ScienceWeek

SCIENCEWEEK

July 28, 2007

Vol. 11 - Number 29

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I thank God I was not made a dextrous manipulator; the most important of my discoveries have been suggested to me by my failures.

-- Humphry Davy (1778-1829)

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Contents (full text below):

1. Paleontology: Variation and Early Evolution

2. Materials Science: Filling a Void

3. Physics: Pierre-Gilles de Gennes (1932-2007)

4. Book Review: Psychology: The Nature of Belief

5. Astrobiology: Photosynthesis in Watercolours

6. Developmental Biology: A Ten Per Cent Solution

7. Inflammatory Disease: Assault on the Guardian

8. Obituary: Horst Tobias Witt (1922–2007)

9. Unravelling the Pathogenesis of Inflammatory Bowel Disease

10. The Spread of Obesity in a Large Social Network over 32 Years

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1.

Science 27 July 2007: Vol. 317. no. 5837, pp. 459 - 460 DOI: 10.1126/science.1145550

Paleontology: Variation and Early Evolution

Gene Hunt

Variation is often said to be the raw material for evolution. In the absence of heritable variation, no mechanism--natural selection included--can cause evolutionary change within populations. That variation is necessary for evolution is uncontroversial, but scientists have long wondered if abundant variation might play a more active role in facilitating or channeling evolutionary change (1, 2). Any evolutionary influence of variation would presumably operate continually, but there have been some indications that during the Early Cambrian (542 to 513 million years ago), the link between variation and evolutionary divergence may have been especially strong.

At roughly the same time as the greatest known burst of biological innovation, the Cambrian Explosion of animal body plans, it appears that species may have been unusually variable in their morphology. Although intriguing, the evidence for this increased Cambrian variability has been somewhat equivocal. However, on page 499 of this issue, Webster (3) presents the results of a novel analysis of trilobite variability that puts this pattern on much firmer empirical footing. He reports that during the heyday of innovation in the Cambrian, trilobite species were in fact unusually variable, more so than at any other time in their history.

Previous suggestions of elevated Cambrian variability involve a variety of taxa, but special emphasis has been placed on trilobites (4, 5), which have by far the richest fossil record during this interval. One commonly cited example is the number of body segments in the thorax of adult trilobites. Within some Cambrian species, this feature is variable, whereas in post-Cambrian trilobites, the number of segments is almost always fixed within species, and often within higher taxonomic levels such as genera and families (6). As interesting as this example is, it applies to only one trait and a small number of trilobite species. More convincing evidence for enhanced variation would require a broader and more systematic survey of characters and traits, but there are formidable obstacles to measuring variation in a meaningful way across very different traits and taxa.

Webster gets around these difficulties by cleverly exploiting a large set of expert observations already in existence. Since the advent of cladistic methods in systematics, specialists generally represent their morphological observations as explicitly defined characters with discretely coded character states. For example, a character might reflect the number of ridges in a defined region of the trilobite head, and there would be different character states corresponding to the presence of one ridge, two ridges, and so on. Systematists not only record the character state attributed to each species in a study but also usually indicate for each character which species were variable. Such coding of species represented by individuals with two or more different character states is called "polymorphic" by systematists.

By tracking the preponderance of polymorphic versus invariant characters over time, Webster was able to document a dramatic pattern: In the early intervals of trilobite evolution (the Early and Middle Cambrian), polymorphism was much more common than in any subsequent period of trilobite history. Because the elevated polymorphism was not limited to any particular kinds of traits, trilobite species during these early intervals were very likely to have been exceptionally variable in their overall morphology. Moreover, this period of elevated polymorphism occurs at the same time that trilobites were diversifying taxonomically and morphologically, suggesting to Webster that elevated variation may have promoted the radiation of trilobites. Although this large data set of observations is not a random sample of trilobite lineages or traits, a variety of sensitivity analyses suggest that whatever its biases, they do not appear to change markedly over time.

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2.

Science 27 July 2007: Vol. 317. no. 5837, pp. 460 - 461 DOI: 10.1126/science.1146517

Materials Science: Filling a Void

Stephanie L. Brock

Porous inorganic materials are widely used as filters and catalysts--applications that involve the transport of molecules or ions to reactive surfaces. Such materials include zeolites and mesoporous solids (both of which have ordered pore structures), as well as dried gel structures such as aerogels (with a disordered pore structure). The materials vary in the number, size, and distribution of pores, but with few exceptions, they are oxides. This "chemical exclusivity" has severely limited their potential applications. Thus, zeolites efficiently absorb calcium and magnesium ions and are therefore effective water-softening agents, but they are largely ineffective for remediation of heavy metal ions, such as mercury or lead.

The problem with oxides is that they prefer to form bonds with small metal ions such as magnesium and zinc. Heavy metals are large and polarizable and cannot be effectively bound by porous oxides. One way to get around this problem involves modifying the surface of the oxide so that it presents a larger, more polarizable binding atom, such as a sulfur group, permitting selective adsorption of heavy metal ions (1). On page 490 of this issue, Bag et al. report another approach (2): They use a sol-gel reaction to construct porous solids that are analogous to oxides but contain the heavier chalcogenides (such as sulfides or selenides) instead of oxide. The resulting chalcogenide aerogels selectively bind heavy metals without requiring modification.

A few methods for making porous chalcogenide aerogels have previously been reported. These methods used either thiolysis chemistry, in which molecular metal precursors are reacted with hydrogen sulfide (3), or the oxidative condensation of preformed metal chalcogenide nanoparticles (4). The method reported by Bag et al. promises additional flexibility because it starts from molecular ions or small clusters of semiconducting metal chalcogenides and uses metal ions as linkers. Both the cluster and the metal ion can be varied to adjust the properties of the resulting material.

This general approach--the linking of chalcogenido clusters with metal ions--has been previously used to prepare mesostructured chalcogenides (5-8). In these studies, surfactants served as templates, organizing the metal chalcogenide component around the micellar structures, analogous to the synthesis of mesoporous aluminosilicate materials (9). However, in contrast to mesoporous aluminosilicates, attempts to remove the surfactant by washing or heating resulted in collapse of the pore structure. The present surfactant-free strategy is simpler, eschewing order completely, yet generating stable porous structures.

Bag et al. use a metathesis (or partner-switching) reaction between a metal chalcogenide salt and tetrachloroplatinate in aqueous solution to obtain a solvent-swollen chalcogenide polymer. Wringing out this "sponge" without collapsing the structure can be achieved by drying from a supercritical solvent, producing an aerogel [a term that refers to the fact that the pore solvent has been replaced by air (10)].

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3.

Science 27 July 2007: Vol. 317. no. 5837, p. 466 DOI: 10.1126/science.1146688

Physics: Pierre-Gilles de Gennes (1932-2007)

Armand Ajdari

Described as the "Isaac Newton of our time" by the Royal Swedish Academy in the citation for his Nobel Prize in Physics in 1991, Pierre-Gilles de Gennes died on 18 May 2007 at the age of 74. Beyond the remarkable lecturer and the advocate of science and scientific research cherished by media and students, Pierre-Gilles de Gennes was above all one of the greatest physicists of the 20th century. The depth and breadth of his scientific achievements are exceptional. In the last year of his life, de Gennes published articles in five different areas, from the motion of dislocations in the quantum regime to the storage of olfactory information in the brain.

De Gennes was born in 1932 to a family of medical doctors. He began his academic career at the Ecole Normale Supérieure in Paris, followed by 4 years at the Commissariat à l'Energie Atomique in Saclay. In his early work, he focused on magnetism, studying the scattering of neutrons in metallic materials close to magnetic transitions, as well as questions regarding spin waves and rare earths. A postdoctoral stay at Berkeley in the group of Charles Kittel followed, before a 2-year stint in the French Navy.

Moving to Orsay in 1961, de Gennes founded an experimental and theoretical effort on superconductors. His work led to important insights into surface superconductivity and into superconductivity without band-gap. Around 1968, de Gennes began to revisit the field of liquid crystals, drawing fruitful formal analogies with superconductors. His insights had a substantial impact on the physical understanding of these materials, which now play an important part in many technologies such as liquid crystal displays.

In 1971, de Gennes was appointed professor at the Collège de France. He then shifted his interest to polymers and to other topics previously categorized as chemistry. Drawing on his creativity, his genius at simplifying problems, and his ability to establish connections with sophisticated formal theories of statistical physics, he demonstrated the power of physics in dealing with these systems. This field is today called soft condensed- matter physics. As he had done previously, de Gennes teamed up with experimentalists at the Collège de France, in Saclay, and in Strasbourg to stimulate his creativity and validate his predictions.

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4.

Science 27 July 2007: Vol. 317. no. 5837, p. 456 DOI: 10.1126/science.1142653

Book Review: Psychology: The Nature of Belief

Reviewed by Scott Atran

Six Impossible Things Before Breakfast: The Evolutionary Origins of Belief

by Lewis Wolpert. Faber and Faber, London, 2006. 243 pp., £14.99. ISBN 9780571209200. Norton, New York, 2007. 255 pp. $25.95. ISBN 9780393064490.

In explaining why he wrote Six Impossible Things Before Breakfast, Lewis Wolpert describes a disturbing encounter with his son's envious belief that father has the advantage in life because he is likely to die sooner and enjoy heaven. In August 2005, while with Muslim mujahedin in Sulawesi, I noticed tears welling up in my traveling companion, Farkhin (who helped bomb the Philippine ambassador's residence in Jakarta and had hosted 9/11 mastermind Khalid Sheikh Mohammed) when he heard of a young man killed in a skirmish with Christian fighters. "Farkhin, you knew the boy?" I asked. "No," he lamented, "but he was only in the Jihad a few weeks; I've been fighting since Afghanistan [late 1980s] and I'm still not a martyr."

In trying to grasp his son's belief as well as the beliefs of people like suicide bombers and today's great clashes among religious and political beliefs, Wolpert draws fresh insight from the biological and evolutionary roots of belief. He surveys a vast domain that begins with children's innate ideas about the differences between how inert objects and animate agents like people interact and ends with the almost miraculous breakaway of scientific beliefs from our intuitive understanding of the world: there are more molecules in a glass of water than glasses of water in the oceans. We find out that other primates lack mental equipment for mind reading. They can't represent or embed another's beliefs in their own thoughts ("John believes that Mary thinks that…"). Thus they can't understand how they or others can have false beliefs or conceive of fiction, God, or scientific truth. And we learn why other animals can't truly imitate or learn a new dance and why homeopathic medicine and psychotherapy involve "beliefs related to witchcraft."

The book's unifying theme is that all belief is ultimately rooted in causal understanding and has its evolutionary origins in the use and manufacture of tools. This lets Wolpert scan the landscape of belief with clarity and direction but leads down the wrong path in key areas. He argues that managing fire "might have been one of the origins of market exchange, and might have led to the advantage of humans knowing about numbers." Yet defining aspects of number, such as the concept of a class of similar classes or of infinite discreteness, relate more to categorization processes and language structure than to causality. We are told "Verbs ranging from 'go' to 'hit' to 'throw' require causal thinking … an essential prerequisite for language development." Now Kanzi, a brilliant bonobo, can use symbolic tokens to reference causal relations between actions and goals; however, Kanzi's strings are usually action-action combinations, such as "chase bite." These strings employ two "predicates" and no subject. No human language allows sentences that have no syntactic arguments and thus cannot express a subject-predicate proposition. Hominid tool play tells us little of testable, scientific interest about linguistic structure, number, or markets.

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5.

Nature 448, 418 (26 July 2007) | doi:10.1038/448418a; Published online 25 July 2007

Astrobiology: Photosynthesis in Watercolours

John Raven

The spectrum of stellar radiation available to an organism is altered by the atmosphere and water on the planet it inhabits. Study of this relationship can outline the limits to photosynthesis.

Water is essential for life 'as we know it', and the search for life 'as we don't know it' elsewhere in the Universe centres on the search for evidence of water1. But the properties of water that make it essential for organisms and their environments can also restrict organisms' activities. An example that has now been re-investigated by Kiang et al.2, 3 and by Stomp et al.4 is the wavelength dependence of the absorption of electromagnetic radiation by water, and also by permanent atmospheric gases. Such studies can inform our understanding of the distribution and pigmentation of photosynthetic organisms on Earth2, 3, 4, and on any life-supporting Earth-like planets in other solar systems.

This biological dark side of water — its absorption of solar electromagnetic radiation — creates habitats that restrict or eliminate the roles of solar radiation in supplying energy for photosynthesis and information to sensory systems. The effective absence of solar radiation deep in large bodies of water such as lakes and oceans has long been recognized, and limits photosynthesis with this energy source to at most the top few hundred metres of water bodies, and to the land surface. The significance of water's wavelength-dependent attenuation of solar radiation for photosynthesis by aquatic organisms has been recognized since the late nineteenth century. Engelmann5, with his theory of complementary chromatic adaptation, suggested in 1883 that the depth at which seaweeds with different pigments grow might be related to the spectrum of incident radiation they receive.

Later work showed that Engelmann had underestimated the role of dissolved and suspended material in modifying the radiation attenuation due to water alone, and that, even when this was taken into account, the quantitative significance of complementary chromatic adaptation of seaweeds in nature was small6. But Engelmann's perception was a great stimulus to study of the photosynthetic pigmentation and the radiation environment of organisms in relation to the absorption of radiation by water. That work has extended to anoxygenic organisms (photosynthetic bacteria)2, 3, 4 — that is, those whose photosynthesis does not generate oxygen — as well as being carried out on the oxygenic organisms considered by Engelmann, and also to other planets that might support life4. On Earth, the advent of anoxygenic organisms preceded that of oxygenic ones.

Kiang et al.2 surveyed the diversity of photosynthetic organisms, and propose constraints on the evolution of the pigments that harvest and transform radiation. One is the wavelength of the peak photon flux in the environment. Another is the longest wavelength that has sufficient energy per photon to bring about the appropriate photochemical reaction (in which photon energy is converted into chemical energy). Organisms that produce oxygen from water, a very energy-intensive reaction, are constrained to using shorter wavelengths than are those that do not produce oxygen. This is the case despite the oxygen producers using two photochemical reactions in series, rather than a single reaction, as seen in anoxygenic organisms. The sorts of photochemistry that can occur, and the pigmentation of the organisms, are greatly influenced by the absorption of solar radiation by water (and oxygen) in the atmosphere and, for aquatic organisms, in the water body in which they live2.

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6.

Nature 448, 420-421 (26 July 2007) | doi:10.1038/448420a; Published online 25 July 2007

Developmental Biology: A Ten Per Cent Solution

John Reinitz

In early embryos, a concentration gradient of the Bicoid protein affects pattern formation. Studies of living embryos reveal a surprising level of accuracy in the Bicoid gradient. But is it accurate enough?

A central idea in developmental biology is Lewis Wolpert's theory of positional information1. This states that a substance present in a concentration gradient induces different developmental fates in cells when present at different concentrations. The first such morphogenetic gradient to be identified was that of the gene transcription factor Bicoid in embryos of the fruitfly Drosophila melanogaster2, 3. This protein is distributed with an exponential profile, with its concentration decreasing towards the posterior pole of the embryo. Although the importance of the Bicoid gradient in specifying cellular fates was established, quantitative puzzles remained. These problems have now been largely solved by Gregor and colleagues4, 5 in two papers in Cell.

A previous study6 had shown that the Bicoid concentration gradient varied far more widely between embryos than did the expression of the hunchback (hb) gene, which is used as a readout of the effect of Bicoid concentration. This and other studies, however, were performed in fixed tissue, where it is impossible to determine absolute protein concentrations or to follow changes in gene expression over time.

Gregor et al.4 tagged Bicoid with enhanced green fluorescent protein (eGFP), which allowed them to directly observe its gradient in live embryos. For this, the authors constructed a genetic line of fruitflies in which the bicoid gene (bcd) was replaced by a functional bcd–egfp fusion gene. They then monitored the gene's protein product by time-lapse microscopy during the blastoderm stage of early embryonic development.

In early Drosophila development, the embryo is a syncytium — it consists of a mass of cytoplasm, with nuclei that are not separated by cell membranes. The nuclei undergo a series of 13 rapid divisions, with the blastoderm forming at about division 10. The authors found that it is at division 9 — before blastoderm formation — that Bicoid–eGFP is first detected. As it is a DNA-binding protein, Bicoid is localized in the nucleus. But as nuclei lose their envelopes during each division, internally stored Bicoid is released into the cytoplasm.

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7.

Nature 448, 421-422 (26 July 2007) | doi:10.1038/448421a; Published online 25 July 2007

Inflammatory Disease: Assault on the Guardian

Richard M. Ransohoff

In multiple sclerosis, the immune system attacks 'self' tissues. Ten years after the discovery of one target of this autoimmunity, work with mice identifies it as a guardian protein produced in response to inflammation.

On page 474 of this issue, Ousman and her co-workers1 describe how autoimmunity to a protein known as alphaB-crystallin (CRYAB) can contribute to inflammatory injury of the central nervous system. They show that autoimmune attack on CRYAB does not directly cause tissue damage. Rather, it worsens the severity of damage by simultaneously eliminating two of the protein's functions — its action as a restraining element for inflammation, and its ability to inhibit programmed cell death of glial cells in the nervous system.

The clinical context for this research is multiple sclerosis (MS), an inflammatory disorder of the human central nervous system. This disease selectively targets myelin, the complex, lipid-rich membrane that enwraps some nerve axons. Its connection with CRYAB began with an experiment that challenged orthodoxy: in 1995, van Noort et al.2 reported CRYAB to be a predominant target of autoimmunity in MS. They discovered CRYAB's significance by isolating myelin proteins from MS autopsy material, and determining these proteins' ability to act as autoantigens in evoking a reaction from T cells. These are major players in the immune system, and both produce and are stimulated by cytokine messenger molecules.

The group's finding2 came as a surprise. During many years of research on autoimmune models of MS (known collectively as experimental autoimmune encephalomyelitis, or EAE), investigators had identified several myelin proteins with encephalitogenic potential. Encephalitogenicity implies that immunization with the protein, or with a peptide derived from it, could elicit an autoimmune reaction, characterized by inflammation, demyelination and weakness of the limbs. Known encephalitogenic agents includedthe principal proteins of myelin — myelin basic protein and myelin proteolipid protein — as well as minor components, such as myelin oligodendroglial glycoprotein (MOG).

Van Noort and colleagues took the road "less traveled by" and focused on myelin from patients with MS. Previously, the usual assumption had been that any autoantigen present in myelin would be a constituent of the healthy tissue. CRYAB was distinctly an outlier, because it is expressed only at low levels in myelin derived from the non-diseased central nervous system3. It belongs to the family of small heat-shock proteins that are produced by all cells in response to stress. CRYAB is also an oddity among heat-shock proteins, however, being expressed selectively in the eye lens, in skeletal and cardiac muscle, and in glial cells, including oligodendrocytes (the cells that produce myelin) and astrocytes.

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8.

Nature 448, 425 (26 July 2007) | doi:10.1038/448425a; Published online 25 July 2007

Obituary: Horst Tobias Witt (1922–2007)

Wolfgang Junge1 & A. William Rutherford

During the second half of the twentieth century, great strides were made in revealing the molecular details of oxygen-generating photosynthesis, the basis of almost all life on Earth. Horst Witt was one of the prime movers behind this revolution in understanding.

Witt was born in 1922 in Bremen, Germany. From his youth he was interested in physics, and while at school he won a prestigious prize for his high-risk, and literally explosive, experiments on supersonic airfoils. On the outbreak of the Second World War, he entered the Luftwaffe, but his scientific aptitude led to his early (and lucky) release to take up research at the University of Göttingen. He received his PhD in solid-state physics in 1950, and then moved to the Max Planck Institute of Physical Chemistry where — like several other brilliant young scientists, including Manfred Eigen — he began to explore the largely hidden beauties of the molecular life sciences.

Witt chose oxygenic photosynthesis as his lifelong research topic. Inspired by the methods pioneered by George Porter and Ronald Norrish, he embarked on work with the technique of flash spectrophotometry. Using algae, in 1955 he discovered reactions of chlorophylls, carotenoids and cytochromes that occurred in microseconds. By 1961, his work, along with the independent discoveries of Lou Duysens and of Bessel Kok, led to a scheme with two photochemical reaction centres in series. At photosystem II, electrons are removed from water, generating a strong oxidant, oxygen. At photosystem I, the electrons are used to produce a strong reductant, NADPH (and thence sugars). The energy difference between the strong oxidant and the strong reductant powers all oxygen-based life.

At that time the two Nobel laureates in the field, biochemist Otto Warburg and spectroscopist James Frank, were fighting their famous battles from ensconced positions. When confronted with Witt's detailed reaction scheme in 1962, Warburg mused: "Could you tell us how the chemical mechanism of photosynthesis can be described on the basis of your spectroscopic observations?" Witt countered with a well-aimed jibe at his eminent critic, the pioneer of oxygen detection, by observing that "it would be difficult to deduce the mechanism of a combustion engine based only on sniffing the exhaust".

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9.

Nature 448, 427-434 (26 July 2007) | doi:10.1038/nature06005

Unravelling the Pathogenesis of Inflammatory Bowel Disease

R. J. Xavier & D. K. Podolsky

Recently, substantial advances in the understanding of the molecular pathogenesis of inflammatory bowel disease (IBD) have been made owing to three related lines of investigation. First, IBD has been found to be the most tractable of complex disorders for discovering susceptibility genes, and these have shown the importance of epithelial barrier function, and innate and adaptive immunity in disease pathogenesis. Second, efforts directed towards the identification of environmental factors implicate commensal bacteria (or their products), rather than conventional pathogens, as drivers of dysregulated immunity and IBD. Third, murine models, which exhibit many of the features of ulcerative colitis and seem to be bacteria-driven, have helped unravel the pathogenesis/mucosal immunopathology of IBD.

The major forms of idiopathic IBD, ulcerative colitis and Crohn's disease are chronic inflammatory disorders of the gastrointestinal tract that have been empirically defined by clinical, pathological, endoscopic and radiological features1. The onset of IBD typically occurs in the second and third decades of life and a majority of affected individuals progress to relapsing and chronic disease. Family aggregation has long been recognized. First-degree relatives of affected individuals have a relative risk of fivefold or greater. The inheritable component seems stronger in Crohn's disease than in ulcerative colitis2, 3. It is of interest that in several countries with historically low rates of IBD, a pattern of rising incidence in the past one to two decades, particularly for Crohn's disease, has occurred, suggesting that environmental factors are also involved.

Key features of ulcerative colitis include diffuse mucosal inflammation that extends proximally from the rectum to a varying degree. In conjunction with severe inflammation and the coincident production of a complex mixture of inflammatory mediators, extensive superficial mucosal ulceration develops. Histopathological features include the presence of a significant number of neutrophils within the lamina propria and the crypts, where they form micro-abscesses (Fig. 1). Depletion of goblet cell mucin is also common. Crohn's disease is characterized by aggregation of macrophages that frequently form non-caseating granulomas (Fig. 1). Although any site of the gastrointestinal tract may be affected, involvement of the terminal ileum is most common and the earliest mucosal lesions in Crohn's disease often appear over Peyer's patches. Unlike ulcerative colitis, Crohn's disease may be patchy and segmental, and inflammation typically transmural.

Genome-wide searches for IBD susceptibility loci performed in the last few years have been highly successful in identifying genes that contribute to disease susceptibility. In initial screening efforts, two groups identified NOD2 (also designated CARD15 and IBD1) as a susceptibility gene in Crohn's disease, using positional cloning and candidate gene approaches4, 5. Since then, several additional susceptibility loci have been implicated in inflammatory bowel disease and confirmed by replication: IBD5, IL23R and ATG16L1 (refs 6, 7, 8, 9, 10, 11, 12, 13, 14). (See Fig. 2 for the full list of genes validated in multiple studies as well as those genes that require additional confirmation). The genetic variants that have been found to confer Crohn's disease risk point to the importance of innate immunity, autophagy and phagocytosis in Crohn's disease pathogenesis. In particular, a number of genes associated with Crohn's disease (IL23R, PTPN2) are also associated with other autoimmune disorders, suggesting that a subset of Crohn's disease patients share common triggers with these conditions. In addition, multiple disease-associated intergenic segments have been identified and replicated in genome-wide association studies. These intergenic regions implicate new genes and pathways—possibly including genes that are expressed within these regions and others that are remotely regulated to modify the disease phenotype. Further understanding of regulatory elements within non-coding genomic regions and gene–gene interactions will lead to a better understanding of the underlying mechanisms that cause disease. Despite early linkage analysis suggesting an important contribution of the MHC complex to IBD susceptibility, in contrast to rheumatoid arthritis and multiple sclerosis, identification of precise genes within the MHC region that confer susceptibility has been problematic. Individual risk genes are discussed below within the context of a consideration of pathophysiologic mechanisms.

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10.

New England Journal of Medicine. Volume 357:370-379, July 26, 2007, Number 4.

The Spread of Obesity in a Large Social Network over 32 Years

Nicholas A. Christakis, M.D., Ph.D., M.P.H., and James H. Fowler, Ph.D.

Background: The prevalence of obesity has increased substantially over the past 30 years. We performed a quantitative analysis of the nature and extent of the person-to-person spread of obesity as a possible factor contributing to the obesity epidemic.

Methods: We evaluated a densely interconnected social network of 12,067 people assessed repeatedly from 1971 to 2003 as part of the Framingham Heart Study. The body-mass index was available for all subjects. We used longitudinal statistical models to examine whether weight gain in one person was associated with weight gain in his or her friends, siblings, spouse, and neighbors.

Results: Discernible clusters of obese persons (body-mass index [the weight in kilograms divided by the square of the height in meters], ?30) were present in the network at all time points, and the clusters extended to three degrees of separation. These clusters did not appear to be solely attributable to the selective formation of social ties among obese persons. A person's chances of becoming obese increased by 57% (95% confidence interval [CI], 6 to 123) if he or she had a friend who became obese in a given interval. Among pairs of adult siblings, if one sibling became obese, the chance that the other would become obese increased by 40% (95% CI, 21 to 60). If one spouse became obese, the likelihood that the other spouse would become obese increased by 37% (95% CI, 7 to 73). These effects were not seen among neighbors in the immediate geographic location. Persons of the same sex had relatively greater influence on each other than those of the opposite sex. The spread of smoking cessation did not account for the spread of obesity in the network.

Conclusions: Network phenomena appear to be relevant to the biologic and behavioral trait of obesity, and obesity appears to spread through social ties. These findings have implications for clinical and public health interventions.

The prevalence of obesity has increased from 23% to 31% over the recent past in the United States, and 66% of adults are overweight.1,2 Proposed explanations for the obesity epidemic include societal changes that promote both inactivity and food consumption.3 The fact that the increase in obesity during this period cannot be explained by genetics4,5 and has occurred among all socioeconomic groups1 provides support for a broad set of social and environmental explanations. Since diverse phenomena can spread within social networks,6,7,8,9,10 we conducted a study to determine whether obesity might also spread from person to person, possibly contributing to the epidemic, and if so, how the spread might occur.

Whereas obesity has been stigmatized in the past, attitudes may be changing.11,12 To the extent that obesity is a product of voluntary choices or behaviors, the fact that people are embedded in social networks and are influenced by the evident appearance and behaviors of those around them suggests that weight gain in one person might influence weight gain in others. Having obese social contacts might change a person's tolerance for being obese or might influence his or her adoption of specific behaviors (e.g., smoking, eating, and exercising). In addition to such strictly social mechanisms, it is plausible that physiological imitation might occur; areas of the brain that correspond to actions such as eating food may be stimulated if these actions are observed in others.13 Even infectious causes of obesity are conceivable.14,15

We evaluated a network of 12,067 people who underwent repeated measurements over a period of 32 years. We examined several aspects of the spread of obesity, including the existence of clusters of obese persons within the network, the association between one person's weight gain and weight gain among his or her social contacts, the dependence of this association on the nature of the social ties (e.g., ties between friends of different kinds, siblings, spouses, and neighbors), and the influence of sex, smoking behavior, and geographic distance between the domiciles of persons in the social network.

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