Since this book was written, many fascinating papers have been published that present results very relevant to the various topics in this book. I will attempt to summarize some of them over the next few weeks so as to bring us up to date. For example, regarding the topic of Chapter 4, “Prenatal origins of adult health and disease”, Sheau-Fang Ng and colleagues at the University of New South Wales in Australia report (Nature 467:963, ’10) that feeding adult male rats a high fat diet increases their weight and body fat, and induces symptoms of diabetes – all of which is expected. The more interesting finding is that the daughters of these males also reproducibly develop a diabetes-like condition. This indicates that the father’s diet alters the development of his sperm. The authors suggest that the mechanism for this effect is an epigenetic alteration of the sperm DNA – not a change in DNA sequence but a chemical modification of the type discussed in Chap. 4. Another interesting question these results raise is whether the daughters will now pass this diabetes condition to their offspring, as has been shown to happen under other circumstances (see also plate 4 in the book). If this transgenerational effect holds true for human fathers, the potential impact for disease is enormous, given the epidemic of obesity we are observing in the developed world.
Regarding the possible role of the bacteria in the gastrointestinal tract in causing or exacerbating some symptoms of autism (Chap. 7), a recent paper from Sydney Finegold and colleagues at the VA Medical Center West in Los Angeles (Anaerobe 16:444, ’10) reports that the “microbiome” assessed in stool samples from severely autistic children has a number of striking differences from stool samples taken from typically developing children. The change in bacterial composition in the gut could be due to stress that the children experience, as it has been shown in mice that social stress can alter the microbiome (Bailey et al., Brain Behavior and Immunity ‘10). On the other hand, it may work in the opposite direction, as changing the composition of bacteria in the gut can alter the level of stress hormone as well as a component of the inhibitory system in the brain. John Bienenstock and colleagues at McMaster University in Canada and John Cryan at the University of Cork in Ireland found that feeding mice Lactobacillus rhamnosus caused them display less anxiety under stressful conditions than mice on a standard diet (Proceedings of the National Academy of Sciences USA 108:16050, ’11). Interestingly, the authors showed that the effect of the bacteria on the brain requires the presence of the vagus nerve, which innervates the GI tract, among other organs. This is similar to the finding discussed in Chap. 2: the ability of infections in peripheral tissues to cause depressive or “sickness behavior” in rodents is mediated in part by the vagus nerve. Regarding autism, a recent and quite large study of 90 autism spectrum disorder (ASD) patients by Laura de Magistris and colleagues at the Second University of Naples reported that 48% of these patients have GI problems, and that the incidence of increased intestinal permeability (“leaky gut”) is 8-fold higher in ASD patients than in controls. This raises the possibility that GI or bacterial products could leak into the circulation and thereby alter behavior of ASD patients by directly or indirectly influencing the brain.