Traditional science regards the body as a collection of cells all carrying identical genetic information. The body cells generate specialized tissues that orchestrate the activity of an entire body. This view has been recently challenged, with new scientific findings showing that the microorganisms we carry in and on our body (microbiome) are not passive passengers. Rather, this huge and diverse community of microbes is intricately linked to the physiological functions of our body, in health and disease.
Each person carries in his body a weight of 2 pounds bacteria. The number of microbes in this volume outnumbers the number of cells in our body, and their genetic complexity is represented by thousands of different bacterial strains. Previously, we scientists thought that these bacteria represent an extra baggage that, at most, may contribute specific metabolites to our body, and protect our body from infection by toxic bacteria.
This simplistic view has been recently contested, prompting us to regard the interactions between bacteria and our cells in a wider context. Furthermore, it turns out that several diseases are not caused by a direct effect on our cells, but rather by disruption of the balance and communication between “our” microbes and our cells. These diseases range from auto-immune diseases to the response of our body to certain anti-cancer drugs. A recent paper in the journal Nature, coming from the lab of Dr. Eran Elinav at the Weizmann Institute, provides yet another unexpected twist in this evolving tale.
Type 2 diabetes is a disease encountered in adults, representing a reduced capacity of the body cells to respond to insulin and take in sugar from the blood (glucose intolerance). It was also shown that obesity may enhance the appearance of type 2 diabetes. To protect from obesity, people in the western world are using large amounts of non-caloric artificial sweeteners (NAS) such as saccharine, sucralose or aspartame.
When lab mice were fed with NAS, they developed glucose intolerance, reflecting the onset of type 2 diabetes. The surprising finding was that this response originated from alterations in the bacteria populating the gut. The response of the mouse cells is interpreted as a secondary outcome of the alteration in the balance of bacterial populations.
Photo by Sunholm via Wikimedia Commons.
The researchers could demonstrate that the primary effect of NAS was on the bacterial population. How? It is possible to grow Lab-mice under sterile conditions following a caesarian birth. Using this process, scientists generate germ-free mice. Mice have the habit of eating the feces of their cage mates. The surprising scientific finding was, that the diabetic defect of a mouse could, be transferred to another germ-free mouse, through their feces. Closer examination revealed that the NAS diet of the original mouse, led to a change in bacterial composition in its intestine. It is not yet clear, however, how this modification elicited the diabetic response in the mouse cells.
Several experiments indicate that these findings are also relevant to humans. The composition of gut bacteria of type 2 diabetes patients shows marked differences from healthy people’s microbial population. Additional findings revealed that when volunteers who do not consume NAS were placed under an NAS diet, their blood sugar levels were elevated within days, and their gut-bacterial-composition was altered. Finally, since the mouse habit of eating feces ignores species barriers, germ-free mice that consumed the feces of the humans who were fed NAS, developed elevated blood-sugar levels.
These findings indicate that a common solution to obesity problems may actually be a cause in the appearance of type 2 diabetes. This will require a serious evaluation of future use of artificial sweeteners.
When a possible cause for a human disease is traced to the bacterial populations we harbor and our inter-relations with them, it provides a hope for cure. The bacterial population in our gut and the diversity it represents, is larger than the genetic complexity of our own cells by orders of magnitude. Yet, because microbes are so different from cells of higher organisms, there are ways of specifically manipulating the bacterial population. This management should not involve total eradication of bacteria by antibiotics, this would be more like a sledgehammer blow. Rather, a gentle probiotic manipulation is required, one that may restore the normal balance of bacterial species.
In the future, we will probably discover more examples of the links between human health and our bacterial populations. Auto-immunity is a prime candidate, but even diseases such as depression may be linked to the microbiome.
This should lead us to view our body as a niche, where in addition to our own cells, we live in a symbiotic manner with our bacterial communities. Those communities represent another essential organ, and as such, the integrity of their composition should be preserved. Following these findings, we should regard the summation of our cells and our microbiome as a “super organism”, containing a genetic diversity that is characteristic to every person.
Benny Shilo is professor of molecular genetics at the Weizmann Institute of Science, where he has served in a variety of leadership, research, and teaching roles for over 30 years. He is also a photographer. His latest book is Life’s Blueprint: The Science and Art of Embryo Creation