I’m sure you’ve heard of the old adage, “You are what you eat.” When it comes to anorexia, our children are what they DON’T eat. As a saying often heard during our childhood years, and usually meant to discourage over-consumption of junk food– it’s fundamentally commonsense, and the truth of it has been proven time and again by scientific research.
The flip side of this equation, however, while equally commonsense, is overlooked by modern medicine despite its profound impact on health.
“You are what you eat” is true.
“You are what you don’t eat” is also true.
As the thousands of research studies on malnutrition and health outcomes that have been conducted over the past century, and each and every one of the anorexia nervosa patients I have ever encountered demonstrates with absolute clarity, the sum of human health is as much about what we don’t eat as it is about what we do.
We must examine both sides of this equation, and the ways in which malnutrition can set off a biological cascade that ultimately evolves into a life-threatening illness.
Through nutrition, and an appreciation of the connections through which nutrition steers the course of physical and mental health, we can unlock doors beyond which lies the hope for the realization of recovery from anorexia nervosa.
The Laws of Nutrition: Defining “Essential”
The field of nutritional science is vast and encompasses a number of sub-fields that differ in terms of scope and research focus. When it comes to human nutrition, however, there is one universal law with which all scientists agree. This has to do with “essential” nutrients.
The law? Well, quite simply: “essential” means essential.
We see the word “essential” tacked on to literature, TV ads, and internet articles, usually in front of lists of nutrients or dietary supplement formulations. More often than not, the significance of this term is ignored or brushed aside.
The human body is an incredible machine and has evolved to be able to manufacture many of the nutrients it needs to function properly. Vitamin D, for example, can be synthesized in our skin upon exposure to natural sunlight; cholesterol, a building block of critically important hormones and signaling molecules, can be made by the liver, intestines, and other tissues throughout the body.
There are many nutrients, however, that the body requires to function optimally but cannot manufacture on its own. These are the “essentials,” and include (among many others) vitamin C, vitamin A, amino acids from protein, essential fatty acids, and minerals such as magnesium, potassium, and selenium.
Essential nutrients must be obtained through the diet; there is no other way for the body to acquire them. This is important to understand as we consider the effects of prolonged self-starvation as well as the malnutrition that results.
When it comes to neurobiology, “essential” assumes an even greater significance, as many nutrients have been identified as being required by the brain. When the brain is deprived of needed nutrients, the stage for anorexia is set.
Malnourished Neurons and Puberty
During puberty, the trajectory of an adolescent’s overall development is determined. Critical physiologic growth takes place at this life stage: adolescents add what amounts to twenty percent of their adult height (even up to ninety-two percent in males), up to fifty percent of their adult bone mineral content and skeletal mass, and fifty percent of their adult weight over the course of puberty. 1-5
Hormones and rapid growth alter metabolism. Changes also occur in systems regulating appetite and weight. The profound changes that occur during puberty are heavily dependent upon the availability and adequate supply of essential nutrients obtained from food.
Good nutrition is also crucial for the developing brain. The brain is the most complex organ in the body, and although it accounts for only two percent of body weight, twenty-five percent of the body’s energy is dedicated to fueling it. 6 There are one hundred billion nerve cells, or neurons, in the brain, and each connects to more than two thousand other neurons.
The brain’s need for nutrients is at an all-time high during adolescence, the same period in which our children are least likely to obtain them through healthy eating. During this critical time window, a malnourished brain in tandem with any number of possible internal and/or environmental variables can coalesce into a “perfect storm.”
And if adolescents start dieting and restricting essential nutrition, the subsequent malnutrition results in nutrient deficiencies that may lead to the entrenchment of some of the symptoms of anorexia nervosa. On average, half of all mental illnesses present by the age of fourteen; most of these, however, go undetected and untreated in this early stage of life. 7
DNA is not destiny; nor are the factors encountered in the physical and sociocultural worlds that we occupy. It is, instead, the interaction between genes and environment that may lead to nutritional deficiency syndrome.
Genetics or Environment
Anorexia often begins a change in one’s diet, which over time becomes increasingly restrictive. But there are millions of people around the world who diet, and of these only a small percentage cross that invisible threshold separating healthy, conscientious dieting with disordered eating and, ultimately, anorexia.
Part of the answer to this problem lies in genetics, the branch of biology dedicated to the study of genes, heredity, and genetic variation. Lifestyle factors, including the food we eat, can profoundly affect gene expression.
Any alteration to the body’s “instruction manual,” or the way in which the manual is or is not being read (expression), can trigger a cascade of changes throughout the biologic system. For example, a research report in the International Journal of Eating Disorders showed that the longer an individual suffers from anorexia nervosa, the more likely he or she is to display alterations to his or her DNA, which then cause alterations in gene expression, which then affect body function, thus entrenching the disease. 8
In other words, when a hypothetical teenager who seems perfectly healthy chooses to diet or adopt a vegan lifestyle, and if there’s been a genetic shift towards behavior linked with anorexia, that teenager may be at a higher risk for ultimately developing anorexia nervosa.
Nutritional Deficiency Syndrome
Approaching anorexia nervosa solely as a psychological disorder does not account for the brain’s response to a shortage of essential nutrients. Regardless of genes, culture, personality traits, family pressures, or the presence or absence of comorbid conditions, the biological results of starving remain the same: a malnourished brain.
Anorexia nervosa is a biological illness fundamentally sustained by starvation and malnutrition, whether self-imposed or the product of genetic, psychosocial, or environmental circumstances. Biology is the single and unchangeable constant linking all cases of anorexia, everywhere.
All those who struggle with this serious disorder, no matter their age, gender, employment status, relationship status, genetic makeup, or medical history, present with significantly imbalanced and abnormal biochemistry, a direct result of self-starvation.
The medical field has pursued treatment after treatment and therapeutic model after therapeutic model for anorexia nervosa over the years, and most focus on psychology as well as increasing patients’ overall caloric intakes.
This kind of approach generally ignores or is slow to correct, one of the root causes of the disorder: nutritional deficiencies arising from prolonged self-starvation that profoundly disrupt normal brain function (otherwise known as nutritional deficiency syndrome).
I have stated that a majority of traditional anorexia treatment models are inadequate as a result of their omission of biology from all considerations. This is demonstrably true; protocols that focus on psychology but exclude biology are fundamentally incomplete.
As with the old saying “you are what you eat,” however, we cannot examine only one half of a two-factored equation and expect the results to satisfactorily resolve the issue at hand.
The sum of human health is as much about intangible factors as it is about quantifiable, measurable, biologic ones. The role of stress in the emergence or persistence of anorexia nervosa has been established for well over a century, and we cannot deny the role of psychology in anorexia any more than we can accept a treatment model that denies biology.
I believe we can stop the rising rates of anorexia nervosa by directly addressing nutritional deficiency syndrome, the root cause of the disorder, and by restoring nutritional balance to the malnourished brain whilst supporting a healthy mind.
This approach, in tandem with already-available behavioral modalities, coalesces a treatment that is both comprehensive and – most importantly – successful!
- Soliman A, De Sanctis V, Elalaily R, Bedair S. Advances in pubertal growth and factors influencing it: can we increase pubertal growth?. Indian J Endocrinol Metab. 2014;18(Suppl 1):S53-S62.
- Patton GC, Viner R. Pubertal transitions in health. Lancet. 2007;369(9567):1130-1139.
- Rogol AD, Roemmich JN, Clark PA. Growth at puberty. J Adolesc Health. 2002;31(6 Suppl):192-200.
- Bailey DA, Martin AD, McKay HA, Whiting S, Mirwald R. Calcium accretion in girls and boys during puberty: a longitudinal analysis. J Bone Miner Res. 2000;15(11):2245-2250.
- Scholl TO. Puberty and adolescent pregnancy. In: Goldman MB, Hatch MC, eds. Women and health. San Diego, CA: Academic Press; 2000: chapter 8.
- Bélanger M, Allaman I, Magistretti PJ. Brain energy metabolism: focus on astrocyte-neuron metabolic cooperation. Cell Metab. 2011;14(6):724-738.
- Kessler RC, Angermeyer M, Anthony JC, et al. Lifetime prevalence and age-of-onset distributions of mental disorders in the World Health Organization’s World Mental Health Survey Initiative. World Psychiatry. 2007;6(3):168-176.
- Booij L, Casey KF, Antunes JM, et al. DNA methylation in individuals with anorexia nervosa and in matched normal-eater controls: a genome-wide study. Int J Eat Disord. 2015;48(7):874-882.
Photo Credits: Photo by Annushka Ahuja