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Commentary: Lactose and ischaemic heart disease: a weak 28-year-old hypothesis.

Ischaemic heart disease (IHD) is one of the more extensively researched diseases and most of its risk factors have been identified by consistent data from different studies. Diet and dietary patterns have been found to be correlated with the risk of IHD, for example, the dietary pattern of fruits and vegetables, whole-meal bread, low fat dairy and little alcohol has an inverse association with the risk, 1 while high intake of red and processed meat, refined grains and sugars, French fries and high fat dairy is associated with increased IHD risk. 2 Milk has been less consistently correlated with IHD and two recent reviews of published literature suggest there is no increased risk. 3,4 Milk is a rather complex food because it is a rich source of protein, saturated fat, calcium and lactose sugar. Saturated fat from dairy products, including whole milk has been found to be related to IHD. 5 Calcium from milk and dairy products is a major source of daily human consumption but the studies have failed to find an association with IHD. 6,7 Lactose is rather specific to unfermented milk and if found related to IHD could specifically point to unfermented milk as the causative nutrient. This is the basis of the paper by Siegel titled: Hypothesis: Is lactose a dietary risk factor for IHD? 8 published 28 years ago in this journal. The association between lactose and IHD was a reasonable and novel hypothesis to pursue three decades ago given the era of increasing awareness of IHD and the search for possible explanations from available data. This was similar to the study by Keys in 1980, 9 which suggested that saturated fat is associated with IHD based on correlational ecological data. However, a closer look at the paper by Segall reveals some methodological problems that undermine the eloquent argument for the observed association between lactose and IHD. This might also explain why no subsequent data was published to support this hypothesis. The paper does present the arguments for a hypothesis rather than a causal association, and therefore an ecological study design for the purpose of promoting such a hypothesis is acceptable. The term ‘ecological fallacy’ was coined in the 1950s and the bias introduced by attempting to apply findings from aggregate or geographical data to the individual-level is well-known. 10 Comparisons of countries without adjustment for important confounders between these countries, which are usually not available from aggregate data, can lead to false conclusions. The well known example of finding higher suicide rates in predominantly Protestant European countries compared with predominantly Catholic countries has been attributed to this fallacy. 11 In his paper, Segall does present the possibility that environmental factors explain the observed association given that the group of countries with high lactose exposure [low prevalence of lactose malabsorption also known as lactose intolerance (LI)] and high IHD were the developed countries with high socioeconomic status. This explanation is then dismissed based on low IHD in Japan and high IHD in the Punjab. The data on LI from the Punjab was based only on 18 subjects, and in the cited IHD study on Punjabis, 91% of the cases were from the high and middle income Punjabi social class, while the unique diet in Japan of fish and seafood high in omega-3 fatty acids (that is mostly protective against IHD) could explain why a country with high socioeconomic status would have low IHD. In a letter to the editor on the inverse association between wine and IHD in European countries, Segall argues about the ‘possible coincidental presence of a geographical factor of unknown identity that explains this association’, 12 an argument that can also explain the findings in the paper on milk and IHD published by Segall.