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Wildfires in Los Angeles. Flooding in Miami. While we were looking elsewhere—or trying to cover our eyes—Minnesota became the second-fastest warming state in the country. The pine forests will swoon. Some of our iconic animals—moose, lynx, loons—will move up north.
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The obesity epidemic is a global issue and shows no s of abating, while the cause of this epidemic remains unclear. Marketing practices of energy-dense foods and institutionally-driven declines in physical activity are the alleged perpetrators for the epidemic, despite a lack of solid evidence to demonstrate their causal role.
While both may contribute to obesity, we call attention to their unquestioned dominance in program funding and public efforts to reduce obesity, and propose several alternative putative contributors that would benefit from equal consideration and attention. Evidence for microorganisms, epigenetics, increasing maternal age, greater fecundity among people with higher adiposity, assortative mating, sleep debt, endocrine disruptors, pharmaceutical iatrogenesis, reduction in Summers fat women adult matures over mpls is the worst of ambient temperatures, and intrauterine and intergenerational effects, as contributing factors to the obesity epidemic are reviewed herein.
While the evidence is strong for some contributors such as pharmaceutical-induced weight gain, it is still emerging for other reviewed factors. Considering the role of such putative etiological factors of obesity may lead to comprehensive, cause specific, and effective strategies for prevention and treatment of this global epidemic. The prevalence of obesity has increased substantially since the mid th century.
Although there seems to have been an accelerated rate of increase somewhere aroundat least in the United States Baskin et al. Within the United States, this increase has occurred in every age, race, sex and socioeconomic group. Although recent evidence suggests that the prevalence of obesity may have begun to asymptote within some segments of the U. Ogden et al. Obesity has not only increased in the United States but also seems to have increased in virtually every country where detailed data are available Caballero, Reasons for this increase are incompletely understood Keith et al.
That is, when we question the strength of the evidence of the big two as contributors, or certainly the chief and near sole contributors to the obesity epidemic, we are not questioning the importance of energy intake and energy expenditure, including physical activity energy expenditure in influencing obesity levels.
Our questioning of the big two stems from two points. First, the evidence supporting various elements of the big two as contributors to individual or population levels of obesity is often quite weak. Second, even though some elements of the big two do very likely play some role in influencing obesity levels, we believe that an unquestioned assumption of their preeminence has led to the possibly ill-advised expenditure of public effort and funds on programs aimed at reducing population levels of obesity that and has also reduced the exploration of other potential causes and the alternative obesity reduction programs that might stem from their identification.
The big two seem to be accorded special status in many dialogues and writings on obesity such that our usual healthy scientific skepticism is held back when considering them. Perhaps this is because the Big Two as explanations for obesity appeal to a prevalent anti-corporate sentiment Crossley, or perhaps because they have an intuitive appeal based, in part, on their simplicity and the fact that they require little specialized knowledge to comprehend and deal with easily observable aspects of life with which all of us are familiar.
Regardless of the cause, as scientists, we should retain our skepticism toward all hypotheses and our open-mindedness to new hypotheses. What are some of the specific facts that enhance our skepticism of the big two as near-omnipotent causes of the obesity epidemic?
We make no pretext of offering an exhaustive consideration of evidence for or against the big two, but rather highlight a few bullet points that reinforce our skepticism. Restaurant Dining. Restaurant dining and fast-food restaurant dining in particular have been considered as major contributors to the obesity epidemic.
Yet, Anderson and Matsa conducted an analysis of a nationally representative sample of 3-day food records and found that while diners at fast food restaurants ate roughly — kcal more during restaurant meals, they largely compensated by eating less at other occasions such that the net increase in energy intake associated with restaurant dining was extremely small i. Physical Education. Some argue that a reduction in the frequency of physical education PE is a major contributor to obesity.
Yet the evidence that PE frequency has decreased is itself questionable Sturm, and some studies in children report that the frequency of participation in sport has increased Salmon et al Regardless of changes in frequency of PE offerings or participation, much evidence suggests that standard PE classes have no appreciable impact on obesity levels Cawley et al. Sidewalks and the Built Environment.
HFCS consumption but not necessarily fructose per se has increased substantially in the last several decades and has been speculated to be a contributor to the obesity epidemic Bray et al ; Welsh et al Yet, a critical review Forshee et al. Vending Machines. Vending machines have been discussed as a threat to childhood overweight and obesity and changes in school policy have been made to reflect this view Sothern et al Yet little to no extant evidence indicates that vending machines have contributed to the problem Faith et al.
These are just a few examples and we do not wish to imply that any of the hypothesized influences described in the bullet points above merit being summarily dismissed. Further research on many aspects of the big two is clearly warranted. Our point is merely that we do not have conclusive evidence that the big two or their individual elements are the preeminent contributors to the obesity. And yes, portion sizes and caloric intake have increased.
Contemporary life has become more sedentary, with more time spent in front of the computer and TV screens and less time engaging in rigorous activity As scientists we believe that we can and should do our part to offer a more sophisticated and data-based view of obesity.
Outside the circle of public health advocacy discussions, scientists widely and readily acknowledge that multiple factors contribute to obesity including but not necessarily limited to genetic, dietary, economic, psychosocial, reproductive, and pharmacologic factors. Our purpose here is to expand upon our brief discussions elsewhere Keith et al.
We introduce one or two additional factors not covered by Keith et al. We do not discuss two factors covered in that article, namely reductions in smoking prevalence and demographic changes, because we believe that they are so well documented and supported that little further review of the evidence is needed at this time. For a useful recent consideration of the influence of smoking reduction on obesity, see Baum While the role of decreased smoking in the obesity epidemic is an important observation, it does not change the fact that smoking is an unhealthful habit that we would not wish to promote.
Similarly, demographic changes may play a role in obesity, but they are not subject to manipulation by reasonable public policy. For these reasons, we do not consider smoking and demographic changes further herein.
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Although there is some variation from one putative cause to another, we generally seek evidence of the following types. Ecological Correlation. This is generally the weakest form of evidence but worth reviewing because it provides a basis for hypothesis generation and can offer additional support to an overall body of evidence. Ecological correlative evidence would typically involve showing that the amount of the putative contributing factor has increased over time during the same period that obesity has increased or is positively correlated with obesity levels across populations e.
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Individual Level Epidemiologic Correlation. This is a somewhat stronger form of evidence because we can, in principle, make better attempts to control for potential confounding factors. Such evidence, though stronger than ecological correlation, can still only demonstrate association and not causation.
Non-Human Experimental Evidence. Such data including that derived from cell line and model organism studies, are usually very convincing because they can provide us with evidence about causation and the mechanisms of action. However, such evidence always leaves extrapolation to humans open to question.
Human Experimental Evidence. Human experimental evidence by experimental we mean studies in which subjects are randomly ased to different levels of the independent variable under study can offer evidence about causation in humans and are likely the best evidence we can obtain. Unfortunately, such evidence is often limited in the present context for several reasons.
First it is often impractical or unethical to randomly as people to be exposed to the factors under study e. Second, even when randomized experiments can be done it is often difficult to do them with sufficient fidelity on a large scale and for a sufficiently long period of time to permit confident conclusions about long-term population effects. Thus, the evidence available in this realm is often limited to small, short-term, or laboratory analogue studies. For each of the putative causes we will review, we seek evidence in each of the described above to provide a picture of the strength or lack thereof of the entire body of evidence.
Although ten different microbes have been reported to cause obesity in various experimental models Pasarica and Dhurandharthe possible contribution of infections in the etiology of human obesity is often overlooked. Considering the etiological role of infections in several other chronic diseases, Dhurandhara relationship between infections and obesity is plausible.
The close interaction between the function of the immune system and adipose tissue adds to this plausibility.
Adipocytes and macrophages share many similar functional characteristics, and they are in fact so similar that preadipocytes have the ability to differentiate into macrophages Charriere et al Therefore, it is plausible for adipose tissue to expand in response to certain infections, as a direct consequence or by shifting of the organism to surplus energy state.
Experimental infection of animal models with obesity-promoting microbes in increased adiposity, demonstrating a direct cause-and-effect relationship.
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These experimental models range from non-human primates to insects and include rodents and chickens. Canine distemper virus CDV was the first reported obesity promoting virus Lyons et al In mice infected with CDV, obesity develops after acute infection has abated and when no virus is detectable. CDV decreases levels of melanin concentrating hormone Veraeten et aland down-regulates leptin receptors in the hypothalamus, Bernard et al which may promote positive energy balance in this model. Other infectious agents have also been examined in this context.
Ten putative contributors to the obesity epidemic
The main effect of RAV-7 that may contribute to adiposity is a decrease in thyroid hormone levels Duff et al In addition, Borna Disease virus has been found to cause obesity in rats Gosztonyi et alby damaging the hypothalamus and by neuroendocrine dysregulations Herden et aland scrapie agents have been reported to induce obesity in mice Kim et al ; Carp et al Although the exact adipogenic mechanism is unknown, Scrapie agents disrupt normal glucose metabolism, with hyperglycemia resulting in disrupted transvascular glucose transport in some regions of the brain Vorbrodt et alwhich may lead to functional dysregulation of hypothalamus and consequential adiposity.
Next, four adenoviruses were reported to promote obesity. Animals experimentally infected with SMAM-1, an avian adenovirus, or three human adenoviruses, adeneovirus AdAd-5, and Ad developed increased adiposity Dhurandhar et al ; ; ; ; ; Whigham et al ; So et al compared to controls despite similar food intake. Originally un-infected cage-mates of the experimentally infected chickens acquired the virus via horizontal transmission and developed visceral adiposity. Paradoxically, the increased adiposity due to SMAM-1 infection was accompanied by a reduction in serum cholesterol and triglycerides.
Like SMAM-1, Ad increases adiposity in experimentally infected chickens, as well as rats, mice and marmosets non-human primates Dhurandhar et al ; ; ; Pasarica et alwithout inducing detectable hyperphagia, and reduces serum cholesterol and triglycerides Dhurandhar et al;Dhurandhar et al; ;. In the rat model, Ad appears to exert both, central and peripheral effects Pasarica et al Ad decreased norepinephrine levels in the paraventricular nucleus, arcuate nucleus, dorso-medial hypothalamus and ventro-medial hypothalamus.
Other neurotransmitters such as dopamine and 5-hydroxyindolacetic acid concentrations were also reduced in some of these brain regions. On the other hand, Ad increased whole body insulin sensitivity and enhanced expression of genes involved in the adipogenic and de-novo lipogenesis pathway such as fatty acid synthase FAS and acetyl-CoA carboxylase ACC-1 Vangipuram et al Just four days following infection, Ad36 spre to adipose tissue, liver, kidney, and brain, lowers inflammatory cytokine levels, and infected rats have increased epididymal fat pad weight Pasarica et al b.
The adipogenic role of Ad36 was recently confirmed independently by another research group Thomas et alwho showed that Ad36 could be used as a tissue engineering tool for building adipose tissue. Recently, more human adenoviruses were tested for their adipogenic potential in animal models. Six subgroups classify adenoviruses by genetic similarity. Adenovirus type 5 Ad-5 induced adiposity in mice So et aland Adenovirus 37 Ad increased adiposity in chickens, whereas other two human adenoviruses Ad-2 and Ad are non-adipogenic in chickens Whigham et al Thus, the adipogenic effect is not shared by all adenoviruses, but appears specific to certain serotypes.
Adipogenic potential of remaining the 45 known human adenoviruses has not been tested.