AstraZeneca’s drug Crestor lowers the risk of heart attacks in apparently healthy adults with no prior history of cardiac disease and normal cholesterol levels, according to the results of a trial known as Jupiter.

Participants in Jupiter did have elevated levels of C-reactive protein (CRP), a non-specific marker for inflammation that identifies people at risk for cardiac events regardless of their cholesterol levels. CRP levels are measured using a $20 dollar blood test that is covered by most insurance policies.

Jupiter was a multicenter, prospective trial involving 17,802 participants in 26 countries that had entered an age where cardiac risk is highest—men over 50 and women over 60. Participants had no signs or symptoms of cardiac disease, and their cholesterol levels were not high enough to prompt treatment using current guidelines. But their CRP levels were high—at least 2.0 milligrams/liter.

Participants were randomized to receive 20 milligrams of Crestor or a placebo. Those who took Crestor experienced a 54% reduction in the risk of heart attack and a 48% reduction in the risk of stroke. They were 46% less likely to require angioplasty or coronary bypass surgery and had 20% lower mortality from all causes. LDL (bad) cholesterol dropped 50% and CRP levels dropped 37% in the Crestor group. Serious adverse events were rare and occurred at the same rate in both groups.

Paul Ridker, a cardiologist at Brigham and Women’s Hospital, was the principal investigator of the Jupiter trial. He presented the results in New Orleans yesterday during a meeting of the American Heart Association. Ridker is listed as an inventor on several CRP assays whose patents are held by the Brigham. He and several co-authors receive grants and other income from AstraZeneca.

“The potential public health benefits are huge,” Ridker told the Washington Post. “It really changes the way we have to think about prevention of heart attack and stroke.” Ridker’s point seems well taken since nearly half of all heart attacks occur in people that have normal cholesterol levels.  JUPITER suggests a broader screening role for CRP, especially in those with normal cholesterol.

However, Stanford cardiologist Mark Hlatky expressed caution to the Wall Street Journal. “Before we expand treatment indications in any drastic way, we need to do due diligence,” he said. “The idea that everybody should get CRP measured is premature and not backed up by good data.”

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The northern bluefin tuna is native to the Atlantic Ocean and the Mediterranean Sea. The source of nearly all the tuna used in sushi, it is particularly revered in Japan where a large specimen can command $100,000 in Tokyo fish markets.

The fish live in deep ocean waters where no country has jurisdiction, and as a result they have been subject to decades of overfishing.

The problem is approaching crisis stage. Brian MacKenzie and colleagues at the Technical University of Denmark reported in particular that even if all bluefin fishing were halted immediately, bluefin populations in both the Atlantic and the Mediterranean will likely collapse within a decade.

Not that the current plan comes anywhere close to an outright ban. In theory, the organization that sets bluefin fishing policies is the Madrid-based International Commission for the Conservation of Atlantic Tunas (ICCAT). Its performance has prompted the Economist to propose that ICCAT actually stands for International Conspiracy to Catch All Tunas.

ICCAT had set a quota of 30,000 metric tons per year even though scientists suggest this is 2-4 times the sustainable amount. In response to the outcry from the scientific community (which must have been tough to hear amid the din arising from sushi restaurants on 6 continents), ICCAT reduced its quota to 25,000 metric tons. Whoop-de-damn-do!

Let’s not even start on the fact that at least 50,000 metric tons are actually landed each year due to illegal fishing and non-existent monitoring.

Oh, and even if ICCAT set a properly aggressive limit and became empowered to enforce it, there’s the problem of how the 46 participating countries would divvy up the catch.

Longitudinal studies in the US and Japan have linked violent video game use to aggressive behavior in children and teens.

Scientists tested for the association in three cohorts: US children aged 9-12, Japanese children aged 12-15, and Japanese children aged 13-18. They published their findings in last week’s issue of Pediatrics.

The investigators found that habitual video gaming early in the school year predicted either getting into a fight at school or being cited by a peer or a teacher for physically aggressive behavior 5-6 months later. The findings held firm after the scientists accounted for gender and a previous history of aggressive behavior. The effect was similar for the US and Japanese youth and was more pronounced in younger children.

“When you find consistent effects across two very different cultures, you’re looking at a pretty powerful phenomenon,” lead author Craig Anderson told the Washington Post. “One can no longer claim this is somehow a uniquely American phenomenon. This is a general phenomenon that occurs across cultures.”

But Anderson hastened to add that violent video game exposure occurs in a larger context of a child’s life. “A healthy, normal, nonviolent child or adolescent who has no other risk factors for high aggression or violence is not going to become a school shooter simply because they play 5 hours or 10 hours a week of these violent video games,” he told the Post.

Extremely violent behavior usually occurs “when there is a convergence of multiple risk factors” such as gang involvement, substance abuse, poverty, and antisocial peers or parents, he added.