117sulfate and mucin are the main sources of sulfate uptaken by B. thetaiotaomicron.
Interestingly, enhanced mucus degradation was considered a couse of reduced gut
lining integrity (Rey et al. 2013 ).
The gastrointestinal tracts of centenarians were recently found to have less
abundant sulfate-reducing bacteria such as Desulfovibrio, but have much plentiful
butyrate-producing bacteria such as Clostradia (Wang et al. 2015 ). Nevertheless,
it is currently inconclusive whether obesity is caused by the dysbiosis between
sulfate-reducing bacteria and butyrate-producing bacteria. However, we can image
that the trace amount of hydrogen sulfide that is released by less abundant sulfate-
reducing bacteria might be beneficial to extend lifespan (Qabazard et al. 2014 ),
but overproduction of hydrogen sulfide by the overgrown sulfate-reducing bacteria
might induce the cancerous alteration (Attene-Ramos et al. 2007 ) and initiate an
adipogenetic process (Tsai et al. 2015 ) directly or indirectly through conversion of
nitrate/nitrite to large-amount NO (Vermeiren et al. 2012 ).
Given that gut bacteria, especially Gā, are responsible of LPS leakage and
inflammation induction, how to prevent such an adverse outcome? The most
important consideration should be prevent the dysbiosis of gut microbiota. For
this purpose, you should maintain a balanced daily diet that contains low fat
and high fiber. If you are an obese person or a patient with type II diabetes, you
should restrict your calorie uptake, and recover your microbiota homeostasis. For
example, it is beneficial to eat more fiber-rich vegetables and fruits to nourish the
butyrate-producing bacteria, but eat less meats or chondroitin sulfate-rich foods to
avoid the overgrowth of sulfate-reducing bacteria.
Interestingly, dietary yeast has been reported to reduce hepatic steatosis, obe-
sity, and type II diabetes in mice (Everard et al. 2014 ) as well as neuroinflamma-
tion in mice (Takata et al. 2015 ), suggesting that yeast might narrow the occupying
space by bacteria, and compromise LPS-induced inflammatory diseases. If this
situation is also confirmed in human, supplementation with dietary yeast as an
probiotic alternative to bacterial prebiotics might be helpful to decrease the risk of
obese, fatty liver, and type II diabetes.
7.3 The Origin of CSC: Next Breakthrough
on Tumorigenesis/Carcinogenesis?
Regardless of debating on the concept of CSC, tumorigenesis/carcinogenesis
must experience the extensive genetic alteration and chromosome instability. It is
known that the chronic inflammation is linked to cancer by rehearing the scenar-
ios of tumor initiation, promotion, malignant conversion, invasion, and metastasis
(Grivennikov et al. 2010 ). How inflammation causes tumor/cancer remains largely
unknown, but many types of tumor/cancer are known to be originated from a long-
term immune activation that upregulates proinflammatory cytokines and triggers
NO burst. Given that NO is implicated in inflammation-originated tumor/cancer,
7.2 Low-Grade Inflammation as an Essential Consequence of Obesity?