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A Comprehensive Review of Complications and New Findings Associated with Anorexia Nervosa

Leah puckett.

1 ACUTE Center for Eating Disorders, Denver, CO 80204, USA; [email protected] (L.P.); [email protected] (D.G.); [email protected] (V.K.); [email protected] (K.C.)

2 Department of Medicine, School of Medicine, University of Colorado, Aurora, CO 80045, USA

Daniela Grayeb

Vishnupriya khatri, kamila cass, philip mehler.

3 Eating Recovery Center, Denver, CO 80230, USA

Anorexia nervosa is a complex and deadly psychiatric disorder. It is characterized by a significant degree of both co-occurring psychiatric diseases and widespread physiological changes which affect nearly every organ system. It is important for clinicians to be aware of the varied consequences of this disorder. Given the high rate of mortality due to AN, there is a need for early recognition so that patients can be referred for appropriate medical and psychiatric care early in the course of the disorder. In this study, we present a comprehensive review of the recent literature describing medical findings commonly encountered in patients with AN. The varied and overlapping complications of AN affect pregnancy, psychological well-being, as well as bone, endocrine, gastrointestinal, cardiovascular, and pulmonary systems.

1. Introduction

Anorexia nervosa (AN) is a complex psychiatric disorder with a high rate of mortality and a relatively low rate of remission [ 1 ]. Using DSM-V criteria, the lifetime prevalence of AN in females is estimated to be as high as 4% [ 2 ]. The lifetime prevalence in males has been estimated to be between 0.1% and 0.3%, although this is likely an underestimate [ 3 ]. AN has a high rate of psychiatric comorbidities including strong associations with mood and anxiety disorders, personality disorders, self-harm and suicidality, as well as substance use disorders [ 4 , 5 ]. In addition, AN leads to widespread medical complications across virtually all organ systems, which contributes to it being one of the highest causes of mortality among psychiatric disorders [ 6 ]. Complications worsen with a lower body mass index (BMI), which indicates a greater severity of disease [ 7 ]. Medical complications have been related to a plethora of complex physiological changes that lead to decreased energy expenditure and include cardiac, bone, obstetric, and gynecological changes, as well as endocrine, gastrointestinal, hematological, electrolyte imbalance, and skin changes [ 4 ].

2. Etiopathogenesis

The etiopathogenesis of AN is still unknown. Although progress has been made in identifying genetic, developmental, psychological, and neurobiological factors that play a role in the development of the disorder [ 8 ], it is evident that, similar to all psychiatric disorders, its origins are multifactorial. AN is familial, with heritability estimates for AN ranging from 0.41 to 0.74 [ 9 , 10 ], and higher heritability estimates have been found when more stringent definitions of anorexia were applied [ 11 ]. Significant genetic correlations have been found among AN and various anthropometric and metabolic traits, including negative correlations with BMI, fasting insulin, and fasting glucose [ 12 ], and therefore metabolic factors, including the gut microbiome, have been considered for understanding the etiology of AN [ 13 , 14 ]. Developmentally, cesarean section, multiple births, low gestational age, congenital malformations of the mouth or digestive system, and older parental age are associated with increased risk of AN [ 15 , 16 ]. Temperamental characteristics associated with lifetime prevalence of AN include perfectionism, obsessionality, reward dependence, negative affectivity, and neuroticism [ 17 , 18 , 19 ]. Neurobiologically, findings of reward processing and reward learning abnormalities indicate reward circuit dysfunction in AN [ 20 , 21 ]. Neuropsychologically, impairments such as set-shifting difficulties and poor central coherence may be related to the pathophysiology of the disorder [ 22 ]. Dieting is the most common precipitating factor for the development of AN, with severe dieting being especially implicated in triggering the onset of AN [ 23 , 24 ].

3. Psychiatric Treatment

There are currently no FDA approved medications for the treatment of AN [ 25 ]. The most established psychological treatment for adolescents with AN is family-based therapy (FBT) [ 26 ]. Randomized controlled trials have shown adolescent FBT to be superior to individual therapy for supporting weight restoration in adolescents. Currently, there are no therapy modalities that have achieved empirical support for adults with AN and no evidence that a particular mode of therapy is more efficacious than another mode of therapy [ 27 ]. Novel approaches are being explored, including treatments focused on neurocognitive factors found to be impaired in individuals with AN, including problems with set-shifting and central coherence [ 28 ]. Treating patients at the appropriate level of care is important. In severe cases, initial medical stabilization, followed by inpatient and residential treatment, is recommended [ 29 ]. Severe AN is defined by a BMI of <15 kg/m 2 . For adolescents, inpatient treatment of AN has been shown to be highly effective, with sustained increases in body weight and decreases in eating disorder symptoms found at one-year follow-up [ 30 ]. Due to a lack of insight into the severity of the disease among patients, involuntary treatment may be indicated [ 31 ].

4. Medical Complications

4.1. endocrine system complications.

Anorexia nervosa (AN) is characterized by alterations in multiple neuroendocrine axes and peptides that signal or regulate energy intake. Some of the endocrine and metabolic abnormalities in patients with AN represent physiological adaptive responses to chronic starvation that are reversible after weight restoration. However, other abnormalities may play a role in disease pathophysiology and sustained neuropsychiatric symptoms. Hormonal changes include growth hormone (GH) resistance with low insulin-like growth factor-1 (IGF-1) levels, hypothalamic hypogonadism, hypercortisolemia, and changes in appetite-regulating hormones such as leptin, ghrelin, peptide YY, and possibly adiponectin [ 32 ]. Changes are seen in the hypothalamic-pituitary axis (HPA) in patients with AN which affect both anterior and posterior derived pituitary hormones.

4.1.1. Hypothalamic-Pituitary-Adrenal Axis

The hypothalamic-pituitary-adrenal axis (HPAA) is in a chronically stimulated state in at least one-third of patients with AN [ 33 ]. Elevated baseline cortisol levels are likely observed during extreme caloric restriction in both healthy individuals and patients with AN. However, reversibility of HPAA dysregulation, even in recovered patients with AN, is not always observed [ 34 ]. Cortisol stimulates gluconeogenesis, and cortisol levels in patients with AN have been shown to be inversely correlated to fasting glucose [ 35 ]. The degree of hypercortisolemia also correlates inversely with BMI and fat mass [ 36 ]. Furthermore, it is associated with the severity of bone loss and depression in patients with AN [ 37 ].

4.1.2. Hypothalamic-Pituitary-Thyroid Axis

Severe weight loss in patients with AN is characterized by the nonthyroidal illness syndrome (also known as euthyroid sick syndrome) seen in patients with systemic illnesses, including chronic starvation. In women with AN, levels of total triiodothyronine (T3) are low. The reverse T3 level is elevated due to increased peripheral deiodination of thyroxine (T4) to reverse T3. Free T4 levels vary from normal to low normal, and TSH levels vary from normal to low normal [ 38 ]. These changes are an adaptive response to a decrease in metabolic rate and energy expenditure, and therefore require no treatment other than weight recovery.

4.1.3. Hypothalamic-Pituitary-Gonadal Axis

Studies of adult women with AN show immature, low amplitude luteinizing hormone (LH) pulses. The altered LH pulsatility manifests as hypothalamic amenorrhea. LH secretory patterns may revert to prepubertal levels of low, nonpulsatile secretion or to a pubertal pattern of entrainment of LH secretion to the sleep cycle. LH and FSH responses to GnRH appear normal, indicating that the reduced pulse frequency is not secondary to pituitary changes but presumably because of changes in the GnRH pulse generator. The gonadotropin secretion is stimulated by both estradiol and leptin, which are both decreased in patients with AN [ 39 ].

4.1.4. Growth-Hormone/Insulin-Like Growth Factor-1 Axis

Anorexia nervosa (AN) is characterized by a nutritionally acquired growth hormone (GH) resistance leading to low concentrations of insulin-like growth factor-1 (IGF-1), which is another essential determinant of reduced bone mineral density. High levels of GH in individuals with AN have a gluconeogenic role in maintaining euglycemia, mediated through increased lipolysis. Weight gain leads to a normalization of GH secretion and GH-binding protein concentrations, which are consistent with adaptation to the individual’s nutritional status [ 40 ].

4.1.5. Hypothalamic Neuropeptides

Hypothalamic neuropeptides such as nesfatin-1, phoenixin, spexin, and kisspeptin affect energy homeostasis and eating behaviors and may also be involved in the pathogenesis of anxiety related to eating disorders [ 41 ].

4.1.6. Vasopressin (or Antidiuretic Hormone, ADH)

Hyponatremia is very common in patients with AN and may lead to complications such as altered levels of consciousness and seizures. Purging behaviors, as seen in the binge eating-purging subtype, are the most common cause, although the syndrome of inappropriate antidiuretic hormone secretion (SIADH) may also be implicated. Central diabetes insipidus (DI), resulting in hypernatremia, has also been reported in patients with AN due to defective vasopressin secretion [ 42 ]; DI can also manifest during the refeeding period as a disorder of osmoregulation between serum osmolality and plasma vasopressin levels [ 43 ].

4.1.7. Oxytocin

Basal levels of oxytocin, a neuropeptide normally produced in the hypothalamus and released by the posterior pituitary, are decreased in patients with AN. Oxytocin plays a role in social bonding, modulation of anxiety and depressive symptoms, and bone metabolism. It is speculated that low oxytocin levels may contribute to alexithymia in women with anorexia nervosa [ 44 ].

4.1.8. Appetite-Regulating Hormones

Gastrointestinal hormones are normal signals to modulate appetite and maintain energy homeostasis. Ghrelin is an orexigenic hormone predominantly produced in the stomach and is thought to act upon the HPA, affecting the secretion of gonadotropin-releasing hormone (GnRH), adrenocorticotropic hormone (ACTH), growth hormone (GH), follicle-stimulating hormone (FSH), and LH. Plasma ghrelin levels are elevated in both AN-restricting (AN-R) and AN-binge eating/purging (AN-BP) subtypes. The increase in a hormone with orexigenic action in patients with AN is paradoxically caused by a central resistance to ghrelin. In patients with AN, the lack of a motivating feeding response to ghrelin, despite hunger sensation, supports an altered reward circuit that may contribute to the disease’s onset and maintenance [ 45 ]. Elevated ghrelin concentrations in patients with AN may be necessary to modulate glucose homeostasis, serving as an adaptive mechanism for maintaining normoglycemia in response to severe undernutrition. The secretion of ghrelin varies with insulin levels, suggesting a reciprocal regulation of these hormones [ 46 ].

Peptide YY (PYY) is an anorexigenic hormone released by the L cells of the distant intestine in response to caloric intake that acts at the hypothalamus to decrease appetite and food ingestion. PYY correlates inversely with BMI and fat mass. Levels of PYY are paradoxically elevated in patients with AN; this would not be adaptive to a state of chronic malnutrition but may play a role in the disorder’s pathogenesis contributing to decreased nutrient intake and disordered eating psychopathology [ 47 , 48 ].

Adipocytokines secreted by adipose tissue, such as adiponectin, leptin, and resistin, have significant roles in regulating energy metabolism and insulin sensitivity [ 49 ]. Leptin, a hormone mainly produced in white adipose tissues, is a valuable marker of long-term energy stores. In patients with AN, there is a marked fall in leptin concentration in proportion to fat mass [ 46 ]. A decrease in serum leptin levels, described in the literature, has been postulated to lead to both amenorrhea and restlessness similar to rat-specific semi-starvation-induced hyperactivity [ 50 ]. However, data concerning serum levels of the other adipocytokines are conflicting. Serum adiponectin has been found to be either increased, normal, or decreased in various studies in AN patients [ 51 , 52 ]. Likewise, serum plasma resistin levels have been found to be either decreased or normal [ 53 , 54 ]. These discrepancies suggest that confounding factors, such as eating behaviors and physical activity level, could interfere with the results and further studies are needed.

4.1.9. Glucose Metabolism

In general, fasting levels of glucose are lower in patients with AN than in healthy controls. Hypoglycemia has been described as one of the causes of sudden death in patients with AN. Liver injury caused by autophagia, hypotension, ischemia, in addition to marked glycogen depletion, seem to be the causes of hypoglycemia. To counteract the effects of hypoglycemia, secretion of both GH and cortisol induce insulin resistance, and thus increase glycemia. Gastrointestinal hormones such as glucagonlike peptide 1 (GLP-1) and amylin stimulate insulin release from pancreatic cells. The plasma levels of GLP-1 and amylin are both found to be low in patients with AN, which seems to be an appropriate adaptive response to starvation in order to prevent further hypoglycemia [ 42 ].

4.2. Refeeding Syndrome

The term refeeding syndrome (RS) has been used to describe the adverse consequences that can occur in all malnourished patients during the early stages of nutrition repletion, whether the method of refeeding is oral, enteral, or parenteral. Patients with AN are at high risk for RS. Refeeding hypophosphatemia (RH) is the most common complication of nutritional restoration for patients with AN. The highest risk of hypophosphatemia seems to be in patients who weigh less than 70% of their ideal body weight or lose weight rapidly [ 55 ]. Other consequences of RS include acute thiamine deficiency resulting in Wernicke’s encephalopathy and Korsakoff syndrome, with the potential for permanent cognitive impairment, hypokalemia, hypomagnesemia, metabolic acidosis, or alkalosis, and fluid overload resulting in cardiac failure. The American Society for Parenteral and Enteral Nutrition (ASPEN) Parenteral Nutrition Safety Committee and the Clinical Practice Committee have developed consensus recommendations for identifying patients with or at risk for refeeding syndrome (RS) and for avoiding and managing the condition. RS diagnostic criteria can be stratified as follows: a decrease in any one, two, or three of serum phosphorus, potassium, or magnesium levels by 10–20% (mild), 20–30% (moderate), or >30% and/or organ dysfunction resulting from a decrease in any of these or due to thiamine deficiency (severe), occurring within 5 days of reintroduction of calories [ 56 ]. In patients with AN, the degree of malnourishment appears to correlate with the severity of RH [ 57 ].

The reintroduction of nutrition leads to a switch from fat to carbohydrate metabolism and an increase in insulin concentration. Insulin stimulates the movement of potassium, phosphate, and magnesium into cells leading to their depletion in the extracellular compartments. Reactivation of carbohydrate metabolism increases degradation of thiamine, a cofactor required for cellular enzymatic reactions in Krebs cycle. Deficiency in all these nutrients can then occur [ 58 ].

Recent studies have provided evidence to support a switch in current care practices for refeeding from a conservative approach to higher calorie refeeding; however, caution should still be applied for more severely malnourished, i.e., <70% average body weight, and/or chronically ill, adult patients [ 59 ].

4.3. Bone Health in Anorexia Nervosa

Of notable concern related to AN are the effects of malnutrition on bone health. Unfortunately, the deleterious effects on bone mineral density (BMD) are not completely reversible despite weight restoration. These effects include decreased height, chronic pain, and increased immediate and lifetime risk of fracture due to inadequate bone accrual and ongoing bone loss [ 60 , 61 ]. A recent cohort study of 344 female patients who were being treated for eating disorder found a significantly lower BMD at the L-spine (16%), femoral neck (18%), and total hip (23%) in patients with active AN. Patients in remission had lower BMD than healthy controls but higher than women with active AN at the L-spine and hip [ 62 ].

Bone mineral density is measured by dual-energy X-ray absorptiometry (DEXA). T scores reflect a comparison with peak bone mass of healthy adults, while Z scores reflect age and sex-matched comparisons. Generally, in younger patients (<50 years old), Z scores are used for reporting. Osteopenia is defined as a BMD between −1.5 and −2.5, while osteoporosis is defined as a BMD < −2.5 [ 63 ].

Males and females with AN are both at risk of bone disease; 80% of females with AN have BMD Z scores < 1, 44% of females have BMD Z scores < 2, and 32% of males with AN have BMD Z scores < 2 [ 64 ]. A previous longitudinal study demonstrated a decrease in BMD over time, with a large mean annual decline of 2.4% at the hip and 2.6% at the spine. While BMD stabilized over the first year after weight restoration and continued to increase over time, it failed to fully normalize [ 64 ]. A recent study that assessed long-term outcomes of bone health in females, at 5 and 10 years after initial diagnosis of anorexia nervosa, demonstrated decreased BMD at the femoral neck and arms and CT evidence of cortical thinning, despite BMI being normal [ 65 ].

Factors associated with an increased risk of low BMD include lower BMI, longer duration of illness and amenorrhea, decreased muscle mass, and lower serum vitamin D levels [ 61 , 66 ]. The risk appears to be increased primarily in patients with restrictive eating disorder patterns. One large community sample found that BN was not a risk factor for low BMD if not associated with restriction [ 67 ]. An additional risk factor for bone disease in patients with AN is adolescent age. An earlier age of onset of AN (<18 years) is associated with a greater decrease in BMD [ 64 ]; 39% of bone mineral content is accrued between ages 10–14 and 95% of peak bone mass is typically reached prior to age 19 in healthy females, a process that is impaired in patients with AN. Adolescent females as well as males demonstrate decreased markers of both bone formation and resorption [ 64 ]. Adult women with AN demonstrate increased bone resorption and decreased bone formation [ 64 ]. This “uncoupling” is indeed the reason for aggressive loss of BMD in patients with AN, notwithstanding their typically young age, in contrast to post-menopausal women with osteoporosis where the only issue is increased resorption.

Bone disease in AN is caused by a complex interplay of physiological changes that occur in the malnourished state in response to energy deprivation which are incompletely understood. Changes in function of the hypothalamic-pituitary-adrenal axis include decreased GNRH leading to decreased LH and FSH and impaired ovulatory function. This leads to decreased estrogen which results in increased bone resorption. Decreases in testosterone and dihydroepiandrosterone (DHEA) are also observed and can further lead to decreased estrogen. In males with AN, low testosterone contributes to decreased BMD [ 68 ] and indeed severe osteoporosis is also a major problem for these males. In addition, GH resistance and increases in CRH, ACTH, and cortisol lead to decreased BMD. Changes in hormones such as leptin which is stored in adipose tissue and alterations in gut hormones further contribute. Collectively, these changes are reflective of the energy-conserving state in AN [ 64 ].

Patients with AN demonstrate a lifetime increased risk of fracture in both males and females. Thirty percent of women with AN report a fracture at one or more sites over a lifetime [ 67 ]. Risk of fractures in females is observed at younger ages, across all sites, whereas risk of fractures in males with AN is seen after age of 40 with an increased rate of vertebral fractures specifically [ 64 ]. Cumulative incidence of any fracture persists 40 years after diagnosis [ 69 ].

Despite the evidence of bone disease as evidenced by both decreased BMD and increased fracture risk in patients with AN, it is unclear if the increased fracture risk seen in AN can be directly associated with BMD measurement. One study, which demonstrated 60% increased fracture risk in women with AN, found fractures occurred even in women with normal BMD. Another 18-month longitudinal study demonstrated that 12.5% of women with AN had asymptomatic vertebral fractures not associated with illness duration, severity of malnutrition, or BMD [ 64 ]. A recent study that demonstrated increased fracture risk in AN did not find a direct association with decreased BMD [ 62 ]. Authors cited potential limitations of DEXA for assessing BMD in patients with AN, including relationships between DEXA and fracture risk taken primarily from post-menopausal populations, altered body composition arising from cycles of weight-loss and weight-gain leading to inaccurate estimate of BMD, and difficulty estimating the cumulative effects of AN given multiple periods of disease relapse and remission [ 62 ]. Further studies need to be conducted to better elucidate how to utilize DEXA in evaluating and reducing fracture risk in patients with AN.

Given the interplay between amenorrhea and bone disease, there has been interest in hormonal treatment of both males and females with AN. Many studies have not demonstrated increased BMD in females with AN who used oral contraceptive pills (OCPs), and there has been concern regarding hormonal treatment in younger patients with AN due to the risk of premature closure of epiphyseal plates [ 64 ]. However, a recent cross-sectional study demonstrated possible benefits. Females with AN using OCPs were found to have improved BMD at whole body, lumbar spine, as well as femoral neck, hip, and radius. The benefits correlated with longer duration of treatment with OCPs and shorter delay in initiating OCP treatment after AN onset. Patients with lower BMI experienced the greatest benefit from use of OCPs [ 70 ]. Yet, most experts do not recommend OCPs to treat low BMD in patients with AN. Previously, physiologic estrogen has been shown to improve BMD at the spine and hip in adolescents with AN [ 71 ]. Another recent small exploratory study that investigated the use of transdermal estrogen in adult women with AN found increased spine BMD [ 72 ], and many experts have recommend transdermal estrogen for younger patients with AN and low BMD. Testosterone therapy may be beneficial for treating males with AN. In older men with osteoporosis, testosterone has been shown to increase BMD, as well as in younger men with hypogonadism. However, there is a lack of data on treatment of bone disease in males with AN [ 68 ].

The mainstay for treatment of bone disease in AN is nutrition and weight restoration. In addition, patients should be instructed to take an adequate amount of calcium and vitamin D to optimize bone health. Studies in patients with AN have demonstrated an association with calcium intake <600 mg/day and lower bone mineral densities, as well as a high prevalence of vitamin D deficiency and insufficiency [ 68 ]. Treatment of bone disease in AN with prescription medication must take into account the risks and benefits of the various potential options. Bisphosphonates, which work by inhibiting bone resorption, are one option. Alendronate has been shown to increase BMD in adolescents treated for one year; however, the improvement compared to controls was not statistically significant. A randomized controlled trial demonstrated improvement in spine and hip BMD in adult women with AN [ 68 ]. Possible adverse effects include congenital abnormalities in women of childbearing age, which are particularly concerning given the long half-life of bisphosphonates [ 68 ]. Other potential side effects are osteonecrosis of the jaw in patients undergoing extensive dental work, gastrointestinal side effects, and atypical femur fractures [ 63 ]. Another treatment option is teriparatide, a recombinant parathyroid hormone analog which improves bone formation. It is given as a daily injectable for at least 2 years which may be impractical for some women. Yet, it has demonstrated significant improvement in BMD (10.5% at the spine) in older women with AN [ 73 ]. Teriparatide is contraindicated in pregnancy and should be avoided in patients with Paget’s disease or unexplained alterations in alkaline phosphatase given a risk of development of osteosarcoma observed in rats [ 63 , 68 ]. Another option is denosumab, a human monoclonal antibody that inhibits osteoclasts and is an injection given every 6 months. This medication has been demonstrated to be effectiveness in post-menopausal women with osteoporosis but has not been studied in AN. BMD decreases quickly after cessation of denosumab, therefore, drug holidays are not recommended with its usage [ 63 , 68 ].

4.4. Gastrointestinal Complications in Anorexia Nervosa

Gastrointestinal (GI) symptoms are common in AN, with over 90% of patients reporting GI complaints. While the pathogenesis of GI complaints are attributed to sequelae of weight loss, there is also a significant functional component to many of the GI complaints by patients with AN [ 74 , 75 ].

A recent systematic literature review, from 1967 to 2019, categorized the most common subjective GI symptoms reported by patients with AN. Among them include constipation, nausea, abdominal pain, abdominal fullness, vomiting, heartburn, epigastric pain, decreased appetite, diarrhea, and dysphagia [ 76 ]. Kessler et al. found that the severity of GI symptoms was more significantly correlated with somatization than with eating disorder severity and did not correlate with BMI [ 77 ]. This supported a previous study by Boyd et al. that also reported an association with anxiety and neuroticism and severity of GI complaints in patients with AN [ 78 ]. A recent literature review (2000–2017) of the medical causes of food-related GI symptoms in eating disorders found that AN patients reported higher food-associated symptoms than average; however, the incidence of celiac disease, an immune-mediated disorder to gluten, was similar among patients with AN and the general population. On the basis of their comprehensive review, Kress et al. predicted that the prevalence of immunological or structural GI disorders was no higher in patients with AN than in the general population, and that GI complaints from patients with AN were more likely to be functional. They advised that further diagnostic workup for persistent symptoms was warranted only after control of purging and restrictive behaviors and weight restoration [ 75 ]. More studies in patients with AN are needed to assess the functional nature of GI complaints and to further evaluate the prevalence of food allergies and intolerances.

Another interesting area of research is the role of intestinal microbiota, i.e., living organisms including prokaryotes, eukaryotes, archaea, and viruses, on the gut-brain axis [ 79 ]. Hata et al. found that transplanting the gut microbiome from patients with AN into germ-free mice resulted in poor weight gain, decreased appetite, decreased food efficiency, increased anxiety-related and compulsive behaviors, and decreased serotonin levels as compared with healthy mice. Compulsive behavior improved after administration of Bacteroides vulgatus (a genus found to be low in AN patients), however, it did not impact weight gain [ 80 ]. Studies in patients with AN have shown a significant reduction in Roseburia species, which was associated with a decreased level of butyrate, i.e., a short-chain fatty acid, that correlated with anxiety and depression disorders. A reduction in Roseburia inulinivorans was correlated with lower insulin levels, which may help patients with AN to preserve euglycemia. Additionally, higher levels of Enterobacteriacee and Methanobrevibacter smithii , an Archaeon capable of extracting more calories from food through the transformation of hydrogen to methane, have been identified in patients with AN as compared with healthy controls. There is experimental evidence that intestinal methane production is linked to slower intestinal transit, predisposing to constipation [ 81 ]. One study showed that, while overall microbial richness increased after weight gain, gut dysbiosis, short chain fatty acid profiles, and GI complaints remained persistent three months after weight gain [ 74 ]. Whether dysbiosis is the cause or effect of AN remains to be seen. Furthermore, fecal microbiota transplant is a promising area of research that might provide treatment and shed more light into this complex system [ 74 , 81 ].

While many of the GI complaints in patients with AN may be functional, there are certain GI complaints that require further investigation. Many case reports have documented superior mesenteric artery (SMA) syndrome (more commonly in AN-R) [ 76 , 82 ]; acute gastric dilation with subsequent gastric wall ischemia, necrosis, and perforation (more commonly in AN-BP); and duodenal dilation (more commonly in AN-R) [ 76 ], which further exacerbate GI symptoms and should remain in the differential diagnosis of abdominal pain in patients with AN.

In addition, there are numerous abnormalities in the liver that occur in AN. Starvation-induced autophagy and apoptosis is the proposed mechanism for liver dysfunction in AN, supported by liver biopsies in patients with AN with aminotransferase > 1900 IU/mL (typically with ALT > AST) [ 83 ]. Independent of body weight, the incidence of hypoglycemia was four to five times higher with liver dysfunction, and hypophosphatemia occurred twice as often with elevated liver function tests in patients with AN [ 84 ]. Severe, acute liver failure in patients with AN is reversible with weight restoration and rarely requires testing for secondary causes of liver dysfunction. An increase in aminotransferases also occurs with refeeding, likely due to excessive hepatic fat and glucose deposition, and can be managed with a reduction in daily caloric amount [ 83 ].

4.5. Cardiovascular Complications in Anorexia Nervosa

Cardiovascular complications have long been implicated in sudden death of patients with AN, which, as previously stated, remains to be one of the deadliest psychiatric disorders [ 85 ]. Research advances over the past few years have progressed our understanding of the static and dynamic cardiac changes in patients with AN.

Studies of cardiac hemodynamics continue to demonstrate the near universal finding of bradycardia, as well as decreased heart rate variability (HRV) in patients with AN [ 85 , 86 ]. Bradycardia is reversed with weight restoration, and permanent pacemaker placement is unwarranted and causes procedural complications [ 85 , 86 ]. As Cotter et al. recommended, society guidelines should be updated to include AN within reversible causes of bradycardia to avoid unnecessary permanent pacemaker placement [ 86 ]. A meta-analysis demonstrated a small increase in resting vagal tone, measured indirectly through HRV [ 87 ]. A decreased HRV has also been seen in patients with AN who underwent continuous cardiac monitoring for a year [ 85 ]. Co-morbid depression further decreased the HRV in patients with AN [ 88 ]. Decreased HRV has been a known independent predictor of mortality in post-myocardial infarction patients for decades [ 89 ]. However, more studies are needed to understand the clinical implication of decreased HRV in patients with AN.

Our understanding of cardiac structure and function in patients with AN continues to progress with comprehensive, modern, and dynamic echocardiographic evaluations and more recently cardiac MRI (CMRI) studies. A retrospective study evaluated Doppler echocardiograms in adult patients with AN with an average BMI of 12 (N = 124) [ 90 ]. All AN patients had subclinical cardiac impairments and 15% had reduced ejection fraction (EF). Interestingly, AN-BP and hypertransaminasemia were independently associated with a reduced EF. Consideration for echocardiogram should be made in patients with AN (especially AN-BP) with hypertransaminasemia to prevent complications of heart failure with refeeding [ 90 ]. Doppler echocardiography used to assess aortic stiffness by pulse wave velocity in adolescent AN patients found increased arterial stiffness [ 91 ]. Whether this portends a higher risk of cardiovascular disease, or if it is reversed with weight restoration, remains to be seen. A meta-analysis of echocardiographic findings in patients with AN revealed a reduction in left ventricular mass, a reduction in cardiac output, diastolic dysfunction, and an association with mitral valve prolapse and pericardial effusion, with a trend toward improvement with weight restoration [ 92 ]. Left ventricular mass was increased in hyperactive patients with AN as compared with non-hyperactive patients with AN but was still significantly lower than in the healthy controls [ 93 ]. Dynamic changes in cardiac function during exercise have been evaluated using stress echocardiography [ 94 ]. Adolescent patients with AN had reduced exercise duration, which was independently associated with BMI, and reduced peak cardiovascular indices as compared with healthy controls, but a normal pattern of cardiovascular response with progressive exercise [ 94 ]. In a study of 40 patients with AN (average BMI 15), 23% of the patients showed evidence of myocardial fibrosis on CMRI as evidenced by late gadolinium enhancement (LGE) as compared with 0% in the control group [ 95 ]. Myocardial fibrosis has been positively correlated to sudden death in the general population, likely due to propensity for arrhythmia formation [ 95 ]. A more recent study did not find evidence of LGE on CMRI in patients with AN. However, the majority of AN patients had recovered weight at the time of CMRI in the study [ 96 ]. More CMRI studies in patients with AN are warranted to better understand the prevalence of myocardial fibrosis and the clinical significance.

Previous studies have reported conflicting results on whether QTc prolongation is inherent in AN [ 97 , 98 , 99 , 100 ]. Recent studies, however, have reported consistent findings of normal QTc in patients with AN, including a meta-analysis of 964 patients and a cohort study of 1026 patients, using a variety of QTc correcting formulas [ 97 , 98 ]. Furthermore, another study found no correlation between QTc > 440 ms and increased risk of cardiac events or all-cause mortality in patients with AN [ 99 ]. QTc prolongation, when present in patients with AN, therefore, should be considered in the context of extrinsic factors such as hypokalemia and/or known QT prolonging medications rather than being summarily attributed to AN [ 97 ]. A dynamic QTc evaluation during exercise showed a longer QTc in patients with AN than healthy controls during peak exercise, returning to normal at rest [ 100 ]. More studies are needed to validate this finding and control for QTc prolonging medications. As the focus shifts from QTc prolongation as a cause of sudden death of patients with AN, a year-long insertable cardiac monitor study revealed bradyarrhythmia, particularly sinus pauses, to be more common and perhaps more relevant for understanding the etiology of sudden cardiac death than ventricular tachyarrhythmias, although more studies are needed [ 85 ].

4.6. Pulmonary Complications in Anorexia Nervosa

Anorexia nervosa can lead to weakness and wasting of respiratory muscles, dyspnea, reduced aerobic and pulmonary capacity, lung parenchyma alterations, and life-threatening consequences [ 101 ]. In recent studies, cases of spontaneous pneumothorax and pneumomediastinum related to starvation have been reported [ 102 , 103 , 104 ]. Different mechanisms for this have been proposed. One proposed mechanism is a traumatic mechanism with vomiting-induced esophageal rupture (Boerhaave syndrome), as has been described in cases of AN. Another proposed mechanism is the Macklin effect, where alveolar rupture may occur due to increased intra-alveolar pressure and low perivascular pressure [ 105 , 106 ]. Air from ruptured alveoli may migrate into the mediastinum, pericardium, peritoneal, and retroperitoneal cavities; subcutaneous tissues; and the epidural space [ 107 ].

Bullae, bronchiectasis, and other structural changes of the lungs may occur as severe complications of AN [ 108 ]. Emphysema-like changes have also been reported in the lungs of chronically malnourished patients because of anorexia nervosa [ 109 ].

Lung infections due to opportunistic organisms and usually nonpathogenic mycobacteria have been described in patients with AN and no history of a preexisting pulmonary disease [ 110 , 111 , 112 ]. However, gastroesophageal disease and other causes of chronic aspiration (self-induced vomiting) may predispose patients with AN to develop bronchiectasis, and thus increase their risk for non-tuberculous mycobacterial infections [ 113 ].

4.7. Hematologic Complications in Anorexia Nervosa

Gelatinous marrow transformation occurs as malnutrition worsens. Specifically, serous fat atrophy in the bone marrow, and normal marrow fat is replaced by a thick mucopolysaccharide substance that impedes the egress of precursor cells from the bone marrow [ 114 , 115 ]. This leads to trilinear hypoplasia with leukemia, anemia, and thrombocytopenia detected in that order of decreasing frequency [ 116 ].

Interestingly, despite frank neutropenia, patients with AN do not appear to be at an increased risk of infection, and thus neutropenic precautions are not needed. Similarly, the use of expensive growth factors is not indicated because the marrow reconstitutes quickly with nutritional rehabilitation. Anemia in patients with AN is typically normocytic, but when the red blood cells indices are abnormal, it is typically macrocytic, although vitamin B₁₂ and folate levels are not low [ 117 ]. Microcytic anemia is rare and requires additional evaluation.

4.8. Obstetric/Gynecologic Complications in Anorexia Nervosa

Amenorrhea occurs in up to 84% of females with AN, related to complex physiological hormonal changes including the aforementioned drop in serum levels of leptin and a decrease in gonadotropin-releasing hormone which leads to decreased LH, FSH, and anovulation [ 118 , 119 ]. This has important consequences on fertility in women with AN, making it more difficult to conceive and increases the likelihood of miscarriage and pregnancy related complications such as preterm birth, cesarean section, microcephaly, small for gestational age, and perinatal mortality if conception does occur. These complications persist in women with a history of AN despite recovery, albeit with overall improvement in fertility potential [ 118 , 120 ]. Thus, women with AN need a higher level of surveillance during pregnancy and delivery [ 120 ].

Despite overall difficulties with fertility in patients with AN, adolescents with AN have a two-fold increase in unplanned pregnancy. A recent review found a lack of evidence for a negative impact on BMD in adolescents and young women with AN treated with combined hormonal contraceptives over a 12–18 month period [ 119 ]. In addition, there may be a protective effect of prolonged usage of OCPs [ 119 ]; however, this remains controversial. Given the high risk of unplanned pregnancies, contraception is an important issue to consider.

5. Conclusions

In summary, the complications of AN are varied and complex, with a significant overlap in pathophysiological mechanisms. The devastating effects of malnutrition perpetuate the eating disorder given exacerbation of physical and psychological discomfort during malnutrition and refeeding. Awareness of current and real medical complications that occur in patients with severe AN can help both clinicians and families to recognize the complexity of the illness and underscores the need for informed care. There is significant emerging research about the widespread medical impact of AN, the understanding of which helps providers to best serve patients who suffer from this disorder.

Author Contributions

L.P., writing—original draft preparation abstract, introduction, bone health, obstetric/gynecologic health, conclusion, writing—review and editing of entire manuscript, project administration; D.G., writing—original draft preparation endocrine, pulmonary complications, writing—review and editing endocrine, pulmonary complications; V.K., writing--original draft preparation GI, cardiac complications, writing—review and editing GI, cardiac complications; K.C., writing—original draft preparation etiopathogenesis and psychiatric treatment, writing—review and editing etiopathogenesis and psychiatric treatment; P.M., conceptualization of entire manuscript, writing—original draft preparation hematologic complications, writing—review and editing entire manuscript, supervision of entire manuscript. All authors have read and agreed to the published version of the manuscript.

This research received no external funding.

Conflicts of Interest

The authors declare no conflict of interest.

Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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Perspective article, a perspective on chronic and long-lasting anorexia nervosa.

• 1 Department of Biomedical and Neuromotor Sciences, Psychiatry, Bologna University, Bologna, Italy
• 2 Department of Psychological Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand
• 3 Department of Biochemistry, Faculty of Medicine, UKM Medical Centre, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia

Anorexia Nervosa (AN) is a severe eating disorder which typically develops in younger females. Many studies focus on this specific population, a majority of which will eventually partially or fully recover. A minority will become chronic despite extensive treatment. These patients are treatment-resistant and may not necessarily benefit from usual treatment. In this article we will reflect on possible mechanisms which may explain the maintenance of disease, and especially on the possible role of affective and anxiety disturbances. We will use, due to the lack of large-scale studies, data from risk and prognostic factors, treatment options and neurobiological correlates in chronic AN patients. Lastly, we will propose how these elements may advise further research and treatments.

Introduction

Anorexia Nervosa (AN) is an eating disorder (ED) which significantly impacts younger females ( 1 ). It is characterized by low energy intake, fear of gaining weight, behavior which interferes with weight gain, and misperceptions regarding the patient's own body weight and shape ( 2 ) which significantly influence self-evaluation and misrepresent the severity of the illness to the patient. It typically develops in younger females, although cases emerging in the elderly population have been described ( 3 ). Two subtypes of AN are common: the binge-eating/purging subtype and the restricting subtype. Regardless of the subtype, patients reach extremely low weights. Affective and anxiety disturbances, such as depression, panic disorder and obsessive-compulsive disorder, are common comorbidities; substance abuse is also relatively frequent in these patients ( 2 ).

While a significant number of patients eventually recover, most reach partial of full remission only a number of years from the development of first symptoms ( 4 ). However, it has been estimated that more than 10% of AN patients ( 4 ) do not actually get better and eventually become chronic, as spontaneous recovery after more than 10 years of illness duration has been found to be rare, although it has been reported ( 5 ). There is, however, a paucity of studies on chronic AN, especially in the older population, possibly due to its relatively high remission rate after a few years of treatment ( 4 ). A definition of chronic AN has been developed, Severe and Enduring Anorexia Nervosa (SE-AN) ( 6 ), and some of its perpetuating factors have been suggested ( 7 ). While this definition is useful to describe peculiarities of chronic patients, due to the relatively broad criteria for SE-AN definition and the young age of emergence of symptoms, few studies actually focus on older-aged, long-standing AN.

We believe a different perspective on chronic, long-standing AN, based on evidence from neurobiological alterations, risk and prognostic factors, and available treatments, could suggest novel strategies to identify cases at higher-risk for chronicity. Patients with Anorexia Nervosa at a higher-risk of chronicity could share features which could be found in the elderly. This could, in turn, inform further studies and help the development of treatments aimed at both the younger and the older population.

In order to better understand chronic, long-standing AN, we will first describe two of its long-term definitions: Anorexia Tarda (AT), a form of Anorexia which occurs in the elderly, and SE-AN, focusing specifically on their limits.

Then, in order to better understand which factors may raise the risk of chronicity, we will look at the evidence regarding chronic cases of AN in order to integrate three areas of investigation: established risk and prognostic factors, which may intuitively influence the course of disease; evidence regarding treatments of chronic AN cases, as their effects (or lack thereof) may help better understand the neurobiological foundation of chronicity in AN; and lastly, evidence regarding neurobiological characteristics of chronic AN patients, in order to understand whether the integration of all three areas of investigation may suggest common features and mechanisms. This could help develop better treatment strategies which could benefit both the younger and the older population.

In conclusion, we will review the relevance and the limits of the available evidence, as the majority of the evidence focuses on the younger population, and we will suggest a different approach for future studies on the matter.

Two Definitions of Chronic and Long-Lasting AN

Although associated with adolescence and young age, eating disorders may occur de novo and even recur in the elderly.

Already in the 1980s, awareness of “Anorexia in the Elderly” was raised as associated with psychiatric and physical comorbidities, or as a reduction in opioid feeding drive and excessive satiety that are a normal part of aging ( 8 ). The term “Anorexia Tarda” (AT) was then coined to differentiate Anorexia associated with depression, dementia, cancer, and other comorbidities from Anorexia as a distinct eating disorder in the elderly ( 9 , 10 ). AT appears to be relatively rare among older women, with a population-based study reporting a 0.17% lifetime risk in women over 45 years old ( 11 ). It has not yet been established whether presentations of AT in older women represent a continuation of a lifelong illness or late onset of the disease: in the most comprehensive review to date ( 12 ), while AT was found to be more common than AN, comorbid depression was found in more than half of the older patients, which is in itself a risk factor for chronicity in AN ( 13 ). AT as a definition suffers from critical limits, as it lacks a consensus regarding age or duration of the illness, nor it differentiates de novo and recurrent cases.

Another definition recently gained traction: Severe and Enduring Anorexia Nervosa (SE-AN). Virtually unknown before 2010, it found its way in dozens of publications in the last decade. It is defined as AN which persists for more than 3–7 years (depending on the author) after appropriate treatments ( 6 , 14 ).

Although this definition may apply to older patients who suffer from chronic anorexia nervosa, if AN emerges in adolescence it is possible that the SE-AN patient can be quite young, and thus data may not necessarily inform clinicians regarding treatment options for older-aged AN patients. As Herpertz-Dahlmann suggested in a recent commentary ( 7 ), definitive data is still lacking regarding AN and specifically SE-AN in order to identify specific risk factors which may have a role in the development of chronic AN over the course of the disease. As noted by Kaplan and Strober ( 15 ), “no predictive study of long-term risk of illness persistence” assessed in a comprehensive manner the role of the risk architecture linked to AN, such as traits, genetics and other phenotypes associated to the illness. Yet, one could argue that factors which have a role in the persistence of AN in patients with decades of illness may already be present in SE-AN patients, as the majority of AN patients go into partial or full remission in less than a decade from the emergence of the illness ( 4 ) and never become SE-AN patients. That would mean that data on SE-AN patients could still be useful to ascertain elements which might sustain AN from a pathophysiological point of view well into the old age. However, this definition has limitations as well, as no consensus has been reached on the duration of the illness (more than 3 or 7 years), and it does not differentiate age of onset, nor whether recurrences should be included.

Why do these patients become chronic, long-standing cases, while the majority of other AN patients eventually go into remission? This uncertainty may stem from a systemic issue. The widespread use of American Psychiatry Association and World Health Organization criteria for psychiatry research allows clinicians to compare patients in a cost-effective manner from all over the world by providing an invaluable common framework for diagnoses. However, a categorical approach primarily based on symptoms and life history may only partially take into account the neurobiological relationship between different diagnoses, traits and characteristics, especially when they present similarly.

Hence, which factors may have a role in fueling the chronicity of AN? In order to better define the characteristics of this population, and in the absence of more targeted studies, a look at established risk and prognostic factors may be useful. In the literature, a number of factors have been identified as negative predictors of illness, and they may be useful to understand chronic AN from a different perspective, as they may have identified common characteristics within the broader AN definition which correlate with a higher rate of chronicity.

What Is the Evidence on Risk and Prognostic Factors in Anorexia Nervosa?

A number of risk and prognostic factors have been found to be involved in AN and its course. In Tozzi et al. ( 16 ) explored patients' perspectives on perceived causes of AN, and found that familial dysfunction (including emotional abuse), adverse experiences related to food (such as dieting, weight loss) and emotional duress (pressure, stress, frustration) were the most common perceived causes; a supportive relationship, personal growth (maturation) and therapy/counseling were the most frequently reported recovery factors. Bulik et al. ( 17 ) found that higher neuroticism raised the risk of developing AN; in Keski-Rahkonen et al. ( 13 ) found that pre-morbid depressive symptomatology predicted lower recovery rates in AN, and found that many unrecovered patients reported perfectionism and dissatisfaction with their partner.

Focusing on SE-AN patients, Le Grange et al. ( 18 ) compared Cognitive-Behavioral Therapy-AN (CBT-AN) and Specialist Supportive Clinical Management (SSCM) and found that lower age, shorter duration of illness, being employed, having better social adjustment and not taking any psychopharmacological medication were predictors of better outcome; eating disorder psychopathology, age, subtype of AN and depression were found as moderators of treatment. Regarding the role of comorbidities, extreme compulsiveness ( 4 ), obsessive-compulsive traits and OCD ( 19 ), depression ( 20 , 21 ), and anxiety ( 22 ) also emerged as negative predictors for full recovery.

While these characteristics inform the clinician, the mechanism through which they relate to the course of the illness is still unclear. Do they correlate with a worse prognosis due to the added burden of a fully separate illness, do they reciprocally impair their healing processes, or maybe their coexistence actually defines a specific phenotype?

Furthermore, many of the aforementioned factors may be of limited use to the clinician who first approaches the patient. Factors such as family dysfunction, emotional abuse, the absence of a supportive relationship and previous, negative experiences related to food may already have affected the prognosis. Comorbidities, such as pre-morbid depressive symptoms or trait perfectionism, can be useful to stratify the risk of chronicity, but as pre-morbid factors they, too, may have already exerted their effect on the prognosis.

Although informative, as this categorical approach helps us clinicians to immediately recognize elements from life histories which may correlate with a higher risk of chronicity, we still do not know how they are related and the mechanism through which they influence the prognosis.

What Is the Evidence on Treatment Options for Chronic, Long-Standing Anorexia Nervosa?

Can treatment options for chronic AN help us better understand the illness? The evidence in the available literature appears to be rather limited.

Despite being the disease with the highest fatality rate in psychiatry ( 23 ), there are still no approved pharmaceutical treatments for Anorexia Nervosa in Europe and in the United States of America. And for severe cases, effective treatment options are even less clear ( 24 ). However, a growing body of research investigated effective treatments for SE-AN.

Therapeutical interventions, in particular of a Cognitive-Behavioral imprint, such as CBT-AN ( 25 ), CBT-Enhanced, and Cognitive Remediation Therapy ( 26 ) appear to yield some results, although due to the uneven definition of SE-AN, mixed treatments and small sample sizes, their impact is still under investigation.

Evidence regarding pharmacological treatments is still quite limited. A trial of Dronabinol, a synthetic cannabinoid, showed evidence of weight gain in SE-AN patients but no change in AN symptoms ( 27 ), and a recent case report detailed full remission after 15 years of illness after a ketogenic diet and IV ketamine ( 5 ). A previous study on ketamine on treatment-resistant ED patients found longer remission of symptoms correlated to lower compulsion scores after ketamine infusions ( 28 ). Regarding brain stimulation therapies, studies on Deep Brain Stimulation found only small improvements in AN symptoms ( 29 ). Thus, data from treatment options for chronic cases is far from definitive, and does not appear to suggest a common pattern of efficacy among treatments, limiting our ability to formulate hypotheses regarding its mechanisms.

What Is the Evidence on the Neurobiology of Anorexia Nervosa?

AN appears to have a significant biological basis, as its heritability has been estimated to be 0.56 ( 17 ), and a growing number of neurobiological alterations have been found to be related to AN.

Dopamine is a neurotransmitter which is notoriously involved in reward mechanisms ( 30 ). Reward pathways have been found to be altered in AN, for example when healthy controls perceived euphoria in a drug-induced spike of dopamine levels, AN patients (even when fully recovered) reported feelings of anxiety and unpleasantness, which may explain why AN patients report food-elicited sensations as aversive from a motivational standpoint ( 31 ). Furthermore, even recovered AN patient appear to have altered reward processing mechanisms, as they find more difficult to process information and feedback ( 32 ), and also to respond to motivational inputs ( 33 ), compared to controls. This difficulty in processing information, feedback and motivation, may alter their capacity to make a fully informed choice regarding their health, a critical issue especially in SE-AN patients ( 34 ). At the same time, AN patients appear to be able to outscore healthy controls in specific measures of cognition ( 35 ).

Serotoninergic systems appear to be altered as well. Polymorphisms of serotonin transporters have long been associated with a higher risk of developing AN ( 36 ). Serotonin is a neurotransmitter made from Tryptophan, which is an essential amino-acid taken from food, and possibly mediates many of the comorbidities that have been associated with AN such as depression ( 37 ), obsessive-compulsive disorder ( 38 ) and anxiety ( 39 ). Since starvation lowers the concentration of Tryptophan, it may be regarded as a control measure to limit neurotransmission ( 40 ), possibly due to an intolerance of symptoms such as thoughts, feelings and emotions of these illnesses. Other imbalances in neurotransmitters, hormones and peptides such as norepinephrine, estradiol, and ghrelin have been found in AN ( 31 , 41 ).

Furthermore, imbalances in brain pathways may also mediate some of AN symptoms. It was found that the ability of AN patients to suppress hunger signals may be due to a reverse direction of signaling between hypothalamus and ventral striatum: in a recent study by Frank ( 42 ), signal in healthy controls was directed from the hypothalamus to the ventral striatum, while in AN patients signal direction was reversed.

How to Integrate the Available Evidence?

While the available evidence still does not allow to define a phenotype of chronic, long-standing AN, due to the lack of rigorous large-scale studies on this population, we may attempt to integrate and interpret the available evidence in order to advise future studies and hypotheses on this population.

The question is: do cases of chronic, long-standing AN suffer from the same disease as patients who will eventually recover from AN, or do they suffer from a different psychopathological disorder which, while manifesting symptoms that meet the categorical criteria for AN, could be described as a distinct diagnostic entity in which eating symptoms mislead the diagnosis, thereby indirectly contributing to a higher resistance to treatment? And if so, what pathopsychological characteristics would this phenotype have?

In order to define this phenotype in the future, neurobiological alterations may be a helpful starting point, as research evidence is rapidly expanding. Nonetheless, evidence from treatment options and risk and prognostic factors may be useful as well, especially for chronic, older-aged AN patients which are not recovered. This is because some of the literature on AN neurobiology struggles with a limitation: to discern alterations that stem from long-term starvation, they compare patients with active illness and in remission (Recovered Anorexia Nervosa, or RECAN), thus in order to avoid the critical confounder of body starvation, alterations which persist after full recovery may actually had been already present before the illness developed, and could be deemed risk factors worth investigating. However, this approach does not necessarily portray the condition of chronic, still unrecovered cases.

In order to better understand which of the many alterations found from neurobiological studies could have a role in the development of chronic AN, risk and prognostic factors may be regarded as elements which fuel a dysregulation in a number of systems and correlate with chronicity. Although a nature vs. nurture argument could be made, considering the significant heritability of AN ( 17 ), it may be suggested that affective and anxiety systems could have a role in the persistence of AN, as among the aforementioned factors are found pre-morbid depressive symptoms, obsessional and obsessive-compulsive tendencies, and familial dysfunction, which is in itself a known risk factor for anxiety and depressive disorders ( 43 , 44 ).

Although further studies are needed to better understand emotions, studies suggest the involvement of many structures in the brain, especially the amygdala, the prefrontal cortex (PFC), the orbitofrontal cortex (OFC), and the insula regarding motivation, interoception, emotions, anxiety and obsessive thoughts ( 45 , 46 ). Thus, it may be suggested that alterations in the neurobiology of AN affect at least some of the structures which are involved in the process of generating emotions.

Studies on effective treatments are still lacking. However, therapy and especially Cognitive-Behavioral approaches seem to be somewhat effective in resistant cases, which may be due to their foundation of treatments which are particularly useful for affective and anxiety disorders. While it may be suggested that the improvement from Dronabinol treatment is mediated by cannabinoid effects on hunger signals ( 27 ), the positive effects found in the two small studies on ketamine ( 27 , 28 ), a substance highly correlated to Esketamine, which was recently approved in Europe and in the United States for treatment-resistant depression, may further suggest a significant role of the depressive-anxiety spectrum on chronic, long-standing AN. Further studies on the significance of these mechanisms could explain why antidepressants are not effective treatments for AN ( 47 ).

Thus, at least part of the available evidence may suggest an involvement of affective and anxiety systems, the dysregulation of which may be worth investigating in chronic, long-standing AN patients.

A Perspective on Chronic AN and Comorbidities, Which Came First: The Chicken or the Egg?

A critical missing element in order to define chronic AN patients is what is fueling the persistence of disease.

In our clinical experience, even general psychiatry services—and more so non-psychiatric medical services—are fast to refer to ED clinics as soon as disordered eating symptomatology is found, especially in younger patients. ED clinics then typically assess the patient and focus on the extent of ED symptoms to discern whether, from a categorical point of view, they can be classified as a true ED. As seen from the available literature on AN, specific ED treatment helps ( 36 ) and in the following months to years the majority of patients get better, and some may even reach full remission of ED symptoms, which is why patients are typically referred to treatment from specialists. As previously mentioned, however, a minority of patients becomes chronic.

The available evidence may suggest an involvement of affective and anxiety systems in the prognosis, which is sometimes found even before the development of symptoms. Nonetheless, the typical age of emergence of ED symptoms, adolescence and young adulthood, is hardly one where communication is clear between patients and their families. The weight loss, however, can be spotted from a distance, and patients are eventually brought to medical attention.

It may be possible that a portion of AN patients who will eventually become chronic first develop a disturbance and then use restriction and refusal of food as means of control of the effects of said disturbance. This could, with time, become a chronic, relatively stable equilibrium which is maintained by food restriction and may be worsened by eating, a process which may also be sustained by recently suggested novel mechanisms, such as imbalances in gut microbiota ( 48 ). As previously mentioned, neurobiological evidence suggests that AN patients react negatively to a number of pleasant stimuli, especially food-related stimuli ( 31 ). If this premise were to be confirmed by future studies, that would explain why treatments who mainly focus on eating symptomatology may not work as well on this specific subpopulation. As a consequence, therapies which encompass egosyntonicity and focus on measures such as motivation, have been proposed in the treatment of chronic AN ( 25 ).

Conclusions

In conclusion, further studies are needed to better define the phenotype of the chronic, older-aged AN patient, as the SE-AN definition may include quite younger patients, and there is a substantial lack of evidence regarding AT. Thus, in order to better define the characteristics of long-lasting AN, a consensus on long-lasting AN and older-age AN, and especially their differences, must be reached. Moreover, the available literature may suggest the involvement of anxiety and affective disorders in the maintenance of AN, especially in long-lasting, chronic patients. However, due to the limited available evidence, further studies on the impact and prevalence of affective and anxiety disorders in AN patients are needed in order to clarify whether AN is (at least in part) masking and controlling symptoms of other disturbances which will eventually fuel the maintenance of disease, especially in chronic and treatment-resistant cases, possibly constituting a separate AN phenotype. It should also be noted that while our article attempts to describe different areas of investigations in chronic AN, it does not constitute a systematic review of the available evidence.

Data Availability Statement

The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author.

Author Contributions

MS, YB, HD, DD, FP, and AA contributed to the conception and design of this manuscript. MS wrote the first draft of the manuscript. All authors contributed to manuscript revision, read, and approved the submitted version.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Publisher's Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

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Keywords: anorexia nervosa, severe and enduring anorexia nervosa, older-age, long-lasting anorexia nervosa, role of emotions, affective and anxiety

Citation: Speciani M, Barak Y, Damanhuri H, De Ronchi D, Panariello F and Atti AR (2021) A Perspective on Chronic and Long-Lasting Anorexia Nervosa. Front. Psychiatry 12:756669. doi: 10.3389/fpsyt.2021.756669

Received: 10 August 2021; Accepted: 11 October 2021; Published: 29 October 2021.

Reviewed by:

Copyright © 2021 Speciani, Barak, Damanhuri, De Ronchi, Panariello and Atti. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Anna Rita Atti, annarita.atti@unibo.it

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Anorexia nervosa: What you need to know

Anorexia means a loss of appetite and inability to eat, often due to a physical illness. Anorexia nervosa is when a person intentionally restricts their food intake.

A note about sex and gender

Sex and gender exist on spectrums. This article will use the terms “male,” “female,” or both to refer to sex assigned at birth. Click here to learn more .

Anorexia nervosa is the name of a mental health condition. It is a serious disease, but, with the right treatment, recovery is possible. It is part of a potentially life threatening mental health disorder that involves emotional challenges, an unrealistic body image, and an exaggerated fear of gaining weight.

In some cases, an individual may lose a significant amount of weight and demonstrate the characteristic behaviors of anorexia but not have very low body weight or body mass index (BMI). Researchers refer to this as atypical anorexia nervosa.

Anorexia nervosa often appears during a person’s teenage years or early adulthood, but it can sometimes begin in the preteen years or later in life.

People often think of anorexia nervosa in connection with people who are female, but it can affect people of any sex or gender. Research suggests that the risk of eating disorders may be higher among transgender people than cisgender people.

Statistics show that females with anorexia outnumber males with the disorder at a ratio of 10 to 1. The effects of the disorder are more likely to be life threatening among males than among females. The reason for this is that males often receive a later diagnosis due to the mistaken belief that it does not affect them.

What is anorexia nervosa?

A person with anorexia nervosa will intentionally restrict their food intake as a way to lose weight or avoid gaining weight. A person with anorexia nervosa will often have an intense fear of weight gain, even if they have severely low body weight.

Dietary restrictions can lead to nutritional deficiencies, which can severely affect overall health and result in potentially life threatening complications.

The emotional and psychological challenges of anorexia nervosa can be hard for a person to overcome.

Therapy includes counseling, nutritional advice, and medical care. Some people may need treatment in the hospital.

There are many myths about eating disorders. These can lead to false assumptions and affect a person’s chances of seeking and getting help.

Learn more about the myths surrounding eating disorders and the real facts.

Anorexia nervosa symptoms

Anorexia nervosa is a complex condition. The main sign is significant weight loss or low body weight. In atypical anorexia nervosa, the person may still have a moderate weight despite substantial weight loss.

A lack of nutrients may lead to other physical signs and symptoms, including:

• severe loss of muscle mass
• listlessness, fatigue , or exhaustion
• low blood pressure
• lightheadedness or dizziness
• low body temperature with cold hands and feet or, possibly, hypothermia
• bloated or upset stomach
• swollen hands and feet
• loss of menstruation or less frequent periods
• infertility
• loss of bone density, increasing the risk of fractures
• brittle nails
• constipation
• irregular or abnormal heart rhythms
• lanugo , which is fine downy hair on the body
• increased facial hair
• bad breath and tooth decay in people who vomit frequently

The person may also demonstrate certain behaviors, such as :

• limiting their overall food intake or the range of foods they consume
• showing excessive concern with weight, body size, dieting, calories, and food
• exercising a lot, taking laxatives , or inducing vomiting
• assessing their body weight and size frequently
• talking about being “fat” or having overweight
• denying feeling hungry or avoiding mealtimes
• developing food rituals, such as eating foods in a specific order
• cooking for others without eating
• withdrawing from friends and social interaction
• showing signs of depression

The person may associate food and eating with guilt. They may seem unaware that anything is wrong or be unwilling to recognize their issues around eating.

Not everyone with the condition will behave in the same way, and some individuals may experience atypical anorexia nervosa, meaning that they will not have low body weight.

Anorexia nervosa causes

Concerns about body weight and shape are often features of anorexia nervosa, but they may not be the main cause. Experts do not know exactly why the condition occurs, but genetic, environmental, biological, and other factors may play a role.

For some people, anorexia nervosa also develops as a way of gaining control over an aspect of their life. As the person exerts control over their food intake, this feels like success, and so, the behavior continues.

Anorexia nervosa risk factors

Several factors can increase a person’s risk for developing anorexia nervosa, including :

• past criticism about their eating habits, weight, or body shape
• a history of teasing or bullying, especially about weight or body shape
• a sense of pressure from society or their profession to be slim
• low self-esteem
• having a personality that tends toward obsession or perfectionism
• sexual abuse
• a history of dieting
• pressure to fit in with cultural norms that are not their own
• historical trauma, such as racism

Biological and genetic factors

A person may also have a higher chance of developing an eating disorder if:

• a close relative has had a similar disorder
• there is a family history of depression or other mental health issues
• they have type 1 diabetes

In 2015, researchers found that people with anorexia nervosa may have different gut microbial communities than those without the condition. This could contribute to anxiety, depression, and further weight loss.

Learn how the COVID-19 pandemic has affected people with eating disorders.

Early diagnosis and prompt treatment increase the chance of a good outcome.

The doctor may ask the person questions to get an idea of their eating habits, weight, and overall mental and physical health.

They may order tests to rule out other underlying medical conditions with similar signs and symptoms, such as malabsorption, cancer, and hormonal problems.

In addition to a physical exam, this may include :

• blood tests, including coagulation tests, a complete blood count , and a comprehensive metabolic profile
• urine tests
• an electrocardiogram
• imaging tests, such as a computed tomography (CT) scan or bone density scan

A psychological evaluation is also necessary to determine if a person meets the diagnostic criteria for anorexia nervosa.

According to the National Eating Disorders Association , the criteria below can help doctors make a diagnosis. However, they note that not everyone with a serious eating disorder will meet all these criteria.

• Restriction of energy intake and significantly low body weight for the person’s age, sex, and overall health.
• Intense fear of gaining weight or becoming fat, despite being underweight .
• Changes in the way the person experiences their body weight or shape, an undue impact of body weight or shape on the person’s self-image, or denial that their current low body weight is a problem.

Anorexia nervosa vs. bulimia nervosa

Anorexia nervosa and bulimia nervosa are both eating disorders and sometimes share certain symptoms, such as an intense fear of gaining weight or a distorted body image.

However, people with anorexia often restrict food intake, exercise excessively, or adopt extreme diet patterns to lose weight.

On the other hand, bulimia nervosa is characterized by recurrent episodes of binge eating or eating large amounts of food, followed by compensatory behaviors to prevent weight gain, such as self-induced vomiting, excessive exercising, consuming laxatives, or fasting.

This cycle can also be present in people diagnosed with the binge-eating/purging subtype of anorexia nervosa.

However, unlike bulimia, anorexia nervosa is also characterized by the significant restriction of energy intake, leading to significantly low body weight for a person’s age, sex, and overall health.

Treatment and recovery

A healthcare professional will make a comprehensive plan to address the individual’s specific needs.

It will involve a team of specialists who can help the person overcome the physical, emotional, social, and psychological challenges that they face.

Strategies include:

• cognitive-behavioral therapy (CBT) , which can help the person find new ways of thinking, behaving, and managing stress
• family and individual counseling, as appropriate
• nutritional therapy, which provides information on how to use food to build and maintain health
• medication to treat depression and anxiety
• supplements to resolve nutritional deficiencies
• hospital treatment, in some cases

It can be challenging for a person with anorexia nervosa to engage in treatment. As a result, the person’s participation in therapy may fluctuate. Relapses can occur, especially during the first 2 years of treatment.

Family and friends can provide crucial support. If they can understand the condition and identify its signs and symptoms, they can support the individual during recovery and help prevent a relapse.

Hospital treatment

The person may need to spend time in the hospital if they have:

• a severely low BMI
• malnutrition
• complications due to inadequate food intake
• a persistent refusal to eat
• a psychiatric emergency

Treatment will allow for a gradual increase in food intake to restore overall health.

Complications

Complications can affect every bodily system, and they can be severe.

They include problems with:

• the cardiovascular system
• the blood, such as a low white or red blood cell count
• the digestive system
• the kidneys
• hormonal imbalances
• bone strength

Some of these issues can be life threatening. In addition to the physical effects of poor nutrition, the person may have an increased risk of suicide.

In fact, anorexia nervosa has the highest mortality rate of all mental health conditions.

For this reason, early diagnosis and treatment are essential.

Eating disorders can be caused by a variety of factors and there is currently no known way to prevent the development of anorexia nervosa.

However, recognizing the symptoms and seeking treatment early can help improve the chances of recovery.

According to the National Eating Disorders Association , prevention programs aimed at reducing factors for eating disorders could also be beneficial.

These programs typically involve changing public policy, encouraging people to question diet culture and the media, promoting body acceptance, and replacing restrictive diets with practices like intuitive eating.

Living with anorexia nervosa

Dr. Maria Rago, Ph.D., the president of the National Association of Anorexia Nervosa and Associated Disorders (ANAD) , offered Medical News Today the following tips for anyone who thinks that they or a loved one may have anorexia nervosa:

• Be kind and respectful rather than judgmental.
• Look into providers of treatment to find good matches, and meet with some of the people to decide who can best help.
• Consider a treatment team — including a dietitian, a therapist, and a psychiatrist — all of whom should specialize in eating disorders.
• Make sure to get all the education and support possible.
• Review the treatment plan and make changes when you think best.

Dr. Rago noted that ANAD has free support groups and mentoring programs for recovery and that they invite people to take advantage of the free services. “The right help can change your life, and even save your life,” she said.

Frequently asked questions

Here are a few common questions about anorexia nervosa.

What is the nervosa part of anorexia?

“Nervosa” is a term rooted in Latin that originally meant “nervous” or “vigorous.” “Anorexia” comes from both Latin and Greek and means “without appetite.”

When originally used to describe a syndrome in the Middle Ages, “anorexia” referred to a refusal to eat, with the goal of religious or spiritual purity. In the 1800s, the term “anorexia nervosa” came to mean a self-imposed food refusal.

What is the difference between anorexia and anorexia nervosa?

Anorexia is a term used to describe the loss of appetite or the inability to eat, which can be caused by many health conditions. On the other hand, anorexia nervosa is an eating disorder in which a person intentionally limits their food intake in an effort to lose weight or prevent weight gain.

What are the warning signs of anorexia?

There are many potential warning signs of anorexia, including feeling preoccupied with food, exercise, or body weight. Experiencing feelings of guilt or shame after eating, avoiding situations that involve food, and withdrawing from friends, hobbies, or activities are a few other possible warning signs.

Anorexia nervosa is an eating disorder and a serious mental health condition. It involves restricting food intake, which can lead to severe nutritional deficiencies.

The effects of anorexia nervosa can be life threatening, but counseling, medication, and treatment for underlying mental health issues can help people with this condition.

If a person has signs of anorexia nervosa, they should seek medical help. Early diagnosis and treatment are more likely to lead to a positive outcome.

Last medically reviewed on June 22, 2022

• Eating Disorders
• Nutrition / Diet
• Obesity / Weight Loss / Fitness
• Psychology / Psychiatry

How we reviewed this article:

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• Berends, T., et al. (2018). Relapse in anorexia nervosa: A systematic review and meta-analysis [Abstract]. https://pubmed.ncbi.nlm.nih.gov/30113325/
• Bulimia nervosa. (n.d.). https://www.nationaleatingdisorders.org/learn/by-eating-disorder/bulimia
• Cost, J., et al. (2020). Medical complications of anorexia nervosa. https://www.ccjm.org/content/87/6/361.long
• Dell'Osso, L., et al . (2016). Historical evolution of the concept of anorexia nervosa and relationships with orthorexia nervosa, autism, and obsessive–compulsive spectrum. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939998/
• Diemer, E. W., et al. (2018). Beyond the binary: Differences in eating disorder prevalence by gender identity in a transgender sample. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5775111/
• DSM-5 changes: Implications for child serious emotional disturbance [Internet]. (2016). https://www.ncbi.nlm.nih.gov/books/NBK519712/
• Duncan, T. K., et al. (2014). Reclamation of power and self: a meta-synthesis exploring the process of recovery from anorexia nervosa. https://www.tandfonline.com/doi/full/10.1080/21662630.2014.978804
• Eating disorders. (2021). https://medlineplus.gov/eatingdisorders.html
• Edakubo, S., et al. (2020). Mortality and risk assessment for anorexia nervosa in acute-care hospitals: A nationwide administrative database analysis. https://bmcpsychiatry.biomedcentral.com/articles/10.1186/s12888-020-2433-8
• Garber, A. K., et al. (2019). Weight loss and illness severity in adolescents with atypical anorexia nervosa. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6889949/
• Kleiman, S. C., et al . (2015). The intestinal microbiota in acute anorexia nervosa and during renourishment: Relationship to depression, anxiety, and eating disorder psychopathology. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4643361/
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Anorexia nervosa and familial risk factors: a systematic review of the literature

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• Antonio Del Casale   ORCID: orcid.org/0000-0003-2427-6944 1 ,
• Barbara Adriani 2 ,
• Martina Nicole Modesti 2 ,
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• Anna Maria Speranza 1  

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Cite this article

Anorexia Nervosa (AN) is a psychological disorder involving body manipulation, self-inflicted hunger, and fear of gaining weight.We performed an overview of the existing literature in the field of AN, highlighting the main intrafamilial risk factors for anorexia. We searched the PubMed database by using keywords such as “anorexia” and “risk factors” and “family”. After appropriate selection, 16 scientific articles were identified. The main intrafamilial risk factors for AN identified include: increased family food intake, higher parental demands, emotional reactivity, sexual family taboos, low familial involvement, family discord, negative family history for Eating Disorders (ED), family history of psychiatric disorders, alcohol and drug abuse, having a sibling with AN, relational trauma. Some other risk factors identified relate to the mother: lack of maternal caresses, dysfunctional interaction during feeding (for IA), attachment insecurity, dependence. Further studies are needed, to identify better personalized intervention strategies for patients suffering from AN.

Highlights:

This systematic review aims at identifying the main intrafamilial risk factors for anorexia nervosa, including maternal ones.

Intrafamilial risk factors identified mostly regard family environment and relational issues, as well as family history of psychiatric diseases.

Family risk factors identified may interact with genetic, environmental, and personal risk factors.

These findings may help develop tailored diagnostic procedures and therapeutic interventions.

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Introduction

Eating behavior encompasses all responses associated with the act of eating and is influenced by social conditions, individual perception, previous experiences, and nutritional status. Additional influencing factors include mass media and idealization of thinness. Anorexia nervosa (AN) is a psychological disorder concerning body manipulation, including fear of becoming fat and self-inflicted hunger. This disorder is interpreted as a response to the social context and a woman’s rejection of fat to deny mature sexuality (Gonçalves et al., 2013 ; Korb, 1994 ) and it was once supposed to have “hysterical” causes (Valente, 2016 ). The current definition of AN provided by the DSM-5 describes it as “a restriction of energy intake relative to requirements such as to lead to a significantly low body weight […]; intense fear of gaining weight or becoming fat, or persistence in behaviors that interfere with weight gain […]; alteration in the way weight or body shape are experienced […]” (Cuzzolaro, 2014 ). The lifetime prevalence of AN is estimated being of 1.4% (0.1–3.6%) in women and 0.2% (0-0.3%) in men (Galmiche et al., 2019 ). The lifetime prevalence rates of anorexia nervosa might be up to 4% among females and 0.3% among males (Van Eeden et al., 2021 ). AN finds its roots in biological, psychological, social, and familial risk factors.

More precisely, heritable risk factors for AN can be found in 48–74% of cases (Baker et al., 2017 ): for example, it has a higher prevalence in female relatives of individuals with AN (Bulik et al., 2019 ). The presence of genetic correlations between AN and metabolic and anthropometric traits may explain why people with AN achieve very low BMIs and may even maintain and relapse to low body weight despite clinical improvement (Bulik et al., 2019 ). On the other hand, psychological risk factors include excessive concerns about weight and figure, low self-esteem, and depression; while social risk factors are related to peer diet, peer criticism, and poor social support (Haynos et al., 2016 ). As far as family is concerned, it has been observed that anorexic girls’ families are often characterized by poor communication with one another, overprotection, conflicts, and hostility (Emanuelli et al., 2003 ; Horesh et al., 2015 ; Sim et al., 2009 ).

Overall, the puzzle of AN risk factors is still obscure and needs deeper investigations as far as some predisposing aspects are concerned, such as intrafamilial risk factors, which have been extensively analyzed but not properly clarified for clinical applications. Because of the multifactorial etiology of AN, intrafamilial risk factors identification can help to establish preventive interventions in at-risk individuals, and to provide tailored treatments from the earliest stages of the disorder. Our main hypothesis is that intrafamilial as well as maternal risk factors play an essential role in the development of the disease.

Therefore, the main objective of this work is to provide a scientific review of the existing literature about familial relational risk factors involved in the development of AN, with the aim of improving: prevention, establishment of an early diagnosis, and development of a tailored treatment.

Methodology

On February the 16th, 2022, a first research was conducted on PubMed with the title/abstract filter, using the terms “anorexia AND risk factors AND family” in the search bar. For eligibility, we included only randomized controlled studies and case-control studies focused on the issue, as well as case-control studies with at least 50 participants. We excluded reviews, single case studies, case reports, other types of articles and other studies that did not focus on the main topic. The system provided 76 articles, of which 24 were ignored for low relevance. Hence, 52 were assessed for eligibility, from which 26 articles were excluded for not respecting the inclusion criteria, and 12 were excluded for not analyzing the research subject specifically. To the remaining 14 articles, 2 were added from citation search.

In the PRISMA diagram below (Fig.  1 ), the articles identified for the review (76) are reported schematically: screened (76), assessed for eligibility (52) and included (16).

PRISMA diagram of the study

The main results of the studies analyzed are summarized in Table  1 .

Despite anorexia having been usually considered an expression of age-specific conflicts intensified by constrictive cultural ideas and certain kinds of familial constellations (Bemporad et al., 1988 ), having our review included studies from 1990 to 2021 and conducted across many countries (i.e. US, Japan, Poland, UK, etc.) we can hypothesize that such a condition just evolves with culture and time, still maintaining certain background issues that we are aiming to emphasize in order to recognize certain red flags.

Eating disorders mark deficits in the ability to be nourished and to symbolize embodied experience. Psychoanalytic theories suggest that mothers who are insufficiently developed leave the child either austerely avoiding intrusion or struggling to digest maternal provisions without becoming lost in them. (Charles, 2021 ). Infantile Anorexia (IA) has been defined as a child’s refusal of food for more than 1 month, between 6 months and 3 years of age; acute and/or chronic malnutrition; parental concern about the child’s eating; mother-child conflict, talk, and distraction during mealtime (Chatoor et al., 1998 ). Maternal risk factors for (IA) we have identified across the review can confirm this widely accepted theory, specifically lack of maternal caresses (Mangweth et al., 2005 ), dysfunctional interaction during feeding in IA (Ammaniti et al., 2010 ), and attachment insecurity (Chatoor et al., 2000 ). Regarding maternal history of psychiatric diseases, it has been noted that maternal depression has an influence on the development of conflicts during mother-child interaction in younger children, while maternal psychoticism predicts mother-child conflict during feeding in older children (Ammaniti et al., 2010 ). This means that depressed mothers engage in less positive interactions with their infants while breastfeeding, with difficulties in empathically recognizing their infant’s affective states at mealtimes (Ammaniti, Ambruzzi et al., 2004 ; Feldman et al., 2004 ).

In addition to the relational risk factors, maternal diet seems to play a role in the development of AN (Haynos et al., 2016 ). This mechanism seems to find its roots early during childhood, since the infant’s weight appears to be inversely related to the mother’s degree of concern about her body shape (Ammaniti, Lucarelli et al., 2004 ). The “modelling theory of AN” (Pike & Rodin, 1991 ) argues that adolescent girls begin the diet by mimicking their dieting mothers. It seems that family concerns about weight and appearance are directly linked to the development of low satisfaction with one’s body, and therefore directly or indirectly related to eating problems (Leung et al., 1996 ).

Maternal risk factors are synthesized in Table  2 .

Enlarging our highlight from the mother to the whole family nucleus, the onset and maintenance of AN seems to be closely related to familial risk factors, and knowing them is crucial to identify the best therapeutic approach in order to target the unhealthy family environment as well as the needs of the patient. In addition, being aware of the familiar background may help in strengthening the hypothesis of genetic correlates within Eating Disorders (ED). Intrafamilial risk factors for the development of ED seem to have a greater impact when they occur early in adolescence (Field et al., 2008 ), but most of them are chronic in time and one can suppose they can be found in a family at any time during the life of the patient.

The major intrafamilial risk factors identified in this review are summarized in the following Table  3 .

Increased food intake in the family (Hilbert et al., 2014 ) seems to play a role in the development of ED. This seems counterintuitive, but the discrepancy between one’s family food intake and peer and media influences on body ideals may contribute to triggering a subtle mechanism by which diet represents a way to affirm oneself in front of the family and reestablish social acceptance.

Perfectionism (Hilbert et al., 2014 ; Pike et al., 2008 , 2021 ) is widely recognized as a familiar risk factor across many studies, and it can be assimilated to higher parental demands (Pike et al., 2008 ). It surely contributes to creating a tense family environment in which the development of oneself is more difficult, therefore inhibiting progressive differentiation of self from other (Charles, 2021 ). Perfectionism itself will become a personal risk factor for the outcome and severity of disease (Longo, Aloi et al., 2021 ) in a way that could be mimicking the family environment.

In general, unhealthy family functioning is predictive of adolescence problems (Lyke & Matsen, 2013 ). General family malfunction is predictive for AD onset during adolescence, and the level of affective expression of the family seems to be relate to ED risk during adolescence (Felker & Stivers, 1994 ), but our review has highlighted that all those features of what could be described as a “toxic” family environment in the common sense play a role in the development of AN. Emotional reactivity (Lyke & Matsen, 2013 ), as well as family taboos regarding nudity and sexuality (Mangweth et al., 2005 ), low familial involvement (Haynos et al., 2016 ), negative affectivity (Pike et al., 2008 , 2021 ), and family discord (Pike et al., 2008 ) may lie in the background in the lives of a future AN patient, and should be recognized as environmental risk factors in order to develop a tailored psychotherapeutic intervention that may involve the family as well as the patient, since it seems clear that the quality of family functioning influences the development (McGrane & Carr, 2002 ) and maintenance of EDs (North et al., 1997 ; Strober et al., 1997 ; Wewetzer et al., 1996 ).

As far as the presence of other disorders in family members is concerned, our review established that a familiar history of almost any psychiatric disorder (Longo, Marzola et al., 2021 ; Pike et al., 2021 ), including depression (Lyon et al., 1997 ), affective disorders (Steinhausen et al., 2015 ), alcohol and drug abuse (Lyon et al., 1997 ) plays a role in the development of AN. Nevertheless, having a sibling with AN increases the risk of developing AN (Machado et al., 2014 ; Steinhausen et al., 2015 ). We can hypothesize that the role of genetics in this mechanism is crucial yet still obscure, and nevertheless, talking about the presence of these diseases in members of the family nucleus, having to cope and live with the difficulties of others’ conditions is what can predispose to AN. In addition, the opposite may happen as well: there is an increased risk for relatives of patients with AN and BN to develop subclinical forms of ED, major depressive disorder, obsessive-compulsive disorder, and anxiety disorders (Lilenfeld et al., 1998 ). What is curious to note is that, on the one hand, having a sibling with AN predisposes to the development of AN (Felker & Stivers, 1994 ; Machado et al., 2014 ; Steinhausen et al., 2015 ), probably because of shared intrafamilial risk factors, therefore underlining the importance of the aim of this review; but, on the other hand, negative family history for ED predicts poor outcome (Ackard et al., 2014 ), probably because of the familiar unpreparedness to cope with such a difficult condition and the discrepancy created between the healthy members and the patient, which remains alone and uncapable of sharing certain issues with the others, so close yet so far from them.

Another risk factor identified is having suffered a relational trauma (Longo, Marzola et al., 2021 ). In general, individuals who have suffered from traumatic events (physical violence, being threatened with a weapon, sexual violence, being a victim of robbery) more frequently develop maladaptive eating behaviors (Field et al., 2008 ). Some evidence also suggests an increase of severe life events in the year preceding the onset of AN (Råstam & Gillberg, 1991 ). Children of mothers who have experienced the loss of a vital member of their family (i.e. older child or partner) in the six months prior to pregnancy have a higher risk of ED than children and infants who have not been exposed to this risk factor (Su et al., 2015 ). Further confirming the possible role of relational trauma as a red flag not only in the development of AN, but also in determining the severity of the disease, patients with AN and comorbid Post Traumatic Stress Disorder (PTSD) show more severe concerns about body shape and weight (Field et al., 2008 ). Having suffered physical and sexual abuse during childhood appears to be related to the onset of psychiatric pathologies in general, and not specifically to the onset of EDs in the young adult (Bruch, 1977 ; McGrane & Carr, 2002 ; Smith et al., 1995 ): therefore, this risk factor needs further investigation to confirm its specific role in the development of AN.

Strength and limits

The strength of this work lies in the comparison between different studies regarding AN showing high level of evidence and providing a complete picture of the constellation of intrafamilial risk factors of anorexia nervosa. There main limit of this study is that few articles from those included are from the very last years, while many other studies were conducted and published earlier (1990–2014), underlining the need of further investigations.

Conclusions

The main intrafamilial risk factors for AN identified from this study are: increased food intake in the family, perfectionism, higher parental demands, emotional reactivity, family taboos regarding nudity and sexuality, low familial involvement, negative affectivity, family discord, dependence, negative family history for ED (as a predictor of poor outcome), family history of depression, positive family history for psychiatric disorders, affective disorders in family members, alcohol and drug abuse, having a sibling with AN, relational trauma. Some other risk factors identified may relate to the role of the mother during childhood especially, and are as follows: lack of maternal caresses, dysfunctional interaction during feeding (for IA), attachment insecurity, dependence, maternal diet.

Complex interactions occur between intrafamilial risk factors and other personal aspects and symptoms, including perfectionism, individual body image issues, social concerns, excessive preoccupation with weight control, stress and adjustment problems, lack of close friends, social prejudice.

In conclusion, further studies are needed to understand more clearly how intrafamilial risk factors for AN interact with other environmental, personal and genetic ones, in order to connect the dots that can lead to an improvement of diagnostic and therapeutic procedures, and to the development of tailored intervention strategies that may target multiple issues in the life of the patient, including intrafamilial mechanisms that may be identified precociously and addressed through familial therapy, for the sake of the whole family nucleus.

Data availability

Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

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Conceptualization: ADC, SV; Data curation ADC, GP; Investigation: SV, BA, MNM, AV, GP; Methodology: ADC; MNM; Supervision: ADC, AMS; Roles/Writing - original draft: ADC, SV, BA, MNM; Writing - review & editing: ADC, MNM.

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Del Casale, A., Adriani, B., Modesti, M.N. et al. Anorexia nervosa and familial risk factors: a systematic review of the literature. Curr Psychol 42 , 25476–25484 (2023). https://doi.org/10.1007/s12144-022-03563-4

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Terminal anorexia nervosa: three cases and proposed clinical characteristics

• Jennifer L. Gaudiani   ORCID: orcid.org/0000-0002-2035-9390 1 ,
• Alyssa Bogetz 2 &
• Joel Yager 2  

Journal of Eating Disorders volume  10 , Article number:  23 ( 2022 ) Cite this article

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Most individuals with eating disorders will either recover, settle into an unrecovered but self-defined acceptable quality of life, or continue to cycle from crisis to relative stability over time. However, a minority of those with severe and enduring eating disorders recognize after years of trying that recovery remains elusive, and further treatment seems both futile and harmful. No level of harm reduction proves achievable or adequately ameliorates their suffering. In this subgroup, many of those with anorexia nervosa will experience the medical consequences of malnutrition as their future cause of death. Whereas anyone who wishes to keep striving for recovery despite exhaustion and depletion should wholeheartedly be supported in doing so, some patients simply cannot continue to fight. They recognize that death from anorexia nervosa, while perhaps not welcome, will be inevitable. Unfortunately, these patients and their carers often receive minimal support from eating disorders health professionals who are conflicted about terminal care, and who are hampered and limited by the paucity of literature on end-of-life care for those with anorexia nervosa.

• Case presentation

Three case studies elucidate this condition. One patient was so passionate about this topic that she asked to be a posthumous co-author of this paper.

Conclusions

Consistent with literature on managing terminal illness, this article proposes clinical characteristics of patients who may be considered to have a terminal eating disorder: diagnosis of anorexia nervosa, older age (e.g. age over 30), previous participation in high quality care, and clear and consistent determination by a patient who possesses decision-making capacity that additional treatment would be futile, knowing their actions will result in death. By proposing the clinical characteristics of terminal anorexia nervosa, we hope to educate, inspire compassion, and help providers properly assess these patients and provide appropriate care. We hope that this proposal stimulates further expert consensus definitions and clinical guidelines for management of this population. In our view, these patients deserve the same attendant care and rights as all other patients with terminal illness, up to and including medical aid in dying in jurisdictions where such care is legal.

As a patient with severe and enduring anorexia nervosa advocating for my legal right to MAID (medical aid in dying), I confronted numerous obstacles and challenges from the medical profession, related not just to the question of whether I should have access to MAID generally, but more so, how my anorexia, a psychiatric condition frequently misunderstood by the medical community, interacted with my decision making capacity and desire to pursue MAID as one potential option knowing that my illness was indeed terminal. –Alyssa

The vast majority of potentially terminal illnesses carry with them thoughtfully considered and evidence-based staging criteria. These criteria allow patients and clinicians to distinguish mild and likely curable presentations of the disease from irreversible, pre-terminal and terminal stages. Medical specialties treating cancer, organ failure, or various infectious diseases have dedicated considerable attention and resources to delineating levels of severity. While preliminary suggestions for labeling severe and enduring anorexia nervosa (SE-AN) [ 1 ] and for staging the disorder have been proposed [ 2 ], generally accepted staging criteria for anorexia nervosa (AN) have not yet been developed. Remarkably, the same diagnostic label (“AN”) and treatment criteria that apply to teenagers only a few months into their disorder are also used for patients who are decades older, who have lived through innumerable admissions to inpatient and residential care facilities, and whose quality of life has been irrevocably damaged by persistent, severe mental and physical illness. The field acknowledges SE-AN as a somewhat distinct clinical condition, but despite thoughtful clinical and research efforts [ 3 , 4 ] the designation has not been formalized as a diagnosis, and consensus regarding criteria for SE-AN remains elusive [ 5 ].

AN carries the second highest mortality rate in the DSM-5 after opioid use disorder, with a death rate estimated at 5–16 times that of the general population. [ 6 , 7 ] Several important recent studies confirm and expand upon these data. A specialized medical inpatient unit in France for those with severe anorexia nervosa evaluated 384 patients admitted over 17 years, with a mean age at admission of 29.4 years old. The standardized mortality ratio (SMR) was 15.9 for women and 22.4 for men, where older age was determined to be a major predictor of mortality. The mean age at death was 41.3 (± 15.3) years, on average two years after hospital admission. The SMR was maximally increased for patients whose first admission to the unit took place while they were between 25 and 35 years old. Specifically, those admitted between 30–34 years old had the highest SMR of 26. Somatic (medical) causes accounted for 43% of deaths, while 11.5% of deaths were caused by suicide. [ 6 ] In a registry-based observational epidemiological study encompassing the entire population of Denmark over 44 years, the SMR for all-cause mortality reached a maximum of about 6 in the age group 20–34 years, and the SMR for suicide in those with AN was 11. Natural causes accounted for two-thirds of death in those with AN. [ 8 ] Finally, a retrospective cohort study evaluated 19,041 individuals with an eating disorder in Ontario, Canada, using administrative healthcare data. The entire cohort, not comprised only of those with AN, had an SMR of 5; they found that potential years of life lost were 6 times higher than expected compared with the Ontario population. Similar to the other studies, peak values for SMRs were observed among adults between 30 and 44 years old, and again the SMRs observed in males were almost two-fold higher than in females. [ 9 ] Importantly, the profound suffering inherent in AN drives the high suicide rate noted in multiple studies, where up to 20% of patients who die prematurely do so by suicide [ 10 ]. Compared with gender- and age-matched groups, patients with AN are 18 times more likely to die by suicide [ 11 ].

Based on these data, AN can unquestionably prove fatal. Despite this fact, the field lacks clinical roadmaps for compassionate, appropriate care for those who will not be able to survive. This does great disservice to patients and their families. By comparison, we do not expect individuals with metastatic lung cancer who have disease progression despite past treatments, which often come with negative sequelae, to keep presenting for those same ineffective treatments. Rather, they are more likely to receive the psychological preparation, connection, and medical and emotional support offered to patients with terminal conditions. Although current laboratory measures and imaging studies by themselves are unable to help us stage patients with AN, based primarily on clinical histories and patients’ narratives we can better understand the clinical course of this illness and the subset of patients with AN who may seek palliative care [ 12 , 13 , 14 ].

There is growing recognition that palliative care may be appropriate for some patients, but the clinical characteristics for terminal anorexia nervosa have not been proposed. Delineating and validating this stage would greatly assist patients, families, and clinicians across disciplines, especially those in palliative and hospice care. Designating terminal AN may more readily enable patients to receive palliative care, hospice care, and emotional and practical resources for loved ones, as well as access to medical aid in dying (MAID) where legal. Therapeutic goals in these situations are to ameliorate suffering and honor the life lived. Of note, MAID is offered to individuals whose death is inevitable within six months from an underlying disease process; it provides patients a choice in how they die, not whether they die. It is not a means of suicide.

In this paper, we describe three cases of exceptional people whose AN was terminal, and who died peacefully with family around them. All three were patients of a private practice outpatient medical clinic specializing in eating disorders in Denver, Colorado. One patient, who had been a medical researcher herself, was so passionate about the topic that she asked to join as a posthumous author on this paper so her voice could be heard. The other two patients’ parents consented to share their son’s/daughter’s stories and reviewed, and all three families edited the relevant story prior to manuscript submission. All families agreed that first names should be used instead of a pseudonym or initials in order to emphasize the truly personal, real-life origin of these stories. Based on these experiences and others [ 12 , 14 ], we conclude by proposing a set of clinical characteristics of those who can be identified as having terminal AN.

Case presentations

Case 1: aaron.

Aaron was a 33-year-old man with a long history of restrictive AN, severe obsessive compulsive disorder (OCD), recurrent major depression, and chronic suicidality. He had been a sensitive child with low self-esteem and perfectionism from a young age. His parents noticed OCD traits from early childhood, but he did not receive this formal diagnosis until years later.

During his freshman year in high school, a health class warned about the risks of “eating junk food.” Aaron began to run regularly and played hours of basketball daily. One by one, he eliminated dietary fats and created food rules. His parents thought this was just a stage, an assessment they came to understand very differently over time, but they eventually recognized his serious problems and established a treatment team. Later in high school, Aaron was hospitalized several times for AN, participated in family therapy, and required his mother’s presence, even at school, to complete meals. Despite graduating as valedictorian of his high school class, he was initially too ill to start college. Later, his attempt to begin college was thwarted by his need for constant supervision of food intake. Aaron’s perfectionism and self-criticism ultimately ended his college career.

Over the next two decades, Aaron spent countless months in medical hospitals and in inpatient and residential eating disorder settings. He repeatedly gained the weight required for discharge so that he could return home, only to inevitably relapse. He felt mortified and guilty about the amount of money his family spent on his treatment, and he was acutely aware of life passing him by.

In his early 30 s, following a long and serious downward spiral during which he refused a higher level of care, his family finally threatened to call 911 if he did not enter treatment. Consequently, he was admitted to an inpatient eating disorder program. After first spending time in a hospital setting for stabilization where he refused to eat, a feeding tube was placed. A court mandate to ensure ongoing treatment was requested and granted on grounds of grave disability from his mental illness, and he spent the next 10 months against his will in inpatient and residential eating disorder care. He cut off communication with his parents but allowed the treatment team to talk with them. Eventually his therapist convinced him to have family sessions over the phone; it was the only time his parents could talk to him.

Aaron’s persistent resistance to treatment throughout his stay at the eating disorder program caused difficulty in maintaining his nutritional stability. He underwent in-depth exposure and response prevention therapy around food as he continued to be tube fed, and he was finally able to sustain his weight with oral food. At that time, he only agreed to eat to avoid the prospect of being administered olanzapine against his will, as he feared this medication would cause him to gain weight.

After Aaron had been fully weight restored for several months, he was stepped down to a partial hospital program (PHP). He immediately restricted intake and proceeded to lose nearly a pound a day, resulting in readmission to residential treatment where, after intensive efforts, he once again achieved his target weight. Aaron struggled with basic activities of daily living due to his OCD. For instance, he resisted using lotion or lip balm as he feared they might be absorbed into his skin as calories. He completed a course of intranasal ketamine in hopes of alleviating his OCD, depression, and suicidality, but ketamine treatments had no meaningful impact.

Author JG (hereafter referred to as “Dr. G”) first met Aaron for an outpatient medical consultation after he had completed this most recent residential treatment and was once again about to step down to PHP. This consultation constituted one component of an organized, comprehensive future discharge plan. In this initial medical visit, after a year of residential treatment, Aaron was medically stable. He desperately missed his eating disorder behaviors, fantasized about eating less and losing weight, and wished his AN would have already taken his life. Aaron mused that his all-or-nothing, perfectionistic temperament made the unknown terrifying, but he felt proud of how rigidly he had previously adhered to his eating disorder rituals, as he believed that few others could achieve a similar degree of calorie restriction. Despite his long history of treatments, including his year of suffering through the long court-mandated treatment, Aaron had never meaningfully changed his eating related attitudes, thoughts, or behaviors. He had absolutely no motivation for recovery.

During the initial consultation, Dr. G informed both Aaron and his emotionally supportive and highly invested parents that she could offer ongoing outpatient medical care along one of two pathways. In one, Aaron would complete PHP, be discharged to home (where he lived with his parents), see a therapist and dietitian regularly, and work on whatever degree of recovery he could bear, aiming toward a quality of life that he called “living productively.” Should he decide that he required a higher level of care, the team would promptly support that choice. On the second pathway, if Aaron relapsed and declined readmission, the outpatient team would no longer battle with him to seek a higher level of care, given the futility of his most recent, autonomy-depriving treatment course. Rather, the family and team would support and comfort him until such time as he required home palliative care and eventually hospice support. Aaron initially felt that these two choices were needlessly stark and binary, and he settled back into PHP.

Two months after the initial consultation, Aaron continued to endure PHP, primarily to honor his commitment to his residential treatment team that he would see through his course of treatment. But he felt no better. He received a course of intravenous ketamine to supplement the intranasal ketamine treatment initiated in the residential program, but he experienced no improvements in mood, hopelessness, or OCD. Just before discharge to his parents’ home, he still hadn’t decided which treatment pathway to choose. He would not accept psychiatric medications, and a team consisting of a physician, therapist, and dietitian was established to care for him at home.

However, starting on the day of his discharge from PHP, Aaron stopped eating altogether, a course of behavior that is rare even in those with severe AN. He drank only water, stating, “I don’t want to die, but my eating disorder is in charge.” A week later, he met with his longstanding outpatient therapist. She was very apprehensive about his ability to remain in the community, and she felt ambivalent concerning what her role might be if he insisted on remaining at home. Aaron told her, “I wish I could eat, but I won't eat; I don't want to die, but I feel hopeless that there's any other pathway.” The therapist worried that she would be forced to have Aaron detained against his will in his home state. A formal decision-making evaluation was performed by a local psychiatrist, and Aaron was found to possess decisional capacity. Consulting with his home therapist, Dr. G proposed that Aaron’s refusal to eat was less about “wanting to die” than simply accepting that he could not live—he was not “attracted to life” [ 17 ]. Dr. G suggested that the proper course at this point would be to proceed with a home palliative care consultation and shift treatment goals to supporting comfort and dignity, as Aaron clearly declined a return to treatment.

During a telemedicine meeting with Dr. G a week later, Aaron asserted, “I don't want to do this for anybody else anymore. It's time to do things only if I want them.” At about this time, Aaron also sought comfort from his therapist and his religious leader, as the prospect of death frightened him, and he was unsure what dying would mean. But he described that being given the choice of what would happen next was empowering – “different, scary, relieving, and right” – in great contrast to repeatedly feeling powerless and demeaned by his many prior chaotic relapses followed by intense pressures to return to treatment. Aaron signed a Do Not Resuscitate (DNR) order and within the next few days was referred to a home palliative and hospice care organization. Dr. G spoke with the organization’s medical director to explain why this brilliant 33-year-old man who was refusing to eat was being referred for palliative care. Aaron hoped that the home palliative care service would help him and his family “process this sorrow and fear.”

Two weeks later, after more than a month of eating nothing and drinking only water, Aaron’s OCD and insomnia were heightened; he worried that by simply smelling his mother’s cooking he might be ingesting those calories. He believed that he might absorb calories from the grocery cart of the person ahead of him at the store. Always reluctant to take medications, he began to consider accepting anxiolytics from the hospice staff, whom he thought were extremely kind.

Aaron noted that by spending no energy forcing himself to eat, he was able to direct energy toward engaging in his faith. His siblings came to visit, and as they talked and laughed, he realized it had been years since they had connected positively. Throughout the course of his eating disorder, every family connection had felt fraught. He summarized his collective family’s response to this pre-terminal phase as, “They were very supportive. They recognize the gravity of this situation. They aren't angry, sad but not fearful.” As he chose to spend his days talking with his parents and sleeping, he noted that he was thinking about others "rather than being so self-absorbed." Imagining his parents’ distress made him sad, and he wanted his parents to keep getting support after his death. "This is one of the hardest things they've had to deal with in their lives."

Even as he rapidly lost weight, Aaron’s body distortions grew worse, and he kept wishing his weight would fall even faster. After almost six weeks without food, Aaron began accepting anxiolytics and antiemetics. He obsessed that someone might have injected his water bottles with calories. When Dr. G asked if he had any words to share for posterity, he expressed words of warning for those who might find themselves in his situation: “OCD will amplify,” “Be prepared for an annoying obsessive brain that might drive you crazy,” and “Just because you aren’t eating doesn’t mean it’s all good now.” He expressed how vital it was to “have people in your life [doctor, parents, family, close friends] whom you trust and can seek reassurance from, who love you unconditionally,” whose comforting words can be “life-saving in terms of giving you peace.” He connected deeply with a feeling that peace comes from God.

After about eight and a half weeks without any food, Aaron was spontaneously vomiting daily and feeling much weaker. Beautifully cared for by home hospice, he began to take low dose morphine for pain and distress. When Aaron’s parents wondered what his death certificate would say about cause of death, Dr. G reassured them that the cause would be anorexia nervosa and malnutrition, not suicide. Often speaking through tears, Aaron’s parents described how they were enjoying a deep loving sweetness with their son that they hadn’t experienced in years, and how they would miss him when he died. They felt compassion for those who lose a loved one abruptly without having time for love, connection, and closure. Often, they saw glimpses of the boy they hadn’t seen in years, as when he looked at photos that made him laugh.

Two weeks later, Aaron passed away with his family surrounding him. Even as they were exhausted and grieving deeply, his parents expressed enormous gratitude for the care he received and for the way they had been able to reconnect with him.

Case 2: Jessica

Jessica was a 36-year-old woman with a history of OCD and AN, purging subtype (laxatives) that began during her junior year of high school, when she tried to lose weight prior to a vacation. This started a pattern of restricting, binge eating, and then overexercising that persisted into college. When her weight, which had remained normal for some time, did eventually drop, she left college for intensive outpatient eating disorder treatment. It was such a difficult experience that from this time on, she mistrusted eating disorders providers. She lamented that she lost most of the fun of college to her eating disorder.

Due to progressive constipation, Jessica began using laxatives, which led to laxative abuse. She soon found that every time she stopped taking laxatives, her weight skyrocketed (due to rehydration and rebound edema). Ultimately, her AN caused her to drop out of nursing school. Jessica experienced her first hip fracture from severe osteoporosis when she was critically emaciated at age 27, requiring her to move home with her parents; the following month she incurred a stress fracture of her shoulder from using crutches. Her parents pursued guardianship as Jessica was refusing a higher level of care, but her medical team refused to release records to the family’s attorney due to HIPAA. Without the option to pursue guardianship with mandated longer-term residential treatment, her parents came to believe this was the critical juncture where recovery might have been possible, but instead her disease became more entrenched. Over the next 7 months, working with her outpatient primary care provider, dietitian, and therapist, she slowly gained a meaningful amount of weight, although she remained very underweight. Following this, she got an excellent job and once again lived independently from her parents, working productively for three years. However, at age 29, her increased anxiety, the side effects of laxative abuse, and the shame of her anorexia caused her to separate herself from her family and to work from home, increasing her isolation. She checked herself into an expert inpatient medical center to stop using laxatives and then spent a week in inpatient eating disorder treatment before leaving against medical advice. Jessica did manage to stay off laxatives for a year but was plagued by edema. Repeatedly, restriction and overexercise would recur, usually accompanied by laxative abuse, which at its worst consisted of taking 100 tablets a day.

During her initial consultation with Dr. G, Jessica memorably stated, “The eating disorder keeps me out of integrity with my values. It doesn't feel good. You believe something but aren't living it. This is the biggest motivation for wanting to change. I really want to live in alignment with my values, honoring my body, feeling things, stopping being unkind to my body.” Although very kind and compassionate towards others, she struggled to show herself the same grace.

Jessica met criteria for immediate admission back to the inpatient medical service, but given her prior negative experiences with treatment, she wanted to attempt to keep working and live near her parents. She agreed to outpatient care with a multidisciplinary team, focusing on harm-reduction goals. Initially, Jessica was able to follow medical and nutritional recommendations faithfully. Then, within three months of initiating outpatient medical care she fell and sustained a pelvic fracture. This was frightening, disabling, and prevented her from taking her calming (and to her, calorie-burning) nature walks. Overcome by managing the challenges of a rapidly changing body on her own and worried about her fracture and bone health, Jessica readmitted herself to specialized inpatient medical care for medical stabilization. Following stabilization, she agreed to transfer to residential care to attempt a full course of eating disorder treatment. However, after two weeks in the residential care program she left against clinical advice, unable to follow the meal plan consistently and feeling extremely distressed by her bodily changes (even though her weight had barely changed).

At home, Jessica again tried hard to follow treatment recommendations at a harm-reduction level (no laxatives, low caloric intake, gentle movement in the outdoors), but once more the distress of bodily changes was too much for her to bear. About a month after leaving the residential program, Jessica first talked about the possibility of palliative care and began talking with her mom about suicidal thoughts. Most nights she would say she hoped she didn’t wake up the next morning. In order to help Jessica resist the laxatives that gave her such severe abdominal pain and nausea, and still hoping to support her in finding an acceptable degree of harm reduction, Dr. G worked with Jessica to use diuretics to manage fluid weight changes. (Notably, this approach would rarely if ever be offered in a more typical eating disorders treatment plan.) Jessica operated within these guidelines and constraints for the next five months, at times thinking she might be able to persist, but more often lamenting that this strategy was still too difficult and painful. By this point, she had been granted indefinite leave from work and moved in with her parents.

About nine months after initial consultation, Jessica acknowledged that it was time for a palliative approach, confessing, “I’m just ready. It's been a long fight. I'm eating so little, and I'm back on the laxatives every couple of days.” She declined intranasal or intravenous ketamine which might have ameliorated her depression, OCD symptoms, and hopelessness. As she felt progressively miserable physically and psychologically, her suicidality increased. She purchased a gun, and one night she drove to a bridge with thoughts of jumping off, but then decided to return home. She had difficulty finding a therapist who understood terminal AN and who could accept her treatment trajectory, but she found and worked with a kind naturopathic doctor who specialized in mental health, and she did experience some benefit from psychiatric medications.

At this point, fearful of suffering a long, drawn-out death from starvation and unwilling to put her parents through the agony of witnessing this decline, Jessica requested referral to a palliative care specialist who assessed patients for medical aid in dying (MAID). Dr. G spoke with Jessica’s parents repeatedly, assuring them that guardianship and forced treatment were likely now to be futile. The parents had done everything possible to help their daughter find an acceptable quality of life. Jessica signed a DNR order. After speaking with the palliative care physician by phone to discuss the case and advocate for Jessica, Dr. G completed the MAID forms as consulting physician, given that Jessica’s prognosis was presumed to be 6 months or less. The palliative care physician prescribed the MAID medications.

About a year after the initial consultation, and about three months after the MAID consultation, Dr. G saw Jessica for the last time via telemedicine. Jessica wrote to Dr. G in an e-mail, “I’ve been back in a place the last several weeks where the emotional pain and the physical and emotional exhaustion of living like this are just too much for me. I’m trying to make it to the end of May, maybe through June to meet my brother’s upcoming baby before I go.” Jessica described her life as filled with unbearable pain and anxiety. Watching people walking around the neighborhood making future plans felt devastating, because she’d “give anything to be in anybody else’s shoes.” Yet when she thought about stopping diuretics, eating enough food, and gaining weight so she could physically live that life, she said, “it feels impossible.”

Jessica waited several weeks to fill the MAID prescription. She then set multiple dates to use it over a couple of months and changed her mind as that date got closer. A month before her death, she started to receive home hospice services. During this time period, she had long conversations with her parents, brother, and friends, noting that she had many happy memories over her life, apologizing for what she had put them all through over the years, and stating that she hated her eating disorder. She told them she realized that, while her eating disorder behaviors made it seem like she hadn’t loved or trusted them at times, she loved them all very much. She repeatedly told her family that she didn’t want to die, that she didn’t want to miss out on future time with her family, friends, and niece and nephew, but she just couldn’t continue to exist this way. The emotional pain and anxiety were unbearable. She couldn’t live a normal life, and she felt her body was too destroyed to recover. Her parents believe that in her last month she was trying to die naturally by barely eating, reducing her fluid intake, and walking for hours daily, even when she had to sit down often to catch her breath. She stopped driving and carried identification in case she collapsed on a walk. She fainted at home several times in the week before her death, including the night before she died. On the day she took the MAID prescription, she stayed in bed, was at peace, and spent time talking with each parent and her brother. Together as a family, they reminisced, laughed, cried, had their “hug circle” as they had called it since her childhood, and felt surrounded by love. Her parents each held a hand, and her brother sat right next to her. During the three doses of the medicine taken over an hour, she was comfortable and conscious. Within ten minutes of taking the final dose, Jessica closed her eyes, and her breathing slowed.

Jessica didn’t choose to live with anorexia. For all the years she endured living within its prison and myriad complications, her parents ultimately felt strongly that she deserved to choose the time, place, and way of her release. They felt that an unexpected blessing of MAID was that it allowed Jessica to live several months longer than she otherwise would have. Knowing she didn’t have to die a violent death by suicide, that she would have a peaceful way out when the pain and anxiety became unbearable, and that she would be able to die with dignity surrounded by loving family, allowed her to hold on longer. As a dying wish to her mother, she shared, “Mom, I'd like you to do something that will help others not go through what I went through."

Case 3: Alyssa

Alyssa, the posthumous author on this paper, was a 36-year-old woman with OCD, depression, and restrictive AN who described herself as having “a type A, neurotic personality: a sensitive, compassionate, loving person who's incredibly self-critical and has wanted to do things 0% or 110% with no gray area.” She first felt suicidal at age 13, when she realized that her body was too large to fit into standard dress sizes for her upcoming Bat Mitzvah. She started therapy at that time and was continually in therapy thereafter. After going through high school at a higher weight, the summer before college she vowed to change her body and began exercising in earnest. In college it was easy to restrict. By the time she returned home for Thanksgiving she had lost a substantial amount of weight. Everyone praised her, and she experienced “a deluge of external validation that was irresistible,” firmly establishing her eating disorder by age 18. Alyssa wrestled with AN throughout the rest of her education and career. A brilliant academic, she became the only non-physician Assistant Director of a major academic medical center residency department, mentoring residents and students, doing research, and publishing in major journals.

After struggling with AN for 15 years, during which she received intermittent outpatient support, Alyssa moved in with her parents and reduced her workload. She was extremely helpful in her mother’s struggle with a cancer diagnosis and often underplayed the significance of her own illness. At age 33, to correct severe hypercalcemia she was admitted to the teaching hospital in which she had previously worked. The family felt that her AN was hardly addressed during that hospitalization, in part due to the fact that institutional expertise for AN was confined to a pediatric program. To them, this felt like a vital missed opportunity to attempt changing her disease trajectory, in particular as the only recommendation on discharge was to seek residential eating disorder care.

Alyssa worked for 7 months to obtain insurance authorization for care in a residential eating disorders program, and to gain enough weight to meet their admission criteria. However, upon admission to that program she was deemed still too underweight (by one pound) and was referred to a specialized inpatient medical program. Being rejected for care after so much work also felt like a missed therapeutic opportunity. After a delay, Alyssa spent several weeks in the specialized hospital program and met the minimal criteria for discharge, departing with the understanding that she would immediately enroll in another residential program. However, after discharge from the hospital she refused to do so and could never accept going to an eating disorders program thereafter.

In the years prior to initial consultation with Dr. G, Alyssa’s outpatient treatment team included a local primary care physician with whom she was very close, a therapist she had been seeing regularly in recent years, and an expert eating disorders therapist who had worked with her and the family over the years. Over a period of three years, Alyssa had intermittently thought about and even phoned Dr. G’s outpatient medical clinic, but she never booked an appointment, indicating that she felt very ambivalent about recovery and was considering a palliative care approach. When she finally presented for an initial consultation, Alyssa identified her goals as follows: “I really want a life, to use my Masters in Social Work degree to help others heal, to find a partner, and to experience pleasure, laughter, joy, and freedom, including from my own brain.” As her main barrier she cited the chronic, longstanding shame and body disgust that persistently kept her from meeting her own needs.

At the time of initial consultation, Alyssa met criteria for inpatient medical hospitalization, although she experienced remarkably few physical symptoms, which reinforced her view that she must be “fine.” She declined a higher level of care. Nonetheless, she saw herself as shamefully thin, more keenly felt given her extended family’s experience of the Holocaust. She wanted to be able to walk down the street without turning heads due to being so emaciated, but concurrently struggled to balance this desire against her strong resistance to gaining weight.

Alyssa agreed to ongoing care with the clinic and accepted referral to an expert registered dietitian. She committed to at least attempt a harm reduction approach in which she would slowly restore weight to a point where she could be more physically, mentally, and professionally functional, and where she could resume her yoga practice. However, she stipulated that she would halt weight restoration if and when her AN thinking could no longer bear it. Over the course of the next year or so, she valiantly succeeded in increasing her caloric intake considerably above her previous severely restrictive baseline. But due to the hypermetabolic state often seen in malnourished patients who increase their caloric intake, she experienced no meaningful weight gain.

Nine months after initial consultation, Alyssa emphatically reflected that her goals had not changed, but she had grave doubts about her ability to achieve them. She described feeling “utterly exhausted” and could no longer muster the strength to keep fighting. She vividly described her daily internal battles, struggling every minute of the day to eat enough of her meal plan and constantly fighting against the extreme headwinds of her AN’s resistance. Once she had eaten, she would bitterly berate and punish herself for having done so. At this point she was not certain that her AN was terminal, but she was moving strongly in that direction and wanted to understand her options.

Dr. G clarified that at any time, Alyssa could choose to pursue full recovery and a higher level of care, could continue fighting as she was, or could consider two options that did not focus on recovery. The first option would be choosing palliative care. This would acknowledge that she would likely not survive and also allow her to consider a "bucket list" of experiences for the time she had left. Palliative care would mean that she could eat what appealed to her, with no pressure applied by the team. The treatment focus would be on finding joy and comfort as much as possible. Dr. G emphasized the value of signing a DNR document to protect Alyssa from the mandates of the healthcare system in the event that she experienced an abrupt decline and/or cardiac arrest. Alyssa was also advised that a home palliative care/hospice evaluation would be useful to oversee her treatment as desired during this stage, for emotional and practical support if needed and to protect her parents from any potential legal repercussions should she pass away at home as an emaciated adult. Dr. G noted that for some patients, this stage can last a long time, and that some can “reset” when pressures to gain weight and threats of mandated treatment are removed. In some cases, this state of reduced external pressure might even lead to renewed ability to engage in meaningful harm reduction and even recovery work.

The second option would be to seek hospice care. Hospice care would be suitable if the torments of her AN and the extraordinary difficulties of moving about the world in a skeletal body were beyond being helped by a palliative care approach. Given her faster metabolism, if Alyssa abandoned her attempts to consume a higher meal plan, she would clearly have a less than six-month prognosis and qualify for hospice care. With this option, Dr. G would refer Alyssa to a home hospice service, anticipating that she would become increasingly frail. The home hospice staff would establish warm relationships with Alyssa and her parents, make sure that anxiety, insomnia, nausea, and/or pain were managed, and provide them all access to psychological and spiritual support as desired. During this time, Alyssa could live her life as she chose. As she became less independent, hospice would provide assistive aids such as a shower chair, bedside commode, and hospital bed. The overall goals would be to maximize Alyssa’s comfort, dignity, and time to connect with family.

During this conversation, Dr. G also noted that Alyssa lived in a location where MAID was legal. If she chose the hospice route—and had interest—a referral for the option of MAID was also possible. Alyssa was informed that she herself would have to administer the MAID medications if she chose to use them; no one else could administer them to her. After completing the required regulatory processes and filling the prescription, MAID medications could be used or not as desired. But, as the human body can be exceptionally resilient even with terminal malnutrition, having the medications at hand would give Alyssa the opportunity, while still having an intact brain, to choose not to suffer through additional weeks of extreme physical discomfort and weakness.

A week after these options were reviewed, Alyssa wrote Dr. G:

After deep reflection and discussion with my parents, I’ve decided it makes sense to initiate the Hospice process (Ie evaluation, etc.) now so my family and I are prepared for what may come. I would value your guidance and help with this….I do not know if they have ever worked with patients like myself… I would love for you to be the PCP overseeing this process regardless of the Hospice we select if, and only if, you are comfortable with this. I want to be clear that my priority is to obtain access to the medications that would support my legal right to die should I wind up choosing this path in the future. I feel strongly that based on our thorough discussion, I am aware of my options and their risks and benefits in light of the trajectory of my illness. Please do let me know what I can do to help facilitate initiation of this process. I am available and happy to help.

In a family meeting the following week, Alyssa’s father, a physician, tearfully shared the principles he and Alyssa’s mother had come to accept during intense conversations with their daughter: She had the right to choose care or no care after having been ill for 18 years. There would be no ultimatums. This disease would probably be the reason that "we lose you." They knew how much she had suffered and continued to suffer, and they understood that at some point the psychological anguish would become unbearable for her. They respected that this could be as bad as physical pain. They accepted that when the anguish became unbearable, Alyssa would have the right to end her life by taking medical aid in dying medications. They agreed that financial planning and end of life planning were worthy tasks. To Dr. G and to Alyssa, these words conveyed deeply reassuring love, compassion, and support.

Alyssa’s parents asked whether any treatments remained that might yet change the outcome of her course, specifically noting that Alyssa had not completed a full residential eating disorder program, never fully restored weight, never tried newer psychedelic options such as ketamine, psilocybin, or MDMA, and hadn’t had a feeding tube. Dr. G acknowledged that all but the feeding tube might ordinarily be undertaken prior to someone’s seeking end of life care for AN. Yet, she had been suffering for so long, and despite many conversations about all these treatment possibilities, Alyssa would not consent to any of them. Therefore, given her clarity of understanding around these issues and her sense that she could not fight anymore, everyone had to accept that they weren’t meaningful options. With regards to a surgical feeding tube in the context of AN rather than due an anatomical impediment, Dr. G noted that if someone restricts the “tube God gave them,” i.e. their esophagus, they would also be very likely to restrict through a surgical feeding tube, so that would not be a long term solution.

An excellent home hospice agency agreed to work with Alyssa and her family, and Dr. G placed a referral for a MAID consultation. The palliative care physician met with Alyssa about MAID. Since the idea of requesting MAID for a patient with AN was so foreign and unnerving to him, he asked Alyssa to be assessed formally for decision-making capacity. After a local psychiatrist confirmed that Alyssa clearly possessed decision-making capacity, the palliative care doctor fully accepted Alyssa’s right to enter home hospice care and could understand the rationale for MAID provision. However, even as he and his team provided empathetic support, he ultimately felt personally unable to write the MAID medication prescription due to his discomfort with the unique presentation. Clarification with the state’s Medical Board and other regulatory entities determined that Dr. G, licensed in this state although based in another state, could serve as prescribing physician, and that Alyssa’s longstanding primary care physician could serve as consulting physician. Dr. G prescribed the MAID medications about six weeks after Alyssa entered hospice care. Four days before her death, eager to contribute to this article, Alyssa sent Dr. G the following (unedited) notes about her thoughts on this complicated topic:

Below I share the considerations I made as I weighed the potential benefits and risks of pursing MAID. I share my experience in hopes of offering a first-hand perspective that may help other patients and physicians as they consider and weigh the option of utilizing MAID, rather than offering a prescriptive decision-making tool or recommending that all patients with terminal SEAN have access to such medication.

Personal considerations:

MAID not pursued in isolation, but rather in the context of being in Hospice care following a terminal dx of anorexia (i.e., estimated 6 months or left to live). I would not have qualified for Hospice care unless my illness was terminal (i.e., not reversible for me in light of physical, mental, emotional damage to my body).

In my individual case, death was inevitable. I clearly understood my prognosis and accepted this. I saw MAID as an opportunity to select a specified time and circumstances for my death. Death itself is fraught with fear, ambiguity, a sense of powerlessness and tremendous anguish, not just for the patient who is dying, but for that patient’s family. Upon deep reflection, I came to see MAID as an opportunity to relieve my suffering and minimize at least some of my family’s suffering related to my death by choosing the when and how of my death, rather than “wait” for sudden death from cardiac arrest or other outcome of my illness or experience a slow and protracted death as my family and I watch my body and mind degrade over days and maybe even weeks of time

I had to ask important questions about my quality of life and whether for me, the quality of my life was more important than the quantity of days I remained alive. I was experiencing extreme physical pain, was unable to walk, could not sit without discomfort, I couldn’t swallow my food, my breath was labored, and I had frequent chest pain. I was not living. I felt like “dead girl barely walking.” For me personally, a longer life spent in bed feeling ill and suffering and dependent on others to provide most of my care was not how I wanted to live. My concerns about this suffering trumped any fear of selecting the route of my death (again, knowing that death was inevitable). Knowing that I could utilize MAID if the suffering became so severe offered me a sense of ease and peace of mind in my final stage of life that I would not have had otherwise

One question that I needed to answer for myself honestly was whether I understood the impact use of MAID would have on my family. I had to confront that my use of MAID would be difficult for them, not just the idea of my using it but how their presence at the end of my death, watching me administer my own medications to die, would be ingrained in their memories of me as their daughter and their sister, and how this story of my passing would affect my family throughout the generations to come (i.e., what stories would they tell about my life and death, how could this be traumatizing or perhaps seen as healing?). Such questions could only be answered through ongoing involvement and discussion with my family members, which we had with my physicians and amongst ourselves

Another important question I asked was how would I want a family member to die if I knew their illness was terminal and death was imminent. Would I see their use of MAID as a compassionate act towards themselves? How would I tell their story? Would I extend the compassion I was asking for from them to them if the situation were reversed? I also asked them individually how they would want to die if they could have the option of choosing?

All in all, a voluntary decision, not made in haste, thoughtful, careful, meticulous. Decision made as arrangements were made for my passing including burial arrangements, financial and family orders.

Decision also heavily considered with spiritual advisors (chaplain, Rabbi, etc.)

Challenges faced:

MAID in general is highly controversial and its use is RARE – even for patients who do receive it, many do not end up using it. Only a handful of physicians who support using it. Makes it unknown and scary for physicians and patients alike; limited research

Makes acceptance of its use more difficult for family members, too

Prescribing MAID (for some physicians) may feel counter to physician identity as healer & fixer; may spark deep internal/ethical/moral debate for individual physicians as they weigh the option of whether to prescribe

Do they see this as an act of compassion for patients who wish to relieve their suffering?

Do they see this as prescribing a means of suicide?

Anorexia specific – for me, a big issue that caused most ethical debate was whether my case of anorexia nervosa was “reversible.” Many physicians misunderstand SEAN (not even an official DSM diagnosis) and that while anorexia nervosa is a psychiatric illness, it comes with severe medical complications that ultimately are the reason for death. Some of the physicians I worked with could not believe my illness was indeed terminal, but rather felt that there would be something that could be done to reverse the physical damage done to my body that would somehow lengthen my life (even if not for very long – i.e., 1 year).

Yes, perhaps I could stay alive for a few months while in the hospital, but I would have to live in the hospital (MDs might see the benefit of this, but could I? NO! This is where my own reflection around quality of life came in)

My personal belief that this is what makes having such an extreme form of AN so agonizing – mental and emotional suffering is compounded by painful physical complications

Gross misunderstanding about anorexia nervosa in general.

Just over a day before she died, Alyssa wrote to Dr. G, “Thank you with all of my heart for helping to make this possible. I view it as a tremendous act of love.” With family and spiritual support surrounding her, Alyssa became unresponsive in the natural course of her malnutrition. Shortly thereafter, she passed away peacefully. She never actually ingested the MAID medication she had at her disposal.

By presenting these three cases, we have intended to convey some of the emotional, moral, and ethical challenges and dilemmas that patients with SE-AN, their families, and their professional caregivers may face at the end of life. Suffering from unrelenting and irredeemable disorders, these patients made difficult choices, ultimately deciding “enough is enough” [ 18 ]. The anguish endured by these patients and their families resulted in part from lack of professional understanding and consensus regarding terminal care for patients with AN. Neither the fields of palliative and hospice care nor eating disorders have provided definitions or guidance regarding what constitutes a terminal condition in AN or proper ways to address patients and their families grappling with this condition.

Accordingly, we present the following proposed clinical characteristics of those with terminal AN for consideration by both fields (Table 1 ). As illustrated by our cases, no set of criteria will apply perfectly to every patient who identifies with having a terminal case of AN. However, based on prior literature on criteria for clinical terminality [ 15 ], high SMR in those who have previously received inpatient care, are older, and have a history of more severely medically compromised presentations [ 6 , 7 , 8 , 9 , 10 , 11 ], and clinical expertise, the authors propose these clinical characteristics. Some deviation within the second and third characteristics is to be expected and must be individualized to the patient situation. However, the first and fourth must be met in full.

Proposed clinical characteristics of patients with terminal anorexia nervosa

A diagnosis of anorexia nervosa . Anorexia nervosa is the only eating disorder that carries a guaranteed medical cause of death from malnutrition should weight loss continue unabated. As a result, consistent with literature on duration of life during hunger strikes resulting in death [ 16 ], a prognosis of less than 6 months can fairly be established when the patient acknowledges further treatment to be futile and stops engaging in active recovery work. A less than six-month prognosis is congruent with current practice around determination of terminal diagnoses. We fully recognize that patients with SE-AN are likely to have other psychiatric conditions as well.

Age of 30 or older . This criterion accommodates for what is clinically seen as a potential “late maturation phase” in which even those who have been sick for a long time may discover a shift in values and desires that motivates recovery as they enter their late 20 s. Every effort should be made to promote full recovery and continuation of life in those younger than 30. However, the SMR data of multiple recent studies showing the highest death rates in those with a history of inpatient admissions, longer duration of AN, and age over 30 years old [ 6 , 7 , 8 , 9 ], taken alongside what functionally has often been a decade or two of exhaustive, ultimately unsuccessful eating disorder treatment, indicates that the age of around 30 as a minimum for terminal AN is reasonable.

Prior persistent engagement in high-quality, multidisciplinary eating disorder care. Worldwide access to expert eating disorder care varies widely, as does the availability of access to expert inpatient, residential, and full day treatment programs for those with eating disorders. Thus, the definition of care identified here must remain somewhat broad. Before someone can decide they cannot recover, they must have participated in high-quality, expert care to the maximum extent that this is available. This provision should motivate policies that allow for transfers of patients out of designated “networks” that lack expertise, with funding coverage provided at a center of excellence. Ideally, at least some of this treatment will have been undertaken at a sufficiently high level of care to provide extensive structure and support, preferably to the point of full weight restoration at least once in the relatively recent past. Congruent with receipt of such care, qualified health care professionals on the team must support the patient in their decision to stop fighting. We acknowledge that many factors may impact patients’ ability to participate in such care, including lack of access to eating disorders expertise, limitations of the healthcare system, and a personal sense—often based on prior treatment experiences—that admission to certain care settings would cause more harm than good.

Consistent, clear expression by an individual who possesses decision-making capacity that they understand further treatment to be futile, they choose to stop trying to prolong their lives, and they accept that death will be the natural outcome. Careful determination of decisional capacity is required in each case [ 19 ]. An individual who wavers in their conviction or expresses different goals to different people is not yet ready to receive the appellation of terminal AN.

Most eating disorders providers have cared for patients with AN who, despite suffering for decades, continue to show extraordinary determination and resilience. These patients still want help, at least with a harm-avoidance strategy if not with outright full recovery. In these cases, every effort must be made to support the patient’s wishes and provide appropriate resources for recovery. There must be no “giving up” on those who still seek to get better. Indeed, the drive to live and ability to find aspects of life worth fighting for can be seen vividly in the majority of those with AN, even in the face of years or decades of illness and suffering. The psychological imperatives of AN that often lead patients to resist or refuse clinically appropriate care, hazarding medical and psychological risk and deterioration, may seem to conflict with a stated desire to keep trying for recovery. However, in honoring patient autonomy, responsive care must always be offered as long as an individual states that this is their wish.

Patients in their earlier and younger years of AN may say they would rather die than gain weight or nourish themselves properly, a characteristic indicating that AN may present as an ego-syntonic mental illness. Nonetheless, the majority of patients with AN ultimately recover, and such expressions of anguish can be met with compassion and appropriate multidisciplinary care. We would not condone accepting a terminal diagnosis in younger patients. Of note, there are no explicit physiologic markers or measurables (weight, degree of weight loss, presence of or degree of organ failure, vital signs) which delineate someone with terminal AN. Even individuals with extreme medical malnutrition may recover fully if they so choose and have access to expert care. By contrast, if all criteria for terminal AN are met, as in the case of Aaron, individuals should not be obliged to demonstrate extreme medical instability before having the right to choose to stop fighting. Furthermore, while the obsessional ruminations of individuals with AN can be perplexing, clinicians should not regard the presence of body distortions and food fears as proof that these patients are unable to understand personal options and make reasoned health care decisions.

How can we determine that patients with severe anorexia nervosa possess the clinical decision-making capacity necessary to permit them to withdraw from treatment? With respect to decision-making capacity, four traditional criteria are usually applied: understanding, appreciation, ability to reason, and communication of decision [ 20 ]. In Dr. G’s estimation, confirmed in the two cases where formal independent assessment by a psychiatrist was performed, each of the patients met these criteria and was therefore capable of deciding to withdraw from conventional treatment. Alyssa’s clear, incisive writing just days before her death beautifully illustrates the insight and cognitive capacity that many patients with AN possess right up to the end of their life.

Clinical, legal, and ethical commentators in the field concur that withdrawal from treatment may be appropriate when further treatment, whether voluntary of involuntary, will provide only brief improvement, and is unlikely to offer sustained quality of life [ 21 , 22 ]. A formal assessment of decision-making capacity may help ameliorate family member fears that such an important decision is being made in an appropriate and ethical manner, especially when AN fears and distortions can seem so irrational. In addition, a formal bioethics evaluation might be valuable, but consideration of this must be balanced against most bioethicists’ lack of experience with patients who have AN, with the risk that their own innate and misguided reaction that “this patient just has to eat” could undermine a qualified patient’s decisions that are supported by their longstanding care team and family. Even medical ethicists must be wary about how their own cognitive and affective biases might influence their recommendations. [ 23 ]

Family members and carers play an immensely important role in the lives of those with AN. They bear witness to the suffering and challenges experienced by those with AN and are usually directly involved in the recovery process in multiple ways (financial/material support/behavioral support/engagement in the therapeutic work, among others). Many dread the day their child legally becomes an adult and can choose to exclude them from the details of recovery work, such that they become the financial supporters of care they are no longer privy to. The exhaustion, fear, love, and hope experienced by family members cannot be overstated. In any case where a patient meets the criteria for terminal AN, it is always preferable to include family members in the discussions and ideally come to a consensus. There may be dissent within a family about whether their loved one should be allowed to make the decision to stop fighting. These three cases illustrated how each family was meaningfully involved in the clinical discussions in the months before each patient’s death. Each family’s ultimate acceptance (through deep grief) of their son or daughter’s prognosis and choice contributed to a heightened sense of connection and love prior to death.

Acknowledging the considerable controversies surrounding MAID for patients with mental disorders [ 24 , 25 , 26 ], we also submit that patients with terminal AN who are severely physiologically compromised, and whose end-of life suffering results from both psychological and physical pain, should be afforded access to medical aid in dying in locations where such assistance has been legalized—just like other patients with terminal conditions.

AN confers an exceptionally high death rate. The lack of acceptance of terminality in AN and the absence of professionally condoned protocols and standard procedures for supporting patients and families through these phases further complicates end-of-life stages for the adults with AN who cannot keep fighting. These represent a small fraction even of the population of those with SE-AN. Per our proposed clinical characteristics, patients must not only decline further recovery-oriented treatment (which is not uncommon at times for those with AN), but also must explicitly and consistently choose to stop trying to prolong their lives, accepting that death will be the natural outcome. When a patient begins talking about the possibility of not being able to survive, every effort should be made to validate such a serious perspective and to offer an individualized and thoughtful series of harm reduction strategies and treatment options that might make life bearable. However, the process of seeking alternatives to death must not be so exhaustive as to disrespect limits the patient sets; while a family might be desperate for their loved one to try an experimental treatment or “just try going to treatment one more time,” they must ultimately accept the patient’s lack of consent for these.

Our proposed clinical characteristics of patients with terminal AN have no bearing on those who wish to keep fighting despite very long-standing and severe disease, even when their eating disorder behaviors seem incongruent with survival. Very specifically, to move toward a designation of terminal AN, an individual must express consistently that they can no longer live with their disease and will no longer maintain a minimum nutritional intake needed to support life. To be clear, each patient is unique and requires careful individual assessment and consideration as to the best approach going forward. Consistent with calls from others regarding the need for better definition and agreement regarding labeling and staging for SE-AN in general [1,2,3,4 5], the authors hope that these cases and characteristics of those with terminal AN will provide a starting point for identification, care, and further discussion. We would strongly encourage the development of expert consensus criteria and clinical guidelines endorsed by both the fields of palliative and hospice care and eating disorders. These brave, suffering individuals deserve no less.

Availability of data and materials

All narrative data and record of e-mails exchanged with patients and families throughout and after their care with the clinic are available.

Abbreviations

• Anorexia nervosa

Dr. Jennifer Gaudiani

Medical Aid in Dying

Obsessive Compulsive Disorder

• Severe and enduring anorexia nervosa

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Acknowledgements

Dr. Gaudiani would like to acknowledge the Gaudiani Clinic’s nurse, Abby Brockman, RN, for her excellent clinical care of these patients and their families.

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Dr. Gaudiani was the internist for the three patients, drafted the article, and reviewed and approved revisions. Ms. Bogetz (deceased patient) contributed to the text and proposed criteria. Dr. Yager consulted with Alyssa and her family, contributed to the text, and provided extensive editing.

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Correspondence to Jennifer L. Gaudiani .

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Consent for publication of these cases was provided by all of the deceased patients’ families and by Alyssa prior to her death, and all families asked that patients’ first names be used in lieu of initials. This case report did not require further ethical approval.

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All three authors consented to publish this article. Ms. Bogetz (posthumous author) consented prior to her death, both verbally and in writing. Written informed consent for publication of their clinical details was obtained from the parents of the other two patients. A copy of the consent forms is available for review by the Editor of this journal as an additional file.

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Alyssa Bogetz: 1985–2021, former patient

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Gaudiani, J.L., Bogetz, A. & Yager, J. Terminal anorexia nervosa: three cases and proposed clinical characteristics. J Eat Disord 10 , 23 (2022). https://doi.org/10.1186/s40337-022-00548-3

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What is anorexia nervosa?

Types of anorexia, am i anorexic, signs and symptoms of anorexia, anorexia causes and risk factors, effects of anorexia, getting help, anorexia treatment, tip 1: understand this is not really about weight or food, tip 2: learn to tolerate your feelings, tip 3: challenge damaging mindsets, tip 4: develop a healthier relationship with food, helping someone with anorexia, anorexia nervosa: symptoms, causes, and treatment.

Are you or a loved one struggling with anorexia? Explore the warning signs, symptoms, and causes of this serious eating disorder—as well as how to get the help you need.

Anorexia nervosa is a serious eating disorder characterized by a refusal to maintain a healthy body weight, an intense fear of gaining weight, and a distorted body image. Anorexia can result in unhealthy, often dangerous weight loss. In fact, the desire to lose weight may become more important than anything else. You may even lose the ability to see yourself as you truly are.

While it is most common among adolescent women, anorexia can affect women and men of all ages. You may try to lose weight by starving yourself, exercising excessively, or using laxatives, vomiting, or other methods to purge yourself after eating. Thoughts about dieting, food, and your body may take up most of your day—leaving little time for friends, family, and other activities you used to enjoy. Life becomes a relentless pursuit of thinness and intense weight loss. But no matter how skinny you become, it’s never enough.

The intense dread of gaining weight or disgust with how your body looks, can make eating and mealtimes very stressful. And yet, food and what you can and can’t eat is practically all you can think about.

But no matter how ingrained this self-destructive pattern seems, there is hope. With treatment, self-help, and support, you can break the self-destructive hold anorexia has over you, develop a more realistic body image, and regain your health and self-confidence.

There are three types of anorexia:

• Restricting type of anorexia is where your weight loss is achieved by restricting calories (following drastic diets, fasting, exercising to excess).
• Purging type of anorexia is where your weight loss is achieved by vomiting or using laxatives and diuretics.
• Atypical anorexia is where you have all the symptoms and dangerous obsessions of anorexia, except you’re not underweight (often due to your genetic makeup). Even though you may still be in a healthy weight range, your dieting or exercise habits put severe stress on your body.

Ask yourself the following questions:

• Do you feel fat even though people tell you you're not?
• Are you terrified of gaining weight?
• Do you lie about how much you eat or hide your eating habits from others?
• Are your friends or family concerned about your weight loss, eating habits, or appearance?
• Do you diet, compulsively exercise, or purge when you're feeling overwhelmed or bad about yourself?
• Do you feel powerful or in control when you go without food, over-exercise, or purge?
• Do you base your self-worth on your weight or body size?

Speak to a Licensed Therapist

BetterHelp is an online therapy service that matches you to licensed, accredited therapists who can help with depression, anxiety, relationships, and more. Take the assessment and get matched with a therapist in as little as 48 hours.

While people with anorexia often exhibit different habits, one constant is that living with anorexia means you're constantly hiding those habits. This can make it hard at first for friends and family to spot the warning signs. When confronted, you might try to explain away your disordered eating and wave away concerns. But as anorexia progresses, people close to you won't be able to deny their instincts that something is wrong—and neither should you. If eating and weight control your life, you don't have to wait until your symptoms have progressed or your health is dangerously poor before seeking help.

Food behavior symptoms

Dieting despite being thin. Following a severely restricted diet. Eating only certain low-calorie foods. Banning “bad” foods such as carbohydrates and fats.

Obsession with calories, fat grams, and nutrition. Reading food labels, measuring and weighing portions, keeping a food diary, reading diet books.

Pretending to eat or lying about eating. Hiding, playing with, or throwing away food to avoid eating. Making excuses to get out of meals (“I had a huge lunch” or “My stomach isn't feeling good”).

Preoccupation with food. Constantly thinking about food. Cooking for others, collecting recipes, reading food magazines, or making meal plans while eating very little.

Strange or secretive food rituals. Refusing to eat around others or in public places. Eating in rigid, ritualistic ways (e.g. cutting food “just so,” chewing food and spitting it out, using a specific plate).

Appearance and body image symptoms

Dramatic weight loss. Rapid, drastic weight loss with no medical cause.

Feeling fat, despite being underweight. You may feel overweight in general or just “too fat” in certain places, such as the stomach, hips, or thighs.

Fixation on body image. Obsessed with weight, body shape, or clothing size. Frequent weigh-ins and concern over tiny fluctuations in weight.

Harshly critical of appearance. Spending a lot of time in front of the mirror checking for flaws. There's always something to criticize. You're never thin enough.

[Read: Body Shaming: Causes, Effects, and Improving Your Body Image]

Denial that you're too thin. You may deny that your low body weight is a problem, while trying to conceal it (drinking a lot of water before being weighed, wearing baggy or oversized clothes).

Purging symptoms

Using diet pills, laxatives, or diuretics. Abusing water pills, herbal appetite suppressants, prescription stimulants, ipecac syrup, and other drugs for weight loss.

Throwing up after eating. Frequently disappearing after meals or going to the bathroom. May run the water to disguise sounds of vomiting or reappear smelling like mouthwash or mints.

Compulsive exercising. Following a punishing exercise regimen aimed at burning calories. Exercising through injuries, illness, and bad weather. Working out extra hard after bingeing or eating something “bad.”

There are no simple answers to the causes of anorexia. Anorexia is a complex condition that arises from a combination of many social, emotional, and biological factors. Although our culture's idealization of thinness plays a powerful role, there are many other contributing factors, including your family environment, emotional difficulties, low self-esteem, and traumatic experiences you may have gone through in the past.

Psychological causes . People with anorexia are often perfectionists and overachievers. They tend to be the “good” daughters and sons who do what they’re told, excel in everything they do, and focus on pleasing others. But while they may appear to have it all together, inside they feel helpless, inadequate, and worthless. Through their harshly critical lens, if they’re not perfect, they’re a total failure.

Family and social pressures . In addition to the cultural pressure to be thin, there are other family and social pressures that can contribute to anorexia. These include participation in an activity that demands slenderness, such as ballet, gymnastics, or modeling. It can also include having parents who are overly controlling, put a lot of emphasis on looks, diet themselves, or criticize their children’s bodies and appearance. Stressful life events—such as the onset of puberty, a breakup, or going away to school—can also trigger anorexia.

Biological causes . Research suggests that a genetic predisposition to anorexia may run in families. If a girl has a sibling with anorexia, she is 10 to 20 times more likely than the general population to develop anorexia herself. Brain chemistry also plays a significant role. People with anorexia tend to have high levels of cortisol, the brain hormone most related to stress, and decreased levels of serotonin and norepinephrine, which are associated with feelings of well-being.

Risk factors for anorexia

• Body dissatisfaction
• Strict dieting
• Low self-esteem
• Emotional difficulties
• Perfectionism
• Troubled family relationships
• History of physical or sexual abuse
• Other traumatic experiences
• Family history of eating disorders

While the causes of anorexia are uncertain, the physical effects are clear. When your body doesn't get the fuel it needs to function normally, it goes into starvation mode and slows down to conserve energy. Essentially, your body begins to consume itself. If self-starvation continues and more body fat is lost, medical complications pile up and your body and mind pay the price.

Source:  National Women's Health Information Center

Deciding to get help for anorexia is not an easy choice to make. It's not uncommon to feel like anorexia is part of your identity—or even your “friend.” You may think that anorexia has such a powerful hold over you that you'll never be able to overcome it. But while change is hard, it is possible.

Admit you have a problem. Up until now, you've been invested in the idea that life will improve—that you'll finally feel good—if you lose more weight. The first step in anorexia recovery is admitting that your relentless pursuit of thinness is out of your control and acknowledging the physical and emotional damage that you've suffered because of it.

Talk to someone. It can be hard to talk about what you're going through, especially if you've kept your anorexia a secret for a long time. You may be ashamed, ambivalent, or afraid. But it's important to understand that you're not alone. Find a good listener—someone who will support you as you try to heal.

Stay away from people, places, and activities that trigger your obsession with being thin. You may need to avoid looking at fashion or fitness magazines, spend less time with friends who constantly diet and talk about losing weight, and stay away from weight loss websites and “pro-ana” sites that promote anorexia.

Seek treatment from trained eating disorder professionals.

Treating anorexia involves three steps:

• Getting back to a healthy weight.
• Starting to eat more food.
• Changing how you think about yourself and food.

[Read: Eating Disorder Treatment and Recovery]

Medical treatment . The first priority in anorexia treatment is addressing and stabilizing any serious health issues. Hospitalization may be necessary if you are dangerously malnourished or so distressed that you no longer want to live. You may also need to be hospitalized until you reach a less critical weight. Outpatient treatment is an option when you’re not in immediate medical danger.

Nutritional treatment . A second component of anorexia treatment is nutritional counseling. A nutritionist or dietician will teach you about healthy eating and proper nutrition. The nutritionist will also help you develop and follow meal plans that include enough calories to reach or maintain a normal, healthy weight.

Therapy . Therapy is crucial to anorexia treatment. Its goal is to identify the negative thoughts and feelings that fuel your eating disorder and replace them with healthier, less distorted beliefs. Therapy can also help you deal with difficult emotions, relationship problems, and stress in a productive, rather than a self-destructive, way.

Along with professional treatment, the following tips can guide you on the road to recovery:

The food and weight-related issues are in fact symptoms of a deeper issue: depression, anxiety, loneliness, insecurity, pressure to be perfect, or feeling out of control. Problems that no amount of dieting or weight loss can cure.

The difference between dieting and anorexia

In order to overcome anorexia, you first need to understand that it meets a need in your life. For example, maybe you feel powerless in many parts of your life, but you can control what you eat. Saying “no” to food, getting the best of hunger, and controlling the number on the scale may make you feel strong and successful—at least for a short while. You may even come to enjoy your hunger pangs as reminders of a “special talent” that most people don't possess.

Anorexia may also be a way of distracting yourself from difficult emotions. When you spend most of your time thinking about food, dieting, and weight loss, you don't have to face other problems in your life or deal with complicated emotions. Restricting food may provide an emotional numbness, anesthetizing you from feelings of anxiety, sadness, or anger, perhaps even replacing those emotions with a sense of calm or safety.

Unfortunately, any boost you get from starving yourself or shedding pounds is extremely short-lived—and at some point, it will stop working for you at all. Dieting and weight loss can't repair the negative self-image at the heart of anorexia. The only way to do that is to identify the emotional need that self-starvation fulfills and find other ways to meet it.

“I feel fat”

While your weight usually remains quite constant over the course of, say, a week, feelings of fatness can fluctuate wildly. Often, feeling fat is a mislabeling of other emotions, such as shame, boredom, frustration, or sadness. In other words, “I feel fat” really means “I feel anxious,” or “I feel lonely.” And those feelings are unlikely to ever be changed by a diet.

Identifying the underlying issues that drive your eating disorder is the first step toward recovery, but insight alone is not enough. Let's say, for example, that following restrictive food rules makes you feel safe and powerful. When you take that coping mechanism away, you will be confronted with the feelings of fear and helplessness your anorexia helped you avoid.

Reconnecting with your feelings can be extremely uncomfortable. It's why you may feel worse at the beginning of your recovery. But the answer isn't to return to the destructive eating habits you previously used to distract yourself; it's to learn how to accept and tolerate all of your feelings—even the negative ones.

Using mindfulness to cope with difficult emotions

When you start to feel overwhelmed by negativity, discomfort, or the urge to restrict food, take a moment to stop whatever you're doing and investigate what's going on inside.

Identify the emotion you're feeling. Is it guilt? Shame? Helplessness? Loneliness? Anxiety? Disappointment? Fear? Insecurity?

Accept the experience you're having. Avoidance and resistance only make negative emotions stronger. Instead, try to accept what you're feeling without judging yourself.

Dig deeper. Where do you feel the emotion in your body? What kinds of thoughts are going through your head?

Distance yourself. Realize that you are NOT your feelings. Emotions are passing events, like clouds moving across the sky. They don't define who you are.

Once you learn how to accept and tolerate your feelings, they'll no longer seem so scary. You'll realize that you're still in control and that negative emotions are only temporary. Once you stop fighting them, they'll quickly pass.

For a step-by-step guide to learning how to manage stress and uncomfortable emotions, check out HelpGuide's free Emotional Intelligence Toolkit .

New ways to find emotional fulfillment

Once you understand the link between your emotions and your disordered eating patterns—and can identify your triggers—you still need to find alternatives to dieting that you can turn to for emotional fulfillment. For example:

If you're depressed or lonely, call someone who always makes you feel better, schedule time with family or friends, watch a comedy show, or play with a dog or cat.

If you're anxious, expend your nervous energy by dancing to your favorite music, squeezing a stress ball, or taking a brisk walk or bike ride.

If you're exhausted, treat yourself with a hot cup of tea, go for a walk, take a bath, or light some scented candles.

If you're bored, read a good book, explore the outdoors, visit a museum, or turn to a hobby you enjoy (playing the guitar, knitting, shooting hoops, scrapbooking, etc.).

People with anorexia are often perfectionists and overachievers. They're the “good” daughters and sons who do what they're told, try to excel in everything they do, and focus on pleasing others. But while they may appear to have it all together, inside they feel helpless, inadequate, and worthless.

If that sounds familiar to you, here's the good news: these feelings don't reflect reality. They're fueled by irrational, self-sabotaging ways of thinking that you can learn to overcome.

Damaging mindsets that fuel anorexia

All-or-nothing thinking. Through this harshly critical lens, if you're not perfect, you're a total failure. You have a hard time seeing shades of gray, at least when it comes to yourself.

Emotional reasoning. You believe if you feel a certain way, it must be true. “I feel fat” means “I am fat.” “I feel hopeless” means you'll never get better.

Musts, must-nots, and have-tos . You hold yourself to a rigid set of rules ( “I must not eat more than x number of calories , “ “I have to get straight A's,” “ I must always be in control.” etc.) and beat yourself up if you break them.

Labeling. You call yourself names based on mistakes and perceived shortcomings. “I'm unhappy with how I look” becomes “I'm disgusting.” Slipping up becomes “I'm a “failure.”

Catastrophizing. You jump to the worst-case scenario. If you backslide in recovery, for example, you assume that there's no hope you'll ever get better.

Put your thoughts on the witness stand

Once you identify the destructive thoughts patterns that you default to, you can start to challenge them with questions such as:

• “What's the evidence that this thought is true? Not true?”
• “What would I tell a friend who had this thought?”
• “Is there another way of looking at the situation or an alternate explanation?”
• “How might I look at this situation if I didn't have anorexia?”

As you cross-examine your negative thoughts, you may be surprised at how quickly they crumble. In the process, you'll develop a more balanced perspective.

Even though anorexia isn't fundamentally about food, over time you've developed harmful food habits that can be tough to break. Developing a healthier relationship with food entails:

• Getting back to a healthy weight
• Starting to eat more food
• Changing how you think about yourself and food

Let go of rigid food rules. While following rigid rules may help you feel in control, it's a temporary illusion. The truth is that these rules are controlling you, not the other way around. In order to get better, you'll need to let go. This is a big change that will feel scary at first, but day by day, it will get easier.

Get back in touch with your body. If you have anorexia, you've learned to ignore your body's hunger and fullness signals. You may not even recognize them anymore. The goal is to get back in touch with these internal cues, so you can eat based on your physiological needs.

Allow yourself to eat all foods. Instead of putting certain food off limits, eat whatever you want, but pay attention to how you feel physically after eating different foods. Ideally, what you eat should leave you feeling satisfied and energized.

Get rid of your scale. Instead of focusing on weight as a measurement of self-worth, focus on how you feel. Make health and vitality your goal, not a number on the scale.

Develop a healthy meal plan. If you need to gain weight, a nutritionist or dietician can help you develop a healthy meal plan that includes enough calories to get you back to a normal weight. While you can do this on your own, you're probably out of touch with what a normal meal or serving size looks like.

Getting past your fear of gaining weight

Getting back to a normal weight is no easy task. The thought of gaining weight is probably extremely frightening, and you may be tempted to resist.

But this fear is a symptom of your anorexia. Reading about anorexia or talking to other people who have lived with it can help. It also helps to be honest about your feelings and fears. The better your family and treatment team understand what you're going through, the better support you'll receive.

Having anorexia can distort the way your loved one thinks—about their body, the world around them, even your motivations for trying to help. Add to that the defensiveness and denial involved in anorexia and you'll need to tread lightly.

Waving around articles about the dire effects of anorexia or declaring, “you'll die if you don't eat!” probably won't work. A better approach is to gently express your concerns and let the person know that you're available to listen. If your loved one is willing to talk, listen without judgment, no matter how out of touch the person sounds.

[Read: Helping Someone with an Eating Disorder]

Think of yourself as an “outsider.” As someone not suffering from anorexia, there isn't a lot you can do to “solve” your loved one's condition. It is ultimately their choice to decide when they are ready.

Encourage your loved one to get help. The longer an eating disorder remains undiagnosed and untreated, the harder it is on the body and the more difficult it is to overcome.

Seek advice from a health professional, even if your friend or family member won't. And you can bring others—from peers to parents—into the circle of support.

Be a role model for healthy eating, exercising, and body image. Don't make negative comments about your own body or anyone else's.

Don't act like the food police. A person with anorexia needs compassion and support, not an authority figure standing over the table with a calorie counter.

Avoid threats, scare tactics, angry outbursts, and put-downs. Anorexia is often a symptom of extreme emotional distress and develops out of an attempt to manage emotional pain, stress, and/or self-hate. Negative communication will only make it worse.

Hotlines and support

National Eating Disorders Association  or call 1-800-931-2237 (National Eating Disorders Association)

Beat Eating Disorders  or call 0345 643 1414 (Helpfinder)

Butterfly Foundation for Eating Disorders  or call 1800 33 4673 (National Eating Disorders Collaboration)

Service Provider Directory  or call 1-866-633-4220 (NEDIC)

More Information

• Almost Anorexic – Is My (or My Loved One’s) Relationship with Food a Problem? - (Harvard Health Books)
• Treatment - Tips on eating disorder treatment. (National Eating Disorders Association)
• Anorexia nervosa - FAQs on anorexia and its treatment. (Office on Women’s Health)
• Anorexia Nervosa - Includes risk factors such as body image, self esteem, and perfectionism. (Eating Disorders Victoria)
• Feeding and Eating Disorders. (2013). In Diagnostic and Statistical Manual of Mental Disorders. American Psychiatric Association. Link
• Anorexia nervosa | Office on Women’s Health. (n.d.). Retrieved July 27, 2022, from Link
• Anorexia Nervosa—Psychiatric Disorders—Merck Manuals Professional Edition. (n.d.). Retrieved July 27, 2022, from Link
• Anorexia Nervosa—StatPearls—NCBI Bookshelf. (n.d.). Retrieved July 27, 2022, from Link
• Lloyd, S., Yiend, J., Schmidt, U., & Tchanturia, K. (2014). Perfectionism in Anorexia Nervosa: Novel Performance Based Evidence. PLoS ONE, 9 (10), e111697. Link
• Moskowitz, Lindsay, and Eric Weiselberg. “Anorexia Nervosa/Atypical Anorexia Nervosa.” Current Problems in Pediatric and Adolescent Health Care 47, no. 4 (April 1, 2017): 70–84. Link
• Harrington, Brian C., Michelle Jimerson, Christina Haxton, and David C. Jimerson. “Initial Evaluation, Diagnosis, and Treatment of Anorexia Nervosa and Bulimia Nervosa.” American Family Physician 91, no. 1 (January 1, 2015): 46–52. Link
• National Eating Disorders Association. “Anorexia Nervosa,” March 31, 2023. Link
• Tozzi, Federica, Patrick F. Sullivan, Jennifer L. Fear, Jan McKenzie, and Cynthia M. Bulik. “Causes and Recovery in Anorexia Nervosa: The Patient’s Perspective.” International Journal of Eating Disorders 33, no. 2 (2003): 143–54. Link
• Woerwag-Mehta, Sabine, and Janet Treasure. “Causes of Anorexia Nervosa.” Psychiatry , Eating disorders, 7, no. 4 (April 1, 2008): 147–51. Link
• Fairburn, C. G., Z. Cooper, H. A. Doll, and S. L. Welch. “Risk Factors for Anorexia Nervosa: Three Integrated Case-Control Comparisons.” Archives of General Psychiatry 56, no. 5 (May 1999): 468–76. Link
• Zipfel, Stephan, Katrin E Giel, Cynthia M Bulik, Phillipa Hay, and Ulrike Schmidt. “Anorexia Nervosa: Aetiology, Assessment, and Treatment.” The Lancet Psychiatry 2, no. 12 (December 1, 2015): 1099–1111. Link

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Eating disorders among teens more severe than ever

Teen eating disorders have never been this rampant — or this severe. 

Hospitalizations for eating disorders spiked during the pandemic, doubling among adolescent girls, according to the Centers for Disease Control and Prevention . While most teens have returned to a normal life of in-person school, sports and social activities, eating disorders, especially anorexia, remain at an all-time high, experts warn.

“The kids are not OK,” said Melissa Freizinger, the associate director of the eating disorder program at Boston Children’s Hospital. “As the pandemic started and then progressed, we kept thinking, ‘Oh, it’s going to get better in 2022. Oh, it’s going to get better in 2023. But it hasn’t.”

Eating disorder-related health visits — which include hospital stays, pediatrician visits, telehealth talk therapy, and everything in between — more than doubled among people younger than 17 in the past five years, according to a recent report from the data company Trilliant Health . From 2018 through mid-2022, visits among this age group  jumped 107.4% across all eating disorders, from around 50,000 visits at the beginning of 2018 to more than 100,000 in 2022. Visits related to anorexia nervosa, which has the highest death rate of any mental illness, jumped 129.26%. 

The pandemic worsened the incidence of anxiety and depression — both are risk factors for triggering or worsening eating disorders.

While eating disorder-related visits dipped slightly after a peak in 2021, they’re nowhere near pre-pandemic levels as adolescents and younger teens cope with the after-effects of Covid, such as grieving for family members who have died, falling behind in school or losing touch with friends.

And the patients coming in with eating disorders are in more serious condition now, with both mental and physical symptoms appearing more urgent, experts say.

“They’re sicker than before, and they’re more complicated than they were before,” said Boston Children’s Freizinger, noting that even after Covid, teens are being hospitalized at an alarming rate. Many require medical stabilization for malnourishment, and their psychiatric symptoms are more severe.

“We all have collective trauma from the pandemic, but many of these kids have PTSD," said Freizinger. "They’re also younger.”

Waitlists for eating disorders treatment 

Seventeen-year-old Lana Elisha Garrido, who was first treated for anorexia at age 13 and then relapsed in December 2021, said she noticed younger patients at the Los Angeles facility where she received intensive treatment five months last year. 

“When I was 13, everyone around me in treatment was an adult,” she said. “Now there’s like 20 people my age.” Garrido, who’s connected with other teens through volunteering with the National Eating Disorder Association (NEDA), said she’s been hearing about monthslong waitlists to begin treatment. 

Despite the pervasive eating disorder stereotype — white, female and underweight — teens from racial and ethnic minority groups, as well as males and teens with larger bodies, develop certain eating disorders at even higher rates, according to research.  

“I feel like a lot of marginalized people out there don’t know what to do or where to go or how to approach treatment,” said Garrido, a first-generation Filipino American whose parents are immigrants.

Over the years, Garrido said she’s noticed that almost all of the doctors in her various treatment facilities have been white, despite living in a city as racially and ethnically diverse as Los Angeles. 

Eating disorders are less likely to be recognized among these underrepresented groups. In one 2006 study, doctors accurately diagnosed 17% of Black women, 41% of Latina women and 44% of white women with identical eating disorder symptoms.

Freizinger added that many eating disorder specialists don’t accept Medicaid or don’t accept insurance at all, which can make treatment access all the more difficult for underrepresented minority groups, especially Black and Hispanic populations who are more likely to have Medicaid or lack health insurance altogether than white Americans. 

These missed diagnoses and treatment access barriers have meant very few research studies into eating disorder disparities, but several slightly older studies suggest certain eating disorders may be more prevalent among minorities. A 2011 JAMA Psychiatry study, for instance, found bulimia was more common among Hispanic teens than white teens, and binge-eating disorder was more common among both Black and Hispanic teens than white teens. In 2013, a survey of high schoolers identified eating disorder behaviors occurred nearly three times as often among transgender students. 

‘The environment pulls the trigger’

Before Covid, Freizinger would typically start seeing patients around a parent’s divorce, a lost loved one or the transition from middle school to high school or high school to college.

“It’s a complicated process with biological, psychological, genetic and social-cultural factors,” she said.

Under typical circumstances, strong social connections can act as protective factors for teens with heightened risks, helping them avoid developing eating disorders.

That changed in 2020. During pandemic lockdowns, young people suddenly lost access to these connections.

Megan Bazzini, now 22, has struggled with anorexia since her early teens. She has since recovered, but said her symptoms worsened during the pandemic.

“Before Covid, if your thing was going out for dumplings with your friends, and you said you didn’t want to do that because of your eating disorder, you’d stop getting invited to hang out,” said Bazzini, who lives in New York City.

During Covid restrictions and lockdowns, those experiences vanished.

“I wasn’t in social situations where I felt like I needed to eat to make other people happy,” she said. “Eating disorders thrive in secret.”

Thinness ideals and social media

However, it's impossible to separate the teen eating disorder crisis from social media, experts insist.

Eighty-four percent of teens reported using social media, and the most popular apps were YouTube, Snapchat and TikTok, according to a survey from the nonprofit Common Sense Media. Experts say these platforms’ algorithms encourage eating disorder behaviors and reinforce negative body image. 

“We’re seeing these algorithms target teens and make the content they see more extreme,” said Dr. Jessica Lin is an adolescent medicine physician who specializes in eating disorders at Cincinnati Children’s. She offered the example of a teen who started watching home exercise videos during the pandemic.

“Suddenly the algorithm says they’re interested in exercise and diet content, and it just keeps showing up and worsening,” she said. “It can just spiral from there.”

After several years in recovery, Garrido says her TikTok feed started recommending what the eating disorder community calls “pro-ana” content, meaning photos and videos glamorizing the eating disorder and encouraging followers to consume fewer calories. Garrido said these videos played a role in her recent relapse.

“I was like, ‘Why am I trying to recover from something someone else wants so desperately?’ Might as well just do it again.’” 

Bazzini has stopped using most social media for this reason. “It’s just awful,” she said.

Social media companies, including TikTok, Meta — which owns Instagram — and Google — which owns YouTube — have been the targets of numerous lawsuits in recent years from parents alleging the platforms caused their teens to develop eating disorders. Last year, the Seattle-based Social Media Victims Law Center filed three lawsuits — two against Meta and one against TikTok — alleging that the apps caused young girls to develop chronic eating disorders .  

To be sure, the companies that run these social media apps have taken some measures to cut down the potentially harmful eating disorder content on their platforms, including adding warning labels or age restrictions to some posts and taking others down altogether.

Recently, YouTube wrote in an update to its community guidelines , “On April 18, 2023, we updated our Eating disorders policy to better protect the community from sensitive content that may pose a risk to some audiences. We may remove imitable content, age-restrict content, or show a crisis resource panel on videos about eating disorders or self-harm topics.”

It’s unclear whether, and to what degree, these lawsuits and policy updates will lessen social media’s role in the teen eating disorder crisis. 

Diagnosing eating disorders

A broader recognition of what it means to have an eating disorder could explain, to some extent, the sharp rise in teen eating disorders. With a shift in the way psychiatrists, psychologists and physicians diagnose them, it’s possible more cases are being recognized, rather than more teens developing new disorders.

In 2013, the American Psychiatric Association's manual of mental disorders — the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, or D.S.M.-5 — included binge eating as an official eating disorder for the first time. The D.S.M.-5 also eliminated a requirement that people lose their periods to be diagnosed with anorexia, and added “atypical anorexia” for people with anorexia who aren’t technically underweight.

This updated manual drove greater recognition of eating disorders, including among boys. 

“With the broadening criteria, we were able to be more aware that males can have eating disorders, specifically anorexia, and that people who live in larger bodies can also develop anorexia,” Lin said. “So there’s definitely been better recognition and better acceptance.”

Dr. Walter Kaye, director of the eating disorders program at the University of California, San Diego, suspects broader criteria may have played into the increase.

“Insurance companies are more likely to support something with a diagnosis behind it," he said.

Similar to the crisis for mental health care for teens , demand for treatment has created a tremendous gap in access , with the number of young people in need of care outpacing the availability of doctors, mental health professionals and facilities.

“Eating disorder care is significantly harder to access right now because of the increase in volume, and that’s where we’re stuck,” Lin said. “For these teens to recover, they need to get into treatment as soon as possible, and we’re still a long way away from having enough providers to help the number of patients we have.”

CLARIFICATION (May 1, 2023: 11:32 a.m. ET): A previous version of this article omitted Dr. Jessica Lin’s job description.   She is an adolescent medicine physician who specializes in eating disorders at Cincinnati Children’s.

NBC News contributor Caroline Hopkins is a health and science journalist who covers cancer treatment for Precision Oncology News. She is a graduate of the Columbia University Graduate School of Journalism.