Researchers have long known that brain diseases like mood disorders and anxiety run in families. In recent years, scientists have identified some of the specific gene variants that increase risk for these illnesses. All of this genetic research can almost make biology seem like destiny.

In fact, when I describe the biological and genetic basis for eating disorders, many people commonly say that it's depressing. That if an ED is biological, you can't get better (once an anorexic, always an anorexic). That any offspring will be doomed to repeat my eating disorder. Yet there is no 'anorexia gene,' no 'bulimia gene.' An eating disorder has been, and will always be, a complex interaction between nature and nurture, genes and environment, chemistry and culture.

Although it's a tad more complicated than this, genes essentially make proteins. Some proteins are so evolutionarily ancient and so important to your body that all humans will have identical copies of these proteins--one from their mother and one from their father. Some proteins have evolved more recently, or have greater flexibility in shape and form and function (the sequence of DNA ultimately determines the shape of a protein; the shape of a protein determines what job it does and how well it does that job). These particular proteins can tolerate small mutations, tiny changes to its shape, and so not all humans will carry the same copy. Several different versions of the gene, known as a polymorphism, exist among humans.

These polymorphisms aren't an on/off switch, an indication that you have the disease or you don't. Rather, they indicate that you are more likely to have an eating disorder, depression, anxiety, schizophrenia. This likelihood is also influenced by your life experiences (and the other way around), which can both increase or decrease your risk of becoming ill.

Researchers have found that genetics isn't destiny for those with anxiety disorders. In a study titled "What is an “Adverse” Environment? Interactions of Rearing Experiences and MAOA Genotype in Rhesus Monkeys" that will appear in the May 1st issue of Biological Psychiatry, researchers found that a rich social environment could protect monkeys from the negative effects of a gene polymorphism linked to anxiety. A press release summarized the research as follows:

There are some circumstances in a child's development – such as abusive parenting – that everyone would agree constitutes "adversity." This study suggests, however, that other, more subtle features of the broader social environment influence development, and that genes that affect our behavioral responses are sensitive to these influences. So even though an infant may be reared with its nurturing mother, the relative absence of other social partners, for both the mother and the infant, can result in the infant developing an anxious style of responding to challenges, particularly if it possesses a "risky" genotype.

Of particular significance, said senior author John Capitanio, Ph.D., is "that animals that were raised in rich, complex settings with mothers, other kin, and peers, were completely protected from the potentially deleterious effects of having the 'risky' form of the MAOA gene."

This isn't to say that genes aren't important--because they most certainly are. But we're just touching the tip of the iceberg with our understanding of how our genes interact with our environment. Any biological children that I have will be at a higher risk of developing an eating disorder. That's just reality. But I can make sure that they understand the dangers and futility of dieting, that they understand the true meaning of healthy eating and the range of shapes and sizes that human bodies come in. I can also step in at the first sign of trouble and make sure that he or she begins eating properly and maintaining an appropriate weight. I don't know for sure that this will protect them, but it can't hurt to try.