Obesity and H1N1

Being Overweight May Make Influenza Worse

© Stephen Allen Christensen

May 20, 2009
New data tie obesity to a higher rate of complications from H1N1 infection. Regardless of this novel flu's relative virulence, obese people may need different treatment.

According to Anne Schuchat, acting director of the Center for Disease Control’s National Center for Immunization and Respiratory Diseases, obesity may play a role in the severity of H1N1 infections.

During a briefing aired on May 19, 2009, she said, “We were surprised by the frequency of obesity among the severe cases that we have been tracking and do think that this is an important result.”

Among 30 H1N1 cases admitted to California hospitals in April and May, 37% had underlying lung problems, and 20% took medications or had other conditions that suppress the immune system. Four patients had diabetes mellitus—another condition that predisposes to complications—and four were obese. (Centers for Disease Control and Prevention. Hospitalized patients with novel influenza A (H1N1) virus infection—California, April-May, 2009. Morbidity and Mortality Weekly Report. May 18, 2009/58[Early Release];1-5)

Prior to this analysis, CDC had not considered obesity to be an independent risk factor for complications of H1N1 infection, but the organization is now considering whether obese individuals should be treated differently when they acquire H1N1, or whether immunization protocols should differ for obese persons.

CDC is investigating a number of theories about why obesity may play a role in the severity of influenza infection. Schuchat proposed one mechanism—hypoventilation due to “Pickwickian syndrome”—that could increase the pulmonary complications of a respiratory infection.

Unfortunately, improving respiratory function (via artificial ventilation and/or oxygenation) may not address all of the issues that face obese patients who contract a novel influenza virus; more insidious processes might also play a role.

Possible Reasons for Increased Severity of Influenza in Obese Individuals

There is ample (and increasing) evidence that obesity interferes with normal immune function:

  • Animal research shows that obesity prevents the body from properly turning on its immune system in response to infection. For example, when infected with influenza, obese mice are 50% less capable of killing the virus when compared to lean mice.
  • Obese mice are ten times more likely to die from influenza infection than mice of normal weight.
  • Obese animals exhibit an impaired ability to express genes and proteins that control several antiviral and pro-inflammatory cytokines, which are essential for dealing with infections in their early stages.
  • Obese animals demonstrate deficiencies in the activity of natural killer cells, which are T lymphocytes that limit viral spread by killing infected cells. (Smith A, et al. Diet-induced obese mice have increased mortality and altered immune responses when infected with influenza virus. J Nutr. 2007;137:1236-43)
  • Leptin modulates several parameters of the immune response, including T cell activity, proliferation of white blood cells, and inflammatory activity. Obesity decreases the sensitivity of peripheral tissues to leptin signals and contributes to impaired immunity. (Claycombe K, et al.A role for leptin in sustaining lymphopoiesis and myelopoiesis. Proceedings of the National Academy of Sciences of the United States of America. 2008;105(6):2017-21)

Americans are among the most obese people in the world. Obesity in adults has increased by 60% during the past two decades; one-third of them are now considered obese. Obesity in American children has tripled in the past 30 years.

In addition to a multitude of other health problems that accompany obesity, it appears that susceptibility to infections—and higher morbidity and mortality from those infections—must now be added to the list.


The copyright of the article Obesity and H1N1 in Diseases/Viruses is owned by Stephen Allen Christensen. Permission to republish Obesity and H1N1 in print or online must be granted by the author in writing.




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