Some chronic diseases may be initiated in susceptible individuals by single “germs,” such as acquired immune deficiency syndrome (AIDS) from human immune deficiency virus (HIV), ulcers from Helicobacter pylori, or Lyme disease from Borrelia burgdorferi, but most major chronic diseases do not have a single cause.

Modifiable factors such as smoking, alcohol, lifestyle (e.g., exercise), and nutrition top lists of contributors to cardiovascular disease, cancer, and obesity/metabolic syndrome/diabetes [1]. The view is weakening that genetic makeup predestines one to disease, as understanding grows of potential remediation of biochemical abnormalities underlying genetic predisposition to ill health [11]. Indeed, a small, shrinking fraction of chronic disease is attributed directly to genetic makeup, as recently discussed for cancer [10] and autism [12]. Instead, gene-environment interactions are very plausibly postulated, such as Apolipoprotein-E 4 interactions with heavy metals associated with Alzheimer’s disease [13] or expression of glutathione genes and mercury body burden [14]. Such observations led to development of the field of toxicogenomics, with Judith Stern of the University of California at Davis stating, “genetics loads the gun, but environment pulls the trigger” [15]. In this context, George Church of Harvard Medical School commented that the conversation has evolved from, “Here is your destiny, get used to it!” to “Here is your destiny, and you can do something about it!” [16].

The related field of epigenetics is also coming into focus. Environmental factors ranging from stress to various chemicals may alter methylation of DNA, which in turn modifies DNA expression. Without altering the genetic code, individuals’ morphology and predisposition to chronic disease are affected by exposures early in life or even exposures in previous generations, predating conception [17–19].