Some truth to “feed a cold, starve a fever”
Research from Yale University in the US has found that there may be some truth to the old wives’ tale that says “feed a cold, starve a fever.” The study, published in Cell, looked at the effects of providing nutrients during infection and found that mice with bacterial infections that were fed died, while those with viral infections that were fed lived. In the first series of experiments, the investigators infected mice with the bacterium Listeria monocytogenes, which commonly causes food poisoning. The mice stopped eating and they eventually recovered. But when the mice were force fed, they died. The researchers then broke the food down by component and found fatal reactions when the mice were given glucose, but not when they were fed proteins or fats. Moreover, giving mice the chemical 2-deoxy-D-glucose (2-DG), which prevents glucose metabolism, was enough to rescue even mice that were fed glucose, allowing them to survive the infection. When the researchers did similar studies in mice with viral infections, they found the opposite effect. Mice infected with the influenza virus A/WSN/33 survived when they were force fed glucose, but died when they were denied food or given 2-DG. Further research showed that different areas of the brain were affected depending on which type of infection the mice died from, indicating that the animals’ metabolic needs differ depending on which part of the immune system had been activated. Lead author Professor Ruslan Medzhitov said that the findings may have immediate implications for the design of clinical trials evaluating the benefits of providing nutrients to patients with sepsis. “Sepsis is a critical problem in hospital intensive care units that defies most modern medical approaches,” he says. “A number of studies have looked at nutrition in patients with sepsis, and the results have been mixed. But these studies didn’t segregate patients based on whether their sepsis was bacterial or viral. The implication is that patients should be stratified by the cause of their sepsis, and trials should be designed based on that.”
Exercise combats alcohol’s cancer risk
An international research collaboration, led by the University of Sydney, has found that exercising at even the basic recommended weekly physical activity levels (at least 150 minutes of moderate intensity activity) may offset some of the harmful effects of drinking alcohol. Published in the British Journal of Sports Medicine, the study found that for alcohol drinkers aged 40 years and over, physical activity may decrease the risks of dying both from cancer and from other causes. The researchers drew on responses from eight nationally representative, continuous and annually repeated population surveillance surveys, carried out in the UK between 1994 and 2006, which looked at the impact of physical activity and alcohol consumption on health outcomes. Participants were asked to consent to linkage of their study data to their National Health Service health records and mortality data. The analysis included 36 370 adults, with a corresponding 5735 deaths and a mean of 353 049 person-years of follow-up (mean follow-up period of 9.7 years [standard deviation, 4.3]). Compared with never having been a drinker, drinking even within the UK 2015 recommended levels (equivalent in Australia to an average of 2.4 standard drinks per day for men and 1.6 drinks per day for women) was associated with a 36% greater risk of death from cancer as well as a 13% greater risk of death from any cause. But this risk was substantially lessened or offset among those who were physically active at the basic recommended level or at the higher level (equivalent to at least 300 minutes of moderate intensity activity per week). In the physically active groups, only harmful levels of drinking were associated with increased risk of cancer death and death from any cause.
New hope for those with “hidden” HIV
Australian research, published in Nature Communications, has raised hopes that doctors may be able to completely purge latent human immunodeficiency virus (HIV) from the cells of infected people who are otherwise successfully controlling the disease with antiretroviral therapy. Although antiretroviral therapy can reduce HIV levels in the body to almost undetectable levels, latent reservoirs of HIV survive by being “invisible” to the body’s immune system. Researchers from the Westmead Institute for Medical Research in Sydney showed that histone deacetylase (HDAC) inhibitors – panobinostat and vorinostat – which work as latency-reversing agents, can activate HIV gene expression from a diverse population of latent HIV-infected cells. The researchers suggest that the drugs could potentially be used in combination with immunotherapy in a “shock-and-kill” strategy to purge the HIV-infected cells. Using advanced sequencing techniques from patients involved in trials of the drugs in Denmark and Melbourne, the researchers were able to analyse the baseline reservoir of HIV and determine which proviruses (virus genomes integrated into the DNA of a host cell) were activated by the HDAC inhibitors, and were then able to discern which of these viruses later contributed to rebound. While the development of this approach is still in its infancy, the research showed that HDAC inhibitors are a promising class of drugs that could potentially allow patients to discontinue antiretroviral treatment and live without fear of viral rebound.
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