Drinking more water associated with numerous dietary benefits, study finds

For people who want to control their weight or reduce their intakes of sugar, sodium and saturated fat, tap water may be what the doctor ordered.

A new study that examined the dietary habits of more than 18,300 U.S. adults found the majority of people who increased their consumption of plain water -- tap water or from a cooler, drinking fountain or bottle -- by 1 percent reduced their total daily calorie intake as well as their consumption of saturated fat, sugar, sodium and cholesterol.

People who increased their consumption of water by one, two or three cups daily decreased their total energy intake by 68 to 205 calories daily and their sodium intake by 78 to 235 milligrams, according to a paper by University of Illinois kinesiology and community health professor Ruopeng An. They also consumed 5 grams to nearly 18 grams less sugar and decreased their cholesterol consumption by 7 to 21 milligrams daily.

"The impact of plain water intake on diet was similar across race/ethnicity, education and income levels and body weight status," An said. "This finding indicates that it might be sufficient to design and deliver universal nutrition interventions and education campaigns that promote plain water consumption in replacement of beverages with calories in diverse population subgroups without profound concerns about message and strategy customization."

An examined data from four waves (2005-12) of the National Health and Nutrition Examination Survey, conducted by the National Center for Health Statistics. Participants were asked to recall everything they ate or drank over the course of two days that were three to 10 days apart.

An calculated the amount of plain water each person consumed as a percentage of their daily dietary water intake from food and beverages combined. Beverages such as unsweetened black tea, herbal tea and coffee were not counted as sources of plain water, but their water content was included in An's calculations of participants' total dietary water consumption.

On average, participants consumed about 4.2 cups of plain water on a daily basis, accounting for slightly more than 30 percent of their total dietary water intake. Participants' average calorie intake was 2,157 calories, including 125 calories from sugar-sweetened beverages and 432 calories from discretionary foods, which are low-nutrition, calorie-dense foods such as desserts, pastries and snack mixes that add variety to but are not necessary for a healthy diet.

A small but statistically significant 1 percent increase in participants' daily consumption of plain water was associated with an 8.6-calorie decrease in daily energy intake, as well as slight reductions in participants' intake of sugar-sweetened beverages and discretionary foods along with their consumption of fat, sugar, sodium and cholesterol.

While An found that the decreases were greater among men and among young and middle-aged adults, he suggested they could have been associated with these groups' higher daily calorie intakes.

The study was published in the Journal of Human Nutrition and Dietetics.

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Materials provided by University of Illinois at Urbana-Champaign. Original written by Sharita Forrest. Note: Content may be edited for style and length.

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Journal Reference:

1. R. An, J. ‎McCaffrey. Plain water consumption in relation to energy intake and diet quality among US adults, 2005-2012. Journal of Human Nutrition and Dietetics, 2016; DOI: 10.1111/jhn.12368

Could Parkinson's disease start in the gut?

Parkinson's disease may start in the gut and spread to the brain via the vagus nerve, according to a study published in the April 26, 2017, online issue of Neurology®, the medical journal of the American Academy of Neurology. The vagus nerve extends from the brainstem to the abdomen and controls unconscious body processes like heart rate and food digestion.

The preliminary study examined people who had resection surgery, removing the main trunk or branches of the vagus nerve. The surgery, called vagotomy, is used for people with ulcers. Researchers used national registers in Sweden to compare 9,430 people who had a vagotomy over a 40-year period to 377,200 people from the general population. During that time, 101 people who had a vagotomy developed Parkinson's disease, or 1.07 percent, compared to 4,829 people in the control group, or 1.28 percent. This difference was not significant.

But when researchers analyzed the results for the two different types of vagotomy surgery, they found that people who had a truncal vagotomy at least five years earlier were less likely to develop Parkinson's disease than those who had not had the surgery and had been followed for at least five years. In a truncal vagotomy, the nerve trunk is fully resected. In a selective vagotomy, only some branches of the nerve are resected.

A total of 19 people who had truncal vagotomy at least five years earlier developed the disease, or 0.78 percent, compared to 3,932 people who had no surgery and had been followed for at least five years, at 1.15 percent. By contrast, 60 people who had selective vagotomy five years earlier developed Parkinson's disease, or 1.08 percent.

After adjusting for factors such as chronic obstructive pulmonary disease, diabetes, arthritis and other conditions, researchers found that people who had a truncal vagotomy at least five years before were 40 percent less likely to develop Parkinson's disease than those who had not had the surgery and had been followed for at least five years.

"These results provide preliminary evidence that Parkinson's disease may start in the gut," said study author Bojing Liu, MSc, of the Karolinska Instituet in Stockholm, Sweden. "Other evidence for this hypothesis is that people with Parkinson's disease often have gastrointestinal problems such as constipation, that can start decades before they develop the disease. In addition, other studies have shown that people who will later develop Parkinson's disease have a protein believed to play a key role in Parkinson's disease in their gut."

The theory is that these proteins can fold in the wrong way and spread that mistake from cell to cell.

"Much more research is needed to test this theory and to help us understand the role this may play in the development of Parkinson's," Liu said. Additionally, since Parkinson's is a syndrome, there may be multiple causes and pathways.

Even though the study was large, Liu said one limitation was small numbers in certain subgroups. Also, the researchers could not control for all potential factors that could affect the risk of Parkinson's disease, such as smoking, coffee drinking or genetics.

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Materials provided by American Academy of Neurology (AAN). Note: Content may be edited for style and length.

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Journal Reference:

1. Bojing Liu, Fang Fang, Nancy L. Pedersen, Annika Tillander, Jonas F. Ludvigsson, Anders Ekbom, Per Svenningsson, Honglei Chen, and Karin Wirdefeldt. Vagotomy and Parkinson disease: A Swedish register–based matched-cohort study. Neurology, April 2017 DOI: 10.1212/WNL.0000000000003961

Low-sodium diet might not lower blood pressure

A new study that followed more than 2,600 men and women for 16 years found that consuming less sodium wasn't associated with lower blood pressure. The new findings call into question the sodium limits recommended by the current Dietary Guidelines for Americans.

Lynn L. Moore, DSc, associate professor of medicine at Boston University School of Medicine, will present the new research at the American Society for Nutrition Scientific Sessions and annual meeting during the Experimental Biology 2017 meeting, to be held April 22-26 in Chicago.

"We saw no evidence that a diet lower in sodium had any long-term beneficial effects on blood pressure," said Moore. "Our findings add to growing evidence that current recommendations for sodium intake may be misguided."

The 2015-2020 Dietary Guidelines for Americans recommends limiting sodium intake to 2,300 grams a day for healthy people. For the study, the researchers followed 2,632 men and women ages 30 to 64 years old who were part of the Framingham Offspring Study. The participants had normal blood pressure at the study's start. However, over the next 16 years, the researchers found that the study participants who consumed less than 2500 milligrams of sodium a day had higher blood pressure than participants who consumed higher amounts of sodium.

Other large studies published in the past few years have found what researchers call a J-shaped relationship between sodium and cardiovascular risk -- that means people with low-sodium diets (as recommended by the Dietary Guidelines for Americans) and people with a very high sodium intake (above the usual intake of the average American) had higher risks of heart disease. Those with the lowest risk had sodium intakes in the middle, which is the range consumed by most Americans.

"Our new results support these other studies that have questioned the wisdom of low dietary sodium intakes in the general population," said Moore.

The researchers also found that people in the study who had higher intakes of potassium, calcium and magnesium exhibited lower blood pressure over the long term. In Framingham, people with higher combined intakes of sodium (3717 milligrams per day on average) and potassium (3211 milligrams per day on average on average) had the lowest blood pressure.

"This study and others point to the importance of higher potassium intakes, in particular, on blood pressure and probably cardiovascular outcomes as well," said Moore. "I hope that this research will help refocus the current Dietary Guidelines for Americans on the importance of increasing intakes of foods rich in potassium, calcium and magnesium for the purpose of maintaining a healthy blood pressure."

Moore says that there is likely a subset of people sensitive to salt who would benefit from lowering sodium intake, but more research is needed to develop easier methods to screen for salt sensitivity and to determine appropriate guidelines for intakes of sodium and potassium in this salt-sensitive group of people.

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Materials provided by Experimental Biology 2017. Note: Content may be edited for style and length.

Overweight/obese people with diabetes at increased risk of brain abnormalities

A new study published in Diabetologia (the journal of the European Association for the Study of Diabetes [EASD]) reveals that overweight and obese individuals with early stage type 2 diabetes (T2D) had more severe and progressive abnormalities in brain structure and cognition compared to normal-weight study participants.

The research conducted by Dr Sunjung Yoon and Dr In Kyoon Lyoo (Ewha Brain Institute, Ewha Womens University, Seoul, South Korea), Hanbyul Cho (The Brain Institute, University of Utah, Salt Lake City, UT, USA), and colleagues in Korea and the USA looked into the effects of being overweight or obese on the brains and cognitive functions of people with early stage T2D.

Chronic T2D is already known to increase the risk of a range of health problems in multiple organs throughout the body. Complications in the brain caused by the disease may accelerate cognitive dysfunction, and even increase the risk of dementia. While the exact mechanism underlying how T2D alters the brain is not fully understood, several metabolic side effects including insulin resistance, poor blood sugar control, and inflammation have been suggested as playing a role.

Obesity is linked to an increased risk of T2D and can often precede its onset. Additionally, being overweight has been linked to metabolic dysfunction, which is independently associated with brain alterations, as well as carrying a risk of further exacerbating metabolic abnormalities arising from T2D. Little is known, however, about the effect on the brain of excess weight or obesity in the presence of T2D.

A group of 150 Koreans between the ages of 30 and 60 were recruited for the study, comprising 50 overweight/obese individuals with T2D, 50 normal-weight individuals with T2D, and 50 normal-weight control individuals without diabetes. Participants were matched for age and sex across the three groups, and diabetic individuals were also matched for disease duration. Individuals with chronic diabetic complications or major medical, neurological, or psychiatric disorders were excluded from the study, and all those with diabetes had been diagnosed within the previous 5 years and had not received stable insulin therapy.

Data about the structure of participants' brains were acquired using magnetic resonance imaging (MRI), which allowed the mean thickness of the cerebral cortex to be measured across its entirety. Participants also underwent cognitive assessments consisting of tests of memory, psychomotor speed, and executive function, as these are known to be affected in people with T2D.

The study found that grey matter was significantly thinner in clusters in the temporal, prefrontoparietal, motor and occipital cortices of the brains of diabetic study participants when compared to the non-diabetic control group. Further thinning of the temporal and motor cortices was also observed in the overweight/obese diabetic group, compared to normal-weight diabetics. The team also discovered region-specific changes which suggested that the temporal lobe has a particular vulnerability to the combined effects of having T2D and being overweight or obese.

Previous studies have already found that being overweight/obese or having T2D both increase the risk of dementia independently of one another. Atrophy of the temporal lobe has also been identified as one of the earliest observable changes in the large-scale structure of the brain in patients with Alzheimer's disease. The alterations to that region of the brain which were observed in this study may be an indication of how being overweight/obese, having T2D, and the risk of developing dementia are linked.

While the study notes that current WHO guidelines that use Body Mass Index (BMI) to classify individuals as overweight or obese do not differ according to ethnic origin, people of Asian ethnicity tend to be more vulnerable to slight increases in BMI, and are at higher risk of T2D than other ethnicities. This vulnerability may be linked to differences at the cellular level as well as a tendency toward insulin resistance, even in lean individuals. The authors note that the potential for ethnic differences in brain vulnerability to T2D and/or obesity may need to be taken into account when interpreting their results.

The authors state: "Furthermore, we found that disease duration-related alterations in cortical thickness and white matter integrity were more prominent in overweight/obese type 2 diabetic individuals than in those with normal weight. A similar trend was also found in psychomotor speed performance. These findings suggest that weight status may play additive roles in T2D-related brain and cognitive alterations."

They add: "Our findings also highlight the need for early intervention aimed to reduce risk factors for overweight or obesity in type 2 diabetic individuals to preserve their brain structure and cognitive function." The authors stress that the importance of managing insulin resistance during early stage T2D may be greater than previously thought.

They caution, however that: "the current study did not recruit overweight/obese individuals without T2D. Therefore, we could not determine the potential effects of overweight/obesity that are completely independent of type 2 diabetes on metabolic, brain and cognitive measures," and suggest that "Further studies using a more elaborate framework are recommended to better describe the independent and combined (additive, synergistic or interactive) effects of T2D and obesity/overweight on the brain."

The authors conclude: "An increased awareness of overweight/obesity-related risk is necessary to prevent and manage type 2 diabetes-related brain atrophy and cognitive dysfunction from early stage T2D onward."

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Materials provided by Diabetologia. Note: Content may be edited for style and length.

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Journal Reference:

1. Sujung Yoon, Hanbyul Cho, Jungyoon Kim, Do-Wan Lee, Geon Ha Kim, Young Sun Hong, Sohyeon Moon, Shinwon Park, Sunho Lee, Suji Lee, Sujin Bae, Donald C. Simonson, In Kyoon Lyoo. Brain changes in overweight/obese and normal-weight adults with type 2 diabetes mellitus. Diabetologia, 2017; DOI: 10.1007/s00125-017-4266-7

Further knowledge required about the differences between milk proteins

New knowledge on milk composition and quality is of essential importance to consumers as well as the industry. There are therefore considerable research efforts in milk worldwide. One of the major topics concerns milk's content of different proteins and their importance to human health. Basically, milk consists of two protein types -- whey and casein. Casein can be further divided into four categories. One of these, beta casein, attracts particular attention. Several beta casein types exist and A1 and A2 are the most common.

It has been suggested that A2-protein milk is a healthier alternative to A1-protein milk, as the latter is claimed to metabolize into potentially detrimental peptides in the intestine. One specific peptide formed during digestion is further claimed to have unfavourable effects on the consumers drinking it. However, the European Food Safety Authority (EFSA) dismissed these claims in 2009 as undocumented.

It is currently debated whether some of the discomfort reported by some milk consumers regarding impact on the gastrointestinal system may be caused by discomfort originating from these detrimental peptides. A2-milk has been labelled a more "original" milk and is closer to breast milk. Foreign companies have succeeded in establishing specialized industries that sell milk that only contains A2-type beta casein. In December 2016, the Danish dairy Thise introduced a Danish variant.

Need for fact-based argumentation

This particular area still requires additional research and there is no scientific evidence to substantiate that one protein type is superior compared to the other, states Professor Lotte Bach Larsen, Department of Food Science at Aarhus University:

- I acknowledge that further research and examination is required within this particular area in order to base the debate on solid, fact-based argumentation. We cannot rule out that some consumers, who feel discomfort when consuming milk, might benefit from drinking solely A2-milk.

In a recently finished investigation, Lotte Bach Larsen and her colleagues from the Department of Food Science cooperated with Norwegian scientists to examine if the two different protein types give rise to different metabolization patterns and thus the formation of potentially bioactive protein fragments. In their examination the scientists used gastric and intestinal juices from humans to study how enzymes in the gastrointestinal tract break down the proteins. The experiment was accomplished in a laboratory model system and using protein types that were purified from milk from cows whose milk contained either solely A1 or A2 variants of the protein.

- The examination demonstrates -- quite as expected -- that a number of different peptides is formed from both protein types, when the milk is metabolized. But, it also turns out that the peptide in question is actually present when both A1 and A2 milk is digested. However, the content of this specific peptide formed from A1 beta casein protein variant by the human digestion enzymes was approx. three times higher than liberated from the A2 beta casein variant. As this study was carried out with purified beta casein variants, there is a need to examine whether there is a difference in content of this specific peptide, if digestion is going on using milk and not simply isolated beta casein proteins. In addition, it would be beneficial to carry out a proper human intervention study on eventual the effects when consuming the two different types of milk, and also examine if the peptide can be measured in the blood, says Lotte Bach Larsen.

A2-milk is the most frequent type

Another interesting aspect when discussing the difference between A1 and A2 milk is the fact that milk containing the A2-type beta casein is actually the most frequent type in Danish dairy cattle. Scientists from the Department of Food Science were able to conclude this fact when they -- in connection with a major research project -- carried out a screening of the protein composition of Danish milk. Actually, the frequency of the A2 protein was almost the same in both Danish Jersey cattle and Danish Holstein cattle.

- It is rather interesting if consumers consider A2 milk to be something unique and special. We should point out that even though most of the Danish milk is mixed, dairy milk will normally contain both types, but with levels of the A2 type over the A1 type, as it seems that A2 is present in highest frequency over the A1 vatiant. If you choose a milk type that specifically contains the A2 protein of the beta casein, you should know that this milk comes from cows that have been screened for the variants and selected for this production, says Lotte Bach Larsen.

She hopes that the future will bring an increased focus on studies in the metabolism of milk proteins in human studies.

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Materials provided by Aarhus University. Note: Content may be edited for style and length.

The swollen colon: Cause of chronic inflammation discovered

Researchers at the University Medical Center of Johannes Gutenberg University Mainz and the German Research Center for Environmental Health, Helmholtz Zentrum München have discovered that too much of the oncogene Bcl-3 leads to chronic intestinal diseases. They describe in Nature Communications exactly how it throws the immune system off-balance.

Chronic intestinal disorders such as ulcerative colitis and Crohn's disease are caused by the body's own immune defense system. Sufferers frequently experience episodic symptoms such as abdominal pain, cramps, and diarrhea. Researchers are still trying to identify the precise underlying origins of these problems. A team led by Dr. Nadine Hövelmeyer and Professor Ari Waisman of the Mainz University Medical Center in collaboration with Dr. Elke Glasmacher of Helmholtz Zentrum München has discovered a new mechanism that causes intestinal inflammation.

"With the help of our cooperation partners, we were able to demonstrate that the level of the Bcl-3 protein, which also plays a role in the development of various cancerous diseases, is elevated in the intestinal tract of colitis patients and is indeed a trigger of the disease," said Dr. Nadine Hövelmeyer, head of the work group at the Mainz-based Institute for Molecular Medicine. According to the study, Bcl-3 develops its effect on intestinal health through interaction with the so-called regulatory T-cells (Tregs). Their main task is to prevent overreaction of the immune system and to develop a level of tolerance towards the body they serve.

Gene blockade in the spotlight

"We were able to demonstrate that Bcl-3 suppresses the activation of Tregs by preventing the necessary genes from being read," explained Dr. Elke Glasmacher, head of the team at the Institute for Diabetes and Obesity in Munich. "Bcl-3 interacts with the transcription factor p50, which is otherwise responsible for activation, and blocks it."

"Consequentially, the regulatory T-cells remain passive, the immune system is no longer regulated, and inflammatory processes begin to take place. Experiments using various models have revealed that elevated quantities of Bcl-3 cause certain cells to migrate to the intestines, where they trigger a severe inflammatory response," Dr. Sonja Reissig, lead author of the publication and research associate at Mainz University Medical Center, pointed out.

"The results represent a major contribution towards our understanding of chronic intestinal inflammation and hopefully over the long-term will help us discover aspects that we can target with new therapies," concluded Hövelmeyer. Her colleague Professor Ari Waisman, Director of the Institute for Molecular Medicine at the Mainz University Medical Center, added: "We are currently focusing on the search for new active agents that will prevent the interaction between Bcl-3 and p50, thus maintaining normal Treg functionality."

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Materials provided by Johannes Gutenberg Universitaet Mainz. Note: Content may be edited for style and length.

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Journal Reference:

1. Sonja Reißig, Yilang Tang, Alexei Nikolaev, Katharina Gerlach, Christine Wolf, Kathrin Davari, Christian Gallus, Joumana Masri, Ilgiz A. Mufazalov, Markus F. Neurath, F. Thomas Wunderlich, Jörn M. Schattenberg, Peter R. Galle, Benno Weigmann, Ari Waisman, Elke Glasmacher, Nadine Hövelmeyer. Elevated levels of Bcl-3 inhibits Treg development and function resulting in spontaneous colitis. Nature Communications, 2017; 8: 15069 DOI: 10.1038/NCOMMS15069

New appetite control mechanism found in brain

Over recent decades, our understanding of hunger has greatly increased, but this new discovery turns things on their head. Up until now, scientists knew that leptin -- a hormone released by fatty tissue, reduces appetite, while ghrelin -- a hormone released by stomach tissue makes us want to eat more. These hormones, in turn, activate a host of neurons in the brain's hypothalamus -- the body's energy control center.

The discovery of NPGL by Professor Kazuyoshi Ukena of Hiroshima University shows that hunger and energy consumption mechanisms are even more complex than we realized -- and that NPGL plays a central role in what were thought to be well-understood processes.

Professor Ukena first discovered NPGL in chickens after noticing that growing birds grew larger irrespective of diet -- suggesting there was more to energy metabolism than meets the eye. Intrigued, the researchers at HU performed a DNA database search to see if mammals might also possess this elusive substance. They found that it exists in all vertebrates -- including humans.

In order to investigate its role, if any, in mammals, Professor Ukena's team fed three groups of mice, on three distinct diets, to see how NPGL levels are altered. The first set of mice was fed on a low-calorie diet for 24 hours. The second group was fed on a high-fat diet for 5 weeks -- and the third lucky group was fed on a high-fat diet, but for an extended period of 13 weeks.

The mice fed on a low calorie diet were found to experience an extreme increase in NPGL expression, while the 5-week high-fat-diet group saw a large decrease in NPGL expression.

Further analysis found that mice possess NPGL, and its associated neuron network, in the exact same locations of the brain as those regions already known to control appetite suppression and energy use.

Professor Ukena proposes that NPGL plays a vital role in these mechanisms -- increasing appetite when energy levels fall and reducing appetite when an energy overload is detected -- together, helping to keep us at a healthy and functioning weight, and more importantly alive!

As NPGL levels greatly increased in mice exposed to a low calorie diet, Professor Ukena believes it is an appetite promoter, working in opposition to appetite suppressing hormones such as leptin. Backing this hypothesis up, it was found that mice directly injected with NPGL exhibited a voracious appetite.

Interestingly NPGL levels, which plummeted in the 5-week-long high-fat-diet mice -- fell back to normal levels in mice who gorged themselves for the longer period of 13 weeks.

It is proposed that exposure to high-fat diets for long periods of time lead to insensitivity to leptin's appetite-suppressing effects, and so NPGL -- even at normal levels -- leads to weight gain and obesity, showing that the body can only do so much to keep our weight in check.

Professor Ukena says that further study is required to understand the interaction of previously known appetite mechanisms with this new kid on the homeostasis block. It does seem however, that we still have a lot to learn about appetite, hunger, and energy consumption. It is hoped that this study into mammalian NPGL adds another piece to the puzzle.

What is certain -- but you knew this already -- is that dieting is difficult. The discovery and study of mammalian NPGL helps explain why, and provides a plausible excuse for those whose good intentions fall short.

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Materials provided by Hiroshima University. Note: Content may be edited for style and length.

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Journal Reference:

1. aichi Matsuura Kenshiro Shikano Takaya Saito Eiko Iwakoshi-Ukena Megumi Furumitsu Yuta Ochi Manami Sato George E. Bentley Lance J. Kriegsfeld Kazuyoshi Ukena. Neurosecretory protein GL, a hypothalamic small secretory protein, participates in energy homeostasis in male mice. Endocrinology, March 2017 DOI: 10.1210/en.2017-00064

Optomizing Health Benefits by Drinking Water at The Correct Time

Most people know by now that drinking water is essential to health, antiaging and longevity. One can survive without food for 40 days, but ones health will gradually deteriorate without water after two days depending on temperature and amount of body water loss.

Benefits of Drinking Water and its Functions in the Body?

75% of brain is water
83% of body’s blood is water
regulates body temperature
removes body waste
help convert food into energy
helps body absorb nutrients
helps carries nutrients and oxygen to cells
helps to maintain normal kidney function
cushions bone, 75% of muscles are water
protects and cushions vital organ

The Key to Optimizing Health from Drinking Water
Forget those who try to sell you alkaline water, or bottled water, as both does not optimize health.

Many bottled water are no better than tap water, and drinking alkaline water has no effect on stomach pH, or on the pH of blood. Filtered water manufacturers claim that alkaline water, which has a pH higher than tap water, can neutralize acid in your blood, boost energy, speed metabolism and even slow the aging process. Most of these claims are unproven, though limited research has shown that alkaline water may reduce bone loss in pre-menopausal women, according to the health department at Columbia University. For a sure way to improve your bone health and maintain healthy pH levels, eat a diet rich in fruits and vegetables, along with plenty of calcium and vitamin D sources, such as fortified milk and salmon. No need to drink alkaline water. 

When to Drink Water
Here’s how to drink water at the correct time to maximize its effectiveness on your Body:
Drink two glasses of water after waking up – helps activate internal organs.
Drink 1 glass 30 Minutes before meal – helps digestion
Drink 1 glass before taking a bath – helps lower blood pressure
Drink 1 glass before sleep – may help to avoid stroke or heart attack.

Weight-bearing exercises promote bone formation in men

Human hormone, protein linked to bone mass are impacted by 12 months of targeted exercise

Osteoporosis affects more than 200 million people worldwide and is a serious public health concern, according to the National Osteoporosis Foundation. Now, Pamela Hinton, associate professor in the Department of Nutrition and Exercise Physiology, has published the first study in men to show that long-term, weight-bearing exercises decrease sclerostin, a protein made in the bone, and increase IGF-1, a hormone associated with bone growth. These changes promote bone formation, increasing bone density.

"People may be physically active, and many times people know they need to exercise to prevent obesity, heart disease or diabetes," Hinton said. "However, you also really need to do specific exercises to protect your bone health."

In the study, men 25- to 60-years-old who had low-bone mass were split into two groups. One group performed resistance training exercises such as lunges and squats using free weights. The other group performed various types of jumps, such as single-leg and double-leg jumps. After 12 months of performing the exercises, Hinton then compared the levels of bone proteins and hormones in the blood.

"We saw a decrease in the level of sclerostin in both of these exercise interventions in men," Hinton said. "When sclerostin is expressed at high levels, it has a negative impact on bone formation. In both resistance and jump training, the level of sclerostin in the bone goes down, which triggers bone formation."

The other significant change Hinton observed was an increase in the hormone IGF-1. Unlike sclerostin, IGF-1 triggers bone growth. The decrease of harmful sclerostin levels and the increase in beneficial IGF-1 levels confirmed Hinton's prior research that found both resistance training and jump training have beneficial effects on bone growth.

To increase bone mass and prevent osteoporosis, Hinton recommends exercising specifically to target bone health. While exercises such as swimming and cycling are beneficial to overall health, these activities do not strengthen the skeleton. Hinton suggests also doing exercise targeted for bone health, such as resistance training and jump training.

The study, "Serum sclerostin decreases following 12 months of resistance- or jump-training in men with low bone mass," was published in Bone.

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Materials provided by University of Missouri-Columbia. Original written by RoseAnn Sorce. Note: Content may be edited for style and length.

How walking benefits the brain

You probably know that walking does your body good, but it's not just your heart and muscles that benefit. Researchers at New Mexico Highlands University (NMHU) found that the foot's impact during walking sends pressure waves through the arteries that significantly modify and can increase the supply of blood to the brain. The research will be presented today at the APS annual meeting at Experimental Biology 2017 in Chicago.

Until recently, the blood supply to the brain (cerebral blood flow or CBF) was thought to be involuntarily regulated by the body and relatively unaffected by changes in the blood pressure caused by exercise or exertion. The NMHU research team and others previously found that the foot's impact during running (4-5 G-forces) caused significant impact-related retrograde (backward-flowing) waves through the arteries that sync with the heart rate and stride rate to dynamically regulate blood circulation to the brain.

In the current study, the research team used non-invasive ultrasound to measure internal carotid artery blood velocity waves and arterial diameters to calculate hemispheric CBF to both sides of the brain of 12 healthy young adults during standing upright rest and steady walking (1 meter/second). The researchers found that though there is lighter foot impact associated with walking compared with running, walking still produces larger pressure waves in the body that significantly increase blood flow to the brain. While the effects of walking on CBF were less dramatic than those caused by running, they were greater than the effects seen during cycling, which involves no foot impact at all.

"New data now strongly suggest that brain blood flow is very dynamic and depends directly on cyclic aortic pressures that interact with retrograde pressure pulses from foot impacts," the researchers wrote. "There is a continuum of hemodynamic effects on human brain blood flow within pedaling, walking and running. Speculatively, these activities may optimize brain perfusion, function, and overall sense of wellbeing during exercise."

"What is surprising is that it took so long for us to finally measure these obvious hydraulic effects on cerebral blood flow," first author Ernest Greene explained. "There is an optimizing rhythm between brain blood flow and ambulating. Stride rates and their foot impacts are within the range of our normal heart rates (about 120/minute) when we are briskly moving along."

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Materials provided by Experimental Biology 2017. Note: Content may be edited for style and length.

Physical activity may ward off heart damage

Physical activity can lower the risk of heart damage in middle-aged and older adults and reduce the levels of heart damage in people who are obese, according to research published in JACC: Heart Failure.

Obesity is associated with structural and functional abnormalities in the heart and subsequent heart failure. Heart failure may be caused by subclinical myocardial damage, in which there is damage to the heart muscle but a patient does not show sign or symptoms.

Researchers examined 9,427 patients aged 45-64 years without cardiovascular disease and a body mass index of more than 18.5 kg/m2. Physical activity was measured through a questionnaire and categorized according to current guidelines as "recommended" (at least 75 minutes per week of vigorous intensity or at least 150 minutes per week of a combination of moderate to vigorous intensity), "intermediate" (1-74 minutes per week of vigorous intensity or 1-149 minutes of a combination of moderate to vigorous intensity), or "poor" (no moderate to vigorous exercise). To measure damage to the heart, researchers assessed levels of high sensitivity troponin T. Elevated levels of this biomarker are considered a marker of heart damage and have been shown to be associated with future heart failure.

Elevated levels of high sensitivity troponin T were observed in 7.2 percent of the total study population. Individuals with lower levels of physical activity were significantly more likely to have elevated levels of high sensitivity troponin suggesting higher heart damage. For example, participants who performed poor and intermediate levels of physical activity were 39 percent and 34 percent more likely to have heart damage than persons who engaged in recommended levels of physical activity.

The researchers subsequently looked at the combined associations of physical activity and obesity with this blood marker of heart damage. Obesity had been previously shown to be strongly associated with elevated levels of high sensitivity troponin, and the combination of obesity and elevated troponin was associated with a significantly increased risk of future heart failure. In the current study, the authors demonstrated that participants with obesity who performed poor levels of exercise had the highest likelihood of having elevated high sensitivity troponin levels. Participants with obesity who performed recommended levels of physical activity had a weaker association with elevated levels of high sensitivity troponin, and after adjustment for traditional cardiac risk factors, this was association was no longer statistically significant. These results suggest physical activity may lessen the association of obesity and heart damage. The authors also found a significant interaction between physical activity and obesity on elevated levels of high sensitivity troponin, which indicates that the protective association of physical activity and heart damage may be stronger among individuals with obesity, a group at particularly high risk for future heart failure.

"The protective association of physical activity against subclinical myocardial damage may have implication for heart failure risk reduction, particularly among the high-risk group of individuals with excess weight," said Roberta Florido, MD, cardiology fellow at Johns Hopkins Hospital and lead author of the study. "Promoting physical activity may be a particularly important strategy for heart failure risk reductions among high risk groups such as those with obesity."

In an accompanying editorial comment, Tariq Ahmad, MD, MPH, FACC, and Jeffrey M. Testani, MD, MTR, said they encourage cardiologists to promote healthy habits rather than simply treating heart failure after it has developed.

"In this report we add to the body of evidence supporting moderate physical activity and its protective effect in the setting of obesity," said JACC: Heart Failure Editor-in-Chief Christopher O'Connor, MD, FACC.

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Materials provided by American College of Cardiology. Note: Content may be edited for style and length.

Treating bloodstream infections with fewer side effects

Patients with bloodstream infections could avoid treatment with a combination of antimicrobial therapies if they are given the right drug as early as possible and if they are classified as at low risk of death. This would reduce the risk of adverse side effects, as well as the likelihood of drug resistance developing in the bacteria that cause the infection -- carbapenemase-producing Enterobacteriaceae (CPE).

The results from the international INCREMENT study, presented at the 27th European Congress of Clinical Microbiology and Infectious Diseases (ECCMID) today (Sunday) and published simultaneously in The Lancet Infectious Diseases, show for the first time that combination therapy is only better than treatment with a single antimicrobial in patients with bloodstream infections caused by CPE if they are at high risk of dying. In these patients combination therapy halved the risk of death, but it made no difference in patients at low risk.

A second presentation on the INCREMENT study showed that it was possible to avoid using carbapenems -- the class of antimicrobial therapies considered as drugs of last resort -- to treat bloodstream infections caused by another type of bacteria called extended-spectrum beta-lactamase producing Enterobacteriaceae (ESBL-E), which are usually resistant to a range of antimicrobial drugs including cephalosporins. The research showed that if patients were treated with other drugs, thought to be active against the infection, and then switched to a better-targeted drug once doctors had identified the bacteria, patients did as well as those who were treated immediately with carbapenems. This finding may help doctors to reduce the use of carbapenems so that they can be reserved for use only for infections that are definitely resistant to all other existing antimicrobial therapies.

When treating patients with potentially life-threatening bloodstream infections, doctors often use a combination of antimicrobial or broad spectrum antimicrobial drugs in order to try to start combating the infection as quickly as possible, but without knowing which treatments the bacteria are actually susceptible to. This means that the drugs may not be well targeted and it can lead to bacteria developing resistance to a range of antimicrobials, including the therapies of last resort.

In the first presentation, Professor Jesús Rodríguez-Baño, Head of the infectious diseases division at the University Hospital Virgen Macarena (Seville, Spain) and President-elect of the European Society of Clinical Microbiology and Infectious Diseases (ESCMID), reported results from 37 hospitals in 11 countries on 437 patients with bloodstream infections caused by CPE -- a group of bacteria that are resistant to carbapenems. They can kill up to about half of patients who develop bloodstream infections.

Before starting antimicrobial treatment, patients were assessed for their risk of death; patients at low risk scored between 0-7 and those at high risk scored between 8-15 on the IMCREMENT-CPE score. Fifty-one percent of the patients were low risk.

At the start of treatment, 343 patients received antimicrobial therapy that was active against the bacteria causing the infection -- either a single antimicrobial drug or a combination. This treatment more than halved the risk of death for the group as a whole. However, combination therapy was only associated with a reduced risk of death (a decrease of 44%) in the high-risk patients, and not in the low-risk patients.

Prof. Rodríguez-Baño said: "Contrary to present recommendations, combination therapy can be avoided in a substantial proportion of patients with bloodstream infections due to CPE. These patients can be identified using the INCREMENT-CPE score and if they are low risk they can be treated with a single active antimicrobial. This helps to avoid the problems that can be associated with combination therapy, such as a higher risk of adverse side effects, the development of resistance by the infection-causing bacteria to more antimicrobials, and the higher cost.

"We hope that, as a result of these findings, clinicians will be able to evaluate patients better so that only those at high risk will be given combination therapy."

In the second presentation, Dr Zaira Palacios Baena, an internal medicine resident at the Hospital Universitario Virgen Macarena (Seville, Spain), told the congress: "There is no consistent evidence about the use of different regimens of treatments for bloodstream infections due to extended-spectrum beta-lactamase producing Enterobacteriaceae. We wanted to assess the impact of starting treatment with drugs that were thought likely to be active against the infection, but before doctors had identified the precise microorganism causing the infection and which drugs it would be susceptible to.

"We found that even if we treated patients with antimicrobial drugs that proved to be inactive against the bug that was causing the infection, it did not increase death rates if we take into account their underlying risk of death and if we switch to a drug that is active against the infection as soon as we know which one will work. Nowadays, with the evolution of technology in the field of microbiology, we can know the susceptibility of a microorganism within 24 hours and then we can start using the right, targeted active treatment. This means that we do not have to start treating patients immediately with carbapenems, but can try out other drugs first before switching to an active antimicrobial, that is not necessarily a carbapenem, if the first drug doesn't work."

Dr Palacios Baena and her colleagues included 855 patients with bloodstream infections caused by ESBL-E who were treated between 2004 and 2012 in the INCREMENT study and who received their first treatment within 24 hours. They assessed the patients' risk of dying within 30 days using the INCREMENT-ESBL score, which takes into account factors such as age, type and source of the infection (most were E.coli or Klebsiella bacteria), the severity of the infection and the presence of other diseases or conditions.

The patients who started antimicrobial therapies before the susceptibility of the infection was known were classified into three groups:

1) patients who were given carbapenems or another broad spectrum antimicrobial therapy called beta-lactamase/beta-lactamase inhibitors; this was called "choice therapy (CT)" and these patients were used as the reference group to compare the other two groups against;

2) patients who were given other antimicrobial drugs, either alone or in combination, that were known to work against ESBL-E in the laboratory, called "alternative therapy (AT)"; and

3) patients who were given antimicrobial therapy that proved to be inactive against the infection, called "inactive therapy (IT)."

The majority of patients (489, 57%) received choice therapy, 83 (10%) received alternative therapy, and 283 (33%) received inactive therapy. A total of 144 patients (17%) died. The death rates for CT patients was 17%, for AT patients it was 19%, and for IT patients, 15.5%. There was no statistically significant difference in death rates between patients who received CT and those who received either AT or IT.

The risk of death in high-risk patients increased by a third for each point on the INCREMENT-ESBL score, and patients who were treated with a targeted therapy that had not been shown to work against the bacteria in laboratory tests (inactive targeted therapy) had a nearly three-fold increased risk of death. Dr Palacios Baena said these were the patients most likely to benefit from early treatment with broad-spectrum drugs known to be active against this type of bacteria.

She said that further research needed to be done to confirm their results before any changes were introduced in the way patients with these bloodstream infections are treated. "We hope these results might help other investigations, and maybe in the future we can stop the threatening development of carbapenem-resistant microorganisms by avoiding the use of carbapenems in selected patients.

"Many deaths can be prevented if we use the antimicrobials available to us appropriately and moderately. It's necessary to strengthen the research into new molecules and the development of old ones. Patients, politicians and the general population must be aware that the use of broad-spectrum antimicrobials needs to be reserved only for when they are really needed, as it is a disaster for patients who develop an infection due to a microorganism that is resistant to carbapenems."

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Materials provided by European Society of Clinical Microbiology and Infectious Diseases. Note: Content may be edited for style and length.

'Connshing syndrome' named as a new cause of high blood pressure

Research led by scientists at the University of Birmingham has revealed a new cause of high blood pressure which could lead to major changes in managing the disease.

High blood pressure, also known as hypertension, often goes unnoticed but if left untreated can increase the risk of heart attack and stroke.

Studies estimate that one in four adults suffer from hypertension, but most patients have no identifiable cause for the condition.

However, it is known that in up to 10 per cent of hypertensive patients the overproduction of the adrenal hormone aldosterone -- a condition known as primary aldosteronism or Conn syndrome -- is the cause of disease.

Now the University of Birmingham-led study has, for the first time, made the important discovery that a large number of patients with Conn syndrome do not only overproduce aldosterone but also the stress hormone cortisol.

Professor Wiebke Arlt, Director of the Institute of Metabolism and Systems Research (IMSR) at the University of Birmingham, said: "Our findings show that the adrenal glands of many patients with Conn syndrome also produce too much cortisol, which finally explains puzzling results of previous studies in Conn patients.

"These previous studies had found increased rates of type 2 diabetes, osteoporosis and depression in Conn patients -- problems typically caused by overproduction of cortisol, also termed Cushing syndrome, and not by too much aldosterone."

The authors of the University of Birmingham-led study, conducted in collaboration with a group of scientists from Germany, decided to name this new cause of hypertension -- the combined overproduction of aldosterone and cortisol -- as Connshing syndrome.

At present, many Conn syndrome patients are treated with drugs that are directed against the adverse effects of aldosterone. However, this leaves the cortisol excess untreated.

Second author of the study, published in JCI Insight, Katharina Lang -- an academic clinical lecturer at IMSR -- said: "These findings are very likely to change clinical practice.

"Patients will now need to undergo more detailed assessment to clarify whether they suffer from Conn or Connshing syndrome.

"Previously, patients with Conn syndrome were never assessed for the overproduction of other hormones but this will now change thanks to the results of this study.

"Also, researchers now will need to investigate whether treating the Connshing patients with an additional drug, which counteracts the cortisol excess, will improve their health outcomes."

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Materials provided by University of Birmingham. Note: Content may be edited for style and length.

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Journal Reference:

1. Wiebke Arlt, Katharina Lang, Alice J. Sitch, Anna S. Dietz, Yara Rhayem, Irina Bancos, Annette Feuchtinger, Vasileios Chortis, Lorna C. Gilligan, Philippe Ludwig, Anna Riester, Evelyn Asbach, Beverly A. Hughes, Donna M. O’Neil, Martin Bidlingmaier, Jeremy W. Tomlinson, Zaki K. Hassan-Smith, D. Aled Rees, Christian Adolf, Stefanie Hahner, Marcus Quinkler, Tanja Dekkers, Jaap Deinum, Michael Biehl, Brian G. Keevil, Cedric H.L. Shackleton, Jonathan J. Deeks, Axel K. Walch, Felix Beuschlein, Martin Reincke. Steroid metabolome analysis reveals prevalent glucocorticoid excess in primary aldosteronism. JCI Insight, 2017; 2 (8) DOI: 10.1172/jci.insight.93136

Medical history reveals multiple sclerosis begins to impact patients sooner

People with multiple sclerosis can show signs of something wrong five years before the onset of disease, much earlier than previously thought, according to a new analysis of health records from people with the condition.

The new research, published in Lancet Neurology, is a first step to identifying red flags to help doctors screen for the disease and start interventions earlier. This could point researchers in a new direction for finding the root cause of the disease.

"Proving that people with multiple sclerosis have already changed their behaviour in the five years before even the earliest medical recognition of the condition is very important because it means we have to look beyond those five years to understand how it is caused," said Helen Tremlett, senior author of the study and a professor in the department of medicine at the Djavad Mowafaghian Centre for Brain Health.

Multiple sclerosis is thought to be an autoimmune disease where the body attacks the protective coating, known as myelin, around brain cells. Once a person is diagnosed with multiple sclerosis, a physician will try to pinpoint the onset of the disease, sometimes known as the patient's first demyelinating event, and can include problems with vision or motor control.

The researchers examined health records of 14,000 people with multiple sclerosis from B.C., Saskatchewan, Manitoba and Nova Scotia over a 20-year period and compared them to the health records of 72,000 people without the disease. They were looking for something called a prodrome, an early set of symptoms that can indicate the onset of a disease.

Prodromes have been identified for other neurological conditions like Alzheimer's and Parkinson's diseases. The recognition of these prodromes has provided clues about how the diseases might begin and has stimulated new research into causes or triggers.

This study of patients from across Canada revealed that there is a phase where people begin to show symptoms before multiple sclerosis is medically recognized. During this phase patients tend to visit their physicians, be admitted to a hospital and fill prescriptions more than the general population.

"There's something going on here that makes this population of people unique," said José Wijnands, first author of the manuscript, a postdoctoral fellow and a Michael Smith Foundation for Health Research trainee.

"When other degenerative brain diseases have a prodrome, it suggests that something may be happening," said Tremlett. "We hope to uncover what this might be in multiple sclerosis."

Going forward, the team of researchers will try to understand why these patients had been using the health-care system differently, and whether there are trends in illnesses reported and prescriptions filled that point to a specific set of symptoms that doctors could use to help identify multiple sclerosis earlier.

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Materials provided by University of British Columbia. Note: Content may be edited for style and length.

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Journal Reference:

1. José M A Wijnands, Elaine Kingwell, Feng Zhu, Yinshan Zhao, Tanja Högg, Karen Stadnyk, Okechukwu Ekuma, Xinya Lu, Charity Evans, John D Fisk, Ruth Ann Marrie, Helen Tremlett. Health-care use before a first demyelinating event suggestive of a multiple sclerosis prodrome: a matched cohort study. The Lancet Neurology, 2017; DOI: 10.1016/S1474-4422(17)30076-5