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   The Scientist >> Magazine >> Features   
      
      
   The Sum of Our Parts   
      
   Putting the microbiome front and center in health care, in preventive   
   strategies, and in health-risk assessments could stem the epidemic of   
   noncommunicable diseases.   
      
   By Janice Dietert and Rodney Dietert | July 1, 2015   
      
   (c) DUNG HOANG   
      
   Looking across generations at how health concerns have changed over the past   
   century is an enlightening exercise. For your ancestors living in the roaring   
   '20s, fear of infectious diseases--including typhoid fever, cholera, and   
   influenza--far outweighed    
   concerns about heart disease or cancer. Autism, Alzheimer's, attention deficit   
   disorder, and Parkinson's disease were virtually unheard of. Allergies, then   
   called hay fever, were around, but not common. Ratchet ahead through the   
   rock-and-roll and disco    
   generations and on to the '80s and '90s, and the fear of cancer grew   
   enormously, while a number of new diseases began to appear on the radar   
   screen. Asthma, autism, lupus, arthritis, inflammatory bowel disease,   
   attention deficit disorder, celiac disease,    
   multiple sclerosis, obesity, and diabetes, among others, became common   
   concerns. Fast-forward another two decades to present day, and it is not a   
   matter of whether you, your friends, or family members have one of these   
   ailments, but which ones and how    
   many.   
      
   In less than 100 years, leading diseases and causes of death have shifted   
   dramatically away from infectious diseases and heavily toward noncommunicable   
   diseases (NCDs), not just in developed countries, but around the globe. NCDs   
   are now the number one    
   killer worldwide, accounting for 63 percent of all mortalities.1 There is no   
   question that environmental variables, including exposure to cigarette smoke,   
   certain dietary factors, and chemicals such as heavy metals, pesticides,   
   endocrine disruptors, or    
   particular drugs, increase one's risk of developing an NCD. Psychosocial   
   stressors also play a role. But any assumption that the ongoing NCD epidemic   
   is due solely to external factors would be missing a key part of the story:   
   the human microbiome. In    
   reality, the NCD epidemic is as much about the ways we have altered our   
   microbiomes in recent decades as it is about our changing external environment.   
      
   Commensal microbes that live on and in us are critical for our health. By cell   
   numbers, we are approximately 90 percent microbial, and the vast majority of   
   the genes expressed in our superorganism are not on our mammalian chromosomes   
   but in the bacteria,    
   archaea, and single-celled eukaryotes that call the human body home. Normally,   
   a robust microbiome would be part of our inheritance, a legacy passed, largely   
   maternally, from generation to generation. But recently that chain has been   
   broken, usually more    
   than once. The increase in cesarean deliveries, the reduced prevalence and   
   duration of breastfeeding, overuse of antibiotics both as prescription drugs   
   and in agriculture, modern urban living surrounded by sanitizers, and a   
   general tendency to limit    
   contact with the environment have changed our relationship with the microbes   
   that are an integral part of our biology. In today's world, our best chance of   
   acquiring microbes might be from touching our computer keyboards and   
   cellphones or frequenting    
   shopping malls, hotel rooms, or doctors' offices--and many are not bugs you   
   want in and on your body.   
      
   In less than 100 years, leading diseases and causes of death have shifted   
   dramatically away from infectious diseases and heavily toward noncommunicable   
   diseases.   
      
   Our microbial gatekeeper   
   The human microbiome plays a critical role as a filter between us and the   
   world. In fact, it is the microbiome that determines our actual exposure to   
   the environment. Substances such as foods, drugs, and environmental   
   chemicals--collectively termed    
   xenobiotics--must first pass through the layers of microbiota on the skin, in   
   the gut, and in the airways where, depending upon the microbes present, the   
   chemicals will be sequestered, excluded, or metabolized before they ever enter   
   our cells. The common    
   gut actinobacterium Eggerthella lenta, for example, can significantly change   
   the potency of the cardiac drug digoxin.2 Likewise, microbiome composition   
   affects the toxicity of certain environmental chemicals such as arsenic, with   
   some sulfur-reducing gut    
   bacteria able to generate highly toxic, thiolated species of arsenic, thereby   
   increasing health risks following exposure.3 And, of course, diverse gut   
   microbes are critical components of our gastrointestinal system, helping us   
   process the otherwise hard-   
   to-digest foods we eat.   
      
   There is also a flip side to the xenobiotic-microbiome relationship: the   
   external environment affects the composition of our microbial populations.   
   Even some xenobiotics that were previously thought to be safe may need to be   
   reexamined in light of    
   effects on the microbiome. For example, commonly used food emulsifiers such as   
   polysorbate 80 and carboxymethylcellulose have been reported to adversely   
   affect the microbiome of rodents, predisposing them to chronic inflammation   
   and elevated risk of    
   metabolic syndrome. In one study, mice that drank the emulsifiers in water   
   showed reduced overall diversity of the gut microbiota, decreased   
   representation of generally beneficial Bacteroidales species, and higher   
   numbers of some potentially pathogenic    
   bacteria, such as Ruminococcus gnavus.4 In some rodent strains, exposure to   
   the emulsifiers also thinned the mucus barrier, reducing the physical distance   
   between bacteria residing on the surface of the barrier and gut epithelial   
   cells by more than 50    
   percent. Such alterations can affect the interactions between bacteria and   
   cells of the innate immune system, increasing the risk of inflammation-driven   
   disease. Not coincidentally, microbiomes that have been impoverished or   
   unbalanced by environmental    
   factors often have a skewed bacterial metabolism, affecting their host's   
   energy utilization, hormone status, and control of inflammation.   
      
      
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