I covered off in Part VII all the reasons why the "obesity epidemic" should always appear inquotation marks to indicate that it is a fallacious concept.
But I want to drive a stake into its heart and cover off in detail the issues of weight being linked higher risks of various diseases.
Class 1, 2 and 3 Obesity
Class 1 Obesity: 5’5” 180-209 lbs. 5’10” 210-244 lbs.
Class 2 Obesity: 5’5” 210-239 lbs. 5’10” 245-284 lbs.
Class 3 Obesity: 5’5” 240 lbs. and up. 5’10” 285 lbs. and up.
Only 4.8% of the population in the U.S. is at Class 3 Obesity [C.L. Ogden et al., 2006]. Generally it is this small sub-population of ‘the obese’ that is now the focus of more intense scrutiny when it comes to negative health outcomes.
And even then, evidence so far is not able to show definitive associations between Class 3 Obesity and disease.
“Until very recently, the health risks of obesity were thought to be well understood, with a straightforward correlation between increasing obesity and increasing risk of health problems such as type 2 diabetes, coronary heart disease, hypertension, arthritis and cancer. It is becoming clear, however, that the location of fat deposition, variation in the secretion of adipokines and other factors govern whether a particular obese person develops such complications.” [A. Walley et al., 2006].
Andrew Walley and his colleagues further state in the discussion of their meta-analysis “being obese does not necessarily mean being ill and, indeed, it is likely that very good health is required to establish and to maintain extreme obesity (emphasis mine).”
Obesity and Diabetes
David Redden and David Allison in a thorough review of the literature on the genetic associations of obesity and diabetes find that none of the studies have been successfully replicated [D. Redden, D. Allison, 2003]. The reason non-replication is significant is that it indicates the original data suggesting a link between obesity and diabetes were flawed in some way. Redden and Allison also provide significant detail on how these flaws may have crept into the studies, one of course being publication bias.
Metabolically healthy obese people are at no greater risk for diabetes or cardiovascular disease than so-called healthy-weight people.
There is great disagreement on how many metabolically healthy obese people there might be, but that is understandable given that $862 million (USD) a year is provided by the National Institutes of Health for obesity research [NIH, 2009]. With small sample size, Martin Brochu and his colleagues found almost 40% of the obese women studied were metabolically normal, using insulin resistance as the marker for metabolic abnormality [M. Brochu et al., 2001].
Jennifer Kuk and her colleagues used the NHANES III results from 6,011 men and women to announce that only 6% are metabolically normal [J. Kuk et al., 2009]. In their conclusions they report that the metabolically normal obese prevalence is anywhere from 6% to 38.4%, depending on the cutoffs used. I question their metabolic abnormality definitions that account for the massive drop in the metabolically normal obese population. I am also puzzled by the fact that the American Diabetes Association is not listed within the acknowledgments, and yet the ADA logo is prominently displayed on Figure 1 synthesizing the results of insulin resistance and also metabolic abnormalities for the obese population under review.
48% of patients with diabetes are not obese [K. Slynkova et al, 2006]. In fact until our war on obesity, diabetes mellitus Type II was considered a disease that predominantly impacted older patients of all sizes.
Shifting the Markers (Yet Again)
In 1997, the standard for diagnosing diabetes was lowered from a fasting blood glucose level of 140 mg/dL to 126 mg/dL. It resulted in an immediate 50% increase in the number of diabetics in the U.S.
“There is wide overlap between healthy persons and persons with diabetes in the fasting plasma glucose range of 126 to 140 mg per dL (7.0 to 7.8 mmol per L). Each year only 1 to 5 percent of persons with impaired glucose tolerance develop manifestations of diabetes.After 10 years, most do not have diabetes or have normal results on retesting.Even among Native Americans, a population at high-risk for diabetes, the 10-year incidence of renal failure occurring in those with a fasting plasma glucose level of less than 140 mg per dL (7.8 mmol per L) is only 8.4 cases per 1,000 person-years.” [S. Woolf, S. Rothemich, 1998].
Obesity and diabetes are not dependably associated, and diabetes itself is likely overly- diagnosed in our populations since the 1997 adoption of lower fasting blood glucose markers. The Centers for Disease Control and Prevention, when publishing data on the National Health and Nutrition Examination Survey (NHANES), found that incidence of diabetes was not increasing and that this was unexpected given increasing prevalence of overweight and obesity [CDC, Morbidity and Mortality Weekly Review, September 5, 2003].
Obesity, Sleep Apnea and Hypertension
Obstructive sleep apnea is repetitive obstruction of the airway such that the person stops breathing while sleeping. The ensuing lack of oxygen forces the person awake. It is associated with daytime sleepiness, due to fragmented and interrupted sleep, and an increased risk of hypertension (high blood pressure). Obstructive sleep apnea is present in approximately 50% of all patients with cardiovascular disease [A. Logan, D. Bradley, 2010].
Thing is, that despite all these wonderful correlations: sleep apnea appears alongside hypertension and cardiovascular disease in such a way that it is clustered by more than just chance, 50% of those with sleep apnea are not obese [I. Mortimer et al., 1998].
In a small study involving non obese men (N=23) with obstructive sleep apnea, prolonged sitting and the fluid displacement from the legs overnight may actually be the source of the condition completely unrelated to body weight [S. Redolfi et al., 2009]. I will be addressing activity levels as the real focus for good health outcomes regardless of body weight in a moment.
Obesity and Cardiovascular Disease
Another set of researchers decided to take NHANES (1999-2004) with a sample of 5,440 participants to assess cardio-metabolic risk factors for the obese population.
Rachel Wildman and her colleagues defined cardio-metabolic abnormalities as: elevated triglycerides, fasting plasma glucose, C-reactive protein (indicating inflammation), insulin resistance and low HDL cholesterol levels. They found 23.5% of those at a normal weight were cardio-metabolically abnormal. 51.3% of overweight (BMI 25-29.9) and 31.7% of obese (above BMI 30) were cardio-metabolically normal. [R. Wildman et al., 2008].
“Despite assertions that obesity causes heart disease, the preponderance of autopsy and coronary angiography studies indicates that obesity is unrelated to cardiovascular disease. In fact, the largest of the angiographic studies -- more than 4,500 subjects, published in 1991 -- revealed that the fattest men and women had the cleanest arteries. The massive International Atherosclerosis Project (1960s) concluded after analysis of 23,000 sets of coronary vessels that there was no relationship between heart disease and body fat.” [G. Gaesser, M. Fumento, 1997].
The Framingham Heart Study original cohort in 1948 included 2,336 men and 2,873 women from Massachusetts who were between the ages of 30 to 62. Subsequent cohorts have been studied since that time as well [W. Kannel et al., 1993]. Lauren Lissner and her colleagues reviewed the Framingham Heart Study results and were able to identify that excess cardiovascular disease mortality rates in the obese could be explained by weight cycling (yo-yo dieting), something I will discuss further in Part IX. [L. Lissner et al., 1991].
And how you come to your obesity is critical in defining cardiovascular disease risk. High birth weight increases the chance of obesity in later life but paradoxically also lowers the risk of cardiovascular disease [A. Singhal et al., 2003].
And finally, in patients with advanced heart failure, obesity is not associated with increased mortality and provides more favorable outcomes. [T. Horwich et al., 2001; G. Fonarow et al., 2007].
Obese people with cardiovascular illness, pneumonia, HIV, high blood pressure, congestive heart failure, type 2 diabetes, cancer and high cholesterol, those needing hemodialysis and those who have undergone heart transplants all have better outcomes than lean people with the same conditions [Healthy Weight Network, Obesity: Risks and Benefits, 2009 (appropriate clinical trials referenced at source)].
The takeaway point from this entire section is that obesity is not an automatic disease state nor does it automatically involve increased risks of diseases and early death.
Furthermore Katherine Flegal and her colleagues’ review of the NHANES data (I, II, and III) suggest unequivocally that being overweight (BMI 25-29.9) generated 86, 094 fewer deaths than expected. That means negative 86,094 deaths (or 86,094 living participants were expected to have died within the study timeframe) [K. Flegal et al., 2005].
Nonetheless, in a complex interplay of the body’s inflammatory responses, clinical data do show that for obesity at its most severe (and under age 70) there is an increase in deaths associated with cardiovascular disease, diabetes, kidney disease, as well as colon, breast, pancreatic, uterine and ovarian cancers. The death risks decrease with age and disappear by age 70 [ibid.]. The jury is still very much out on whether inflammation precedes the development of this type of extreme obesity and the accompanying illnesses or whether the increase of fat tissue causes heightened inflammatory responses [P. Dandona et al., 2003; A. Berg et al., 2005]
And even with the cancers associated with obesity, death may be more likely to occur because both overweight and obese patients receive inadequate screening and in particular intentionally inadequate chemotherapeutic dosing [J. Griggs et al., 2005].
Before I get into the presumed value of exercise for all sizes, I want to turn my attention to some of the societal, political and prejudicial aspects of fat.
Childhood Obesity and Social Services
Last month social workers in Ohio removed a 200 lb. 8-year old boy from his home stating that the mother had not been doing enough to control his weight [U.S. News, November 28, 2011].
The news coverage states the boy was at risk for such diseases as diabetes and high blood pressure. He came to the attention of the authorities in 2010 when he was hospitalized with severe breathing problems and was diagnosed with sleep apnea for which he uses a continuous positive airway pressure (CPAP) machine at night now.
It appears as though the only definitive diagnosis is sleep apnea. If he does not currently suffer from diabetes or high blood pressure (which I suspect given the parents’ lawyers’ statements), then it is shocking his medical team would allow for his removal into State care. And even if he currently suffers from diabetes and/or high blood pressure, these are independent health issues that cannot be resolved through weight loss in any case.
It also appears as though this boy’s medical team has not learned from the experience of Anamarie Regino of New Mexico. In 2001, she too was yanked away from her parents by social services accusing the mother of not following strict calorie restriction. At the time Anamarie was 3 years old, was 3’6” tall and weighed 124 lbs. To this day a concrete diagnosis eludes Anamarie’s case, but at age 7 she had the bones of a 14 year old, suffers from asthma and sleep apnea (sound familiar?) and she has various mild disabilities. Anamarie Regino is now 14 years old and her weight gain tapered off as she grew.
Anamarie did not improve appreciably in foster care and was subsequently returned to her parents several months later at which point they monitored the mother’s every move for at least another year. Now, diagnosed with a “genetic predisposition to gain weight”, Anamarie is faring well with treatment for insulin resistance and a CPAP machine, but of course is still morbidly obese. Sadly Anamarie’s mother passed away on October 7, 2011 making the removal of Anamarie from her mother at age 3 even more tragic, given how little time they were to have together as a family in the end. [http://www.abqjournal.com/main/2011/10/08/news/coping-with-a-loss.html/attachment/anamarie-regino]. For a more detailed look at Anamarie’s case, consider reading: The Obesity Myth, by Paul Campos.
Whatever causes this extreme level of childhood obesity, it is not overfeeding by parents. Shame on the entire medical community for not exercising sufficient curiosity, humbleness and empathy to clearly state that no definitive diagnosis is available and therefore no cause has yet been identified.
Those currently struggling with restrictive eating behaviors, fully a third of our population, are also harmed by this ‘war on obesity’. So pervasive is the unbridled hatred of being naturally anything other than thin, these decisions to put fat taxes on foods and remove children from parents only reinforce tremendous anxiety about what we all eat.
Exercise: What it Does and Does Not Do
The best thing about being physically active is that it can remediate all health issues that are usually associated with obesity without any appreciable weight loss. Even better, physical activity does not require triathlete level activity, rather the equivalent of about 30 minutes of brisk walking every single day.
Exercise and Hypertension
Exercise lowers blood pressure [J. Halliwill, 2001; J.R. MacDonald, 2002]. And the post-exercise hypotensive period is long and most pronounced for patients diagnosed with hypertension. Changes in diet (not to be confused with restriction of calories at all) can also reverse hypertension, namely the addition of fruits and vegetables into the diet [L.J. Appel et al., 1997].
Exercise, Insulin Sensitivity and Fat Metabolism
Obese women experienced marked improvements in both carbohydrate and lipid metabolism after aerobic exercise sessions of 90 minutes (at 55% of maximum aerobic power), 4 to 5 times a week over a 6-month period [B. Lemarche et al., 1992].
Even modest exercise programs (walking at intensity 45–55 or 65–75% heart rate reserve, frequency 3–4 or 5–7 days/week, duration 30 min/session) with absolutely no weight loss improved both glucose and fat metabolism in previously sedentary adults [G. Duncan et al., 2003].
“These data suggest that exercise training is accompanied by a significant reduction in insulin resistance, as indicated by well-validated surrogate measures. These data also suggest that moderate-intensity exercise is as effective as high-intensity exercise when 400 kcal are expended per session.”[G. O’Donovan et al., 2005].
Exercise and Cardiovascular Disease
Even in mid-life, a modest increase in activity is associated with decreased mortality [J. Myers, 2003].
“Patients with newly diagnosed heart disease who participate in an exercise program report an earlier return to work and improvements in other measures of quality of life, such as more self-confidence, lower stress, and less anxiety. Importantly, by combining controlled studies, researchers have found that for heart attack patients who participated in a formal exercise program, the death rate is reduced by 20% to 25%.” [ibid.]
Exercise and ‘Weight-Prevalent’ Cancers
Although they have not yet identified the biological mechanisms involved in the protective effect of exercise with colorectal cancer, it nonetheless exists. [J. Quadrilatero, L. Hoffman-Goetz 2003; G. Macfarlane, A. Lowenfels; 1994; J. Meyerhardt et al., 2006]
Exercise provides more modest protection against endometrial cancer [S. Olson et al., 1997] and a reasonable lowering of risk of death from breast cancer [M. Holmes et al., 2005].
Exercise and Weight Loss
Following a regular exercise program results in a 5-8% loss in weight on average. Obviously, someone who is BMI 30 is not going to become BMI 20 through exercise intervention.
The biggest mistake we have made in our modern society is to assume that we can mess with our bodies’ optimal weight set points. Losing weight through calorie restriction can certainly provide more than 5% weight reduction, but it fails on two counts: 1) it is not sustainable and 2) is damages the body.
It should also be noted that the modest benefits of 30 minutes of brisk walking on morbidity and mortality are irrelevant when compared to the massive detriment of exercise dependence that is common for those with eating disorders.
Please note that systematic review data is now available on this site under: Papers.