March 21st, 2007 by Dr. Val Jones in News
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As spring approaches, we can expect a new onslaught of pollen, bugs, and mud puddles. Mosquito eggs will hatch in stagnant water, and a new generation of hungry little disease vectors will be lurking in wooded areas, awaiting their first meal.
Luckily for those of us who live in North America, those annoying mosquito bites are unlikely to infect us with malaria.
A team of scientists committed to eradicating malaria (one of my personal favorite parasites) has taken a new approach to reducing transmission rates: creating a strain of malaria-immune mosquitoes.
I had been under the mistaken impression that mosquitoes lived in perfect harmony with malaria parasites, but apparently the organisms can make them quite ill as well. Not ill enough to die immediately (hence their ability to spread the disease) but ill enough to die prematurely.
So if we could create a malaria immune mosquito, we could give them a survival advantage over their peers, thus slowly influencing the mosquito population in favor of the new strain. This could result in a new population of mosquitoes who could not harbor malaria.
In humans, malaria parasites have learned how to attach themselves to red blood cell proteins and incubate inside the cells. In mosquitoes, the parasites latch on to a protein (called SM1) on the surface of epithelial cells of their gut lining. Through the miracle of genetic engineering, we’ve managed to alter the SM1 proteins in certain mosquitoes, making them immune to invasion by parasites they ingest through infected blood.
Although the immune mosquitoes are not ready for prime time release in malaria endemic countries (the research only showed that the scientists could genetically engineer resistance to one strain of malaria), it sure would be interesting to see if we could use mosquitoes themselves to fight a disease that claims the lives of over one million people per year.
This is a rare case of a problem becoming the solution!
This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
February 21st, 2007 by Dr. Val Jones in News
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Malaria is caused by a crafty little parasite that has become resistant to many medicines. But now researchers at Northwestern University have discovered a chink in its armor – a blood pressure medicine called propranolol. Who knew that a common beta-blocker used to treat hypertension might provide the death blow to such a scourge?
Usually, malarial parasites infect their host’s blood stream through a mosquito bite, and then congregate in the liver and pounce on red blood cells as they pass by. They have a way of adhering to the red blood cells via certain surface receptors (beta 2 adrenergic receptors linked to Gs proteins). They latch on to the red cells and then burrow into the cell and hijack it in order to reproduce inside it. Then, like the horror movie Alien, once they’re fully grown (into “schizonts”) they burst out of the cells and roam free to repeat the process all over again.
Now propranolol happens to block the Gs proteins, which effectively makes it impossible for the parasites to attach themselves to the red blood cells (which they need to use to reproduce themselves).
So what’s the caveat to of all this? Well, folks don’t know they have been infected with malaria until they have symptoms, and the symptoms include high fevers and low blood pressure… so giving someone a medicine that lowers their blood pressure even further might not be a good idea.
The other caveat is that propranolol works like a charm in the test tube, and in mice, but we haven’t yet tried it out in humans who have malaria.
Still, it seems to me that a little bit of propranolol might go a long way to preventing malarial infections in at risk populations. I’ll be interested to see what further studies show!
And if you’re interested, I’ll create a few more blog posts about parasites and other creepy crawly human invaders… Just let me know if you can handle more of this!
This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
February 10th, 2007 by Dr. Val Jones in News
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A small pheromone study made a big splash in the media this week, announcing that male sweat contains a chemical that causes arousal in females.
The media’s sensationalization of the study made me feel dubious about the science behind it. I thought to myself, here we go again – some shoddy research and a lot of hand waving… I was determined enough to get the story straight, that I paid my $15 to the Journal of Neuroscience to get my hands on the original data. And I’m glad I did because my suspicions were NOT confirmed.
Claire Wyart et al. at UC Berkeley designed this study well. They took great pains to control the variables, account for confounders, and provide the appropriate environment for the study. “All testing was performed in a temperature and humidity controlled, stainless-steel-coated, 5 x 8 foot room equipped with HEPA (high-efficiency particulate air) and carbon filtration.” Wyart’s team also made meticulous note of previous research on the subject. They also repeated the study just to make sure that their findings were reproduceable. A total of 48 women participated.
In this double blind, placebo-control study they found that exposure to one of the chemicals in male sweat, androstadienone (AND), produced increased cortisol levels, elevated mood, and increased sexual arousal (when combined with provocative videos) up to an hour after the AND was inhaled.
Now, instead of focusing on the enhanced sexual arousal observation (that triggered the media blitz), Wyart suggested an interesting twist: what if AND could be used as a therapy for those suffering from cortisol deficiency (Addison’s disease)? Current standard therapy requires cortisol replacement which may cause peptic ulcers, osteoporosis, weight gain, mood disorders, and other pathologies. But AND is a potential “natural” solution.
Of course, I’m somewhat skeptical of this alternative since Addison’s is generally caused by an autoimmune attack on the adrenal gland cells – and I’m not sure that stimulating what’s left of them (with AND) would result in enhanced cortisol production. Still, Wyart raises an interesting point: what if we could learn how to positively influence the endocrine system with scent stimulation? Could this be a new method of treatment for women with anxiety, depression, or low libido but with far fewer side effects than our current methods?
Well, it’s too early to tell, but I think Wyart’s on to something. As she notes in her research article, AND is only one of hundreds of chemicals found in human sweat, and it is unclear if it is the most potent chemical in the arousal arena. It will be interesting to see if AND is eventually added to perfumes, cosmetic products, and the like as a means of tricking the body into feeling happier, sexier, and more balanced. Science meets aromatherapy? What do you think?
This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
January 18th, 2007 by Dr. Val Jones in News
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In 1918, a man died of a vicious strain of “Spanish Flu” and was buried in the Alaskan tundra. Almost a century later, scientists found his well preserved body poking through some permafrost and decided to take tissue samples to a Canadian laboratory to thaw out the virus that killed the man.
Sounds like the beginning of a made-for-TV, horror movie, doesn’t it? Well, I wish it were fiction. This is a true story.
So why did the scientists revive this infectious menace? To see what it would do to modern day macaque monkeys, of course.
The BBC news reports:
“Symptoms appeared within 24 hours of exposure to the virus, and the subsequent destruction of lung tissue was so widespread that, had the monkeys not been put to sleep a few days later, they would literally have drowned in their own blood.”
Um… gross?
The scientists say,
“This research provides an important piece in the puzzle of the 1918 virus, helping us to better understand influenza viruses and their potential to cause pandemics.”
The BBC continues:
“Analysis at the University of Wisconsin-Madison (UW-M) revealed that a key component of the immune system, a gene called RIG-1 appeared to be involved.
Levels of the protein produced by the gene were lower in tissue infected with the 1918 virus, suggesting it had a method of switching it off, causing immune defenses to run wild. This ability to alter the body’s immune response is shared with the most recent candidate for mutation into a pandemic strain, the H5N1 avian flu.”
There is a final word from Dr. Jim Robertson, a British virologist:
“Many influenza virologists remain nervous about creating and experimenting with a reconstructed 1918 Spanish flu virus.”
Yeah, I’m nervous too.
This post originally appeared on Dr. Val’s blog at RevolutionHealth.com.
