My colleagues and I appreciate the thoughtful comments of Dr. Lanou regarding our recent report showing dairy acceleration of weight and fat loss secondary to energy restriction (1) and are pleased to clarify the key points she has raised. First, with regard to diets and dietary compliance, as indicated in the paper, diets for all treatment arms were constructed to provide comparable levels of macronutrient and fiber content, and these were achieved; Table 2 of the paper shows no significant differences in macronutrient distribution across the three treatment arms. The Table does not include dietary fiber, but the target level was 8–12 g/d, and the actual level achieved averaged 9.4 g/d, with no significant differences among the groups. We regret the omission of this information from the text of the manuscript. With regard to compliance with the dietary protocol, the 32 subjects who completed the study were adherent with respect to maintaining the 500 ± 100 kcal/d energy deficit as assessed by complete diet diaries throughout the study. Furthermore, all subjects were sedentary at study initiation and maintained this pattern throughout the study. Dr. Lanou has raised two important issues with regard to the potential role of vitamin D in cows’ milk. One of these is linked to the mechanism of action of calcium-rich foods in suppressing adiposity: suppression of 1α,25(OH)2D3 levels, as we have recently reviewed (2). Dr. Lanou cites our previous work (3) to show that vitamin D3 has “been shown to inhibit fat breakdown in human fat cells in vitro” and uses this as the basis for caution to be exercised regarding recommendations for cows’ milk consumption. The key flaw in this argument is that it fails to recognize that dietary vitamin D3 does not have any known effect on adipocyte lipid metabolism; it is only the hormone 1α,25(OH)2D3 that exerts regulatory effects on adipocyte function, and increased dietary vitamin D3 consumption does not lead to increased 1α,25(OH)2D3 unless normal regulatory systems are substantially overloaded (i.e., vitamin D toxicity). The issue of the role of vitamin D3 in prostate cancer deserves careful consideration. Although much has been made of a proposed association between prostate cancer risk and milk consumption (4), it is important to recognize that most of the data in support of this association are derived from an observational study (The Health Professionals Follow-Up Study), which clearly cannot infer causality. In addition, further analysis of this study failed to confirm the association of calcium intake and prostate cancer (5), whereas a prospective randomized controlled trial indicated that dietary calcium decreased, rather than increased, prostate cancer risk (6). Moreover, the putative mechanism of action of 1α,25(OH)2D3 in protecting the prostate is based on in vitro studies of pharmacological levels of either 1α,25(OH)2D3 or its analogues in stimulating apoptosis. These studies should be interpreted with considerable caution in light of our recent observations that indicate that, although pharmacological doses of 1α,25(OH)2D3 do indeed promote apoptosis in another cell system (human adipocytes), physiological concentrations exert the opposite effect (7). Accordingly, in the absence of other compelling data, we cannot infer that the physiological elevations in 1α,25(OH)2D3 that occur in response to low-calcium diets will protect the prostate, and the lone randomized clinical trial evaluating the effects of dietary calcium on prostate cancer risk suggests that the opposite may be the case (6). Finally, Dr. Lanou's cautionary note that weight loss does not occur in clinical trials originally designed to evaluate skeletal end-points is inaccurate, because she has overlooked the work of Heaney and colleagues (8, 9, 10), who have analyzed data from nine studies, including three controlled trials and six observational studies of calcium intake in which body weight could be assessed as a secondary outcome. Overall, increased calcium intake was consistently associated with reduced indices of adiposity (body weight, body fat, and/or weight gain). The aggregate effect was that each 300-mg increase in daily calcium intake was associated with a 3-kg lower body weight in adults and a 1-kg decrease in body fat in children. These observations are strongly supported by a substantial body of observational studies that support a role for dietary calcium and dairy foods in controlling excess adiposity (2) and that are now further supported by randomized controlled clinical trial data (1).
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Open Access
Dec 1, 2009
Ronald P Kühnlein 
