2016 Edited to Add: When I first began writing here I generated a searchable database for references and I have since done away with that option. This entire series remains to be edited to include the full references within each piece. As time allows, this series will be edited to include complete references at the end of each part in the series.
We have now come to the final entry of this nine part series on fat. While it is not possible to undo such a culturally dominant philosophy as the abhorrence of fat in our society with a few blog entries, I hope that for those who have persevered reading the series that it has challenged you to re-evaluate all the assumptions upon which your own fear and contempt of fatness may be based.
In this final section we will visit all the damage that trying to lose weight has wrought upon our society in recent decades.
When Pigs Fly
“…contrary to frequent medical insistence on the desirability of dieting, there are many undesirable facets, for there is an almost inevitable weight gain after dieting so that ‘the major treatment for obesity may also be the major cause of obesity (emphasis in original).” [S. Wooley, O. Wooley, 2004]
I will get into the medical dangers of weight loss after discussing the largest elephant in the living room, namely that dieting does not work and is unsustainable.
Restrictive caloric intake has a 95-97% failure rate for maintaining permanent weight loss beyond 5 years [D.M. Garner, S.C. Wooley, 1991; G.K. Goodrick, J.P. Foreyt, 1991]. Obviously these data do not include those who develop eating disorders. With that kind of spectacular failure rate, what on earth possesses not just the population at large, but in particular the medical and health communities to persist with weight loss as a possible solution for any health issue that may arise?
Were weight loss any other kind of intervention meant to improve health outcomes, then success rates of 3-5% would be considered coincidental and therefore statistically insignificant. 3-5% isn’t even large enough to be considered some kind of placebo effect.
Proof positive that you cannot take the human out of human beings no matter how much education you provide or how much evidence-based science you drill into them.
What follows is a laundry list of medical risks associated with losing weight and also being at a low weight. But before we get into those details, let’s consider first the sociocultural reasons why we may continue to think that weight loss is viable and safe despite all the evidence to the contrary.
Metaphors as Masochism
(technically the title is a simile)
In the previous section the image is of a hot air balloon of a pig with wings, obviously meant to conjure up the saying “When pigs fly.” That’s a metaphor for the unlikelihood of something happening. Two peas in a pod? A metaphor for two people who are very close.
We utter on average six metaphors per minute [J. Geary, 2009]. Metaphors pepper our speech because they are an efficient way to stuff a lot more meaning into a single phrase. Aristotle referred to metaphor as “giving the thing a name that belongs to something else.” I won’t get into the distinction of categorical and comparison forms of metaphor or extended forms of metaphor such as allegories or parables. Rather, I would like to look at linguistic and non-linguistic metaphor as it relates to our bodies.
Turns out we are phenomenally wired for metaphors. Oops, that’s another metaphor – we aren’t really “wired” as living creatures
We often use our bodies as the basis of metaphors to explain thought. The mind uses the body to make sense of abstract concepts.
“Why do we look up to those we respect, stoop to the level of those we disdain and think warmly about those we love? Why do we hide dirty secrets or wash our hands of worries? Why do we ponder weighty subjects and feel a load lift after we have made a decision? Why do we look back on the past and forward to the future?” [S. Carpenter, Wired Magazine, Jan. 2011]
But what of the metaphors (or similes) the mind uses to make sense of its own body?
“I’m slow as molasses”, “He’s dog tired” or “She’s bouncing off the walls” would all be examples where physical states are described using other physical objects in our world: molasses, how a dog sleeps and bouncing off walls as a ball might do.
We use a tremendous amount of metaphor when we are attempting to explain symptoms in a health consultation. We are trying to explain how something is wrong with our bodies as we understand them.
The pain is stabbing, the head is foggy, the insides are squeezed, the throat is burning…are just some examples of common metaphors in health consultations.
Here are common metaphors and I won’t need to tell you to what they pertain:
Slug, pig, porker, whale, hippo, walrus and cow.
“Many [of my generation] still believe it is possible to “just turn off the television.” They are scornful, disdainful, sure of their own immunity to the world I talk about. No one really believes the ads, do they? Don’t we all know these are just images, designed to sell products? Scholars in the audience may trot out theory about cultural resistance and “agency.” Men may insist that they love fleshy women. [Then] I simply catch the eye of a twenty-year-old in the audience. They know. They understand that you can be as cynical as you want to be about the ads—and many of them are—and still feel powerless to resist their messages.”
[Susan Bordo, Unbearable weight: feminism, Western culture, and the body, University of California Press, 2003]
Metaphors of course are not merely language-based. Consider the following image:
Most of you will instantly be able to classify this as “heroin chic”. I can think of half a dozen other equally subversive metaphors: rocker chic, schoolgirl chic, biker chic, baby girl chic, slutty chic (just add any questionable word to “chic”).
Superficially these variations of ‘chic’ are all style metaphors—the idea that we express our ‘individuality’ visually in a conformist and tribal way to signal to others as much as we can about our affiliations, our identity, our likes and dislikes, and our relative value when measured against others.
What does heroin chic say about someone who adopts the imagery? What style metaphor could a young woman adopt today that does not embed some variation on the themes of vulnerability,
hyper-sexualization, and pre-pubescent immortality? Or for that matter young men?
The issue with visual metaphors is that they communicate much more than what our cognitive minds will consciously process. The old adage “A picture is worth a thousand words” should really be “A single picture cannot be replaced by even an infinite number of words”
Both men and women in almost all cultures today are encouraged to see the body as a machine that needs constant intervention to run smoothly. For many, the body is also a measuring stick and its physical manifestation is how we measure our worth and value. The body must be worked on, otherwise it will simply veer towards overblown, unmanageable, deteriorating and failing states.
These are such powerful and pervasive metaphors that shape our relationship with our bodies that we don’t even realize that new metaphors might even be feasible, let alone desirable.
What does any of this have to do with weight loss? Everything. Despite the absolute falseness of the metaphor that our bodies are machines that must be governed, controlled and manipulated to function, we still want to believe that fairy-tale. We believe on that horrible, deep, irretrievable and beyond-words metaphorical level. To not do so means we are fat, lazy, stupid and sick hippos, cows, pigs, porkers, whales, walruses or slugs.
Increased Risk of Illness and Death
There are two aspects to the increased risk of illness and death when it comes to weight loss: 1) losing the weight and 2) being at a low BMI.
In analyzing 3,152 participants (BMI ≥25) from the Finnish Twin Study (1974) using in depth surveys applied in 1975 and 1981, researchers were able to unequivocally show that intentional weight loss during that six year period resulted in increased long-term mortality compared to those intending to lose weight and not doing so, and also compared to those with unintentional weight loss [T. Sørensen et al., 2005].
They also found that excess mortality was higher for those with intentional weight loss who reported using dieting as their method of weight reduction as opposed to those reporting the use of exercise. [ibid.] Unlike many other studies of this ilk, Sørensen and colleagues ensured that the intention to lose weight was identified prior to weight loss actually occurring whereas most other studies have relied on usually inaccurate post-event self-reports.
The risks for surgical site infections are significantly correlated with weight loss in the six months prior to surgery [D.L. Malone et al., 2002]. And surgical site infections are a predictor of increased mortality independent of other risk predictors.
In a study to determine the impacts of lifetime weight gain on the presence of breast cancer, researchers assessed 1,065 breast cancer patients, 964 surgical controls and 981 neighborhood controls at age 18, most of adult life and recently. Patients with breast cancer at age 60+ had gained more weight throughout adult life than healthy controls, however patients with premenopausal breast cancer had gained less weight than healthy controls through adult life [F. Lubin et al., 1985]. Although survival rates vary, generally younger premenopausal breast cancer patients have lower survival rates [H-O. Adami et al., 1986].
In a large study of Swedish men who lost weight, particularly those who were overweight or obese, their risk of non-cancer mortality increased during the 16-year follow-up period [P.M. Nilsson et al., 2002].
Women who had lost more than 8.55% of their maximum lifetime weight to become lean had increased mortality rates when compared to lifetime weight stable lean women [C. Rumpel et al., 2010].
Older women [65+] who lose weight, are underweight, or weight-cycle are all at increased risk for death [M.W. Reynolds et al., 1999].
In both men and women who had lost more than 15% of maximum body weight there was an increased risk of death from all causes, regardless initial BMI status [D.D. Ingram, M.E. Mussolino, 2010].
“Weight fluctuation is associated with a higher risk of all-cause and cardiovascular disease mortality in the US population, even after adjustment for pre-existing disease, initial BMI and the exclusion of those in poor health or incapacitated.” [V.A. Diaz et al., 2005]
Low Body Mass Index
Being underweight involves increased length of stay in hospital intensive care units and impaired functional status upon discharge when compared with average, overweight and obese patients [A. Tremblay et al., 2003].
Those with rheumatoid arthritis are far more likely to experience cardiovascular death with BMI <20, after controlling for age, sex, cardiac history, diabetes, smoking status, hypertension and malignancies [H.M. Kremers et al., 2004].
Being in the lower 50th percentile of weight was an independent and strong predictor of death within 12 months from the outset of the study period for those undergoing maintenance hemodialysis [J. D. Kopple et al., 1999].
One of several variables impacting mortality following outpatient pulmonary rehabilitation was low BMI [D.A. Gerardi et al., 1996]. The most significant variable for mortality in this case was slow timed walking distance following outpatient pulmonary rehabilitation.
Subarachnoid hemorrhage (a risk factor for those with atherosclerotic diseases) is positively associated with smoking and hypertension and body mass index was inversely associated – meaning leanness increased the risk [P. Knekt et al., 2004].
Low BMI is a significant independent predictor of reduced survival in both young and old hospitalized patients [F. Landi et al., 2000].
Thrown in for good measure, the National Health and Nutritional Examination Survey (NHANES I) show that diets that omitted several food groups were associated with increased mortality rates [A. Kant et al., 1993].
Patients undergoing coronary bypass surgery are at higher risk of both complications and death when they are BMI<20 [B. Reeves et al., 2003].
For Japanese men and women low BMI (<18.5) was associated with both total stroke and intraparenchymal hemorrhage in those with cardiovascular disease [R. Cui et al., 2005].
There are higher mortality rates for patients with chronic heart failure in both those with average or low BMI levels [A. Oreopoulos et al., 2008].
Complications and death associated with percutaneous coronary intervention are higher for patients at or less than BMI 25 and also for those higher than BMI 35 [S. Ellis et al., 1996].
Mirror, Mirror: Dangers of Weight Cycling
And if weight loss and low weights weren’t bad enough, then for goodness’ sake don’t yo-yo diet (weight cycling).
Interestingly, yo-yo dieting or weight cycling is not a marker of the eating disorder spectrum. Despite the fact that most on the eating disorder spectrum initially lose a lot of weight and those who recover regain the weight, this is not actually weight cycling.
Weight cycling disproportionately happens to those who are naturally ‘overweight’ or ‘obese’ and not on the eating disorder spectrum.
Basically those on the eating disorder spectrum who do not recover fall into two broad categories: those who maintain starvation or energy deficit status and those who attempt to maintain energy deficit status but nonetheless experience reactive eating that usually returns them to average BMI ranges.
There is no voluntary respite period in their efforts to continue to restrict for anorexics, bulimics, orthorexics and those with anorexia athletica. They continue unceasingly to either maintain a lower-than-optimal weight, or they are never-endingly trying to return to a lower-than-optimal weight. Generally there is much confusion between what constitutes weight cycling and reactive eating.
Weight cycling involves purely sociocultural pressures on those who are not on the eating disorder spectrum. In other words there is no underlying biological pre-determination to pursue weight loss for weight-cyclers.
Reactive eating occurs for both weight cyclers and those on the eating disorder spectrum who do not maintain constant energy deficits. Confusing right?
Distinguishing Weight Cycling and Reactive Eating
Let’s take two women: one who is on the eating disorder spectrum and the other who is not. For argument’s sake we’ll say they are both optimally meant to be BMI 26 (‘overweight’).
Both hate their bodies (big surprise) and decide to restrict calories and increase exercise to lose a lot of weight.
Six months later, after restricting calories to an unwavering 1200 calories per day and exercising faithfully six days a week for 90 minutes, they have both lost 35 pounds and are BMI 20.
Let’s assume that the one with an active eating disorder really wants to keep going, but she finds that she is starting to “binge” (reactively eating to make up energy deficits) from time to time. In response, she ups her exercise to 7 days a week and increases both intensity and duration. To no avail, her weight starts to creep back up because she finds she succumbs to evening sessions of eating a day’s worth of calories and then some.
She has now moved from active anorexia to active restriction/reactive eating cycles combined with anorexia athletica. Soon she becomes bulimic in her desperation to try to drop the weight back to BMI 20 and begins abusing laxatives, diuretics and starts purging.
Meanwhile our non-eating disorder subject feels outwardly very good about her new socially acceptable weight and this has been reinforced by countless compliments from family and friends. Nonetheless, her life is busy and she decides that she now has to adjust to that ephemeral concept of “maintenance” intake. She has really missed enjoying her favorite foods. She admits that she is hungry a lot. She certainly doesn’t want to lose more.
She starts to reintegrate normal social functions and interactions. Having fun with the girls out once again includes actually eating what everyone else is eating, rather than rigidly sticking to a salad with no dressing.
Soon she finds the weight is creeping back up. She continues with a reasonable exercise schedule but does not up the intensity or duration in response to a few extra pounds.
Within six months beyond hitting BMI 20, our non-eating disorder subject is back to BMI 25. She is still out walking with friends on weekends and juggling her usually busy schedule but she now feels disappointed. She feels she is a failure for having ‘allowed’ her weight to slide back up to almost its original pre-diet level but she plans to start a new diet soon.
Both women in this saga experienced a biological need to eat more because their bodies were working to return to their optimal weight set points (nothing anyone can do about that). That drive is called reactive eating. They are reacting to insufficient energy in, for their body’s needs.
However, the one with an eating disorder is continuing to try to restrict calories and as such the reactive eating is more intense. The one without an eating disorder is upping her calories and no longer trying to restrict. Eventually when her body is energy balanced again, the reactive eating stops. For the one with an eating disorder, it doesn't end because she is constantly trying to restrict each time a binge happens.
Neither one has experienced weight-cycling so far. Which one do you think goes on to develop weight cycling issues?
It’s the one without the eating disorder.
Weight Cycling In Detail
I have hopefully covered off in other blog posts (and more in ones to come as well) the serious health issues that accompany an untreated eating disorder, so in this post we focus exclusively on weight-cycling which is a very unhealthy outcome for usually ‘overweight’ and ‘obese’ people who constantly put themselves on new restrictive calorie diets because our society hates fat people.
A more accurate term for weight cycling would really be weight spiraling.
We pick up with our non-eating disordered woman now that she is at BMI 25, having started at BMI 26. She is as good as her word, and she starts a new diet and exercise regime to get back to BMI 20 again in time for bikini season. Let’s say her name is Matalin.
Within another 6 months of yet another round of grueling starvation and exercise, Matalin returns to BMI 20 yet again. Then she’s off on vacation with her family by July to enjoy all her hard work. By September she’s jumped to BMI 22, but she is now thinking that perhaps that is a more reasonable range. By January however she is BMI 26.7.
Nonetheless, positive thinker that she is, Matalin is back on her diet and exercise regime by that following August. She doesn’t want to spend another summer like she just did all embarrassed and covered up at the beach.
It takes 9 months to get to BMI 20.8 this time around and only 3 months post-diet to get back to BMI 26 and by month 6, post-diet, she is at BMI 28—the highest weight she has ever been in her life.
Ten years in the future for Matalin, with this kind of weight cycling, or spiraling, and she is now BMI 34. In those intervening years, she’s gone on fasts, used various pills, tried the grapefruit diet, the low-fat diet, the no-carb diet…everything and anything. She is now dealing with a host of health issues and is on anti-depressants having recently been diagnosed with depression.
Each time she gave up on one ridiculous unmaintainable diet after another, her weight climbed ever higher. After one particularly horrible experience when she was out walking for exercise and a bunch of guys in a car screamed at her to go back home because she was too fat to live, she stopped even getting out for walks. She bought a treadmill for home but as a social person she found it too boring and it sits in the basement covered with the kids’ stuff now.
Icing on the cake? (pun intended) Her doctor tells her she needs to lose weight as a solution for her misattributed weight-assigned health issues: high cholesterol, hypertension and a pre-diabetic fasting glucose response.
And this is playing out in millions of people’s homes across the world. Ostensibly, it's difficult to differentiate between the behaviors of our non-eating disorder weight-cycling individual and someone with an eating disorder (an anxiety disorder wherein food is misidentified as a threat within the threat identification system in the brain).
Weight Cycling Health Issues
So how does someone like Matalin overshoot her body’s original optimal weight set point (BMI 26) by weight cycling?
It appears as though starvation (dieting) suppresses a resting metabolic rate, for survival, and repeated cycles of starvation result in a more permanently suppressed metabolic rate despite adequate energy intake during non-starvation periods of weight cycling.
Using the Finnish Twin Cohort study, mentioned earlier, researchers were able to identify that average weight gain was only weakly associated with weight-loss attempts, but that major weight gain was strongly associated with weight-loss attempts. Those experiencing the greatest weight gain after weight loss were initially young men and middle-aged women. There appears to be some genetic factors also involved as to whether major weight gain will occur post weight-loss attempts, but these factors are unidentified at this point. These results were present after controlling for several confounders as well [M. Korkeila et al., 1999].
In a study involving 692 female adolescents, weight-loss attempts predicted elevated increase in weight and onset of obesity over the 4-year study period [E. Stice et al., 1999].
No matter their starting weight, the young women in the study had a 3.24 times greater chance of obesity onset than non-dieters. The risk was no greater for girls who started overweight than those who were underweight or normal weight at baseline [ibid.].
So when your 13-year old daughter decides she is going to diet because her thighs are getting too big, do you tell her that she’s over 3 times more likely to overshoot her body's optimal weight set point that way than if she just didn’t diet at all? I’m thinking it might be a good idea.
And like Matalin in our scenario above, in the Women’s Ischemic Syndrome Evaluation (WISE) multicenter study of 485 women, those who reported weight cycling in their lives had high-density lipoprotein (HDL – “good cholesterol”) levels that were anywhere from 7% to 27% lower than their non weight cycling counterparts (dependent upon the amount of weight lost and gained) [M.B. Olson et al., 2000].
Adolescent wrestlers, who regularly weight cycle to “make weight” for matches end up with significantly lower resting metabolic rates (RMR) than non-cyclers (154.6 vs. 177.2 kJ/m2/h) [S. Nelson Steen et al., 1988]. A subsequent study suggests that only two cycles do not result in lower RMR [W.D. Schmidt et al., 1990]
Bone mineral density was studied in 169 premenopausal women, pairwise matching was done (non-cycler vs. cycler) and results suggested that lower spine and distal radius bone mineral density loss occurs for weight cyclers [M. Fogelholm et al., 1997].
In an indirect relationship, weight cycling is strongly predictive of higher BMI and that, in turn, was strongly predictive of the development of type 2 diabetes. However weight cycling was not independently predictive of developing type 2 diabetes [A. E. Field et al., 2004].
A small study (N=30) suggests that weight cycling also causes redistribution of body fat to the upper body fat compartments. The overweight women with a history of weight cycling had significantly thicker subcutaneous adipose (fat) tissue of the upper body than overweight non-weight cycling controls. They also had significantly less subcutaneous adipose layers on their legs than normal weight women [S.J. Wallner et al., 2004].
Weight cycling is more common in women than in men, and it seems associated with more doctor visits and poor self-perceived health [M. Lahti-Koski et al., 2005].
And as we have seen with Matalin, epidemiological studies show increased BMI is associated with both major depression and suicide ideation for women [K.M. Carpenter et al., 2000]. Specifically among women, obesity is related to major depression and this relationship increases among those of high socio-economic status [A. J. Stunkard et al., 2002].
“Weight cycling is also linked to increased gallbladder surgery, renal cancer, oxidative DNA damage in mammary tissue (suggesting increased risk for breast cancer) and depletion of fatty acids.” [G. Gaesser, Weight, Weight Loss, and Health: A Closer Look at the Evidence, 2003 (further references in original)]
Weight Cycling and Progressive Weight Gain
Why did Matalin overshoot her optimal weight each and every time that she stopped dieting? She likely wore out facets of her body’s complex homeostatic capability.
A similar process occurs with chronic stress (coming up in the next section) and its impact on the immune system. For many, chronic stress progressively suppresses the immune response. Initially, stress stimulates the immune response and that of course has value for short-term survival. However, the system works to return to its baseline as it cannot function long term at 110% of its optimal state.
Depending on a number of genetic and environmental factors, especially in the presence of chronic stress, patients can find themselves not returning to 100% immune function. Chronic stress can force the body to try to keep modulating the immune response such that some become immunosuppressed and others develop autoimmune disease. In the first circumstance the body pushes the immune system to function at lower than optimal rates and in the second the body pushes the immune system above its optimal state [R.M. Sapolsky, 2004].
If we restrict calories, leptin levels respond to temporarily provide enhanced survival capability. Just as our bodies are well-adapted to short-term stress stimuli and yet poorly adapted to chronic stress stimuli, we are well-adapted to face a famine, but less well-adapted to manage chronic cycles of famine.
As I mentioned in post VI, there is a small group of people extremely well-adapted to cycles of chronic famine and their predisposition has been nicknamed “the thrifty gene”. It appears for some who embark on chronic cycles of famine they are able to trigger physiological changes that mimic what we see in those with the thrifty gene: much lower resting metabolic rates, a predisposition to both leptin and insulin resistance and an economy of physical movement in day-to-day existence.
Some individual case studies suggest that given enough time and a complete cessation of calorie deficit practices, leptin resistance resolves and an accompanying return to an original optimal weight set point is achieved.
Does stress factor into gaining weight? Yes. However, not for everyone.
In a study of 7965 male and female British civil servants, those in the leanest quintile lost weight with high job strain and low job control (the quintessential public service employment experience), whereas those in the highest quintile (above BMI 27) were impacted by the same stressful work environment with weight gain [M. Kivimäki et al., 2006].
Glucocorticoids are a class of steroid hormones released in our bodies when we are under stress. Glucocorticoids increase appetite for about 2/3 of all of us and decrease it for the other third. Now we all know that calorie intake is not correlated to BMI (from post VI in this series on fat).
“Therefore, with chronic stressors, corticosterone seems to act in brain in an excitatory rather than an inhibitory fashion. We believe, under conditions of chronic stress, that there is an indirect glucocorticoid feedback that is mediated through the effects of the steroid ± insulin on metabolism. Increased energy stores feedback on brain to inhibit hypothalamic CRF and decrease the expression of dopamine-β-hydroxylase in the locus coeruleus. These changes would be expected to decrease the level of discomfort and anxiety induced by chronic stress. Moreover, central neural actions of glucocorticoids abet the peripheral effects of the steroids by increasing the salience and ingestion of pleasurable foods.” [M.F. Dallman et al., 2006].
Under normal conditions glucocorticoids and insulin act in balance to support energy intake and metabolism (along with a host of other hormones). It appears under conditions of chronic stress the system changes somewhat and it allows for weight gain in those prone to hyperphagic responses (over-eating) with increased glucocorticoids in the system. Critically this kind of weight gain leads to a disproportionate amount of subcutaneous abdominal fat being laid down, more of a marker of oncoming health issues than weight gain not related to chronic stress.
Chronic stress has particular features: unpredictability, lack of control, difficult or impossible to resolve, and persistent over time. Working for an organization that is complex, where the job offers little authority but much accountability, the deliverables are out of one’s control and the organization periodically ‘downsizes’ to increase productivity (to shareholder delight), would be a quintessential chronic stressor.
Of course, this kind of chronic stress even without weight gain causes all manner of health issues that have been wrongly correlated with weight gain itself, namely hypertension, heart disease and diabetes [T. G. Pickering, 2001; D.S. Krantz, M.K. McCeney, 2002; R.P. Robertson, 2004].
And finally, it is highly likely that for women in particular, even more so for those of higher socioeconomic status, weight gain in and of itself is a chronic stressor.
A good book to read to understand chronic stress, its implications and possible ways to moderate it, is Robert Sapolsky’s: Why Zebras Don’t Get Ulcers.
“As you read this, about 100 million sleep-deprived Americans are driving cars and trucks, operating hazardous machinery, administering medical care, monitoring nuclear power plants and even piloting commercial jets.” [J.E. Brody, Personal health; Health alarm for a sleep-deprived society, NYTimes, 1994].
Lack of sleep that is a contributing factor to many serious health issues, and it also appears to be associated with weight gain.
“Recent chronic partial sleep deprivation experiments, which more closely replicate sleep loss in society, demonstrate that profound neurocognitive deficits accumulate over time in the face of subjective adaptation to the sensation of sleepiness.” [J. Durmer et al., 2005]
Sleep deprivation, rather than obesity, could more feasibly be described as an epidemic. And we adapt to the sensation of sleepiness such that we do more neurocognitive and broader physical damage over time.
Preschoolers need 12-15 hours of sleep, yet regularly get 9.5 hours (naps included) in a recent US-based study, and sleep deprivation is a serious problem for school-aged kids as well, never mind adults [C. Acebo et al., 2005].
In a study where 2,281 children ages 3-12 years at baseline were re-evaluated 5 years later to assess correlations of sleep patterns and overweight, those who slept less, went to bed later, or got up earlier at baseline assessment had higher BMIs 5 years later and were more likely to be overweight [E. K. Snell et al., 2007].
A meta-analysis of 655 separate studies of children and adults confirms that there is a consistent risk of obesity in short sleepers (children and adults). But what comes first? A predisposition to overweight that causes shortened sleep, shortened sleep that causes overweight, or some third factor related to both traits?
Shortened sleep lowers leptin levels, but like everything in our bodies, it’s not quite that simple. Lack of sleep also messes with the amplitude of the diurnal rhythm of leptin. That amplitude (intensity) of the rhythm contributes to increase the satiety signal [K. Spiegel et al., 2004].
Leptin, as many of you now know, is a critical gating hormone in our bodies. It supports homeostasis, appetite, metabolic rate, bone formation, blood formation and normal neurotransmitter and hormone functions. When we starve, leptin levels plummet and this triggers the body to lower the metabolic rate and increase appetite cues. When we overindulge, leptin shoots up and this triggers the body to increase metabolic rate and decrease appetite cues.
Sleep deprivation doesn’t just make us hungrier because leptin levels are lower than normal, but it also messes with heart rate variability, thyroid hormone levels and cortisol levels. A well-rested person has an inverse relationship of leptin and cortisol in her system [ibid.]. With sleep deprivation that inverse relationship is curtailed in the evening and cortisol levels increase the amount of energy the body stores rather than uses, and preferentially stores it as subcutaneous abdominal fat [R.M. Sapolsky, 2004].
Bariatric Surgery and Other Implements of Torture
There are two forms of bariatric surgery: gastric banding (implanting a device) and gastric bypass surgery.
The trend is towards laparoscopic procedures rather than open procedures and may progress soon to endoscopic procedures.
Malabsorptive procedures include: biliopancreatic diversion, jejunoileal bypass and endoluminal sleeve. Restrictive procedures include: vertical banded gastroplasty, adjustable gastric band, sleeve gastroectomy, intragastric balloon and gastric plication. [Weight-control Information Network, National Institutes of Health, 2012].
Bariatric surgery has a complication rate equivalent to that of cholecystectomy (removal of the gallbladder [E.H. Livingston, 2001]. Given that at least a third of all cholecystectomy patients continue to suffer pain and gastrointestinal symptoms post-surgery, a complication rate of this level is concerning.
“…all of these procedures, to variable degrees, alter the anatomy and physiology of the gastrointestinal tract. This fact, along with postoperative dietary changes, makes these patients vulnerable to a multitude of potential complications.” [S.A. Shikora et al., 2007]
And to spell it out what the complications look like:
“Based on previous meta-analyses, most of the top 10 complications from bariatric surgery are gastrointestinal: dumping, vitamin/mineral deficiencies, vomiting (and nausea), staple line failure, infection, stenosis (and bowel obstruction), ulceration, bleeding, splenic injury, and perioperative death. Two other gastrointestinal complications of bariatric surgery are indirect consequences of the surgery: bacterial overgrowth and diarrhea.” [T.L. Abel, A. Minocha; 2006].
There has been a 2.5-fold increase in bariatric surgery procedures from 1987-2001. Of the 3,328 bariatric procedures reviewed in one meta-analysis, the 30-day mortality rate was 1.9% and was associated with surgical inexperience [D.R. Flum, E.P. Dellinger, 2004].
Apologies to all neurosurgeons, but it’s my humble opinion that gastric and intestinal surgeries are more complex and more poorly understood than even many brain surgeries.
To make the determination that interfering with your body’s ability to absorb energy based on the presence of a socially unacceptable level of adipose tissue, displays a profound level of cultural dysfunction.
Many who look to develop fat acceptance in our society refer to these procedures as stomach amputations. I prefer to call them gastric mutilations. Similar to the practice genital mutilation of females in cultures that believe a woman who experiences sexual pleasure will be unfaithful, we mutilate the stomachs of (predominantly) obese females in our culture because we believe a woman who is fat is not only undesirable, but also despicable and a subversive influence on others (especially her children).
Of course the argument for these surgeries and all their accompanying risks is that they lower mortality from what would be expected if the obese patient does not undergo the surgery. The reduction is from a 16% mortality rate for obese controls compared to an 11% mortality rate for those who underwent bariatric surgery [ibid.]. It ends up being a 5% relative reduction in the chance of dying from health issues that are wrongly attributed to excess adiposity in the first place—not exactly a persuasive argument for surgery to me.
But if we’ve learned one thing in this series it is that correlation provides no proof of causation. Given that bariatric surgery patients are told that their post-surgery weight loss is also dependent on changes in lifestyle habits [Mayo Clinic], then a 5% reduction in mortality rate may have nothing to do with the surgery itself and everything to do with the fact that the patient gets out and starts being active.
Other torture implements for the fat include diet pills (both prescription and over-the-counter) and diuretics. While less invasive than bariatric surgery, they are dangerous in their own ways. And the question still remains: are any of us actually assessing the relative risks of fatness vs. the treatments of fatness when deciding to take medication that messes with such an exquisitely complex system as our balance of energy?
Low Birth Weights
I won’t go into too much detail here because I have covered off this topic in more detail in my post on Reproductive Health I: Fertility & Pregnancy, but one of the serious ramifications of restricting calories for women who decide to have children is the greater risk that their baby is of low birth weight when born. Low birth weight pre-disposes the child to metabolic syndrome in later life [V. Nobili et al., 2008; C. Li et al., 2001].
By comparison, a high birth weight increases the risk of obesity in later life but paradoxically decreases cardiovascular disease. It appears as though this may be due to high birth weight somehow being associated with later development of fat free (or lean) mass [A. Singhal et al., 2003].
The German occupation of the Netherlands in 1944 allowed researchers to determine that famine for pregnant women who were in the first two trimesters was more likely to result in obese subjects with metabolic syndrome (at age 19 at follow-up), than for the subjects whose mothers had faced the same famine while in the third trimester of pregnancy [W.H Dietz, 1994]. Given that today women are far more likely to be restricting calories at any given time, feasibly women expose their fetuses to starvation prior to them becoming aware that they are pregnant in that critical first trimester.
What Can We Do?
Now we are at the end of this long series on fat. Do we feel less contempt or fear? Likely not.
But we should nonetheless keep striving for a neutral interaction with our own fatness and the fatness of others.
If there is only one thing that I hope you as the reader retain from this series, it is the necessity of ceasing all forms of restrictive eating and excessive energy-deficit-creating behaviors.
What are you supposed to do if you are naturally not BMI 18.5 (which will be true for 99% of us)? Use all the tools at your disposal to accept your body and reframe your mind’s misunderstanding so that you no longer view your body as something to be beaten into submission. Get counseling, read books and seek like-minded people to reinforce your efforts.
Your body is not a home that you renovate as you see fit, it is your very existence. We went horribly wrong in western culture many years ago with the conceptualization of mind and body as distinct entities. There is no mind without body. Is there a spirit part of us? I cannot answer that. But I can say that neither your mind nor your body would exclusively house your spirit, if there is one to be had, because we are indivisible creatures. The energy we absorb and release is not neatly partitioned and we are not machines, circuits or computers.
We need to watch our metaphors.
Please note that systematic review data is available for review under Papers.