Por primera vez el Gobierno norteamericano ha desoído las recomendaciones de su propia Agencia del Medicamento, que le aconsejaba vender la píldora del día después en las farmacias y en los supermercados, sin receta médica y sin comprobaciones por parte del farmacéutico. Hasta ahora, la píldora, conocida como Plan B, se vende con receta médica a los menores de 17 años y sin receta a todos los demás. Todos los que quieran adquirirla deben presentarle al farmacéutico una prueba de su edad, como un pasaporte o carné de conducir.
La comunidad científica y la Agencia del Medicamento le habían recomendado a Barack Obama eliminar esos filtros, para venderla libremente a todos los que la desearan, algo que el presidente ha ignorado. Por decisión del presidente, se seguirá pidiendo receta a los menores de 17 y prueba de edad a todos los que quieran adquirirla. La píldora Plan B se vende por unos 50 dólares (unos 37 euros al cambio actual) y contiene altas dosis de la hormona conocida como progestágeno sintético. Si la mujer la ingiere hasta 72 horas después del encuentro sexual puede evitar la ovulación y prevenir un embarazo no deseado. Esa píldora no tiene efecto sobre una mujer que ya esté embarazada.
El gobierno de George W. Bush se opuso a venderla sin receta. Finalmente lo permitió, reticentemente, en 2006, y sólo para mayores de 18 años. Entonces, sin embargo, el asunto ya estaba en los tribunales. Una orden judicial obligó a Obama a rebajar esa edad a los 17 años en julio de 2009. Entonces, comenzó un nuevo proceso de investigación por el cual la Agencia del Medicamento trató de averiguar si sería seguro vender el tratamiento sin restricciones en farmacias y supermercados. "Según la información que se envió a la agencia, [ésta] determinó que el producto es seguro y efectivo en mujeres adolescentes, y que las mujeres adolescentes entienden que el producto no es para uso rutinario, y que no las protege contra enfermedades de transmisión sexual", dijo el miércoles la jefa de la agencia, Margaret Hamburg.
Hamburg le pidió formalmente al gobierno que permitiera la venta libre de Plan B, junto a los preservativos y los espermicidas. Las evidencias científicas, sin embargo, no sirvieron para convencer a la Casa Blanca, a sólo un año de una campaña de reelección del presidente Obama, en la que éste deberá apelar no sólo a sus bases, sino también a los votantes más conservadores y religiosos. La Secretaria de Sanidad, Kathleen Sebelius, se justificó en un comunicado.
"La edad media de comienzo de la menstruación femenina en EE UU es de 12,4 años", dijo Sebelius. "Sin embargo, el 10% de las niñas pueden tener hijos a los 11,1 años. Es sabido que hay diferencias cognitivas y de comportamiento entre niñas adolescentes que son más mayores y las niñas más jóvenes que ya están en edad reproductiva. Si hubiera aprobado esa recomendación, ese producto hubiera estado al alcance de todas las niñas, en todas las edades reproductivas, sin receta médica".
El presidente Obama apoyó la decisión de su ministra de Sanidad en una rueda de prensa, este jueves. "Yo, que tengo dos hijas [de 13 y 10 años] estoy convencido de que debemos asegurarnos de que este asunto se gestiona con el necesario sentido común", dijo. "Es lógico que no se quiera vender la píldora a niñas de 10 o de 11 años que acudan a un supermercado y quieran comprarla, junto a chicles y pilas, porque es permitirles comprar un medicamento que, si no se usa de forma adecuada, puede tener efectos adversos".
En un cambio de tornas, los grupos conservadores han alabado al presidente Obama y la base demócrata en el Congreso le ha acusado de ignorar la ciencia y dejarse llevar por argumentos religiosos. "El proceso de investigación de la Agencia del Medicamento fue exhaustivo y concienzudo", dijo la representante demócrata Diana DeGette. "La información que se envió al Departamento de Sanidad dejaba claro que Plan B es segura y efectiva para los usos para los que se la ha destinado. El acceso a métodos anticonceptivos seguros y fiables es una parte esencial de la sanidad".
**Publicado en "EL PAIS"
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Traductor
09 December 2011
Combination of everolimus and exemestane improves survival for women with metastatic breast cancer
In an international Phase III randomized study, everolimus, when combined with the hormonal therapy exemestane, has been shown to dramatically improve progression-free survival, according to research from The University of Texas MD Anderson Cancer Center. The study, known as Breast Cancer Trials of Oral Everolimus (BOLERO-2), was presented Dec. 7 at the 2011 CTRC-AACR San Antonio Breast Cancer Symposium by Gabriel Hortobagyi, M.D., professor and chair of MD Anderson's Department of Breast Medical Oncology. Earlier findings were simultaneously reported in the New England Journal of Medicine.
Everolimus, an immunosuppressant agent first used to prevent rejection of organ transplants, also has anti-angiogenic properties. It inhibits the mammalian target of rapamycin (mTOR) protein, a central regulator of tumor cell division and blood vessel growth in cancer cells; the mTOR pathway is activated in hormone-resistant breast cancer, explained Hortobagyi. Currently, the oral agent is approved for both the treatment of kidney cancer and pancreatic neuro-endocrine tumors, with MD Anderson's research leading the way for the latter's usage approval by the FDA.
Preliminary BOLERO-2 data were first presented at ESMO and showed a significant progression-free survival benefit; these updated findings represent six additional months of patient follow-up, Hortobagyi explained.
"This study is based on the concept that we now know more about the resistance mechanisms to endocrine therapy and the experimental arm of BOLERO-2 uses a dual-attack on treatment refractory hormone receptor-positive breast cancer: it simultaneously inhibits the estrogen-signaling pathway with the aromatase inhibitor, exemestane, and the PI3-kinase/AKT/mTOR pathway with the use of everolimus," Hortobagyi said. "For the first time in a large Phase III trial, we have demonstrated that this dual-attack is more effective than a single endocrine treatment for patients who have received prior endocrine therapy."
The international Phase III trial enrolled 724 metastatic breast cancer patients, all of whom were post-menopausal, had hormone receptor-positive disease and evidence of progressive disease. In a two-to-one ratio, 485 women were randomized to receive the combination of everolimus (10 mg daily), and exemestane, an aromatase inhibitor, and compared to 239 women who received exemestane and placebo. All were previously treated with and progressed on letrozole and anastrozole, with the majority of women extensively treated with prior therapies. The median age of the women enrolled was 62 years; the study's primary endpoint was progression-free survival.
In patients receiving the everolimus combination, researchers found a progression-free survival of 7.4 months, compared to 3.2 months in those who took exemestane alone, a finding Hortobagyi describes as "highly significant." The clinical benefit rate -- complete responses, partial responses and stability exceeding six months -- was 50.5 percent in those in the combination arm, compared to 25.5 percent in those who received the hormonal therapy alone. Adverse effects, such as shortness of breath, hyperglycemia, mouth sores and fatigue, were all higher in the combination group, but were manageable and did not disrupt patients' quality of life, the researchers found. Survival data are still being analyzed.
Because aromatase inhibitors are associated with bone loss and fractures, as a safety measure, Hortobagyi and the researchers assessed patients for bone-turnover markers. The addition of everolimus was found to significantly reduce the level of such markers -- an interesting area for future study, noted Hortobagyi.
"Over the years, our treatment approach for such women with metastatic breast cancer has been sequential use of as many hormone therapies as possible, keeping metastatic disease under control for as long as possible. These findings may allow us to change our approach. In this group of heavily pre-treated patients, all of whom progressed on prior endocrine therapy, the addition of this mTOR inhibitor resulted in significant prolongation of progression-free survival and an improved response rate, with only a modest addition of toxicity," said Hortobagyi.
Hortobagyi believes that these findings may be practice-changing for women who meet the criteria for BOLERO-2. Additional studies are planned with everolimus in breast cancer, including in combination with an aromatase inhibitor in the adjuvant setting, as well as additional clinical trials in the metastatic setting.
In addition to Hortobagyi, authors on the international study include: Jorge Baselga, M.D., Massachusetts General Hospital Cancer Center and Harvard Medical School, and the NEJM study's corresponding author; Martine Piccart, M.D., Jules Bordet Institute; Hope S. Rugo, M.D., University of California, San Francisco, Helen Diller Family Comprehensive Cancer Center; Howard Burris, M.D., Sarah Cannon Research Institute; Mario Campone, M.D., Institut de Cancérologie de l'Ouest; Shinzaburo Noguchi, M.D., Osaka University; Michael Gnant, M.D., Comprehensive Cancer Center, Medical University of Vienna; Kathleen Pritchard, M.D., Sunnybrook Odette Cancer Centre; Luc Vittori, Zhiying Xu, Ph.D., Pabak Mukhopadhyay, Ph.D., Tarek Sahmoud, M.D., Ph.D. and David Lebwohl, M.D., the last five of Novartis Pharmaceuticals.
The trial was funded, in part, by Novartis. Hortobagyi reports receiving research funds from, as well as having served as a consultant for, Novartis.
**Source: University of Texas M. D. Anderson Cancer Center
Everolimus, an immunosuppressant agent first used to prevent rejection of organ transplants, also has anti-angiogenic properties. It inhibits the mammalian target of rapamycin (mTOR) protein, a central regulator of tumor cell division and blood vessel growth in cancer cells; the mTOR pathway is activated in hormone-resistant breast cancer, explained Hortobagyi. Currently, the oral agent is approved for both the treatment of kidney cancer and pancreatic neuro-endocrine tumors, with MD Anderson's research leading the way for the latter's usage approval by the FDA.
Preliminary BOLERO-2 data were first presented at ESMO and showed a significant progression-free survival benefit; these updated findings represent six additional months of patient follow-up, Hortobagyi explained.
"This study is based on the concept that we now know more about the resistance mechanisms to endocrine therapy and the experimental arm of BOLERO-2 uses a dual-attack on treatment refractory hormone receptor-positive breast cancer: it simultaneously inhibits the estrogen-signaling pathway with the aromatase inhibitor, exemestane, and the PI3-kinase/AKT/mTOR pathway with the use of everolimus," Hortobagyi said. "For the first time in a large Phase III trial, we have demonstrated that this dual-attack is more effective than a single endocrine treatment for patients who have received prior endocrine therapy."
The international Phase III trial enrolled 724 metastatic breast cancer patients, all of whom were post-menopausal, had hormone receptor-positive disease and evidence of progressive disease. In a two-to-one ratio, 485 women were randomized to receive the combination of everolimus (10 mg daily), and exemestane, an aromatase inhibitor, and compared to 239 women who received exemestane and placebo. All were previously treated with and progressed on letrozole and anastrozole, with the majority of women extensively treated with prior therapies. The median age of the women enrolled was 62 years; the study's primary endpoint was progression-free survival.
In patients receiving the everolimus combination, researchers found a progression-free survival of 7.4 months, compared to 3.2 months in those who took exemestane alone, a finding Hortobagyi describes as "highly significant." The clinical benefit rate -- complete responses, partial responses and stability exceeding six months -- was 50.5 percent in those in the combination arm, compared to 25.5 percent in those who received the hormonal therapy alone. Adverse effects, such as shortness of breath, hyperglycemia, mouth sores and fatigue, were all higher in the combination group, but were manageable and did not disrupt patients' quality of life, the researchers found. Survival data are still being analyzed.
Because aromatase inhibitors are associated with bone loss and fractures, as a safety measure, Hortobagyi and the researchers assessed patients for bone-turnover markers. The addition of everolimus was found to significantly reduce the level of such markers -- an interesting area for future study, noted Hortobagyi.
"Over the years, our treatment approach for such women with metastatic breast cancer has been sequential use of as many hormone therapies as possible, keeping metastatic disease under control for as long as possible. These findings may allow us to change our approach. In this group of heavily pre-treated patients, all of whom progressed on prior endocrine therapy, the addition of this mTOR inhibitor resulted in significant prolongation of progression-free survival and an improved response rate, with only a modest addition of toxicity," said Hortobagyi.
Hortobagyi believes that these findings may be practice-changing for women who meet the criteria for BOLERO-2. Additional studies are planned with everolimus in breast cancer, including in combination with an aromatase inhibitor in the adjuvant setting, as well as additional clinical trials in the metastatic setting.
In addition to Hortobagyi, authors on the international study include: Jorge Baselga, M.D., Massachusetts General Hospital Cancer Center and Harvard Medical School, and the NEJM study's corresponding author; Martine Piccart, M.D., Jules Bordet Institute; Hope S. Rugo, M.D., University of California, San Francisco, Helen Diller Family Comprehensive Cancer Center; Howard Burris, M.D., Sarah Cannon Research Institute; Mario Campone, M.D., Institut de Cancérologie de l'Ouest; Shinzaburo Noguchi, M.D., Osaka University; Michael Gnant, M.D., Comprehensive Cancer Center, Medical University of Vienna; Kathleen Pritchard, M.D., Sunnybrook Odette Cancer Centre; Luc Vittori, Zhiying Xu, Ph.D., Pabak Mukhopadhyay, Ph.D., Tarek Sahmoud, M.D., Ph.D. and David Lebwohl, M.D., the last five of Novartis Pharmaceuticals.
The trial was funded, in part, by Novartis. Hortobagyi reports receiving research funds from, as well as having served as a consultant for, Novartis.
**Source: University of Texas M. D. Anderson Cancer Center
Premature babies harbor fewer, but more dangerous microbe types
One of the most comprehensive studies to date of the microbes that are found in extremely low-birthweight infants found that hard-to-treat Candida fungus is often present, as well as some harmful bacteria and parasites. Researchers at the Duke University Medical Center and Nicholas School of the Environment looked at the microbes in 11 premature infants and found much less diversity than in full-term infants.
"The babies' guts were taken over by microbes we know are dangerous if they get into the blood," said senior author Patrick Seed, MD, PhD, assistant professor of pediatrics at Duke. "Even after the babies were no longer on antibiotics, healthier bacteria didn't appear in the babies very quickly. This may be one reason why premature babies are so vulnerable to infections."
All of the premature children were placed on antibiotic treatments after birth, which would wipe out some types of bacteria and yeast, but once they were off the antibiotics and taking food, the researchers expected to see more diversity of bacteria in the babies' developing digestive systems than they found.
The findings were published in PLoS One open-access journal on December 8, 2011.
Five infants had blood infections while three had necrotizing enterocolitis, an infection-related death of bowel tissue, said Seed, who is also with the Jean and George Brumley Jr. Neonatal-Perinatal Research Institute and the Duke Center for Microbial Pathogenesis.
Seed said that while the study babies were colonized mainly by organisms that were found in stool specimens, in some cases they also had infections with Staphylococcus epidermidis, a form of staph infection, that was abundant in many of the babies' digestive tracts.
The bacteria and yeast in the premature babies' digestive tracts are known causes of devastating infections in these babies. The gut seems to be a reservoir for some organisms that form infections, Seed said. Previous to this work, "we only knew the tip of the iceberg," he said.
The researchers used genomic (DNA) typing of the bacteria, fungi, and parasites to determine which types were present.
It's not clear if the newborns are picking up these early infections from their mother's milk, blood, or in other ways, or if the pathogens are from the environment surrounding the infants.
"It's important to know where these pathogens come from so that doctors can possibly manipulate the babies' environment or their digestive systems," Seed said. He noted that other studies had shown value for giving babies probiotic substances to tip the internal balance toward more favorable bacteria, necessary for immunity and better health.
Seed stressed that certain bacteria and other microbes are helpful for growing babies and their immune systems, so it is important not to do any damage by creating an antiseptic environment.
"It's a question of balance," Seed said. "As vulnerable as these babies are, we still wouldn't want to wipe out all of the bacteria, even all of the potentially harmful bacteria."
*Source: Duke University Medical Center
"The babies' guts were taken over by microbes we know are dangerous if they get into the blood," said senior author Patrick Seed, MD, PhD, assistant professor of pediatrics at Duke. "Even after the babies were no longer on antibiotics, healthier bacteria didn't appear in the babies very quickly. This may be one reason why premature babies are so vulnerable to infections."
All of the premature children were placed on antibiotic treatments after birth, which would wipe out some types of bacteria and yeast, but once they were off the antibiotics and taking food, the researchers expected to see more diversity of bacteria in the babies' developing digestive systems than they found.
The findings were published in PLoS One open-access journal on December 8, 2011.
Five infants had blood infections while three had necrotizing enterocolitis, an infection-related death of bowel tissue, said Seed, who is also with the Jean and George Brumley Jr. Neonatal-Perinatal Research Institute and the Duke Center for Microbial Pathogenesis.
Seed said that while the study babies were colonized mainly by organisms that were found in stool specimens, in some cases they also had infections with Staphylococcus epidermidis, a form of staph infection, that was abundant in many of the babies' digestive tracts.
The bacteria and yeast in the premature babies' digestive tracts are known causes of devastating infections in these babies. The gut seems to be a reservoir for some organisms that form infections, Seed said. Previous to this work, "we only knew the tip of the iceberg," he said.
The researchers used genomic (DNA) typing of the bacteria, fungi, and parasites to determine which types were present.
It's not clear if the newborns are picking up these early infections from their mother's milk, blood, or in other ways, or if the pathogens are from the environment surrounding the infants.
"It's important to know where these pathogens come from so that doctors can possibly manipulate the babies' environment or their digestive systems," Seed said. He noted that other studies had shown value for giving babies probiotic substances to tip the internal balance toward more favorable bacteria, necessary for immunity and better health.
Seed stressed that certain bacteria and other microbes are helpful for growing babies and their immune systems, so it is important not to do any damage by creating an antiseptic environment.
"It's a question of balance," Seed said. "As vulnerable as these babies are, we still wouldn't want to wipe out all of the bacteria, even all of the potentially harmful bacteria."
*Source: Duke University Medical Center
El pescado reduce el riesgo cardiaco en las mujeres jóvenes
Las mujeres jóvenes podrían reducir significativamente su riesgo de contraer enfermedades cardiovasculares mediante un hábito tan sencillo como comer más pescado rico en ácidos grasos omega 3, según una nueva investigación danesa centrada en este grupo de población.
En comparación con las mujeres que siguen una dieta rica en estos ácidos grasos, aquellas que no comen nunca o casi nunca pescado pueden presentar un riesgo hasta un 90% mayor, de acuerco con los resultados presentados en la revista 'Hypertension: Journal of the American Heart Association'.
Los investigadores, del Instituto Statens Serum en Copenhague (Dinamarca), usaron los datos de una encuesta sobre embarazos, en la que se recogieron datos de 49.000 mujeres danesas de entre 15 y 49 años y se indagó en sus hábitos alimenticios, estilo de vida e historial familiar. Las participantes tuvieron un seguimiento medio de ocho años, a partir de 1996. En este tiempo se registraron cinco muertes debidas a causas cardiovasculares sin ningún diagnóstico previo.
Además, se produjeron 328 episodios provocados por la hipertensión, 146 cerebrovasculares y 103 infartos cardiacos. Todos estos problemas resultaron ser mucho más frecuentes entre las mujeres que comían poco pescado.
"Por lo que sabemos, este ha sido el primer estudio de este tamaño que se ha centrado exclusivamente en mujeres en edad de tener hijos", señala la doctora Marin Strøm, del Centro de Programación Fetal de la citada institución danesa. "El pescado es la única fuente de la que podemos obtener cantidades importantes de los ácidos grasos omega 3", explica Strøm a ELMUNDO.es.
Hay que tener en cuenta que las mujeres con dietas pobres en pescado también presentaban , en general, mayores tasas de otros factores de riesgo, como obesidad, tabaquismo o consumo de alcohol. Aunque también eran, como media, más jóvenes y más físicamente activas.
-Beneficios a corto y largo plazo
"El mayor desafío de hacer llegar esta clase de mensajes sobre salud a las poblaciones más jóvenes radica en que se cree que los beneficios se producen a muy largo plazo, quizás en 30 o 40 años. Pero nuestro estudio muestra que este no es el caso. Hemos visto una fuerte asociación con la enfermedad cardiovascular en las mujeres que estaban aún en sus treintena tardía", explica la doctora Strøm.
El estudio específico de las mujeres es importante porque, aunque su sistema cardiovascular es parecido al de los hombres, existen también algunas diferencias, según los autores del trabajo. "Por ejemplo, la inflamación, el colesterol y los niveles de triglicéridos pueden tener un mayor influjo negativo entre mujeres", señala Strøm, quien, sin embargo, reconoce: "Pensamos que estos ácidos grasos pueden ser también beneficiosos para otros grupos".
Las mujeres que tomaban suplementos de omega 3 fueron excluidas del estudio, con el fin de observar el efecto beneficioso de tomar estos ácidos grasos únicamente en su forma natural, a través del pescado. Algunos de los productos ricos en omega 3 son el atún, la caballa, el bacalao, el salmón, el mero o el arenque.
**Publicado en "EL MUNDO"
En comparación con las mujeres que siguen una dieta rica en estos ácidos grasos, aquellas que no comen nunca o casi nunca pescado pueden presentar un riesgo hasta un 90% mayor, de acuerco con los resultados presentados en la revista 'Hypertension: Journal of the American Heart Association'.
Los investigadores, del Instituto Statens Serum en Copenhague (Dinamarca), usaron los datos de una encuesta sobre embarazos, en la que se recogieron datos de 49.000 mujeres danesas de entre 15 y 49 años y se indagó en sus hábitos alimenticios, estilo de vida e historial familiar. Las participantes tuvieron un seguimiento medio de ocho años, a partir de 1996. En este tiempo se registraron cinco muertes debidas a causas cardiovasculares sin ningún diagnóstico previo.
Además, se produjeron 328 episodios provocados por la hipertensión, 146 cerebrovasculares y 103 infartos cardiacos. Todos estos problemas resultaron ser mucho más frecuentes entre las mujeres que comían poco pescado.
"Por lo que sabemos, este ha sido el primer estudio de este tamaño que se ha centrado exclusivamente en mujeres en edad de tener hijos", señala la doctora Marin Strøm, del Centro de Programación Fetal de la citada institución danesa. "El pescado es la única fuente de la que podemos obtener cantidades importantes de los ácidos grasos omega 3", explica Strøm a ELMUNDO.es.
Hay que tener en cuenta que las mujeres con dietas pobres en pescado también presentaban , en general, mayores tasas de otros factores de riesgo, como obesidad, tabaquismo o consumo de alcohol. Aunque también eran, como media, más jóvenes y más físicamente activas.
-Beneficios a corto y largo plazo
"El mayor desafío de hacer llegar esta clase de mensajes sobre salud a las poblaciones más jóvenes radica en que se cree que los beneficios se producen a muy largo plazo, quizás en 30 o 40 años. Pero nuestro estudio muestra que este no es el caso. Hemos visto una fuerte asociación con la enfermedad cardiovascular en las mujeres que estaban aún en sus treintena tardía", explica la doctora Strøm.
El estudio específico de las mujeres es importante porque, aunque su sistema cardiovascular es parecido al de los hombres, existen también algunas diferencias, según los autores del trabajo. "Por ejemplo, la inflamación, el colesterol y los niveles de triglicéridos pueden tener un mayor influjo negativo entre mujeres", señala Strøm, quien, sin embargo, reconoce: "Pensamos que estos ácidos grasos pueden ser también beneficiosos para otros grupos".
Las mujeres que tomaban suplementos de omega 3 fueron excluidas del estudio, con el fin de observar el efecto beneficioso de tomar estos ácidos grasos únicamente en su forma natural, a través del pescado. Algunos de los productos ricos en omega 3 son el atún, la caballa, el bacalao, el salmón, el mero o el arenque.
**Publicado en "EL MUNDO"
Women advised to avoid ZEN bust-enhancing supplements because of possible cancer risk
Women who use bust-enhancing dietary supplements containing the mycoestrogen zearalenone (ZEN), a naturally occurring toxin that widely contaminates agricultural products, could be increasing their risk of breast cancer. That is the warning from breast health experts in a paper published online ahead of print publication in the January issue of IJCP, the International Journal of Clinical Practice. "No clinical trials have been published on the use of potent oestrogens like ZEN in bust-enhancing products and their use should be discouraged because of the lack of evidence of their long-term safety" says Professor Ian Fentiman, consultant breast surgeon at Guy's and St Thomas' NHS Foundation Trust, London.
The use of ZEN to increase bust size is just one of the key concerns raised by the review focussing on the affects of ZEN and its derivatives on the human reproductive system and breast cancer. It also included the use of ZEN to fatten up livestock, its use in hormone replacement therapy and oral contraceptives, its links with premature puberty and its possible effects on breast cancer.
"ZEN is a toxic non-steroidal mycoestrogen produced by fungi that widely contaminates agricultural products, such as crops, eliciting oestrogenic responses by mimicking the female sex hormones" explains Professor Fentiman.
Using ZEN in animal feed has been associated with a wide range of reproductive anomalies in livestock, including diminished fertility and infertility, reduced litter size and smaller offspring and negative effects on the reproductive organs.
International studies have suggested links between consumption of ZEN-fed animals and products and precocious (early) puberty in young females.
These include an epidemic of premature breast development and early puberty in Puerto Rico, linked to dairy and meat products, and studies from Hungary and Italy where female children with precocious puberty had increased ZEN levels in their serum.
"In fact the European Union has banned using ZEN to fatten up cattle, a technique used in the USA since 1969, because of its links with precocious puberty" says Professor Fentiman.
"Recently it has been suggested that some ZEN derivatives can increase the growth of hormone-dependent breast tumours. It has also been reported that, depending on the dose, ZEN can either promote or prevent breast cancer. So the jury on whether its links with breast cancer are positive or negative is well and truly out at this stage."
-The authors drew a number of conclusions from their review:
There is a lack of information on the human metabolism of ZEN and disagreement on the mechanisms of ZEN oestrogenic action in human tissue.
The presence of this mycoestrogen in cereals, milk, and meat, and the possibility of ZEN involvement in the development of new breast tumours, warrant further investigation.
Future studies should investigate the effects of ZEN on the growth stimulation of hormone-dependent cancers and identify the key genes that promote hormone-dependent cancers.
ZEN promotes programmed cell death and reduces the proliferation of cancer cells when administered at certain doses.
Although ZEN is a common diet toxic mycoestrogen, the potential risk to human health appears to only occur when it is absorbed in concrete concentrations or over a long period of time.
A molecular biomarker of dietary exposure to ZEN and its derivatives will allow the detection and control of harmful food intake.
The interaction of ZEN with anti-oestrogens and anticancer agents and antioxidants requires further investigation.
**Source: Wiley-Blackwell
The use of ZEN to increase bust size is just one of the key concerns raised by the review focussing on the affects of ZEN and its derivatives on the human reproductive system and breast cancer. It also included the use of ZEN to fatten up livestock, its use in hormone replacement therapy and oral contraceptives, its links with premature puberty and its possible effects on breast cancer.
"ZEN is a toxic non-steroidal mycoestrogen produced by fungi that widely contaminates agricultural products, such as crops, eliciting oestrogenic responses by mimicking the female sex hormones" explains Professor Fentiman.
Using ZEN in animal feed has been associated with a wide range of reproductive anomalies in livestock, including diminished fertility and infertility, reduced litter size and smaller offspring and negative effects on the reproductive organs.
International studies have suggested links between consumption of ZEN-fed animals and products and precocious (early) puberty in young females.
These include an epidemic of premature breast development and early puberty in Puerto Rico, linked to dairy and meat products, and studies from Hungary and Italy where female children with precocious puberty had increased ZEN levels in their serum.
"In fact the European Union has banned using ZEN to fatten up cattle, a technique used in the USA since 1969, because of its links with precocious puberty" says Professor Fentiman.
"Recently it has been suggested that some ZEN derivatives can increase the growth of hormone-dependent breast tumours. It has also been reported that, depending on the dose, ZEN can either promote or prevent breast cancer. So the jury on whether its links with breast cancer are positive or negative is well and truly out at this stage."
-The authors drew a number of conclusions from their review:
There is a lack of information on the human metabolism of ZEN and disagreement on the mechanisms of ZEN oestrogenic action in human tissue.
The presence of this mycoestrogen in cereals, milk, and meat, and the possibility of ZEN involvement in the development of new breast tumours, warrant further investigation.
Future studies should investigate the effects of ZEN on the growth stimulation of hormone-dependent cancers and identify the key genes that promote hormone-dependent cancers.
ZEN promotes programmed cell death and reduces the proliferation of cancer cells when administered at certain doses.
Although ZEN is a common diet toxic mycoestrogen, the potential risk to human health appears to only occur when it is absorbed in concrete concentrations or over a long period of time.
A molecular biomarker of dietary exposure to ZEN and its derivatives will allow the detection and control of harmful food intake.
The interaction of ZEN with anti-oestrogens and anticancer agents and antioxidants requires further investigation.
**Source: Wiley-Blackwell
Científicos de Houston descubren que la capacidad de recordar se multiplica si se inhibe una determinada molécula
Recordar el cumpleaños de tu padre o el nombre de una persona que te acaban de presentar, retener el camino de vuelta al hotel en una ciudad nueva, conservar intactos los recuerdos de la infancia de tus hijos o lo que estudiaste en el colegio. ¿Por qué hay personas cuya memoria es prodigiosa y otros que no pueden confiar en ella ni para el más ínfimo detalle? Un equipo de científicos del Baylor College of Medicine (BCM) de Houston (Texas) parece haber encontrado una molécula en cuya ausencia la memoria de los mamíferos se multiplica.
La molécula en cuestión es la PKR, estudiada durante años por su labor como protectora de los mamíferos contra infecciones virales. Pero el equipo liderado por el doctor Mauro Costa-Matiolli, profesor de neurociencia en BCM, observó que la actividad de esta molécula aparecía modificada cuando un paciente presentaba algún tipo de desorden cognitivo, por lo que comenzaron a estudiar su función en el cerebro.
El resultado fue asombroso. «Descubrimos que cuando inhibimos genéticamente la molécula PKR, aumentamos la excitabilidad de las células del cerebro y potenciamos el aprendizaje y la memoria», explica el doctor.
Durante el estudio, el equipo del BCM utilizó dos tipos de ratones. Unos con PKR en el cerebro y otros en los que esta molécula había sido inhibida. Lo que observaron fue que los ratones sin PKR tenían una especie de «súper memoria» comparados con el otro grupo de roedores. Una de las pruebas que realizaron fue comprobar la memoria espacial de los ratones para encontrar una plataforma siguiendo indicadores visuales. Los ratones normales tuvieron que repetir varias veces el ejercicio para recordar el emplazamiento de la plataforma, mientras que los ratones sin PKR aprendieron la ruta tras una única prueba.
Tras descubrir su efecto en el cerebro, la investigación se orientó a detallar el funcionamiento de este proceso molecular. Encontraron que cuando se inhibe la molécula PKR, el aumento de actividad sináptica (la comunicación entre neuronas) es producida por el interferón gamma, otra molécula relacionada con el sistema inmunitario. «Los resultados muestran que dos moléculas conocidas por su papel en el sistema inmunológico regulan el tipo de actividad cerebral que conduce a la formación de la memoria a largo plazo en el cerebro adulto», detalla Costa-Mattioli.
-Aplicación a los humanos
La verdadera revolución de este estudio, publicado en la revista científica «Cell», es que prueba que el proceso inhibidor de PKR que se realizó en los roedores se puede reproducir en los humanos. Para hacerlo universal haría falta desarrollar la «pastilla crece-memoria», un medicamento que incluiría la pequeña molécula encargada de bloquear la molécula PKR.
Costa-Mattolli es consciente de que el desarrollo de una píldora así puede tardar años y que encontrará diversos obstáculos para su aprobación en la Administración de Alimentos y Medicamentos de Estados Unidos. A pesar de ello, el mejorar la actividad cerebral de millones de personas es una meta apremiante. «Más investigación es sin duda necesaria para traducir estos resultados en terapias efectivas, pero para nosotros sería un placer si nuestro estudio contribuyese a ese fin», puntualizó el científico.
**Publicado en "ABC"
La molécula en cuestión es la PKR, estudiada durante años por su labor como protectora de los mamíferos contra infecciones virales. Pero el equipo liderado por el doctor Mauro Costa-Matiolli, profesor de neurociencia en BCM, observó que la actividad de esta molécula aparecía modificada cuando un paciente presentaba algún tipo de desorden cognitivo, por lo que comenzaron a estudiar su función en el cerebro.
El resultado fue asombroso. «Descubrimos que cuando inhibimos genéticamente la molécula PKR, aumentamos la excitabilidad de las células del cerebro y potenciamos el aprendizaje y la memoria», explica el doctor.
Durante el estudio, el equipo del BCM utilizó dos tipos de ratones. Unos con PKR en el cerebro y otros en los que esta molécula había sido inhibida. Lo que observaron fue que los ratones sin PKR tenían una especie de «súper memoria» comparados con el otro grupo de roedores. Una de las pruebas que realizaron fue comprobar la memoria espacial de los ratones para encontrar una plataforma siguiendo indicadores visuales. Los ratones normales tuvieron que repetir varias veces el ejercicio para recordar el emplazamiento de la plataforma, mientras que los ratones sin PKR aprendieron la ruta tras una única prueba.
Tras descubrir su efecto en el cerebro, la investigación se orientó a detallar el funcionamiento de este proceso molecular. Encontraron que cuando se inhibe la molécula PKR, el aumento de actividad sináptica (la comunicación entre neuronas) es producida por el interferón gamma, otra molécula relacionada con el sistema inmunitario. «Los resultados muestran que dos moléculas conocidas por su papel en el sistema inmunológico regulan el tipo de actividad cerebral que conduce a la formación de la memoria a largo plazo en el cerebro adulto», detalla Costa-Mattioli.
-Aplicación a los humanos
La verdadera revolución de este estudio, publicado en la revista científica «Cell», es que prueba que el proceso inhibidor de PKR que se realizó en los roedores se puede reproducir en los humanos. Para hacerlo universal haría falta desarrollar la «pastilla crece-memoria», un medicamento que incluiría la pequeña molécula encargada de bloquear la molécula PKR.
Costa-Mattolli es consciente de que el desarrollo de una píldora así puede tardar años y que encontrará diversos obstáculos para su aprobación en la Administración de Alimentos y Medicamentos de Estados Unidos. A pesar de ello, el mejorar la actividad cerebral de millones de personas es una meta apremiante. «Más investigación es sin duda necesaria para traducir estos resultados en terapias efectivas, pero para nosotros sería un placer si nuestro estudio contribuyese a ese fin», puntualizó el científico.
**Publicado en "ABC"
Breakthrough in regulating fat metabolism
Scientists at Warwick Medical School have made an important discovery about the mechanism controlling the body's 'fat switch', shedding new light on our understanding of how proteins regulate appetite control and insulin secretion. This research, led by Professor Victor Zammit, Head of Metabolic and Vascular Health at Warwick Medical School, found that the enzyme known as 'Carnitine palmitoyltransferase 1A' (CPT1) has a switch which is thrown depending on the composition and curvature of its cellular membrane. This is the first time such a mechanism has been described and may possibly be unique, reflecting the importance of this protein to cellular function.
CPT1 is the key protein that regulates fatty acid oxidation in the liver and is critical for metabolism. Its activity determines whether individuals suffer from fatty liver in one extreme or ketosis in the other. Professor Zammit explained: "Knowing that the CPT1 enzyme can switch and what controls it will ultimately lead to a better understanding of why some people appear to have a speedy metabolism and others struggle to curb their appetite.
"We are making great inroads to understanding the science behind our metabolism and how at cellular level it changes according to the influence of different factors -- be they nutritional or hormonal."
The importance of this work on clinical practice is that, having discovered the molecular mechanism, it should now be possible to design drugs that flick the switch of CPT1 in one way or the other, depending on the requirements of individual patients and the tissue that needs to be affected. For example, drugs can be developed for patients suffering from diabetic keto acidosis, a condition when insufficient insulin caused the body to start breaking down fat, so that the enzyme is inhibited to oxidize fewer fatty acids.
"This would be a major breakthrough in tackling the obesity crisis we now face," added Professor Zammit.
The research, conducted in association with the University of Southern California, Los Angeles, USA has been published in Journal of Biological Chemistry.
**Source: University of Warwick
CPT1 is the key protein that regulates fatty acid oxidation in the liver and is critical for metabolism. Its activity determines whether individuals suffer from fatty liver in one extreme or ketosis in the other. Professor Zammit explained: "Knowing that the CPT1 enzyme can switch and what controls it will ultimately lead to a better understanding of why some people appear to have a speedy metabolism and others struggle to curb their appetite.
"We are making great inroads to understanding the science behind our metabolism and how at cellular level it changes according to the influence of different factors -- be they nutritional or hormonal."
The importance of this work on clinical practice is that, having discovered the molecular mechanism, it should now be possible to design drugs that flick the switch of CPT1 in one way or the other, depending on the requirements of individual patients and the tissue that needs to be affected. For example, drugs can be developed for patients suffering from diabetic keto acidosis, a condition when insufficient insulin caused the body to start breaking down fat, so that the enzyme is inhibited to oxidize fewer fatty acids.
"This would be a major breakthrough in tackling the obesity crisis we now face," added Professor Zammit.
The research, conducted in association with the University of Southern California, Los Angeles, USA has been published in Journal of Biological Chemistry.
**Source: University of Warwick
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