Common knowledge is often based on good science. It is thus reassuring that most of our fellow citizens accept the well-researched idea that diet influences health.

Discussions of exactly what diet produces what health effect can get cantankerous, though, so two recent publications are welcome additions to the debate.

It’s been known for some time that calorie-restricted diets prolong life and lead to fewer cancers. Researchers from MIT now tell us why this is so (Nature 458 [9 April 2009], 725–731).

If the cellular enzyme phosphatidylinositol-3-kinase is highly active, then dietary restriction does not provide protection from cancer formation. PI3K is involved in insulin-mediated signaling, so this is the likely target for nutrient restriction’s beneficial effects.

Best of all, therapeutic or preventative strategies might be able to take advantage of this pathway without the unappealing prospect of actually getting people to eat less.

The other discovery comes from the Medical College of Georgia (Cancer Research 69 [1 April 2009], 2826–2832). Thangaraju et al. offer a molecular explanation of why high fiber diets provide protection from colon cancer.

It turns out that bacteria in the colon eat roughage and produce the simple organic molecule butyrate. The butyrate in turn activates the uncolorfully named receptor GPR109A, which triggers programmed cell death (apoptosis). Voila, cancer cell expires.

So the overall lesson is to cut calories and eat more fiber. You’ve probably already heard this in the common knowledge category, but now it is buttressed by science.

But I’ve always wondered: if you truly are what you eat, why would anybody eat nuts?

A new journal is usually a sign of vitality and excitement in any field. And if that journal reaches the caliber of the venerable Nature family of publications, the excitement hits an even higher energy level.

And so the arrival of Nature Chemistry—surely cause for excitement—does not disappoint. The inaugural issue has everything from microtubes, to attoreactors, to molecular rotors. In other words, something for everyone, except normal people (smile).

Seriously, I couldn’t stop reading it. The special section called “The Future of Chemistry” is from a collection of eminent chemists speculating on frontier possibilities from synthesis, to tools, to complex systems. There are also book reviews (sometimes better, and certainly faster, than reading the book), job postings (essential in these times), and Nature’s indispensable “News and Views.”

There are even regular research papers, all up to Nature’s high editorial and scientific standards.

Best of all, you can peruse the premiere issue on the Web for free. And if you love print, you can subscribe for 25% off.

Such a deal, and one even a frugal chemist could love.

Bacterial resistance to antibiotic medicines is commonplace, is spreading worldwide, and is a major threat to human health.

There are strains of bacteria resistant to every known drug. Don’t catch one of these beasties unless you’re sure your last will and testament is in good order.

The medicinal chemist’s reaction to drug resistance is to create new drugs (in fact, this is the medicinal chemist’s reaction to everything….). To be truly effective, a new drug would act on a new target and not merely be a structural variation on an existing medicine.

One exciting new target for antimicrobials has been fatty acid biosynthesis. Fatty acids are essential components of bacterial membranes, and thus of life. Best of all, the pathway to fatty acid creation is different in bacteria than in humans. Voila, a target that could lead to drugs that kill microbes but leave patients’ own biochemistry untouched.

Nature has even provided a lead compound: platensimycin. It comes from a soil fungus, is a potent inhibitor of fatty acid biosynthesis, and has been the model for development of a whole new class of desperately needed synthetic antibiotics.

Whoops. A new report from a collaborative Parisian group (Nature 458 [5 March 2009], 83–86) reveals a flaw in the reasoning for this type of antibacterial agent. Sure, if you inhibit fatty acid formation it kills the bacterium. But if the bug has another source of fatty acids, it simply doesn’t care that its own synthetic mechanism is impeded.

Soil doesn’t have a ready source of fatty acids so platensimycin is very effective in that environment. But higher organisms have blood, which is well stocked with fatty acids, and thus such antibiotics just don’t work in real patients (who happen to be rats in this study).

Don’t be too nihilistic about drug development, though. There might be ways to avoid fatty acid uptake by nasty bacteria or to combine such inhibitors with other drugs in a more potent combination.

Never underestimate scientific ingenuity!

What really grosses you out? Snakes or spiders, perhaps. Or putrid, rotting, stinky food. Or people who hurt, take advantage of, or exploit other people.

Each of these trigger our sense of disgust, defined in the dictionary as “profound aversion or repugnance excited by something offensive.”

You might think that the disgust we feel toward rotten food—ignited by a reaction to the chemicals emitted—is different from the moral disgust we feel about things like slavery or incest. Maybe not, at least according to a collaborative research effort from the University of Pennsylvania and the University of Virginia.

Writing in Science these investigators compared detailed facial expressions in subjects experiencing either unpleasant liquids or unfair treatment in a money game (323 [27 February 2009], 1222–1226). They conclude that both types of disgust result in the same facial motor activity, and offer this as “evidence for the oral origins of disgust.”

It is intriguing to think that an ancient chemical-sensing mechanism that exists to avoid toxic substances could evolve into a more modern system of moral judgment. It’s a parsimonious argument—and evolutionarily favored if different types of disgust use the same biological machinery.

Still, I’m not convinced. Just because different inputs result in a common output doesn’t necessarily mean that the same processing occurred in between, or even that other collateral outputs (behaviors, in this case) might not be more pertinent. So I’ll wait for a more molecular mechanistic explanation before I conclude that holding my nose in disgust is the same reaction no matter what the offense.