Cytokine dysregulation is believed to play a key role in the remodeling of the immune system at older age, with evidence pointing to an inability to fine-control systemic inflammation, which seems to be a marker of unsuccessful aging. This reshaping of cytokine expression pattern, with a progressive tendency toward a pro-inflammatory phenotype has been called “inflamm-aging.” Despite research there is no clear understanding about the causes of “inflamm-aging” that underpin most major age-related diseases, including atherosclerosis, diabetes, Alzheimer’s disease, rheumatoid arthritis, cancer, and aging itself. While inflammation is part of the normal repair response for healing, and essential in keeping us safe from bacterial and viral infections and noxious environmental agents, not all inflammation is good. When inflammation becomes prolonged and persists, it can become damaging and destructive. Several common molecular pathways have been identified that are associated with both aging and low-grade inflammation. The age-related change in redox balance, the increase in age-related senescent cells, the senescence-associated secretory phenotype (SASP) and the decline in effective autophagy that can trigger the inflammasome, suggest that it may be possible to delay age-related diseases and aging itself by suppressing pro-inflammatory molecular mechanisms or improving the timely resolution of inflammation. Conversely there may be learning from molecular or genetic pathways from long-lived cohorts who exemplify good quality aging. Here, we will discuss some of the current ideas and highlight molecular pathways that appear to contribute to the immune imbalance and the cytokine dysregulation, which is associated with “inflammageing” or parainflammation. Evidence of these findings will be drawn from research in cardiovascular disease, cancer, neurological inflammation and rheumatoid arthritis.

Maternal vitamin D insufficiency is associated with childhood rickets and longer-term problems including schizophrenia and type 1 diabetes. Whilst maternal vitamin D insufficiency is common in mothers with highly pigmented skin, little is known about vitamin D status of Caucasian pregnant women. The aim was to investigate vitamin D status in healthy Caucasian pregnant women and a group of age-matched non-pregnant controls living at 54 -558N. Vitamin D insufficiency: Vitamin D supplementation: PregnancyVitamin D is essential to maintain bone health, playing a key role in bone mineralisation (1) , with severe vitamin D deficiency in children resulting in rickets (2) . As stores of vitamin D in newborns are dependent on maternal vitamin D status (3) , vitamin D deficiency during pregnancy leads to infant vitamin D deficiency and thus to increased risk of rickets (4) . More recent evidence suggests that in addition to causing poor mineralisation of the skeleton, vitamin D insufficiency is linked to other non-skeletal health outcomes (5,6) . 25-Hydroxyvitamin D (25(OH)D) is the storage form of vitamin D and circulating plasma concentrations of 25(OH)D are an indicator of vitamin D status. There is a lack of consensus on definitions regarding adequate vitamin D status and various cut-off levels have been used to define levels of deficiency: severe deficiency ,12·5 nmol/l (7)

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