The mechanisms behind these beneficial effects on risk factors are largely unknown. In evaluations of multivariate correlation, diet emerged as a stronger explanatory variable than any other relevant variable for variations in dynamic insulin sensitivity, AUCins
0–120, log C-reactive protein and diastolic blood pressure. The observed effects on risk factors thus seem to be primarily caused by diet. However, it is conceivable that this dietary effect on risk factors is a result of differences in other variables induced by dietary assignment. An important finding in this regard is the divergence of the weight curves between the two groups after 3 months of feeding. The Paleolithic group was thus lighter and had a lower energy intake at the end of the study than the Cereal group, despite a threefold larger ration by weight. The diverging weight curves could be interpreted in several ways. They could be interpreted as food restriction in the Paleolithic group, which could explain the observed effects on risk factors [
28]. Neither group was fed their respective diet
ad libitum but was rather allocated rations on a group basis judged sufficient to achieve healthy animals by an experienced experimental pig farmer. This procedure was chosen due to concerns about the unfamiliar Paleolithic diet as swine feed, and the fact that feeding
ad libitum is not the custom in Swedish swine production. The diverging weight curves between the groups could thus possibly be caused by differences in subjectively allocated rations (e.g. difference in energy intake), which could lead to food restriction in the Paleolithic group. However, food restriction typically lowers mean body temperature by 1–2°C [
29], and we found no significant difference in mean body temperature between the two groups, indicating that there was not a substantial food restriction in the Paleolithic group as compared to the Cereal group. In fact, the mean weight in the Paleolithic group is well within the normal range of pigs [
30]. The diverging weight curves are thus probably not caused by food restriction in the Paleolithic group but instead could be interpreted as obesity in the Cereal group in analogy with human classification of individual weight based on statistical health effects [
31]. The significant difference in subcutaneous fat thickness between groups and the high correlation between weight and subcutaneous fat thickness supports this notion. Obesity in humans is associated with increased insulin resistance, high blood pressure and high levels of C-reactive protein [
23], and could explain the observed effects on risk factors. The difference between the two diets regarding obesity promotion could still be due to differences in subjectively allocated rations, but could alternatively be due to properties of a cereal based swine feed which possibly disturb the regulation of satiation [
3], satiating properties of a Paleolithic diet [
2] and differing effects between the diets on energy metabolism [
2]. The satiating properties of a Paleolithic diet could be due to differences in macronutrient diet composition, such as the low protein content of cereals in the Cereal group diet. The Paleolithic group thus ate relatively more protein and less carbohydrates, which through satiating, thermogenic and other properties could account for the results of the study [
32,
33], although results from studies on the association between protein intake and diseases of affluence have been contradictory [
34]. In future studies of Paleolithic diets it would be valuable to match diets for macronutrient composition. The latter alternative explanations for the diverging weight curves is supported by our epidemiological findings in humans from Kitava, Papua New Guinea, where a non-western lifestyle has been connected to leanness despite food being available
ad libitum [
13]. The diverging weight curves would then suggest that the beneficial effects on risk factors could be due to differences between diets regarding obesity promotion. Alternatively, obesity could be a marker for other effecting mechanisms, such as leptin resistance, and the diverging weight curves would then suggest that the beneficial effects on risk factors could be due to differences between diets regarding promotion of leptin resistance [
3].