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Humans create ecologically simplified landscapes that favour some wildlife species, but not others.Here, we explore the possibility that those species that tolerate or do well in human-modified environments, or 'synanthropic' species, are predominantly the hosts of zoonotic emerging and re-emerging infectious diseases (EIDs). We do this using global wildlife conservation data and wildlife host information extracted from systematically reviewed emerging infectious disease literature. The evidence for this relationship is examined with special emphasis on the Australasian, South East Asian and East Asian regions. We find that synanthropic wildlife hosts are approximately 15 times more likely than other wildlife in this region to be the source of emerging infectious diseases, and this association is essentially independent of the taxonomy of the species. A significant positive association with EIDs is also evident for those wildlife species of low conservation risk. Since the increase and spread of native and introduced species able to adapt to human-induced landscape change is at the expense of those species most vulnerable to habitat loss, our findings suggest a mechanism linking land conversion, global decline in biodiversity and a rise in EIDs of wildlife origin.

This compelling account charts the relentless trajectory of humankind, and its changing survival and disease patterns, across place and time from when our ancient ancestors roamed the African Savannah to today's populous, industrialised, globalising world. This expansion of human frontiers - geographic, climatic, cultural and technological - has encountered frequent setbacks from disease, famine and dwindling resources. The social and environmental transformations wrought by agrarianism, industrialisation, fertility control, social modernisation, urbanisation and mass consumption have profoundly affected patterns of health and disease. Today, as life expectancies rise, the planet's ecosystems are being damaged by the combined weight of population size and intensive economic activity. Global warming, stratospheric ozone depletion and loss of biodiversity pose large-scale hazards to human health and survival. Recognising this, can we achieve a transition to sustainability? This and other profound questions underlie this chronicle of expansive human activity, social change, environmental impact and their health consequences.

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Objective: The world's climate will continue to change because of human influence. This is expected to affect health, mostly adversely. We need to compare the

Background The evidence associating diet and risk of multiple sclerosis (MS) is inconclusive. Objectives The aim of this study was to investigate associations between a Mediterranean diet and risk of a first clinical diagnosis of central nervous system demyelination (FCD), a common precursor to MS. Methods We used data from the 2003–2006 Ausimmune Study, an Australian multicenter, case-control study examining environmental risk factors for FCD, with participants matched on age, sex, and study region (282 cases, 558 controls; 18–59 y old; 78% female). The alternate Mediterranean diet score (aMED) was calculated based on data from a food-frequency questionnaire. We created a modified version of the aMED (aMED-Red) where ∼1 daily serving (65 g) of unprocessed red meat received 1 point. All other components remained the same as aMED. Conditional logistic regression (254 cases, 451 controls) was used to test associations between aMED and aMED-Red scores and categories and risk of FCD, adjusting for history of infectious mononucleosis, serum 25-hydroxyvitamin D concentrations, smoking, education, total energy intake, and dietary underreporting. Results There was no statistically significant association between aMED and risk of FCD [per 1-SD increase in aMED score: adjusted odds ratio (aOR): 0.89; 95% CI: 0.75, 1.06; P = 0.181]. There was evidence of a nonlinear relation between aMED-Red and risk of FCD when a quadratic term was used (P = 0.016). Compared with the lowest category of aMED-Red, higher categories were significantly associated with reduced risk of FCD, corresponding to a 37% (aOR: 0.63; 95% CI: 0.41, 0.98; P = 0.039), 52% (aOR: 0.48; 95% CI: 0.28, 0.83; P = 0.009), and 42% (aOR: 0.58; 95% CI: 0.35, 0.96; P = 0.034) reduced risk of FCD in categories 2, 3, and 4, respectively. Conclusions A Mediterranean diet, including unprocessed red meat, was associated with reduced risk of FCD in this Australian adult population. The addition of unprocessed red meat to a Mediterranean diet may be beneficial for those at high risk of MS.

The evidence associating red meat consumption and risk of multiple sclerosis is inconclusive. We tested associations between red meat consumption and risk of a first clinical diagnosis of central nervous system demyelination (FCD), often presaging a diagnosis of multiple sclerosis. We used food frequency questionnaire data from the 2003–2006 Ausimmune Study, an incident, matched, case-control study examining environmental risk factors for FCD. We calculated non-processed and processed red meat density (g/1,000 kcal/day). Conditional logistic regression models (with participants matched on age, sex, and study region) were used to estimate odds ratios (ORs), 95% confidence intervals (95% CI) and p- values for associations between non-processed ( n = 689, 250 cases, 439 controls) and processed ( n = 683, 248 cases, 435 controls) red meat density and risk of FCD. Models were adjusted for history of infectious mononucleosis, serum 25-hydroxyvitamin D concentrations, smoking, race, education, body mass index and dietary misreporting. A one standard deviation increase in non-processed red meat density (22 g/1,000 kcal/day) was associated with a 19% reduced risk of FCD (AOR = 0.81; 95%CI 0.68, 0.97; p = 0.02). When stratified by sex, higher non-processed red meat density (per 22 g/1,000 kcal/day) was associated with a 26% reduced risk of FCD in females ( n = 519; AOR = 0.74; 95%CI 0.60, 0.92; p = 0.01). There was no statistically significant association between non-processed red meat density and risk of FCD in males ( n = 170). We found no statistically significant association between processed red meat density and risk of FCD. Further investigation is warranted to understand the important components of a diet that includes non-processed red meat for lower FCD risk.