Chapter 22: Feeding and Eating Disorders

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Welcome back to The Deep Dive.

Today we're tackling a really significant topic, feeding and eating disorders.

We've gone straight to the source, pulling from a key chapter in

comprehensive textbook of psychiatry.

It's dense stuff.

It absolutely is.

And look, our goal here is to give you the essential framework because these disorders, they're marked by these persistent disturbances in eating or feeding behaviors and the impact is profound.

Physical health,

medical stability, how people function day to day.

Yes, psychosocial functioning too.

Right, and early identification isn't just important, it's critical.

The medical side of things can get dangerous really fast.

Exactly.

So think of this as your quick start guide.

We want to pull out the core psychiatric concepts, those strict diagnostic criteria, the theories behind them, and crucially the treatment approaches.

We want to make it clear and quick to grasp.

Okay, so to lay it out, the DSM -5 and the newer DSM -5 -TR, they list six main diagnoses.

You've got anorexia nervosa or AN, bulimia nervosa, BNN, binge eating disorder, BED, then avoidant restrictive food intake disorder, that's ARFID, and finally PICA and rumination disorder.

And what about cases that don't quite fit?

Oh yeah, those fall into two broader categories.

Other specified feeding or eating disorder, OSFED, or unspecified USF, kind of catch -alls.

Okay, let's dive into the definitions then, starting with probably the most well -known, anorexia nervosa.

What are the three core components we absolutely need to know for AM?

Okay, three key things.

First,

significantly low body weight, and that's judged based on their age, sex, developmental path, physical health context.

Not just a number on a scale.

Exactly.

Second, this intense fear of gaining weight or becoming fat or persistent behavior that actively interferes with weight gain even though they're underweight.

And the third.

And third, this is the really tricky part, a disturbance in the way they experience their body weight or shape, or undue influence of body weight or shape on how they see themselves, their self -worth.

That's the psychological piece, isn't it?

Where their value as a person gets completely tied up in being thin.

Precisely.

It's that body image distortion.

They might feel overweight even when they're objectively, civilly underweight.

And often, the source material highlights this, they fail to recognize just how medically serious their low weight is.

It's like the illness blinds them to the danger.

Now, I know the criteria for AIN have changed a bit.

Didn't they used to require amenorrhea, the loss of periods?

They did, yeah.

That was a significant change in DSM -5.

They removed it.

Why was that?

Well, basically, research found that women who met all the other criteria for AIN but still menstruated, they didn't really differ in the course of their illness or their prognosis compared to those who did lose their periods.

Plus removing it obviously helps with diagnosing men or pre -pupil girls or women on hormonal contraceptives.

They also took out that specific mention of 85 % of ideal body weight.

Oh, right.

Why?

To stop clinicians from using it as this rigid, arbitrary cutoff.

Weight needs context.

Makes sense.

Okay, so if that profound low weight is the hallmark of AIN, what happens if you have the binging and purging cycle but without being severely underweight?

That leads us to bulimia nervosa, right?

Exactly.

Bulimia nervosa, or BN, is characterized by that cycle.

Yeah.

Recurrent episodes of binge eating.

Followed by recurrent inappropriate compensatory behaviors to prevent weight gain.

Think self -induced vomiting, misusing laxatives or diuretics, excessive exercise, fasting.

And the key difference from AIN is their weight.

Yes.

People with BN typically maintain a body weight that's at or above the minimum normal level.

Okay, let's nail down that term binge eating.

The DSM -5TR is pretty specific, isn't it?

It needs two things.

Yes.

Two crucial components have to be there.

First, eating in a period of time, an amount of food that is definitely larger than what most people would eat in a similar period under similar circumstances.

So an objectively large amount.

Objectively large.

Got it.

And second.

And second, a sense of lack of control over eating during the episode.

Feeling like you just can't stop eating or control what or how much you're eating.

That loss of control piece seems critical.

But wait, you said objectively large.

So someone could feel totally out of control, but if the amount wasn't technically large enough,

they might not meet the DSM -5 criteria.

You've got your finger right on a point of ongoing discussion and, frankly, controversy in the field.

We can circle back to that.

But sticking with DSM for now.

Okay.

If you take that definition of binge eating, the large amount plus the loss of control, but you remove the compensatory behaviors like purging or excessive exercise, then you arrive at binge eating disorder, BED.

Right, the third of the big three.

Correct.

People with BED have those recurrent binge eating episodes, but they don't regularly use those inappropriate compensatory behaviors afterwards.

And like BN, their weight is typically normal or more often they're in the overweight or obese range.

And how often do these behaviors need to happen for BN or BED diagnosis?

For both BN and BED, the criteria specify that the binge eating and for BN, the compensatory behaviors too, occur on average at least once a week for three months.

That frequency threshold was actually lowered in DSM -5.

Oh, it used to be higher.

Yeah, it was twice a week.

But research showed that people binging once a week weren't clinically that different.

Interesting.

Okay, so let's shift gears slightly.

What about eating disturbances where the motivation isn't about body shape or weight?

That brings us to ARFID, right?

Exactly.

Avoidant Restrictive Food Intake Disorder, ARFID.

This is characterized by eating or feeding disturbance, like apparent lack of interest in food,

avoidance based on sensory characteristics, or concern about aversive consequences of eating.

Like choking.

Like fear of choking or vomiting, yes.

And this disturbance leads to a persistent failure to meet appropriate nutritional or energy needs.

So you see significant weight loss, nutritional deficiency, dependence on supplements, or marked interference with psychosocial functioning.

But the crucial distinction from AN or BN is?

The reason for the restriction.

It is not driven by any distress about body shape or weight.

That's the key differentiator.

It could be extreme picky eating based on texture, a past traumatic event involving food, or just a profound lack of interest.

Got it.

And briefly, the other two, pica and rumination disorder.

Right, pica is the persistent eating of non -nutritive, non -food substances.

Things like paper or soil, chalk, paint, over a period of at least one month.

And it has to be inappropriate to the developmental level and not part of a culturally supported practice.

And rumination disorder involves repeated regurgitation of food over at least a month.

The food might be re -chewed, re -swallowed, or spat out.

Importantly, it can't be diagnosed if the symptoms occur exclusively during the course of AN, BN, BED, or ARFID.

Makes sense.

Now let's get into the why.

What actually causes these disorders?

The book talks about a confluence model.

Yes, the confluence model is a really helpful way to think about it.

It suggests that it's not one single thing, but rather a coming together of factors.

You have predisposing traits, maybe genetic vulnerabilities, certain personality factors.

Then something precipitating happens, like starting a diet, puberty stress, a life transition.

That triggers the onset.

And then maintaining factors keep the illness going, like the physiological effects of starvation itself, or the binge -perch cycle becoming entrenched.

Let's look at AN specifically.

We know genetics play a role you mentioned, up to 11 times higher risk if a first -degree relative has it.

What about the psychological profile?

For AN, the textbook points to a cluster of traits often seen before the illness starts.

High levels of perfectionism, often high self -discipline, significant harm avoidance.

Harm avoidance, meaning?

Like being very cautious, inhibited, worried about negative consequences,

and critically, a high degree of cognitive inflexibility, a real rigidity in thinking, difficulty shifting sets, or seeing alternative perspectives.

That sounds like it would make recovery incredibly hard.

It does.

And it ties into this neurobiological idea called the habit hypothesis.

Okay, tell me about that.

The idea is that initially, restricting food might be a conscious goal -directed behavior, the goal being weight loss.

But over time, through repetition, it shifts from being controlled by the prefrontal

goal -directed areas to becoming more automatic, habitual, driven by the dorsal striatum.

It becomes less of a choice and more of an ingrained, almost reflexive pattern.

Wow, like the brain wires itself into the disorder.

How does the profile for bulimia nervosa compare?

Is it different from AN?

Oh, quite different in some key ways.

While AN is often associated with that rigidity and control, BN tends to be linked more with high impulsivity and novelty seeking.

Impulsivity, okay.

Yeah.

And biologically, there's some evidence mentioned for things like delayed gastric emptying, maybe in a large stomach capacity, and potentially reduced response to CCK.

That's a hormone that signals fullness or satiety.

These could contribute to the tendency to binge.

And then the cycle just keeps itself going.

Exactly.

The restriction leads to intense urges to binge.

The binge leads to guilt and distress, which triggers the purge or other compensatory behaviors, followed by renewed commitment to restrict and round it goes.

It sounds utterly exhausting.

Okay, let's talk numbers.

Epidemiology.

Which of these is actually the most common?

I was a bit surprised.

Yeah.

Counterintuitively, maybe.

Binge eating disorder, BED, is the most prevalent eating disorder overall.

Lifetime prevalence is estimated around 1 to 3 % in women and maybe 0 .5 to 1 % in men.

It's also the one with the least disparity between genders.

More common than anorexia or bulimia?

Yes.

Anorexia nervosa has a lifetime prevalence of around 1 .4 % in women and 0 .2 % in men.

But worryingly, the incidence, the rate of new cases seems to be increasing, particularly in that high -risk group of 15 to 19 -year -old females.

That's concerning.

And ARFID.

Any demographic notes there?

Interestingly, ARFID might actually be more common in males than females, which is different from AN, BN, and BED, where females are

Okay, let's loop back to diagnosis for a minute and that controversy about defining a binge.

You mentioned DSM versus ICD.

Right.

So DSM5TR insists on the binge being objectively large, plus the feeling of loss of control.

But the ICD11, which is used more internationally, has actually removed the requirement for the amount of food to be objectively large.

They focus primarily on the subjective experience of loss of control over eating.

So, under ICD11, someone eating a normal amount of food but feeling completely out of control could still meet criteria for a binge episode.

Potentially, yes, if the loss of control is the prominent feature.

It reflects this ongoing debate.

Is it the quantity or the feeling of being unable to stop that really defines the psychopathology?

Clinicians often use probing questions, like the one suggested in Table 22 -2 in the textbook, asking things like, was the amount unusually large for you?

How long did it last?

Did you feel you couldn't stop once you started?

That couldn't stop part really captures the essence.

Okay.

And to really highlight the difference between AN and ARFID, can you walk us through that case example of Kay, the 11 -year -old?

Sure.

So Kay was an 11 -year -old girl presenting with significant weight loss below the 7th percentile.

Her food restrictions started years earlier after an episode where she felt nauseous and vomited.

Okay.

This led her to develop an intense persistent fear of vomiting.

She became extremely anxious about eating, especially outside the home, worried it would make her sick.

Mealtimes were incredibly stressful.

So she was restricting significantly, losing weight.

Sounds like AN.

But here's the key.

When specifically asked about her body image, Kay adamantly denied any concerns about her shape or weight.

She didn't want to be thin.

In fact, she expressed a strong desire to gain weight and be healthy.

Her restriction was purely driven by the fear of the aversive consequence vomiting.

That nails the distinction.

Low weight isn't enough.

For AN, you need that specific drive for thinness or fear of fatness.

Okay.

Let's talk about the physical toll.

The medical pathology is serious.

Extremely serious.

Mortality rates are significantly elevated in AN.

The textbook quotes figures up to six times higher than the general population and also elevated in BN, mostly due to medical complications.

What are some of the most critical physical consequences we need to watch for in AN?

Starvation affects every organ system.

You see profound slowing of the heart rate.

That's birdycardia, low blood pressure, hypotension, temperature regulation issues, feeling cold.

Some develop lingo that find downy hair on the body.

Like the body's trying to keep warm.

Exactly.

And one of the most worrying long -term effects is the loss of bone mineral density.

This leads to osteopenia or even osteoporosis.

And that bone loss may not be fully reversible even after weight restoration.

That's devastating.

And for bulimia, what are the immediate dangers there?

With BIN, especially involving purging like vomiting or laxative abuse,

the biggest acute risk is electrolyte disturbances, particularly hypokalemia, low potassium.

And that's dangerous because?

Because potassium is critical for heart function.

Low potassium can cause serious, potentially fatal cardiac arrhythmias.

It's a medical emergency.

You also see gentle enamel erosion from stomach acid, sometimes swollen salivary glands, the parotid glands.

Russell's calluses on the knuckles from inducing vomiting is sometimes seen, but not always.

So close medical monitoring is non -negotiable.

Labs, ECGs.

Absolutely essential.

Checking electrolytes, kidney function, thyroid function, getting a baseline ECG to look for things like a prolonged QTC interval, which increases a rivnia risk.

Okay.

Moving towards treatment.

It's notoriously challenging for anorexia, partly because the illness is often described as egosyntonic.

Can you unpack that term for us?

Egosyntonic means that parts of the illness, particularly the restrictive behaviors, the weight loss, the sense of control, are experienced by the person as consistent with their self -image or even as positive achievements.

They might feel proud of their discipline.

So they don't necessarily want to get better, at least not fully.

Exactly.

It creates this profound ambivalence about recovery.

Part of them might recognize the dangers or the impact on their life, but another part clings to illness.

This makes engaging in treatment incredibly difficult.

So faced with that ambivalence, what's the first step in treatment?

The immediate primary goal has to be nutritional rehabilitation and weight restoration to get them out of medical danger.

This usually happens in a structured setting.

Calorie prescriptions traditionally started quite low, maybe 1500 to 1800 kilo a day, gradually increasing.

But there's emerging evidence, as the chapter notes, that starting higher, perhaps around 2000 kilo a day, might actually be safer and lead to faster weight gain without increasing risks, aiming for about two to five pounds per week gain in inpatient settings.

But isn't there a risk if you refeed too quickly, refeeding syndrome?

Yes, absolutely.

That's a critical concern.

Refeeding syndrome is a potentially lethal complication caused by rapid shifts in fluids and electrolytes, especially phosphate, when nutrition is reintroduced after prolonged starvation.

It can cause cardiac failure, respiratory failure, seizures.

So refeeding must be done carefully with close medical monitoring, especially phosphate levels.

Okay.

What about psychotherapy for AM?

For adolescents, the strongest evidence supports family -based therapy, FBT,

often called the Maudsley method.

Here, the parents are empowered and supported to take temporary charge of their child's refeeding process at home.

So the family becomes part of the treatment team?

Very much so.

For adults with AM, the evidence is less definitive.

Several approaches like specialized forms of CBT, like CBTE, interpersonal psychotherapy, IPT, and acceptance and commitment therapy, ACT, show modest benefits.

But no single therapy has emerged as clearly superior for adults yet.

And medications.

I would have thought antidepressants would be standard, but you mentioned earlier they aren't always effective for AM.

That's correct.

For patients who are actively underweight with AN,

standard antidepressants like SSRIs have generally not been shown to be effective for the core symptoms of AN, meaning aiding weight gain or reducing the eating disorder thoughts.

They might help with co -occurring depression or anxiety, but not the AN itself.

Is there anything that does help pharmacologically?

There is some evidence mentioned in the chapter for the atypical antipsychotic olanzapine.

It seems to help promote some modest weight gain and maybe reduce obsessional thinking about food and weight, typically used at lower doses like 5 to 10 milligrams per day.

But it's not a cure -all and has side effects.

Okay.

Now let's switch to bulimia and binge eating disorder.

Is the treatment approach different?

Yes.

Quite different, especially regarding psychotherapy effectiveness.

For bulimia nervosa, cognitive behavioral therapy, CBT, specifically enhanced CBT, CBTE, is considered the gold standard, the first line treatment.

Why is CBT so effective for BN?

It's highly structured.

It directly targets the cycle.

Phase 1 focuses on establishing regular eating patterns and stopping the binge purge behaviors.

Later phases work on identifying triggers, challenging the distorted thoughts about shape and weight, and developing relapse prevention skills.

IPT is also effective, but tends to work more slowly than CBT.

And medication for BN?

Here, SSRIs are effective.

Specifically,

fluoxetine Prozac is FDA approved and is the medication of choice.

Importantly, it's usually needed at a higher dose than typically used for depression, 60 milligrams per day, to effectively reduce binging and purging frequency, even in people who aren't depressed.

50 milligrams, okay, that's important.

And any meds to avoid.

Yes, a crucial contraindication.

The antidepressant bupropion, well, buterin, should not be used in patients who purge, because it lowers the seizure threshold and purging itself can cause electrolyte shifts that also increase seizure risk.

Good to know.

Finally, what about binge eating disorder?

Again, CBT is highly effective for BED, leading to binge abstinence in a significant number of patients, often over 50 percent.

IPT and DBT skills can also be helpful.

Does CBT for BED help with weight loss too?

That's a key point.

While CBT is excellent for stopping the binges, it's generally not effective as a standalone treatment for weight loss.

Weight management might require separate or additional interventions.

Pharmacologically, the stimulant medication Lisdexamphetamine, VIVANS, is FDA approved for the short -term treatment of moderate to severe BED in adults.

Some antidepressants might also help reduce binge frequency.

So, just to wrap up the main points, we've covered these six distinct syndromes, each needing a tailored approach.

We saw how diagnosis really hinges on things like weight status, that key AN versus BN difference, and the motivation behind restriction for ARFID, and etiology is complex, that interplay of genetics, psychology, environment.

It's a lot to take in, but understanding that framework is so important.

That brings us to the end of this deep dive.

Thank you for joining us and navigating this complex chapter with us.

We really hope breaking it down like this gives you a clear, usable understanding of these often misunderstood and, as we've heard, medically serious disorders.

Absolutely.

Now, as always, we want to leave you with a final thought to mull over.

Considering the evidence that some physical consequences, like the devastating bone density loss and anorexia nervosa, might not fully reverse even after someone recovers weight,

and that some neuropsychological impacts might linger long -term, what does that really tell us about the potentially irreversible physiological costs of these illnesses?

And how might fully acknowledging those lasting impacts change how we approach early detection, intervention intensity, and maybe even our definition of full recovery?

That's a heavy but crucial question.

Something to think about.

A warm thank you from the entire Last Minute Lecture Team.

We'll see you on the next Deep Dive.