From TIME:

About a year ago, the makers of Red Bull, the famous caffeine-loaded energy drink, decided to come out with a soda, unsurprisingly named Red Bull Cola. The shared name implied the same big kick. But could the cola's boost — supposedly "100% natural" — come from something else? Officials in Germany worry that they've found the answer — cocaine. And now they have prohibited the soda's sale in six states across the country and may recommend a nation-wide ban.

"The [Health Institute in the state of North Rhine Westphalia] examined Red Bull Cola in an elaborate chemical process and found traces of cocaine," Bernhard Kuehnle, head of the food safety department at Germany's federal ministry for consumer protection, told the German press on Sunday. According to this analysis, the 0.13 micrograms of cocaine per can of the drink does not pose a serious health threat — you'd have to drink 12,000 L of Red Bull Cola for negative effects to be felt — but it was enough to cause concern.

Red Bull has always been upfront about the recipe for its new cola. Its website boasts colorful pictures of coca, cardamom and Kola nuts, along with other key "natural" ingredients. The company insists, however, that coca leaves are used as a flavoring agent only after removing the illegal cocaine alkaloid. "De-cocainized extract of coca leaf is used worldwide in foods as a natural flavoring," said a Red Bull spokesman in response to the German government's announcement. Though the cocaine alkaloid is one of 10 alkaloids in coca leaves and represents only 0.8% of the chemical makeup of the plant, it's removal is mandated by international antinarcotics agencies when used outside the Andean region.

In Germany, the Red Bull spokesman insisted that his company's product, along with others containing the coca-leaf extract are considered safe in Europe and the U.S. And already, some experts have come to Red Bull's defense. "There is no scientific basis for this ban on Red Bull Cola because the levels of cocaine found are so small," Fritz Soergel, the head of the Institute for Biomedical and Pharmaceutical Research in the city of Nuremberg, tells TIME. "And it's not even cocaine itself. According to the tests we carried out, it's a nonactive degradation product with no effect on the body. If you start examining lots of other drinks and food so carefully, you'd find a lot of surprising things," he says.

But the problem is when it comes to coca and cocaine, it's not just a health concern, but a legal one. Since 1961, trade of coca outside the Andean region — where people have chewed or brewed coca in tea to stave off hunger and exhaustion for centuries — has been prohibited unless the cocaine alkaloid is removed. Few companies in the world have authorization to trade in the leaf and most are pharmaceutical companies that perform this decocainizing process. The most prominent is New Jersey-based Stepan Chemical Company which has been reported to supply Coca-Cola with its narcotic-free derivative.

But no one knows where Red Bull Cola's coca leaves come from or where they are processed. Red Bull did not respond to immediate requests for comment and Rauch Trading AG, the Austria-based food company that actually manufactures Red Bull Cola was quick to tell TIME that they are not allowed to speak about the product. Meanwhile, Bolivia, which has lots of coca leaves to sell, is getting a kick out of the fact Red Bull Cola admits to using coca in any form (since Coca-Cola evades the question). Ironically, the drink is not actually available yet in Bolivia. But, the locals say, this is a great opportunity to show that coca isn't harmful — with or without the cocaine alkaloid.

From HealthDigestNews.com:

Naltrexone is the generic name for a drug, approved by the FDA in 1984, used to treat alcohol and opioid addiction. Opioids are generally pain-management agents such as morphine, codeine, oxycodone, and fentanyl. Opioids also include heroin and methadone, as well as our own naturally occurring endorphins.

Naltrexone is an opiate receptor antagonist; that is, it blocks cellular opiate receptors. As such, it removes the pleasurable feelings associated with alcohol and opioid abuse. In fact, the drug does such a good job of blocking the receptors that many heroin addicts would stop taking naltrexone, since it simply made them feel terrible all the time. As such, methadone became the drug of choice in the treatment of heroin addiction.

Neurologist Bernard Bihari MD, who at the time was treating heroin addicts with naltrexone, discovered that a substantial number of them—who also suffered from AIDS—had extremely low levels of endorphins. He postulated that this may have been the reason they turned to heroin in the first place. While opioid (and thus endorphin) receptors are found throughout the body, they are especially prevalent on immune system related cells.

Since many diseases stem from some sort of immune dysfunction, Bihari wondered if low endorphin levels were a factor. In 1985, Bihari discovered that a low dose of naltrexone (LDN) blocks the endorphin receptors for only about an hour, the net result being that the body responds by secreting much more of the endorphins—often by a factor of five.

Within a few years, he was seeing the therapeutic benefits of LDN in patients with such varied conditions as lymphoma, lupus, and pancreatic cancer. But, as good as these results seemed to be, they were not observed in a controlled clinical study.

The first study of LDN published in a US-based medical journal would come in 2007, with Dr. Jill Smith's article in the American Journal of Gastroenterology entitled "Low-dose naltrexone therapy improves active Crohn's disease" (e-published in January, print published in April). Smith and her team found that 67% of the patients went into remission and fully 89% showed some therapeutic benefit. This encouraging work led to an NIH grant and a Phase II placebo-controlled clinical trial, currently in progress.

In September, 2008, results were published for a Phase II clinical trial in Italy in which LDN was used to combat multiple sclerosis (MS). Again, the results were highly promising. Since MS is thought to result from an autoimmune process whereby T cells mistake myelin—the coating around nerve cell fibers in the brain and spinal chord—for a foreign invader and attack it, many assumed that MS was the consequence of an overactive immune response. These results, though, would argue against that theory.

In 2007, Burton Berkson MD, PhD and associates published an article in Integrative Cancer Therapies entitled "Reversal of signs and symptoms of a B-cell lymphoma in a patient using only low-dose naltrexone." Berkson's 2006 article in the same journal entitled "The long-term survival of a patient with pancreatic cancer with metastases to the liver after treatment with the intravenous alpha-lipoic acid/low-dose naltrexone protocol" described the incredible turnaround of a patient previously diagnosed as terminal in 2002.

LDN is inexpensive with virtually no harmful side effects. However, since it is no longer a proprietary drug, the pace of rolling out clinical trials for the off-label effects described in this article will probably be slow, as will its acceptance by mainstream medicine. Still, there is nothing to prevent a patient from taking an FDA approved drug for an off-label indication, and this practice goes on all the time.