Categoría: Preventive medicine

Limoneno: valor nutricional de cáscara de limón


Limoneno (limonene en inglés)

El limoneno es una sustancia natural que se extrae de los cítricos. Es la sustancia que da olor característicos a las naranjas y los limones. Pertenece al grupo de los terpenos.
El limoneno levógiro (-) se extrae de la cáscara de la naranja y le confiere su olor característico.
El limoneno dextrógiro (+) es un líquido aceitoso que puede extraerse fácilmente de la cáscara del limón y es el responsable de su olor.

Pues hay varios artículos en MedLine (PubMed)  http://www.ncbi.nlm.nih.gov/pubmed/ sobre diferentes efectos biológicos de limón y cítricos como naranja, especialmente en su cáscara, que es la que tiene mayor contenido de limoneno.

Los resúmenes a continuación son los que se obtienen con términos de búsqueda limonene and cancer and trial and humans 

  1. Life Sci. 2013 Jul 10;92(24-26):1151-6. doi: 10.1016/j.lfs.2013.04.013. Epub 2013 May 7. Oral administration of d-limonene controls inflammation in rat colitis and displays anti-inflammatory properties as diet supplementation in humans. d’Alessio PA(1), Ostan R, Bisson JF, Schulzke JD, Ursini MV, Béné MC.  Author information:  (1)Biopark Cancer Campus, University Paris Sud-11, 94807 Villejuif, France. endocell@wanadoo.fr  AIMS: To further explore the anti-inflammatory properties of d-Limonene. MAIN METHODS: A rat model was used to compare evolution of TNBS (2,5,6-trinitrobenzene sulfonic acid)-induced colitis after oral feeding with d-Limonene compared to ibuprofen. Peripheral levels of TNF-α (Tumor Necrosis Factor alpha) were assessed in all animals. Cell cultures of fibroblasts and enterocytes were used to test the effect of d-Limonene respectively on TNFα-induced NF-κB (nuclear factor-kappa B) translocation and epithelial resistance. Finally, plasmatic inflammatory markers were examined in an observational study of diet supplementation with d-Limonene-containing orange peel extract (OPE) in humans. KEY FINDINGS: Administered per os at a dose of 10mg/kg p.o., d-Limonene induced a significant reduction of intestinal inflammatory scores, comparable to that induced by ibuprofen. Moreover, d-Limonene-fed rats had significantly lowered serum concentrations of TNF-α compared to untreated TNBS-colitis rats. The anti-inflammatory effect of d-Limonene also involved inhibition of TNFα-induced NF-κB translocation in fibroblast cultures. The application of d-Limonene on colonic HT-29/B6 cell monolayers increased epithelial resistance. Finally, inflammatory markers, especially peripheral IL-6, markedly decreased upon OPE supplementation of elderly healthy subjects submitted or not to 56 days of dietary supplementation with OPE. SIGNIFICANCE: In conclusion, d-Limonene indeed demonstrates significant anti-inflammatory effects both in vivo and in vitro. Protective effects on the epithelial barrier and decreased cytokines are involved, suggesting a beneficial  role of d-Limonene as diet supplement in reducing inflammation.  Copyright © 2013 Elsevier Inc. All rights reserved.  PMID: 23665426  [PubMed – indexed for MEDLINE]
  2. Cancer Prev Res (Phila). 2013 Jun;6(6):577-84. doi: 10.1158/1940-6207.CAPR-12-0452. Epub 2013 Apr 3. Human breast tissue disposition and bioactivity of limonene in women with early-stage breast cancer.  Miller JA(1), Lang JE, Ley M, Nagle R, Hsu CH, Thompson PA, Cordova C, Waer A, Chow HH.  Author information:  (1)The University of Arizona Cancer Center, 1515 N Campbell Ave, Tucson, AZ 85724, USA. jam1@email.arizona.edu  Limonene is a bioactive food component found in citrus peel oil that has shown chemopreventive and chemotherapeutic activities in preclinical studies. We conducted an open-label pilot clinical study to determine the human breast tissue disposition of limonene and its associated bioactivity. We recruited 43 women with newly diagnosed operable breast cancer electing to undergo surgical excision to take 2 grams of limonene daily for two to six weeks before surgery. Blood and  breast tissue were collected to determine drug/metabolite concentrations and limonene-induced changes in systemic and tissue biomarkers of breast cancer risk  or carcinogenesis. Limonene was found to preferentially concentrate in the breast tissue, reaching high tissue concentration (mean = 41.3 μg/g tissue), whereas the major active circulating metabolite, perillic acid, did not concentrate in the breast tissue. Limonene intervention resulted in a 22% reduction in cyclin D1 expression (P = 0.002) in tumor tissue but minimal changes in tissue Ki67 and cleaved caspase-3 expression. No significant changes in serum leptin, adiponectin, TGF-β1, insulin-like growth factor binding protein-3 (IGFBP-3), and  interleukin-6 (IL-6) levels were observed following limonene intervention. There  was a small but statistically significant postintervention increase in insulin-like growth factor I (IGF-I) levels. We conclude that limonene distributed extensively to human breast tissue and reduced breast tumor cyclin D1 expression that may lead to cell-cycle arrest and reduced cell proliferation. Furthermore, placebo-controlled clinical trials and translational research are warranted to establish limonene’s role for breast cancer prevention or treatment.  PMCID: PMC3692564 PMID: 23554130  [PubMed – indexed for MEDLINE]
  3. Altern Med Rev. 2007 Sep;12(3):259-64. D-Limonene: safety and clinical applications.  Sun J(1).  Author information:  (1)Thorne Research, PO Box 25, Dover, ID 83825, USA. jidong@thorne.com  D-limonene is one of the most common terpenes in nature. It is a major constituent in several citrus oils (orange, lemon, mandarin, lime, and grapefruit). D-limonene is listed in the Code of Federal Regulations as generally recognized as safe (GRAS) for a flavoring agent and can be found in common food items such as fruit juices, soft drinks, baked goods, ice cream, and pudding. D-limonene is considered to have fairly low toxicity. It has been tested for carcinogenicity in mice and rats. Although initial results showed d-limonene increased the incidence of renal tubular tumors in male rats, female rats and mice in both genders showed no evidence of any tumor. Subsequent studies have determined how these tumors occur and established that d-limonene does not pose a mutagenic, carcinogenic, or nephrotoxic risk to humans. In humans, d-limonene has demonstrated low toxicity after single and repeated dosing for up to one year. Being a solvent of cholesterol, d-limonene has been used clinically to dissolve cholesterol-containing gallstones. Because of its gastric acid neutralizing effect and its support of normal peristalsis, it has also been used for relief of heartburn and gastroesophageal reflux (GERD). D-limonene has well-established chemopreventive activity against many types of cancer. Evidence from a phase I clinical trial demonstrated a partial response in a patient with breast cancer and stable disease for more than six months in three patients with colorectal cancer.  PMID: 18072821  [PubMed – indexed for MEDLINE]
  4. Drug Metab Pharmacokinet. 2004 Aug;19(4):245-63. Cancer prevention by natural compounds.  Tsuda H(1), Ohshima Y, Nomoto H, Fujita K, Matsuda E, Iigo M, Takasuka N, Moore MA.  Author information:  (1)Department of Molecular Toxicology, Nagoya City University Graduate School of  Medical Sciences, Japan. htsuda@med.nagoya-cu.ac.jp  Increasing attention is being paid to the possibility of applying cancer chemopreventive agents for individuals at high risk of neoplastic development. For this purpose by natural compounds have practical advantages with regard to availability, suitability for oral application, regulatory approval and mechanisms of action. Candidate substances such as phytochemicals present in foods and their derivatives have been identified by a combination of epidemiological and experimental studies. Plant constituents include vitamin derivatives, phenolic and flavonoid agents, organic sulfur compounds, isothiocyanates, curcumins, fatty acids and d-limonene. Examples of compounds from animals are unsaturated fatty acids and lactoferrin. Recent studies have indicated that mechanisms underlying chemopreventive potential may be combinations of anti-oxidant, anti-inflammatory, immune-enhancing, and anti-hormone effects, with modification of drug-metabolizing enzymes, influence on the cell cycle and cell differentiation, induction of apoptosis and suppression of proliferation and angiogenesis playing roles in the initiation and secondary modification stages of neoplastic development. Accordingly, natural agents are advantageous for application to humans because of their combined mild  mechanism. Here we review naturally occurring compounds useful for cancer chemoprevention based on in vivo studies with reference to their structures, sources and mechanisms of action.  PMID: 15499193  [PubMed – indexed for MEDLINE]
  5. Exp Biol Med (Maywood). 2004 Jul;229(7):567-85. Studies of the isoprenoid-mediated inhibition of mevalonate synthesis applied to  cancer chemotherapy and chemoprevention.  Mo H(1), Elson CE.  Author information:  (1)Department of Nutrition and Food Sciences, Texas Woman’s University, Denton, TX 76204, USA. hmo@mail.twu.edu  Pools of farnesyl diphosphate and other phosphorylated products of the mevalonate pathway are essential to the post-translational processing and physiological function of small G proteins, nuclear lamins, and growth factor receptors. Inhibitors of enzyme activities providing those pools, namely, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase and mevalonic acid-pyrophosphate decarboxylase, and of activities requiring substrates from the pools, the prenyl protein transferases, have potential for development as novel chemotherapeutic agents. Their potentials as suggested by the clinical responses  recorded in Phase I and II investigations of inhibitors of HMG CoA reductase (the statins), of mevalonic acid-pyrophosphate decarboxylase (sodium phenylacetate and sodium phenylbutyrate), and of farnesyl protein transferase (R115777, SCH66336, BMS-214662, Tipifarnib, L-778,123, and, prematurely, perillyl alcohol) are dimmed by dose-limiting toxicities. These nondiscriminant growth-suppressive agents induce G1 arrest and initiate apoptosis and differentiation, effects attributed to modulation of cell signaling pathways either by modulating gene expression, suppressing the post-translational processing of signaling proteins and growth factor receptors, or altering diacylglycerol signaling. Diverse isoprenoids and the HMG CoA reductase inhibitor, lovastatin, modulate cell growth, induce cell cycle arrest, initiate apoptosis, and suppress cellular signaling activities. Perillyl alcohol, the isoprenoid of greatest clinical interest, initially was considered to inhibit farnesyl protein transferase; follow-up studies revealed that perillyl alcohol suppresses the synthesis of small G proteins and HMG CoA reductase. In sterologenic tissues, sterol feedback control, mediated by sterol regulatory element binding proteins (SREBPs) 1a and 2, exerts the primary regulation on HMG CoA reductase activity at the transcriptional level. Secondary  regulation, a nonsterol isoprenoid-mediated fine-tuning of reductase activity, occurs at the levels of reductase translation and degradation. HMG CoA reductase  activity in tumors is elevated and resistant to sterol feedback regulation, possibly as a consequence of aberrant SREBP activities. Nonetheless, tumor reductase remains sensitive to isoprenoid-mediated post-transcriptional downregulation. Farnesol, an acyclic sesquiterpene, and farnesyl homologs, gamma-tocotrienol and various farnesyl derivatives, inhibit reductase synthesis and accelerate reductase degradation. Cyclic monoterpenes, d-limonene, menthol and perillyl alcohol and beta-ionone, a carotenoid fragment, lower reductase mass; perillyl alcohol and d-limonene lower reductase mass by modulating translational efficiency. The elevated reductase expression and greater demand for nonsterol products to maintain growth amplify the susceptibility of tumor reductase to isoprenoids, therein rendering tumor cells more responsive than normal cells to isoprenoid-mediated growth suppression. Blends of lovastatin, a potent nondiscriminant inhibitor of HMG CoA reductase, and gamma-tocotrienol, a potent isoprenoid shown to post-transcription-ally attenuate reductase activity with specificity for tumors, synergistically affect the growth of human DU145 and LNCaP prostate carcinoma cells and pending extensive preclinical evaluation, potentially offer a novel chemotherapeutic strategy free of the dose-limiting toxicity associated with high-dose lovastatin and other nondiscriminant mevalonate pathway inhibitors.  PMID: 15229351  [PubMed – indexed for MEDLINE]
  6. Eur J Cancer. 2000 Jun;36(10):1292-7. The state-of-the-art in chemoprevention of skin cancer.  Stratton SP(1), Dorr RT, Alberts DS.  Author information:  (1)Arizona Cancer Center, College of Medicine, University of Arizona, Tucson, AZ  85724, USA. stratton@azcc.arizona.edu  The incidence of skin cancer (both melanoma and non-melanoma) continues to grow at an alarming rate. Our chemoprevention strategies include the development of novel agents evaluated by (1) preclinical mechanistic studies in models of ultraviolet (UV) radiation-induced skin carcinogenesis; (2) clinical studies of immunohistochemical surrogate endpoint biomarkers in high-risk patients; and (3)  randomised, placebo-controlled phase I, II and III clinical chemoprevention trials. Recent clinical results validate this development model. Molecular targets of chemopreventive strategies for melanoma and non-melanoma skin cancers  include the ras and activator protein-1 (AP-1) signal transduction pathways. A transgenic murine melanoma model has been developed for evaluating potential agents in vivo. Agents at various stages of study include the green tea catechin  epigallocatechin gallate (EGCG), the limonene derivative perillyl alcohol, the ornithine decarboxylase inhibitor alpha-difluoromethylornithine (DFMO), selenium, retinoids and salicylates. New chemopreventive agents that can be used to complement sunscreens may result in decreased incidence, morbidity and mortality  of skin cancer.  PMID: 10882869  [PubMed – indexed for MEDLINE]
  7. Cancer Chemother Pharmacol. 1998;42(2):111-7. Phase I and pharmacokinetic study of D-limonene in patients with advanced cancer. Cancer Research Campaign Phase I/II Clinical Trials Committee.  Vigushin DM(1), Poon GK, Boddy A, English J, Halbert GW, Pagonis C, Jarman M, Coombes RC.  Author information:  (1)Department of Medical Oncology, Charing Cross Hospital, London, UK. d.vigushin@cxwms.ac.uk  PURPOSE: D-Limonene is a natural monoterpene with pronounced chemotherapeutic activity and minimal toxicity in preclinical studies. A phase I clinical trial to assess toxicity, the maximum tolerated dose (MTD) and pharmacokinetics in patients with advanced cancer was followed by a limited phase II evaluation in breast cancer. METHODS: A group of 32 patients with refractory solid tumors completed 99 courses of D-limonene 0.5 to 12 g/m2 per day administered orally in 21-day cycles. Pharmacokinetics were analyzed by liquid chromatography-mass spectrometry. Ten additional breast cancer patients received 15 cycles of D-limonene at 8 g/m2 per  day. Intratumoral monoterpene levels were measured in two patients. RESULTS: The MTD was 8 g/m2 per day; nausea, vomiting and diarrhea were dose limiting. One partial response in a breast cancer patient on 8 g/m2 per day was maintained for 11 months; three patients with colorectal carcinoma had prolonged  stable disease. There were no responses in the phase II study. Peak plasma concentration (Cmax) for D-limonene ranged from 10.8+/-6.7 to 20.5+/-11.2 microM. Predominant circulating metabolites were perillic acid (Cmax 20.7+/-13.2 to 71+/-29.3 microM), dihydroperillic acid (Cmax 16.6+/-7.9 to 28.1+/-3.1 microM), limonene-1,2-diol (Cmax 10.1+/-8 to 20.7+/-8.6 microM), uroterpenol (Cmax 14.3+/-1.5 to 45.1+/-1.8 microM), and an isomer of perillic acid. Both isomers of perillic acid, and cis and trans isomers of dihydroperillic acid were in urine hydrolysates. Intratumoral levels of D-limonene and uroterpenol exceeded the corresponding plasma levels. Other metabolites were trace constituents in tissue. CONCLUSIONS: D-Limonene is well tolerated in cancer patients at doses which may have clinical activity. The favorable toxicity profile supports further clinical  evaluation.  PMID: 9654110  [PubMed – indexed for MEDLINE]
  8. Drug Metab Dispos. 1996 May;24(5):565-71. Identification and characterization of limonene metabolites in patients with advanced cancer by liquid chromatography/mass spectrometry.  Poon GK(1), Vigushin D, Griggs LJ, Rowlands MG, Coombes RC, Jarman M.  Author information:  (1)Cancer Research Campaign Centre for Cancer Therapeutics, Charing Cross Hospital.  Limonene is a farnesyl transferase inhibitor that has shown antitumor properties. The drug had been given orally to cancer patients. Plasma and urine samples collected from the patients were examined by reversed-phase HPLC-atmospheric pressure chemical ionization and electrospray ionization MS. The drug underwent rapid conversion to hydroxylated and carboxylated derivatives. Characterization and structural elucidation of the metabolites were achieved by LC/MS and NMR. Five major metabolites were detected in the plasma extracts, namely limonene-1,2-diol, limonene-8,9-diol, perillic acid, an isomer of perillic acid,  and dihydroperillic acid. Urinary metabolites comprised the glucuronides of the two isomers of perillic acid, dihydroperillic acid, limonene-8,9-diol, and a monohydroxylated limonene.  PMID: 8723738  [PubMed – indexed for MEDLINE]
  9. JAMA. 1996 May 1;275(17):1349-53. Chemoprevention of breast cancer.  O’Shaughnessy JA(1).  Author information:  (1)Medicine Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.  PMID: 8614122  [PubMed – indexed for MEDLINE]
  10. J Cell Biochem Suppl. 1995;22:139-44. Prevention and therapy of mammary cancer by monoterpenes.  Gould MN(1).  Author information:  (1)Department of Human Oncology, University of Wisconsin-Madison 53792, USA.  Monoterpenes, found in a wide variety of plants, are a major component of plant essential oils. The unsubstituted monocyclic monoterpene limonene has been shown  to prevent carcinogen-induced mammary cancer at both the initiation and the promotion/progression stages. This terpene also causes the complete regression of the majority of advanced rat mammary cancer when added to the diet. Modification  of limonene by hydroxylation at various positions increases both its chemopreventive and therapeutic efficacy. For example, the naturally occurring hydroxylated limonene analog perillyl alcohol is 5-10 times more potent than limonene and has a similar therapeutic index. Several cellular, metabolic and molecular activities are associated with terpene exposure. These include induction of phase I and II hepatic detoxification enzymes, selective inhibition  of protein isoprenylation, inhibition of CoQ synthesis, and induction of the mannose 6-phosphate/IGFII receptor and TGF beta. Due to the therapeutic efficacy  of monoterpenes in experimental model systems, clinical evaluation of this class  of compounds has begun in advanced cancer patients. A Phase I trial of limonene is in progress in the UK. Efforts in the US will target perillyl alcohol for Phase I testing. Pre-IND toxicology is currently being completed. Phase I trails  are anticipated to begin in the Spring of 1995. We feel that the results of these therapeutic trials, if positive, will facilitate the development of current terpenes and more potent analogs for future chemoprevention trials.  PMID: 8538191  [PubMed – indexed for MEDLINE]
  11. Clin Nutr. 2015 Jul 15. pii: S0261-5614(15)00188-0. doi: 10.1016/j.clnu.2015.06.010. [Epub ahead of print]Impact of diet and nutraceutical supplementation on inflammation in elderly people. Results from the RISTOMED study, an open-label randomized control trial. Ostan R1, Béné MC2, Spazzafumo L3, Pinto A4, Donini LM4, Pryen F5, Charrouf Z6, Valentini L7, Lochs H8, Bourdel-Marchasson I9, Blanc-Bisson C9, Buccolini F10, Brigidi P11, Franceschi C12, d’Alessio PA13.
    BACKGROUND & AIMS:
    Eating habits may influence the life span and the quality of ageing process by modulating inflammation. The RISTOMED project was developed to provide a personalized and balanced diet, enriched with or without nutraceutical compounds, to decrease and prevent inflammageing, oxidative stress and gut microbiota alteration in healthy elderly people. This paper focused on the effect on inflammation and metabolism markers after 56 days of RISTOMED diet alone or supplementation with three nutraceutical compounds.
    METHODS:
    A cohort of 125 healthy elderly subjects was recruited and randomized into 4 arms (Arm A, RISTOMED diet; Arm B, RISTOMED diet plus VSL#3 probiotic blend; Arm C, RISTOMED diet plus AISA d-Limonene; Arm D, RISTOMED diet plus Argan oil). Inflammatory and metabolism parameters as well as the ratio between Clostridium cluster IV and Bifidobacteria (CL/B) were collected before and after 56 days of dietary intervention, and their evolution compared among the arms. Moreover, participants were subdivided according to their baseline inflammatory parameters (erythrocytes sedimentation rate (ESR), C-Reactive Protein, fibrinogen, Tumor Necrosis Factor-alfa (TNF-α), and Interleukin 6) in two clusters with low or medium-high level of inflammation. The evolution of the measured parameters was then examined separately in each cluster.
    RESULTS:
    Overall, RISTOMED diet alone or with each nutraceutical supplementation significantly decreased ESR. RISTOMED diet supplemented with d-Limonene resulted in a decrease in fibrinogen, glucose, insulin levels and HOMA-IR. The most beneficial effects were observed in subjects with a medium-high inflammatory status who received RISTOMED diet with AISA d-Limonene supplementation. Moreover, RISTOMED diet associated with VSL#3 probiotic blend induced a decrease in the CL/B ratio.
    CONCLUSIONS:
    Overall, this study emphasizes the beneficial anti-inflammageing effect of RISTOMED diet supplemented with nutraceuticals to control the inflammatory status of elderly individuals.
    KEYWORDS:
    Ageing; Diet; Inflammation; Nutraceutics; Probiotics; d-Limonene

Sigue leyendo

Material sobre contaminación electromagnética por Alejandro Melo Florián MD, FACP


Hola a todos:

DNA

El tema de la contaminación electromagnética requiere más conocimiento por parte de los usuarios, aquí se comparten algunos sitios de interés relacionados con este tema candente, de gran impacto en la salud pública:



Conferencia de Alejandro Melo Florián MD sobre contaminación electromagnética  http://es.slideshare.net/guest8dd35a/contaminacin-electromagntica-upload-presentation



Daño genotóxico, implica daño del ADN, es uno de los primeros pasos cuando va a ocurrir una neoplasia o cáncer: https://librarymedical.wordpress.com/2015/06/30/genotoxic-damage-by-radiofrequency/


Por qué se deben mantener los celulares lejos del cuerpo: https://www.facebook.com/notes/alejandro-melo-flori%C3%A1n/los-celulares-se-deben-tener-lejos-del-cuerpo-devra-davis/740882445975114



Los campos electromagnéticos son agentes cancerígenos, de acuerdo a la Academia norteamericana de medicina ambiental https://librarymedical.wordpress.com/2014/12/28/declaracion-de-academia-americana-de-medicina-ambiental-sobre-campos-electromagneticos/



El pulso electromagnético es el fenómeno físico que ocurre cuando se marca el móvil, es una microonda que libera gran cantidad de energía, que se libera a los tejidos orgánicos que estén en la cercanía. https://librarymedical.wordpress.com/2014/11/15/el-pulso-electromagnetico-pem/



Estudios clínicos serios del 2014 apoyan los hallazgos anteriores de una asociación entre intenso del uso del teléfono móvil y los tumores cerebrales. El pulso electromagnético de mayor intensidad que causa estrés en el ADN está justo cuando se marca y cuando se contesta, en estos momentos se debe tener alejado de la cabeza. https://librarymedical.wordpress.com/2014/11/15/evidencia-sobre-uso-celulares-y-cancer-cerebral/


Registro de tumores cerebrales en EEUU. Estos registros son estadísticas oficiales.  https://librarymedical.wordpress.com/2015/06/30/registro-de-tumores-cerebrales-en-ee-uu-2006-2010/


Electropolución de la telefonía móvil. https://alejandromeloflorian.wordpress.com/2015/03/21/electropolucion-y-la-nocividad-de-la-telefonia-movil/



Contaminación electromagnética. https://alejandromeloflorian.wordpress.com/2012/04/24/contaminacion-electromagnetica/



Luz LED y efectos en melatonina: https://cerebromenteconciencia.wordpress.com/2015/08/17/luz-led-y-efectos-en-melatonina/



Colección en sitio web Scoop.it sobre temas de contaminación electromagnética presentes en la red, http://www.scoop.it/t/electromagnetic-fields-contamination (Nota: requiere tener cuenta para poder entrar)




Noticias del mundo de la medicina en: https://alejandromeloflorian.wordpress.com/

More information about HONcode

Notas médicas y varias en Facebook


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Publicado originalmente en: https://librarymedical.wordpress.com/2015/05/04/notas-medicas-y-varias-en-facebook/

A continuación se listan artículos varios en página de notas de Facebook. Se presentan de forma organizada según temática, lo cual hace más fácil la consulta de referencia.

De práctica médica

Reflexiones sobre la práctica médica

Médicos en EE.UU. desencantados con la atención a pacientes

El nuevo rol del médico

Faltan médicos especialistas?

Bibliotecas virtuales

Memes: genes de la cultura

Temas sobre salud pública

Sensatez y publicidad a medicamentos.

Cómo usan los pacientes Internet

Temas sobre neurociencia

Mind, meditation, consciousness and quantum mechanics

Material sobre memoria

Lo que hace por el cerebro la escritura a mano

Comentarios sobre el paradigma holográfico y la conciencia

Teoría de la mente, por Antonio Damasio

Estimulación cortical contralateral usando mano no dominante

Temas sobre envejecimiento

Temas sobre Envejecimiento Exitoso

Estudio Comparativo ALLHAT


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Este estudio clínico es de los que a uno como clínico le gustaría ver más en el sentido de establecer si los nuevos medicamentos funcionan mejor que los antiguos. El contexto es que hay que tener en cuenta que muchos de los estudios clínicos que se presentan son solamente comparativos vs. placebo y los nuevos medicamentos que suelen tener unos costos muchos más elevados para los sistemas de salud, deberían justificar que tienen significativamente más beneficios que los ya existentes, para poder justificar en general los mayores costos que tienen. Escribo esto a propósito de material escrito por Marcia Angell MD, editora en jefe durante más de 20 años de la muy prestigiosa y reconocida New England Journal of Medicine.

angell.480 (1) Marcia Angell.

Este estudio se llama ALLHAT,con un número de eventos importantes, que confiere suficiente poder estadístico al estudio, a pesar de las diferencias en los niveles de presión arterial logrados, tampoco se pudieron establecer resultados estadísticamente significativos en términos de prevenci ón de mortalidad total e infarto de miocardio entre las tres medicaciones, y en prevención de eventos cerebrovasculares entre clortalidona y amlodipina. Sólo la clortalidona mostró un perfil más favorable que las otras dos medicaciones para proteger del desarrollo de insuficiencia cardíaca, y comparando con lisinopril, de accidentes cerebrovasculares. En este punto deberíamos preguntarnos por qué diferencias de PA estadísticamente significativas no se traducen en reducciones de eventos cardiovasculares duros, hecho perfectamente demostrado a partir tanto de estudios epidemiológicos como de ensayos clínicos controlados.

El estudio ALLHAT fue desarrollado en forma oficial por el Instituto Nacional del  Corazón, Pulmón y Sangre de los Estados Unidos, incluyó pacientes hipertensos arteriales estadios 1 y 2 de más de 55 años de edad con un factor de riesgo cardiovascular, y comparó clortalidona, amlodipina y lisinopril. La clortalidona redujo la presión arterial sistólica m ás que la amlodipina y el
lisinopril; la amlodipina redujo la presión diastólica m ás que la clortalidona y el lisinopril; la amlodipina redujo la presión sistólica m ás que el lisinopril; no hubo diferencias entre clortalidona y lisinopril para la diastólica. Estos resultados no concuerdan con los de los ensayos clínicos controlados publicados previamente, en los que se demostró equipotencia entre las diversas familias
de medicamentos, como ha ocurrido en los estudios INSIGHT y STOP 2, por ejemplo.

En el estudio ALLHAT han quedado claramente establecidos los efectos metabólicos de las distintas medicaciones, los cuales indudablemente también interfieren en el desarrollo de eventos duros. La clortalidona aumenta los niveles promedio de glicemia y la incidencia de diabetes mellitus, presenta mayores niveles de colesterol total promedio y de pacientes con hipercolesterolemia, y reduce significativamente la potasemia promedio, aumentando el porcentaje de pacientes con hipokaliemia. La amlodipina no modificó las glicemias promedio de la población en estudio durante los 4 años del mismo, aunque en este grupo desarrollaron
diabetes mellitus más pacientes que con lisinopril; por otra parte, no mostró diferencias con esta última droga en los niveles de colesterol plasmático total y kaliemia. Finalmente, el lisinopril fue la única de las tres drogas que redujo las glicemias promedio y tuvo significativamente menor desarrollo de diabetes mellitus. Por lo expuesto, quizás las diferencias en t érminos de reducción de PA puedan ser contrarrestadas por diferencias en efectos metabólicos, y esto pueda explicar los resultados neutros en la mayoría de los puntos finales duros.

CONCLUSIONES 

El estudio ALLHAT no mostró diferencias estadísticamente significativas entre las tres medicaciones en términos de prevención de mortalidad total e infarto de  miocardio.

Además, corrobora la presunción de que los bloqueantes de los canales de calcio no previenen el desarrollo de insuficiencia cardíaca en pacientes hipertensos arteriales, pero sorprende ostensiblemente que los inhibidores de la enzima convertidora  no tengan este efecto, según ALLHAT,  ya que en metaanálisis previos se habían observado beneficios comparables con diuréticos y/o betabloqueadores, e inclusive mayor beneficio con inhibidores ECA.

Referencias

http://www.fac.org.ar/1/revista/03v32n2/actual/act01/piskorz.PDF

http://clinical.diabetesjournals.org/content/21/3/102.full

 

Lactancia materna y alergia en lactantes


Abstract

Short-term breastfeeding or no breastfeeding, early exposure to the complex dietary proteins, such as cow-milk proteins and cereals, or to berries, fruit and roots have been implicated as risk factors for β cell autoimmunity, clinical type 1 diabetes, or both.

Importancia del tema 

Los niños que no reciben Lactancia Materna exclusiva, sino que se alimentan de fórmula común de leche vaca (CMF  sigla en inglés para Cow Milk Formula), reciben 106 veces más carga antigénica oral (es decir, muchas más probabilidades de desarrollar una respusta inmune anormal) al comparar frente a los niños alimentados exclusivamente con leche materna.

Por lo tanto, los esfuerzos se han centrado en las posibilidades de reducir la carga alergénica temprana  (entiéndase como tal cargal, la proteína de leche de vaca, que es una proteína ajena al organismo y extraña al sistema inmune del lactante) para aquellos lactantes no amamantados plenamente, mediante la modificación de la fórmula infantil, con el objetivo de prevenir la alergia alimentaria temprana, especialmente en niños con alto riesgo de enfermedad atópica Este término atópica se refiere a alergia, que suele manifestarse como dermatitis atópica (la famosa “costra de leche” que algunas veces presentan los lactantes en etapas tempranas de la vida) a veces como rinitis alérgica que es empeorada por el polvo de la casa, la caspa de mascotas como perros, gatos en los domicilios, a veces como  asma bronquial.

 .90343 (1)  Entiendo mucho mejor la afirmación de un profesor de pediatría: “La leche de vaca solo es buena para los terneros”.

La administración de leche de vaca en niños en forma temprana SE DEBE EVITAR, porque puede inducir alergia (manifestada primero como dermatitis atópica) luego como rinitis alérgica (los niños empiezan respiración oral, hacen maloclusión dental, con el costo consiguiente de los varios años de ortodoncia) y después la inexorable marca atópica suele terminar en asma. Sí, asma.

Como si no fuera poco, la leche de vaca con su carga proteica es capaz de actuar sobre el sistema inmune del lactante y hace que se produzcan anticuerpos contra las células beta del páncreas, órgano endocrino importante y esta situación puede manifestarse como DIABETES MELLITUS que requiere administración de insulina de por vida, en muchas ocasiones.

bombaAtomica La leche de vaca en un recién nacido tiene un efecto semejante al de inducir una “detonación” en el sistema inmune, cuando lo que se necesita es que dicho sistema se “despierte” gradualmente.

Fuente de esta información.

  1. von Berg A, Filipiak-Pittroff B, Krämer U, Link E, Bollrath C, Brockow I, Koletzko S, Grübl A, Heinrich J, Wichmann HE, Bauer CP, Reinhardt D, Berdel D; GINIplus study group. Preventive effect of hydrolyzed infant formulas persists until age 6 years: long-term results from the German Infant Nutritional Intervention Study (GINI). J Allergy Clin Immunol. 2008 Jun;121(6):1442-7. http://www.ncbi.nlm.nih.gov/pubmed/18539195
  2. Rosenbauer J, Herzig P, Kaiser P, Giani G. Early nutrition and risk of Type 1 diabetes mellitus–a nationwide case-control study in preschool children. Exp Clin Endocrinol Diabetes. 2007 Sep;115(8):502-8. http://www.ncbi.nlm.nih.gov/pubmed/?term=17853333
  3. Knip M, Virtanen SM, Becker D, Dupré J, Krischer JP, Åkerblom HK; TRIGR Study Group. Early feeding and risk of type 1 diabetes: experiences from the Trial to Reduce Insulin-dependent diabetes mellitus in the Genetically at Risk (TRIGR). Am J Clin Nutr. 2011 Dec;94(6 Suppl):1814S-1820S. http://www.ncbi.nlm.nih.gov/pubmed/21653795

Gaseosas y obesidad


efectos-secundarios-gaseosas

Impuestos son una medida para frenar el consumo de los refrescos. Además de tener el inconveniente que castigan al consumidor, la publicidad continua. Igual  la restricción debería ser para el productor porque lo que se va a lograr en la primera forma, es aumentar más las arcas del productor.

Con una propuesta de imponerle a la gaseosa un impuesto entre 50 y 100 pesos, el ministro de salud quiso iniciar el debate para reducir los niveles de obesidad que se registran el país.
En una conferencia médica sobre “Ciudades Saludables” celebrada en Medellín, el ministro lanzó la propuesta que según él está siendo adoptada en varios países.
La preocupación principal tiene que ver con los alarmantes niveles de obesidad y de enfermedades como diabetes tipo 2 que se registran el país y enfermedades asociadas al consumo de gaseosas.

Para el ministro esto tendría dos objetivos principales, el primero un plan de choque contra la obesidad y la diabetes y el segundo que los recursos derivados del impuesto sean utilizados por las entidades regionales para planes de atención y prevención en salud.

Un refresco regular de 591 mililitros contiene 227 calorías, de acuerdo con el Departamento de Agricultura de Estados Unidos (USDA, por sus siglas en inglés). Esa bebida tiene más del 10% del total de calorías que una mujer adulta necesita para mantener un peso saludable, de acuerdo con las pautas de dieta de la USDA. Mientras tanto, aproximadamente uno de cada cuatro estadounidenses obtiene al menos 200 calorías al día de bebidas azucaradas. Estas cifras, junto con trabajos como el de Stanhope, ofrece municiones a los médicos y funcionarios públicos de salud, que dicen que los refrescos deben ser tratados como el enemigo público de la salud número uno.

“Las bebidas gaseosas y las que contienen azúcar son la respuesta más fácil en (la razón de los problemas) de la salud pública hoy en día”, dice el médico David Ludwig, director de la Fundación New Balance del Centro de la Prevención de la Obesidad, en el Hospital Infantil en Boston, Estados Unidos. “Muchos niños están consumiendo 300 calorías por día o más, sólo en bebidas que contienen azúcar. Compara el reto de darle tres vasos de bebidas azucaradas, contra que reciban dos horas de actividad física moderada”.

“Si cambias de refresco de cola a agua, es fácil”, dice Elizabeth Mayer-Davis, una profesora en la Universidad de Carolina del Norte en Estados Unidos y recién presidenta de la Asociación Americana de Diabetes en Estados Unidos. “No tienes que hacer grandes cambios complicados en cómo cocinas y compras, y todo eso. Y el número de calorías que puedes ahorrar, puede ser sustancial”.

Lecturas complementarias

http://qcpages.qc.cuny.edu/~redwards/Papers/edwards-comment-10-657R1.pdf

http://www.alternativaregional.com/bebidas-gaseosas-el-enemigo-principal-en-la-lucha-contra-la-obesidad#sthash.8Cg1XVby.dpuf

Fuente de la figura:

http://refugiofitness.wordpress.com/2014/04/03/los-efectos-negativos-de-tomar-gaseosas/