Sorry, life attack prevented Science Friday from going off on time.  I had to move into the Director’s office at work (which is exactly the same as my old office, only with a better view), so that the new scientist that is coming to save me by taking over some of my old responsibilities (which only makes room for the new responsiblities, unfortunately) could move in without having to sweep my cookie crumbs out of her desk drawers.

 And while we are on the subject of cookies…

Moira asks:

OK.. I have a life science question for you: If your parents are overweight, how do you beat the genetic side of being overweight? Is there a hormone/vitamin that will help trick the body in to reducing stored fat and beat the genes?

This is because this weight watchers thing has me only losing about 1 lb a week on average. I’m seeing a distinct decrease in the rate at which I’m losing weight in proportion to the time I’ve been on the program.

So can you flex your life science muscle on that? And yes, I’m all about raw data.

When we start to look at the genetics of any given trait (such as body weight), even when we move past the question of genetics vs. environment and focus ourselves purely on genetics, things inevitably get more complex than we bargained for.  Weight, and because medical genetics tends to use “abnormal” to define “normal”, lets use the term obesity (discard the negative connotation for a moment and just focus on the medical definition), is one of those things that quickly becomes a tangled nest of genetic interactions.  Considering the bulk of scientific research on the subject (pun intended), if it were as simple as a couple of metabolic pathways to be tweaked, we’d have a pill for it by now.

And we don’t.  So here is your first take-home lesson – If a weight loss drug offers you a silver bullet for weight control, they’re lying.  Period.  And as both a dieter and a life scientist, I can tell you that one pound a week is not bad.  Any more than 1-2 lbs a week usually involves water.

To follow format with the last Science Friday, I am going to focus on the genetics first, and put the environment off until last.  Because the environment is ultimately the part you can control – the genetics just direct you to the “how” of doing it.

 First, there are some assumptions that even experts have about the role of our genes in obesity that have turned out to be inaccurate.   Our initial assumption is that people who tend toward being obese have inborn differences in metabolism from those who are thin.  It has been popular to make the assumption that food intake between a thin and a heavy person is the same, it’s just the heavy person metabolizes it more slowly.  That is pretty obviously the case, but here’s the thing – this is rarely because of an inborn difference in genetics.  Changes in metabolism are most often the result of the onset of obesity, not the cause.

If we look at extreme cases of obesity to give us clues, what we find is that when we can trace the difference to genetics, to cases where we can identify single genes that are responsible, the genes affected are involved in satiety, not metabolism.  In other words, in a very small (and I want to emphasize that this is a VERY small) subset of the morbidly obese the genetic pathway that tells them that they have had enough food and to STOP eating is disrupted.  As a result their eating habits are aberrant.  So it IS what they are eating, and not because they metabolize it any differently than you or I.  The message from the stomach to the brain that says ‘Put down the fork and walk away from the plate” just doesn’t get processed like it should. 

So the question is, why has this “defect” persisted?

We tend to think of the way our biology works in terms of how we live our current lifestyle.  But our current lifestyle is a blink in the evolution of our species.  What is “maladaptive” to us now makes perfect sense in the context of tens of thousands of years of evolutionary selection.

Enter environment.

Evolution is the result of the environment exerting selective pressures on a species (in this case, us), that cause a subset (who have a natural genetic variation) to be more successful than their compatriots.  Success being defined as more likely to reach breeding age and/or producing more viable offspring.  Eventually the subset becomes the dominant, and if environmental conditions change, the cycle repeats itself.  If lifecycles are short, this change can happen very quickly (for instance, you can selectively breed a tailless boxer in five generations, each generation taking about a year).  But in humans, where lifecycles and time to “likely breeding age” are long, it can take a long, long time to respond to a change in selection pressure. 

Back in our days on the savannah, food supplies were limited and the necessary energy expenditure to find it was substantial.  It made sense that when you found it, you filled the tank to capacity, so to speak.  So, a slow satiety response was positively adaptive.  You would need the stored energy to search out the next feast.

Keep in mind that I mentioned that only a small, small number of obesity cases can be tracked to variations in only one of the genes involved in satiety.  For the great majority of people for whom the tendency to be overweight is genetic (and it is estimated that 40 to 70% of our weight tendencies ARE inherited), it is a combination of many genes that produces the final weight “setting”.  Which means, while it is “programmed” in your genes, there’s a lot of room for variation in what we inherit.  That’s why in so many cases, siblings vary widely in their final body type.  While we probably get our tendencies from our parents, it’s difficult to distill exactly what that means.

And back to the environment…

If we look at some of the most recently published information on dietary tendency in Western countries, we find something interesting.  The trend for fat and overall calorie consumption in these “developed” countries over the last several years is, contrary to what the media would like you to believe, downward.  In other words, we are consuming less fat and fewer calories each year, on the average, than we did the last.  And yet, obesity continues to rise.

We know what we are supposed to be eating.  And by and large we ARE doing something about it.  But caloric control is only one part of the equation.

We were designed to store energy against future expenditure.  But as the daily occupations in Western society slip further toward the sedentary, we are approaching the bottom limits of our fight against satiety.  We have to start EXPENDING.  We cannot beat our genes, we can only use them the way they were supposed to be used.

So, there you go.   The “magic bullet” for maintaining healthy weight is exactly what it has always been – “eat less, move more”.  Except we are only getting half of it right.