Though unknown, the causes of these urban-rural differences have been hypothesized to include, e.g., infections, diet, toxic exposures, social class, or an artefact due to selective migration.
Other pathogenic mechanisms of TRPC6 mutation that have been hypothesized include altered channel regulation, altered interaction with other slit diaphragm proteins, and altered protein turnover [ 3].
The biologically plausible associations that have been hypothesized include total energy consumption, altered androgen metabolism, oxidative stress, specific fatty acid consumption and pesticide intake.
It has been hypothesized that CTCs include putative precursors that initiate distal metastases.
Extrinsic factors contributing to resistance have also been hypothesized, including multidrug resistance and microenvironmental factors [14], [15].
Various mechanisms underlying these associations have been hypothesized, including fetal undernutrition, genetic susceptibility and postnatal accelerated growth.
Although the natural history of prostate cancer is currently unknown, multiple etiologies have been hypothesized, including genetic defects [4], [5], [6].
Some mechanisms to explain the healthful effects related to caffeine on preventing the MetS have been hypothesized, including sympathetic over activation, antagonism of adenosine receptors, increased norepinephrine release, a sympathomimetic agent that is capable of increasing energy expenditure, and promoting the loss of body fat [ 55, 56].
Several reasons for poor compliance have been hypothesized, including disease symptoms (e.g., grandiosity, paranoia, problems with accurate recall), treatment-emergent side effects, substance abuse, lack of support systems to encourage medication compliance, psychostressors, and poor patient-provider relationships [ 14, 15].
