From ScienceDaily website (see original article)
Oct. 30, 2013 — Making fat cells immortal might seem like a bad idea to most people, but for a team of University of Iowa scientists it was the ideal way to study how the interaction between bacteria and fat cells might contribute to diabetes.
The connection between fat, bacteria, and diabetes is inflammation, which is the body's normal reaction to infection or injury.
Inflammation is beneficial in small, controlled doses but can be extremely harmful when it persists and becomes chronic.
"The idea is that when fat cells (adipocytes) interact with environmental agents -- in this case, bacterial toxins -- they then trigger a chronic inflammatory process," says Patrick Schlievert, Ph.D., UI professor and head of microbiology and co-senior author of a new study published in the journal PLOS ONE.
"We know that chronic inflammation leads to insulin resistance, which can then lead to diabetes.
So people are very interested in the underlying causes of chronic inflammation."
The UI researchers used immortalized fat cells to show that bacterial toxins stimulate fat cells to release molecules called cytokines, which promote inflammation.
By immortalizing fat cells the UI team created a stockpile of continuously dividing, identical cells that are necessary for repeat experiments to validate results, explains Al Klingelhutz, Ph.D., UI microbiologist and co-senior author of the study.
Previous studies have shown that a toxin called lipopolysaccharide (LPS) produced by E. coli bacteria that reside in the human gut, triggers fat cells to produce pro-inflammatory cytokines, and this interaction has been proposed to contribute to the development of diabetes.
The UI team focused on a different bacterium, Staphylococcus aureus (staph), which appears to be important in the context of diabetes for two reasons. First, as people become obese and then progress into diabetes they become very heavily colonized with staph bacteria.
Secondly, staph is the most common microbe isolated from diabetic foot ulcers, one of the most common and health-threatening complications of diabetes.
All staph bacteria make toxins called superantigens -- molecules that disrupt the immune system.
Schlievert's research has previously shown that superantigens cause the deadly effects of various staph infections, such as toxic shock syndrome, sepsis, and endocarditis.
The new UI study shows that superantigens from staph bacteria trigger fat cells to produce pro-inflammatory molecules.
Moreover, the study found that superantigens synergized with LPS from E. coli to magnify fat cells' cytokine responses, amplifying the inflammation, which could potentially boost the likelihood of developing diabetes.
"The E. coli that resides in our gut produces LPS and every day a small amount of this toxin gets into our circulation, but it is generally cleared from the circulation by the liver.
However, people colonized by staph bacteria are also chronically exposed to superantigens, which shut down the LPS detoxification pathway," Schlievert explains.
"That creates a synergy between the 'uncleared' LPS and the superantigen.
All these two molecules do is cause inflammation and cytokine production. So in essence, their presence together creates a perfect storm for inflammation."
The findings suggest that by promoting chronic inflammation through their effect on fat cells, staph superantigens may play a role in the development of diabetes.
In addition, the chronic inflammation caused by the superantigens may also hinder wound healing in diabetic foot ulcers.
The ulcers, which affect 15 to 25 percent of people with diabetes, are notoriously difficult to heal and can often lead to amputation.
Why immortalize fat cells?
The UI team created immortalized fat cells for their research because primary fat cells (taken directly from fat tissue) are not very useful for lab experiments.
Once the primary cells are grown in a dish, they quickly stop dividing and can't be used for repeated experiments.
In contrast, the immortalized fat cells allow experiments to be repeated multiple times on identical cells ensuring consistent, reproducible results.
Klingelhutz and his team immortalized immature precursor fat cells by adding in two genes from HPV (the virus that causes cervical cancer) along with a gene for part of an enzyme that controls the length of cells' telomeres -- the pieces of DNA that protect chromosome tips from deterioration.
These immortal precursor cells could then be "grown up" in petri dishes and differentiated into normal fat cells.
"The immortal fat cells are a great experimental tool that will allow us to investigate the mechanisms of the inflammation and allow us to test ways to potentially inhibit the response," says Klingelhutz. "That would be a goal in the future."
sabato 2 novembre 2013
giovedì 24 ottobre 2013
Controlling Triggers of Age-Related Inflammation Could Extend 'Healthspan'
From ScienceDaily website (see original article)
Oct. 21, 2013 — Inflammation is the common denominator of many chronic age-related diseases such as arthritis, gout, Alzheimer's, and diabetes. But according to a Yale School of Medicine study, even in the absence of a disease, inflammation can lead to serious loss of function throughout the body, reducing healthspan -- that portion of our lives spent relatively free of serious illness and disability.
Published as the cover article in the October issue of Cell Metabolism, the study found that immune sensor Nlrp3 inflammasome is a common trigger of this inflammation-driven loss of function that manifests itself in insulin-resistance, bone loss, frailty, and cognitive decline in aging.
As the elderly population increases, clinicians are seeing a spike in age-related diseases, but scientists did not fully understand the role of inflammation. What is commonly known is that as we age, our cells change, leading the immune system to produce chronic, low-level inflammation throughout the body.
Aging is also a major risk factor for multiple chronic diseases, but according to the researchers, biomedical enterprise spends billions of dollars to tackle each age-dependent disease separately.
"This is the first study to show that inflammation is causally linked to functional decline in aging," said lead author Vishwa Deep Dixit, professor of comparative medicine and immunobiology at Yale School of Medicine.
"There are multiple cellular triggers of inflammation throughout the body, but we've pinpointed Nlrp3 as the specific sensor that activates inflammation with age."
"If aging is indeed a common factor for multiple diseases, the unanswered question is, can we identify the triggers of aging that cause low-level inflammation so that 'switching off' the trigger can slow the onset of multiple chronic diseases that are age-dependent at their onset," Dixit added. "Since aging affects us all, if this goal can be achieved, it is likely to significantly improve the healthspan and may also lower healthcare costs as the aging population increases in the U.S."
Dixit and his colleagues investigated the normal aging process of mice that were free of diseases, and fed a normal diet.
The research team found that immune sensor Nlrp3 inflammasome is activated in response to aging.
They then tested mice to determine if reducing the activity of Nlrp3 inflammasome lowers inflammation, and aging-associated decline in function.
Results showed that animals with lower Nlrp3 activation were protected from many age-related disorders such as dementia, bone loss, glucose intolerance, cataracts, and thymus degeneration.
Functionally, the mice also performed better, were less frail, and ran for longer durations.
The researchers also tested another immune sensor called caspase11, which is activated in response to certain infections, and found that it was not linked to the age-related inflammation process.
"Now that we've identified this mechanism in the Nlrp3 sensor, we might be able to manipulate this immune sensor to delay, or reduce inflammation," Dixit said.
"This could lead to the possibility of prolonging healthspan, potentially leading to an old age relatively free of disease or disability."
Dixit said additional studies are needed to explore whether the Nlrp3 mechanism can be safely manipulated without impairing the immune system.
He points out that although there are several anti-inflammatory drugs available, none seem to be effective in expanding the healthspan.
"One of our long-term goals is to develop therapies or specific diets that could dampen the excessive inflammation process as a means to prevent chronic diseases," he said.
Oct. 21, 2013 — Inflammation is the common denominator of many chronic age-related diseases such as arthritis, gout, Alzheimer's, and diabetes. But according to a Yale School of Medicine study, even in the absence of a disease, inflammation can lead to serious loss of function throughout the body, reducing healthspan -- that portion of our lives spent relatively free of serious illness and disability.
Published as the cover article in the October issue of Cell Metabolism, the study found that immune sensor Nlrp3 inflammasome is a common trigger of this inflammation-driven loss of function that manifests itself in insulin-resistance, bone loss, frailty, and cognitive decline in aging.
As the elderly population increases, clinicians are seeing a spike in age-related diseases, but scientists did not fully understand the role of inflammation. What is commonly known is that as we age, our cells change, leading the immune system to produce chronic, low-level inflammation throughout the body.
Aging is also a major risk factor for multiple chronic diseases, but according to the researchers, biomedical enterprise spends billions of dollars to tackle each age-dependent disease separately.
"This is the first study to show that inflammation is causally linked to functional decline in aging," said lead author Vishwa Deep Dixit, professor of comparative medicine and immunobiology at Yale School of Medicine.
"There are multiple cellular triggers of inflammation throughout the body, but we've pinpointed Nlrp3 as the specific sensor that activates inflammation with age."
"If aging is indeed a common factor for multiple diseases, the unanswered question is, can we identify the triggers of aging that cause low-level inflammation so that 'switching off' the trigger can slow the onset of multiple chronic diseases that are age-dependent at their onset," Dixit added. "Since aging affects us all, if this goal can be achieved, it is likely to significantly improve the healthspan and may also lower healthcare costs as the aging population increases in the U.S."
Dixit and his colleagues investigated the normal aging process of mice that were free of diseases, and fed a normal diet.
The research team found that immune sensor Nlrp3 inflammasome is activated in response to aging.
They then tested mice to determine if reducing the activity of Nlrp3 inflammasome lowers inflammation, and aging-associated decline in function.
Results showed that animals with lower Nlrp3 activation were protected from many age-related disorders such as dementia, bone loss, glucose intolerance, cataracts, and thymus degeneration.
Functionally, the mice also performed better, were less frail, and ran for longer durations.
The researchers also tested another immune sensor called caspase11, which is activated in response to certain infections, and found that it was not linked to the age-related inflammation process.
"Now that we've identified this mechanism in the Nlrp3 sensor, we might be able to manipulate this immune sensor to delay, or reduce inflammation," Dixit said.
"This could lead to the possibility of prolonging healthspan, potentially leading to an old age relatively free of disease or disability."
Dixit said additional studies are needed to explore whether the Nlrp3 mechanism can be safely manipulated without impairing the immune system.
He points out that although there are several anti-inflammatory drugs available, none seem to be effective in expanding the healthspan.
"One of our long-term goals is to develop therapies or specific diets that could dampen the excessive inflammation process as a means to prevent chronic diseases," he said.
giovedì 5 settembre 2013
Sudden Decline in Testosterone May Cause Parkinson's Disease Symptoms in Men
From ScienceDaily website (see original article)
July 26, 2013 — The results of a new study by neurological researchers at Rush University Medical Center show that a sudden decrease of testosterone, the male sex hormone, may cause Parkinson's like symptoms in male mice.
The findings were recently published in the Journal of Biological Chemistry.
One of the major roadblocks for discovering drugs against Parkinson's disease is the unavailability of a reliable animal model for this disease.
"While scientists use different toxins and a number of complex genetic approaches to model Parkinson's disease in mice, we have found that the sudden drop in the levels of testosterone following castration is sufficient to cause persistent Parkinson's like pathology and symptoms in male mice," said Dr. Kalipada Pahan, lead author of the study and the Floyd A. Davis endowed professor of neurology at Rush.
"We found that the supplementation of testosterone in the form of 5-alpha dihydrotestosterone (DHT) pellets reverses Parkinson's pathology in male mice."
"In men, testosterone levels are intimately coupled to many disease processes," said Pahan.
Typically, in healthy males, testosterone level is the maximum in the mid-30s, which then drop about one percent each year.
However, testosterone levels may dip drastically due to stress or sudden turn of other life events, which may make somebody more vulnerable to Parkinson's disease.
"Therefore, preservation of testosterone in males may be an important step to become resistant to Parkinson's disease," said Pahan.
Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of Parkinson's disease.
Nitric oxide is an important molecule for our brain and the body.
"However, when nitric oxide is produced within the brain in excess by a protein called inducible nitric oxide synthase, neurons start dying," said Pahan.
"This study has become more fascinating than we thought," said Pahan.
"After castration, levels of inducible nitric oxide synthase (iNOS) and nitric oxide go up in the brain dramatically.
Interestingly, castration does not cause Parkinson's like symptoms in male mice deficient in iNOS gene, indicating that loss of testosterone causes symptoms via increased nitric oxide production."
"Further research must be conducted to see how we could potentially target testosterone levels in human males in order to find a viable treatment," said Pahan.
July 26, 2013 — The results of a new study by neurological researchers at Rush University Medical Center show that a sudden decrease of testosterone, the male sex hormone, may cause Parkinson's like symptoms in male mice.
The findings were recently published in the Journal of Biological Chemistry.
One of the major roadblocks for discovering drugs against Parkinson's disease is the unavailability of a reliable animal model for this disease.
"While scientists use different toxins and a number of complex genetic approaches to model Parkinson's disease in mice, we have found that the sudden drop in the levels of testosterone following castration is sufficient to cause persistent Parkinson's like pathology and symptoms in male mice," said Dr. Kalipada Pahan, lead author of the study and the Floyd A. Davis endowed professor of neurology at Rush.
"We found that the supplementation of testosterone in the form of 5-alpha dihydrotestosterone (DHT) pellets reverses Parkinson's pathology in male mice."
"In men, testosterone levels are intimately coupled to many disease processes," said Pahan.
Typically, in healthy males, testosterone level is the maximum in the mid-30s, which then drop about one percent each year.
However, testosterone levels may dip drastically due to stress or sudden turn of other life events, which may make somebody more vulnerable to Parkinson's disease.
"Therefore, preservation of testosterone in males may be an important step to become resistant to Parkinson's disease," said Pahan.
Understanding how the disease works is important to developing effective drugs that protect the brain and stop the progression of Parkinson's disease.
Nitric oxide is an important molecule for our brain and the body.
"However, when nitric oxide is produced within the brain in excess by a protein called inducible nitric oxide synthase, neurons start dying," said Pahan.
"This study has become more fascinating than we thought," said Pahan.
"After castration, levels of inducible nitric oxide synthase (iNOS) and nitric oxide go up in the brain dramatically.
Interestingly, castration does not cause Parkinson's like symptoms in male mice deficient in iNOS gene, indicating that loss of testosterone causes symptoms via increased nitric oxide production."
"Further research must be conducted to see how we could potentially target testosterone levels in human males in order to find a viable treatment," said Pahan.
Migraines Associated With Variations in Structure of Brain Arteries
From ScienceDaily website (see original article)
July 26, 2013 — The network of arteries supplying blood flow to the brain is more likely to be incomplete in people who suffer migraine, a new study by researchers in the Perelman School of Medicine at the University of Pennsylvania reports.
Variations in arterial anatomy lead to asymmetries in cerebral blood flow that might contribute to the process triggering migraines.
The arterial supply of blood to the brain is protected by a series of connections between the major arteries, termed the "circle of Willis" after the English physician who first described it in the 17th century.
People with migraine, particularly migraine with aura, are more likely to be missing components of the circle of Willis.
Migraine affects an estimated 28 million Americans, causing significant disability.
Experts once believed that migraine was caused by dilation of blood vessels in the head, while more recently it has been attributed to abnormal neuronal signals.
In this study, appearing in PLOS ONE, researchers suggest that blood vessels play a different role than previously suspected: structural alterations of the blood supply to the brain may increase susceptibility to changes in cerebral blood flow, contributing to the abnormal neuronal activity that starts migraine.
"People with migraine actually have differences in the structure of their blood vessels -- this is something you are born with," said the study's lead author, Brett Cucchiara, MD, Associate Professor of Neurology.
"These differences seem to be associated with changes in blood flow in the brain, and it's possible that these changes may trigger migraine, which may explain why some people, for instance, notice that dehydration triggers their headaches."
In a study of 170 people from three groups -- a control group with no headaches, those who had migraine with aura, and those who had migraine without aura -- the team found that an incomplete circle of Willis was more common in people with migraine with aura (73 percent) and migraine without aura (67 percent), compared to a headache-free control group (51 percent).
The team used magnetic resonance angiography to examine blood vessel structure and a noninvasive magnetic resonance imaging method pioneered at the University of Pennsylvania, called Arterial spin labeling (ASL), to measure changes in cerebral blood flow.
"Abnormalities in both the circle of Willis and blood flow were most prominent in the back of the brain, where the visual cortex is located.
This may help explain why the most common migraine auras consist of visual symptoms such as seeing distortions, spots, or wavy lines," said the study's senior author, John Detre, MD, Professor of Neurology and Radiology.
Both migraine and incomplete circle of Willis are common, and the observed association is likely one of many factors that contribute to migraine in any individual.
The researchers suggest that at some point diagnostic tests of circle of Willis integrity and function could help pinpoint this contributing factor in an individual patient.
Treatment strategies might then be personalized and tested in specific subgroups.
July 26, 2013 — The network of arteries supplying blood flow to the brain is more likely to be incomplete in people who suffer migraine, a new study by researchers in the Perelman School of Medicine at the University of Pennsylvania reports.
Variations in arterial anatomy lead to asymmetries in cerebral blood flow that might contribute to the process triggering migraines.
The arterial supply of blood to the brain is protected by a series of connections between the major arteries, termed the "circle of Willis" after the English physician who first described it in the 17th century.
People with migraine, particularly migraine with aura, are more likely to be missing components of the circle of Willis.
Migraine affects an estimated 28 million Americans, causing significant disability.
Experts once believed that migraine was caused by dilation of blood vessels in the head, while more recently it has been attributed to abnormal neuronal signals.
In this study, appearing in PLOS ONE, researchers suggest that blood vessels play a different role than previously suspected: structural alterations of the blood supply to the brain may increase susceptibility to changes in cerebral blood flow, contributing to the abnormal neuronal activity that starts migraine.
"People with migraine actually have differences in the structure of their blood vessels -- this is something you are born with," said the study's lead author, Brett Cucchiara, MD, Associate Professor of Neurology.
"These differences seem to be associated with changes in blood flow in the brain, and it's possible that these changes may trigger migraine, which may explain why some people, for instance, notice that dehydration triggers their headaches."
In a study of 170 people from three groups -- a control group with no headaches, those who had migraine with aura, and those who had migraine without aura -- the team found that an incomplete circle of Willis was more common in people with migraine with aura (73 percent) and migraine without aura (67 percent), compared to a headache-free control group (51 percent).
The team used magnetic resonance angiography to examine blood vessel structure and a noninvasive magnetic resonance imaging method pioneered at the University of Pennsylvania, called Arterial spin labeling (ASL), to measure changes in cerebral blood flow.
"Abnormalities in both the circle of Willis and blood flow were most prominent in the back of the brain, where the visual cortex is located.
This may help explain why the most common migraine auras consist of visual symptoms such as seeing distortions, spots, or wavy lines," said the study's senior author, John Detre, MD, Professor of Neurology and Radiology.
Both migraine and incomplete circle of Willis are common, and the observed association is likely one of many factors that contribute to migraine in any individual.
The researchers suggest that at some point diagnostic tests of circle of Willis integrity and function could help pinpoint this contributing factor in an individual patient.
Treatment strategies might then be personalized and tested in specific subgroups.
martedì 20 agosto 2013
Esagerare con il pesce grasso può far male al cuore
Dalla rubrica Salute - Corriere della Sera (vedi articolo originale)
Il pesce fa bene al cuore, su questo ci sono ormai ben pochi dubbi.
Eppure se si esagera e se ne mangia troppo anche salmone e compagnia possono far male, aumentando il rischio di aritmie gravi come la fibrillazione atriale.
Lo dimostra una ricerca danese presentata a EHRA EUROPACE 2013, secondo cui l'ideale sarebbe un apporto “medio” dei preziosi acidi grassi omega-3 del pesce: introdurne troppi o troppo pochi è ugualmente dannoso per la funzionalità del cuore.
STUDIO – I dati sono stati raccolti da Thomas Rix dell'ospedale universitario danese di Aalborg su oltre 57mila persone dai 50 ai 64 anni che facevano parte del Danish Diet, Cancer and Health Study, un'indagine nata per indagare il ruolo della dieta nello sviluppo dei tumori.
Attraverso questionari si sono raccolte informazioni precise sull'alimentazione dei partecipanti, ricostruendo il consumo di pesce e da questo l'introito quotidiano medio di acidi grassi omega-3; tutti sono stati poi seguiti per oltre 13 anni registrando i casi di fibrillazione atriale occorsi nel frattempo, poco meno di 3500 nell'arco del periodo di osservazione.
Quindi, si sono confrontate le diete di chi si era ammalato e degli altri, scoprendo che rispetto a chi non mangiava mai o pochissimo pesce (da zero a 0,38 grammi al giorno di omega-3) chi lo consumava in quantità moderate (da 0.39 a 0.53 grammi o da 0.54 a 0.73 grammi al giorno) aveva un rischio di fibrillazione atriale dal 9 al 13 per cento inferiore.
All'aumentare degli omega-3, però, non si è visto un progressivo ridursi del pericolo di aritmie, anzi: i partecipanti con un consumo elevato (oltre 0.73 ma entro 0.99 grammi al giorno) avevano un rischio ridotto di appena il 4 per cento, quelli che mangiavano moltissimo pesce (oltre 1 grammo al giorno di omega-3) avevano addirittura una probabilità di aritmie del 3 per cento superiore a chi non lo consumava mai o pochissimo.
PESCE – La «dose» di pesce che garantisce il minimo rischio è quella che apporta circa 0.63 grammi di omega-3 al giorno, ovvero circa due porzioni a settimana di pesci ricchi di grassi “buoni” come salmone, acciughe, sgombri e simili.
«La riduzione del 13 per cento del rischio di aritmia con questi livelli di consumo si può spiegare con effetti diretti antiaritmici degli omega-3, a cui si aggiungono proprietà antinfiammatorie e di riduzione del pericolo di ischemia cardiaca che contribuiscono alla salute del cuore – osserva Rix –. Questo dato conferma osservazioni precedenti secondo cui mangiare pesce da una a quattro volte a settimana riduce di quasi un terzo il pericolo di fibrillazione atriale rispetto a consumarlo meno di una volta al mese.
Più difficile spiegare i meccanismi biologici connessi all'incremento del rischio di aritmia in chi mangia molto pesce, invece: possiamo solo supporre che il bilancio fra gli effetti di inibizione o al contrario di promozione della fibrillazione atriale si modifichi in base alle altre patologie eventualmente presenti, ma non abbiamo idea del motivo reale.
Saranno necessari ulteriori ricerche per capire perché troppi omega-3 possano essere deleteri; tuttavia, questi dati potrebbero spiegare perché l'uso di questi composti per la prevenzione delle patologie cardiovascolari abbia dato risultati contraddittori, in passato».
Il pesce fa bene al cuore, su questo ci sono ormai ben pochi dubbi.
Eppure se si esagera e se ne mangia troppo anche salmone e compagnia possono far male, aumentando il rischio di aritmie gravi come la fibrillazione atriale.
Lo dimostra una ricerca danese presentata a EHRA EUROPACE 2013, secondo cui l'ideale sarebbe un apporto “medio” dei preziosi acidi grassi omega-3 del pesce: introdurne troppi o troppo pochi è ugualmente dannoso per la funzionalità del cuore.
STUDIO – I dati sono stati raccolti da Thomas Rix dell'ospedale universitario danese di Aalborg su oltre 57mila persone dai 50 ai 64 anni che facevano parte del Danish Diet, Cancer and Health Study, un'indagine nata per indagare il ruolo della dieta nello sviluppo dei tumori.
Attraverso questionari si sono raccolte informazioni precise sull'alimentazione dei partecipanti, ricostruendo il consumo di pesce e da questo l'introito quotidiano medio di acidi grassi omega-3; tutti sono stati poi seguiti per oltre 13 anni registrando i casi di fibrillazione atriale occorsi nel frattempo, poco meno di 3500 nell'arco del periodo di osservazione.
Quindi, si sono confrontate le diete di chi si era ammalato e degli altri, scoprendo che rispetto a chi non mangiava mai o pochissimo pesce (da zero a 0,38 grammi al giorno di omega-3) chi lo consumava in quantità moderate (da 0.39 a 0.53 grammi o da 0.54 a 0.73 grammi al giorno) aveva un rischio di fibrillazione atriale dal 9 al 13 per cento inferiore.
All'aumentare degli omega-3, però, non si è visto un progressivo ridursi del pericolo di aritmie, anzi: i partecipanti con un consumo elevato (oltre 0.73 ma entro 0.99 grammi al giorno) avevano un rischio ridotto di appena il 4 per cento, quelli che mangiavano moltissimo pesce (oltre 1 grammo al giorno di omega-3) avevano addirittura una probabilità di aritmie del 3 per cento superiore a chi non lo consumava mai o pochissimo.
PESCE – La «dose» di pesce che garantisce il minimo rischio è quella che apporta circa 0.63 grammi di omega-3 al giorno, ovvero circa due porzioni a settimana di pesci ricchi di grassi “buoni” come salmone, acciughe, sgombri e simili.
«La riduzione del 13 per cento del rischio di aritmia con questi livelli di consumo si può spiegare con effetti diretti antiaritmici degli omega-3, a cui si aggiungono proprietà antinfiammatorie e di riduzione del pericolo di ischemia cardiaca che contribuiscono alla salute del cuore – osserva Rix –. Questo dato conferma osservazioni precedenti secondo cui mangiare pesce da una a quattro volte a settimana riduce di quasi un terzo il pericolo di fibrillazione atriale rispetto a consumarlo meno di una volta al mese.
Più difficile spiegare i meccanismi biologici connessi all'incremento del rischio di aritmia in chi mangia molto pesce, invece: possiamo solo supporre che il bilancio fra gli effetti di inibizione o al contrario di promozione della fibrillazione atriale si modifichi in base alle altre patologie eventualmente presenti, ma non abbiamo idea del motivo reale.
Saranno necessari ulteriori ricerche per capire perché troppi omega-3 possano essere deleteri; tuttavia, questi dati potrebbero spiegare perché l'uso di questi composti per la prevenzione delle patologie cardiovascolari abbia dato risultati contraddittori, in passato».
lunedì 8 luglio 2013
Cancer Risks Double When Two Carcinogens Present at 'Safe' Levels, Epigenetics Study Finds
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."
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."
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.
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