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I’ve been away so sorry for the delay in replying to comments and emails. I have just responded now to the lovely responses I have found in my comments and email.

My emails reminding me about comments also seems to have stopped turning up (gotta love technology) so that hasn’t helped either.

Although I don’t post as much now, my email is always open and I will always respond to any letters. And once I sort out the commenting issue on posts, I’ll be quicker at responding there too.

 

 

and I mean, ALWAYS. Never give up.

From NEDC Newsletter 2016

Eating disorders are complex mental illnesses. To date, no single cause has been identified. Rather, widespread research suggests that the onset of an eating disorder is unique to the individual and often involves the integration of multiple factors (Culbert, Racine, & Klump, 2015; Rikani et al., 2013). Understanding these known risk factors has the potential to improve treatment methods, determine high risk groups for prevention programs and reduce stigma (Striegel-moore & Bulik, 2007). Current literature explores genetic, psychological and socio-cultural influences.

Genetic Vulnerability

The genetic link to eating disorders has been a consistent focus in scientific literature. Previous findings from family and twin studies indicate that eating disorders have a hereditary component (Trace, Baker, Pe, & Bulik, 2013). In particular, one study found that first-degree relatives of individuals with Anorexia Nervosa are 11 times more likely to develop the illness than relatives of individuals without the disorder (Strober, Freeman, Lampert, Diamond, & Kaye, 2000). This suggests that genetics can influence an individual’s vulnerability to eating disorders.

The onset of eating disorders, specifically Anorexia Nervosa and Bulimia Nervosa, typically occurs during adolescence (Hudson, Hiripi, Pope, & Kessler, 2007; Striegel-moore & Bulik, 2007). The complex hormonal, physical and neural changes associated with puberty increase the likelihood of adolescent engagement in disordered eating behaviours (Klump, 2013). Given such, puberty is recognised as a significant risk period.

Although there has been decades of research exploring the genetics of eating disorders, the biological causes are still not well understood. This may be because the majority of studies involve small sample sizes and are often conducted during the acute or recovery phase of an eating disorder (Trace et al., 2013). The QIMR Berghofer Medical Research Institute in Queensland are currently undertaking the largest international investigation into the cause of Anorexia Nervosa. This study, known as the Anorexia Nervosa Genetic Initiative (ANGI), seeks to identify the specific genes associated with Anorexia Nervosa in the hopes of better understanding the causes and finding a potential cure.

Psychological Factors

A connection between certain personality traits and eating disorders has been identified. Research into Anorexia Nervosa and Bulimia Nervosa has shown that obsessive compulsive personality disorder, low self -esteem and perfectionism are considerable risk factors for disordered eating behaviours and attitudes (Culbert et al., 2015; Egan, Wade, & Shafran, 2011). A recent investigation into childhood obsessive compulsive personality traits found that the presence of perfectionism and inflexibility in early life can predict the later development of an eating disorder (Southgate, Tchanturia, Collier & Treasure, 2008). Personality types are also important to consider when treating an eating disorder, as obsessive compulsive tendencies may continue to drive restrictive and rigid behaviours. Given such, Egan et al. (2011) argues that traits such as perfectionism should be treated alongside an eating disorder, in order to effectively reduce disordered eating symptoms.

The cognitive, behavioural and interpersonal changes that accompany eating disorders can make it difficult to discern the psychological causes from the psychological effects. For example, the co-existence of depression and anxiety with eating disorders has raised debate as to whether such conditions precede or are a direct outcome of an eating disorder.

Socio-Cultural Influences

Socio-cultural influences play a considerable role in the development of eating disorders. Mass media, such as television, magazines and advertising, airbrush and alter images to portray unrealistic representations of the male and female body (Perloff, 2014; Striegel-moore & Bulik, 2007). Predominant images suggest that beauty is associated with thinness for females and a lean, muscular body for males. Individuals who internalise this ‘thin’ ideal and strive for the ‘perfect’ body, are at a greater risk of developing body dissatisfaction, which can lead to dieting and other disordered eating behaviours (Culbert et al., 2015). More recent research has explored the impact of social media on body image and eating behaviours. Andsager (2014) argues that the introduction of Facebook and Instagram has increased our exposure to photo-shopped images and thin ideals. Although a direct link to eating behaviours is yet to be established, the appearance-focused nature of social media platforms has been shown to cultivate body image concerns and reduce self-esteem (Perloff, 2014).

Additionally, there is growing evidence that the ways in which weight, shape and size are discussed in the home have a strong impact on self-esteem and dieting behaviours (Loth et al., 2014). Culbert et al. (2015) propose that environmental and psychological factors interact with and influence the expression of genes to cause eating disorders. Further research into this relationship is needed.

Modifiable Risk Factors

Identifying potential risk factors for eating disorders is beneficial in shaping effective prevention and early intervention programs. Research indicates that prevention programs with the most favourable outcomes are those which focus on reducing modifiable risk factors (Jacobi, Hayward, Zwaan, Kraemer, & Agras, 2004). Low self-esteem, body dissatisfaction, dieting behaviours and internalisation of the thin ideal have been acknowledged as variable factors associated with the onset of eating disorders.

The aetiology of eating disorders is becoming a growing field of research. Although limited conclusive evidence has been recorded, understanding possible influences can inform best practice and encourage effective management of eating disorders.

References

Andsager, J. L. (2014). Research Directions in Social Media and Body Image. Sex Roles, 71, 407–413.

Culbert, K. M., Racine, S. E., & Klump, K. L. (2015). Research Review : What we have learned about the causes of eating disorders – a synthesis of sociocultural , psychological , and biological research. Journal of Child Psychology and Psychiatry, 11, 1141–1164.

Egan, S. J., Wade, T. D., & Shafran, R. (2011). Perfectionism as a transdiagnostic process : A clinical review. Clinical Psychology Review, 31(2), 203–212.

Hudson, J. I., Hiripi, E., Pope, H. G., & Kessler, R. C. (2007). The Prevalence and Correlates of Eating Disorders in the National Comorbidity Survey Replication. Journal of Biological Psychiatry, 61, 348–358.

Jacobi, C., Hayward, C., Zwaan, M. De, Kraemer, H. C., & Agras, W. S. (2004). Coming to Terms With Risk Factors for Eating Disorders : Application of Risk Terminology and Suggestions for a General Taxonomy. Psychological Bulletin, 130(1), 19–65.

Klump, K. L. (2013). Puberty as a critical risk period for eating disorders : A review of human and animal studies. Hormones and Behavior, 64(2), 399–410.

Loth, K. A., Ph, D., D, R., Maclehose, R., Ph, D., Bucchianeri, M., … D, R. (2014). Predictors of Dieting and Disordered Eating Behaviors From Adolescence to Young Adulthood. Journal of Adolescent Health, 55(5), 705–712.

Perloff, R. M. (2014). Social Media Effects on Young Women ’ s Body Image Concerns : Theoretical Perspectives and an Agenda for Research, 363–377.

Rikani, A. A., Choudhry, Z., Choudhry, A. M., Ikram, H., Asghar, M. W., Kajal, D., … Mobassarah, N. J. (2013). A critique of the literature on etiology of eating disorders. Annals of Neurosciences, 20(4), 157–161.

Southgate, L., Tchanturia, K., Collier, D., & Treasure, J. (2008). The development of the childhood retrospective perfectionism questionnaire (CHIRP) in an eating disorder sample. European Eating Disorders Review, 16(6), 451-462.

Striegel-moore, R. H., & Bulik, C. M. (2007). Risk Factors for Eating Disorders. American Psychologist, 62(3), 181–198.

Strober, M., Freeman, R., Lampert, C., Diamond, J., & Kaye, W. (2000). Controlled family study of anorexia nervosa and bulimia nervosa: Evidence of shared liability and transmission of partial syndromes. The American Journal of Psychiatry, 157(3), 393–401.

Trace, S. E., Baker, J. H., Pe, E., & Bulik, C. M. (2013). The Genetics of Eating Disorders. Annual Review of Clinical Psychology, 9, 589–620.

I’ve written in brief about heart problems with anorexia, but it’s any eating disorder that can also produce severe heart problems. This is the hidden killer for many. I found that not knowing Sophie’s true heart rate until she was in hospital to be a very critical issue. The GP and others treating her before her first hospital admission, didn’t mention heart problems either. Nor did they do a full check on heart rate – lying down, sitting, standing. There was never a moment that they measured drop rate. They also never mentioned the heart rate overnight, when it normally drops. For those with anorexia this is very very critical. Many have their heart rate drop into emergency intensive care zones during this time and never know it. It happened to us and thousands of others. The scary side – heart failure – and not even knowing that it was getting the heart was getting that low.

As we coasted towards our second hospital admission, this time I was more than aware. Our specialist doctor did the proper heart rate tests, but I pushed our GP to do the same (and still struggled for them to understand how important this was). I also took Sophie’s heart rate late at night and in the early morning before she got up. It gave me a very real idea of what her heart was dropping to overnight, it gave me more mileage with the GP and getting her pushed onto the critical admission list.

The article below also outlines the different types of heart problems that arise with eating disorders. I didn’t know that last two and frankly, we should all be told these things regardless when we are in treatment care. I’ve put just the heart information here, but the full article that covers more general information about anorexia is available: http://www.everydayhealth.com/columns/jared-bunch-rhythm-of-life/for-both-men-and-women-anorexia-nervosa-is-increasing-and-the-effects-on-the-heart-can-be-severe/

Anorexia and the Heart

Here are four broad patterns in which the heart is affected with both short- and long-term exposure to anorexia nervosa:

1. Loss of heart muscle. Just like the skeletal muscles in your arms and legs that you can see, the heart muscle loses mass. In patients with longstanding anorexia the heart walls thin and weaken. The heart chambers then enlarge. The pumping function of the heart declines and with it, blood pressure falls. Organs that are very sensitive to blood pressure and blood flow such as the kidneys and liver then begin to fail. Fortunately with weight gain and replenishment of essential vitamins and minerals the heart muscle often recovers.

2. Abnormal heart rhythms. A number of abnormal heart rhythms can occur with anorexia. One is that the heart beats slowly, a pattern called bradycardia. This is a particular problem in people who have weak heart muscles. Normally if the heart function weakens and less blood is pumped with each beat, the heart has to increase the number of beats per minute to maintain the same average blood flow. With anorexia, if the energy stores in the heart are so depleted that the heart rhythm cannot increase to compensate for a weakened heart failure, blood pressure falls more quickly and organ failure develops rapidly.

Another concern is fast abnormal heart rhythms. People tend to be most sensitive to these types of rhythms if they follow a pattern of binge eating and purging. This can result in dangerous shifts and loss of body electrolytes such as sodium, potassium, and magnesium. The electrical aspects of the heart that create heartbeats are critically dependent on these electrolytes. When they fall, chaotic electrical patterns can develop in the lower heart chambers that result in cardiac arrest.

3. Loss of the autonomic regulation of the heart and blood vessels. Our bodies do a lot of things that we are unaware of to help us function. For example, the simple act of sitting or standing requires multiple complex changes in the body. Among these are constricting of the blood vessels to raise blood pressure, and a subtle elevation of the heart rate and contractility of the heart. In people with anorexia these reflexes can be impaired or lost. This can result in profound drops in blood pressure when attempting to sit, stand, or walk. People with anorexia can experience severe lightheadedness, fainting spells, and even cognitive changes.

4. Mitral valve prolapse. The heart valve between the upper and lower chambers on the left side of the heart is called the mitral valve. It closes when the lower heart chamber contracts to pump blood throughout the body. The changes in the heart muscle mass compared the structure of the heart valve can affect the closing of the valve. The mitral valve then can close less tightly and prolapse into the upper heart chamber. In people with anorexia about 20 percent will have mitral valve prolapse. Unfortunately, the heart valve condition appears to persist even after weight gain.

I am seeing more patients with anorexia in my clinic. To a physician, low body weight and in particular the pattern of muscle loss are noticeable signs. Most of my patients with anorexia eat a low to low-normal calorie content in a day, but then exercise excessively. Despite being very underweight they still discuss weight loss goals they hope to attain. More recently, I have encountered a surge in misuse of “natural” therapies to cleanse or purge the colon or work as a diuretic. These therapies are every bit as dangerous when misused as prescription laxatives and diuretics, and can lead to severe mineral and electrolyte depletion a

no more meds

 Medication freeYes we are still here! But our journey means the blog is not something that now gets a lot of posts. I debated with making it an advocacy, education blog etc but that was never the point of this blog. There are better forums for the advocacy ED awareness but not here. This is our story, Sophie’s story and I do not want to detract from that. It is also our story told from my view in most cases rather than my daughter’s. Now she is 21 and well, the story is now ALL hers. I am merely a by-stander and whatever or wherever her future takes her, the story is her’s alone now.

As a quick update, she is now medication free. No more anti-depressant!!!! A huge move forward after being on it for 5.5years. Soph has been toying with the idea for several months, but cautious of her anxiety and depression bouts that possibly the medication might be helping. But considering the depths of the ’bouts’ I do wonder just how much the medication was really helping. Teenagers change so much in every way (psychologically, emotionally, physically) as they become adults, that what was started at 15 is very probably not overly useful at 21. Many anti-depressants can also stop working as effectively long-term.

So med free. I demanded she take the weaning off process SLOWLY. INCREDIBLY.SLOWLY. Got the ‘awww mum’ whole drama. But I didn’t want the cold turkey, medication backlash that happens. Coming off medication like these means months before she will be fully herself and functioning without drug related responses. Her brain and body will need to change and readjust to normal state for many processes. She is in effect a very different person from the child at 15. Not just because she is now adult, but also because of the long term medication. The anorexia alone has made her a different person. The medication has made it a bigger difference from then to now. Too many psychological, mental and emotional changes that is over and above normal growth and change.

She’s been med free for about a month. Too early yet to tell how she will go. Life needs to happen for her to see if she can manage herself. She is still home on uni break for a few more weeks, then back to reality. This time round she has been home for almost 4 months, so it will be a bigger drop back into uni life and her living reality. But she is brave and courageous for taking the step that needed to be taken. A new freedom and learning who she is now without any props is the only way to go!

Having been on the receiving end of many of these phrases and been made to feel like it is my burden alone to carry, it is time many of our called Christian favourite pull-out phrases go under the microscope. We tout these out making us feel like we have responded in a caring, Christian manner when in fact we have only added to the isolation and pain. Some of the responses below aren’t even biblical. Like many other sayings, they have come about from home spun, pull yourself up theology. I never want to be on the receiving end of these again, nor do I want to ever find myself saying them to someone in painful, messy, traumatic circumstances. Instead I hope to offer practical help, just turn up with the cleaning gear, the meal, the hug and never ever offer empty phrases or wait to be asked to help out. It also means forgiving those, who in their narrowness and inabilities, didn’t intentionally mean to harm. And hope through grace and maturity will grow to be more caring and embracing of pain in others.

communicating across the boundaries of faith & culture

crisis

  1. God will never give you more than you can handle. While some may believe it is theologically correct, depending on your definitions, it is singularly unhelpful to the person who is neck-deep in a crisis, trying to swim against a Tsunami. A wonderful phrase recently came from Support for Special Needs. They suggest changing this from “God will never give you more than you can handle” to “Let me come over and help you do some laundry.” This strikes me as even more theologically correct.
  2. It gets better. Yes, yes it does. But right then, it’s not better. And before it gets better, it may get way worse.
  3. When God shuts a door, he opens a window. Maybe, but maybe not. Maybe he just shuts a door. Maybe there is no window. There was no window for Job. There was a cosmic battle that raged as he sat in distress. There…

View original post 1,145 more words

This research sparked a big response on a group I belong to and how so many of our children who have an eating disorder, are also double jointed and flexible.It may be something my readers also relate to and recognise in their children or themselves.

It’s an interesting concept and one that further research would be good to continue. Unfortunately they didn’t link to the actual research papers, but the news post is available on Scientific American.

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Joint flexibility is an oft-coveted trait that provides a special advantage to dancers and athletes, but there can be too much of this good thing. A growing body of research suggests a surprising link between high levels of flexibility and anxiety. A study published last year in the journal Frontiers in Psychology is among the most recent to confirm the association, finding that people with hypermobile joints have heightened brain activity in anxiety regions.

Joint hypermobility, which affects approximately 20 percent of the population, confers an unusually large range of motion. Hypermobile people can often, for instance, touch their thumb to their inner forearm or place their hands flat on the floor without bending their knees. The trait appears to be genetic and is a result of variation in collagen, the main structural protein of connective tissue.

Being double-jointed has long been linked with an increased risk for asthma and irritable bowel syndrome, among other physical disorders. “Joint hypermobility has an impact on the whole body and not just joints,” says Jessica Eccles, a psychiatrist and researcher at the University of Sussex in England. It was only a matter of time before scientists also looked at whether joint hypermobility was linked to mental disorders. The investigation began in 1993 and heated up in 1998 when researcher Rocío Martín-Santos, now at the Hospital Clinic of the University of Barcelona, and her colleagues discovered that patients with anxiety were 16 times more likely to have lax joints. Their findings have since been replicated numerous times in large populations.

A 2012 brain-imaging study conducted by Eccles and her colleagues found that individuals with joint hypermobility had a bigger amygdala, a part of the brain that is essential to processing emotion, especially fear. In the 2014 study, which was conducted by Eccles and her associates in collaboration with researchers from Spain, hypermobile participants displayed heightened neural reactivity to sad and angry scenes in brain regions implicated in anxiety. Researchers have also linked the condition with increased consumption of chocolate, tobacco and alcohol—items that are often used in an attempt to self-medicate anxiety.

Joint hypermobility may also be associated with an exaggerated fight-or-flight reaction. Eccles and her colleagues recently found support for this idea in a study of 400 psychiatric patients. They uncovered a simple yet powerful mechanism behind the link: the collagen abnormalities that make joints especially flexible seem to affect blood vessels, making patients prone to an accumulation of blood in the veins of the legs. This pooling may lead to exaggerated cardiovascular responses to maintain the output of blood from the heart. When the heart has to work extra hard just to circulate blood, it brings the entire body to the verge of a fight-or-flight reaction, requiring very little to set off panic.

Eccles hypothesizes that these patients might benefit in particular from beta blockers, drugs that ease anxiety by reducing symptoms of the body’s fight-or-flight response. She hopes that future studies will investigate such targeted treatments for double-jointed people. In the meantime, the findings are an important reminder for clinicians to consider the possibility that a patient’s mental disorder could have purely physical origins.

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