This month, Sydney Spiesel discusses toilet training, getting rid of lice, preventing liver cancer in Africa, staving off the avian flu, and the drawbacks of antibacterial soap. (Click here and here for the October and September roundups.)
Toilet Training: Spiesel’s Third Law of Pediatrics
State of the Science: This month’s health news featured The Return of 19th-Century Toilet Training. The past era’s steely core (rigid control of a child’s bodily functions) now comes wrapped in velvet (it’ll be done warmly and lovingly). Potty training isn’t training at all—it’s just freedom from diapers.
Theory:Slate’s Emily Bazelon has already pointed out some of the downsides of the diaper-free movement. This seems a perfect opportunity to introduce my (as yet unproven but common-sensel) Third Law of Pediatrics: The average age of toilet training around the world is directly proportional to latitude. The farther kids live from the equator, the slower they are in general to toilet train. Cold weather to the north or far south means more layers of clothes, and more clothes makes it harder for children to deal with toileting independently. They need to get a parent’s attention, and then that parent has to hike them into the john (please, no letters from all you thoughtlessly named Johns). Confronted with this sequence a few times, most kids quickly conclude that it’s not worth the trouble and then must be talked down from that stance.
Tip: The corollary to my Third Law (frankly more useful than the law itself, though not in November) is this: Toilet train in the summer. If it’s at all possible, let your kid run around naked in the backyard. After a week or two of running around without a wet diaper, most kids are powerfully motivated and no coaching is needed. In the United States, the right moment for most kids seems to be around the age of 2½. As Chinese parents have learned, clothing that facilitates independence can uncouple toilet training from latitude.
Bonus Tip: In the war between the generations, it’s best if children never learn that they have the atom bomb. Be low-key, patient, and nonintrusive as you gently facilitate your child’s acquisition of this skill.
Lice: How to get rid of them
Disclaimer: I once almost had a vested interest in the subject that follows. Alas, it was not to be … more on that below.
State of the Pest: The height of fall means football season for some but head lice season for many parents. Yuck! As the weather turns, children come indoors, crowd together, and share pillows and hats and hairbrushes. Which means that soon they’re also sharing an extremely annoying though completely harmless external parasite. The head louse, unlike its cousin the body louse, never carries any human illness. It just makes you itch and itch.
If you’ve spotted a louse, that pretty much guarantees there are more in hiding. The bugs have largely become resistant to all the chemicals—”pediculocides”—incorporated in treatment shampoos and rinses. So are their eggs, called “nits.” Because the nits firmly cement themselves to individual hairs, and because hairs are firmly attached to scalps, nits rarely pass from person to person. But they can keep an infection going once it starts.
Strategy: Getting rid of lice is time-consuming and painstaking, partly because of their life cycle. I recommend that parents begin by shampooing a child’s hair with any kind of shampoo and water as hot as is comfortable. (The bugs definitely don’t like heat.) Follow this with a commercial product that loosens nits. Then comb out the bugs and nits with a good-quality fine-toothed nit comb (I have tried Pronto brand loosener and lice comb and thought they worked well; others recommend Clear brand. The National Pediculosis Society—which, I should say, doesn’t agree with my recommendations—sells its own comb). Don’t worry, though, you’ve missed some.
Next comes old-fashioned nit-picking. Inspect the hairs by hand and pick out any additional nits you spot. I find it helpful to use a binocular magnifier from a hobby shop—the professional ones are too expensive—and a really bright light to help with the job. Don’t worry, you’ve still missed some.
Next, drown the remaining pests by applying oil to the hair. Any kind of oil will probably do, but olive oil has the benefit of leaving the hair shiny (and it’s a bit classier). Apply the oil liberally, really wetting the hair and rubbing it down well into the scalp, where the bugs hang out. Then cover the head with a shower cap and leave it on overnight. The next morning, any lice on the head should be dead. But the nits you missed won’t be and must be removed. So shampoo the oil out and nitpick again. You still won’t succeed in getting all the nits out, no matter how hard you try, though you will get almost all of them. The few remaining ones will hatch. So you need to repeat the overnight-oil, shampoo, and nit removal cycle probably three or four times, with one or two days between cycles.
After 11 days or so you will have drowned all the possible hatchlings. Things that may have head lice in them—hats and pillows—can be disinfected by putting them in a sealed bag for two to three days to allow any wandering bugs to die. (A louse out of the egg can’t live off the scalp for more than 24 to 48 hours, since it requires heat and food—they are bloodsuckers—to survive.) If you’re in a hurry, dry cleaning or hot-water washer-and-dryer treatment will kill them faster.
My contribution to lice-ology: I developed a shampoo that makes lice and nits glow, and thus easy to find and remove. It is an invention sadly never picked up by a manufacturer, even though Calvin Trillin thought it almost worth a Nobel Prize nomination. Frankly, though I am proud of my idea and it works very well, it is a convenience, not a necessity. The world has done just fine without it.
Peanuts: Preventing them from molding—and preventing liver cancer
State of the Science: Liver cancer is a common and serious problem in parts of Africa where people eat a lot of peanuts and corn stored under hot and humid conditions. A common mold (Aspergillus flavus) that grows on peanuts and corn produces aflatoxin, a cancer-causing toxin. Aflatoxin contamination is not a problem in the United States because production, storage, and inspection standards are routinely high. In Africa, however, aflatoxin from the mold is almost certainly the explanation for the high rate of liver cancer (hepatitis B plays a role, too). Though there are some experimental methods for eliminating aflatoxin from foods—exposure to ammonia may work—none are practical for farmers in the developing world.
Prognosis: Now a study by P.C. Turner and colleagues, mostly working at the University of Leeds in England, has shown that low-cost, low-tech interventions can significantly lower the aflatoxin contamination of African staple foods. The fixes: using the sun to fully dry peanuts laid out on fiber mats (instead of an earthen floor); sorting the dried nuts and discarding moldy or damaged ones and then storing the good ones in natural fiber bags (instead of plastic). The most expensive suggestion was to raise the stored peanuts with $10 wooden pallets and to sprinkle a little locally made insecticide underneath. The total cost for all the interventions is about $50 per household for the first year and less in subsequent years since most of the supplies can be reused. It’s worth noting, though, that the annual per capita gross national product is only about $1,100 in Guinea, where the experiment was performed.
Benefits: It’s hard to imagine a more cost-effective intervention. Farmers will become healthier and more productive; their children will be protected from the growth-retarding effects of aflatoxin; their animals will fare better, improving the protein available in the food supply; and fewer resources will be needed to care for the sick. Not glamorous, but awfully worthwhile.
Avian Flu: How we’ll someday catch it
State of the Science: Influenza is a virus that is constantly undergoing change. It’s commonly assumed that this innate instability—or “hypermutability”—is the reason that the current avian flu (H5N1) will mutate and target human populations. But when H5N1 someday transforms into a virus that moves efficiently from human to human, the change probably won’t be the result of random mutation.
Prognosis: Some winter day, a farm worker somewhere who is suffering from ordinary human flu will come in close contact with infected birds and catch avian flu virus from them. Both strains of flu virus will multiply in his cells. Inevitably, in one or more of those cells, the eight segments of the bird virus will get mixed up with the eight strands of the human virus and a new virus with some avian and some human gene segments packaged together will be produced. Most of the flu viruses that will result from random intermingling of avian and human flu genes won’t pose a problem because the accidental combinations most often will fail. But sooner or later a new flu virus that incorporates both human infectivity genes and avian virulence genes will emerge as a result of this process of genetic reassortment. And that is the scenario to be anticipated with dread.
What to do: Public health officials already are wisely trying to isolate domestic birds so they are not exposed to the infected wild birds carrying the avian flu virus in ever-widening circles. European countries have started to require that their domestic birds be kept indoors at all times. Additionally, many of those countries have also wisely closed their borders to all bird importation.
Public health officials also should concentrate on immunizing farm workers against conventional human flu, so as to decrease the chance that they will be infected with both avian and human strains of this virus. Realistically, this will be difficult to accomplish. Many farm workers in Asia, Africa, and South America are isolated and hard to reach. And so far, the international funds and the will required for this kind of immunization program have been lacking. But if we can stave off the dangerous genetic reassortment I’ve described, we might have enough time to develop new vaccines and antivirals in time to stop the global pandemic that a human-to-human strain of avian flu could cause.
Antibacterial soap: Why not to use it
State of the Science: Antibacterial soaps have been very popular with germophobic consumers despite evidence that these antibacterial chemicals don’t do anything useful. Readers of this column will remember that giving bars of soap to desperately poor squatters in Karachi made an enormous difference in preventing infectious disease, but it mattered not whether the soap bar was plain or contained an added antibacterial ingredient. Other studies have come to the same conclusion.
The real question isn’t whether antibacterial soaps do any good. My guess is that probably about 80 percent (to take a guess) of all nonprescription products don’t either. Antibacterial soaps, though, might actively cause harm, as the FDA’s Nonprescription Drug Advisory Panel considered last month. Stuart Levy of Tufts University has shown that the use of these products can lead to the development of bacteria that resist their antibacterial effects. And research by others suggests that antibacterial additives to household cleaners can cause germs to become resistant to antibiotics.
Theory: Antibiotics are different in every way—origin, composition, mode of action—from the chemicals we might add to soap to inhibit bacteria. So how could exposure to them suddenly promote resistance to antibiotics? Research by John Beaber, Bianca Hochut, and Matthew Waldor, working together at Tufts, provides an elegant and frightening answer. They found that if even a few bacteria are carrying genes that protect them from antibiotics, physical or chemical damage can trigger them to share that resistance with nearby germs. The bacteria respond to the damage by sending an internal SOS, which activates the bacteria to pass on its antibiotic resistance to other germs it comes in contact with.
Caveat: I began by saying that antibacterial additives sometimes unexpectedly confer protection for bacteria against unrelated antibiotics. And then I talked about how an SOS mechanism can stimulate damaged bacterial cells to pass on bacterial resistance. By putting these two ideas next to each other, I hinted that one thing might explain the other. It might. But honesty compels me to reveal that this is only speculation. We really won’t know if antibacterial soap additives set off the chain of events I’ve described until that experiment is done. Still, I’d avoid antibacterial soaps—at best, they are useless, and at worse they may actually increase the risk of infections that don’t respond to treatment with antibiotics.