Angelina Jolie had her breasts surgically removed because a test discovered that she carried a mutant gene, BRCA1, and feared developing breast cancer. [BR = breast. CA = cancer]
This, of course, is entirely a matter between her, her family and her medical advisers.
But there is a public issue here too. News coverage contain some misconceptions about genes. The connection to emotions is via the central role of chance, fortune or luck in our lives.
Genes determine what and who we are and DNA determines genes. Most people seem to subscribe to this view. Genes are now regarded as the causes of all manner of medical conditions. Find the underlying gene, fix it and the problem is solved.
So widespread is this view that while much attention has been paid to Jolie’s courage, the expense of genetic screening (and its patenting and commercialization), very little attention has been given to the assumptions behind the diagnosis. That’s what I want to do here for this common view about genes is wrong.
Organisms, small and large, develop as a consequence of interactions between their genes, the environment in which they live (i.e., other kinds of organisms), and random molecular interactions within individual cells. Gene mutations or variations are tested for acceptability by that environment, those organisms. Some survive, others do not. This is natural selection.
Certainly, genes are one set of causal agents, but the causation works the other way too. The social and natural environment in which we live can damage genes and their DNA. Ingesting airborne pollutants can do it. So can being grindingly poor and oppressed. This environmentally caused genetic damage can be passed on to the next generation. Why does does this type of gene damage receive so little attention?
The causes of an organisms life are a complex combination of ‘internal’ and ‘external’ forces—although the very distinction is problematic. In no sense is the environment external to us. It is active in shaping what happens within cells. Random cellular movements and chance molecular events add another layer of complexity. We should, then, beware of simple, unitary causation.
BRCA1/2 are oncogenes, genes that regulate cell division. Mutations in these genes make cell division less stable and more likely to occur at a pathologically high rate—but how this works is unknown. Because it is unknown oncologists talk in terms of risk, chance or probability, not causation.
According to Angelina Jolie’s article in the New York Times, inheriting the BRCA1 gene increased her chance of breast cancer to 87% and increased her chance of ovarian cancer to 50%. But 87 and 50 per cent of what? My local weather forecast tells me there is a 60% chance of precipitation tonight. Again, 60% of what? It may rain. It may not. Meteorologists don’t know for sure because several conditions have to be met for it to rain. It’s the same with breast cancer.
Mutations in these genes (BRCA1/2) are not the cause of breast cancer, they are one of several predisposing conditions. Without an explanation of the causal link between the gene mutation and the cancer there is always the possibility that the cancer may be caused by something else. It probably is.
Indeed, when we look to the small print we find a very equivocal diagnosis. Here is what the National Cancer Institute says about BRCA1/s gene mutations:
It is important to note, however, that most research related to BRCA1 and BRCA2 has been done on large families with many individuals affected by cancer. Estimates of breast and ovarian cancer risk associated with BRCA1 and BRCA2 mutations have been calculated from studies of these families. Because family members share a proportion of their genes and, often, their environment, it is possible that the large number of cancer cases seen in these families may be due in part to other genetic or environmental factors. Therefore, risk estimates that are based on families with many affected members may not accurately reflect the levels of risk for BRCA1 and BRCA2 mutation carriers in the general population. In addition, no data are available from long-term studies of the general population comparing cancer risk in women who have harmful BRCA1 or BRCA2 mutations with women who do not have such mutations. Therefore, the percentages given above are estimates that may change as more data become available. Source (my emphasis).
Note family members share genes ‘and, often, their environment’. What might these ‘other genetic or environmental factors’ be?
Let me also add that there are other, more natural, ways of counteracting a mutant BRCA1 gene than a double mastectomy.
I do not know enough about Angelina Jolie’s condition to comment, beyond ‘A person often meets his destiny on the road he took to avoid it’. (Jean de La Fontaine, writing in the 17th century)
I do know, however, that the commerce of medicine exerts an influence on diagnosis. Some medical conditions are practically invented so as to create a market for pharmaceuticals. The genes BRCA1/2 are cloned and patented by Myriad Genetics of Salt Lake City (one of the ‘discoverers’ of these genes). The outcome of litigation on this is pending.
And emotions? For students of the course, look up ‘luck and emotions’ in the index of Ben-Ze’ev’s The Subtlety of Emotions and discovery the emotionality of luck, fortune, chance for yourselves.
NB. The featured image is of a cancer cell about to disappear down a lymph duct.
For those wanting to know more about the debate over the causality of genes, Richard Lewontin is a good place to start for he is the leading critic of biological determinism. For a brief flavour of this debate see What Genes Can’t Tell Us: An Exchange among William D. Foulkes, Hugh Young Rienhoff Jr., and Philip D. Hansten, reply by Richard C. Lewontin. The New York Review of Books, May 26, 2011.