One thing I believe to have learned over the years is that those readers who are interested in anorexia nervosa seem to have little interest in obesity, which they regard as an lifestyle choice irrelevant to them, while those who study obesity often ask themselves what this rare condition (AN) has to do with their vastly more prevalent (read: important) condition of obesity (OB)? Well, as it turns out, quite a lot.

And by the way, it’s worth repeating at the outset, neither condition is one of choice. Who would choose them?

So let’s start with the simplest similarities between these two groups: those with anorexia nervosa and those with obesity. Both AN and OB are complex neurobiological disorders with widespread metabolic consequences.

Both have strong genetic and epigenetic underpinnings. People with both conditions can be exposed to and influenced by obesogens in the environment. Thus, a patient who is starved and thin during the years of their AN can develop the same higher body weight issues later in life, when exposed to obesogens.

And as we’ve learned from collaboration with Dr. Emily Cooper of the Diabesity Research Foundation, these similarities also relate to the metabolic consequences of dieting or restricting calories.  It turns out that OB patients almost always have a history of self-imposed - and invariably encouraged! - diets or have engaged in periods of fruitless and harmful restricting (fruitless since the weight almost always comes back, plus some).  

Patients with AN by definition engage in restricting (with or without purging). And it turns out that the response of the brain to dietary suppression is remarkably similar in both groups. And this really should surprise no one.

The brain hates low food intake. And it will exact its “revenge” for it. Even hours of restricting or dieting can result in a drop in leptin - a protein that, among other things, acts as a signal to the brain that the food supply is endangered - which in turn can cause a decrease in the base metabolic rate in order to conserve energy. To do this the brain turns down our “oven”, the thyroid gland, and slows the caloric burn rate.  It also puts the brakes on reproduction, affecting both female and male hormones.  It cranks up hormones designed to increase appetite such as ghrelin, which, according to Dr Cooper, has further central nervous system and peripheral inhibitory impacts on thyroid and reproductive function.

Dieting serves to increase ghrelin, which increases insulin and decreases postprandial glucose, a condition known as postprandial hypoglycemia (PPHG), something we often see in our patients with AN. And at Kartini Clinic we know this because we do extensive metabolic testing (part of Weight Restoration 2.0).

Our lab testing has shown that a remarkable number of young patients who are otherwise recovering nicely from AN have PPHG, which in turn suppresses leptin despite adequate weight restoration, and inhibits resumption of menstruation (in females AN patients).  This in turn has serious implications for bone health and cognitive (brain) function.

But wait, the news about dieting gets worse! Ghrelin is elevated in dieting and can stay elevated a long time after resumption of eating -- according to the Diabesity Research Foundation, 62 months or more. So recovering from dieting/restricting is remarkably similar whether your starting point was fat, thin or average. And both groups also suffer from terrible social stigmatization, though ironically, in my experience, the two groups often seem to have remarkably little sympathy for each other.

As I mentioned, another shared vulnerability is environmental obesogens.  Obesogens are chemicals in our environment that trigger metabolic derangements whose end point is to raise body weight.  These changes can be immediate and/or epigenetic, which may even make them heritable (a sobering thought).

Most of you will have heard of bisphenol-A, a plastic additive that has been put in products from baby bottles to cash register receipts, food containers, the lining of cans of food, etc. and which apparently can be absorbed through skin contact.  Consumer pressure to limit the use of these additives has caused several companies (e.g.Tupperware, Kirkland/Costco) to remove them.  Recently, however, there has been some controversy about whether the chemicals replacing them actually may be as bad.

Arsenic is cited as another obesogen.  And while arsenic sounds like something you would not want to ingest, it’s where we are exposed to it that’s interesting -- and terrifying.  In an article in Consumer Reports, entitled Will a gluten-free diet really make you healthier? we learn that an unexpected effect of not eating wheat is the increased consumption of rice, which increases our exposure to arsenic. It turns out that a “local” (California) rice is among the lowest in arsenic.  Good to know!

Another obesogen is nicotine, and I mention it because of its paradoxical influence on body weight: children exposed to smoking and nicotine in utero are frequently born small for gestational age, and it isn't until they are adults that the effects of intra-uterine nicotine exposure are seen in increased rates of obesity and metabolic syndrome.

There are several smartphone apps designed to help us monitor these additives, much like those for monitoring pesticides in food (e.g. “the Dirty Dozen”), though they are not all equally user-friendly.  I typed in a few of my stand-by cosmetics into an app called “Think Dirty”.  I first typed Chanel #5 perfume (presumably French) and found that it has a rating of 9 out of 10 (10 is the worst)!  So how about my Clarins face cream?  A 10; Neutrogena sunblock lotion?  8. And further random cosmetic counter options: La Mer’s Cream de la Mer? 9; Bobbi Brown rouge? 9; L’Oreal lipstick “tickled pink”? 10;  Perricone MD face moisturizer (developed by a well known physician no less)? 9; his “concealer concealer”? 10.  Of the Shampoos chosen at random: Organic Root Stimulator shampoo was a 10; Vidal Sasson Pro was a 9; Head and Shoulders Shampoo was a 10.  Take a look for yourselves.  It’s pretty concerning.

The message is: whether you have AN or suffer from OB, you are equally exposed and no matter your starting weight, the end point can be obesity and metabolic disorders.  Oh, and by the way, no amount of dieting will prevent the increase in body size (to say nothing of endocrine disruption) caused by environmental obesogens-- in fact, via the leptin changes outlined above, dieting will actually make it worse.

Are obesogens the sole concerns of extreme organic farmers, health food nuts and “orthorexic” individuals?  Definitely not.  My own study of weight homeostasis in humans has prompted me to re-think many things.  It’s time we move beyond simple weight restoration in AN to Weight Restoration 2.0 and waaay beyond dieting and exercise as a treatment for OB.

Real health is what we should be after.  We need to get informed; as providers and consumers we need to attempt to stay up with the science.  We need to go where the science takes us despite the inconvenience and discomfort such a re-think may prompt.  We are all on this journey together.