Abstract
The reduction of excessive weight remains a major public health challenge, with control currently limited to a calorie reduction strategy. Currently, attempts are being made at revisiting the fibre hypothesis based on the African studies of Denis Burkitt, that the lack of dietary fibre in the modern diet was responsible for the occurrence of obesity and many of the other non-communicable diseases of what he called “Western civilization”. However, the dilemma is that Burkitt himself stressed that other peoples of his day, such as the Maasai, remained healthy without consuming such high fibre diets. Equally, the present obesity epidemic is accompanied by diseases of a malfunctioning immune system and of poor mental health that do not seem to be adequately explained simply by a deficiency of dietary fibre. Though unknown in Burkitt’s day, an increasing degradation of a mutualistic intestinal microbiome would offer a better fit to the observed epidemiology, especially if the microbiome is not effectively passed on from mother to child at birth. Taking the broader view, in this article we posit a view of the microbiome as a cofactor of mammalian evolution, in which a maternal microbial inheritance complements the parental genetic inheritance of the animal, both engaging epigenetic processes. As this would require the microbiome to be fully integrated with the animal as it develops into an adult, so we have a meaningful evolutionary role for the microbiome–gut–brain axis. By a failure to correctly establish a microbiome–gut interface, the inhibition of maternal microbial inheritance sets the scene for the future development of non-communicable disease: compromised immune system function on the one hand and dysfunctional gut–brain communication on the other. The basic principle is that the fully functioning, diverse, microbiome achieves interkingdom communication by the generation of messenger chemicals, semiochemicals. It is envisaged that the in situ detection of these as yet ill-defined chemical entities by means of an ingestible sensor would indicate the severity of disease and provide a guide as to its amelioration.
Highlights
The control of obesity has been a major unmet medical need for more than a century [1].In the wake of the failure of 20th century behavioural and dietary treatments [2] the economic cost of the on-going obesity epidemic is substantial and is steadily increasing [3].The aetiology remains unknown but, for whatever the underlying reason, has traditionally been ascribed to either eating too much food or doing too little exercise
We suggest the following reasons: diversity of maternal microbial inheritance allows the microbiome of the child to alter with the manifold variations of its own genetic inheritance, as observed for blood group antigens, for example [29]; diversity allows the microbiome to express the full range of mobile genetic elements liberated from external microbes by the action of phage viruses [30]; and redundancy, in the engineering sense of the word, means that the failure of one set of microbes, for whatever reason, allows a second set to take over and perform the same function
The effect of a degraded microbiome–gut–brain axis is to increase the propensity for the development of non-communicable disease as a child develops into an adult [51]
Summary
The control of obesity has been a major unmet medical need for more than a century [1]. While there is little doubt that obesity is fundamentally due to eating too much food that is too digested, what constitutes too much for each individual is a matter of intense current research, including the twin principles of the “personal fat threshold” [11], and of the microbes inherent within the “personalised nutrition” concept [12] This present article considers the role of the intestinal microbes in rendering the population as a whole more vulnerable to weight gain, within the context of the other non-communicable diseases that are steadily rising across the modern world [8]. In the context of the ongoing interest in the microbiome, with the body and its attendant microbes acting as one unit, we first decided to revisit the earlier account of Denis Burkitt
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