In
biological terms, the word “environment” means the host of influences, besides
DNA, which affect our inherited genes, turning them on and off, and having
marked consequences for human development and health. These influences include
viruses, neo-natal injury, exposure to toxic substances, auto-immune processes
(where cells mysteriously destroy each other) or changes involved in aging.
They also include the effects of countless variables arising from our
interactions with others and with the world around us.
Two theories
are now an important focus of research – the virus theory and the
neuro-developmental theory.
Virus Theory: The fact that similar risk factors
operate for both schizophrenia and mood disorders suggests that these illnesses
have some
common infectious causes. There is the well-documented fact that an excess of
births occur, in the winter and spring months, of people who later develop these
illnesses. This means there may be a seasonal “slow virus” involved. Mothers
may have caught the virus during pregnancy; the virus could affect the fetal
brain, but pathological changes would not show up until many years after birth.
Being raised
in a city is another shared risk factor for people who develop these illnesses;
areas of dense population mean that viruses are more easily transmitted.
Moreover, pregnant women known to have viral infections, or compromised immune
systems due to malnutrition, are at much greater risk of having children who
develop these illnesses.
Recent
studies at the National Institute of Mental Health have yielded the first
antibody evidence that the common parasitic infection, toxoplasmosis, doubles
or triples the risk for schizophrenia. Pregnant women can get this infection
quite easily from undercooked meat, unwashed, hands, or from handling cat
litter. The risk for schizophrenia stems from the mother’s immune system
antibody response which can affect the fetus.
Neuro-developmental Theory: There is growing consensus among
researchers that schizophrenic illness results from damage to the frontal
lobes, in utero or during early childhood, which lies dormant until the late
teens when the frontal cortex of the brain reaches full development. In other
words, as one researcher recounts, the illness “begins before birth, spares the
brain through childhood, only to erupt in psychotic breakdowns and profound
disability at the beginning of productive life.” This “silent lesion” could be
hereditary, or the result from epigenetic factors such as birth complications,
head injuries (both of which occur at an unusually high rate in schizophrenia),
viruses, toxins, or auto-immune reactions – all of which could affect a
vulnerable neonatal brain.
It is now
widely believed that central nervous system maturation plays a crucial role in
this illness in late adolescence, as frontal and limbic circuits do not reach
functional maturity until early adulthood. In this sense, then, schizophrenia
is an organic brain disease resulting from an early injury whose consequences
are there, from the beginning, but do not “unfold” or make a behavioral impact,
until the time when cortical connections fully develop. Various perinatal forms
of neuro-developmental damage may also occur in bipolar disorder and
depression.
An awareness
of the effects of brain biology, genetics, and environmental factors could
hopefully lead to a greater understanding of people with mental illness. It
could lead families and people with mental illness to actively seek treatment.
It can reassure people that mental illness is not caused by character weakness,
the devil, or poor parenting. It is a treatable condition. There is hope.
