BackgroundBreast cancer, the leading cancer type in women worldwide, is affected by reproductive and nonreproductive factors. Estrogen and progesterone influence the incidence and progression of breast cancer. The microbiome of the gut, a complex organ that plays a vital role in digestion and homeostasis, enhances availability of estrogen and progesterone in the host. Thus, an altered gut microbiome may influence the hormone‐induced breast cancer incidence. This review describes the current understanding of the roles of gut microbiome in influencing the incidence and progression of breast cancer, with an emphasis on the microbiome‐induced metabolism of estrogen and progesterone.Recent FindingsMicrobiome has been recognized as a promising hallmark of cancer. Next‐generation sequencing technologies have aided in rapid identification of components of the gut microbiome that are capable of metabolizing estrogen and progesterone. Moreover, studies have indicated a wider role of the gut microbiome in metabolizing chemotherapeutic and hormonal therapy agents and reducing their efficacy in patients with breast cancer, with a predominant effect in postmenopausal women.ConclusionThe gut microbiome and variations in its composition significantly alter the incidence and therapy outcomes of patients with breast cancer. Thus, a healthy and diverse microbiome is required for better response to anticancer therapies. Finally, the review emphasizes the requirement of studies to elucidate mechanisms that may aid in improving the gut microbiome composition, and hence, survival outcomes of patients with breast cancer.

Compartmental models that dynamically divide the host population in categories such as susceptible, infected and immune constitute the mainstream of epidemiological modelling. Effectively such models treat infection and immunity as binary variables. We constructed an individual based stochastic model that considers immunity as a continuous variable and incorporates factors that bring about small changes in immunity. The small immunity effects (SIE) comprise cross immunity by other infections, small increments in immunity by sub clinical exposures and slow decay in the absence of repeated exposure. The model makes qualitatively different epidemiological predictions including repeated waves without the need for new variants, dwarf peaks (peak and decline of a wave much before reaching herd immunity threshold), symmetry in the upward and downward slopes of a wave, endemic state, new surges after variable and unpredictable gaps, new surge after vaccinating majority of population. In effect the SIE model raises alternative possible causes of the universally observed dwarf and symmetric peaks and repeated surges, observed particularly well during the Covid-19 pandemic. We also suggest testable predictions to differentiate between the alternative causes for repeated waves. The model further shows complex interactions of different interventions that can be synergistic as well as antagonistic. The model suggests that interventions that are beneficial in the short run can also be hazardous in the long run.

Calcium Citrate Malate’s (CCM) health benefits were patented over three decades ago. It is involved in calcium retention, in children and adolescents. In adulthood, it is seen to promote the maintenance of bone health. In conjunction with vitamin D, CCM also decreases the risk of bone fracture in aged people and ensures that postmenopausal women’s health is made better. CCM, unlike other supplements, does not need to be taken along with a meal and is seen to deliver benefits to individuals of any age group. CCM is usually used when the person has achlorhydria where the gastric acid secretion is reduced and there is an absence of an acidic environment (required by calcium carbonate). Calcium citrate Malate possesses outstanding bioavailability properties and is a useful extension to the calcium available presently, either for direct supplementation or for food fortification.

The recent SARS-CoV-2 pandemic has witnessed the emergence of various virus variants. While the phenomenon of immunity-evading variants is known in other viruses like influenza, there is limited understanding of the ecological and evolutionary processes involved in this succession. Due to the availability of large-scale epidemiological data collected and shared publicly during the Covid-19 pandemic, it becomes possible to explore evolutionary questions that also have implications for public health. We propose multiple alternative hypotheses regarding the origin and spread of these variants and evaluate them based on epidemiological data. Our analysis indicates that the invasion of novel variants is primarily limited by selection rather than mutation. Moreover, the repeated waves observed during the pandemic are not solely caused by the emergence of new variants. Instead, there is a significant overlap between conditions that lead to a wave and those that favor the selection of partially immune-evading variants. This association may contribute to the rise of a new wave alongside the invasion of a new variant. However, the association is not strong enough to support a causal role of the new variant. The dynamic interplay between epidemiological processes and selection on viral variants carries important implications for public health and can guide future policies aimed at effectively controlling infectious epidemics.

The recent pandemic caused by SARS-Cov-2 has witnessed an evolving succession of variants of the virus. While the phenomenon of invasion by immunity evading variants is known for other viruses such as influenza, the dynamics of the ecological and evolutionary process in the succession is little known. Since during the Covid-19 pandemic, large scale epidemiological data were collected and made available in the public domain, it is possible to seek answers to a number of evolutionary questions, which will also have public health implications. We list multiple alternative hypotheses about the origin and invasion of the variants and evaluate them in the light of epidemiological data. Our analysis shows that invasion by novel variants is selection limited and not mutation limited. Further novel variants are not the necessary and sufficient causes of the repeated waves during the pandemic. Rather there is substantial overlap between the conditions leading to a wave and those favoring selection of a partial immune evading variant. This is likely to lead to an association between invasion by new variant and the rise of a new wave. But the association is not sufficiently strong and does not support a causal role of the new variant. The dynamics of interaction between epidemiological processes and selection on viral variants have many public health implications that can guide future policies for effective control of infectious epidemics.