Is Obesity a Disease?

Abstract

Obesity is a well-known risk factor for many chronic diseases as well as early mortality. However, since body mass index does not distinguish between fat mass, fat-free mass, and lean mass, individuals with similar body mass indices may have very different body composition and physiological function. Further, how a person became obese appears as important, if not more important, than their actual amount of fat. Genomics, level of toxicant load, amount of exercise, and ratio of omega 6/3 fatty acid ratio are greater determinants of disease risk than adipose mass.

Obesity and Disease Risk

The research is clear that obesity is a significant risk factor for many chronic diseases. This is well demonstrated in Table 1 from the US Centers for Disease Control. In general, people who are obese have increased levels of many inflammatory molecules, decreased insulin sensitivity, abnormal blood lipids—the list is long. However, obesity is not a monolithic condition. Weight and body mass index (BMI) are poor measures of what is happening physiologically, and how a person becomes obese, including genomic susceptibility, plays a huge role in actual disease risk.

Table 1.

Obesity Significantly Increases Risk for Many Diseases¹

All-causes of death (mortality) High blood pressure (hypertension) High low-density lipoprotein (LDL) cholesterol, low high-density lipoprotein (HDL) cholesterol, or high levels of triglycerides (dyslipidemia) Type 2 diabetes (T2DM) Coronary heart disease Stroke Gallbladder disease Osteoarthritis (a breakdown of cartilage and bone within a joint) Sleep apnea and breathing problems Some cancers (endometrial, breast, colon, kidney, gallbladder, and liver) Low quality of life Mental illness such as clinical depression, anxiety, and other mental disorders Body pain and difficulty with physical functioning

Since BMI does not distinguish between fat mass, fat-free mass, and lean mass, individuals with similar BMIs may have very different body composition and physiological function.

Storing Fat Is a Normal, Healthy Physiological Process

As humans evolved as a species, periods of feast and famine were common. We developed efficient systems to store fat for when food was sparse and mood-elevating ketone metabolism for when we had to live off our fat stores but needed to keep searching for food. Storing fat is a normal, healthy, survival-promoting physiological process. So why all the strong disease associations?

Environmental Toxicants Are a Major Factor in Obesity/Disease Risk

While digging through research for my editorial in volume 15, issue 4, “Is the Diabetes Epidemic Primarily Due to Toxins?”² I was struck by the growing number of researchers who have started calling many of the environmental toxicants “diabetogens” and “obesogens.” They are finding that a large number of persistent organic pollutants (POPs) are independent risk factors for many chronic diseases, especially diabetes and obesity (see my editorial in volume 12, issue 2, “Persistent Organic Pollutants (POPs)—A Serious Clinical Concern”³ for further discussion).

Especially interesting is the work of Ducky Lee, MD, PhD, and her colleagues who discovered not only a strong association between body load of POPs and obesity, but also the striking observation that the normally robust association between obesity and diabetes was absent in obese people who had the lowest levels of POPs.⁴ Her research group is now even suggesting that accumulating adipose tissue is a strategy to dilute fat-soluble toxins and helps explain some of the paradoxes in obesity research.⁵

Amount of Exercise More Important Than Amount of Adipose Tissue

I then looked at risk of cardiovascular disease (CVD) in obese people—and found a similarly surprising result: The normally strong relationship between obesity and CVD is essentially eliminated in those who exercise vigorously (thanks to my friend Wayne Jonas, MD, who brought this to my attention).⁶

The Ratio of Omega 6/3 Fatty Acids in Adipose Tissue Makes a Big Difference

Not only does a diet high in omega-6 fatty acids—especially arachidonic acid—promote inflammation, which aggravates virtually all the metabolic problems found in obesity, but inadequate omega-3 fatty acids levels promote fat deposition and decrease both muscle mass and bone density.^7,8

Obviously, all 3 of the above need to be fleshed out much more deeply, but that is beyond the scope of this editorial. Nonetheless, the problem of defining exactly what obesity is, along with these observations, started me down the path of wondering if focusing on excessive body mass is distracting us from the actual causes of the apparent increased risk of disease normally associated with obesity.

What Really Is Obesity?

Although popular, BMI is unhelpful and likely misleading. Not only does it have the obvious challenge of not differentiating between fat mass and protein mass, it can mask a normal weight individual who has high fat mass. Clearly, body fat percentage is a better measure but it does not consider the omega 6/3 ratio of the fat and does not necessarily indicate metabolic abnormality. Some researchers are suggesting 4 phenotypes of obese individuals: (1) normal weight obese (NWO); (2) metabolically obese normal weight (MONW); (3) metabolically healthy obese (MHO); and (4) metabolically unhealthy obese or “at risk” obese. They also suggest the term adiposopathy, or “sick fat.”⁹

Normal Weight Obese

Inflammation

Normal weight with a high body fat percentage (≥23.5% in men, ≥29.2% in females) and low muscle mass. These individuals have increased oxidative stress and chronically upregulated inflammatory status, which lead to a higher risk of cardiometabolic diseases and sarcopenic obesity. These people have elevated plasma levels of interleukin (IL)-1α, IL-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α.¹⁰ The metabolic dysfunctions are worse in those with specific single nucleotides polymorphisms (SNPs):

• 174G/G (IL-6 promoter). Results in higher levels of IL-6 and increased insulin resistance.¹¹

• IL-15Rα (IL-15 receptor-a) and MTHFR 677C-->T (methylenetetrahydrofolate reductase). Results in lower metabolic rate and increased water retention.¹²

• G/A-308 (TNF-α). Associated with sarcopenic obesity.¹³

Metabolically Obese Normal Weight

Insulin Resistance

Normal weight with elevated blood pressure, low insulin sensitivity, and dyslipidemia.^14,15 These individuals have elevated risk of diabetes. They may also have a higher amount of visceral fat leading to higher blood levels of inflammation cytokines (TNF-α and IL-6) and even more insulin resistance.¹⁶

Metabolically Healthy Obese

Healthy

Excess body fat, but metabolically healthy. Approximately 20% to 30% of obese adults do not show the metabolic complications typically associated with obesity. MHO individuals have high insulin sensitivity, normal blood pressure, no signs of chronic inflammation, and a normal lipid profile.¹⁷ Inflammation increases only when there is a lot of excessive adipose tissue mass. There is no consensus as to how metabolic normality should be defined, so the reported prevalence of MHO ranges from 2% to 50%, depending on the specific criteria used and the population studied.^18,19

Metabolically Unhealthy Obese

High Disease Risk

Obese for both anthropometric parameters (BMI ≥ 30 kg/m²) and fat mass percentage (PBF > 30%) and metabolic abnormalities such as MetS, T2DM, and atherosclerotic CVD.²⁰ This phenotype is linked to higher visceral adiposity than subcutaneous adiposity and consequently to increased fatty acids release into the portal circulation and major deposition in liver.²¹ This is the phenotype with the strongest disease risk and likely accounts for most of the disease associations found with obesity.

Summary

Although commonly used, the term obesity and the BMI as measurement of obesity are of very limited benefit clinically. The research appears clear that the causes of the obesity are much better measures of risk than the excessive adipose tissue itself. However, specific polymorphisms have an impact on the strength of these risk factors and a large enough mass of adipose tissue will itself induce metabolic abnormalities.

Bottom line, except for those who are morbidly obese (about 10% of the population), carrying around extra fat—even a lot of it—does not significantly increase disease risk as long as they (and probably must be all 3): have a low body burden of toxins, exercise vigorously (both aerobic and strength), and eat a diet with a healthy omega 6/3 fatty acid ratio.

In This Issue

Associate Editor Jeffrey Bland, PhD, leads off this issue with another of his provocative commentaries, this one on the role of lymphatic drainage in cardiovascular disease. I had never heard of this hypothesis before, but everyone who has experienced the benefits of massage will instantly understand the importance of this concept. While highly technical, this is a fascinating read.

John Weeks brings us a great review of the cost-effectiveness research documenting the importance of holistic care provided by properly trained nurses. I also find encouraging his review of the work of other organizations to demonstrate cost effectiveness.

Managing Editor Craig Gustafson interviewed Matthew Baral, ND, who will be a keynote speaker at the upcoming annual conference of the American Association of Naturopathic Physicians. I found his discussion of natural settings and healing profoundly inspirational. When I built my first personal computer in 1977, one of the earliest programs I wrote (in assembly language for those who are curious) was to produce active fractal and Mandelbrot designs on my color monitor. Many fascinating hours watching how nature’s beautiful designs evolve from varying starting parameters.

Margaret G. Gasta, MS, RDN; Crystal M. Gossard, MS, CNS; Christy B. Williamson, MS, CNS; Keren E. Dolan, MS; Heather J. Finley, MS, RD, LD, CEDRD; Cathleen M. Burns, MS, RD, LDN; Emily C. Parker, MS, RD; Jessica M. Pizano, MS, CNS; and Elizabeth A. Lipski, PhD, CNS, CCN, BCHN, IFMCP, bring us the fifth portion of their review of probiotics and disease, this time focusing on EENT and respiratory conditions.

The concept of supplemental lysine for herpes simplex prevention has been controversial for decades. Venthan J. Mailoo, BSc(Hons), MBBS and Sanketh Rampes, provide a welcome review the latest research. I think their assertion of a critical dosage threshold and importance of dietary arginine help bring clarity to this challenging problem.

Rajdeep Singh, MD, and my friend Assistant Editor Gerard E. Mullin, MD, provide us an excellent case report documenting the benefits of fully integrated care for a patient suffering serious disease from small intestine fungal overgrowth. This is a compelling example of how some patients truly need both conventional drugs and sophisticated nutritional intervention to solve complex problems.

Long-time readers may recall the article by Lara Pizzorno in volume 13, issue 6, “Canaries in the Phosphate-Toxicity Coal Mines.”²² Jaime Uribarri, MD, in his interview by Craig, speaks powerfully about how the many dietary phosphate natural sources and additives to packaged foods are causing far more metabolic dysfunction and disease than is recognized by most clinicians.

Associate Editor Bill Benda, MD, brings into question the value of political correctness in primary care. So much that is irrelevant to medicine has been heaped upon practitioners that less and less time is available to actually provide the healing patients are seeking.

Joseph Pizzorno, ND, Editor in Chief

drpizzorno@innovisionhm.com

http://twitter.com/drpizzorno

Biography