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 ====== Anorexia ======
+{{:anorexia_ppt.pptx|}}
+{{ :powerpoint-anorexia-1-728.jpg?300 |}}
 ----
-====== Overview ======
+======= Overview =======
-==== Introduction ====
+====== Introduction ======
-Hutchinson- Gilford Progeria syndrome, also known as Progeria, is a rare fatal genetic disease affecting 1 in 4 million babies globally. As of 2014, there were 118 confirmed cases of progeria globally. It is responsible for accelerated aging throughout their childhood, commencing at age 1, resulting in scleroderma, reduced joint mobility, hair loss and more (Progeria101/FAQ, 2018). These symptoms will appear at age 1, The disease progresses atherosclerosis which raises the probability of a heart attack or stroke (Genetics Home Reference, 2018).
+Anorexia nervosa (AN) is a life threatening mental illness that typically begins around puberty but can occur at any age. It is characterized by persistent behaviours that interfere with maintaining an adequate weight for health, a powerful fear of gaining weight or becoming fat, disturbance in how the person experiences their weight and shape and the individual not fully appreciating the seriousness of their condition. If these characteristics are seen over a period of a least three months an individual can be diagnosed with anorexia (Nedic, 2014).
-==== History ====
+Persistent behaviours that interfere with maintaining an adequate weight for health includes: restricting food, compensating for food intake through intense exercise, and/or purging through self-induced vomiting or misuse of medications like laxatives, diuretics, enemas, or insulin. In the past anorexia used to be specifically associated with weight loss, making it difficult to recognize in children and adolescents. Weight gain is needed in children and adolescents in order to support healthy growth and development. Therefore, failing to gain weight or grow is just as concerning as weight loss (Nedic, 2014).
+The powerful fear of gaining weight or becoming fat is common in individuals with anorexia. Individuals may feel this fear ever if they are maintaining a weight that is too low for their health. Often this fear will result in individuals using a variety of techniques to evaluate their body size or weight - behaviour known as body checking. Frequent weighing, obsessive measuring of body parts and the persistent use of mirrors to check for "fat" are common techniques used to body check (Nedic, 2014).
+There is a disturbance in how the person experiences their weight and shape meaning that the person overestimates their body size, they usually evaluate it negatively. Individuals feel that their weight and shape matter more than anything else about them (Nedic, 2014).
-Progeria is an extremely rare genetic disease of childhood characterized by dramatic, premature aging with death occurring on average at the age of 13, usually from heart attack or stroke (Kashyap et al., 2014). Hutchinson-Gilford progeria syndrome (HGPS) is the most severe form of the disease and the classic type. The disease was named after the doctors who first described it in England; in 1886 by Dr. Jonathan Hutchinson and in 1897 by Dr. Hastings Gilford. The term progeria is derived from the Greek work geras, meaning old age (DeBusk, 1972).
+Typically, an individual with anorexia does not fully appreciate the seriousness of their condition as it has been linked to cardiac arrest, suicidality, and other causes of death. Anorexia was previously associated with the loss of menstrual periods which made it difficult or impossible to identify in males or in pre-pubescent children or teens, however this is no longer necessary for diagnosis (Nedic, 2014).
-In 1886, the syndrome was first reported by Hutchinson of a 6-year-old boy whose overall appearance was that of an old man. Hutchinson described the case as “congenital absence of hair and its appendages” (DeBusk, 1972). It was a year later that Gilford described a second patient with similar clinical findings. To date, there are only 100 patients with HGPS that have been described in literature (Kashyap et al., 2014). These two boys were further described in 1897 and 1904 by Gildford, who was the one to proposal the term “progeria” and described the post-mortem characteristics (DeBusk, 1971). Little research was done on the disease until the 1990’s due to the rarity of the disease, causing it to be frequently diagnosed erroneously in patients with some of the features such as alopecia and skin of aged appearance (DeBusk, 1972). However, there are three features present in early life; mid-facial cyanosis, skin resembling scleroderma, and glyphic nasal tip, which all facilitate an early diagnosis of HGPS (DeBusk, 1972).
-<box 80%| > {{ :screen_shot_2018-03-02_at_3.52.29_am.png?300 |}} </box|
+====== History ======
-Figure 1: Dr. Jonathan Hutchinson was the first doctor to describe a case of progeria in 1886.
->
-<box 80%| > {{ :screen_shot_2018-03-02_at_3.52.34_am.png?300 |}} </box| Figure 2: Dr. Hastings Gilford described the second case of progeria in 1887. He was the individual to purpose the term progeria and describe the post-mortem characteristics. >
+Though not termed as anorexia nervosa at the beginning, this condition has been seen since the Hellenistic era and has continued through the Middle Ages (Pini et al., 2016). During these times, it was focused on religious fasting, spiritual purity and self- sacrifice. The term, anorexia nervosa was first established by Sir William Gull in 1873; Sir William Gull made observations of this condition and presented it to the British Medical Association in Oxford, England (Pini et al., 2016). At the same time, French physician, Ernest- Charles Lasègue also published details of cases the same year that the term was created, his work concentrated more on the psychological symptoms and examined the role of parental and family interactions (Pini et al., 2016). Anorexia nervosa was the first eating disorder to be placed into the first DSM edition and it was not until 1980 that the body image disturbance criteria was a diagnostic criterion (Pini et al., 2016). In the DSM 5, it is now under the “other specified feeding or eating disorder” along with bulimia nervosa (BN), binge eating disorder (BED), avoidant/restrictive food intake disorder (ARFID), rumination disorder and pica (Pini et al., 2016).
+<box 50%| > {{ :anorexia_gull.png?200 |}} </box|
+Figure 1: Sir William Gull, an English physician that established the term anorexia nervosa. >
+<box 50%| > {{ :anorexia_miss_a.png?200 |{{ :screen_shot_2018-03-02_at_3.52.34_am.png?300 |}} </box| Figure 2: “ Miss A” one of the earliest cases pictured in 1866 and in 1870 after treatment of anorexia nervosa as published by the medical papers of Sir William Gull >
+====== Etiology ======
+Anorexia nervosa has no specific origin as it is difficult to separate whether the starvation causes the cascade in the body or whether it is the anorexia condition itself. Three major aspects have been highlighted as areas of special interest including the biology, psychology and environmental factors.
+Looking at the biology of the condition, it is seen that heritability can have a major influence in its development. The incidence rates of heritability can be influenced by from 50%-75% through various assessments (Bulik, 2010). It should also be noted that there is no direct link of a gene affecting however a cascade if genes have not been identified. The serotonin pathway as described in the pathophysiology has been highlighted as a key factor in the progression of anorexia nervosa (Kaye et al., 2009).
+The psychology behind the condition indicated that those with a tendency of obsessive-compulsive personality traits are individuals with an increased probability of developing this. Anorexia nervosa alleviates the propagation of anxious behaviours in lieu of a continuous fear of food and gaining weight (Rothenburg, 1988).
+Environmental factors, especially through the influence of western culture, drives the desire to be thin as it represents success and worth. The media often perpetuates a culture of continuous scrutiny over one’s body, idolizing the thin (Mayo Clinic, 2018).
 ====== Epidemiology ======
-HPGS is an extremely rare genetic disorder affecting about 1 in 4 million live births, if unreported or misdiagnosed cases are taken into account. The reported prevalence rate of the disease is 1 in 8 million births, based on the number of cases (Coppedè, 2013). According to the Progeria Research Foundation database, there are an estimated 350-400 children living with progeria worldwide at any one time. As of January 2018, there are a recorded 114 children living with progeria worldwide with numbers steadily increasing as the years go by (http://www.progeriaresearch.org/prf-by-the-numbersprf.html).
+The  lifetime prevalence, incidence rates and 5 year recovery rates were calculated from data from 2882 women from 1975-1979 birth cohorts of Finnish twins (Keski-Rahkonen et al., 2007). The incidence in women aged 15 to 19 years was 270 per 100,000 person- years (Keski-Rahkonen et al., 2007). The 5 year clinical recovery rate was 66.8% at which complete or nearly complete psychological recovery was seen (Keski-Rahkonen et al., 2007). Western countries have a higher prevalence than non- Western countries (Keski-Rahkonen et al., 2007).
-   HPGS affects all races; cases of progeria have been discovered in 45 different countries. However, 97% of affected patients are white. Males are affected 1 ½ times more often than females. The disease was thought to be autosomal recessive in the past, however observations made an autosomal recessive inheritance very unlikely and favour a sporadic, dominant mutation. The mutation results in life spans for progeria syndrome to be in the second/third decades of life, with the majority of patients dying of cardiovascular or cerebrovascular disease between 7 and 27 years of age (Sarkar and Shinton, 2001).
+The average prevalence in Western Europe and North America is 0.3% (National Eating Disorder Information Centre, 2018) . The lifetime prevalence in females is 0.9% and in males is 0.3%; note lifetime prevalence is defined as the proportion of individuals in a population that at some point in their life have experienced the disease (National Eating Disorder Information Centre, 2018). The prevalence of AN in Canada is 0.3% in adolescent and young women (National Eating Disorder Information Centre, 2018).
-<box 80%| > {{ :screen_shot_2018-03-02_at_4.02.11_am.png?300 |}}</box| Figure 3: Number of children and countries that PRF has identified with cases of progeria over the years. >
-<box 80%| > {{ :screen_shot_2018-03-02_at_4.02.19_am.png?300 |}} </box| Figure 4: The 45 different countries that PRF has identified with cases of progeria as of January 1st, 2018. >
+<box 70%| > {{ :anorexia_incidence_rates.png?600 |}} </box| Figure 3: Incidence rates and 95% confidence intervals of anorexia nervosa (AN), bulimia nervosa (BN) and eating disorder not otherwise specified (EDNOS) by year for females aged 10- 49 years in the UK. >
+<box 70%| > {{ :anorexia_incidence_rates_male.png?600 |}} </box| Figure 4: Incidence rates and 95% confidence intervals of anorexia nervosa (AN), bulimia nervosa (BN) and eating disorder not otherwise specified (EDNOS) by year for males aged 10- 49 years in the UK. >
 ==== Risk Factors ====
-It has been found that there are several risk factors for developing anorexia. These include: perfectionism, negative self-evaluation, obesity, family history of anorexia, affective disorder, substance abuse, obsessive-compulsive disorder and a stress/trigger. It was also found that a lot of these risk factors were correlated to being risk factors of other psychological conditions (Fairburn, Cooper, Doll & Welch, 1999). It should also be mentioned that all of the aforementioned risk factors are not known in detail - their significance is unknown at this point. Social determinants, culture and family also play a role, and vary significantly ("Anorexia Nervosa-What Increases Your Risk", 2018).
+It has been found that there are several risk factors for developing anorexia. These include: perfectionism, negative self-evaluation, obesity, family history of anorexia, affective disorder, substance abuse, obsessive-compulsive disorder and a stress/trigger. It was also found that a lot of these risk factors were correlated to being risk factors of other psychological conditions and that they could have been acquired genetically (Fairburn, Cooper, Doll & Welch, 1999). It should also be mentioned that all of the aforementioned risk factors are not known in detail - their significance is unknown at this point. Social determinants, culture and family also play a role, and vary significantly ("Anorexia Nervosa-What Increases Your Risk", 2018).
-<box 80%| > {{ :eatingdisorders-300x281.jpg?300 |}} </box| Figure 5: The main 3 categories of risk factors of anorexia. >
+<box 50%| > {{ :eatingdisorders-300x281.jpg?300 |}} </box| Figure 5: The main 3 categories of risk factors of anorexia. >
-<box 80%| > {{ :picture-11.png?300 |}} </box| Figure 6: Perfectionism is a major risk factor for developing anorexia. >
+<box 50%| > {{ :picture-11.png?300 |}} </box| Figure 6: Perfectionism is a major risk factor for developing anorexia. >
@@ Line 52: / Line 67: @@
 Some common symptoms for patients with anorexia are: extreme weight loss, fatigue, insomnia, dizziness or insomnia, constipation and abdominal pain, low blood pressure, and dehydration. Lastly, some patients present with bulimic symptoms - binging and purging ("Anorexia nervosa - Symptoms and causes", 2018).
+Several complications can arise from AN including gastrointestinal, cardiovascular, pulmonary and skeletal system complications (Mitchell & Crow, 2006). Gastric dilation, mucosal necrosis, delayed gastric emptying, gastric motor dysfunction, constipation, pancreatitis, and perforated ulcers (Mitchell & Crow, 2006). Cardiovascular complications include arrhythmias, acrocyanosis, tachycardia, bradycardia, and hypotension (Mitchell & Crow, 2006). Lastly, skeletal complications include decreased bone mineral density, which leads to osteopenia and other bone- related complications (Mitchell & Crow, 2006).
-<box 70%| > {{ :anorexia-symptoms.jpg?300 |}} </box| Figure 7: This figure shows the symptoms that people with anorexia may present with. >
+<box 50%| > {{ :anorexia-symptoms.jpg?300 |}} </box| Figure 7: This figure shows the symptoms that people with anorexia may present with. >
@@ Line 60: / Line 76: @@
 ====== Pathophysiology ======
-=== Background ===
+=== Biological Effects ===
-The nuclear lamina is a filamentous protein layer that provides mechanical support to the inner nuclear membrane (Gonzalez, 2011). The functions of the nuclear lamina include nuclear positioning, chromatin organization, nuclear pore complex organization, nuclear envelope breakdown and reassembly during mitosis, DNA replication, DNA damage response and cell cycle progression, transcriptional control and apoptosis (Gonzalez, 2011).
-The main components of the nuclear lamina are type V intermediate filaments known as lamins that contain a central α- helical rod surrounded by globular N and C terminal domains; the C terminal region contains the nuclear localization sequences (Gonzalez, 2011). As proteins they form coiled- coil dimers that can associate head to tail. These protofilaments then create the final lamin filaments. Lamins can be classified into two types: A- type and B- type. A -type lamins are basic and type B is acidic. Type A are encoded by the LMNA gene with its two isoforms being Lamin A and C. B type lamins are therefore encoded by the LMNB1 and LMNB2 genes (Gonzalez, 2011).
-Lamin A is affected in Progeria so an understanding of the normal transcriptional and translational mechanisms of this protein is essential (Gonzalez, 2011). In cells containing the normal LMNA gene, prelamin A undergoes post- translational modifications before it is found in its mature Lamin A form. Firstly, the cysteine in the C – terminal CaaX motif is farnesylated by farnesyltransferase. Rce1, an endoprotease then cleaves the three terminal amino acids. Then the newly- available cysteine is then methylated by carboxyl methyltransferase, ICMT. Lastly to create mature Lamin A, 15 C- terminal residues that include the farnesylated and carbosymethylated C- terminal cysteine are cleaved by another endoprotease, Zmpste24/ FACE-1 (Gonzalez, 2011).
+Research demonstrates that women with AN will usually overestimate their own body dimensions whereas healthy women will usually tend to underestimate them. The cognitive-affective component of a disturbed body image comprises of negative-body related attitudes and emotions (Vocks et a, 2010). Although it seems that in Western cultures discontent with one’s shape and weight is common those that have eating disorders seem to exceed those of healthy women in terms of body dissatisfaction.
-=== Genetics ===
+Although AN is characterized as an eating disorder, it remains unknown whether there is a primary disturbance of appetitive pathways, or whether there could be other causes such as anxiety or obsessive preoccupation with weight gain.
-Hutchinson- Gilford Progeria syndrome is commonly caused by a single de novo silent mutation in codon 608 of the LMNA gene (Gonzalez, 2011). The mutation in HGPS is a nucleotide substitution from cytosine to thymine at position 1824 (Goldman et al., 2004). This substitution causes for the partial activation of a cryptic splice site (Goldman et al., 2004). It causes deletion of 150 nucleotides in exon 11 (Goldman et al., 2004). This causes for a 50 amino acid deletion near the C- terminus of the protein, which includes the Zmpste24 cleavage site (Pollex & Hegele 2004). This causes for a mutant prelamin A to remain farnesylated throughout the lifespan of the protein (Pollex & Hegele, 2004). The mutant protein that results from this is known as progerin (Pollex & Hegele, 2004). Around 80% of HGPS cases contain this mutation that is known as the LAΔ50 mutation. Evidence has suggested that transfection of progerin or a non-cleavable form of prelamin A causes for nuclear abnormalities (Pollex & Hegele, 2004). During mitosis, the abnormal association of progerin causes a delay in the onset and progression of cytokinesis and impairs the targeting of lamina components to the nucleus of daughter cells (Gonzalez, 2011). In addition, it can change the entry of the cell into S- phase mediated by hyperphosphorylation of the retinoblastoma gene product (pRB) by cyclin D1/cdk4 (Gonzalez, 2011). Progerin accumulation also causes abnormal chromosome segregation and binucleation (Gonzalez, 2011). It also promotes DNA- damage, changes in DNA repair, causes for genomic instability as well as interfering with nuclear architecture. This leads to premature cell death (Gonzalez, 2011).
+<box 70%| >  {{ :anorexia_patho1.png?500 |}} </box| Figure 8:  If they have a personality or temperament predisposition trait it can contribute to one’ vulnerability of developing anorexia. It is usually seen that it becomes intensified during adolescence. >
- Additional heterozygous mutations for atypical Progeria patients have also been revealed. R644C affects the C- terminus, E578V also in the C- terminus and T10I within the N- terminal globular domain seen in Seip syndrome (Pollex & Hegele, 2004). The most common hypothesis for the inheritance of this disorder is sporadic autosomal dominant (Pollex & Hegele, 2004).
-=== Genomic Instability ===
+=== Serotonin Function ===
-Hutchinson- Gilford Progeria syndrome is commonly caused by a single de novo silent mutation in codon 608 of the LMNA gene (Gonzalez, 2011). The mutation in HGPS is a nucleotide substitution from cytosine to thymine at position 1824 (Goldman et al., 2004). This substitution causes for the partial activation of a cryptic splice site (Goldman et al., 2004). It causes deletion of 150 nucleotides in exon 11 (Goldman et al., 2004). This causes for a 50 amino acid deletion near the C- terminus of the protein, which includes the Zmpste24 cleavage site (Pollex & Hegele 2004). This causes for a mutant prelamin A to remain farnesylated throughout the lifespan of the protein (Pollex & Hegele, 2004). The mutant protein that results from this is known as progerin (Pollex & Hegele, 2004). Around 80% of HGPS cases contain this mutation that is known as the LAΔ50 mutation. Evidence has suggested that transfection of progerin or a non-cleavable form of prelamin A causes for nuclear abnormalities (Pollex & Hegele, 2004). During mitosis, the abnormal association of progerin causes a delay in the onset and progression of cytokinesis and impairs the targeting of lamina components to the nucleus of daughter cells (Gonzalez, 2011). In addition, it can change the entry of the cell into S- phase mediated by hyperphosphorylation of the retinoblastoma gene product (pRB) by cyclin D1/cdk4 (Gonzalez, 2011). Progerin accumulation also causes abnormal chromosome segregation and binucleation (Gonzalez, 2011). It also promotes DNA- damage, changes in DNA repair, causes for genomic instability as well as interfering with nuclear architecture. This leads to premature cell death (Gonzalez, 2011).
-   Additional heterozygous mutations for atypical Progeria patients have also been revealed. R644C affects the C- terminus, E578V also in the C- terminus and T10I within the N- terminal globular domain seen in Seip syndrome (Pollex & Hegele, 2004). The most common hypothesis for the inheritance of this disorder is sporadic autosomal dominant (Pollex & Hegele, 2004).
+The 5-HT serotonin system has been studied in individuals that have AN, to suggest that it is possible that this neurotransmitter system plays a role in many symptoms of anorexia such as enhanced satiety, impulse control and mood.
+<box 70%| > {{ :anorexia_patho2.png?600 |}} </box| Figure 9: Individuals that are more vulnerable to the development of an eating disorder may have an imbalance in the postsynaptic 5-HT(1A) and 5-HT(2) receptor activity (Kaye et al, 2009). >
+It has been said that these might contribute to an increase in satiety and a more anxious harm-avoidant temperament. Individuals with Anorexia are said to have a reduction in dysphoric mood. Starvation is associated with an increase in postsynaptic 5-HT1A receptor binding potential. Additionally the binding of the 5-HT-2A receptor is positively correlated with harm avoidance in individuals that suffer from AN (Kaye et al, 2009).  Individuals with AN will usually pursue starvation ass an attempt to avoid the dysphoric mood that comes as a consequence due to this increased stimulation of postsynaptic 5-HT1A and 5-HT2A receptors and therefore makes eating and weight gain aversive (Kaye et al , 2009).
+=== Anterior Insula ===
+The anterior insula is involved in the idea of interoceptive processing which explores the feelings of pain, temperature itch etc.  The integration of these internal feelings allows to gain a sense of the physiological condition of the entire body. Altered insula activity supports the idea that individuals with AN have an altered sense of self. As mentioned those that have anorexia experience a strong conflict between the biological need for food and an acquired aversive association with the food.  Individuals do not recognize the symptoms of malnutrition, so they do not respond to hunger and they do not have the motivation to change. This is all due the idea of disturbed interoceptive awareness (Kaye et al, 2009).
+Individuals who have AN will usually experience an aversive visceral sensation when they are exposed to food or a form of food-related stimuli. This creates a bias towards the reward-related properties of food and creates a more negative emotion. This minimizes the exposure to food stimuli (Kaye et a, 2009).
+<box 70%| > {{ :anorexia_patho3.png?500 |}} </box| Figure 10: The different effects of the presentation of food in individuals who are healthy and individuals with anorexia nervosa. >
@@ Line 85: / Line 105: @@
 ====== Current Treatments ======
-Unfortunately today there are no treatments for Progeria. Physicians and healthcare providers’ main goals right now are to delay or reduce symptoms. This can be achieved by: small doses of aspirin, preventative medications, physical and occupational therapy, nutrition and dental care. Common with Progeria, small doses of Aspirin attempt to reduce the risk of heart attacks and strokes. Preventative medications that can help lower cholesterol, blood pressure, and reduce the chance of getting a blood clot can all be prescribed if the individual seems to be at risk. Physical and occupational therapy can help an individual maintain healthy movement capability and nutrition and dental care for being overall healthy (Mayo Clinic, 2018). Progeria is commonly screened phenotypically or through medical history at the physician’s office. A genetic test for the LMNA mutations can be ordered if the physician deems this appropriate (Sinha, Raghunath & Ghosh, 2018).
+Through research, it is clearly exemplified that anorexia nervosa is merely not an eating disorder but dives into deep-seeded issues an individual may have. The first step includes the acceptance of their disorder and familial assistance prepares individuals for the upcoming services.
+A psychiatrist is beneficial for the prescription of medications including antidepressants as several individuals experience anxiety in accordance with the eating disorder (Kaye et. al 1999). Enlisting the services of a nutritionist will be of benefit as managing the fear of food will be adequately guided by a professional ensuring the appropriate quality and quantities of food are provided.
+<box 70%| > {{ :anorexia_treatment.png?300 |}} </box| Figure 11: This image compiles a list of services an individual with anorexia nervosa may use to treat the condition. >
-For potential future treatments, there are many different angles of approach. Genetics currently is a big area of research for this disease. Anything from early detection capability, to actual cures, genetics is a significant field to target. Additionally, there is also a lot of interest in reducing the severity of symptoms, common with individuals with Progeria. First, heart and blood vessel disease is a target of interest. Farnesyltransferase inhibitors (FTIs), which are drugs for treating cancer, are being investigated to whether they can help vasodilate blood vessels and reduce weight gain (Mayo Clinic, 2018). In 2012, 25 children with Progeria underwent a clinical trial that showed these results (Gordon et al., 2012). FTIs also have shown in mouse models to improve nuclear shape and reduce the negative effects of built up prelamin A. Lonafarnib, an FTI, certainly gives confidence for developing a potential cure to Progeria (Sinha, Raghunath & Ghosh, 2018).
+The implementation of cognitive behavioural therapy will use psychotherapy as a means to address the underlying thoughts behind the condition. This will recognize those symptoms and assist in a healthy method of alleviating those notions (Kaye et al. 1999). Managing a long term eating disorder will be a difficult challenge however with the enlistment of these services, recovery will be possible.
-(a is Progerin cell, d is a healthy cell - treated with FTI - Capell reference)
 ======Conclusion======
-With the description of the history, diagnosis, symptoms, risks, pathophysiology, etiology, epidemiology, and treatments there are clear outlines of progeria however further research is required. The future implications of progeria details a focus on increasing the lifespan of diagnosed individuals. Although there are not specific treatments available, the future developments are promising. With the use of models and genetics, the advancements to create a clinical trial are near (Swahari and Nakamura, 2016).
+The causes of anorexia nervosa are not completely understood by medical and psychological professionals, it is acknowledged that an array of biological, social, genetic, and psychological factors play a role in increasing the risk of its onset. The societies we live in have strong beliefs and attitudes toward just about everything. Different groups within a given society adapt these beliefs, attitudes and behaviours altering our beliefs and attitudes toward ourselves and our bodies. Our feelings and behaviour also affect our physical make-up and health. The first step in the recovery process is realizing that our food- and weight-related behaviours are hurting us, rather than helping us. Once an individual is able to realize this, help can be found or offered in a variety of days. Family members and friends may also benefit from information and help. It is possible to prevent the development of food and weight fixation and eating disorders. It is also possible to prevent existing eating disorders from getting worse. It begins with learning and improving our own self-esteem and body image, to working with others and making positive societal changes.
 ===== References =====
-Capell, B., Erdos, M., Madigan, J., Fiordalisi, J., Varga, R., & Conneely, K. et al. (2018). Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome. PNAS. Retrieved 24 February 2018, from http://www.pnas.org/content/102/36/12879
-Coppedè, F. (2013). The epidemiology of premature aging and associated comorbidities. Clinical interventions in aging, 8, 1023. DeBusk, F. L. (1972). The Hutchinson-Gilford progeria syndrome: report of 4 cases and review of the literature. The Journal of pediatrics, 80(4), 697-724.
+Anorexia nervosa - Symptoms and causes. (2018). Mayo Clinic. Retrieved 26 March 2018, from https://www.mayoclinic.org/diseases-conditions/anorexia/symptoms-causes/syc-20353591
-De Sandre-Giovannoli, A., Bernard, R., Cau, P., Navarro, C., Amiel, J., Boccaccio, I., … & Lévy, N. (2003). Lamin a truncation in Hutchinson-Gilford progeria. Science, 300(5628), 2055-2055.
+Anorexia Nervosa-What Increases Your Risk. (2018). WebMD. Retrieved 26 March 2018, from https://www.webmd.com/mental-health/eating-disorders/anorexia-nervosa/anorexia-nervosa-what-increases-your-risk
-Goldman, R., Shumaker, D., Erdos, M., Eriksson, M., Goldman, A., & Gordon, L. et al. (2004). Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome. Proceedings Of The National Academy Of Sciences, 101(24), 8963-8968.
+Bulik CM, Thornton LM, Root TL, et al. Understanding the relation between anorexia nervosa and bulimia nervosa in a Swedish national twin sample. Biol Psychiatry. 2010;67:71-77.
-Gonzalez, J. (2011). A-type lamins and Hutchinson-Gilford progeria syndrome: pathogenesis and therapy. Frontiers In Bioscience, S3(1), 1133.
+Dell’Osso, L., Abelli, M., Carpita, B., Pini, S., Castellini, G., Carmassi, C., & Ricca, V. (2016). Historical evolution of the concept of anorexia nervosa and relationships with orthorexia nervosa, autism, and obsessive–compulsive spectrum. Neuropsychiatric disease and treatment,12, 1651.
-Gonzalo, S., & Kreienkamp, R. (2015). DNA repair defects and genome instability in Hutchinson–Gilford Progeria Syndrome. Current Opinion In Cell Biology, 34, 75-83.
+Diagnosis of anorexia nervosa. (2018). Healthdirect.gov.au. Retrieved 26 March 2018, from https://www.healthdirect.gov.au/diagnosis-of-anorexia-nervosa
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