This week saw the launch of a new pill called Ateronon which, according to the press release, ‘is expected to revolutionise approaches to heart health’. Ateronon, we are told, ‘is the first formula proven to halt the oxidation of low-density lipoprotein (LDL) cholesterol, recognized as the key process of atherosclerotic build-up’. The active ingredient is lycopene, a pigment that occurs naturally in tomatoes. Lycopene isn’t very absorbable, but Nestle discovered that it can be made more absorbable by combining it with whey protein to make ‘lactolycopene’.
The new pill has been developed under license from Nestle by Cambridge Theranostics Ltd. The promotional material talks a lot about the legendary Mediterranean diet, which has been linked to a lower risk of heart disease. Because it’s made entirely from naturally occurring ingredients, it’s being treated as a food supplement and not a drug, meaning much less rigorous testing. Ateronon will be available over the counter from next month.
Does it work? Presumably they’ve published some research showing that it does. I put ‘ateronon’ into PubMed.
Your search for ateronon retrieved no results. However, a search for ‘afternoon’ retrieved the following  items.
I decided to leave trawling through those results to find out whether the afternoon can prevent heart disease for another day. I tried ‘lactolycopene’ instead. Two results, one of which was relevant: a 2002 paper, looking at 33 people, which found that you get a similar amount of lycopene from the lactolycopene supplement as you get from tomato paste.
Evidence that lactolycopene could prevent heart attacks and strokes remained elusive, so I tried getting hold of Cambridge Theranostics. I didn’t get an answer, so I tried their PR company, and someone helpfully sent me some documents. One was an ‘expert report’ by Prof Alf A. Lindberg, dated 2006. It describes a pilot phase I study of 18 people with angina. After two months of taking lactolycopene, lipoprotein oxidation (a biochemical process linked with atherosclerosis) was blocked in all 18 patients. Seventeen of them showed clinical improvements, as measured by a questionnaire.
Another document they sent me described two studies by Dovgalevsky and Petyaev which involved giving lactolycopene to coronary heart disease patients. One had 12 subjects, the other 10. In both studies, lipoprotein oxidation was blocked in patients given lactolycopene. The patients also experienced ‘improvements in the clinical status as assessed by a validated clinical questionnaire’.
So the evidence for Ateronon’s efficacy is three small studies in which taking lactolycopene led to reduced lipoprotein oxidation and clinical improvements measured by a questionnaire. None of the studies tested more than 18 people. None of the studies tested healthy people. None of the studies tested whether lactolycopene can prevent heart attacks, strokes, or any actual disease. None of the studies has been published in a peer-review journal. Perhaps most criminally, none of the studies compared lactolycopene with another drug or a placebo.
Maybe lactolycopene can prevent atherosclerosis. In fact I very much hope it does. But at the moment, the claims being made for Ateronon have not come close to being proven.