artimg5

Increasing dietary fiber reduces risk of developing diabetes

Consuming greater quantities of dietary fiber reduces the risk of developing type 2 diabetes, new research confirms. Over 360 million people worldwide are estimated to be affected by diabetes, and this number is projected to increase to more than 550 million by 2030, with serious consequences for the health and economy of both developed and developing countries.

 

New research published in Diabetologia (the journal of the European Association for the Study of Diabetes) indicates that consuming greater quantities of dietary fiber reduces the risk of developing type 2 diabetes.

Over 360 million people worldwide are estimated to be affected by diabetes, and this number is projected to increase to more than 550 million by 2030, with serious consequences for the health and economy of both developed and developing countries. While previous research has found an association between increased dietary fiber intake and a reduced risk of developing type 2 diabetes, most of these data come from the United States, and amounts and sources of fiber intake differ substantially between countries. In this article the authors evaluated the associations between total fiber as well as fiber from cereal, fruit, and vegetable sources, and new-onset type 2 diabetes in a large European cohort across eight countries, in the EPIC-InterAct Study. They also conducted a meta-analysis where they combined the data from this study with those from 18 other independent studies from across the globe.

Dagfinn Aune, a PhD student affiliated with the Norwegian University of Science and Technology and Imperial College London, analysed data from EPIC-InterAct together with colleagues. The EPIC-InterAct study is the world’s largest study of new-onset type 2 diabetes, and is coordinated by the MRC Epidemiology Unit at Cambridge University. EPIC-InterAct includes 12,403 verified incident cases of type 2 diabetes, and, for comparison, a sub-cohort of 16,835 individuals deemed representative of the total cohort of the European Prospective Investigation into Cancer and Nutrition (EPIC) study including some 350,000 participants.

The authors divided the study participants into four equally sized groups from lowest to highest fiber intake, and assessed their risk of developing type 2 diabetes over an average of 11 years’ follow-up.

They found that participants with the highest total fiber intake (more than 26 g/day) had an 18% lower risk of developing diabetes compared to those with the lowest total fiber intake (less than 19g/day), after adjusting for the effect of other lifestyle and dietary factors. When the results were adjusted for body mass index (BMI) as a marker of obesity, higher total fiber intake was found to be no longer associated with a lower risk of developing diabetes, suggesting that the beneficial association with fiber intake may be mediated at least in part by BMI. In other words, dietary fiber may help people maintain a healthy weight, which in turn reduces the chances of developing type 2 diabetes.

When the authors evaluated the different fiber sources, they found that cereal fiber had the strongest inverse association: those with the highest levels of cereal and vegetable fiber consumption had a 19% and 16% lower risk of developing diabetes respectively, compared with those with the lowest consumption of these types of fiber. Again, these associations disappeared when the results were adjusted for BMI. By contrast, fruit fiber was not associated with a reduction in diabetes risk. Cereals accounted for 38% of the total fiber intake, and were the main source of fiber in all the countries involved in the study (with the exception of France where vegetables were the main source).

The authors also undertook a meta-analysis, where they pooled the data from this EPIC-InterAct study with those from 18 other independent studies (eight in the United States, four in Europe, three in Australia, and three in Asia). The meta-analysis included over 41,000 new-onset cases of type 2 diabetes and found that the risk of diabetes fell by 9% for each 10g/day increase in total fiber intake, and by 25% for each 10g/day increase in cereal fiber intake. They did not find a statistically significant relationship between increasing either fruit or vegetable fiber and reducing diabetes risk.

Dagfinn Aune said: “Taken together, our results indicate that individuals with diets rich in fiber, in particular cereal fiber, may be at lower risk of type 2 diabetes. We are not certain why this might be, but potential mechanisms could include feeling physically full for longer, prolonged release of hormonal signals, slowed down nutrient absorption, or altered fermentation in the large intestine. All these mechanisms could lead to a lower BMI and reduced risk of developing type 2 diabetes. As well as helping keep weight down, dietary fiber may also affect diabetes risk by other mechanisms — for instance improving control of blood sugar and decreasing insulin peaks after meals, and increasing the body’s sensitivity to insulin.”

Professor Nick Wareham, senior author on the paper and Director of the MRC Epidemiology Unit, University of Cambridge, added: “This work adds to the growing evidence of the health benefits of diets rich in fiber, in particular cereal fiber. Public health measures globally to increase fiber consumption are therefore likely to play an important part in halting the epidemics of obesity and of type 2 diabetes.”

Story Source:

The above story is based on materials provided by Diabetologia. Note: Materials may be edited for content and length.

ObesityKidsTaste_m_0921

Does Sweet Taste Sensitivity Affect the Development of Diabetes?

The decrease in sweet taste sensitivity which can lead to an increase in sugar intake might be a factor driving people with prediabetes to overt diabetes. Researchers assessed the sweet taste sensitivity in pre-diabetics in comparison with diabetics and with normoglycemic controls.

Forty pre-diabetics, 40 diabetics and 34 normoglycemic controls participated in the study. The three groups were matched for age, sex and BMI. The division into groups was based on their glycated hemoglobin levels. The detection and recognition thresholds were determined by the multiple forced-choice method using sucrose solutions prepared in 1/4 log dilutions. The intensities of perceived sensations for a series of suprathreshold concentrations of sucrose solutions prepared in ½ log dilution were determined by rating on a visual analogue scale. Statistical analyses were performed by SPSS version 21.

The mean (SD) detection thresholds of diabetic, pre-diabetic and normoglycemic groups were 0.025 (0.01), 0.018 (0.01) and 0.015 (0.01) respectively with a significant increase in diabetic group compared to normoglycemic group (p = 0.03). The mean recognition thresholds were not different among the three groups. When the intensity ratings for suprathreshold concentrations of sucrose were compared between the three groups, for all suprathreshold concentrations tested, significant differences were observed across the four concentrations (p < 0.001) and between groups in suprathreshold ratings (p < 0.05). Further analysis showed that the diabetic group had significantly lower suprathreshold ratings than the normoglycemic group (p < 0.001). Although all mean suprathreshold intensity ratings of the pre-diabetic group were between the normoglycemic and diabetic groups, the differences were not significant.

This is the first study to demonstrate the sweet taste sensitivity in pre-diabetics. The findings of the present study do not support the hypothesis of decreased sweet taste sensitivity of pre-diabetics. However, the results confirm the previous findings of blunted taste response in diabetics. The observation of pre-diabetics having intermediate values for all taste thresholds and suprathreshold ratings warrants a future investigation with a larger pre-diabetic sample recruited with more specific screening criteria to test this hypothesis further.

Source: http://www.diabetesincontrol.com/does-sweet-taste-sensitivity-affect-the-development-of-diabetes/

artimg2

Could diabetes protect against ALS?

A reduced risk of amyotrophic lateral sclerosis, or ALS – the most common motor neuron disorder, fatal for its sufferers – has been found among people with type 2 diabetes.

 

The study, published in JAMA Neurology, set out to examine the association between diabetes- and obesity-related hospital admissions and the risk of a diagnosis with ALS.

The study “observed a significantly protective association with diabetes, but not obesity, on risk of ALS.”

Marianthi-Anna Kioumourtzoglou, ScD, of the Harvard T.H. Chan School of Public Health in Boston, MA, conducted the study with coauthors, using data from Danish national registers for 3,650 patients diagnosed with ALS between 1982 and 2009.

The average age at diagnosis was 65.4 years and the patients were compared with 365,000 healthy controls. Some 9,294 patients were identified as having diabetes, 55 of whom were subsequently diagnosed with ALS.

The authors say the findings are in agreement with previous reports of a protective association between vascular risk factors and ALS. They conclude:

“We conducted a nationwide, population-based study and observed an overall protective association between diabetes and ALS diagnosis, with the suggestion that type 2 diabetes is protective and type 1 diabetes is a risk factor.

“Although the mechanisms underlying this association remain unclear, our findings focus further attention on the role of energy metabolism in ALS pathogenesis.”

Rare but fatal disease Motor neuron diseases are progressive neurological disorders in which motor neurons – the cells that control the essential voluntary muscle activity allowing us to speak, walk, breathe and swallow – are destroyed.

ALS is the most common of these conditions – also known as classical motor neuron disease or Lou Gehrig’s disease (American baseball player Lou Gehrig died of the disease in 1941), it is ultimately a fatal disorder that disrupts signals to all voluntary muscles.

Background evidence cited in the paper says around half of patients with ALS – which is rare, having an incidence rate of between 1.5 and 2.5 for every 100,000 people in the population every year – die within 3 years of its onset.

ALS was the subject of appeals for fundraising and greater awareness in the summer of 2014 – when the ice bucket challenge swept through social media.

Several possibilities if the link is causal The latest study is a retrospective, population-based one, looking back over data to find links, so it was not of a prospective design that might have proven cause-and-effect links.

The authors discuss the potential etiology of the link, however: “If the protective association with diabetes results from some causal association with an aspect of diabetes rather than as a result of correlation with something else, then several possibilities could be surmised.”

Possibilities discussed include that diabetes medications may be protective against ALS, metabolic factors resulting from diabetes could have a role, or that high concentrations of uric acid that have been associated with diabetes have also been linked to “lower incidence of other neurodegenerative diseases and prolonged survival in ALS.”

In January, scientists uncovered a cell mechanism that plays a key role in ALS.

Source: http://www.hsph.harvard.edu/news/hsph-in-the-news/type-2-diabetes-may-protect-against-als/

artimg6

New way of preventing diabetes-associated blindness

Reporting on their study with lab-grown human cells, researchers say that blocking a second blood vessel growth protein, along with one that is already well-known, could offer a new way to treat and prevent a blinding eye disease caused by diabetes.

 

Reporting on their study with lab-grown human cells, researchers at The Johns Hopkins University and the University of Maryland say that blocking a second blood vessel growth protein, along with one that is already well-known, could offer a new way to treat and prevent a blinding eye disease caused by diabetes.

A summary of the study appears online May 25 in Proceedings of the National Academy of Sciences.

The disease, diabetic retinopathy, is the most common cause of vision loss in working-age adults in the United States. Diabetic eye disease occurs when the normal blood vessels in the eye are replaced over time with abnormal, leaky, fragile blood vessels that leak fluid or bleed into the eye, damaging the light-sensitive retina and causing blindness. Forty to 45 percent of Americans with diabetes have diabetic retinopathy, according to the National Eye Institute.

Laser-sealing eye blood vessels can save central vision, but this often sacrifices peripheral and night vision, according to Akrit Sodhi, M.D., Ph.D., an assistant professor of ophthalmology at the Johns Hopkins University School of Medicine. Several recently developed drugs — bevacizumab, ranibizumab and aflibercept — can help treat these blood vessels by blocking the action of VEGF, a so-called growth factor released as part of a chain of signals in response to low oxygen levels, which stimulates the growth of new, often abnormal, blood vessels. But studies have shown that although these drugs slow progression to proliferative diabetic retinopathy, it does not reliably prevent it.

Looking for an explanation, postdoctoral fellow Savalan Babapoor-Farrokhran, M.D., and Kathleen Jee, a student at the school of medicine who will begin her residency in ophthalmology at the Wilmer Eye Institute at Johns Hopkins next year, tested levels of VEGF in samples of fluid from the eye taken from healthy people, people with diabetes who did not have diabetic retinopathy and people with diabetic retinopathy of varying severity.

While levels of VEGF tended to be higher in those with proliferative diabetic retinopathy, some of their fluid had less VEGF than did the healthy participants. But even the low-VEGF fluid from patients with proliferative diabetic retinopathy stimulated blood vessel growth in lab-grown cells.

“The results suggested to us that although VEFG clearly plays an important role in blood vessel growth, it’s not the only factor,” Sodhi says.

A series of experiments in lab-grown human cells and mice revealed a second culprit, a protein called angiopoietin-like 4. When the researchers blocked the action of both VEGF and angiopoietin-like 4 in fluid from the eyes of people with proliferative diabetic retinopathy, it markedly reduced blood vessel growth in lab-grown cells.

If a drug can be found that safely blocks the second protein’s action in patients’ eyes, it might be combined with the anti-VEGF drugs to prevent many cases of proliferative diabetic retinopathy, Sodhi suggests.

The team is now investigating whether angiopoietin-like 4 might also play a role in other eye diseases, such as macular degeneration, which destroys the central portion of the retina.

Story Source:

The above story is based on materials provided by Johns Hopkins Medicine. Note: Materials may be edited for content and length.

artimg4

Long life: Balancing protein and carb intake may work as well as calorie restriction

Cutting calories through dietary restriction has been shown to lower cholesterol, improve insulin sensitivity, and even prolong life in mammals. Now, new research publishing on May 28th in Cell Reports shows that, at least in mice, low protein, high carbohydrate diets can provide benefits similar to those obtained with calorie restriction.

“We’ve shown that when compared head-to-head, mice got the same benefits from a low protein, high carbohydrate diet as a 40% caloric restriction diet,” says senior author Stephen Simpson, Academic Director of the University of Sydney’s Charles Perkins Centre. “Except for the fanatical few, no one can maintain a 40% caloric reduction in the long term, and doing so can risk loss of bone mass, libido, and fertility.”

The investigators compared three 8-week diets varying in protein-to-carbohydrate ratio under conditions where food was restricted or food was available at all times. Of the three, low protein, high carbohydrate (LPHC) diets offered when food was always available delivered similar benefits as calorie restriction in terms of insulin, blood sugar, and cholesterol levels, despite increased food intake.

Even though the mice on LPHC diets ate more when food was always available, their metabolism was higher than that of mice on the calorie-restricted diet, and they did not gain more weight. Calorie restriction did not provide any additional benefits for LPHC mice.

Additional research is needed to determine how LPHC diets affect long-term metabolic health and survival, as well as to what extent the type and quality of proteins and carbohydrates matter. “An important next step will be to determine exactly how specific amino acids, the building blocks of proteins, contribute to overall health span and lifespan,” says lead author Samantha Solon-Biet, also of the Charles Perkins Centre.

If the study’s results apply to humans, adjusting protein and carbohydrate intake could lead to healthier aging in a more realistic manner than drastically cutting calories. “It still holds true that reducing food intake and body weight improves metabolic health and reduces the risk of diseases like type 2 diabetes, obesity, and fatty liver disease,” says Simpson. “However, according to these mouse data and emerging human research, it appears that including modest intakes of high-quality protein and plenty of healthy carbohydrates in the diet will be beneficial for health as we age.”

Story Source:

The above story is based on materials provided by Cell Press. Note: Materials may be edited for content and length.

artimg1

Experts reflect on the past, present and future of diabetes.

Over the past 50 years, treatment and outcomes for diabetes have changed dramatically. At a recent symposium, experts looked back at how lives have changed over the past 5 decades and what remains to be addressed over the next 5.

 

The symposium was held at the American Diabetes Association’s (ADA) 75th Scientific Sessions.

“There are things that have happened over the past 50 years that clearly make life a lot better for people,” says Dr. Fred Whitehouse, of the Henry Ford Health System in Detroit, MI. “There’s been a lot of change, most of it for the better, but what people want is a cure and we don’t have that yet.”

Dr. Whitehouse has overseen many changes in how people with diabetes have been treated. When he first started treating people with the condition, the only form of treatment was the injection of animal insulin, obtained from cows or pigs, which could sometimes cause adverse reactions.

Nowadays, human insulin is used, produced by microorganisms and delivered through a variety of different systems including insulin pumps. There are now fewer adverse reactions and no fear of supplies running out, Dr. Whitehouse says, with methods of delivery that are more accurate than ever before.

Glucose levels can also be tracked more accurately. Previously, diabetes control could only be assessed by analyzing the levels of sugar in urine. There are many more options available to patients now, including the noninvasive A1C test that measures average levels over 3 months, “showing whether a person is on the right road or not,” states Dr. Whitehouse.

As methods for treating and tracking the disorder have improved for patients, so too has the collective understanding of diabetes shared by researchers and clinicians. It takes a long time for research to make a clinical impact and recent years have seen the results of 50 years of hard work.
Dr. Daniel Porte, Jr., a professor at the University of California-San Diego, describes one of the most recent discoveries in the field:

“This year, amazingly enough to me, it was discovered that insulin sent to the central nervous system not only feeds back to the brain, it also affects glucose production. It regulates the islet cells, so there is a complete integration of the endocrine system and the nervous system. It took 40 years to discover this.”

Originally, the endocrine and nervous systems were believed to function completely independently of each other, with glucose the sole regular of insulin.

In 50 years, ‘complications of diabetes should become historical memories’ Dr. Porte states that with diabetes research, it is crucial to be patient. “For example, the drugs we use now to treat diabetes were first studied 30 to 40 years ago. And there are many more than the one or two that were being used back in the 1970s.”
Such research not only leads to an improved understanding of diabetes but of other conditions as well. “We now believe that perhaps impaired insulin action in the central nervous system leads to the behavioral changes we see in Alzheimer’s patients,” Dr. Porte explains.

Dr. Michael Brownlee, associate director for biomedical sciences at the Albert Einstein College of Medicine’s Diabetes Research Center in New York City, NY, states that diabetes is such a serious health problem due to its complications. His research on the mechanisms that cause complications such as eye and kidney disease has led to great change.

“Prior to the Diabetes Control and Complications Trial (DCCT) study that was published [in 1993], the general dogma was that diabetes caused both metabolic changes and complications, which had nothing to do with each other. They were just two parallel manifestations of the disease,” he says.

“Now it’s known that prolonged high glucose levels increase the risk for eye and kidney complications associated with diabetes, and maintaining tighter control of blood glucose levels reduces that risk.”

Although the landscape of diabetes treatment and research has changed radically over the past 50 years, physicians are still only able to manage the disease rather than cure it. Dr. Robert Ratner, chief scientific & medical officer for the ADA, outlines what needs to be done:

“The next 50 years must elucidate the mechanisms by which both type 1 and type 2 diabetes occur, along with those critical steps at which we might intervene to prevent disease. Treatments must provide optimal glucose and metabolic control, without the risk of hypoglycemia, and complications of diabetes should become historical memories.”

If research and treatment can progress at the same rate over the next 5 decades as it has over the past 5, who is to say what can be accomplished?

 

Source: http://www.medicalnewstoday.com/articles/295011.php