The Interplay Between Environmental Chemical Exposures and Obesity Proceedings of a Workshop (2016) / Chapter Skim
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5 Other Possible Contributors to Obesity
5 Other Possible Contributors to Obesity
Pages 77-110
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From page 77... ...
The first was reported in 1982 in Science magazine: canine distemper virus, which causes obesity in mice. A variety of other pathogens, including viruses, scrapie agents, bacteria, and even parasites, cause obesity in different animal models, he said.
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From page 78... ...
Ad36 has been associated with a significantly greater prevalence of obesity in a large number of animal models, including chickens, mice, rats, and marmosets. In one experiment with marmosets, for example, the infected animals gained fat about three times as much as the uninfected animals after 6 months.
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From page 79... ...
A great deal of fat accumulated in the liver tissue of the control mice and the Ad2infected mice, while the Ad36-infected mice had much less fat accumulation; indeed, the levels of fat in the livers of Ad36-infected mice fed the high-fat diet were much closer to the fat levels seen in control mice fed the standard chow diet, which have very little fat in their livers (Krishnapuram et al., 2011)
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From page 80... ...
The combined effect is to increase the proliferation of adipocyte progenitors, leading to their differentiation and to lipid accumulation. One interesting finding, Dhurandhar said, is that Ad36 increases glucose uptake by cells.
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From page 81... ...
An obese pperson may nnot remem mber what haappened 3 orr 5 years agoo to trigger tthe obesity, ffor examp ple, whether th here was an in nfection arouund the time oof the onset. A second challeenge is the prresence of muultiple etiologgical factors ffor obesityy, such that itt is very difficcult to attribuute obesity to any one factoor.
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From page 82... ...
So, Dhurandhar said, he and his colleagues have set out to uncover similar indirect evidence to answer the question of whether infections cause obesity. They began by looking for people whose blood held neutralizing antibodies against Ad36, which indicated that they had been exposed to the virus at some time in the past.
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From page 83... ...
This result is very similar, Dhurandhar noted, to the results of the experiments in mice that were infected with Ad36. A 10-year prospective study of 1,400 men and women found similar results.
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From page 84... ...
To me, it does look like an infectious disease spreading through the United States." Discussion Lynn Goldman of the Milken Institute of Public Health at George Washington University opened the discussion session with a question about the modes of transmission of Ad36. Is there, for example, maternal–fetal transmission?
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From page 85... ...
Linda Birnbaum of the National Institutes of Environmental Health Sciences (NIEHS) asked if it would be worthwhile to do studies looking at what happens when people are exposed both to infectious agents and to environmental chemicals, because it is known that environmental exposures can alter susceptibility to infectious agents.
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From page 86... ...
"In the era of electronic health records and health information exchanges," he said, "we have a new kind of substrate to look at the way health is played out in the delivery of normal clinical care that incorporates the work of lots of unnamed collaborators seeing patients every day and lots of patients who have entrusted us with their data." Bailey began by describing two studies that laid the groundwork for the study of antibiotics and obesity. The first was a cohort study in the United Kingdom that followed more than 10,000 children from birth
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From page 87... ...
Surveys and parental recall were used to estimate environmental exposures for the children, while growth parameters were measured directly and obesity rates could be estimated directly at several time points up through 7 years of age (Trasande et al., 2013)
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From page 88... ...
, the researchers found that the two agreed very well. In particular, their estimates of the prevalence of obesity among the children in the pilot study sample matched the obesity rates from NHANES quite closely, which gave them confidence that it was reasonable to use data from the clinical records to measure obesity in populations of children receiving both well-child care and acute care.
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From page 89... ...
The data showed that the vast majority of the antibiotic prescriptions were for common childhood infections, such as ear infections, pneumonia, or sinus infections. To determine obesity rates, the researchers collected data on BMI for 3 years beginning at 24 months of age.
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From page 90... ...
Hispanic ethnicity but not membership in other racial and ethnic groups was associated with increased obesity. Public insurance coverage -- a rough indicator of a lower socioeconomic status -- was also associated with an increased risk of obesity, although there was no difference in obesity rates between children in urban versus suburban practices.
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From page 91... ...
It is important to underscore that there may be unintended effects at work here." It remains to be seen exactly what is mediating the association between antibiotics and obesity risk, if indeed the antibiotics are playing a causal role. Because the obesity occurs well after the antibiotic use, the association cannot explained by temporary deflections in a child's growth trajectory or by perturbations in the gut microbiome at the time of exposure, he said.
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From page 92... ...
She began by showing a couple of videos, one made in 1970 and one made much more recently, of doctors saying that it is calories, not sugar per se, that people have to be careful of -- that as long as you keep the total calories low enough you do not gain weight and that sugar itself poses no risks. Erkin-Cakmak said that this view is too simplistic and that science has something else to say.
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From page 93... ...
Forty percent of people in the United States who are of normal weight also suffer metabolic dysfunction, she said -- again, type 2 diabetes, hyperlipidemia, and hypertension. The prevalence is less among those who are of normal weight than among those who are obese, but the metabolic dysfunction is still a problem.
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From page 94... ...
While visceral fat is not good, liver fat is even worse and is associated with poor health. For example, a study done in South Korean adults found that nonalcoholic fatty liver disease was a
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From page 95... ...
This is why alcoholics suffer from hypertriglyceridemia, high blood levels of triglycerides. Some of the newly synthesized lipids, very low density lipoproteins, participate in the generation of liquid droplets that are stored in the liver, which results in alcoholic fatty liver disease.
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From page 96... ...
The researchers found that those who consumed one or more cans of sugar-sweetened beverage per day had a 29 percent greater risk of developing diabetes, after adjusting for energy intake and BMI. In an international study looking at diet and diabetes, researchers used data from the Food and Agriculture Organization on the total number of calories consumed and the consumption of fruits, oil, sugar, meat, cereals, roots, nuts, and vegetables.
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From page 97... ...
Given all of these different forms of evidence pointing to the role of fructose in metabolic syndromes and particularly in diabetes, ErkinCakmak concluded by saying that understanding of the role of diet in disease must change. Discussion In the discussion session following the presentation, Linda Birnbaum of NIEHS asked if there is any information about what fructose consumption might do to the microbiome.
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From page 98... ...
For saccharin, this is 5 milligrams per kilogram of body weight, or about the amount in three sodas sweetened with saccharin. For sucralose, the ADI is equivalent to five sodas per day, and for acesulfame potassium the ADI is equivalent to about 30 sodas per day.
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From page 99... ...
"There are things that we really don't understand yet." In the intestine, endocrine cells have sweet taste receptors that respond to sugars by increasing the level of incretin hormones. These hormones lead to an increase in insulin levels and thus a decrease in blood glucose levels.
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From page 100... ...
From Fowlerr et al., 200 08. in weight gain is not particularly noticeaable -- only an additional 3 pounds for that 5-ffoot-6-inch, 155-pound p erson.
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From page 101... ...
In mature adipocytes, artificial sweeteners cause a decrease in lipolysis, or the breakdown of lipids, so that more lipids accumulate in the cells. There is also decreased lipolysis in human mesenchymal stem cells.
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From page 102... ...
There were a variety of differences: the artificial sweetener users had higher BMIs and higher levels of hemoglobin A1C, for example. Everything was a little worse for that group, Rother said, but she added that she did not find the human data in that paper to be particularly convincing, other than showing that the microbiome in people who consume artificial sweeteners looks different from the microbiome in those who do not, which is not particularly surprising.
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From page 103... ...
They carried out oral glucose tolerance tests with 22 healthy adolescents and young adults ranging in age from 12 to 25 years in which changes in the blood levels of glucose and certain hormones were tested at various points in time after the subject was given a large dose of glucose. Before giving them the glucose and starting the test, they gave the subjects either mineral water or a diet soda with sucralose and acesulfame potassium.
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From page 104... ...
All of them gained weight, of course, because they were growing children, but the sugar-sweetened group gained more weight than the children who received the drink with the artificial sweetener. The main problem with the study, Rother said, is that there was no group of children who drank just water, so it is impossible to know how children who drink diet sodas would fare versus those who drink just water, but the experiment did clarify one thing: "We know now that if you drink soda, you gain weight beyond what you should gain," Rother said.
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From page 105... ...
On the other hand, there are clear data showing that, in vitro, artificial sweeteners lead to more adipogenesis, less lipolysis, and more insulin secretion than sucrose. It is also clear that artificial sweeteners can affect the intestinal microflora and, in lab animals at least, that they can lead to higher glucose levels and greater weight gain.
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From page 106... ...
Second, he said, while research usually involves isolating one factor out of many and examining how it affects other things, in nature various factors work together and thus need to be considered in conjunction with one another. He mentioned as an example a study of animal models of celiac disease that found four different factors had to exist at the same time for the celiac disease to be expressed.
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From page 107... ...
Bailey replied that in the health services study that he and his colleagues did, they found no association between obesity and such infections as colds or upper respiratory infections. Furthermore, once the use of antibiotics was taken into account in the multivariate analysis, such infections as inner ear infections were not associated separately with obesity.
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From page 108... ...
Linda Birnbaum of NIEHS responded that it is not necessary to wait for 100 percent understanding and certainty before taking action. A lot of information is available from mechanistic studies, animal studies,
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From page 109... ...
2005. Human adenovirus-36 is associated with increased body weight and paradoxical reduction of serum lipids.
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From page 110... ...
2014. Artificial sweeteners induce glucose intolerance by altering the gut microbiota.
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