[ExI] 'capitalism' genes was breeding cats

[Damien Broderick]

On 6/9/2010 7:23 PM, Damien Broderick wrote:

>> If behavior does not come ultimately
>> from genes, then were*does*  it come from?
>
>  From a complex interaction between genetic instructions, phenotypic
> expressions of those instructions in a given environment, and culture

example:


"New Associations between Diabetes, Environmental Factors Found by Novel 
Analytic Technique"
by
Krista Conger


May 20, 2010; (Stanford) -- Got diabetes? If so, you probably know that 
the adult-onset form of the disease can be triggered by, among other 
things, obesity and a fatty diet. You’re also more likely to develop 
diabetes if other family members have it. But a new study by researchers 
at the Stanford University School of Medicine suggests that you should 
also begin looking suspiciously at other aspects of your life ­ like 
your past exposure to certain pesticides or chemicals and even one form 
of Vitamin E.

          In fact, the association of some of these so-called 
“environmental” cues with diabetes surpasses that of the best genetic 
markers scientists have identified for the disease.

          Identifying relationships between a person’s environment (such 
as tobacco exposure) and specific health repercussions (such as cancer) 
is nothing new. Epidemiological studies of large groups of people have 
been doing just that for decades. But they are limited in their ability 
to assess the hundreds or even thousands of variables that comprise the 
intricate fabric of our everyday lives. (What’s your risk of heart 
disease if you smoke sparingly and eat fatty foods, but are also a 
marathoner?) They’re also not open-ended: The researcher has to begin 
with presuppositions about possible relationships. (Does Folic Acid 
prevent birth defects?)

          In this new study, the scientists relied instead on an 
unconventional approach that treats environmental variables as “genes.” 
That conceptual shift allowed them to use some of the same techniques 
initially developed to identify the many sections of DNA throughout the 
genome that might contribute to disease development. Bioinformatics 
expert Atul Butte, M.D., Ph.D., Assistant Professor of Pediatric Cancer 
Biology, compared the data generated by the new approach to the amount 
and types of information gleaned from a DNA microarray.

          “This approach catapults us from being forced to ask very 
simple, directed questions about environment and disease into a new 
realm in which we can look at many, many variables simultaneously and 
without bias,” said Butte, who is also director of the Center for 
Pediatric Bioinformatics at Lucile Packard Children’s Hospital. “In the 
future, we'll be able to analyze the effect of genes and environment 
together, to find, perhaps, that a specific gene increases the risk of a 
disease only if the person is also drinking polluted well water.”

          Specifically, in this study, Butte and his coworkers used the 
technique to identify a previously known association between people with 
Type-2 Diabetes and a class of organic compounds called  polychlorinated 
biphenyls (PCB's), commonly used for many applications until the late 
1970's. They also uncovered a strong, but unexpected, relationship 
between diabetes and high levels of a form of Vitamin E called Gamma 
Tocopherol, which is prevalent in fruits, vegetables, nuts and milk.

          The scientists are careful to caution, however, that an 
association doesn't necessarily mean that Vitamin E or pollutants cause 
Type-2 Diabetes, and that more research is needed to fully understand 
these complex relationships.

          Butte is a senior author of the research published May 20th in 
the on-line journal PLoS ONE. The genetic studies on which the research 
is based are called “genome wide association studies” or GWAS. In a nod 
to its origin, the scientists coined the term “environment wide 
association studies,” or EWAS, for the new technique. They expect that 
EWAS will be useful in the analysis of many complex diseases.

          “We've known for decades that environmental factors play a 
major role in diseases like diabetes, cancer and heart disease,” said 
Jeremy Berg, PhD, director of the National Institute of General Medical 
Sciences, which partially supported the work. “By enabling us to measure 
the impact of these factors, this new approach will shed light on how 
genes and the environment influence our health and could provide 
insights into new ways to control some of our nation’s most serious 
health problems.”

          Graduate student Chirag Patel conceived of, designed and 
executed the computer software for the EWAS. He, Butte and associate 
professor of medicine Jayanta Bhattacharya, M.D., Ph.D., used existing 
population studies conducted from 1999 to 2006 by the U.S. Centers for 
Disease Control and Prevention as part of the National Health and 
Nutrition Examination Survey. The researchers realized that the 
databases contained a goldmine of information, including the levels of 
pollutants and vitamins in subjects’ blood and urine as well as clinical 
measurements such as fasting blood sugar levels.

          In all, the scientists analyzed the relationship of 266 unique 
environmental variables to the likelihood that a person’s fasting blood 
sugar level was 126 mg/dL or higher (between 70 and 110 mg/dL is 
considered normal). Higher-than-normal blood sugar levels after an 
overnight fast are a telltale sign of diabetes. They adjusted for the 
subjects’ age, gender, body mass index, socioeconomic status and 
ethnicity. Finally, they grouped related variables into 21 classes ­ 
such as dioxins, polychlorinated biphenyls, phthalates, etc. ­ similar 
to how individual genes are assigned to chromosomal units in GWAS.

          Butte and his colleagues found that people with relatively 
higher levels of the pesticide-derivative heptachlor epoxide (a chemical 
whose use stopped in the ’80s but is still prevalent in food, soil and 
water) in their blood were more likely than those with lower levels to 
also have high fasting blood sugar levels (Odds Ratio = 1.7). The same 
was true for those with high levels of PCB's (OR = 2.2) and the 
Gamma-Tocopherol form of Vitamin E (OR = 1.5). In contrast, high 
beta-carotene levels were slightly protective (OR = 0.6).

          Scientists have recently made large strides in measuring 
genetic associations to complex disease, but are still far from using 
genes to predict risk for complex chronic diseases or even plan 
preventive measures. On the other hand, our environmental profile is 
potentially more modifiable and also may provide a more complete model 
of disease risk when combined with genetic information.

          “Studying relationships between a person’s environment and 
their disease burden in this manner is going to be far more impactful,” 
said Butte. “We can now imagine what it might be to look at everything 
in the environment, in the same way that we've been doing with the 
genome for the past decade. Imagine one day wearing a chip on your 
clothing that assesses your exposure to hundreds or thousands of 
environmental toxins. You could bring that in to your annual physical 
and you and your doctor could incorporate the information into 
discussions about disease risk and prevention.”

          The researchers are planning to conduct similar EWAS studies 
focused on other diseases, including cancers. They'll also try to 
reproduce the data from the National Health and Nutrition Examination 
Survey studies on specific populations in California.