and absorption of fats. It is not clear whether binding bile acids is the main mechanism. or whether it achieves its effect by binding to the intestinal mucosa. In any case, the fat-blocking effect is relatively modest, and chitosan does not cause side-effects such as the unpleasant and sometimes dramatic side-effects seen with the pharmaceutical inhibitors of fat absorption such as orlistat (gastro-intestinal disturbances, anal leakage, steatorrhea, fecal incontinence). It also has much less inhibitory effect on absorption of fat-soluble vitamins, essential fatty acids and drugs which rely on lipophilicity for absorption. Never the less, Chitosan capsules or tablets should not be taken before taking vitamins or essential fatty acids; the best approach is to take the vitamins and essential fatty acids in the morning, then to take the Chitosan product before lunch and dinner, several hours afterwards.

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