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The external environment's effects upon genes can influence disease, and some of these effects can be inherited in humans. Studies investigating how environmental factors impact the genetics of an individual's offspring are difficult to design. However, in certain parts of the world in which social systems are highly centralized, environmental information that might have influenced families can be obtained. For example, Swedish scientists recently conducted investigations examining whether nutrition affected the death rate associated with cardiovascular disease and diabetes and whether these effects were passed from parents to their children and grandchildren (Kaati et al., 2002). These researchers estimated how much access individuals had to food by examining records of annual harvests and food prices in Sweden across three generations of families, starting as far back as the 1890s. These researchers found that if a father did not have enough food available to him during a critical period in his development just before puberty, his sons were less likely to die from cardiovascular disease. Remarkably, death related to diabetes increased for children if food was plentiful during this critical period for the paternal grandfather, but it decreased when excess food was available to the father. These findings suggest that diet can cause changes to genes that are passed down though generations by the males in a family, and that these alterations can affect susceptibility to certain diseases. But what are these changes, and how are they remembered? The answers to questions such as these lie in the concept of epigenetics.

Existing mouse models of lethal Ebola virus infection do not reproduce hallmark symptoms of Ebola hemorrhagic fever, neither delayed blood coagulation and disseminated intravascular coagulation, nor death from shock, thus restricting pathogenesis studies to non-human primates. Here we show that mice from the Collaborative Cross exhibit distinct disease phenotypes following mouse-adapted Ebola virus infection. Phenotypes range from complete resistance to lethal disease to severe hemorrhagic fever characterized by prolonged coagulation times and 100% mortality. Inflammatory signaling was associated with vascular permeability and endothelial activation, and resistance to lethal infection arose by induction of lymphocyte differentiation and cellular adhesion, likely mediated by the susceptibility allele Tek. These data indicate that genetic background determines susceptibility to Ebola hemorrhagic fever.

Your mother's DNA may have determined your eye color, but some traits that you thought came from her may instead have come from the DNA of bacteria she passed on to you soon after birth, a new study finds. The study found that a mother mouse can pass along to her offspring a susceptibility to intestinal disorders, such as inflammatory bowel disease, by way of a gut-residing bacterium called Sutterella, the researchers reported in the journal Nature on Feb. 16.

The United States is now experiencing what promises to be one of the worst outbreaks of measles since the virus was declared eliminated from the country in 2000.  It began in early January at Disneyland Resort in Anaheim, California, and has since spread to 14 states and infected 84 people, according to the U.S. Centers for Disease Control and Prevention (CDC). Measles, caused by a paramyxovirus from the genus Morbillivirus, is one of the most contagious diseases in the world, infecting more than 90% of susceptible hosts that come in contact with an afflicted individual. In the absence of widespread vaccination, the average person with measles will infect an average of 12 to 18 other people; in contrast, Ebola is typically transmitted to 1.5 to 2.5 people.

Many factors are known to be important in disease causation and these can include an individual's age, gender, genetic make-up and environmental factors that they have been exposed to, such as infectious agents or chemicals.

dice rolling game lesson plan for multifactorial disease cardiovascular risk

NIH Genetic Variation Activity- Are you susceptible? Dice rolling game to model cardiovascular risk. -pdf for handouts

2 min video intro of risk factors/ complexity of disease -poor audio but good examples