Anorexia and Dietary Fat: Brain Function, Hunger and Satiety

Part 2 of a 3-part series: 2 reasons to eat a lot more fat in recovery.

Posted Mar 06, 2020 | Reviewed by Kaja Perina

I concluded the first part of this series on dietary fat by suggesting that everyone in recovery from anorexia should eat more of it. Why? The first piece of the puzzle is the frequently observed correlation between fat intake and illness severity and persistence:

  • “Illness duration is negatively correlated with the amount of fat in the diet, and this becomes significant in the more chronic patients” (Lobera and Ríos, 2009)
  • “The [treatment] failure group consumed significantly less total fat than the [treatment] success group” (Schebendach et al., 2011)
  • “Gastrointestinal symptoms were more common in fat-phobic anorexia nervosa than non-fat-phobic anorexia nervosa patients” (Lee et al., 2012)

These are just correlations, so the causal link could be either way round (low-fat diets increase illness severity/persistence, or illness severity/persistence results in a low-fat diet), or there might be no causal link, with the correlation caused by something else (low-fat diets and illness severity/persistence are both consequences of some other factor, e.g. not wanting to recover). All are possible, but the hypothesis that not eating enough fat prevents recovery has been proposed by several researchers. Relapse risk after short-term weight restoration is a common focus here, for example in a paper on "Eating behavior in anorexia nervosa: Before and after treatment":

  • If your diet consists of less fat, more “non-nutritive beverages” (water, black tea/coffee, diet drinks), and less energy density overall than it should, “persistence of this dietary pattern may contribute to difficulty maintaining weight”. (Mayer et al., 2011)
  • “The reduced overall intake and persistent behavioral avoidance of fat may contribute to the risk of relapse, and therefore is a potential target for treatment intervention.” (Mayer et al., 2011)

Evidence suggests that people who have had acute treatment aimed at weight restoration often revert back to generally lower-calorie but also specifically lower-fat diets after they stop using the hospital meal plan, once their weight is supposedly “normalised” or “restored” (Mayer et al., 2011). A large part of the problem here may be the widespread clinical habit of setting of highly optimistic, not to say irresponsibly low, thresholds for “normal” weight. Any treatment regime that involves reducing people’s energy intake once they reach an arbitrary BMI level is setting people up for relapse.

There are many reasons why this dubious strategy may be employed. Many of them reduce, I think, to a mixture of clinicians’ well-meaning but misguided accommodations of their patient’s anxieties about “unnecessary” weight gain, in combination with their own unaddressed weight stigma and strong pressure to demonstrate treatment "success" by setting thresholds low. If these factors are combined with an unreflective acceptance of the “fat is bad” dietary science dogma, then recommendations to actively reduce dietary fat in order to slow and stop continued weight gain below a minimal "healthy" level may well ensue.

This is exactly what happened for me: excellent as my therapist was in many ways, when I got anxious about my BMI increasing up towards 25 (and eventually beyond), her response was: try switching your whole milk for semi-skimmed (and stop having desserts and second helpings). I did that for a bit, before realising just how neatly that route was leading me back to where I’d just clawed my way out of.

Whether clinically encouraged or not, reversion to the classic anorexic way of eating is a clear sign that the process of recovery has not been sustained, and it is a brilliant way to make full-blown relapse happen. If this reversion does take place, and a patient goes back to the old low-fat ways, is the risk of relapse elevated just because overall energy intake is low? Or is there a greater risk associated specifically with reducing fat in the diet? And if the lack of fat is a significant contributor to the problem, what might be the mechanisms responsible?

Fat is Crucial to Brain Function

It seems clear that fat is doing more than just contributing generic calories. The most obvious form of damage a low-fat diet may do is to normal brain functioning:

“Abnormal patterns of FAs [fatty acids] in AN, coupling to the documented importance of FAs in the development of a healthy and functional brain, suggest that lipid dysregulation is involved in the pathogenesis of AN.” (Nguyen et al., 2019)

Dietary fat is needed to support the normal function of the human brain. For example, brain lipids determine the location and function of proteins in the neuronal membrane, and thereby regulate the throughput of signals through the synapses between neurons. They can also leave the membrane as transmitters and relay signals from the membrane to other cells or compartments within cells (Müller et al., 2015). More generally, fats are essential to the role of neuronal membranes as “dynamic platforms” for multiple vital brain functions (Aureli et al., 2015). So in a basic and profound sense, the less fat you have in the diet, the more damage you are doing yourself. In other areas of mental illness, links have been found between fatty acid profiles and anxiety and depression, with proposals now being made for the development of lipid-based therapies (Müller et al., 2015). If fatty acids have long been depleted through semi-starvation, systematic restoration of them must obviously be part of recovery.

If this fails to happen, because fat intake is never increased enough, or because it’s temporarily increased and then not sustained, full recovery will not happen: neural regeneration will not be completed, therefore neither cognitive nor physical regeneration will be. Fat intake, therefore, may well be not just a common and significant manifestation of the failure to effect real change in a recovery effort from anorexia, but an important cause of that failure.

Fat is Crucial in Hunger and Satiety Regulation

There may be a second strand to the importance of dietary fat in recovery from anorexia, and that relates to the normalization of feelings of satiety, or fullness, as malnutrition abates. During illness, you may dislike or fear the feeling of being full. This may be partly because you tend towards non-nutritious high-volume things that prevent true satiety from ever arriving but create a sometimes uncomfortable feeling of being filled up. You may do this partly because you’re scared of feeling hungry and losing control of your eating, which paradoxically may be more likely precisely because you’re avoiding truly satiating foods. In this context, I find it interesting to reflect on the fact that satiety, although it’s meant to convey that “just right” feeling so elusive in anorexia and recovery, is an oddly underused word – rather similar to the absence in English of a word for neither slim/thin nor fat but just right. In general terms, distortion of hunger and satiety signalling is probably universal in anorexia (Ramoz et al., 2015), because anorexia (and other eating disorders) involves behaviors in which responding naturally to bodily signals is replaced by imposition of other reasons for eating and not eating. Recovery, correspondingly, involves learning to experience, trust, and act on those long-discounted signals again.

So what is the role of fat in this relearning process? Overall, the research on the relative contributions of fat, protein, and carbohydrates to satiety in healthy populations consistently rank protein highest (Chambers et al., 2015; Ortinau et al., 2014; Warrilow et al., 2019); fats (depending on type) and carbohydrates compete for joint second. This chimes with the anorexic rationale for fat avoidance: it’s so easy to eat way more calories when they come as fat, and they don’t even fill me up how they should. However, as in most areas of dietary science, meaningful methods are hard to come by. In particular, there are three notable issues. First, it’s nearly impossible to assess the relative effects of the three macronutrients in real-world settings while holding everything else constant: fat doesn’t come along on its own in actual foods that people eat, for example, and the three main macronutrient groups have different effects in combination with each other, and with other nutrients like fibre. Second, controlled experiments are hard to do, so most data are long-term observational data drawing conclusions based on participants’ entire lifestyles beyond their reported diets. Third, satiety and hunger are not unidimensional more-or-less experiences: they have many context-dependent qualities that fan outwards into fear and pleasure, liking and wanting, satisfaction and desire, what you have been eating and what you will go on to eat. And I think fat plays profound if not always totally tangible roles on all of these dimensions.

In my own experience, and to judge from anecdotal evidence from a lot of people whose successful or (much more often) failed recoveries I’ve observed, high levels of fat in the diet are crucial to everything about the normalisation of eating habits: from modulating hunger and satiety, to broadening variety, to relaxing cognitive hang-ups. Satiety, I think, is the starting point for a lot of these benefits. A striking feature of the effects of diets that involve high fat (and protein) consumption tends to be enhanced satiety (Hu et al., 2016). Diets involving overall calorie restriction and therefore higher carbohydrate-to-fat ratios (because fat provides over double the calories per gram that carbohydrate or protein does) make people reliably hungry; diets that increase fat and protein relative to carbohydrates do not. In recovery from an illness that involves learning to experience and trustingly act on hunger again, this quality of dietary fat is paramount.

In this post back in 2012, I proposed a narrow version of a claim about the benefits of increasing fat in the diet: that eating more fat helps satiety and energy levels achieve stability. Here I’d like to broaden out this claim and say that eating more fat is crucial to normalising dietary choices, as one part of normalising overall eating behaviour, which is what makes full recovery possible.

This chimes with the impressive results obtained in treatment methods that emphasise behaviour change as opposed to weight restoration or psychological exploration—especially in the Mando method, which focuses specifically on eating speed and satiety signalling as drivers of global normalisation of eating behaviours. (The food they provide for patients is described as “ordinary Swedish food”, and isn’t particularly high-fat—the example they give is “mixed vegetables and grilled chicken cubes” [Södersten et al., 2017, p. 183]—but my prediction would be that they’d get even better results if they increased the fat quotient.) Weight restoration comes along for free if you get the behaviours sorted.

And regardless of what your particular geographical and social milieu may currently espouse by way of “normality”, it is a fact that normalising your eating habits in a meaningful way—let’s say, optimising your eating habits for health in its most encompassing sense—depends on you eating a lot of fat, especially if you strongly resist that idea. This is true because of the effects of dietary fat on brain function and satiety, as well as in the wider realms in which health in its fullest sense can be cultivated through systematic inclusion of more fat in the diet.

I’ll explore these in the third and final post in this series.


Aureli, M., Grassi, S., Prioni, S., Sonnino, S., & Prinetti, A. (2015). Lipid membrane domains in the brain. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids1851(8), 1006-1016. Paywall-protected journal record here.

Chambers, L., McCrickerd, K., & Yeomans, M. R. (2015). Optimising foods for satiety. Trends in Food Science & Technology41(2), 149-160. Open-access full text here.

Hu, T., Yao, L., Reynolds, K., Niu, T., Li, S., Whelton, P., ... & Bazzano, L. (2016). The effects of a low-carbohydrate diet on appetite: A randomized controlled trial. Nutrition, Metabolism and Cardiovascular Diseases26(6), 476-488. Open-access full text here.

Lee, S., Ng, K. L., Kwok, K. P., Thomas, J. J., & Becker, A. E. (2012). Gastrointestinal dysfunction in Chinese patients with fat-phobic and nonfat-phobic anorexia nervosa. Transcultural Psychiatry49(5), 678-695. Direct PDF download here.

Lobera, I. J., & Ríos, P. B. (2009). Choice of diet in patients with anorexia nervosa. Nutricion Hospitalaria24(6), 682-687. Full-text PDF here.

Mayer, L. E., Schebendach, J., Bodell, L. P., Shingleton, R. M., & Walsh, B. T. (2012). Eating behavior in anorexia nervosa: Before and after treatment. International Journal of Eating Disorders45(2), 290-293. Open-access full text here.

Müller, C. P., Reichel, M., Mühle, C., Rhein, C., Gulbins, E., & Kornhuber, J. (2015). Brain membrane lipids in major depression and anxiety disorders. Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids1851(8), 1052-1065. Open-access full text here.

Nguyen, N., Dow, M., Woodside, B., German, J. B., Quehenberger, O., & Shih, P. A. B. (2019). Food-Intake Normalization of Dysregulated Fatty Acids in Women with Anorexia Nervosa. Nutrients11(9), 2208. Open-access full text here.

Ortinau, L. C., Hoertel, H. A., Douglas, S. M., & Leidy, H. J. (2014). Effects of high-protein vs. high-fat snacks on appetite control, satiety, and eating initiation in healthy women. Nutrition Journal13(1), 97. Open-access full text here.

Ramoz, N., Versini, A., Grouselle, D., Bonnet, F., Pham, A., Criquillion-Doublet, S., ... & Gorwood, P. (2015). Hunger and satiety signals in anorexia nervosa: Neuroendocrinological and genetic analyses. European Psychiatry30, 361. Paywall-protected journal record here.

Schebendach, J. E., Mayer, L. E., Devlin, M. J., Attia, E., Contento, I. R., Wolf, R. L., & Walsh, B. T. (2011). Food choice and diet variety in weight-restored patients with anorexia nervosa. Journal of the American Dietetic Association111(5), 732-736. Open-access full text here.

Södersten, P., Bergh, C., Leon, M., Brodin, U., & Zandian, M. (2017). Cognitive behavior therapy for eating disorders versus normalization of eating behavior. Physiology & Behavior174, 178-190. Open-access full text here.

Warrilow, A., Mellor, D., McKune, A., & Pumpa, K. (2019). Dietary fat, fibre, satiation, and satiety—a systematic review of acute studies. European Journal of Clinical Nutrition73(3), 333-344. Paywall-protected journal record here.