Saturday, May 11, 2013

Remember the Hypothalamus?



I’m thrilled to see the hypothalamus back in the news.  I've been intrigued for years with this pea-sized area deep in the brain that plays such an important role in our relationship to food.  Indeed, the title of a New York Times article that appeared on Sunday (April 28, 2013), “The Brain:  Our Food Traffic Controller,” echoed a title from the same paper I quoted in the late 1960s:  “Obesity is Traced to Signal Failure” (January 23, 1968).  Back then, long before the days of imaging, it was found that the hypothalamus provided “internal eating cues” to tell us when to eat and when to stop.  The mechanism might get out of whack and “set so high that normal amounts of food no longer satisfy.”  The old source proposed a complimentary theory that, without appropriate signals from within, people might become overly dependent on “external eating cues” instead.  To me, that meant diets, paying too much attention to other people’s idea of what we ought to eat.  And, I’m still convinced the stubborn, long-term and constantly escalating problem of overeating owes a great deal to this. 

An approachable synonym for the hypothalamus was coined in those days:  “appestat.”  I pictured a switch on the wall to regulate heat in the winter and thought the workings of the human brain had to be more elegant than that.  The term is defined now as:  “the neural center in the brain that regulates appetite and is thought to be in the hypothalamus.” My italics emphasize the difficulty in pinning down exactly what goes on in there when we eat.  And that’s what Kathleen A. Page and Robert S. Sherwin, authors of this Sunday’s piece, are working on.

Page and Sherwin call the hypothalamus a “primitive brain region” that evolved to support survival in a time when food was scarce and obtaining it was a lot more labor-intensive than a trip to either McDonald’s or Whole Foods.   As scientists and endocrinologists, they have been focusing on observable responses in the human brain to glucose and to fructose.  For example, they find that glucose – an energy source vital to brain activity – while calorically equal to fructose (no commercial pun intended), does not taste as sweet as its relative, and yet is associated with greater feelings of fullness and satisfaction.  Fructose, on the other hand, gets screened out somehow by the liver; not much of it reaches the brain, so the “appetite and reward areas remain active.”  Thus, the notion that sugar is sugar may be nutritionally accurate, but neurologically, it may be worth another look.

I find this stuff fascinating.  New technology allows even the layperson an appreciation of the elegance and complexity we all know is there.  According to Page and Sherwin, the hypothalamus constantly monitors blood glucose, hormones, and various contributors to metabolism that are intricately involved in energy maintenance, appetite and satisfaction.  The “integrated circuit” they outline includes “brain areas that control taste, reward, memory, emotion and higher-level decision making.” They question how this wealth of new information can be used to help combat the epidemic of obesity, but seem in no rush to judgment.  The work is just starting.

Dr. Norman Jolliffe at Columbia University’s School of Public Health wrote a piece available on the web entitled “How to Reset Your ‘Appestat’ and Reduce Hunger.” I cheer the following quote from his first paragraph: “Infants do not have the natural ability to overeat. Overeating is a learned behavior that needs to be unlearned to reduce hunger.”  Wow!  I couldn't have said it better, and I’m so glad he did.
Then, he loses me – fast.  “Eat less food more often to reduce hunger;”  “Choose lean proteins and healthy fats to keep your appetite at bay;” “Skip simple carbohydrates that cause sharp drops in blood glucose and cravings for more;” “Exercise often, but not for weight loss;” and “Skip the scale.”  There is not a single suggestion here without merit – even though 7 meals a day absolutely does not work for me, and I personally find the Atkins diet onerous.  What I do object to – have always objected to – is the list of guidelines that are nothing but “external cues” as far as I can see.  Jolliffe makes an exquisite case for each item on his programme.  Clearly, it works for him.  But, how can one re-activate one’s own primal, evolutionarily-tested internal cues while following someone else’s?  Sorry to criticize, but I think that’s the wrong way to go.

It’s not going to be so quick and easy to glean solutions to overeating from what we have begun to learn about the brain, I think Page and Sherwin would agree. One statement in particular suggests to me an area in which more study would be useful.  They write:  “When food is restricted, the hypothalamus sends signals that increase your desire to ingest high calorie foods.”   Wow!  I knew that.  My body knows that.  I couldn't have said it better, and I’m so glad they did.

So, how about doing a bunch of studies that follow brain activity under dietary restriction?  Does restriction trigger deprivation signals all by itself, without regard to what is forbidden? Let’s see what the brain does in the context of diet regimens of various kinds.  Let’s take a closer look at the mechanisms of desire. In those gorgeous scanned images of indigo, gold and magenta, could we observe the mechanism in the brain that makes going off a diet a sure thing?
  
I want to know what happens in the hypothalamus when one is made to feel chronically guilty or afraid about food choice.  How do we store in our memory and constantly reinforce the admonition that foods are fattening, unhealthful, or bad?  For example, would the phrase “Sugar is indeed toxic” trigger a stronger or weaker signal in my brain to eat more or less of it?  I only quote Mark Bittman here because he’s one food writer whose opinions I truly value.  Conversely, does a sense of self-righteousness about healthful choices affect satisfaction levels in a positive or perhaps in a negative way?  Do these effects last?  How are satisfaction levels affected by limited or unlimited choice?  Could we study how hypothalamic activity is conditioned, as well as the reversal of it?  Could we examine conflict of interest arising between “internal” and “external” cues?

I don’t think we’ll ever free up the channels to our “Food Traffic Controller” until we answer some questions like these.  They may not be tops on the agenda for endocrinologists, but they are certainly relevant to the issue of obesity, to health and to pleasure in eating – which is of course the object of the exercise. 

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