Obesity and Some Behavioral Biology

All right, weight regulation is really damn complex.  I am going to admit that upfront.  It involves many of the things we’ve talked about on this website in reference to brains—the body, multiple brain systems, complex interactions, and so forth.  Sure, most of the research does not include much context or culture or even environmental interaction, but then again, the research is aimed at getting at some basic biology, at understanding the mechanisms and processes involved in weight regulation.

So, what do we have?  In no particular order other than my impressions from reviewing the literature, (1) the importance of body-based systems in appetite and weight regulation, (2) the usefulness of allostasis in understanding weight, energy, eating and activity regulation; (3) satiation and appetite as more important in obesity than energy balance, which generally plays a modifying role; (4) the need to consider weight gain and weight loss separately; (5) the role of physical activity might play in driving weight regulation; and (6) the considerable limitations of “will power” to affect any of the above points, due to how our brains and bodies are set up and the considerable mismatch between our western ideology of self and how we actually work.

In this post I’ll cover stuff on the first four.  See Greg’s comment on Genetics and Obesity for more on #5-Activity, and for now, I hope that the ability of cognitive control over hormone release and lower brain systems should at least be fairly obvious.  (As for getting all this done by yesterday, I had a senior colleague spring a surprise guest lecture on me—so that meant dropping lots of on-going stuff to get that ready… Excuses, excuses.) 

So, body-based systems.  Two hormones, leptin and ghrelin, play a powerful role in shaping energy regulation, eating and weight.  The trick is that leptin is released by white adipose tissue (fat) and gherlin by the stomach and intestine.  Both have direct effects in our brains, overturning our general view of the brain as a master organ.  Leptin and gherlin act in concerted fashion, like many regulatory systems in the body (e.g., sympathetic and parasympathetic peripheral nervous systems).  For example, Zigman and Elmquist (2003) (pdf) liken them to the Yin and Yang of body weight control.  They characterize leptin as “a molecular signal of energy abundance” and gherlin as “an important indicator of energy insufficiency.”  In mice, increasing circulating leptin can decrease food intake, while gherlin stimulates feeding.  However, neither has proven broadly effective as dietary drugs, because weight and energy regulation are not driven by one sole hormone except in rare genetic deficiency cases.

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Trust your hand, not your eyes

Blogging on Peer-Reviewed ResearchDaniel forwarded me a link to the story, The Hand Can’t Be Fooled, Study Shows, from Science Daily. The story is a short piece about research by Ben-Gurion University of the Negev Psychologist Tzvi Ganel and his colleagues on how the “Ponzo” illusion affects visual perception. The “Ponzo” illusion occurs when two equal line segments appear to be of different lengths because they are superimposed on a pair of converging lines; like two lines hovering over train-tracks disappearing into the distance appear to be of different lengths, as you can see from this illustration I took from the BBC. Ponzo illusion

Ganel and his colleagues ‘hooked participants’ index finger and thumb to computerized position tracking equipment and asked them to grasp the objects with their fingers. Even thought the object appeared to be larger (or smaller) than it really was, the size of their grasp reflected the object’s real rather than apparent size. For good measure, the researchers arranged the illusion so that the object that appeared to be the smaller of the two was actually the larger of the two.’

Ganel argues that the experiment provides compelling support for the ‘two visual systems’ hypothesis put forward by Mel Goodale and David Milner about a decade ago (see Goodale and Milner 1992; Milner and Goodale 1995; for an overview, see Goodale and Humphrey 2001). According to Goodale and Milner, one visual system processes input for object and color recognition, recognizes objects no matter what the perspective of the viewer, and uses conscious parts of the brain; another visual system judges spaces, movement and object trajectories in egocentric space in order to control body movement, and does not necessarily access conscious thought. I’ve written about the two visual systems hypothesis elsewhere in a book chapter that just came out (Downey 2008), so Daniel probably recognized that I’m a bit of a fan of the ‘tectopulvinar’ (motion control) visual system. (For a quick overview of the two systems, this is a good set of diagrams and explanation.)

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Wednesday Round Up #2

On Brains

Susan Greenfield, Bewitched by Bacchae
Meaning, neuronal connections, and Euripides—perfect!

Robert Krulwich and Jad Abumrad, Radio Lab: Into the Brain of a Liar
How big was your fish?  Big-time liars have “more connections in the part of their brains responsible for complex thinking”

Charles Choi, Tiny Brain-Like Computer Created
This chip has dendrites!

Lauran Neergard, Study: Creativity Jazzes Your Brain
Stick a keyboard and a jazz musician in an fMRI, and this is what you get

The Internet

Gamespot, Study Uncovers MMORPG Gender-Swapping Epidemic
“54 percent of all males and 68 percent of all females “gender swap”–or create online personas of their opposite sex”

David Pogue, How Dangerous Is the Internet for Children?
Not as dangerous as the media sometimes says.  Surprise, the context of how you manage the Internet and your children at home makes a big difference in how they interpret what’s online

General Interest

Penepole Green, What’s In a Chair?
Psychiatrists’ offices matter!

Also see Vaughan’s take on this article at Mind Hacks

Nicholas Cristakis, Social Networks Are Like The Eye
The dynamics of social networks

Kevin Lewis, Uncommon Knowledge: Surprising Insights from the Social Sciences
The Boston Globe’s own round up

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Glucose, Self Control and Evolution

Galliott et al. published a 2007 article entitled “Self Control Relies on Glucose as an Energy Source: Willpower Is More Than Self Control” (pdf here). Recently Vaughan at Mind Hacks and Dave at Cognitive Daily have taken up the topic with some creative posts.  Vaughan writes that Resisting Temptation Is Energy Intensive, focusing on the role of attention and the prefrontal cortices.  Dave posts on Practicing Self-Control Takes Real Energy, and includes a recreation of the research procedure (with video) and an informative summary.  I also mentioned some of this research in a previous post on Willpower as Mental Muscle.

What I want to add today is that this sort of research has implications for our understanding of brain evolution and for social problems like obesity and addiction.  Focusing attention and using one part of your brain against another part, that takes significant energy.  The brain is already our most energy-intensive organ, so adding the demands of “self control” on top of that is likely to have presented some adaptive issues in the past.  Put differently, it’s unlikely to expect that we’ve evolved to be able to maintain self control over extremely long periods of time (say, months), simply because such problems rarely presented themselves in the past (there were few adaptive benefits) and because the energetic costs of doing so would have been quite high.

Diets are often marked by periods of effortful weight loss, followed by a slide back, where weight is regained.  That pattern is not simply a matter of mind over matter, of willpower so we can match a cultural and cognitive ideal.  It’s hard for people to maintain sustained mental efforts, it costs energy, and there’s little evolutionary reason to expect everybody’s brains to suddenly begin cooperating with what our culture tells us we should be able to do.

Sapir-Whorf hypothesis was right… about adults

Blogging on Peer-Reviewed ResearchNature recently carried a short piece, Perception coloured by language (written by Kerri Smith), on several research papers, including one by Paul Kay at the University of California, Berkeley (well, actually, Kay is also the co-author on another of the three papers, too). The original article, in the Proceedings of the National Academy of Sciences (US), is not openly accessible, but the abstract is here (Franklin et al. abstract). We’ve had a number of related posts on Neuroanthropology, including Daniel’s Language and Color, and my piece that the title of this one references, Sapir-Whorf hypothesis is right… sort of?

The subject of language learning’s effect on the brain is an especially important one for a number of reasons to us at Neuroanthropology (other than our tendency to flog the occasional dead horse); not only is language a frequent surrogate for more amorphous concepts like ‘culture,’ but it is also one of the capacities that, due to the work of Chomsky, is frequently believed to have innate foundations in the brain. Chomsky’s discussion of a language function innate in all human brains provides one of the foundational texts for much broader, sweeping assertions about ‘massive modularity’ in the brain covering a wide variety of functions.

Work by Kay’s team focused on the brain hemisphere used to classify colours. They tested subjects by showing them coloured targets randomly in their visual fields, and then seeing how long subjects could shift attention to the targets. As Smith writes:

It is well known that in adults, perception of colour is processed predominantly by the left hemisphere, which is also where most people process language. Studies have shown that the language one speaks can have an impact on the colour one sees.

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Glutamate and Schizophrenia

The NY Times has an article, Daring to Think Differently about Schizophrenia, about research on glutamate, schizophrenia, and drug development.  In addiction research, there is also increasing consideration of the role of glutamate, moving beyond the dopamine-centered models.  Glutamate-targeted drugs “might help to treat the cognitive and negative symptoms of schizophrenia. Drugs currently on the market do little to treat those symptoms.”  Here are some early quotes from the article:

Dr. Schoepp and other scientists had focused their attention on the way that glutamate, a powerful neurotransmitter, tied together the brain’s most complex circuits. Every other schizophrenia drug now on the market aims at a different neurotransmitter, dopamine.”

“Glutamate is a pivotal transmitter in the brain, the crucial link in circuits involved in memory, learning and perception. Too much glutamate leads to seizures and the death of brain cells. Excessive glutamate release is also one of the main reasons that people have brain damage after strokes. Too little glutamate can cause psychosis, coma and death.  ‘The main thoroughfare of communication in the brain is glutamate,’ says Dr. John Krystal, a psychiatry professor at Yale and a research scientist with the VA Connecticut Health Care System.”