Kermit Was Right: It's Not Easy Being Green

Global warming has killed off at least 70 frog species by exacerbating outbreaks of a deadly fungal disease, providing the first scientific evidence that world-wide climate change decreases ecological diversity, according to a study published this month in the journal Nature.

The international team of scientists suggests that approximately two-thirds of all harlequin frog species, endemic to Central and South America, have disappeared after falling victim to a chytrid fungus that thrives as a result of temperature increases that have occurred since 1970. Scientists have been keen to understand what has caused these extinctions, and while global warming has been a popular buzz word, this is the first time that researchers have demonstrated that it has, indeed, played a key part.

"Disease is the bullet killing frogs, but climate change is pulling the trigger," says J. Alan Pounds, the lead researcher and a Resident Scientist at the Monteverde Cloud Forest Preserve in Costa Rica, in a prepared statement.

After comparing extinction rates to tropical sea surface and air temperatures for each year, the researchers found that, as tropical temperatures increased, extinction rates did too – something they found confounding, because the fungus actually flourishes at more moderate temperatures.

The scientsts were able to resolve this "climate-chytrid paradox" after discovering that as tropical temperatures increase, evaporation from the oceans does too, resulting in increased cloud formation where the frogs live. Because clouds have a moderating effect on temperature, cloudy days are actually cooler on average, while the nights are warmer. And because the fungus, which is lethal to frogs, thrives in the more temperate cloudy climate, it has managed to wipe out frog populations in large numbers.

In 2004, the Global Amphibian Assessment published that nearly one-third of the world's frogs, toads and salamanders are close to extinction – but amphibians are not the only animals being endangered. Scientists also suggest that global-warming induced epidemics threaten musk oxen in the Arctic and sub-Arctic as well as pine trees in the Rocky Mountains.

Because this research implicates global warming as an undeniable threat to ecological diversity, Pounds considers it imperative to address the problem immediately. "There is clearly an urgent need for a rapid transition to cleaner energy sources," he says in a prepared statement. "I reiterate the call for a bold initative, on the order of the Manhattan and Apollo projects, to put an end to humanity's dependence on fossil fuels." ☼

Tea, It Does The Body Good

Like most sleep-deprived students, I spend what feels like hours each day waiting in line for my daily dose of caffeine. To keep myself from nodding off, I often reflect upon the drinks that the people in front of me order, enjoying the sneak peek I’m having into their private lives.

A Venti Hot Chocolate with Whipped Cream? I bet she wears “Hello Kitty” t-shirts and squeals whenever she sees a puppy.

One thing I’ve learned from doing this (aside from the fact that people really don’t like being stared at) is that it’s a rare day when someone orders a tea. Now, I’m not talking about a Nonfat Chai Latte or a Green Tea Frappuccino: I’m talking about a good old, plain cup of tea.

In an over-stimulating consumer culture that revolves around the concept of “the individual,” I realize that the idea of plain tea is not all that appealing when other possibilities include Grande White Chocolate Peppermint Mochas with One and a Half Pumps of Syrup.

But in my opinion, there are some pretty clear reasons to opt for the tea. Aside from being delicious, a cup of tea is a lot easier on the wallet and the waistline than a mocha, and ordering a tea saves you from having to shuffle over to the other side of the counter and wait another five minutes while giving the barista your cruelest “where’s-my-frigging-coffee-I’m-late-for-class” look.

But even more importantly, tea is actually quite good for you.

For one thing, tea contains strong antioxidants. Antioxidants act like mops in our bodies, soaking up toxins called free radicals that can, if left to their own devices, cause cellular and genetic damage.

Green and black teas contain particular types of antioxidants called polyphenols, which are so amazing they really should be crowned the Jack Bauer of plant compounds. Scientific studies suggest that polyphenols can lower the levels of “bad” (LDL) cholesterol in your blood, reduce your risk for a heart attack and promote weight loss by suppressing your appetite and increasing your metabolism. (While caffeine is also associated with weight loss, the effects observed from tea go far beyond what is expected from the caffeine alone.)

A polyphenol called EGCg, found in abundance in green tea and half as much so in black tea (but not, however, in coffee), has also been shown to exhibit protective effects against breast, prostate, lung, pancreatic, colon and stomach cancers in animal models. Originally it was thought that the antioxidative activity of EGCg was responsible for this, but research has since suggested that EGCg prohibits cancer development and tumor growth using a number of more specific, but as yet unconfirmed, mechanisms. Some of its effects are only sustained if you drink seven or eight cups of green tea per day though – so drink up.

Green tea has also been associated with increased calmness and concentration, the effect of a particular component called theanine which facilitates the generation of alpha waves in the brain. Alpha waves help reduce stress and anxiety, all the while increasing focus and concentration. Highly creative people produce a lot of alpha waves when faced with a problem they need to solve, for example.

There’s more: tea consumption has been associated with a lowered risk for HIV, arthritis, chronic liver disease, Parkinson’s disease, Alzheimer’s and even bad breath.

Even better, there are no known disadvantages to drinking lots of tea – unless you are trying to have a baby or are already pregnant. EGCg inhibits folic acid, a vitamin necessary for embryo development. But that’s it.

Convinced yet?

I’m still sensing resistance, and I bet I know why: you’re afraid because tea doesn’t have as much caffeine as coffee, right? Yes, it’s true – black tea has about half the caffeine of coffee, and green tea is even a little weaker still, although it depends, of course, on how long the tea is steeped. But I have news for you: research suggests that there is no noticeable difference in how alert one feels after drinking a cup of tea versus a cup of coffee, even though they contain different amounts of caffeine. Although researchers cannot yet explain why this is the case, “caffeine level per se does not affect the short term response to tea or coffee,” the study says.

With all these benefits, it’s no wonder that world-wide tea consumption is estimated to be second only to water. Only America seems to be lagging behind, and maybe it is Starbucks’ fault for marketing the heck out of its coffee drinks (and do you blame them? Check out the profit margins on those things!). But the next time you’re zoning out in the coffee queue, wondering whether you actually have the $4 you need for that latte, consider being good to your body: how about a nice, hot cup of tea? ☼

The Only Cure for Pandemic Flu is Prevention

(Article is also published here.)

Many people assume that the “threat” of bird flu is nothing more than another fear-mongering tactic concocted by our government and perpetuated by the media. After all, the bird flu is so-called because it’s really good at infecting birds – not humans. But since 1997, the bird flu strain known as H5N1 has managed to jump species to humans almost 150 times, and because our immune systems are not used to fighting it, bird flu is especially deadly: more than half the people who have been infected have died.

In order to become a real threat to us, though, bird flu needs to “learn” how to spread easily between people. Although there has not been more than one case of this happening to date, viruses like H5N1 are notoriously good at mutating, or modifying their genetic information, and can also recombine or merge with human flu strains. The fear is that, through one of these two mechanisms, bird flu could acquire the ability to spread human-to-human. And with each new person that the virus infects comes a new opportunity for the virus to achieve this.

If it happens – and the World Health Organization suggests it is only a matter of time, either with H5N1 or a similar viral subtype – the WHO predicts that the virus could kill between two and 7.4 million people worldwide.

Wait, you say. By the time it happens, we will have effective antiviral drugs and vaccines to keep us healthy, right?

Probably not. The most promising antiviral drug, Tamiflu, which also happens to be associated with serious side effects, would be only potentially effective, and only if administered before or within the first 48 hours of infection.* Dr. Margaret Chan, the WHO’s Representative of the Director-General for Pandemic Influenza, admits in this month’s WHO Bulletin that “no one knows if it will be effective against the pandemic strain and it should not be regarded as a silver bullet.”

Even if Tamiflu does work, our government is planning to stockpile only enough to treat approximately seven percent of the US population. In fact, due to the risk of antiviral resistance, which renders a drug completely ineffective, it could be counter-productive to treat too many people anyway. Three people infected with bird flu in Vietnam died because the virus became Tamiflu-resistant.

What about vaccines, then? Unfortunately, an effective vaccine must be closely matched to the pandemic strain that emerges, but we don’t yet know what that will look like. The French pharmaceutical company Sanofi Pasteur has begun clinical trials for a vaccine against H5N1 viral strains isolated in 2004, but there is a decent chance that the pandemic strain will be different enough to render it useless. Even if it does end up working, “commercial production cannot begin prior to the emergence and characterization of the pandemic virus,” Chan explains in the WHO Bulletin – a process that will take approximately six months. Given the WHO’s speculation that a pandemic virus would “encircle the globe within three months,” this is not very reassuring. Indeed, Chan admits that “it is highly unlikely that there will be any large quantities of pandemic vaccine available during the first wave of a pandemic.”

The bottom line is, we need to stamp out bird flu before acquires the ability to spread easily among people. And because the risk grows with every animal infected, we need to do this now. But how?

Eradication of bird flu can only be achieved by building the infrastructure necessary to monitor outbreaks and cull infected animals. Farmers around the world need to be educated about bird flu, taught how to properly handle their livestock and encouraged to report potential outbreaks. And because a farm that reports an outbreak might lose all of its poultry, governments need to be able to compensate their farmers appropriately for doing so. Wealthier governments like ours can help by providing poor countries with the financial means necessary to do all of these things.

Fortunately, it appears that our administration has recently realized this too. While earlier US efforts focused on flu prophylaxis and treatment, last week marked a noticeable shift towards prevention. An international conference held in Beijing last week raised $1.9 billion to fight bird flu, and the US was the most generous donor. Our government agreed to provide $334 million in grants to poorer Asian countries, some of which had refused previous loan offers due to fears that they would not be able to repay them.

Indeed, the success of the fight against pandemic flu will depend more on global cooperation than on the efforts of individual countries. It makes sense for wealthier countries to use a fraction of the money they would inevitably spend dealing with the pandemic on a serious effort to prevent it from happening in the first place. ☼

*As I mentioned, Tamiflu may only be potentially effective against a future pandemic flu, and some are skeptical of its efficacy as an antirval drug in general. But nevertheless, fears over pandemic flu have skyrocketed Tamiflu's sales in the past six months, making it one of the most sought-after drugs in the world -- with the US government as one of its biggest consumers.

Interestingly, few realize that Secretary of Defense Donald Rumsfeld is a major shareholder in Gilead Sciences, the company that first developed oseltamivir (the generic name for Tamiflu). The California-based company now licenses the drug to the pharmaceutical company Roche, who manufactures and sells it under its well-known name.

Because Roche has to pay royalties to Gilead Sciences, our Secretary of State is making a fortune. It has been estimated that Tamiflu sales have increased Rumsfeld's net worth by over $1 million just in the past six months.

Where's The Vaccine 40 Million People Are Dying For?

In 1997, President Clinton challenged the scientific community with a lofty goal: to develop an AIDS vaccine by 2007. With just two years left, experts agree that there is no chance a vaccine will be available by then – highly unfortunate, since by current estimates, 40 million people worldwide suffer from HIV / AIDS, including one out of every three people in regions of sub-Saharan Africa. What, exactly, has made AIDS vaccine development so difficult, and how far away is it?

First, it helps to understand how immune responses and vaccines work. If I sneeze and a friend of mine breathes in the virus, her immune system recognizes that the virus is not something normally found in her body. It then reacts by making many copies of specific proteins called antibodies that bind to and neutralize the virus in what is called an antibody-mediated immune response.

Unfortunately, despite the vitamin C she takes every morning, my friend’s body requires time to make these antibodies at first, and by the time there are enough, the virus may already have found its way into her cells and begun replicating. Her body then initiates a different immune response, called a cell-mediated response, in which other immune cells attack and kill her virus-infected cells.

Often, the combination of these two types of immune responses is enough to clear an infection, as in the case of a cold. (A cold is not very fun, but it only lasts a few days.) Unfortunately, HIV has a number of built-in defenses, and the body cannot kill it off on its own.

In order to be effective, an HIV vaccine would have to boost immune responses sufficiently to prevent, or at least significantly limit, HIV infection. But researchers are currently debating one fundamental question about HIV vaccine design: what kind of immune response would it need to spark?

Most vaccines work by initiating an antibody-mediated response, one that attacks viruses (or other pathogens) before they have the chance to enter cells and replicate. This type of vaccine presents the body with innocuous particles having a structure similar to the virus or to a protein produced by it. The body then creates antibodies against the particles – the same antibodies that would attack the real virus. These vaccine-induced antibodies remain in the system, primed for attack, so that when the body encounters the “real thing” in the future, it effectively eliminates the virus before it can establish an infection.

Such a vaccine is particularly difficult to design for HIV because the virus has a highly complex structure, exists in different forms called clades and has the ability to modify its genetic information within the body. A vaccine that induces the production of antibodies against one form of HIV, for instance, does not prepare the body to fight against another. The 2005 AIDS Vaccine Advocacy Coalition Report states, “Anyone who has been tenacious enough to follow AIDS vaccine research over the past two decades knows that the ability to make a vaccine that could induce effective antibodies against circulating strains of HIV remains one of the great unsolved mysteries.”

Because eliminating the virus before it enters cells is so difficult, most researchers have instead focused on developing a vaccine that induces a cell-mediated response, killing already infected cells. This can be done by injecting particles called vectors that have been engineered to carry various viral components inside them. These viral components lead to the activation of particular immune cells which become primed to attack body cells if they ever become infected with HIV. This approach can slow the development of infection and potentially eliminate HIV from the body altogether.

Currently, most of the HIV vaccines being clinically tested – there are over 30 – elicit only this cell-mediated immune response. Some scientists fear that ignoring the antibody-based approach is a bad move. “To have a highly effective vaccine, the broadly neutralizing antibody remains the Holy Grail,” explains Gary Nabel, Director of the Vaccine Research Center at the National Institutes of Health in Bethesda, Maryland, in an interview published in the International Aids Vaccine Initiate Report. If he’s right, then it will be back to square one: researchers will have to find antibodies capable of attacking multiple forms of HIV and will have to incorporate these into a new vaccine.

So, how and when will the scientific community know if, indeed, the cell-mediated response is enough? Scientists are hoping that one recently designed vaccine will answer that question. The New Jersey-based pharmaceutical company Merck has recently begun large-scale efficacy trials in the US, Australia, Caribbean and Latin America for its new HIV vaccine, which uses a cold virus as a vector containing three HIV proteins from one particular clade. Results from this trial are expected in 2008, and they will indicate whether research has been moving in the right direction. “The next three years will bring important decisions for the AIDS vaccine pipeline,” states the 2005 AIDS Vaccine Advocacy Coalition Report.

This is not to say that a vaccine is potentially three years away – to the contrary, the AVAC report admits, “We know that an AIDS vaccine is not around the corner and that making time-bound predictions only serves to raise unrealistic expectations.” Even if the Merck trial is successful, the vaccine will have to enter full scale clinical trials, which will take years even if all goes well. And if the Merck vaccine is not effective, then the scientific community has a lot of work to do. But Nabel is optimistic nonetheless: “We are in the midst of an incredible renaissance in the field of HIV vaccines,” he says in the International Aids Vaccine Initiate Report interview. “The science and technology that we can now apply to advance the field is unprecedented.” ☼