(Source: http://www.drmirkin.com/men/high-blood-sugar-linked-to-prostate-enlargement-low-testosterone-and-prostate-cancer.html)
Metabolic syndrome and type II diabetes are characterized by high blood sugar, insulin, and triglycerides, low HDL and a fatty liver and obesity. Of 490 male adults, average age 58 years old, 37 percent with lower urinary tract obstruction (LUTS) had metabolic syndrome (Adv Urol, published online Jan 23, 2014). Of those with:
• mild LUTS, 37.4 percent had metabolic syndrome,
• moderate LUTS , 46.5 percent had metabolic syndrome and
• severe LUTS, 54.1 percent had metabolic syndrome.
The patients with metabolic syndrome had much larger prostates than those who did not have that syndrome. Obese men and those with higher levels of the bad LDL cholesterol also had larger prostates.
Low Testosterone and Prostate Cancer Linked to Metabolic Syndrome
Of 1,150 men aged 30 years or older, the lower the testosterone, the more likely a man is to have metabolic syndrome. (Urology, published online October 08, 2013). The researchers defined Metabolic Syndrome as a waist circumference of 85 cm or more plus any two of the following: triglyceride 150 mg/dl or higher, good HDL cholesterol level below 40 mg/dL, taking statins, systolic blood pressure of 130 mm Hg or higher, diastolic blood pressure of 85 mm Hg or higher, taking high blood pressure medications, fasting blood sugar 110 mg/dL or higher, or use of a drug to lower high blood sugar.
Men who had any three of the risk factors for metabolic syndrome are one and a half times more likely to develop prostate cancer than those who do not have metabolic syndrome (European Urology, published online February 24, 2014).
Metabolic Syndrome and Diabetes
Metabolic syndrome means you are on your way to becoming diabetic. Diabetes is a disease in which high blood sugar levels damage every cell in your body. When blood sugar levels rise too high (high blood sugar), the pancreas releases large amounts of insulin (high insulin), which converts sugar to a type of fat called triglycerides (high triglycerides). Then your body uses up its good HDL cholesterol to carry triglycerides from the bloodstream to the liver (low HDL). Next, the extra triglycerides carried to the liver are stored in the liver to form a fatty liver. The triglycerides are also stored in your body to make you fat (overweight). These are the components of both metabolic syndrome and Type II diabetes.
Visualizzazione post con etichetta diabetes. Mostra tutti i post
Visualizzazione post con etichetta diabetes. Mostra tutti i post
mercoledì 27 aprile 2016
sabato 2 novembre 2013
Bacteria and Fat: A 'Perfect Storm' for Inflammation
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."
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."
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.
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 8 febbraio 2013
Excess Sugar Linked to Cancer
From Science Daily website (see original article).
Feb. 1, 2013 — Sugars are needed to provide us with energy and in moderate amounts contribute to our well-being. Sustained high levels of sugars, as is found in diabetics, damages our cells and now is shown that can also increase our chance to get cancer: "The dose makes the poison" as Paracelsus said.
It is well known that obesity is a leading cause of diabetes, a disease where the body fails to control blood sugar levels.
High blood sugar levels are characteristic in obesity and diabetes.
What is less well known is that diabetes and obesity are also linked to an increase in cancer risk.
That is, the diabetic population has up to double chances to suffer pancreatic or colon cancer among others, according to well sustained epidemiological studies.
With obesity in British and Spanish children reaching 16%, the highest in Europe, this epidemic has major health implications.
How obesity or diabetes increase cancer risk has been a major health issue.
Scientists led by Dr. Custodia Garcia-Jimenez at the University Rey Juan Carlos in Madrid have uncovered a key mechanism that links obesity and diabetes with cancer: high sugar levels, which increase activity of a gene widely implicated in cancer progression.
Dr Garcia Jimenez's laboratory was studying how cells in the intestine respond to sugars and signal to the pancreas to release insulin, the key hormone that controls blood sugar levels.
Sugars in the intestine trigger cells to release a hormone called GIP that enhances insulin release by the pancreas.
In a study published in Molecular Cell, Dr Garcia Jimenez's team showed that the ability of the intestinal cells to secrete GIP is controlled by a protein called β-catenin, and that the activity of β-catenin is strictly dependent on sugar levels.
Increased activity of β-catenin is known to be a major factor in the development of many cancers and can make normal cells immortal, a key step in early stages of cancer progression.
The study demonstrates that high (but not normal) sugar levels induce nuclear accumulation of β-catenin and leads to cell proliferation.
The changes induced on β-catenin, the molecules involved and the diversity of cancer cells susceptible to these changes are identified.
Dr. Custodia García said "We were surprised to realize that changes in our metabolism caused by dietary sugar impact on our cancer risk.
We are now investigating what other dietary components may influence our cancer risk. Changing diet is one of easiest prevention strategies that can potentially save a lot of suffering and money."
Colin Goding, Professor of Oncology at the University of Oxford, UK said 'Previously we were unsure about how increased blood sugar found in diabetes and obesity could increase cancer risk.
This study identifies a key molecular mechanism through which high blood glucose would predispose to cancer.
It opens the way for potential novel therapies aimed at reducing cancer risk in the obese and diabetic populations.'
Estimations published by the World Health Organisation (WHO): Obesity predisposes to diabetes and its prevalence is doubling every 20 years worldwide.
More than 1 in 10 adults worldwide (12%) are obese (BMI>30).
1 in 6 children in UK and Spain suffer obesity.
Diabetes caused 4.6 million deaths in 2011, more than 2 deaths per hour in Spain, more in USA. Worldwide, 1 in 10 adults (10%) suffered from diabetes in 2010 and more than one-third of individuals with diabetes are unaware they suffer from the disease.
The national cost of diabetes or cancer is in the order of billions of pounds or euros in Spain or England.
More than half (63%) of premature deaths worldwide are due to non communicable diseases (NCD) of which cancer and diabetes are among the 4 causes more frequent.
At least 1 in 3 of the main cancers (27-39%) can be prevented by improving diet, physical activity and body composition.
Feb. 1, 2013 — Sugars are needed to provide us with energy and in moderate amounts contribute to our well-being. Sustained high levels of sugars, as is found in diabetics, damages our cells and now is shown that can also increase our chance to get cancer: "The dose makes the poison" as Paracelsus said.
It is well known that obesity is a leading cause of diabetes, a disease where the body fails to control blood sugar levels.
High blood sugar levels are characteristic in obesity and diabetes.
What is less well known is that diabetes and obesity are also linked to an increase in cancer risk.
That is, the diabetic population has up to double chances to suffer pancreatic or colon cancer among others, according to well sustained epidemiological studies.
With obesity in British and Spanish children reaching 16%, the highest in Europe, this epidemic has major health implications.
How obesity or diabetes increase cancer risk has been a major health issue.
Scientists led by Dr. Custodia Garcia-Jimenez at the University Rey Juan Carlos in Madrid have uncovered a key mechanism that links obesity and diabetes with cancer: high sugar levels, which increase activity of a gene widely implicated in cancer progression.
Dr Garcia Jimenez's laboratory was studying how cells in the intestine respond to sugars and signal to the pancreas to release insulin, the key hormone that controls blood sugar levels.
Sugars in the intestine trigger cells to release a hormone called GIP that enhances insulin release by the pancreas.
In a study published in Molecular Cell, Dr Garcia Jimenez's team showed that the ability of the intestinal cells to secrete GIP is controlled by a protein called β-catenin, and that the activity of β-catenin is strictly dependent on sugar levels.
Increased activity of β-catenin is known to be a major factor in the development of many cancers and can make normal cells immortal, a key step in early stages of cancer progression.
The study demonstrates that high (but not normal) sugar levels induce nuclear accumulation of β-catenin and leads to cell proliferation.
The changes induced on β-catenin, the molecules involved and the diversity of cancer cells susceptible to these changes are identified.
Dr. Custodia García said "We were surprised to realize that changes in our metabolism caused by dietary sugar impact on our cancer risk.
We are now investigating what other dietary components may influence our cancer risk. Changing diet is one of easiest prevention strategies that can potentially save a lot of suffering and money."
Colin Goding, Professor of Oncology at the University of Oxford, UK said 'Previously we were unsure about how increased blood sugar found in diabetes and obesity could increase cancer risk.
This study identifies a key molecular mechanism through which high blood glucose would predispose to cancer.
It opens the way for potential novel therapies aimed at reducing cancer risk in the obese and diabetic populations.'
Estimations published by the World Health Organisation (WHO): Obesity predisposes to diabetes and its prevalence is doubling every 20 years worldwide.
More than 1 in 10 adults worldwide (12%) are obese (BMI>30).
1 in 6 children in UK and Spain suffer obesity.
Diabetes caused 4.6 million deaths in 2011, more than 2 deaths per hour in Spain, more in USA. Worldwide, 1 in 10 adults (10%) suffered from diabetes in 2010 and more than one-third of individuals with diabetes are unaware they suffer from the disease.
The national cost of diabetes or cancer is in the order of billions of pounds or euros in Spain or England.
More than half (63%) of premature deaths worldwide are due to non communicable diseases (NCD) of which cancer and diabetes are among the 4 causes more frequent.
At least 1 in 3 of the main cancers (27-39%) can be prevented by improving diet, physical activity and body composition.
Loneliness, Like Chronic Stress, Taxes the Immune System, Researchers Find
From Science Daily website (see original article).
Jan. 19, 2013 — New research links loneliness to a number of dysfunctional immune responses, suggesting that being lonely has the potential to harm overall health.
Researchers found that people who were more lonely showed signs of elevated latent herpes virus reactivation and produced more inflammation-related proteins in response to acute stress than did people who felt more socially connected.
These proteins signal the presence of inflammation, and chronic inflammation is linked to numerous conditions, including coronary heart disease, Type 2 diabetes, arthritis and Alzheimer's disease, as well as the frailty and functional decline that can accompany aging.
Reactivation of a latent herpes virus is known to be associated with stress, suggesting that loneliness functions as a chronic stressor that triggers a poorly controlled immune response.
"It is clear from previous research that poor-quality relationships are linked to a number of health problems, including premature mortality and all sorts of other very serious health conditions.
And people who are lonely clearly feel like they are in poor-quality relationships," said Lisa Jaremka, a postdoctoral fellow at the Institute for Behavioral Medicine Research at Ohio State University and lead author of the research.
"One reason this type of research is important is to understand how loneliness and relationships broadly affect health.
The more we understand about the process, the more potential there is to counter those negative effects -- to perhaps intervene.
If we don't know the physiological processes, what are we going to do to change them?"
The results are based on a series of studies conducted with two populations: a healthy group of overweight middle-aged adults and a group of breast cancer survivors.
The researchers measured loneliness in all studies using the UCLA Loneliness Scale, a questionnaire that assesses perceptions of social isolation and loneliness.
Jaremka will present the research January 19 at the Society for Personality and Social Psychology annual meeting in New Orleans.
The researchers first sought to obtain a snapshot of immune system behavior related to loneliness by gauging levels of antibodies in the blood that are produced when herpes viruses are reactivated.
Participants were 200 breast cancer survivors who were between two months and three years past completion of cancer treatment with an average age of 51 years.
Their blood was analyzed for the presence of antibodies against Epstein-Barr virus and cytomegalovirus.
Both are herpes viruses that infect a majority of Americans.
About half of infections do not produce illness, but once a person is infected, the viruses remain dormant in the body and can be reactivated, resulting in elevated antibody levels, or titers -- again, often producing no symptoms but hinting at regulatory problems in the cellular immune system.
Lonelier participants had higher levels of antibodies against cytomegalovirus than did less lonely participants, and those higher antibody levels were related to more pain, depression and fatigue symptoms.
No difference was seen in Epstein-Barr virus antibody levels, possibly because this reactivation is linked to age and many of these participants were somewhat older, meaning reactivation related to loneliness would be difficult to detect, Jaremka said.
Previous research has suggested that stress can promote reactivation of these viruses, also resulting in elevated antibody titers.
"The same processes involved in stress and reactivation of these viruses is probably also relevant to the loneliness findings," Jaremka said. "Loneliness has been thought of in many ways as a chronic stressor -- a socially painful situation that can last for quite a long time."
In an additional set of studies, the scientists sought to determine how loneliness affected the production of proinflammatory proteins, or cytokines, in response to stress.
These studies were conducted with 144 women from the same group of breast cancer survivors and a group of 134 overweight middle-aged and older adults with no major health problems.
Baseline blood samples were taken from all participants, who were then subjected to stress -- they were asked to deliver an impromptu five-minute speech and perform a mental arithmetic task in front of a video camera and three panelists.
Researchers followed by stimulating the participants' immune systems with lipopolysaccharide, a compound found on bacterial cell walls that is known to trigger an immune response.
In both populations, those who were lonelier produced significantly higher levels of a cytokine called interleukin-6, or IL-6, in response to acute stress than did participants who were more socially connected.
Levels of another cytokine, tumor necrosis factor-alpha, also rose more dramatically in lonelier participants than in less lonely participants, but the findings were significant by statistical standards in only one study group, the healthy adults.
In the study with breast cancer survivors, researchers also tested for levels of the cytokine interleukin 1-beta, which was produced at higher levels in lonelier participants.
When the scientists controlled for a number of factors, including sleep quality, age and general health measures, the results were the same.
"We saw consistency in the sense that more lonely people in both studies had more inflammation than less lonely people," Jaremka said.
"It's also important to remember the flip side, which is that people who feel very socially connected are experiencing more positive outcomes," she said.
Jan. 19, 2013 — New research links loneliness to a number of dysfunctional immune responses, suggesting that being lonely has the potential to harm overall health.
Researchers found that people who were more lonely showed signs of elevated latent herpes virus reactivation and produced more inflammation-related proteins in response to acute stress than did people who felt more socially connected.
These proteins signal the presence of inflammation, and chronic inflammation is linked to numerous conditions, including coronary heart disease, Type 2 diabetes, arthritis and Alzheimer's disease, as well as the frailty and functional decline that can accompany aging.
Reactivation of a latent herpes virus is known to be associated with stress, suggesting that loneliness functions as a chronic stressor that triggers a poorly controlled immune response.
"It is clear from previous research that poor-quality relationships are linked to a number of health problems, including premature mortality and all sorts of other very serious health conditions.
And people who are lonely clearly feel like they are in poor-quality relationships," said Lisa Jaremka, a postdoctoral fellow at the Institute for Behavioral Medicine Research at Ohio State University and lead author of the research.
"One reason this type of research is important is to understand how loneliness and relationships broadly affect health.
The more we understand about the process, the more potential there is to counter those negative effects -- to perhaps intervene.
If we don't know the physiological processes, what are we going to do to change them?"
The results are based on a series of studies conducted with two populations: a healthy group of overweight middle-aged adults and a group of breast cancer survivors.
The researchers measured loneliness in all studies using the UCLA Loneliness Scale, a questionnaire that assesses perceptions of social isolation and loneliness.
Jaremka will present the research January 19 at the Society for Personality and Social Psychology annual meeting in New Orleans.
The researchers first sought to obtain a snapshot of immune system behavior related to loneliness by gauging levels of antibodies in the blood that are produced when herpes viruses are reactivated.
Participants were 200 breast cancer survivors who were between two months and three years past completion of cancer treatment with an average age of 51 years.
Their blood was analyzed for the presence of antibodies against Epstein-Barr virus and cytomegalovirus.
Both are herpes viruses that infect a majority of Americans.
About half of infections do not produce illness, but once a person is infected, the viruses remain dormant in the body and can be reactivated, resulting in elevated antibody levels, or titers -- again, often producing no symptoms but hinting at regulatory problems in the cellular immune system.
Lonelier participants had higher levels of antibodies against cytomegalovirus than did less lonely participants, and those higher antibody levels were related to more pain, depression and fatigue symptoms.
No difference was seen in Epstein-Barr virus antibody levels, possibly because this reactivation is linked to age and many of these participants were somewhat older, meaning reactivation related to loneliness would be difficult to detect, Jaremka said.
Previous research has suggested that stress can promote reactivation of these viruses, also resulting in elevated antibody titers.
"The same processes involved in stress and reactivation of these viruses is probably also relevant to the loneliness findings," Jaremka said. "Loneliness has been thought of in many ways as a chronic stressor -- a socially painful situation that can last for quite a long time."
In an additional set of studies, the scientists sought to determine how loneliness affected the production of proinflammatory proteins, or cytokines, in response to stress.
These studies were conducted with 144 women from the same group of breast cancer survivors and a group of 134 overweight middle-aged and older adults with no major health problems.
Baseline blood samples were taken from all participants, who were then subjected to stress -- they were asked to deliver an impromptu five-minute speech and perform a mental arithmetic task in front of a video camera and three panelists.
Researchers followed by stimulating the participants' immune systems with lipopolysaccharide, a compound found on bacterial cell walls that is known to trigger an immune response.
In both populations, those who were lonelier produced significantly higher levels of a cytokine called interleukin-6, or IL-6, in response to acute stress than did participants who were more socially connected.
Levels of another cytokine, tumor necrosis factor-alpha, also rose more dramatically in lonelier participants than in less lonely participants, but the findings were significant by statistical standards in only one study group, the healthy adults.
In the study with breast cancer survivors, researchers also tested for levels of the cytokine interleukin 1-beta, which was produced at higher levels in lonelier participants.
When the scientists controlled for a number of factors, including sleep quality, age and general health measures, the results were the same.
"We saw consistency in the sense that more lonely people in both studies had more inflammation than less lonely people," Jaremka said.
"It's also important to remember the flip side, which is that people who feel very socially connected are experiencing more positive outcomes," she said.
Iscriviti a:
Post (Atom)