Background: Anticholinergic and sedating medications are generally contraindicated in those with cognitive decline. We examined trends in medication use by patients at initial presentation to a rural and remote memory clinic (RRMC) between March 2004 and June 2015 to determine whether patterns of medication use have changed. Methods: The first 444 patients seen at the RRMC between 2004 and 2015 were included in this analysis. Medication lists were collected at the patient’s initial visit, and it was noted whether patients were taking anticholinergic or potentially sedating drugs. Statistical analysis (Spearman’s correlation) was conducted to examine trends in medication use over time. Results: Patients were on a mean of 5.18 medications (standard deviation, 3.46). Ninety-one patients (20.5%) were taking at least one anticholinergic medication. There was a decline (25.0% in 2004 to 12.5% in 2014) in percentage of patients presenting with anticholinergic medications over the 11 years of this study (Spearman’s correlation coefficient =−0.64, p=0.035). The prevalence of drugs acting on the central nervous system trended toward an increase, but this was not statistically significant. Sixty-three patients (14.2%) presented to the RRMC already taking a cholinesterase inhibitor. Conclusions: The most encouraging statistic to come from this study is a decline in anticholinergic medication use in this rural population. Prescribers must be properly informed to ensure that the number of medications per patient does not continue to rise, that medications are used only as necessary, and that potentially deleterious medications are avoided.

Although the clinical benefits of dietary supplementation with n-3 polyunsaturated fatty acids (PUFA) has been recognised for a number of years, the molecular mechanisms by which particular PUFA affect metabolism of cells within the synovial joint tissues are not understood. This study set out to investigate how n-3 PUFA and other classes of fatty acids affect both degradative and inflammatory aspects of metabolism of articular cartilage chondrocytes using an in vitro model of cartilage degradation. Using well-established culture models, cartilage explants from normal bovine and human osteoarthritic cartilage were supplemented with either n-3 or n-6 PUFA, and cultures were subsequently treated with interleukin 1 to initiate catabolic processes that mimic cartilage degradation in arthritis. Results show that supplementation specifically with n-3 PUFA, but not n-6 PUFA, causes a decrease in both degradative and inflammatory aspects of chondrocyte metabolism, whilst having no effect on the normal tissue homeostasis. Collectively, our data provide evidence supporting dietary supplementation of n-3 PUFA, which in turn may have a beneficial effect of slowing and reducing inflammation in the pathogenesis of degenerative joint diseases in man.

The number of elderly individuals is growing rapidly worldwide and degenerative diseases constitute an increasing problem in terms of both public health and cost. Nutrition plays a role in the ageing process and there has been intensive research during the last decade on B vitamin-related risk factors in vascular and neurological diseases and cancers. Data from epidemiological studies indicate that subclinical deficiency in most water-soluble B vitamins may occur gradually during ageing, possibly due to environmental, metabolic, genetic, nutritional and pathological determinants, as well as to lifestyle, gender and drug consumption. Older adults have distinct absorption, cell transport and metabolism characteristics that may alter B vitamin bioavailability. Case–control and longitudinal studies have shown that, concurrent with an insufficient status of certain B vitamins, hyperhomocysteinaemia and impaired methylation reactions may be some of the mechanisms involved before a degenerative pathology becomes evident. The question that arises is whether B vitamin inadequacies contribute to the development of degenerative diseases or result from ageing and disease. The present paper aims to give an overview of these issues at the epidemiological, clinical and molecular levels and to discuss possible strategies to prevent B vitamin deficiency during ageing.