I realized that apart from one relatively short post on exercise, I have not synthesized much of the scattered responses I have given to questions about activity and exercise in recovery.
I get asked very often about the necessity of quitting all exercise and exertion while in recovery, so I will try to pull all the information together in this blog post as a one-stop location for future reference.
Of the few science-based recovery programs out there, none support the continuance of exertion or exercise during recovery.
Id Iom: Flickr.com
Anorexia Athletica/Exercise Bulimia
As a refresher, the eating disorder spectrum includes: anorexia nervosa, cycles of restriction/reactive eating, bulimia nervosa, orthorexia nervosa and anorexia athletica (also known as exercise bulimia). Other facets may include diabulimia and drunkorexia.
I have not addressed diabulimia to date and perhaps at some point in the future I will do a post on the topic. Diabulimia is something that may occur for those with Type I diabetes mellitus and a co-occurring eating disorder. As I have mentioned in the past, whenever an eating disorder patient uses any maladaptive behavior to try to alleviate the anxiety that comes from needing to nourish herself, then those behaviors become facets of the condition itself.
Some facets are more socially reinforced than others and exercise is certainly perceived as a life-affirming, stress-relieving behavior that can have no down side. It is why anorexia athletica tends to sneak up on the patient and is easily overlooked by concerned friends and family for quite some time, until the injuries and damage start to pile up.
The risk of developing or reinforcing anorexia athletica is one of the most compelling reasons to cease exercise when you are attempting to recover from an eating disorder. However, it is not the only reason and I’ll get into more details on that as we go along in this post.
As we are bombarded with messages of needing to exercise more and eat less, most who have a genetic predisposition to develop an eating disorder often begin that first diet with an accompanying focus to exercise hard as well.
However, there are also those who activate an eating disorder initially by either planned or unplanned restriction of food intake alone (dieting or illness).
In both circumstances the increase in food intake needed to restore weight and repair damage tends to ratchet up anxiety. In response, it is very easy to apply the maladaptive anxiety-modulation of exercise. The cycle is quickly reinforced and soon the amount of food the eating disorder will “allow” you to consume is inextricably tied to how much you move around to burn off those calories.
Non-Exercise Activity Thermogenesis (NEAT)
Do you prefer to stand when doing things that most people do while sitting? Do you try to avoid sitting? Do you fidget? Do others comment that you always seem to be on the go? If you answer “yes” to any of these questions, then these behaviors are non-exercise activity issues within the context of an eating disorder.
Non-exercise activity thermogenesis (NEAT) is basically all activity that is not exercise that “we undertake as vibrant, independent beings”. 1 NEAT dominates our entire metabolic homeodynamic ability to maintain weight, health and wellbeing. NEAT includes getting out of bed, brushing your teeth, standing, sitting, typing…you get the idea.
NEAT is known to drop precipitously for non-ED folks who are dieting and it increases just as significantly in trial studies where non-ED folk are overfed in laboratory settings. 2,3,4 There is one particularly memorable photograph of the subjects of the Minnesota Starvation Experimentall lying down on the ground as they neared the end of the 3-month period of semi-starvation— too exhausted to sit up or do anything. 5 How much NEAT drops or increases is variable from individual to individual, although fairly constant within each individual throughout a lifetime.
In Levine’s trial (n=16) the variation in the change in NEAT ranged from 700 calories down to -100 calories when the subjects were overfed 1000 calories above their normal baseline intake every day.
The higher the NEAT increased during the overfeeding period, the lower the weight increase that occurred. Remember, however, that in these purposeful overfeeding trials, subjects all return to their pre-trial weight within 2-4 weeks after the end of the trial. 6 Levine theorizes that we each have ingrained NEAT levels and that we also have significant seasonal variations as well.
So now you’re probably thinking, or perhaps more accurately some ED-powered elements of your brain are thinking: “So then if I move around more because I’m eating more, then that’s normal and why should I force myself to lie around and be a lazy slob all day? — That’s not normal when I have to eat so much in recovery!”
Not so fast. Turns out that your NEAT is a bit messed up and it has failed to throttle back in the face of massive restriction of energy in the first place.
In fact, your NEAT is inextricably linked to the persistence of having an eating disorder.
Problematically NEAT appears to increase in those with eating disorders when they are actively restricting intake. The more you fail to provide your body with enough energy to function, the more you are compelled to keep moving, creating even greater energy deficits, driving more compulsion to move…(Dal Capo ad Infinitum, or repeat to infinity.)
I had a colleague who would regularly heap derision on the administrative cost-cutting mantra of “we’ll just have to do more with less”. His response was always, “and that inevitably leads to doing everything with nothing.” His retort is quite comparable to the spiral of an eating disorder.
Neuropeptide Y and Hyperactivity
Neuropeptide Y (NPY) is “considered the most potent orexigenic neuropeptide known." 7 Essentially the presence of NPY generates increased appetite, hunger and feeding (orexigenesis). When energy deprived, the levels of NPY increase in our central nervous system.
The investigation of NPY in anorexic and bulimic patients is one of several areas that Walter Kaye, a leading researcher in the field of eating disorders, has covered in numerous published papers. While it does appear that NPY and other central nervous system neuropeptides are altered in both anorexic and bulimic patients when compared to healthy controls, Kaye and colleagues have determined that the alterations are due to restriction and not causing restrictive behaviors. 8
Increased NPY levels in semi-starved animals and non-ED humans lead to lowered NEAT and increased food intake. For reasons not yet known, increased NPY in those with eating disorders leads to increased activity and decreased food intake.
In other words, NPY levels increase for all of us if we are semi-starved, but for those with a genetic predisposition for an eating disorder, the result is increased activity. In fact, the drive to be active decreases as an eating disordered individual re-feeds. 9
Both neuropeptide Y (NPY) 10 as well as dopamine-orexin 11 interactions have been implicated in the anomalous response of those with an eating disorder when the body needs more energy. There are even some intriguing new investigations in progress as to whether antibodies specific to these orexigenic (driving the need to eat) neuropeptides and neurotransmitters may play a causative role in that drive to keep moving and stop eating that marks an active eating disorder. 12Generally it looks as though those with active eating disorders produce orexigenic neuropeptides and neurotransmitters as do healthy controls, but the response is anorectic (eat less/move more).
Exercise Is Not As Great As You Tell Others It Is
I am usually told in no uncertain terms by many with eating disorders that they are not exercising to try to limit any weight gain. They assure me, and everyone else, that it has nothing to do with body image or food intake at all. They are merely exercising because they love it; it makes them feel strong and healthy; and it improves their mood.
Studies unfortunately suggest that you are desperately trying to believe your own advertising when you swear that the exercise you do is all good.
Turns out that those with eating disorders, through both self-reports and objectively assessed moderate-to-vigorous physical activity observation, are more likely to engage in exercise to regulate negative affect. Fitness and health are less important for ED patients than they are for non-ED controls. 13
In another study, best predictors for identifying exercisers who also had an eating disorder were if they agreed with the following statements:
being annoyed if exercise interrupted
others feel you exercise a lot
feeling bad if unable to exercise a certain amount
feeling that you have/had problems with exercise. 14
Ironically, high levels of depression were more likely with both AN and BN patients who exercised excessively, and levels of anxiety and somatization were particularly high but only with excessively exercising anorexics [E Peñas-Liedó et al., 2002]. The irony of those data is that exercise for non-eating disordered patients tends to ease depression and not exacerbate it.
A community-based study in Australia had the following outcome:
“Exercising to improve appearance or body tone, and feelings of guilt following the postponement of exercise, were the exercise variables most strongly associated with elevated levels of eating disorder psychopathology and, in turn, reduced quality of life.” 15
Yet another comparative evaluation of how eating disordered patients engage in exercise when compared to healthy controls:
“The anorexic group were significantly more hyperactive, exercised more frequently and engaged in a wider variety of exercise behaviours. They were also more likely to exercise in secret and were more compulsive about exercising. They displayed a ‘negative addiction’ to exercise, and gave control of their negative mood states as their major reason for undertaking it.” 16
It also appears that a significant increase in patients’ activity levels at least a year prior to diagnosis with an eating disorder suggests that exercise alone may play a triggering role in the onset of eating disorders. 17
That bears repeating because I have had many patients who have used the fact that their long-held active lifestyle predates their eating disorder and they use this fact as a reason to assume their exercise habits are not linked to the restrictive behaviors in their case.
I could go on, but the takeaway here is that while someone with an eating disorder is readily able to spout all the generally understood benefits of exercise, he or she is not experiencing any of those benefits.
I will address a bit later on in this post the ways in which you can help yourself stop being an apologist for exertion and start becoming an advocate for your own health and recovery.
Next we’ll revisit the logistics of why continuing exercise and pursuing an active lifestyle can sabotage your recovery effort…
Heart, Nerves and Safety
Those with eating disorders are most likely to die of either cardiac complication or suicide. 18,19
Exertion (exercise and/or moderate to intense activity) both during an active period of restriction and during the recovery effort, are dangerous and possibly life threatening. Also keep in mind that active restriction does include cycles of restriction/reactive eating, bulimia, orthorexia and not just anorexia.
The heart’s ability to function normally is hit hard on three fronts with restrictive behaviors: physical damage to the muscle, electrolytic imbalances and de-myelination of the nerves.
It is wise to be very, very conservative and assume that your medical care may or may not catch that you are in danger of having your heart fail during exertion.
I often use Harriet Brown’s article, She’s Not That Skinny. Is She? as a tragic but important example of how the risks can be overlooked even by eating disorder specialists.
Being of average or above-average weight does not automatically mean that the risks to your heart have resolved, especially if you are engaging in cycles of restriction/reactive eating, sub-clinical starvation, and/or purging, laxative and/or diuretic use.
Heart: The Muscle
When you restrict intake relative to your body’s actual energy needs, then it makes up the energy deficit by pilfering energy from everything in your body, not just your fat organ, but also muscles, bones, all other organs etc.
Our society believes that dieting is benign and is merely about trimming down ‘excess’ fat on our frames. The reality is that fat is not a storage compartment, but a critical hormone producing organ and the body also does not discriminate when it comes to trying to make up the energy deficits either.
In addition to the heart muscle being destroyed in the process of the body catabolizing energy from all the cells throughout the body, it is also possible that the volume of blood in your body is reduced such that the heart muscle has to work too hard to get the blood moving through the circulatory system.
Physical damage to your heart from an eating disorder will usually be identifiable by an experienced technician reviewing an echocardiogram.
Heart: The Electrolytes
Restriction, and in particular compensatory behaviors of purging, laxative and diuretic use all mess with the balance of electrolytes in your body.
Electrolytes support the electrical signal that causes the heart to contract strongly and rhythmically.
Electrolyte imbalances may or may not be apparent even in an electrocardiogram (ECG or EKG), as the fluctuations may not be present at the time you undergo the screening. The same holds true for blood screening as a way to isolate electrolyte imbalances as well. Somewhat more dependable is wearing a holter monitor and going about your usual daily life as the readout will capture any fleeting fluctuations that may occur at certain times and not at others.
Heart: The Arrhythmias
Arrhythmias can occur both as a result of heart muscle damage and/or electrolyte imbalances. The common arrhythmias that are present for those with eating disorders are tachycardia and bradycardia. The arrhythmias are the symptoms that you will notice and that will likely compel you to go investigate them further with your physician.
Bradycardia is a resting heart rate of below 60 beats per minute (bpm), although usually in practice physicians will use the marker of 55 bpm. There is a marked distinctive readout for bradycardia associated with eating disorders (on an ECG) that is distinct from a low resting heart rate for an energy-balanced non-ED athlete. 20,21 Unfortunately, because doctors themselves can sometimes be on the eating disorder spectrum or they are unfamiliar with the dangers of bradycardia when it is present due to restriction, they can brush aside a low resting heart rate on the assumption that you are a healthy athlete. 22,23,24
As an aside, there is very little good trial data on the topic of eating disorders in medical professionals. If you are interested, Eating Disorders in Doctors: Out of the Shadows, by Betsy Bates Freed (article from Clinical Psychiatry, Vol. 40, No. 12) and an interview with Dr. Jennifer Gaudiani are some recent discussions on eating disorders within the medical community that may mean we’ll see some clinical research sometime in the future.
However, if you fail to let your doctor know that you are not eating enough to support your energy expenditure, then he or she cannot automatically be expected to investigate troubling bradycardia, especially when you reaffirm that you are just a very active person.
Tachycardia is a sensation of your heart speeding up even when you are at rest. You are most likely to notice this if you are lying down or seated quietly. It can also feel as if your heart skipped a beat, or it seems irregular in some way.
Orthostatic hypotension (feeling faint when going from lying to sitting or sitting to standing) is also a circulatory issue that will present with eating disorders.
Any one of these symptoms has to be taken very seriously. Take it easy. Stop exercising. See your doctor.
Heart: The Nerves
While the arrhythmias will resolve fairly quickly in your recovery process, the nerves need more time and energy in. Of all the heart-related symptoms that put your life at risk, it is the nerves that require of you that you don’t just rush back to exercise the minute that your doctor gives you the all clear (see the article above by Harriet Brown).
The body is busily catabolizing all your cells when you create daily energy deficits and it strips the myelin from your nerves as part of this energy compensation. As I have often quoted before, researcher Janice Russell likens this process to throwing the antique furniture on the fire to keep the house warm.
Myelin is the fatty sheath that covers most nerves throughout your body and it is responsible for the speed and accuracy of electrical conductance along those nerves. And it is nerves that send the signal for the heart to regularly and predictably contract to keep your circulatory system in good working order.
So while your heart muscle may show no signs of damage, your electrolyte balance has been confirmed with blood work, and your ECG results have given you the “all clear”, the re-myelination of your nerves needs time, lots of energy intake (dietary fats in particular) and rest.
Safety
Because de-myelination occurs throughout the body, it also renders you more prone to injury: you don’t move as smoothly and are not as coordinated as you will be once you are in full remission and the nervous system has fully healed.
Furthermore, if you are dealing with functional hypothalamic amenorrhea (a lack of a menstrual cycle as a result of restriction and insufficient energy intake relative to expenditure), then exertion and exercise will also increase the risk of fracture.
Remember too that if you are on oral contraceptives (the pill) then you are not experiencing a menstrual cycle in a biological sense. Obviously do not come off of contraception if you are using it as birth control, but do keep in mind that you may be underweight for what is your body’s optimal weight set point and therefore you may develop osteoporosis (albeit at a slightly slower rate) while you continue to actively restrict and exercise. In other words you too might be prone to stress fractures.
And finally, being underweight is relative and not absolute. You could be BMI 27 and develop fatal heart fibrillation because you are underweight and physically damaged relative to what your body needs to be, to be optimally healthy.
You can also feel fairly confident that if it has crossed your mind that you are somehow not sick enough to need to rest and restore energy in your body then you already know that you are indeed “sick enough”. The term “sick enough” is only a concept that pops up for those with eating disorders.
Although I only have my own empirical evidence on that, maybe someday the “not sick enough” refrain will form the basis of a clinical survey that will unequivocally confirm that only those with eating disorders will identify with the phrase at all.
Right, a brief recap on why exertion is to be avoided during recovery from an eating disorder:
Anorexia athletica is merely another facet of an eating disorder and will grab you by the throat and prevent your remission if you maintain exercise while attempting to recover.
The NPY reception in your central nervous system robs you of a normal NEAT feedback loop such that the more you need energy in your body, the more you are compelled to expend it through heightened exertion. It means that exertion actually feeds the eating disorder.
All the fun, enjoyable, relaxing, mood-modulating and overall health benefits of exercise are not available to you. While you may tell people that you love it, the scientific data say the opposite. The dominant motivators for exertion for you are trying to feel better when you feel bad and feeling worse when you fail to do enough.
Exercise is dangerous to your health and life when you are in recovery.
Please remember you should never attempt a recovery effort without involving medical professionals.
Anorexia Athletica vs. Exercise Dependence
The scientific literature on exercise dependence, with or without the coexistence of an eating disorder, lacks solid consensus at this point. Often the delineation used is primary or secondary exercise dependence— secondary dependence referring to exercise being secondary to the eating disorder pathology.
In a study of 203 triathletes where all subjects completed both the Exercise Dependence Questionnaire the Eating Attitudes Test, 34% had eating disorders. 25 Exercise dependence among the same group of triathletes was 52%. Interestingly amateur athletes are more likely to have primary or secondary exercise dependence when compared to their professional counterparts. 26 However, it could be that professionals are unable to maintain professional status when exercise dependence is present, as injury and ill health may remove them from competition far more quickly.
There is much fussing about in the literature using the DSM classifications for eating disorders while failing to include comparative healthy controls when attempting to identify prevalence of hyperactivity and excessive exercise in one facet of an eating disorder as opposed to another (i.e. AN vs. BN and their various purging/non-purging subtypes).
The prevalence, all facets and subtypes included, ranges between 54-84%. 27 Of the few studies that exist where eating disorders are removed from the equation, it appears that primary exercise dependence may hit rates of 17% or less.
One study of adult female exercisers (n=43) suggested that, in the absence of an eating disorder, primary exercise dependence lacked personality characteristics or levels of psychological distress that distinguished it at all from healthy controls. Although, the researchers did allow for the fact that menstrual abnormalities were present for primary exercise dependent subjects, which would warrant attention [D Bamber et al., 1999]. 28,29,30
Bamber’s study in 2003 (n=56 female) did not isolate a single case of primary exercise dependence, as all had co-occurring eating disorder symptoms. In 2000, Bamber and her colleagues also identified a priori female exercisers who were diagnosed with primary exercise dependence, secondary exercise dependence, eating disorder without exercise dependence and a healthy control. They were interviewed in depth and their taped interviews were subsequently analyzed from a social constructionist perspective. Those who had been identified as primary exercise dependent either showed no evidence of exercise dependence at all, and if they did display facets of exercise dependence it was only in the presence of eating disorder traits as well. 31
So although a bit of arm waving is required right now to make sense of this, if you find postponing exercise generates distress and if you are driven to exercise to try to rectify food intake or ease anxiety, then your exercise behaviors are the result of an eating disorder.
Upping The Intake Doesn’t Work
Many ask me if they cannot just increase their food intake to somehow make up the difference of the expenditure associated with their exercise.
Our bodies do not work mechanistically. A better analogy is that a body has adaptive and quite sophisticated triage rules. Triage is a system used in emergency environments to try to maximize the number of survivors. The body also tries to maximize its ability to survive by prioritizing biological functions in times of energy depletion and deficit.
If an energy deficit exists in the body thanks to a period of restrictive eating or under eating relative to excessive energy expenditure, then replenishing the energy of daily exertion on top of the basal metabolic requirements (which are suppressed*) will take precedence over replenishing the overall energy deficit throughout all the cells in your body.
*Metabolic rate is suppressed when the body does not have enough energy (food) coming in to support all the biological functions in your body. The metabolism is not broken and is in fact performing its life-saving ability until such time as you are energy balanced when you reach remission.
Basically your body is saying to itself: “Well if she’s going to drag me out for a run every morning then there’s no way I’m going to be trying to figure out how to reverse bone mineral density loss, or repair the heart muscle and I’ll keep the biological functions suppressed so that there’s enough energy to handle the godforsaken run along with staying alive until tomorrow.”
I have mentioned in other posts how glucocorticoids (cortisol) impact how your body uses the energy you take in. Stress varies both the levels and pulse rates of glucocorticoids such that your body will preferentially move energy into storage while continuing to suppress biological functions. Exertion and activity are huge stressors for an energy-depleted body.
Even if you could eat enough to truly support regular exercise, on top of the energy needed to stay alive and the energy needed to restore weight and repair damage, the body is stressed by the exertion to the point where you are going to tread water and fail to reach a full remission.
Now let’s move on to the good news. Replacing exertion and exercise in your life while you are in active recovery will greatly improve the chance of a permanent and deeply fulfilling remission.
Exercise Is Not the Be All and End All Anyhow
Living a healthy, fulfilling, generally disease-free and long life is not realized through exercise.
The problem with all the epidemiological data that suggest the more vigorously you exercise the longer you live, is they fail to integrate all the confounding factors that are involved. An epidemiological study simply follows a very large number of people over decades and then uses fancy pants statistical manipulations to attempt to extract correlates from extemporaneous life influences.
I have covered off some of the confusions that result in arbitrarily pulling out two correlates while overlooking other factors in several historical threads on the forums.
Exercise is specifically a forced, conscious and repetitive set of activities engaged in primarily for fitness or strength outcomes. Vigorous exercise correlates well with lower incidence of cardiac disease and death. However vigorous exercise is also correlated with lower cognitive performance later in life. 32 Exercise positively correlates with a lower incidence of bowel cancer and yet also correlates equally well with gut ischemia causing cramping, bloating, nausea, and bloody diarrhea in athletes. 33
And for all those who believe that strength training and toning is perhaps a reasonable choice in recovery because less demand is placed on the heart, that kind of training may be inversely correlated with longevity (meaning more muscle building equals shorter lifespan). 34
There is a complex interplay of many facets that will provide people with long and healthy lives: community, strong friendships, stability, resilience, a nice smattering of luck, some genetic input, most things within your locus of control throughout your life (higher socioeconomic status), regular activity (not exercise sessions), regular routine, and undying interest in learning and doing, and some kind of sense of purpose.
And that’s good news for those of you who now have to replace exercise and exertion in your life with other fulfilling and life affirming activities.
Before we get to that I will actually copy a couple of responses I made on forum threads with regards to extracting correlates such that causation is assumed, but is not confirmed. The first pertains to the French Paradox and the second to the longevity of Okinawans ostensibly being ascribed to hara hachi bu (eating to 80% fullness).
The French Paradox
The root of the French paradox is supposedly that despite the fact the traditional French diet is very high in saturated fats, the rates of coronary heart disease (CHD) (and accompanying death rates from CHD) are lower than in other European countries or the US.
The rates of smoking in France are not much different from those in the States (35% to 25% respectively) and for women it is exactly the same in both countries.
"...in France, coronary causes can be considered as noninitial causes of death in a large proportion of cases, which is at variance with reporting habits in other countries. However that may be, strictly defined coronary death rates in French national statistics, both in the past and nowadays, should be considered as negatively biased estimates at the population level and cannot be used validly in ecological correlation studies." 35
And therein lies some of the concern regarding whether a paradox does indeed exist— if CHD death rates are underreported in France then "poof!" goes the paradox.
"…we can now say that CHD rates are not so low in France, animal fat intake not so high, and the diet-heart concept not so unique that the existence of a “French paradox” may be sustained any longer, except as cultural fantasy or a marketing ploy." 36
The French diet (which by the way is disappearing in the fast food/less sleep modern world in which we are all homogenized) is not just about food, or wine, or smoking. It is about human connection, about tradition, about food (not nutrients or nutraceuticals) and about a way of life.
Human beings are healthier and live longer if they concern themselves with their kin, their friends, their community and the enjoyment of food within those contexts.
Okinawan Hara Hachi Bu
Okinawan women are disproportionately long-lived and the population has a higher-than-average number of centenarians. Okinawa is the most southerly prefecture in Japan. The philosophy of eating to 80% full (hara hachi bu) is touted as being responsible for the longevity seen in this population…
“In fact it is not 20% fewer calories. It is estimated to be between 10-15% lower than Americans however there is a big, big catch to this: the data are provided by self-estimated reports that are then rolled into the Japanese Public Health Center-based prospective study of which there is Cohort I and II data available.
In fact it is called the self-administered food frequency questionnaire.
Now, this is where we get into challenges when it comes to ways of life. A very interesting multi-center study was conducted on the prevalence of extremely restricted diets for pregnant women in South and Southeast Asian communities. The study set out to actually confirm whether such restrictions were occurring and whether it resulted in unhealthy outcomes for the fetus and newborn. Rather than relying on self-reports, the researchers monitored and weighed food. It turned out that none of the prescriptive restrictions (to which the women were supposed to adhere for cultural reasons), were closely held by the pregnant women at all. In fact, they ate as they always had. Keep in mind that the sociocultural concepts were that to eat these foods would endanger the child.
What the researchers were able to determine is that the concept of severe restriction (to support the developing fetus according to cultural dictates) also allowed for the pregnant woman to be removed from all obligations of physical labor that supported the larger family and community. They were essentially on complete rest. This to some extent minimized their energy requirements, but it also allowed for them to be excused precisely because they were supposedly not eating many forbidden foods (although they were eating them all as they normally would).
In another Indian caste where the women are the sole income earners doing incredibly physically demanding road work, the women all eat their lunches at cafes, spending about half of their income on these lunches. They could return home to eat and likely save significant money, but to do so would likely compromise their ability to take in sufficient energy to support their labor-intensive work because at home it is their obligation to place husband and family first for nutritional needs.
These complex sociocultural interplays of how women get sufficient nutrients despite the outward appearance that they do not, is especially common in rural communities and poor communities.
Interestingly in the Okinawan self-reports, it is the younger individuals who report calorie restriction of 10-15% below what their requirements would be. In a society where elders are revered and yet the back-breaking heavy labor (namely fishing) is managed by the younger individuals in the community, we cannot definitively confirm that the dietary restriction is in fact in place.
In other words, the need to appear to be deferential to cultural requirements is like a communal lie that everyone is in on to allow for nutritional requirements to be met but not in such a way that it would blatantly seem to undermine other values held dear within the culture.
There is no question that women in Okinawa disproportionately live to a great age. In Sardinia Italy, it is the men who disproportionately live to a great age. There are several "bluezones" (you can check out Blue Zones Cities) that have been identified where communities appear to have a higher proportion of their population living to their 100th decade.
The problem with these epidemiological studies is that there is no way to identify correlations from causes. These communities have many facets that ensure a lifetime of activity, an integral and revered role within the culture well into old age, close familial and social interactions that are solid throughout life, diets that are distinct based on the region but generally high in local, nutrient-rich vegetables and plants, and some likely relevant genetic mutations as well.
So far, calorie restriction has shown to have no value in humans and this may have something to do with our size, relatively slower metabolism and existing length of life. CR has real positive impact for longevity for mice and rats but has not been transferrable as a technique for extending life in humans.
So essentially, there is no confirmation that Okinawans do in fact eat as per their guidelines of Hara Hachi Bu, however it may be an inherent philosophy that ties the community together in a way that has tremendous health benefits even though there may not be any calorie restriction actually happening at all.
Replace and Distract
I received a Lego® kit as a gift just recently. It's a small one found here on the Lego Site.
I know. It’s pretty exciting to have waded through thousands of words in this post to get to a high point of seeing proof that my Lego skill equals that of most six year olds.
There’s a point to this side story actually. When my son was young I used to help him assemble various Lego kits but of course my role was relegated to pointing out the piece in question and sitting on my hands to resist the urge to snatch it away with the eager/have-no-patience cry of “Here, let me do it!”
So this one wasmy first start-to-finish Lego success. But the best part was how much fun I had putting the thing together. Really.
There is some evidence that the reduced use of our hands in modern life has had a hand (pun intended) in increased rates of mental illness such as anxiety and major depressive disorders. Kelly Lambert addresses the research pertaining to this theory in her book Lifting Depression: A Neuroscientist’s Hands-On Approach to Activating Your Brain’s Healing Power. I have not read this book, and the reviews suggest it may have a bit of a pop-neurology feel to it, but the references attached to her work will likely stand up under scrutiny.
Because the use of arts and crafts in occupational therapy has gone in phases and is currently half-embraced and half-shunned, it has never received thorough scientific assessment. Sinikka Pollanen synthesizes what data exist in her published report: Craft as context in therapeutic change. Canadian Karen Ribeiro previously covered off a similar review in Occupation-as-means to mental health: A review of the literature, and a call for research.
The best way to describe occupational therapy is the practice of applying daily life activities in a guided way that supports healing and a return to full participation in interdependent (communal) and independent (self-directed) living.
Knit, sew, collage, paper-toll, scrapbook, paint, sculpt, photograph, draw, sketch, embroider, quilt, decorate, crochet, weave, spin, thread, glue, paste, embellish, carve, bind, emboss, fold, marble, mâché, cobble, felt, concoct…build things with Lego®!
Arts and crafts will successfully replace exercise sessions and also distract you from the pent up anxiety that not exercising will generate in the initial phases of recovery. It also will allow you to modulate negative affect (bad mood) upwards and broaden a sense of yourself and an innate sense of accomplishment.
Stopping exercise sessions with nothing but yourself and your thoughts to keep you company will inevitably make you want to crawl out of your skin in short order. Researchers in the exercise dependence field recommend replacing the exertion with other non-exertion-based activities and distracting yourself from the times in the day when you are likely to want to indulge in exertion-based activities. 37
The first thing I always suggest as a great replacement is sleep. That would of course be second in line to the best of all replacements: food! If you happen to be an early morning exerciser, then simply sleep in.
For some, the usual morning wakeup is needed and provides some grounding. In that case, still set the alarm, but do 30 minutes of slow yoga stretching, or mindfulness exercises, breathing exercises, or just sitting quietly in the kitchen with a nice mug of something hot (and ideally full of calories too).
Distraction can help alleviate the negative mood, irritability and anxiety that you feel because you are not exercising. Have family breakfasts. Set up a mid-morning get together with a friend for a coffee and a muffin. Have a strategy for busyness at the times when you are most likely to want to exercise.
Enroll in activities (non-exertion) that you may have had some interest in in the past. Crafts, languages, learning new software packages: flip through what's on offer at a local community center to get inspired.
Getting out in the nature is mentally valuable. In fact there is now a whole sub-section of study on green activity. There are three kinds of green activities: appreciative, consumptive and motorized. Not surprisingly appreciative green activities improve environmental behaviors. 38
Access to a garden or a green area a short distance from home is associated with less stress. 39 All green spaces improve mood, with the greatest self-esteem improvements realized for those who are mentally ill. Water in the green space generated greater positive effects in both self-esteem and improved mood, and mood improved within 5 minutes of being outside. 40
My favorite study on this topic is Elizabeth Nisbet and John Zelenski’s ingenious trial of getting subjects to forecast the benefits they might experience by crossing the campus via the outdoor pathways, or an indoor tunnel-based path to get to classes:
“…we found that although outdoor walks in nearby nature made participants much happier than indoor walks did, participants made affective forecasting errors, such that they systematically underestimated nature’s hedonic benefit.” 41
It is not about exercise and it’s not even about sunlight helping you to manufacture vitamin D. In fact the positive effect sunlight has on mood has been shown to be regulated through the eye. 42 Just get outside without breaking a sweat.
How slowly can you go around the block? Make that your task. See if you can get it to 15-20 minutes for one block. Take in absolutely everything in your surroundings. Note every change. Bring a camera and take a picture of the same view each day so you can then compare after your walk whether you actually missed a detail from one day to the next or not.
Consider gardening on a patio or deck— allowing you to be outside and connected to some of the benefits of gardening without the more strenuous aspects of hauling mounds of dirt etc. Set up a bird feeder. Sit out and admire your handiwork growing in the pots and watch the birds.
For those who have followed the Homeodynamic Recovery Method Guidelines to a full remission, no one has returned to rigorous, planned and repetitive exercise and most have expressed surprise that they feel no drive to do so. While a broad array of rewarding activities will be a regular part of your life in remission, exercise will cease to have any hold on you.
If one kind of replacement strategy doesn't work, then try another. Basically enter the process with curiosity about what things you could include in your life to broaden your horizons, rather than entering the process with trepidation assuming you will simply be pacing the floors with nothing better to do.
Identity is not what you do, or don’t do. It is who you are. Find out who you are through the process of recovery.
1. Levine, James A. "Non-exercise activity thermogenesis (NEAT)." Nutrition reviews 62, no. suppl 2 (2004): S82-S97.
2. Leyton, G. B. "Effects of slow starvation." The Lancet 248, no. 6412 (1946): 73-79.
3 Keys, Ancel, Josef Brožek, Austin Henschel, Olaf Mickelsen, and Henry Longstreet Taylor. "The biology of human starvation.(2 vols)." (1950).
4. Levine, James A., Norman L. Eberhardt, and Michael D. Jensen. "Role of nonexercise activity thermogenesis in resistance to fat gain in humans." Science 283, no. 5399 (1999): 212-214.
5. Keys, Ancel, Josef Brožek, Austin Henschel, Olaf Mickelsen, and Henry Longstreet Taylor. "The biology of human starvation.(2 vols)." (1950).
6. Pasquet, Patrick, and Marian Apfelbaum. "Recovery of initial body weight and composition after long-term massive overfeeding in men." The American journal of clinical nutrition 60, no. 6 (1994): 861-863.
7. Achterberg, E. J. M. "The Y of hYperactivitY in Anorexia Nervosa: Role of neuropeptide Y in hyperactivity associated with Anorexia Nervosa." (2009).
8. Bailer, Ursula F., and Walter H. Kaye. "A review of neuropeptide and neuroendocrine dysregulation in anorexia and bulimia nervosa." Current Drug Targets-CNS & Neurological Disorders 2, no. 1 (2003): 53-59.
9. ibid.
10. A. Inui, “Eating behavior in anorexia nervosa—an excess of both orexigenic and anorexigenic signalling?” Molecular Psychiatry 6, no. 6 (2001): 620-624.
11. Anton J. W. Scheurink, Gretha J. Boersma, Ricard Nergårdh, and Per Södersten, “Neurobiology of hyperactivity and reward: Agreeable restlessness in Anorexia Nervosa,” Physiology & Behavior 100, no. 5 (2010): 490-495.
12. Sergueï O. Fetissov, Maria Hamze Sinno, Quentin Coquerel, Jean Claude Do Rego, Moïse Coëffier, Danièle Gilbert, Tomas Hökfelt, and Pierre Déchelotte, “Emerging role of autoantibodies against appetite-regulating neuropeptides in eating disorders,” Nutrition 24, no. 9 (2008): 854-859.
13. Martinsen, Marianne, Solfrid Bratland-Sanda, Audun Kristian Eriksson, and Jorunn Sundgot-Borgen. "Dieting to win or to be thin? A study of dieting and disordered eating among adolescent elite athletes and non-athlete controls." British Journal of Sports Medicine 44, no. 1 (2010): 70-76.
14. Boyd, Catherine, Suzanne Abraham, and Georgina Luscombe. "Exercise behaviours and feelings in eating disorder and non‐eating disorder groups." European Eating Disorders Review 15, no. 2 (2007): 112-118.
15. Mond, Jonathan Matthew, Phillipa J. Hay, Bryan Rodgers, Cathy Owen, and Pierre JV Beumont. "Relationships between exercise behaviour, eating‐disordered behaviour and quality of life in a community sample of women: when is exercise ‘excessive’?." European Eating Disorders Review 12, no. 4 (2004): 265-272.
16. Long, Clive G., Jenny Smith, Marie Midgley, and Tony Cassidy. "Over-exercising in anorexic and normal samples: Behaviour and attitudes." Journal of Mental Health 2, no. 4 (1993): 321-327.
17. Davis, Caroline, Elizabeth Blackmore, Debra K. Katzman, and John Fox. "Female adolescents with anorexia nervosa and their parents: a case-control study of exercise attitudes and behaviours." Psychological medicine 35, no. 03 (2005): 377-386.
18. Misra, Madhusmita, Avichal Aggarwal, Karen K. Miller, Cecilia Almazan, Megan Worley, Leslie A. Soyka, David B. Herzog, and Anne Klibanski. "Effects of anorexia nervosa on clinical, hematologic, biochemical, and bone density parameters in community-dwelling adolescent girls." Pediatrics 114, no. 6 (2004): 1574-1583.
19. Neumärker, Klaus‐Jürgen. "Mortality and sudden death in anorexia nervosa." International Journal of Eating Disorders 21, no. 3 (1997): 205-212.
20. Swenne, I., and P. T. Larsson. "Heart risk associated with weight loss in anorexia nervosa and eating disorders: risk factors for QTc interval prolongation and dispersion." Acta Paediatrica 88, no. 3 (1999): 304-309.
21. Krantz, Mori J., William T. Donahoo, Edward L. Melanson, and Philip S. Mehler. "QT interval dispersion and resting metabolic rate in chronic anorexia nervosa." International Journal of Eating Disorders 37, no. 2 (2005): 166-170.
22. http://www.scielo.br/pdf/rbem/v37n1/03.pdf
23. https://bmcresnotes.biomedcentral.com/articles/10.1186/1756-0500-5-84
24. http://www.omicsonline.org/open-access/body-image-and-eating-behavior-among-medical-students-eating-disorders-among-medical-students-2161-1165-1000256.php?aid=78851
25. Blaydon, Michelle J., and Koenraad J. Lindner. "Eating disorders and exercise dependence in triathletes." Eating disorders 10, no. 1 (2002): 49-60.
26. ibid.
27. Davis, Caroline, S. H. Kennedy, E. Ravelski, and M. Dionne. "The role of physical activity in the development and maintenance of eating disorders." Psychological medicine 24, no. 04 (1994): 957-967.
28. Veale, David. "Does primary exercise dependence really exist." Exercise addiction: Motivation for participation in sport and exercise (1995): 1-5.
29. Bamber, D. J., Ian M. Cockerill, Sue Rodgers, and D. Carroll. "Diagnostic criteria for exercise dependence in women." British Journal of Sports Medicine 37, no. 5 (2003): 393-400.
30. Allegre, Benjamin, Marc Souville, Pierre Therme, and Mark Griffiths. "Definitions and measures of exercise dependence." Addiction Research & Theory 14, no. 6 (2006): 631-646.
31. Bamber, Diane, Ian M. Cockerill, and Douglas Carroll. "The pathological status of exercise dependence." British journal of sports medicine 34, no. 2 (2000): 125-132.
32. Tierney, Mary C., Rahim Moineddin, Angela Morra, Judith Manson, and Jennifer Blake. "Intensity of recreational physical activity throughout life and later life cognitive functioning in women." Journal of Alzheimer's Disease 22, no. 4 (2010): 1331-1338.
33. De Oliveira, Erick Prado, and Roberto Carlos Burini. "The impact of physical exercise on the gastrointestinal tract." Current Opinion in Clinical Nutrition & Metabolic Care 12, no. 5 (2009): 533-538.
34. Fry, A. C., and C. A. Lohnes. "Acute testosterone and cortisol responses to high power resistance exercise." Human physiology 36, no. 4 (2010): 457-461.
35. http://www.dialogues-cvm.com/document/dcvm49.pdf
36. ibid.
37. Kerr, John H., Koenraad J. Lindner, and Michelle Blaydon. Exercise dependence. Routledge, 2007.
38. Tarrant, Michael A., and Gary T. Green. "Outdoor recreation and the predictive validity of environmental attitudes." Leisure Sciences 21, no. 1 (1999): 17-30.
39. Nielsen, Thomas Sick, and Karsten Bruun Hansen. "Do green areas affect health? Results from a Danish survey on the use of green areas and health indicators." Health & place 13, no. 4 (2007): 839-850.
40. Barton, Jo, and Jules Pretty. "What is the best dose of nature and green exercise for improving mental health? A multi-study analysis." Environmental science & technology 44, no. 10 (2010): 3947-3955.
41. Nisbet, Elizabeth K., and John M. Zelenski. "Underestimating nearby nature affective forecasting errors obscure the happy path to sustainability." Psychological science 22, no. 9 (2011): 1101-1106.
42. Rosen, Leora N., and Norman E. Rosenthal. "Seasonal variations in mood and behavior in the general population: a factor-analytic approach." Psychiatry research 38, no. 3 (1991): 271-283.