Every year America’s inflamed and strained swallow 29 billion doses of over-the-counter (OTC) aspirin and non-aspirin pain relievers called non-steroidal anti-inflammatory drugs (NSAIDs).

Our doctors write more than 500 million prescriptions for them. It is almost axiomatic that a session with the doctor ends with a prescription for something.

But the problem with these painkillers is they’re harsh and they cause little micro-bruises on the stomach lining. They also inhibit certain messenger chemicals called prostaglandins that would otherwise stimulate repair of tissues. With every dose, the micro-bruises increase. Even a tiny baby aspirin so many people take to prevent a second heart attack, just 80 mg, causes micro-bleeding.

NSAID use is also associated with leaky gut syndrome when food and other toxins pass easily directly into the bloodstream due to the poor repair processes that fail to protect the mucosal integrity of the gastrointestinal lining. All this makes a discovery by British researchers at the Department of Gastroenterology, Imperial College School of Medicine, London, quite relevant.

They found that the growth hormone (GH) from colostrum, the first milk produced before and the first 6 hours after birth, repairs the NSAID-damaged gut and can actually undo it—and they aren’t talking about experimental evidence; they’ve done a clinical trial.

Scientists examined whether bovine colostrum (BC) could reduce the rise in gut permeability caused by NSAIDs in volunteers taking prescription drugs. Healthy male volunteers participated in a randomized crossover trial comparing changes in gut permeability before and after five days of indomethacin therapy. In healthy volunteers, indomethacin caused a 3x increase in gut permeability whereas no increase in permeability was seen when colostrum was co-administered.

“These studies provide preliminary evidence that bovine colostrum, which is already currently available as an over-the-counter preparation, may provide a novel approach to the prevention of NSAID-induced gastrointestinal damage in humans.