About this Research Topic
During evolution, mankind has gone through alternating periods of famine/abundances, determined by seasons and environmental conditions changes, with consequent modifications in the metabolism efficiency. Adaptability and adjustment to these changes have helped us to survive as a species. Currently, in developed countries radical diet fluctuations are extremely rare, and, in this sense, human metabolism is largely "unchallenged". It is hard to assess whether or not this represents a favorable aspect. Obesity and type 2 diabetes mellitus (T2DM) are approaching epidemic proportions, especially as a consequence of poor quality nutrients, and, at least in part, inadequate nutrition leads to osteoporosis and/or increased bone fragility as well. If these concepts were to be ideally applied to a growing skeleton or in the reparative/remodeling phase the effect would be even more striking. Thus, the unchallenged human metabolism is probably not such a favorable feature, as in terms of human health the issue is not only the quantity of ingested food, but also the quality and its nutrients combination.
The old dogma attributing the physiological role of the human skeleton to a mere repository for calcium and phosphate ions is now outdated, and research over the past two decades demonstrated that our skeleton plays an important role in energy metabolism through “local” hormonal connection, such as leptin and insulin/IGF-1 and osteocalcin-related pathways, together with other organs involved in the metabolic control. Moreover, such hormonal/molecular pathways have been suggested to be fundamental in maintaining energy homeostasis, by controlling and coordinating both fuel uptake, from nutrition, and energy expenditure in all the organs of the body. Due to the common cellular origin of osteoblasts, myocytes, and adipocytes, the hypothesis that the skeleton has a role in energy metabolism results unsurprising. However, questions regarding how fuel sensing/utilization can be properly managed by all these cells, and which underlying molecular mechanisms are involved, remain to be answered. Furthermore, it is currently unclear how human bone cells contribute to global energy, glucose utilization, and homeostasis, and vice-versa.
As a matter of fact, general systemic metabolic impairments are associated with diabetes mellitus and the aging process, and both substantially contribute to skeletal fragility and/or osteoporotic fractures, as suggested by animal models and in vivo human studies revealing the close interaction between whole body metabolism and skeletal health. Several clinical studies, narrative reviews and/or metanalysis-systemic reviews, have, from time to time, hypothesized-suggested that nutrients such as minerals, vitamin complexes, antioxidants, trace elements, play more or less fundamental roles for the health of our skeleton, but it is still lacking in this landscape an overview that can, in part, unite all the underlying metabolic pathways. Even if the effect of individual nutrients is difficult to analyze, due to the presence of a real ‘mixtures of nutrients’ in our diet, some preliminary data indicate that administration of these nutrients either individually or globally, as a mixture of supplements, may improve bone mineral density and/or strength in postmenopausal women affected by osteoporosis.
Nevertheless, we do not have any certainty about a real effectiveness of single or of mix nutrients in preventing fragility fractures.
Within the past several years, the strong relationship between diet and health has been recognized and accepted by the mainstream nutrition community, dramatically increasing the interest in the physiological role of bioactive compounds present in plants over the last decade.
With the term of “Osteodietology”, we aim to define a specific branch of human nutrition aimed at studying and identifying the potential roles that nutrients, including among these even trace elements, may have in the development and maintenance of a healthy, capable human skeleton. We also focus on which part these nutrients play to achieve and maintain adequate levels of bone strength, in order to prevent/reduce fragility fracture events, and the clinical consequences related to them.
In this special issue, we would like to include all the figures involved in clinical, dietary, basic and translational research, animal models, in vivo and in vitro studies, interested, to various degrees, in this specific sector of the health of the human skeleton, with the aim of encouraging a multitasking force in which different health providers/caregivers can create a virtuous “osteodietological” path.
For this reason, contributions focused on this topic under the most varied forms of submission will be welcome, from narrative reviews, to multisystem/metanalysis reviews, clinical trials, peculiar case reports, cell/molecular biology/genetic, and animal/cell model studies.
We also hope that this editorial initiative can serve as an example, an incentive, for the creation of networks/subnetworks dedicated to “osteodietology”, as well as for a future design of research programs, basic, translational and clinical, aimed at expanding knowledge in this field of human health with the potential to provide both support to the current pathophysiological knowledge underlying bone fragility and new integrative/supplementary or even therapeutic strategies.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.