Aproximación crítica a las políticas públicas en salud indígena, medicina tradicional e interculturalidad en México (1990-2016) / A critical examination of public policies related to indigenous health, traditional medicine, and interculturality in Mexico (1990-2016)

RESUMEN En los últimos 26 años, el gobierno mexicano desarrolló múltiples discursos y actividades sobre la denominada "salud intercultural" dirigidos, en especial, a los pueblos originarios de México (alrededor de 62, de acuerdo al criterio lingüístico), y construyó establecimientos de salud (puestos de salud, clínicas y hospitales) en los que propuso la aplicación de indicadores de pertinencia cultural en algunos estados como Puebla, Nayarit, Oaxaca, Chiapas, Querétaro y Jalisco (mínimos e insuficientes). Sin embargo, la salud indígena y la atención médica institucional siguen siendo precarias en cuanto a recursos humanos y materiales (personal sanitario, medicamentos, etc.), y discriminatorios con relación a la forma y al contenido de la atención que se brinda. En este artículo, detallamos algunas de las intervenciones del gobierno que suponen un avance institucional sobre el tema de interculturalidad en salud pero que, en el fondo, significan la continuidad de políticas arbitrarias y excluyentes.

ABSTRACT Over the last 26 years, the Mexican government has developed a number of activities and discourses around what has been called "intercultural health," directed especially at indigenous peoples in Mexico (some 62, according to linguistic criteria). In this way, the government has built health care institutions (rural centers, clinics, and hospitals) in states like Puebla, Nayarit, Oaxaca, Chiapas, Queretaro, and Jalisco, proposing the implementation of cultural pertinence indicators (which are minimal and inadequate). Nevertheless, the health conditions among indigenous populations and the quality of health care provided by public institutions continue to be precarious in terms of human and material resources (health personnel, drugs, etc.) and discriminatory with respect to the form and content of the provided services. This paper describes some of the governmental interventions that purport to be institutional improvements in the field of interculturality, but that actually represent the continuity of arbitrary and exclusive policies.

[A critical examination of public policies related to indigenous health, traditional medicine, and interculturality in Mexico (1990-2016)]. / Aproximación crítica a las políticas públicas en salud indígena, medicina tradicional e interculturalidad en México (1990-2016).

Over the last 26 years, the Mexican government has developed a number of activities and discourses around what has been called "intercultural health," directed especially at indigenous peoples in Mexico (some 62, according to linguistic criteria). In this way, the government has built health care institutions (rural centers, clinics, and hospitals) in states like Puebla, Nayarit, Oaxaca, Chiapas, Queretaro, and Jalisco, proposing the implementation of cultural pertinence indicators (which are minimal and inadequate). Nevertheless, the health conditions among indigenous populations and the quality of health care provided by public institutions continue to be precarious in terms of human and material resources (health personnel, drugs, etc.) and discriminatory with respect to the form and content of the provided services. This paper describes some of the governmental interventions that purport to be institutional improvements in the field of interculturality, but that actually represent the continuity of arbitrary and exclusive policies.

En los últimos 26 años, el gobierno mexicano desarrolló múltiples discursos y actividades sobre la denominada "salud intercultural" dirigidos, en especial, a los pueblos originarios de México (alrededor de 62, de acuerdo al criterio lingüístico), y construyó establecimientos de salud (puestos de salud, clínicas y hospitales) en los que propuso la aplicación de indicadores de pertinencia cultural en algunos estados como Puebla, Nayarit, Oaxaca, Chiapas, Querétaro y Jalisco (mínimos e insuficientes). Sin embargo, la salud indígena y la atención médica institucional siguen siendo precarias en cuanto a recursos humanos y materiales (personal sanitario, medicamentos, etc.), y discriminatorios con relación a la forma y al contenido de la atención que se brinda. En este artículo, detallamos algunas de las intervenciones del gobierno que suponen un avance institucional sobre el tema de interculturalidad en salud pero que, en el fondo, significan la continuidad de políticas arbitrarias y excluyentes.

Contribution of TNF-alpha and nuclear factor-kappaB signaling to type 2 iodothyronine deiodinase activation in the mediobasal hypothalamus after lipopolysaccharide administration.

To determine whether signaling through TNF and/or nuclear factor-kappaB contributes to bacterial lipopolysaccharide (LPS)-induced activation of type 2 iodothyronine deiodinase (D2) in tanycytes lining the floor and infralateral walls of the third ventricle, the effect of a TNF antagonist on D2 gene expression and LPS-induced Ikappa-Balpha expression in tanycytes were studied. Animals treated with soluble, rat, polyethylene glycol-conjugated TNF receptor type 1 (4 mg/kg body weight) before a single ip injection of LPS showed a significant reduction in circulating IL-6 levels but no effect on LPS-induced D2 mRNA in the majority of tanycytes with the exception of a subpopulation of alpha tanycytes in the wall of the third ventricle. LPS induced a rapid increase in Ikappa-Balpha mRNA in the pars tuberalis and a delayed response in alpha tanycytes but absent in all other tanycyte subsets. The LPS-induced increase in Ikappa-Balpha in the pars tuberalis was associated with increased TSHbeta gene expression in this tissue, but cAMP response element-binding protein (CREB) phosphorylation was observed only in a subset of alpha tanycytes. These data suggest that TNF and nuclear factor-kappaB signaling are not the primary, initiating mechanisms mediating the LPS-induced D2 response in tanycytes, but may contribute in part to sustaining the LPS-induced D2 response in a subset of alpha tanycytes. We hypothesize that in addition to TSH, other factors derived from the pars tuberalis may contribute to LPS-induced D2 activation in tanycytes.

Induction of type 2 iodothyronine deiodinase in the mediobasal hypothalamus by bacterial lipopolysaccharide: role of corticosterone.

To determine whether endotoxin-induced activation of type 2 iodothyronine deiodinase (D2) in the mediobasal hypothalamus is dependent on circulating levels of corticosterone, the effect of bacterial lipopolysaccharide (LPS) on D2 gene expression was studied in adrenalectomized, corticosterone-clamped adult, male, Sprague Dawley rats. In sham-adrenalectomized animals, LPS (250 microg/100 g body weight) increased circulating levels of corticosterone and IL-6, as well as tanycyte D2 mRNA in the mediobasal hypothalamus. Adrenalectomized, corticosterone-clamped animals showed no significant rise in corticosterone after LPS, compared with saline-treated controls but increased IL-6 levels and tanycyte D2 mRNA similar to LPS-treated sham controls. To further clarify the potential role of corticosterone in the regulation of D2 gene expression by LPS, animals were administered high doses of corticosterone to attain levels similar to that observed in the LPS-treated group. No significant increase in D2 mRNA was observed in the mediobasal hypothalamus with the exception of a small subpopulation of cells in the lateral walls of the third ventricle. These data indicate that the LPS-induced increase in D2 mRNA in the mediobasal hypothalamus is largely independent of circulating corticosterone and indicate that mechanisms other than adrenal activation are involved in the regulation of most tanycyte D2-expressing cells by endotoxin.

Importance of melanocortin signaling in refeeding-induced neuronal activation and satiety.

To identify regions in the hypothalamus involved in refeeding and their regulation by alpha-MSH, adult rats were subjected to a 3-d fast, and 2 h after refeeding, the distribution of c-Fos-immunoreactive neurons was elucidated. Compared with fed and fasted animals, a significant increase (P < 0.001) in the number of c-Fos-immunoreactive cells was identified in refed animals in the supraoptic nucleus, magnocellular and ventral parvocellular subdivisions of the hypothalamic paraventricular nucleus (PVNv), and the dorsal and ventral subdivisions of the dorsomedial nucleus (DMNd and DMNv, respectively). Refeeding shifted the location of c-Fos-labeled neurons from the medial to lateral arcuate where c-Fos was induced in 88.7 +/- 2.2% of alpha-MSH-containing neurons. alpha-MSH-containing axons densely innervated the PVNv, DMNd, and DMNv and organized in close apposition to the majority of refeeding-activated c-Fos-positive neurons. To test whether the melanocortin system is involved in induction of c-Fos in these regions, the melanocortin 3/4 receptor antagonist, agouti-related protein (AGRP 83-132), was administered to fasting animals just before refeeding. Compared with artificial cerebrospinal fluid, a single intracerebroventricular bolus of agouti-related protein (5 microg/5 microl) not only significantly increased the total amount of food consumed within 2 h but also nearly abolished refeeding-induced c-Fos expression in the PVNv and DMNd and partially reduced c-Fos immunoreactivity in the DMNv. We conclude that refeeding activates a subset of neurons in the PVN and DMN as a result of increased melanocortin signaling and propose that one or more of these neuronal populations mediate the potent anorexic actions of alpha-MSH.

Analysis of the stress response in rats trained in the water-maze: differential expression of corticotropin-releasing hormone, CRH-R1, glucocorticoid receptors and brain-derived neurotrophic factor in limbic regions.

Glucocorticoids and corticotropin-releasing hormone (CRH) are key regulators of stress responses. Different types of stress activate the CRH system; in hypothalamus, CRH expression and release are increased by physical or psychological stressors while in amygdala, preferentially by psychological stress. Learning and memory processes are modulated by glucocorticoids and stress at different levels. To characterize the kind of stress provoked by a hippocampal-dependent task such as spatial learning, we compared the expression profile of glucocorticoid receptor (GR), pro-CRH and CRH-R1 mRNAs (analyzed by RT-PCR), in amygdala, hippocampus and hypothalamus and quantified serum corticosterone levels by radioimmunoassay at different stages of training. mRNA levels of brain-derived neurotrophic factor (BDNF) were also quantified due to its prominent role in learning and memory processes. Male Wistar rats trained for 1, 3 or 5 days in the Morris water-maze (10 trials/day) were sacrificed 5-60 min the after last trial. A strong stress response occurred at day one in both yoked and trained animals (increased corticosterone and hypothalamic pro-CRH and CRH-R1 mRNA levels); changes gradually diminished as the test progressed. In amygdala, pro-CRH mRNA levels decreased while those of BDNF augmented when stress was highest, in yoked and trained animals. Hippocampi, of both yoked and trained groups, had decreased levels of GR mRNA on days 1 and 3, normalizing by day 5, while those of pro-CRH and CRH-R1 increased after the 3rd day. Increased gene expression, specifically due to spatial learning, occurred only for hippocampal BDNF since day 3. These results show that the Morris water-maze paradigm induces a strong stress response that is gradually attenuated. Inhibition of CRH expression in amygdala suggests that the stress inflicted is of physical but not of psychological nature and could lead to reduced fear or anxiety.