From ScienceDaily website (see original article)
June 28, 2013 — Science knows that arsenic and estrogen can cause cancer. At certain very low levels, the chemicals offer little to no threats to human health.
However, new research conducted by Texas Tech University scientists has found that low doses of both chemicals together -- even at levels low enough to be considered "safe" for humans if they were on their own -- can cause cancer in prostate cells.
The combination of the two chemicals was almost twice as likely to create cancer in prostate cells, the research found.
The study published online in the peer-reviewed journal The Prostate.
Kamaleshwar Singh, an assistant professor at The Institute of Environmental and Human Health (TIEHH) at Texas Tech said the findings could have an impact on health regulations regarding the "safe" doses of these chemicals and others.
Most regulations are set by testing one chemical at a time on cells. Very few if any have looked at multiple chemicals at the same time.
"The majority of cancers are caused by environmental influences," Singh said.
"Only about 5 to 10 percent of cancers are due to genetic predisposition. Science has looked at these chemicals, such as arsenic, and tested them in a lab to find the amounts that may cause cancer.
But that's just a single chemical in a single test. In the real world, we are getting exposed to many chemicals at once."
Singh said he became interested in studying two chemicals at once after looking at arsenic's carcinogenic properties in a previous paper.
Because cigarette smoke and well water in some areas, including India, Mexico and even Lubbock county, can contain arsenic, Singh and his doctoral student, Justin Treas, wondered how the carcinogenic properties might change when paired with the presence of another carcinogenic chemical.
The two focused on estrogen because of the chemical's abundance. Many plastics, such as food can liners and bisphenol A (BPA), release small amounts of chemicals that mimic estrogen in the body.
"Co-exposure was creating a greater impact," Singh said. "That was one of the important findings of our study.
The next thing we wanted to know is how these two chemicals are creating a greater effect."
Unlike stronger chemicals that do major damage to the DNA in a cell, such as benzene, arsenic and estrogen aren't major mutagens Singh said.
Instead, their presence tends to stop certain genes from expressing. The process is called DNA hypermethylation.
In the experiment, human prostate cells were treated about once a week for six months with arsenic, estrogen and a combination of the two.
Many of the tests involved levels of arsenic, estrogen or both at levels considered safe by the Environmental Protection Agency.
Treas said the two chemicals stopped the MLH1 gene, which is responsible for sending the signal to start the self-destruct sequence when a cell is damaged. Because the self-destruct couldn't activate, the cells became cancerous after exposure.
"With the lower dose not killing the cell, it's causing damages that go under the cell's radar," Treas said. "We found when you have two compounds together, lower doses could be more serious problem."
lunedì 8 luglio 2013
sabato 22 giugno 2013
Dietary Fructose Causes Liver Damage in Animal Model
From ScienceDaily website (see original article)
June 19, 2013 — The role of dietary fructose in the development of obesity and fatty liver diseases remains controversial, with previous studies indicating that the problems resulted from fructose and a diet too high in calories.
However, a new study conducted in an animal model at Wake Forest Baptist Medical Center showed that fructose rapidly caused liver damage even without weight gain.
The researchers found that over the six-week study period liver damage more than doubled in the animals fed a high-fructose diet as compared to those in the control group.
The study is published in the June 19 online edition of the American Journal of Clinical Nutrition.
"Is a calorie a calorie? Are they all created equal? Based on this study, we would say not," said Kylie Kavanagh, D.V.M., assistant professor of pathology-comparative medicine at Wake Forest Baptist and lead author of the study.
In a previous trial which is referenced in the current journal article, Kavanagh's team studied monkeys who were allowed to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period.
Not surprisingly, the animals allowed to eat as much as they wanted of the high-fructose diet gained 50 percent more weight than the control group.
They developed diabetes at three times the rate of the control group and also developed hepatic steatosis, or non-alcoholic fatty liver disease.
The big question for the researchers was what caused the liver damage.
Was it because the animals got fat from eating too much, or was it something else?
To answer that question, this study was designed to prevent weight gain.
Ten middle-aged, normal weight monkeys who had never eaten fructose were divided into two groups based on comparable body shapes and waist circumference.
Over six weeks, one group was fed a calorie-controlled diet consisting of 24 percent fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose, approximately 0.5 percent.
Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. The high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), similar to what many people eat, while the control group's diet was made from healthy complex carbohydrates and soy protein.
Every week the research team weighed both groups and measured their waist circumference, then adjusted the amount of food provided to prevent weight gain.
At the end of the study, the researchers measured biomarkers of liver damage through blood samples and examined what type of bacteria was in the intestine through fecal samples and intestinal biopsies.
"What surprised us the most was how quickly the liver was affected and how extensive the damage was, especially without weight gain as a factor," Kavanagh said.
"Six weeks in monkeys is roughly equivalent to three months in humans."
In the high-fructose group, the researchers found that the type of intestinal bacteria hadn't changed, but that they were migrating to the liver more rapidly and causing damage there.
It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30 percent higher rate, Kavanagh said.
One of the limitations of the study was that it only tested for fructose and not dextrose.
Fructose and dextrose are simple sugars found naturally in plants.
"We studied fructose because it is the most commonly added sugar in the American diet, but based on our study findings, we can't say conclusively that fructose caused the liver damage," Kavanagh said.
"What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.
"The liver damage began even in the absence of weight gain.
This could have clinical implications because most doctors and scientists have thought that it was the fat in and around tissues in the body that caused the health problems."
The Wake Forest Baptist team plans to begin a new study using the same controls but testing for both fructose and dextrose over a longer time frame.
June 19, 2013 — The role of dietary fructose in the development of obesity and fatty liver diseases remains controversial, with previous studies indicating that the problems resulted from fructose and a diet too high in calories.
However, a new study conducted in an animal model at Wake Forest Baptist Medical Center showed that fructose rapidly caused liver damage even without weight gain.
The researchers found that over the six-week study period liver damage more than doubled in the animals fed a high-fructose diet as compared to those in the control group.
The study is published in the June 19 online edition of the American Journal of Clinical Nutrition.
"Is a calorie a calorie? Are they all created equal? Based on this study, we would say not," said Kylie Kavanagh, D.V.M., assistant professor of pathology-comparative medicine at Wake Forest Baptist and lead author of the study.
In a previous trial which is referenced in the current journal article, Kavanagh's team studied monkeys who were allowed to eat as much as they wanted of low-fat food with added fructose for seven years, as compared to a control group fed a low-fructose, low-fat diet for the same time period.
Not surprisingly, the animals allowed to eat as much as they wanted of the high-fructose diet gained 50 percent more weight than the control group.
They developed diabetes at three times the rate of the control group and also developed hepatic steatosis, or non-alcoholic fatty liver disease.
The big question for the researchers was what caused the liver damage.
Was it because the animals got fat from eating too much, or was it something else?
To answer that question, this study was designed to prevent weight gain.
Ten middle-aged, normal weight monkeys who had never eaten fructose were divided into two groups based on comparable body shapes and waist circumference.
Over six weeks, one group was fed a calorie-controlled diet consisting of 24 percent fructose, while the control group was fed a calorie-controlled diet with only a negligible amount of fructose, approximately 0.5 percent.
Both diets had the same amount of fat, carbohydrate and protein, but the sources were different, Kavanagh said. The high-fructose group's diet was made from flour, butter, pork fat, eggs and fructose (the main ingredient in corn syrup), similar to what many people eat, while the control group's diet was made from healthy complex carbohydrates and soy protein.
Every week the research team weighed both groups and measured their waist circumference, then adjusted the amount of food provided to prevent weight gain.
At the end of the study, the researchers measured biomarkers of liver damage through blood samples and examined what type of bacteria was in the intestine through fecal samples and intestinal biopsies.
"What surprised us the most was how quickly the liver was affected and how extensive the damage was, especially without weight gain as a factor," Kavanagh said.
"Six weeks in monkeys is roughly equivalent to three months in humans."
In the high-fructose group, the researchers found that the type of intestinal bacteria hadn't changed, but that they were migrating to the liver more rapidly and causing damage there.
It appears that something about the high fructose levels was causing the intestines to be less protective than normal, and consequently allowing the bacteria to leak out at a 30 percent higher rate, Kavanagh said.
One of the limitations of the study was that it only tested for fructose and not dextrose.
Fructose and dextrose are simple sugars found naturally in plants.
"We studied fructose because it is the most commonly added sugar in the American diet, but based on our study findings, we can't say conclusively that fructose caused the liver damage," Kavanagh said.
"What we can say is that high added sugars caused bacteria to exit the intestines, go into the blood stream and damage the liver.
"The liver damage began even in the absence of weight gain.
This could have clinical implications because most doctors and scientists have thought that it was the fat in and around tissues in the body that caused the health problems."
The Wake Forest Baptist team plans to begin a new study using the same controls but testing for both fructose and dextrose over a longer time frame.
venerdì 31 maggio 2013
Phthalates -- Chemicals Widely Found in Plastics and Processed Food -- Linked to Elevated Blood Pressure in Children and Teens
From ScienceDaily website (see original article)
May 22, 2013 — Plastic additives known as phthalates (pronounced THAL-ates) are odorless, colorless and just about everywhere: They turn up in flooring, plastic cups, beach balls, plastic wrap, intravenous tubing and -- according to the Centers for Disease Control and Prevention -- the bodies of most Americans.
Once perceived as harmless, phthalates have come under increasing scrutiny.
A growing collection of evidence suggests dietary exposure to phthalates (which can leech from packaging and mix with food) may cause significant metabolic and hormonal abnormalities, especially during early development.
Now, new research published this Wednesday in The Journal of Pediatrics suggests that certain types of phthalates could pose another risk to children: compromised heart health.
Drawing on data from a nationally representative survey of nearly 3,000 children and teens, researchers at NYU Langone Medical Center, in collaboration with researchers at the University of Washington and Penn State University School of Medicine, have documented for the first time a connection between dietary exposure to DEHP (di-2-ethyhexylphthalate), a common class of phthalate widely used in industrial food production, and elevated systolic blood pressure, a measure of pressure in the arteries when the heart contracts.
"Phthalates can inhibit the function of cardiac cells and cause oxidative stress that compromises the health of arteries.
But no one has explored the relationship between phthalate exposure and heart health in children" says lead author Leonardo Trasande, MD, MPP, associate professor of pediatrics, environmental medicine and population health at NYU Langone Medical Center.
"We wanted to examine the link between phthalates and childhood blood pressure in particular given the increase in elevated blood pressure in children and the increasing evidence implicating exposure to environmental exposures in early development of disease."
Hypertension is clinically defined as a systolic blood-pressure reading above 140 mm Hg.
It's most common in people over 50 years old, although the condition is becoming increasingly prevalent among children owing to the global obesity epidemic. Recent national surveys indicate that 14 percent of American adolescents now have pre-hypertension or hypertension.
"Obesity is driving the trend but our findings suggest that environmental factors may also be a part of the problem," says Dr. Trasande.
"This is important because phthalate exposure can be controlled through regulatory and behavioral interventions."
Researchers from NYU School of Medicine, the University of Washington and Penn State University School of Medicine examined six years of data from a nationally representative survey of the U.S. population administered by the National Centers for Health Statistics of the Centers for Disease Control and Prevention.
Phthalates were measured in urine samples using standard analysis techniques.
Controlling for a number of potential confounders, including race, socioeconomic status, body mass index, caloric intake and activity levels, the researchers found that every three-fold increase in the level of breakdown products of DEHP in urine correlated with a roughly one-millimeter mercury increase in a child's blood pressure.
"That increment may seem very modest at an individual level, but on a population level such shifts in blood pressure can increase the number of children with elevated blood pressure substantially," says Dr. Trasande.
"Our study underscores the need for policy initiatives that limit exposure to disruptive environmental chemicals, in combination with dietary and behavioral interventions geared toward protecting cardiovascular health."
May 22, 2013 — Plastic additives known as phthalates (pronounced THAL-ates) are odorless, colorless and just about everywhere: They turn up in flooring, plastic cups, beach balls, plastic wrap, intravenous tubing and -- according to the Centers for Disease Control and Prevention -- the bodies of most Americans.
Once perceived as harmless, phthalates have come under increasing scrutiny.
A growing collection of evidence suggests dietary exposure to phthalates (which can leech from packaging and mix with food) may cause significant metabolic and hormonal abnormalities, especially during early development.
Now, new research published this Wednesday in The Journal of Pediatrics suggests that certain types of phthalates could pose another risk to children: compromised heart health.
Drawing on data from a nationally representative survey of nearly 3,000 children and teens, researchers at NYU Langone Medical Center, in collaboration with researchers at the University of Washington and Penn State University School of Medicine, have documented for the first time a connection between dietary exposure to DEHP (di-2-ethyhexylphthalate), a common class of phthalate widely used in industrial food production, and elevated systolic blood pressure, a measure of pressure in the arteries when the heart contracts.
"Phthalates can inhibit the function of cardiac cells and cause oxidative stress that compromises the health of arteries.
But no one has explored the relationship between phthalate exposure and heart health in children" says lead author Leonardo Trasande, MD, MPP, associate professor of pediatrics, environmental medicine and population health at NYU Langone Medical Center.
"We wanted to examine the link between phthalates and childhood blood pressure in particular given the increase in elevated blood pressure in children and the increasing evidence implicating exposure to environmental exposures in early development of disease."
Hypertension is clinically defined as a systolic blood-pressure reading above 140 mm Hg.
It's most common in people over 50 years old, although the condition is becoming increasingly prevalent among children owing to the global obesity epidemic. Recent national surveys indicate that 14 percent of American adolescents now have pre-hypertension or hypertension.
"Obesity is driving the trend but our findings suggest that environmental factors may also be a part of the problem," says Dr. Trasande.
"This is important because phthalate exposure can be controlled through regulatory and behavioral interventions."
Researchers from NYU School of Medicine, the University of Washington and Penn State University School of Medicine examined six years of data from a nationally representative survey of the U.S. population administered by the National Centers for Health Statistics of the Centers for Disease Control and Prevention.
Phthalates were measured in urine samples using standard analysis techniques.
Controlling for a number of potential confounders, including race, socioeconomic status, body mass index, caloric intake and activity levels, the researchers found that every three-fold increase in the level of breakdown products of DEHP in urine correlated with a roughly one-millimeter mercury increase in a child's blood pressure.
"That increment may seem very modest at an individual level, but on a population level such shifts in blood pressure can increase the number of children with elevated blood pressure substantially," says Dr. Trasande.
"Our study underscores the need for policy initiatives that limit exposure to disruptive environmental chemicals, in combination with dietary and behavioral interventions geared toward protecting cardiovascular health."
lunedì 6 maggio 2013
Melanoma Succumbs To Natural Plant Substance Gossypin In Lab Tests
For the first time, using lab tests on cell cultures and mice, researchers in the US have shown that gossypin, a naturally-occurring substance found in plants, may be an effective treatment against melanoma, the deadliest form of skin cancer.
Hareesh Nair of the Texas Biomedical Research Institute, and colleagues, write about their findings in the April issue of Molecular Cancer Therapeutics.
In their background information they explain that previous studies have shown gossypin, a flavone originally isolated from the hibiscus plant (H. vitifolius), suppresses inflammation and cancer.
However, the underlying molecular activity has not been clear.
In this study, they show that the substance inhibits the action of two gene mutations that commonly occur in people with melanoma, as Nair explains in a press statement:
"Our results indicate that gossypin may have great therapeutic potential as a dual inhibitor of mutations called BRAFV600E kinase and CDK4, which occur in the vast majority of melanoma patients."
According to the American Cancer Society, every year, about 76,000 people are diagnosed with melanoma, the least common form of skin cancer, but the one responsible for the most deaths.
There is currently no single drug or combination that treats all types of melanoma.
For their study, Nair and colleagues tested the effect of gossypin on melanoma in cell cultures and also in live mice.
In the cell culture experiments they found that gossypin stopped cancer cell growth in melanoma cell lines that contained the two gene mutations and stopped the growth of various human melanoma cells.
They suggest gossypin stunted the activity of the mutations by binding with them directly "as confirmed by molecular docking studies".
Gossypin treatment also reduced tumor volume and increased survival rate in mice transplanted with human melanoma tumors containing the two mutated genes.
The authors conclude that:
"In summary, this study identified gossypin as a novel agent with dual inhibitory effects for BRAFV600E kinase and CDK4 for treatment of melanoma."
Nair says the findings "open a new avenue for the generation of a novel class of compounds for the treatment of melanoma".
He and his team now plan to do further studies to understand how the body absorbs and metabolizes gossypin.
The study was funded by the Texas Biomedical Forum and the Robert J. Kleberg, Jr. and Helen C. Kleberg Foundation.
sabato 4 maggio 2013
Crescono le allergie alimentari e cutanee nei bambini
Tratto da Repubblica Salute
Uno studio degli statunitensi "Centers for Disease Control and Prevention (CDC)", che ha comparato le risposte date da genitori nei periodi 1997-1999 e 2009-2011, lancia l’allarme sulle allergie alimentari e cutanee nei bambini, che starebbero aumentando rapidamente.
È bene sottolineare però che i ricercatori non hanno avuto modo di verificare se si trattasse di un'opinione personale o di una diagnosi medica e non hanno avuto accesso ai dati clinici dei bambini. Se i dati raccolti venissero confermati da indagini più approfondite, il fenomeno sarebbe allarmante.
MA È VERA ALLERGIA? - Con un incremento del 50 per cento rispetto alla fine degli anni '90, oggi negli Usa un bambino su 20 soffrirebbe di allergie alimentari e uno su 8 di allergie cutanee come la dermatite atopica e l'eczema.
Non sono stati invece registrati significativi aumenti delle patologie respiratorie allergiche, come la rinite allergica (comunemente chiamata raffreddore da fieno), ritenuta spesso un sintomo predittivo dell'asma nell'età adulta.
Il sospetto è che l'incremento di queste patologie sia dovuto al fatto che i bambini, vivendo in case sempre più pulite, siano diventati più sensibili agli allergeni o che i genitori pongano oggi maggiore (forse persino troppa) attenzione a qualunque reazione cutanea dei propri figli e siano facilmente, e spesso erroneamente, portati a parlare di allergia.
«Non abbiamo una risposta» è la laconica dichiarazione di Lara Akinbami, a capo del team che ha condotto lo studio.
Ma se da un lato è certo che esiste un aumento delle allergie, anche se è decisamente difficile quantificarlo e spiegarlo, dall’altro lato è altrettanto vero che esiste anche una psicosi da allergie.
Come ha sottolineato Morton Galina, allergologo pediatrico dell'Atlanta's Emory School of Medicine, «visitiamo spesso bambini che non sono affatto allergici all'alimento indicato dai loro genitori».
Per esempio, spesso la comparsa dell'orticaria viene erroneamente attribuita al cibo, quando la causa è più semplicemente un virus.
QUALI SPIEGAZIONI? - L'abuso di disinfettanti e antibiotici nelle case americane rovescia la teoria secondo la quale l'esposizione a microbi e batteri a partire dalla prima infanzia abbia un certo effetto preventivo sullo sviluppo delle allergie.
A sostegno di questa teoria vi è un dato raccolto da altre ricerche che sostengono che i bambini che vivono negli Stati Uniti, ma sono nati all'estero (dove è generalmente minore l’impiego di disinfettanti) da genitori stranieri, hanno tassi molto più bassi di allergie cutanee e alimentari.
Un'altra ipotesi riguarda le grandi aree urbane, dove i casi di allergia infantile sono decisamente più numerosi: gli inquinanti dispersi nell'aria metropolitana potrebbero essere i veri responsabili dell'insorgere delle patologie allergiche.
Inoltre vengono guardate con sospetto anche le nuove tecniche di coltivazione e l'allevamento del bestiame, come l'ibridazione del frumento e la somministrazione di antibiotici ai bovini.
Infine, persino la medicina ha dovuto rivedere quello che era considerato praticamente un dogma: per molto tempo, infatti, è stato consigliato alle famiglie con storie di eczema o allergie alimentari di avvicinare il più tardi possibile i propri figli ad alimenti potenzialmente pericolosi come noccioline, latte e uova.
Negli ultimi anni è stata invece invertita completamente la rotta, poiché ci si è accorti che il ritardo nell'assaggio dei cibi era una probabile causa di allergia.
È bene ricordare che l'allergia alimentare è una patologia decisamente rischiosa che in taluni casi può comportare choc anafilattico e addirittura la morte in chi ne soffre, se inavvertitamente o inconsapevolmente consuma alimenti non indicati.
ALLERGIE POVERE E RICCHE - Nel corso della ricerca sono emerse significative indicazioni che mettono in relazione la classe sociale e le patologie allergiche.
I bimbi nati in famiglie ad alto reddito soffrono maggiormente di allergie respiratorie e alimentari rispetto ai loro coetanei meno abbienti, a loro volta più colpiti da quelle cutanee.
Infine esiste anche una chiara indicazione etnica: il 17 per cento dei bambini afro-americani ha problemi dermatologici, contro il 12 per cento dei bianchi e il 10 degli ispanici.
Uno studio degli statunitensi "Centers for Disease Control and Prevention (CDC)", che ha comparato le risposte date da genitori nei periodi 1997-1999 e 2009-2011, lancia l’allarme sulle allergie alimentari e cutanee nei bambini, che starebbero aumentando rapidamente.
È bene sottolineare però che i ricercatori non hanno avuto modo di verificare se si trattasse di un'opinione personale o di una diagnosi medica e non hanno avuto accesso ai dati clinici dei bambini. Se i dati raccolti venissero confermati da indagini più approfondite, il fenomeno sarebbe allarmante.
MA È VERA ALLERGIA? - Con un incremento del 50 per cento rispetto alla fine degli anni '90, oggi negli Usa un bambino su 20 soffrirebbe di allergie alimentari e uno su 8 di allergie cutanee come la dermatite atopica e l'eczema.
Non sono stati invece registrati significativi aumenti delle patologie respiratorie allergiche, come la rinite allergica (comunemente chiamata raffreddore da fieno), ritenuta spesso un sintomo predittivo dell'asma nell'età adulta.
Il sospetto è che l'incremento di queste patologie sia dovuto al fatto che i bambini, vivendo in case sempre più pulite, siano diventati più sensibili agli allergeni o che i genitori pongano oggi maggiore (forse persino troppa) attenzione a qualunque reazione cutanea dei propri figli e siano facilmente, e spesso erroneamente, portati a parlare di allergia.
«Non abbiamo una risposta» è la laconica dichiarazione di Lara Akinbami, a capo del team che ha condotto lo studio.
Ma se da un lato è certo che esiste un aumento delle allergie, anche se è decisamente difficile quantificarlo e spiegarlo, dall’altro lato è altrettanto vero che esiste anche una psicosi da allergie.
Come ha sottolineato Morton Galina, allergologo pediatrico dell'Atlanta's Emory School of Medicine, «visitiamo spesso bambini che non sono affatto allergici all'alimento indicato dai loro genitori».
Per esempio, spesso la comparsa dell'orticaria viene erroneamente attribuita al cibo, quando la causa è più semplicemente un virus.
QUALI SPIEGAZIONI? - L'abuso di disinfettanti e antibiotici nelle case americane rovescia la teoria secondo la quale l'esposizione a microbi e batteri a partire dalla prima infanzia abbia un certo effetto preventivo sullo sviluppo delle allergie.
A sostegno di questa teoria vi è un dato raccolto da altre ricerche che sostengono che i bambini che vivono negli Stati Uniti, ma sono nati all'estero (dove è generalmente minore l’impiego di disinfettanti) da genitori stranieri, hanno tassi molto più bassi di allergie cutanee e alimentari.
Un'altra ipotesi riguarda le grandi aree urbane, dove i casi di allergia infantile sono decisamente più numerosi: gli inquinanti dispersi nell'aria metropolitana potrebbero essere i veri responsabili dell'insorgere delle patologie allergiche.
Inoltre vengono guardate con sospetto anche le nuove tecniche di coltivazione e l'allevamento del bestiame, come l'ibridazione del frumento e la somministrazione di antibiotici ai bovini.
Infine, persino la medicina ha dovuto rivedere quello che era considerato praticamente un dogma: per molto tempo, infatti, è stato consigliato alle famiglie con storie di eczema o allergie alimentari di avvicinare il più tardi possibile i propri figli ad alimenti potenzialmente pericolosi come noccioline, latte e uova.
Negli ultimi anni è stata invece invertita completamente la rotta, poiché ci si è accorti che il ritardo nell'assaggio dei cibi era una probabile causa di allergia.
È bene ricordare che l'allergia alimentare è una patologia decisamente rischiosa che in taluni casi può comportare choc anafilattico e addirittura la morte in chi ne soffre, se inavvertitamente o inconsapevolmente consuma alimenti non indicati.
ALLERGIE POVERE E RICCHE - Nel corso della ricerca sono emerse significative indicazioni che mettono in relazione la classe sociale e le patologie allergiche.
I bimbi nati in famiglie ad alto reddito soffrono maggiormente di allergie respiratorie e alimentari rispetto ai loro coetanei meno abbienti, a loro volta più colpiti da quelle cutanee.
Infine esiste anche una chiara indicazione etnica: il 17 per cento dei bambini afro-americani ha problemi dermatologici, contro il 12 per cento dei bianchi e il 10 degli ispanici.
giovedì 2 maggio 2013
Autismo, schizofrenia, ADHD, bipolarismo e depressione condividono gli stessi geni
Da Repubblica Salute (28/02/13).
Autismo e schizofrenia pari non sono, su questo non c'è dubbio alcuno.
Ma uno studio pubblicato sulla prestigiosa rivista medica Lancet ora getta nuova luce sui fattori in comune di queste due malattie e di altre tre: sindrome da deficit di attenzione e iperattività (ADHD), disturbo bipolare e depressione.
Tutte queste malattie condividono infatti alcuni rischi d'origine genetica.
A dimostrarlo è appunto un'enorme studio del Psychiatric Genomics Consortium, un ente a cui collaborano ricercatori in 19 paesi, che ha analizzato 61mila individui, alcuni che soffrivano di questi disturbi e altri no.
"Queste malattie, che oggi consideriamo nettamente diverse le une dalle altre, potrebbero avere confini molto più smussati", spiega il dottor Jordan Smoller del Massachusetts General Hospital, uno dei medici a capo del progetto.
I ricercatori hanno trovato quattro regioni di dna collegato a tutti e cinque i disturbi, e in particolare le variazioni di due geni che regolano il flusso di calcio nelle cellule cerebrali, meccanismo chiave con cui i neuroni dialogano.
Secondo i ricercatori, queste variazioni possono essere uno dei processi precursori dell'insorgere della malattia.
E chiarire questo funzionamento può avere importanti ripercussioni nella diagnosi di questi disturbi.
Perché il problema con le malattie mentali è proprio un'identificazione adeguata.
Se per le malattie fisiche esistono esami specifici, in psichiatria questo è più aleatorio.
"E dobbiamo migliorare la nostra comprensione di ciò che va storto biologicamente per diagnosticarle al meglio", spiega Bruce Cuthbert del National Institute on Mental Health, che ha finanziato lo studio.
Va detto chiaramente per non generare false aspettative: questo studio non porterà nell'immediato alcun beneficio ai pazienti e alle loro famiglie.
Queste malattie insorgono per un complesso numero di fattori di rischio e di geni, e questi individuati oggi sono solo una parte del mix.
Autismo e schizofrenia pari non sono, su questo non c'è dubbio alcuno.
Ma uno studio pubblicato sulla prestigiosa rivista medica Lancet ora getta nuova luce sui fattori in comune di queste due malattie e di altre tre: sindrome da deficit di attenzione e iperattività (ADHD), disturbo bipolare e depressione.
Tutte queste malattie condividono infatti alcuni rischi d'origine genetica.
A dimostrarlo è appunto un'enorme studio del Psychiatric Genomics Consortium, un ente a cui collaborano ricercatori in 19 paesi, che ha analizzato 61mila individui, alcuni che soffrivano di questi disturbi e altri no.
"Queste malattie, che oggi consideriamo nettamente diverse le une dalle altre, potrebbero avere confini molto più smussati", spiega il dottor Jordan Smoller del Massachusetts General Hospital, uno dei medici a capo del progetto.
I ricercatori hanno trovato quattro regioni di dna collegato a tutti e cinque i disturbi, e in particolare le variazioni di due geni che regolano il flusso di calcio nelle cellule cerebrali, meccanismo chiave con cui i neuroni dialogano.
Secondo i ricercatori, queste variazioni possono essere uno dei processi precursori dell'insorgere della malattia.
E chiarire questo funzionamento può avere importanti ripercussioni nella diagnosi di questi disturbi.
Perché il problema con le malattie mentali è proprio un'identificazione adeguata.
Se per le malattie fisiche esistono esami specifici, in psichiatria questo è più aleatorio.
"E dobbiamo migliorare la nostra comprensione di ciò che va storto biologicamente per diagnosticarle al meglio", spiega Bruce Cuthbert del National Institute on Mental Health, che ha finanziato lo studio.
Va detto chiaramente per non generare false aspettative: questo studio non porterà nell'immediato alcun beneficio ai pazienti e alle loro famiglie.
Queste malattie insorgono per un complesso numero di fattori di rischio e di geni, e questi individuati oggi sono solo una parte del mix.
mercoledì 1 maggio 2013
Connection Between Inflammatory Stimulus and Parkinson's Disease Examined
From ScienceDaily website
Apr. 29, 2013 — Parkinson's disease (PD) is a progressive degenerative disease affecting a person's ability to coordinate and control their muscle movement.
What starts out as a tremor in a finger will eventually lead to difficulty in writing and speaking, and ultimately the inability to walk without assistance.
Since the 1950s research has shown that people with Parkinson's have decreased levels of the chemical dopamine in their brains, which is involved in sending messages to the part of the brain that controls coordination and movement.
Subsequent research has found that dopamine-generating cells, known as dopaminergic neurons, are also absent in a specific area of the brain in those with PD.
The precise cause or causes of PD is unknown, but there is a consensus that an inflammatory event or episode is involved in the initiation of neurodegeneration, and that chronic neuroinflammation is a sustaining and exacerbating reason for the loss of the dopaminergic neurons.
A new study conducted by a team of Texas researchers brings the understanding of inflammation's role a step further.
They have found that a single, high-dose exposure of an experimental inflammatory agent in an animal model causes changes in brain tissue that are similar to those associated with the development of the disease.
The study was conducted by Roger Bick and his colleagues Marie-Francoise Doursout, Michael S. Schurdell, Lauren M. Young, Uzondu Osuagwu, Diana M. Hook, Brian J. Poindexter, Mya C. Schiess, and Diane L. M. Bick, all at The University of Texas Health Science Center at Houston (UTHealth), Houston, TX.
Dr. Schiess presented the team's findings at last week's Experimental Biology 2013 meeting, held at the Boston Convention and Exhibition Center, Boston, Mass.
Their poster presentation was entitled, "Inflammatory cells and cytokines in the olfactory bulb of a rat model of neuroinflammation; Insights into neurodegeneration?" The full study will appear in an upcoming edition of the Journal of Interferon & Cytokine Research.
Methodology
In the study, the researchers examined inflammatory cell and cytokine production in brain tissue from a lipopolysaccharide (LPS)-treated rat model that mimics many of the neuropathologic changes associated with PD.
Concurrently, they monitored the appearance of glial cell line-derived neurotrophic factor (GDNF), a neuronal protective agent, and circulating nitric oxide (NO) levels. They also examined the immune system associated cells in the olfactory bulb of the brain. It is known that Parkinson's starts with this mechanism.
Twelve male Sprague-Dawley rats were treated with intravenous LPS in saline, 12 control rats were treated with saline, and all were maintained for up to 48 hours before euthanasia and brain removal.
Brains were removed from both groups at defined times, blood and other tests were conducted, and images of various sections of the brain, including the olfactory bulb, cortex and cerebellum, were taken using fluorescent microscopy.
Results and Conclusions
In general, the researchers found that a single injection of LPS elicited a systemic inflammatory response in the rats, as indicated by an elevation in certain circulatory cytokines. Tissue taken from the olfactory bulb showed the presence of immune associated cells.
Individual cytokines within the olfactory bulb showed an increase in certain types of cytokines.
Taken together, the complete analysis indicated that the single dose of LPS stimulated an inflammatory response that closely resembled the hallmarks of the development of the disease.
The results suggest an involvement of both the peripheral and the central nervous system immune components in response to inflammation and inflammatory episodes.
As a result, the researchers suggest:
(1) inflammation initiates an immune response;
(2) the presence of continuing and increasing pro-inflammatory mechanisms results in a process whereby cellular protective mechanisms are overcome and the more susceptible cells, such as the dopaminergic neurons, enter into cell death pathways; and
(3) this leads to a series of events that are a key part of the progression of PD.
Next Steps
Neuroinflammation is a significant problem for those with PD, and it persists throughout the course of this debilitating illness.
Understanding of the essential processes behind it is the best pathway to finding therapeutic approaches to address it.
This study highlights an opportunity to better understand the role inflammation plays in the process.
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