Obesity Science In Context

There are currently two blog series underway on on this site: the review of UCSD EDC2014 presentations and the systematic review of weight gain correlates in the scientific literature.

These reviews will hopefully allow for readers to come to their own conclusions. But for those who might be interested, this post is an edited compilation of recent e-mail responses from me to Elizabeth Watson, so that you might have some insight regarding my assessments and theories on the data currently under review. Please note that I use the term "obesity" only as a reflection of the scientific literature I reference in this post.

Epsos.de: Flickr.com
Epsos.de: Flickr.com

The adipose organ (fat) acts in response to metabolic assault on the body from environmental factors (still poorly understood and largely unstudied) and its ability to do so is health reinforcing. The onset of obesity (not inherited natural weight variations — different thing) and almost the entire scientific literature on obesity in general, confuses correlation with causation.

The size of the adipose organ in its un-assaulted state has a wide range of normal size across our populations. An ‘obese’ person is not automatically walking around with a fat organ that is responding to metabolic assault. Some are, many are not.

And when a fat organ purposefully enlarges beyond the body’s inherited optimal weight set point (which sits on a bell-shaped curve of incidence in our population), then the morbidity and mortality outcomes for the fatter individuals are superior to those of average-weighted individuals dealing with equivalent metabolic assault and resulting disease.

Much as it vexes the weight loss industry, a fat person with heart disease (and a host of other progressive diseases) has a better quality of life and longer life than a disease-matched individual who is of average weight. When patients with these conditions are studied in groups of non-obese and obese, then the outcomes reveal a protective element to a larger than average adipose organ size in the presence of various metabolic and life threatening illnesses. It’s called the obesity paradox because everyone is sure obesity is a disease and so the paradox is that obesity confers additional health protection in the presence of several disease states.

It’s mildly amusing to read the contortions of language that are used in systematic reviews associated with this protective facet of an enlarged fat organ. A just one example: “We found an apparently inverse association between overweight or obesity and mortality in critically ill adults, while severe obesity was not significantly related to this outcome.” 1 Or, in plain English: the fatter the patient, the less likely they were to die and this even held true, to a lesser extent, for extremely fat patients too.

As for the attempted prevention of obesity, it is likely exacerbating health outcomes across our populations. Weight loss efforts, as well attempting to maintain a weight level below inherited set point, fail. Studies that suggest health screening markers improve in patients with metabolic chronic conditions if they lose weight always avoid the punchline: 0.003% rate of success in maintaining significant weight loss out five years. And there are no longitudinal studies to show whether these attempts to lose weight actually worsen quality of life and mortality incidence in patients who repeatedly attempt to lose weight, as directly prescribed by their physician, because it will ameliorate markers that denote the presence of a risk factor for future onset of disease. And shifting markers is not the same as improving either quality or length of life either.

Obesity is not a risk factor for disease. It is most certainly not a disease.  And in those who are dealing with an adipose organ increase in size, then that change might be a response wherein the enlargement is occurring as a way to buffer the body from the damage associated with the underlying condition in question.

Does obesity cause metabolic syndrome, diabetes, high blood pressure, and all other manner of chronic conditions that merely reflect a marginal increased risk of future onset of actual disease states? I welcome you to show me the evidence, because I’ve spent five and a half years up to my eyeballs in this stuff and I’m not seeing it.

My central point always remains that those with eating disorders cannot indulge in accepting sociocultural myths that are avidly supported by the financial interests of the medical industrial complex for their wars on cancer, obesity, diabetes, high-blood pressure, bad cholesterol and the like. The morbidity and mortality outcomes for an eating disorder are often hotly disputed. Nonetheless, the eating disorder spectrum is considered the deadliest of the mental illnesses out there no matter the mortality statistics you might care to use.

Natural Selection Theory

What benefit could there be for having an endocrine organ capable of enlarging in size in response to certain environmental pressures?

We already know that we’ve got a very small subsection of our population prone to extreme obesity (about 5% of the population). We also know that this subsection tends to correlate with those populations residing in extremely hostile environments (Pima Indians, Inuit, etc.) where extreme metabolic efficiency would likely have been selected for over time. This predisposition to extreme metabolic efficiency was nicknamed the “thrifty gene” but of course it’s not a straightforward genotype with some handy-dandy lone-gene mutation that we can point to. Nonetheless, these individuals with highly efficient adipose endocrine organs are likely optimized for lower-than-optimal energy intake.

It’s one of the great misunderstandings of human evolution that we believe we are optimized for famine. The vast majority of us is not. If you take a look at the middens (garbage heaps) of Paleolithic cultures throughout Europe and pretty much anywhere except sub-Saharan Africa, the Arctic, and the deserts of North America, we positively gorged and had access to endless supplies of sea and river-based foods. Famine was a relatively recent experience for Homo sapiens with the shift to settled agrarian and hierarchical social structure and it’s questionable that that shift has had much time to act on us in any appreciable way (evolutionarily speaking).

We’ve spent all this time assuming that fat was a tissue designed to store up excess energy for famine. But in famine, the entire body is catabolized— fat mass and fat free mass. Everyone is taught that exercise negates fat-free mass loss during energy intake restriction, but in fact it lowers the rate of fat-free mass loss only very modestly. 2

Now that we know fat is not a tissue but our largest endocrine organ, we need to put a new lens on what possible natural selection pressures allow for a significant percentage of our population to, under innumerable and still poorly understood environmental pressures, have that endocrine organ enlarge and that this enlargement appears, on the face of it, to offer up very measurable improved morbidity and mortality outcomes in the presence of several chronic metabolic disease states.

Traits that are naturally selected for are rarely universally good or bad. Mother nature kluges together what she can and she goes with the raw material at hand, so to speak.

The natural selection pressures on our current population of endocrine disruptors in the environment and across-the-board sleep deprivation levels, may preferentially select for those with adipose endocrine organs able to enlarge to produce higher levels of metabolic hormones capable of modulating the impacts of unrelenting stress responses in the face of environmental pressures.

Evolutionary fitness is exclusively defined by the ability to pass those genes along (procreation). That we didn’t have ultra-processed foods in Paleolithic times is as true as the fact that early hominins had to spend 6-8 hours chewing raw food to extract sufficient energy to survive. If you’ve read Dr. Richard Wrangman’s work (book: Catching Fire) then you know that our big brains and small guts could not be supported with raw food. It was the ability of hominin ancestors to make additional energy available through cooking that is likely largely responsible for the presence of Homo sapiens on the planet now.

Except for the fact that ultra-processed foods will not be around long enough to have an impact on our further central nervous system development (because petroleum and its by-products are a finite resource— necessary in ultra-processed food production), we might have experienced our next great evolutionary leap as a result. We do not have some magical point in the past at which we stopped evolving. We are as in it now as we ever were.

We’ve been exposed to massive surplus in our food supplies since we learned how to cook which is why we see the commensurate explosion in our numbers and accompanying utter exhaustion of the marine food chains around the world. We’re the only animals on the planet optimized for the net energy benefits of eating cooked food over raw.

Life Span, Metabolic Conditions & the Fat Organ

Homo sapiens are, depending on the material you want to review, optimized for a life span of somewhere between 75 and 92 years. 3,4 Our theoretical maximum life span has been pegged at somewhere between 113-124 years. 5

It’s easy to confuse life expectancy with expected life span. Life expectancy has increased but that actually reflects a drastic lowering of infant mortality rates combined with the eradication of several transmissible diseases as well. In fact, if you survive childhood, you were as likely to live to your 70s or 80s in Paleolithic times as today. When human populations shifted to agrarian lives, there was an added burden on life expectancy from transmissible diseases that were added to already high infant mortality from nomadic human existence.

For many, many years primatologists simply assumed that menopause in human females reflected living beyond biologically programmed years. It took some serious study on the part of female primatologists to shift the alpha-male focus to uncover that menopause appears to be very much a naturally selected facet of human beings that greatly enhances the survival of that individual’s progeny.

A great book on the topic of shared parenting and its impact on human evolution is Mothers and Others: Evolutionary Origins of Mutual Understanding by Sarah Blaffer Hrdy. If a child-bearing age woman in modern nomadic tribes has her mother available for alloparenting duties, the survival of her children is greatly enhanced.

Natural selection on human beings is multi-generational. And this leads me to a plausible theory surrounding the natural selection of fat organ enlargement correlated with specific metabolic conditions that were, until the medical industrial complex got its hands on it, predominantly conditions of old age.

“Forced expansion of adipose tissue by transgenic overexpression of the adipokine adiponectin prevents metabolic disease despite massive obesity.” 6

Many fattists cannot conceive of there being any value to being fat because, how are you going to go hunting and gathering when you are too big to move? Biomechanical impacts of obesity are heavily hyped in the scientific literature. But there are marked modifications to gait that protect the knees and hips of those who are above BMI 40. 7,8 And even in a thorough systematic review and meta-analysis of hip osteoarthritis and body mass index, the relative risk increase associated with higher BMI is 1.11— that’s magnificently relevant in a statistical sense, but not much of a risk increase at all in a real world sense. 9 Osteoarthritis is not a fat-only condition; it’s predominantly an aging condition. Furthermore, as adiposity increases as you age, then your usefulness in camp as grandma or grandpa may have relegated you to the babysitting of your own progeny’s progeny and not a lot of trudging around for berries or meat in any case.

Let’s get back to adiponectin for a moment. Adiponectin is one of several hormones produced by your fat organ. Interestingly, it is implicated in longevity.

With aging, there is an increased prevalence of type 2 diabetes, cardiovascular disease (CVD), Alzheimer's disease, and cancer. However, exceptionally long-lived humans, that is, those older than 95 years, have survived to more than double their life expectancy at birth, and have often been spared these age-related diseases. Indeed, offspring of centenarians have 50% lower prevalence rates of these diseases than do the control groups, suggesting that they may inherit protection against these major causes of mortality” 10

The authors of the above paper go on to identify two common variants of the adiponectin genotypes that may be implicated in this hyper-longevity in some humans.

Go ahead and just try to find clinical trials that actually compare lean and obese diabetic patients and their inflammatory and adipokine (or adipocytokine) markers. There’s one.

And now it gets weird because the adiponectin levels for the diabetic obese subjects were lower than that of the diabetic lean subjects. So how can obesity be providing better morbidity and mortality outcomes in the presence of diabetes when compared to lean counterparts with the same condition?

The acylation stimulating protein (ASP) and complement C3 (ASP precursor) were as high, or greater, in the lean diabetic group compared to the obese diabetic group. 11 ASP is a hormone produced by adipocytes to stimulate insulin secretion. This is a tiny study with only eight or nine subjects in each distinct group (control, obese, diabetic obese and diabetic lean individuals). There’s not much we can really glean and at present for every trial implicating one particular adipokine in various metabolic conditions and their correlation (or not) to obesity, there’s another suggesting the opposite.

It would be my prediction that these variations of inter-relating adipokine levels in obese vs. lean subjects must somehow be implicated in the improved morbidity and mortality outcomes for the obese subjects when compared to their lean counterparts.

What I can say with absolute certainty is that the lens of scientific inquiry has a short focal length and is entirely zoomed in on the fallacy that obesity itself causes metabolic chronic conditions. I’d go so far as to say it’s very charitable to refer to such inquiry as “scientific” in origin at all.

How many of you were aware that approximately half of the type II diabetic population is over the age of 70? 12 It might possibly be the same number of you who are aware that the risk of breast cancer is highest for women over the age of 80. These are chronic conditions predominantly affecting the elderly— even today with the barrage of electric light (sleep deprivation), endocrine disruptors and mimickers and toxins floating about our daily lives.

Can I currently prove that obesity that appears in response to metabolic chronic conditions, or essentially conditions directly associated with aging, occurs as a way to prolong quality and length of life? No. Nor can I prove that obesity that appears in response to the universal condition of aging has been naturally selected for in our populations because it conferred such survival advantage— directly to progeny in fact. But given that hundreds of researchers have so valiantly poured their souls into “obesity = disease” with ostensibly nothing to show for it, maybe it’s time to start some new lines of inquiry by applying new testable theories into the mix.

Essentially I’m bored with the “obesity bad” stuff — I want some curious and single-minded investigation that goes beyond "obesity bad" and looks at "obesity why?” and “obesity, what benefit?"

1. H Oliveros, E Villamor, Obesity and Mortality in Critically Ill Adults: A Systematic Review and Metaanalysis, Obesity, Vol.16(3), pp.515-521, 2008.

2. JS Garrow, CD Summerbell, Meta-analysis: effect of exercise, with or without dieting, on the body composition of overweight subjects, European journal of clinical nutrition, Vol.49(1), pp.1-10, 1995.

3. H Kaplan, K Hill, Jane Lancaster, A Magdalena Hurtado, A theory of human life history evolution: diet, intelligence, and longevity, Evolutionary Anthropology Issues News and Reviews, Vol.9(4), pp.156-185, 2000.

4. HS Kaplan, AJ Robson, The emergence of humans: The coevolution of intelligence and longevity with intergenerational transfers, Proceedings of the National Academy of Sciences, Vol.99(15), pp. 10221-10226, 2002.

5.  K Aarssen, L De Haan, On the maximal life span of humans." Mathematical Population Studies, Vol.4(4), pp. 259-281, 1994.

6.  CN Lumeng, Carey N., AR Saltiel, Inflammatory links between obesity and metabolic disease, The Journal of clinical investigation, Vol.121(6), pp.2111-2117, 2011.

7. S-u Ko, Seung-uk, S Stenholm, L Ferrucci, Characteristic gait patterns in older adults with obesity—Results from the Baltimore Longitudinal Study of Aging, Journal of biomechanics, Vol.43(6), pp.1104-1110, 2010.

8. P DeVita, T Hortobágyi, Obesity is not associated with increased knee joint torque and power during level walking, Journal of biomechanics, Vol.36(9), pp.1355-1362, 2003.

9. L Jiang, J Rong, Y Wang, F Hu, C Bao, L Xia, Y Zhao, The relationship between body mass index and hip osteoarthritis: a systematic review and meta-analysis, Joint Bone Spine, Vol.78(2), pp.150-155, 2011.

10 G Atzmon, TI Pollin, J Crandall, K Tanner, CB Schechter, PE Scherer, M Rincon et al., Adiponectin levels and genotype: a potential regulator of life span in humans, The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, Vol.63(5), pp. 447-453, 2008.

11. Y Yang, HL Lu, J Zhang, HY Yu, HW Wang, MX Zhang, K Cianflone, Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes, International journal of obesity, Vol.30(3), pp. 439-446, 2005.

12. JL Ubink-Veltmaat, HJG Bilo, KH Groenier, ST Houweling, RO Rischen, B Meyboom-de Jong, Prevalence, incidence and mortality of type 2 diabetes mellitus revisited: a prospective population-based study in The Netherlands (ZODIAC-1), European journal of epidemiology, Vol.18(8), pp. 793-800, 2003.