Why the new paper by Christakis and Fowler on friendship makes me queasy

I am a neuroscientist, and as a neuroscientist I have a strange belief that most of who we are comes from our brains. My entire career is based around understanding the neural basis of behavior which, I think, is pretty justifiable.

So when I see paper looking at the genetics of behavior, I expect to see at least one or two genes that are directly involved in neural function. A dopamine receptor, probably, or maybe some calcium channels that are acting up. And in one recent paper looking at schizophrenia, that’s exactly what we find! A D2-like dopamine receptor and some glutamate genes. My world is consistent.

But then we get a paper about friendship from Christakis and Fowler who find that friends are more likely to be genetically related to you than chance. So that means that your close friend? Basically a fourth cousin. What Christakis and Fowler have found is a few sets of genes that seem like they might influence friendship. The most important is an olfactory gene which just reeks of pheromones (or possibly hygiene). But the next most important genes? They have to do with linoleic metabolism and immune processes!

Now what am I, as a neuroscientist, supposed to do with that? How do I reconcile my neural view of the world with one where metabolic processes are influencing decisions?

Perhaps I can quiet my mind a little. In a past blog post, I wrote about how social status causes changes in genes related to immune processes. So maybe I can squint and say that okay, really this is an epiphenomenon relating to social status.

But if I’m going to understand behavior – what do I have to know? Do I have to understand literally all of biology? That traits and choices are being affected by what seem to be totally non-brain factors? That my philosophical position of the extended mind is maybe true? That makes me a little queasy.

(End massively speculative rant.)


Christakis NA, & Fowler JH (2014). Friendship and natural selection. Proceedings of the National Academy of Sciences of the United States of America, 111 (Supplement 3), 10796-10801 PMID: 25024208

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Eric Kandel on biological psychiatry

The new (?) science of mind:

In a recent study of people with depression, Professor Mayberg gave each person one of two types of treatment: cognitive behavioral therapy, a form of psychotherapy that trains people to view their feelings in more positive terms, or an antidepressant medication. She found that people who started with below-average baseline activity in the right anterior insula responded well to cognitive behavioral therapy, but not to the antidepressant. People with above-average activity responded to the antidepressant, but not to cognitive behavioral therapy. Thus, Professor Mayberg found that she could predict a depressed person’s response to specific treatments from the baseline activity in the right anterior insula.

These results show us four very important things about the biology of mental disorders. First, the neural circuits disturbed by psychiatric disorders are likely to be very complex.

Second, we can identify specific, measurable markers of a mental disorder, and those biomarkers can predict the outcome of two different treatments: psychotherapy and medication.

Third, psychotherapy is a biological treatment, a brain therapy. It produces lasting, detectable physical changes in our brain, much as learning does…

Matthew State, at the University of California, San Francisco, has discovered a remarkable copy number variation involving chromosome 7. An extra copy of a particular segment of this chromosome greatly increases the risk of autism, which is characterized by social isolation. Yet the loss of that same segment results in Williams syndrome, a disorder characterized by intense sociability.

This single segment of chromosome 7 contains about 25 of the 21,000 or so genes in our genome, yet an extra copy or a missing copy has profound, and radically different, effects on social behavior.

The second finding is de novo point mutations, which arise spontaneously in the sperm of adult men. Sperm divide every 15 days. This continuous division and copying of DNA leads to errors, and the rate of error increases significantly with age: a 20-year-old will have an average of 25 de novo point mutations in his sperm, whereas a 40-year-old will have 65. These mutations are one reason older fathers are more likely to have children with autism and schizophrenia.

The State paper is here. Of course, we should all remember the nature vs nurture debates: the expression of these genes are often influenced by the (social) environment.  I would argue that this intersection will be the most fruitful line of medical research in the coming decades.

On the trail of genetic gastronomy

If I told you that our diets were shaped by our environments, would you be surprised?  If I said that what we ate was shaped by what we liked, would you be surprised by that either?  I should think the answer is no to both questions.  But still, thinking as a neuroscientist the question becomes: what is the neurological basis for why we like the food that we do?  Why do some people enjoy cilantro and some think that it tastes of soap?

It’s clear that our diet has shaped our evolution – just look at the relatively recent emergence of lactose tolerance in European populations.  It is a small leap to assume that the recipes we use may shape how we taste as well – and thus how we experience the world.  A news article in Nature explores the science of taste and recipes:

The Silk Road offers a potential paradise for such genetic exploration. The route traverses massive mountain ranges such as the Pamir and the Tian Shan in central Asia and passes through pockets of the nomadic tribes who originally populated the region, as well as ethnically diverse groups descended from traders who settled en route, often near the roadside inns called caravanserais. These populations did not tend to share their genes, but they did share recipes. Cuisines are remarkably similar along much of the Silk Road — variations on tandoor breads, noodles with vegetable or mutton sauces, and dried or fresh fruit. This means that differences in food preferences between groups are likely to be down to variations in genes rather than in dietary cultures, making them even more appealing to the geneticists…

The scientists have already identified eight variants in known genes, including one for an ion channel involved in sensing spicy-hotness, which are associated with a taste for particular foods. And they have found that variants of the gene for the TAS1R2 protein, part of a sweetness receptor, are associated with a strong liking for vodka and white wine…

There may be bigger scientific stories hiding in the data. Gasparini says that the team is seeing an emerging association in Tajikistani populations between an olfactory receptor gene and both sensitivity to bitter tastes and a tendency to mistake smells. If the finding holds up, it will be the first demonstrated genetic link between smell and taste perception, and it could help to explain how signals from different senses combine to sculpt individual food preferences.