‘No Asians working here’: racialized otherness and authenticity in gastronomical Orientalism

Orientalist discourse relies on the relational epistemology in which the authenticity of the self co-emerges with the authenticity of the other. The cultural definition of authentic ethnic cuisine is discursively constructed through the identification of racialized otherness which also implies the ‘de-racialized’ cultural competency of cosmopolitan consumers. A critical discourse analysis of online restaurant reviews in selected US cities reveals that claims to authenticity in the gastronomical experience involving East Asian cuisine are predicated on the deployment of a racialized Orientalist narrative. We examine five themes: (1) racialized authentic otherness, (2) generalized racial temperament, (3) Orientalist destinations, (4) the authenticity of whiteness, and (5) self-Orientalism by the racialized alterity. We conclude that the production of a racial signification of the ‘Oriental other’ is linked to the authenticity of cultural otherness which, in turn, is connected to the authenticity of the consumer experience.     

‘Structure liberates?’: mixing for mobility and the cultural transformation of ‘urban children’ in a London academy

Abstract

This paper explores how the creation of a socially and ethnically mixed student body relates to mobility within the context of Beaumont Academy. This authoritarian school opened in 2004 under the ethos ‘structure liberates’. Based in a predominantly deprived, ethnic minority area of London, Beaumont seeks to culturally transform its students. With its outstanding GCSE results, the school has been championed as a blueprint for reform, yet the cultural implications underlying this approach remain unexamined. The ethos pathologizes the surrounding area while essentializing itself as an ‘oasis in the desert’ liberating students through discipline. The paper explores how mobility is embodied by students and the alterations or eliminations necessary to achieve it. These alterations produce raced and classed positions and bring them into focus, highlighting who needs to ‘adjust’ themselves to accrue value. Uncritical celebrations of mixed-ness conceal structural inequalities lingering beneath the rhetoric of happy multiculturalism and aspirational citizenship. These inequalities are exacerbated by a marketized education system.     

Is impaired energy regulation the core of the metabolic syndrome in various ethnic groups of the USA and Taiwan?

Background

The metabolic syndrome (MetS) concept is widely used in public health and clinical settings without an agreed pathophysiology. We have re-examined the MetS in terms of body fuels, so as to provide a coherent cross-cultural pathogenesis.

Methods

National Health and Nutrition Examination Survey (NHANES 2001-2) with n = 2254 and Taiwanese National Health Interview Survey (NHIS) sub-set for hypertension, hyperglycemia and hyperlipidemia assessment (TwSHHH 2002), n = 5786, were used to compare different ethnicities according to NCEP-ATPIII (NCEP-tw) criteria for METS. Exploratory factor analysis (EFA) using principal components (PC) was employed to differentiate and unify MetS components across four ethnicities, gender, age-strata, and urban-rural settings.

Results

The first two factors from the PC analysis (PCA) accounted for from 55.2% (non-Hispanic white) to 63.7% (Taiwanese) of the variance. Rotated factor loadings showed that the six MetS components provided three clusters: the impaired energy regulation (IER) components (waist circumference, WC, fasting triglycerides, TG, and fasting plasma glucose, FPG), systolic and diastolic blood pressures (BPs), and HDL-cholesterol, where the IER components accounted for 25-26% of total variance of MetS components. For the three US ethnic subgroups, factor 1 was mainly determined by IER and HDL-cholesterol, and factor 2 was related to the BP components. For Taiwanese, IER was determinant for both factors, and BPs and HDL-cholesterol were related to factors 1 and 2 respectively.

Conclusions

There is a MetS core which unifies populations. It comprises WC, TG and FPG as a core, IER, which may be expressed and modulated in various second order ways.

     

There is no ‘Conundrum’ of InsP6

Indirect assays have claimed to quantify phytate (InsP₆) levels in human biofluids, but these have been based on the initial assumption that InsP₆ is there, an assumption that our more direct assays disprove. We have shown that InsP₆ does not and cannot (because of the presence of an active InsP₆ phosphatase in serum) exist in mammalian serum or urine. Therefore, any physiological effects of dietary InsP₆ can only be due either to its actions in the gut as a polyvalent cation chelator, or to inositol generated by its dephosphorylation by gut microflora.We are grateful to Dr Vucenik for bringing up a number of interesting points.It is true that we have not quantified the dietary intakes of our human donors any more (but also hardly any less) than has been done by those groups claiming that InsP₆ is present in bodily fluids. As a qualitative observation we should point out that in fact all our donors for ref. [1] do have a regular intake of dietary cereals and indeed, one is a strict vegetarian on a high cereal diet. But it is quantification that reveals this to be a specious issue. The limits of detection in our two relevant publications [1,2] for InsP₆ in plasma and urine were, respectively, around two and three orders of magnitude lower than the levels claimed to be present by Grases et al. [3] in the fluids of experimentally phytate-deprived human subjects. These numbers make the argument that we could not detect any InsP₆ simply because we chose donors on the ‘wrong’ diet untenable.So how have those many claims that InsP₆ is present in body fluids come about? For most of them, the simple answer appears to be that the assays used are indirect and are based entirely on the assumption that InsP₆ is present in the first place. Thus, for example, Valiente and co-workers [4,5] and Chen and co-workers [6,7] measured organic phosphate remaining after a series of fractionations of urine samples and simply assumed it was due to InsP₆, as did March et al. measuring inorganic phosphate after a similar protocol [8]. Grases co-workers [9] have used extensively a less indirect assay, which, after initial ion chromatography and dephosphorylation by a phytase, measures myo-inositol by mass spectrometry, but nevertheless the assay starts with the assumption that InsP₆ is there and that this is what they are quantifying. More recently, direct quantification of InsP₆ in plasma by mass spectrometry has been claimed [10] on the basis that there are peaks in plasma at m/z 624 running near where InsP₆ standards elute in two different HPLC separations [10,11]. But no evidence is presented to show even that these peaks are the same compound, let alone any data to establish firmly that InsP₆ is present, e.g. a minimal requirement of m/z quantified to two decimal places with allowance for C₁₃ content or a full disintegration fingerprint (see also [12]). Any quantified misidentification is likely to have a stochastic element to it, and it is noteworthy that Perelló & Grases have stated [11, p. 255]: ‘…we have found some humans and rats having undetectable [InsP₆], probably depending on their diet or other unknown factors’. In the light of the preceding discussion, we can offer a simpler explanation: the InsP₆ was never there in the first place.In contrast to these claims we have, using two entirely independent specific and sensitive assays with quantified spiking recovery, unambiguously shown that InsP₆ is not present in plasma or urine. This is crucial and central to the whole debate about the actions of dietary InsP₆, because it means that InsP₆ never enters the blood. It is only absorbed after being dephosphorylated, principally to inositol (see [1,2] for further discussion). Ironically, the most direct evidence for this lies in Dr Vucenik''s own data in experiments examining the fate of radioactive InsP₆ fed to animals, in which only inositol was detected in the blood [13]. This particular study was, as Dr Vucenik points out in her letter, conducted on mice. However, exactly the same conclusion (i.e. InsP₆ does not enter the circulation from the gut) is equally clear in her earlier study [14], which she did not cite and which was indeed on rats; does this omission ‘reflect poorly’ on Dr Vucenik''s own ‘report and the author''s credibility in culling scientific data’?In short, dietary InsP₆ can have only two fates: it can stay in the gut, ultimately to be defecated [15], and while it is there it can chelate metal ions to alter their uptake from the gut into the body. This is no ‘straw-man’ and is certainly the most likely explanation for all of the effects of InsP₆ on cultured cells, which comprise the majority of the reports cited by Dr Vucenik. Alternatively, InsP₆ can be converted to inositol (principally by the gut microflora [15]) and be taken up as such into the circulation; were any InsP₆ to get into the blood it would in any case be rapidly dephosphorylated by the phosphatase activity we have shown to be present in human plasma [1].For animal studies, we have raised the possibility [1,2] that it is the inositol so generated (Vitamin Bh, harmless as far as we know) that is the active mediator of any reported beneficial effects of dietary InsP₆. We note that most of the websites touting InsP₆ as a dietary supplement advocate inositol as an important (essential?) co-supplement; that the only human cancer study highlighted as important by Dr Vucenik that we could examine [16] did not administer InsP₆ alone, but only in conjunction with inositol; and that in the few studies where the separate contributions of inositol and InsP₆ have been considered, there are data suggesting that it may be the inositol that matters (e.g. fig. 1 of [17]). Moreover, we are not the only ones to suggest this idea. In the Discussion of their paper (on mice) in which InsP₆ was shown not to enter the blood from the gut [13], Dr Vucenik and her colleagues state: ‘Inositol may be responsible for the antitumor actions observed in both chemopreventitive and efficacy studies of IP₆ … A question remains as to whether the activity of IP₆ in animal models can be replicated by administration of inositol alone because only inositol was detected in plasma and tumor after oral gavage’. Precisely.Finally, returning to InsP₆ itself, which, incidentally, is officially classified by the FDA as a ‘fake’ cancer cure (http://www.fda.gov/drugs/guidancecomplianceregulatoryinformation/enforcementactivitiesbyfda/ucm171057.htm), our data lead inevitably to the conclusion that while InsP₆ might impact on the gut environment and thus indirectly on its microflora [2,12], its only plausible direct action on the body will be to inhibit cation uptake from the diet. Although InsP₆ binds trivalent cations with a higher affinity than divalents [18], it is nevertheless comparatively non-specific in this action. Administering chemicals to the diet to manipulate ion uptake is not unknown in modern medicine; for treatment of iron disorders such as haemochromatosis, as an alternative to injection of Desferral, oral administration of the closely related chelator Deferasirox is now sometimes recommended [19]. But Deferasirox is a highly iron-specific chelator, administered under close medical supervision for a directly iron-related pathology. Recommending unmonitored, widespread administration of InsP₆ to address a veritable multitude of different pathologies [20] seems to us to be an entirely different matter.In a well-fed human, where the cation to InsP₆ ratio in the diet is high, InsP₆ may very well do no harm (it is, after all, a natural component of our diet) and there is much evidence to support this idea, as argued by Dr Vucenik. But if InsP₆ is not impacting on cation uptake from the diet to do any harm it is difficult to understand how at exactly the same time it can impact on the same uptake to do good. (See reference [21] for the studies Dr Vucenik requested ‘unequivocally demonstrating the toxicity of pure Ca-Mg-InsP₆ as it occurs naturally’ in humans with low dietary cation uptake.) In the light of the above discussion and our rigorous data, we stand unreservedly by our original closing statement [1]: ‘…that chronically altering cation absorption from the gut by artificially loading the diet with a non-specific chelator … in the hope that it might impact indirectly on cancer or other pathologies seems highly inadvisable’.     

Volunteering,Dana, and the Cultivation of ‘Good People’ in Thailand

The article explores a popular volunteer movement in Thailand and its connection to Buddhist morality and contemporary Thai politics. The article argues that volunteering in Thailand is often conceived of as a gift in various ways: as a form of dana or selfless giving; a gift from ‘good people’ to those defined as ‘in need’ in society and a gift to the Thai nation as a whole. Indeed, when volunteering is said to be a gift to the Thai nation, it is not necessarily because of its ability to redistribute resources, but because of its perceived ability to cultivate moral values and ‘good people’ for the Thai nation. The paper explores the implications that stem from presenting volunteering as a gift, with a strong emphasis on morality and ‘good people’, and how this popular discourse on volunteering may contribute to the maintenance of political status quo in Thailand, particularly in the context of the ongoing political struggles in recent years.     

Understanding the Role of the ‘Self’ in the Social Priming of Mimicry

People have a tendency to unconsciously mimic other''s actions. This mimicry has been regarded as a prosocial response which increases social affiliation. Previous research on social priming of mimicry demonstrated an assimilative relationship between mimicry and prosociality of the primed construct: prosocial primes elicit stronger mimicry whereas antisocial primes decrease mimicry. The present research extends these findings by showing that assimilative and contrasting prime-to-behavior effect can both happen on mimicry. Specifically, experiment 1 showed a robust contrast priming effect where priming antisocial behaviors induces stronger mimicry than priming prosocial behaviors. In experiment 2, we manipulated the self-relatedness of the pro/antisocial primes and further revealed that prosocial primes increase mimicry only when the social primes are self-related whereas antisocial primes increase mimicry only when the social primes are self-unrelated. In experiment 3, we used a novel cartoon movie paradigm to prime pro/antisocial behaviors and manipulated the perspective-taking when participants were watching these movies. Again, we found that prosocial primes increase mimicry only when participants took a first-person point of view whereas antisocial primes increase mimicry only when participants took a third-person point of view, which replicated the findings in experiment 2. We suggest that these three studies can be best explained by the active-self theory, which claims that the direction of prime-to-behavior effects depends on how primes are processed in relation to the ‘self’.     

The Fate of the Method of ‘Paradigms’ in Paleobiology

An earlier article described the mid-twentieth century origins of the method of “paradigms” in paleobiology, as a way of making testable hypotheses about the functional morphology of extinct organisms. The present article describes the use of “paradigms” through the 1970s and, briefly, to the end of the century. After I had proposed the paradigm method to help interpret the ecological history of brachiopods, my students developed it in relation to that and other invertebrate phyla, notably in Euan Clarkson’s analysis of vision in trilobites. David Raup’s computer-aided “theoretical morphology” was then combined with my functional or adaptive emphasis, in Adolf Seilacher’s tripartite “constructional morphology.” Stephen Jay Gould, who had strongly endorsed the method, later switched to criticizing the “adaptationist program” he claimed it embodied. Although the explicit use of paradigms in paleobiology had declined by the end of the century, the method was tacitly subsumed into functional morphology as “biomechanics.”     

‘For her protection and benefit’: the regulation of marriage-related migration to the UK

This paper argues that a two-tier system has evolved dividing intra-UK/EU marriages from extra-UK/EU marriages. For the former, marriage is a contract between two individuals overseen by a facilitating state. For the latter, marriage has become more of a legal status defined and controlled by an intrusive and obstructive state. I argue that this divergence in legislating regulation is steeped in an ethnicized imagining of ‘Britishness’ whereby the more noticeably ‘other’ migrants (by skin colour or religion) are perceived as a threat to the national character. The conceptualization of women as legally ‘disabled’ citizens (1870 Naturalisation Act) for whom a state must act as responsible patriarch, is a fundamental part of this imagining of the nation. The paper therefore examines the social (gendered and ethnicized) assumptions and political aims embedded within the legislation.     

Variation of the parameters of natural reproduction and Crow’s indices in the ethnic groups of Dagestan

Using the 2002 All-Russian population census data, the parameters of differential fertility as a component of natural selection (Crow??s indices) have been calculated for women of seven age cohorts of the seven most numerous ethnic groups of the Republic of Dagestan. It has been shown that in the population of Dagestan in the second half of the 20th century the intensities of two types of selection tended to decrease, viz., intragroup selection relaxed in each ethnic group due to considerable reduction of interfamily variance in fertility and intergroup selection relaxed due to reduction of interethnic differences in fertility. A reduction of the average number of offspring (k) was observed in all ethnic groups, suggesting the spread of birth regulation practices (abortion and contraception). Nevertheless, all Muslim groups (aboriginal Dagestan ethnic groups and Azerbaijanis) are still characterized by an extended pattern of reproduction (2.7 < k < 3.3); in Russians k = 2.1. Interethnic differentials in natural reproduction rates, along with migration processes, account for the dynamics of the ethnic composition and gene-pool structure of the population of the Republic of Dagestan.     

‘Respiratory protection’ of the nitrogenase in dinitrogen-fixing cyanobacteria

Several filamentous and unicellular cyanobacteria were grown photoautotrophically with nitrate or dinitrogen as N-sources, and some respiratory properties of the cells or isolated plasma (CM) and thylakoid (ICM) membranes were compared. Specific cytochrome c oxidase activities in membranes from dinitrogen-fixing cells were between 10- and 50-times higher than those in membranes from nitrate-grown cells, ICM of heterocysts but CM of unicells being mainly responsible for the stimulation. Whole cell respiration (oxygen uptake) of diazotrophic unicells paralleled increased cytochrome oxidase activities of the isolated membranes. Mass spectrometric measurements of the uptake of isotopically labeled oxygen revealed that (low) light inhibited respiration of diazotrophic unicells to a much lesser degree than that of nitrate-grown cells which indicates the prevailing (respiratory) role of CM in the former. Normalized growth yields of diazotrophic unicells grown in continuous light were significantly higher than those of cells grown in a 12/12 hrs light/dark cycle. Mass spectrometry showed that overall nitrogen uptake by the former was higher than by the latter; in particular, and in marked contrast to the time course of nitrogenase activity (acetylene reduction) there was no appreciable nitrogen uptake or protein synthesis during dark periods; likewise, there was no 14-CO₂ fixation, nor chloropholl synthesis, nor cell division in the dark. By contrast, growth in continuous light gave sustained rates of nitrogen and carbon dioxide incorporation over the whole time range. Our results will be discussed in terms of respiratory protection as an essential strategy of keeping apart nitrogenase and oxygen, either atmospheric or photosynthetically produced within the same cell.     

No evidence for ‘skewed’ inactivation of the X-chromosome as cause of Leber's hereditary optic neuropathy in female carriers

Leber’s hereditary optic neuropathy (LHON) is a maternally inherited disorder of the optic nerves. It has been proposed that the specific mutations in the mitochondrial DNA (mtDNA) that are associated with LHON require and X-chromosomally encoded permissive factor in order to become expressed. This would explain both the preponderance of male patients and the fact that most carriers of specific mtDNA mutations remain unaffected. Although linkage studies have been negative so far, the existence of such a factor has not been ruled out. We investigated the genealogical data of 24 large LHON pedigrees and concluded that the presumed X-linked factor would be recessively inherited and that at least 57% of the affected females would be heterozygous. Therefore, these females must be the victim of nonrandom X-chromosomal inactivation (skewed lyonization). However, analysis of X-chromosomal methylation patterns in 16 LHON-affected females revealed substantial skewing in only 15%–20% of cases, which is not significantly different from the patterns in 49 controls. Moreover, we found the frequency of LHON in daughters of affected heterozygous females to be twice to three times as high as in daughters of unaffected heterozygous females, which cannot be explained by an X-chromosomally inherited factor. We conclude that the results of our investigations do not support the hypothesis that LHON is a digenic disease with an X-linked factor being the main cause of loss of vision in the presence of relevant mtDNA mutations. Received: 1 June 1995 / Revised: 20 September 1995     

Culturalizing politics,hyper-politicizing ‘culture’: ‘White’ vs. ‘Black Turks’ and the making of authoritarian populism in Turkey

This paper focuses on the uses and abuses of two terms, ‘White’ and ‘Black Turk’, which have been significant in the ways modern Turkish society and national identity have been defined and contested in recent decades. Initially emerging in social analysis in the 1990s, ‘White Turk’ was a metaphor for and critique of the class culture, subjectivity and worldviews of the ‘new middle classes’ in a period of rapid integration to neoliberalism and globalized capitalism. Over time, both White and Black Turks have come to be used as part of a politics of identity and a politics of authenticity to characterize who are seen as the ‘authentic self’ and inauthentic others of national identity and to assert different visions for the future of Turkish society. White Turk has been adopted as an identity by outspoken members of the media and business elite, whereas its binary opposite, Black Turk, has been appropriated by Islamist politicians of the Justice and Development Party (AKP) as a metaphor to characterize the marginalization and purported oppression of their conservative Muslim constituency. As White and Black Turks were adopted as self-proclaimed identities, they provided a basis for a culturalist depiction of Turkish society, contributing over time to an increasingly divisive politics. Even though the AKP initially used the reference to White and Black Turks to appeal to specific demands for inclusion, as it increased its grip on power, it also (hyper)politicized the terms to articulate nativist claims to authenticity. In recent years, this nativist populism has been used to justify increasing authoritarianism and to delegitimize belonging and political participation of those deemed inauthentic others of the body politics.