Draft Report Compiled by
In This Issue:
1. With worrisome animal research, more focus needed on effects of cannabis on human development
2. Omega-3 fatty acid stops known trigger of lupus
3. Consumption of a bioactive compound from Neem plant could significantly suppress development of prostate cancer
4. Component of red wine, grapes can help to reduce inflammation, study finds
5. For women, caffeine could be ally in warding off dementia
6. Mix and match microbes to make probiotics last
7. Certain alternative therapies may help patients with bowel disorders
8. New research delimits the possible causes of celiac disease
9. New animal research explores red raspberries in supporting healthy weight and motor function
10. Vitamin E may prevent pneumonia in nonsmoking elderly men
11. Antibacterial and antiinflammatory properties of bovine colostrum
12. Fewer indications of ADHD in children whose mothers took vitamin D during pregnancy
13. Running triggers production of a molecule that repairs the brain in animal models
14. Researchers find 2 distinct genetic subtypes in Crohn’s disease patients
With worrisome animal research, more focus needed on effects of cannabis on human development
September 30, 2016
In this new era of legalized marijuana, far too little research has been conducted on the effect of cannabis on the development of human embryos, say researchers at Georgetown University Medical Center who scoured medical literature on the topic and found what they say is worrisome animal research.
Their study, in the journal BioMed Central (BMC) Pharmacology and Toxicology, suggests an urgent need for human epidemiological and basic research that examines the link between maternal cannabinoid use, either smoked or eaten in candy bars, and the health of newborns. Cannabinoids are chemicals like THC, the primary psychoactive compound in marijuana, that act on cannabinoid receptors in neurons, repressing the normal release of neurotransmitters.
“We know from limited human studies that use of marijuana in early pregnancy is associated with many of the same risks as tobacco, including miscarriage, birth defects, developmental delays and learning disabilities, but animal research suggests the potential for many more developmental issues linked with the drug,” says the study’s senior investigator, G. Ian Gallicano, PhD, associate professor of biochemistry and molecular & cellular biology at Georgetown.
Gallicano says one reason for limited research is that the classification of marijuana as a Schedule I drug creates challenges to conducting research.
“All of the model systems point to the notion that cannabinoids affects many aspects of human development because THC and other chemicals alter molecular pathways that shouldn’t be disrupted during development of a fetus,” he says.
“We also know that THC is a promising agent for treating cancer, because it negatively affects tumor growth and can cause the death of cancer cells. Embryo development has similarities to tumor formation — it turns on growth pathways that are necessary for development,” Gallicano says. “The fact that THC seems to stop cancer growth suggests how damaging the chemical could be for a fetus.”
The study grew from a project of four current Georgetown medical students (Joseph Friedrich, Dara Khatib, Keon Parsa, and Ariana Santopietro) for a course, Sexual Development and Reproduction, taught by Gallicano. They undertook the analysis given that although four states have legal recreational marijuana use and 24 allow use of medical marijuana, little research has been conducted on outcomes from use of the drug in pregnancy and biological mechanisms that cause these issues.
The students reviewed the scientific literature for studies on cannabinoids and embryonic development published between 1975 and 2015. They cite the following findings:
• THC lasts in the body for weeks, especially in maternal tissues that act as reservoirs for THC and other cannabinoids, according to studies of pregnant dogs. Human cells studies have shown that THC has a half-life of eight days in fat deposits and can be detected in blood for up to 30 days;
• THC readily crosses the human placenta, which can slow clearance of the drugs while prolonging fetal exposure;
• THC levels in smoked marijuana have increased nearly 25-fold since 1970, and can be substantially stronger in edible preparations of cannabis;
• THC and other cannabinoids interfere with use of folic acid (vitamin B9), which has long been known to be essential for normal development and growth of the human placenta and embryo. Deficiencies in folic acid are linked to low human birth weight, increased risk of spontaneous abortion, and neural tube defects such as spina bifida.
• Cannabinoid signaling plays important roles in development of a mouse embryo. It is required for proper pre-implantation development, embryo transport to the uterus, and implantation.
• In post-implantation development, cannabinoid signaling functions in a multitude of pathways, including, but not limited to blood vessel growth, fate of embryonic stem cells, and normal cognitive development. For example, disruption of one key neural pathway, BDNF, has been linked to increased risk of congenital malformations and impaired cognition, including autism and low IQ in humans.
The authors also say the harms found in animal studies cited in this study do not include the damaged induced from the act of smoking marijuana.
Omega-3 fatty acid stops known trigger of lupus
September 29, 2016
A team of Michigan State University researchers has found that consuming an omega-3 fatty acid called DHA, or docosahexaenoic acid, can stop a known trigger of lupus and potentially other autoimmune disorders.
DHA can be found in fatty, cold-water fish and is produced by the algae that fish eat and store in their bodies. It can be found in fish oil supplements as well, used by more than 30 million Americans.
“What we discovered was when lupus was triggered by crystalline silica, a toxic mineral also known as quartz that’s linked to human autoimmunity, DHA blocked the activation of the disease,” said Melissa Bates, one of the study’s lead authors and a doctoral student in MSU’s Department of Food Science and Human Nutrition and the Institute of Integrative Toxicology.
The findings have been published in PLOS ONE.
The preclinical study looked at the effect of DHA on lupus lesions in the lungs and kidneys of female mice that were already genetically predisposed to the disease. Their results were overwhelmingly positive.
“Ninety-six percent of the lung lesions were stopped with DHA after being triggered by the silica,” said Jack Harkema, another study author and pulmonary pathologist. “I’ve never seen such a dramatic protective response in the lung before.”
Lupus is considered a genetic disease and is triggered not only by inhaling crystalline silica toxicants, but also by other environmental factors such as sun exposure. Quartz is the most common, and most dangerous, form of crystalline silica and is often found in the agriculture, construction and mining industries where workers can breathe in the mineral dust.
“Lupus is the body’s immune system attacking itself and it can damage any part of the body including skin, joints and organs,” said James Pestka, a University Distinguished Professor of food science and human nutrition, who also co-led the research with Bates and Harkema.
Although it’s still unknown exactly why DHA is able to prevent the onset of lupus, the researchers said this study provides scientists with a better model for looking at just how much DHA is needed to ward off the environmental trigger of the disease.
“Cells in the lung can gobble up the silica, but it’s so toxic, it kills these cells,” Harkema said. “When they die, signals are sent out to the immune system that something is wrong. The body then produces such a strong response that it also starts to target healthy cells.”
According to Harkema, the DHA could be changing the way these cells, also known as macrophages, react to the silica in the lungs and somehow alter the immune system’s response.
“Our next step is to figure out exactly what’s happening,” he said.
One theory is the DHA helps cells send an anti-inflammatory signal to the body so it doesn’t overcompensate and trigger an autoimmune response. Another thought is somehow the DHA allows the cells to swallow up and remove the toxic silica from the lung without dying, preventing any inflammatory signals from being sent.
“What we do know is this study is a clear indication that eating DHA can prevent this one type of environmental triggering of lupus,” Pestka said. “It can suppress many of the disease’s signaling pathways, which current drugs on the market now try to target and treat.”
Consumption of a bioactive compound from Neem plant could significantly suppress development of prostate cancer
September 29, 2016
Oral administration of nimbolide, over 12 weeks shows reduction of prostate tumor size by up to 70 per cent and decrease in tumor metastasis by up to 50 per cent
A team of international researchers led by Associate Professor Gautam Sethi from the Department of Pharmacology at the Yong Loo Lin School of Medicine at the National University of Singapore (NUS) has found that nimbolide, a bioactive terpenoid compound derived from Azadirachta indica or more commonly known as the neem plant, could reduce the size of prostate tumor by up to 70 per cent and suppress its spread or metastasis by half.
Prostate cancer is one of the most commonly diagnosed cancers worldwide. However, currently available therapies for metastatic prostate cancer are only marginally effective. Hence, there is a need for more novel treatment alternatives and options.
“Although the diverse anti-cancer effects of nimbolide have been reported in different cancer types, its potential effects on prostate cancer initiation and progression have not been demonstrated in scientific studies. In this research, we have demonstrated that nimbolide can inhibit tumor cell viability — a cellular process that directly affects the ability of a cell to proliferate, grow, divide, or repair damaged cell components — and induce programmed cell death in prostate cancer cells,” said Assoc Prof Sethi.
Nimbolide: promising effects on prostate cancer
Cell invasion and migration are key steps during tumor metastasis. The NUS-led study revealed that nimbolide can significantly suppress cell invasion and migration of prostate cancer cells, suggesting its ability to reduce tumor metastasis.
The researchers observed that upon the 12 weeks of administering nimbolide, the size of prostate cancer tumor was reduced by as much as 70 per cent and its metastasis decreased by about 50 per cent, without exhibiting any significant adverse effects.
“This is possible because a direct target of nimbolide in prostate cancer is glutathione reductase, an enzyme which is responsible for maintaining the antioxidant system that regulates the STAT3 gene in the body. The activation of the STAT3 gene has been reported to contribute to prostate tumor growth and metastasis,” explained Assoc Prof Sethi. “We have found that nimbolide can substantially inhibit STAT3 activation and thereby abrogating the growth and metastasis of prostate tumor,” he added.
The findings of the study were published in the April 2016 issue of the scientific journal Antioxidants & Redox Signaling. This work was carried out in collaboration with Professor Goh Boon Cher of Cancer Science Institute of Singapore at NUS, Professor Hui Kam Man of National Cancer Centre Singapore and Professor Ahn Kwang Seok of Kyung Hee University.
Neem — The medicinal plant
The neem plant belongs to the mahogany tree family that is originally native to India and the Indian sub-continent. It has been part of traditional Asian medicine for centuries and is typically used in Indian Ayurvedic medicine. Today, neem leaves and bark have been incorporated into many personal care products such as soaps, toothpaste, skincare and even dietary supplements.
The team is looking to embark on a genome-wide screening or to perform a large-scale study of proteins to analyse the side-effects and determine other potential molecular targets of nimbolide. They are also keen to investigate the efficacy of combinatory regimen of nimbolide and approved drugs such as docetaxel and enzalutamide for future prostate cancer therapy.
Component of red wine, grapes can help to reduce inflammation, study finds
September 28, 2016
A component of red wine and grapes can help control inflammation induced by a bacterial pathogen that is linked to upper respiratory tract inflammatory diseases such as asthma, chronic obstructive pulmonary diseases (COPD) and middle ear infection (otitis media), according to a study by researchers at Georgia State University.
The findings, published in the online journal Scientific Reports, identify a novel mechanism that resveratrol, a compound found naturally in some plant foods such as grapes, uses to alleviate inflammation in airway disease. The results suggest this compound could offer health benefits and be used to develop new, effective anti-inflammatory therapeutic agents.
“We showed that an important component in red wine and also grapes called resveratrol can suppress inflammation,” said Dr. Jian-Dong Li, a senior author of the study, director of the Institute for Biomedical Sciences at Georgia State and a Georgia Research Alliance Eminent Scholar. “It has been shown that resveratrol can suppress inflammation, but how it regulates inflammation still remains largely unknown. We found that resveratrol suppresses a major bacterial pathogen causing otitis media and COPD by upregulating or increasing the production of a negative regulator called MyD88 short.”
Resveratrol belongs to a group of compounds called polyphenols that are thought to act like antioxidants and protect the body against damage. It has long been considered a therapeutic agent for various diseases, including inflammatory diseases. In the study, resveratrol was effective against inflammation caused by nontypeable Haemophilus influenzae (NTHi), a major respiratory pathogen.
An appropriate amount of inflammation in the body is beneficial for defense against bacterial infection, but uncontrolled inflammation leads to inflammatory diseases. Upper respiratory tract inflammatory diseases such as asthma and COPD affect more than half a billion people worldwide and are characterized by chronic inflammation that is aggravated by respiratory pathogens such as NTHi. Asthma results in 250,000 deaths annually and is the leading cause of hospitalizations in children younger than 15 in the United States. COPD is the third leading cause of death in the U.S., and the World Health Organization predicts it will be the fifth most significant contributor to worldwide disease by 2020. Otitis media is the most common bacterial infection and also the leading cause of conductive hearing loss in children.
Antibiotics are routinely used to treat NTHi infections, but the increasing numbers of antibiotic-resistant bacterial strains and the limited success of currently available pharmaceuticals used to manage the symptoms of these diseases present an urgent need for the development of non-antibiotic therapeutics.
This study found for the first time that resveratrol decreases NTHi-induced expression of pro-inflammatory mediators in airway epithelial cells and in the lungs of mice by enhancing MyD88 short, a negative regulator of inflammatory signaling pathways. MyD88 short is considered a “brake pedal protein” because it can tightly control inflammation induced by this respiratory pathogen. It could be a critical target with significant therapeutic potential for suppressing inflammation associated with chronic airway disease.
The researchers also found that resveratrol has anti-inflammatory effects after NTHi infection, which demonstrates its therapeutic potential.
“The findings help us to shed light on developing new therapeutic strategies by targeting or pharmacologically upregulating MyD88 short production,” Li said. “We could use resveratrol to suppress inflammation or develop resveratrol derivatives that could be pharmacological agents to suppress inflammation using the same strategy.”
Public Release: 3-Oct-2016
For women, caffeine could be ally in warding off dementia
Oxford University Press USA
Among a group of older women, self-reported caffeine consumption of more than 261 mg per day was associated with a 36 percent reduction in the risk of incident dementia over 10 years of follow-up. This level is equivalent to two to three 8-oz cups of coffee per day, five to six 8-oz cups of black tea, or seven to eight 12-ounce cans of cola.
“The mounting evidence of caffeine consumption as a potentially protective factor against cognitive impairment is exciting given that caffeine is also an easily modifiable dietary factor with very few contraindications,” said Ira Driscoll, PhD, the study’s lead author and a professor of psychology at the University of Wisconsin-Milwaukee. “What is unique about this study is that we had an unprecedented opportunity to examine the relationships between caffeine intake and dementia incidence in a large and well-defined, prospectively-studied cohort of women.”
The findings come from participants in the Women’s Health Initiative Memory Study, which is funded by the National Heart, Lung, and Blood Institute. Driscoll and her research colleagues used data from 6,467 community-dwelling, postmenopausal women aged 65 and older who reported some level of caffeine consumption. Intake was estimated from questions about coffee, tea, and cola beverage intake, including frequency and serving size.
In 10 years or less of follow-up with annual assessments of cognitive function, 388 of these women received a diagnosis of probable dementia or some form of global cognitive impairment. Those who consumed above the median amount of caffeine for this group (with an average intake of 261 mg per day) were diagnosed at a lower rate than those who fell below the median (with an average intake of 64 mg per day). The researchers adjusted for risk factors such as hormone therapy, age, race, education, body mass index, sleep quality, depression, hypertension, prior cardiovascular disease, diabetes, smoking, and alcohol consumption.
Public Release: 3-Oct-2016
Mix and match microbes to make probiotics last
IMAGE: This visual abstract depicts the findings of Maldonado-Gómez et al., who show that an orally administered bacterial strain persists long term in a subset of individuals. Engraftment depended on individualized… view more
Credit: Maldonado-Gómez et al./Cell Host & Microbe 2016
Scientists have tried to alter the human gut microbiota to improve health by introducing beneficial probiotic bacteria. Yet commercially available probiotics do not establish themselves in the gut. A study published September 29 in Cell Host & Microbe suggests that it is possible to alter the microbial ecosystem in the human gut for at least 6 months by introducing a single, ecologically appropriate bacterial strain.
The study suggests that matching the right bacterial strain to the gut environment is crucial for making a real change. “If we appreciate the gut microbiota as a complex ecosystem whose composition is governed by strict ecological processes, we can potentially very specifically modulate its composition by introducing a specific strain into it,” says senior author Jens Walter, Associate Professor and Chair for Nutrition, Microbes and Gastrointestinal Health at the University of Alberta, Canada. “This opens the possibility of reintroducing a missing bacterium with a health outcome in mind.”
An international research team tested the persistence of a bacterial strain called Bifidobacterium longum AH1206 in the human gut. This bacterium is on the human gut hit list. It is one of the top 50 most common among the hundreds of species of bacteria typically found in the human gut. “It is a core member of the human microbiome,” Walter says. Bifidobacterium longum is also one of the first dominant bacterial species to establish in the infant gut, especially when infants are breast-fed, which emphasizes the importance and safe intrinsic nature of the strain.
This differentiates it from the probiotics found in grocery and health stores. The bacteria in these products were selected not for their suitability to live in the human gut, but rather for their ease of production in an industrial setting, according to Walter. Microbes that grow in the human gut are much harder to grow in culture at the scales needed for mass production.
Walter likens attempts to grow these industrial strains of bacteria in the human gut to trying to grow strawberries in a tropical rainforest. “They don’t take over because what’s already there is a lot better adapted, and therefore fitter. Incoming organisms are simply outcompeted,” he says.
“Instead of planting strawberries, we planted a real jungle plant in the rainforest, an organism that is a lot more adapted to that ecosystem,” says Walter.
In a double-blind, placebo-controlled trial of 22 people, half of the participants took daily doses of Bifidobacterium longum AH1206 probiotics while the other half took a placebo. After 2 weeks, they switched. Walter and colleagues tracked changes in the gut microbiome over time, looking at the bacterial and genetic composition. 30% of those who took a probiotic with this bacterial strain experienced lasting colonization of the strain and were deemed to be “persisters”; their guts were still colonized by the Bifidobacterium longum AH1206 strain 6 months after they had stopped taking the probiotic.
The data showed that the guts of persisters differed from those who did not have long-lasting affects from the probiotic. Prior to treatment, the persisters had lower levels of the species Bifidobacterium longum or genes found in similar strains. That is, the persisters had an opening in the ecosystem that no existing bacterial strains were vying for. “Competition in ecosystems is especially harsh amongst closely related species because they have the same resource requirements,” says Walter. “It goes back to the theories proposed by Darwin.”
The findings suggest that in people who have lost or never acquired a certain valuable strain of gut bacteria due to use of an antibiotic or some other event, it could be possible to repopulate the gut ecosystem. In addition, “since we can differentiate persisters from non-persisters, we could potentially personalize probiotic treatments,” Walter says.
Public Release: 3-Oct-2016
Certain alternative therapies may help patients with bowel disorders
A new review looks at the evidence behind the effectiveness of complementary or alternative therapies–including probiotics, prebiotics, synbiotics, fiber, and herbal medicinal products–for the treatment of bowel disorders such as irritable bowel syndrome (IBS), functional constipation, and ulcerative colitis.
The review’s authors note that most available studies are biased by several drawbacks; however, probiotics, synbiotics, psyllium, and some herbal medicinal products (primarily peppermint oil) seem to be effective in ameliorating IBS symptoms. Synbiotics and fiber seem to be beneficial in patients with functional constipation, and the non-pathogenic strain Nissle 1917 of Escherichia coli may be effective in maintaining remission in patients with ulcerative colitis.
“Patients with common functional bowel disorders such as chronic idiopathic constipation and irritable bowel syndrome who cannot find benefit or have adverse effects with the use of traditional drug therapies, or do not want to use them, should be told that alternative medicines are available that may be effective,” said Dr. Diego Curro, lead author of the British Journal of Pharmacology study. “Also, patients with mild clinical forms of ulcerative colitis should be informed that they might use, with caution, an alternative probiotic treatment to prevent relapse.”
Public Release: 3-Oct-2016
New research delimits the possible causes of celiac disease
The amount of gluten could be a more important clue than breast-feeding or the timing of the introduction of gluten for continued research into the causes of celiac disease (gluten intolerance). This is one of the findings from several extensive studies of children with an increased genetic risk of celiac disease conducted by researchers at Lund University in Sweden.
Sweden is a high-risk country for the development of celiac disease in early life. Currently, the only known and effective treatment for the disease is for patients to follow a gluten-free diet for the rest of their lives. It is still unclear why gluten intolerance occurs, but researchers all over the world have long focused their efforts on factors such as breast-feeding, dietary habits, the timing of the introduction of gluten and geographical origin. A new doctoral thesis from Lund University includes studies covering all these aspects.
“Our findings indicate that the amount of gluten triggers the disease. We have also observed that the dietary habits among the children we studied vary from one country to another, and that there are reasons to analyse the significance of this variation more closely. More in-depth studies could perhaps contribute to explaining why Swedish children develop celiac disease earlier than children in other countries”, says Carin Andrén Aronsson, a dietician and doctoral student at Lund University, continuing:
“The timing of the introduction of gluten, on the other hand, does not seem to be of great significance. We conducted a very extensive study which confirms similar conclusions from previous, smaller studies.”
All the research in the doctoral thesis is based on small children born with an increased genetic risk of developing celiac disease. Some of the most important conclusions are:
Swedish children whose reported daily intake of gluten was high (more than five grams) up to the age of two years had twice the risk of developing coeliac disease compared to children who consumed a smaller amount. The results from the same sub-study also show that children with celiac disease ate more gluten. The risk of developing the autoimmunity which gives rise to celiac disease was highest in Sweden compared to the other countries in the study (Finland, Germany and USA). The result held after adjustment for some of the most important causes of celiac disease (carrying the risk gene, previous diagnosis in the family and gender). Breast-feeding (starting point/duration), the timing of the first introduction of solid foods and the type of diet varied among the countries studied. European children were first introduced to potatoes and root vegetables while American children were first given rice and root vegetables. There was no apparent connection between the duration of the period of breast-feeding and the risk of developing celiac disease. The timing alone of the introduction of gluten in the diet is not an independent risk factor for subsequent development of gluten intolerance.
The issues surrounding gluten intolerance will continue to occupy Carin Andrén Aronsson after the public defence of her thesis.
“We will investigate the significance of the amount of gluten in a large new study. Is the gluten intake of Swedish children different from that of children in other countries? We will expand the study with children from the other participant countries and increase the follow-up period in comparison with our previous studies, from two to five years. We will also investigate whether the addition of probiotics (beneficial bacteria) to the diet has any effect on the risk of developing celiac disease”, explains Carin Andrén Aronsson, before adding:
“With more knowledge about the significance of diet, I hope it will become possible to personalise the diet instead of having general dietary guidelines as we have today.”
The basis for the studies in the doctoral thesis is a cohort of up to 8 700 children in four countries: Sweden, Finland, Germany and the USA. The children are part of an international research project, TEDDY (The Environmental Determinants of Diabetes in the Young), whose aim is to determine the reasons why children get type 1 diabetes and/or coeliac disease. The principal funding body behind the study is the National Institutes of Health,(NIH) in the US.
“It is a very major and resource-intensive endeavour to determine the causes of celiac disease. Thanks to the children in the TEDDY study, we can conduct several studies of significance to research”, explains Carin Andrén Aronsson.
Public Release: 5-Oct-2016
New animal research explores red raspberries in supporting healthy weight and motor function
The latest issue of the Journal of Berry Research includes two new animal studies that investigate the effects of raspberry consumption in helping to support healthy weight and motor function (strength, balance and coordination). Future studies are needed to support the results found in these studies.
One-cup of frozen red raspberries has only 80 calories, is an excellent source of vitamin C, and provides nine grams of fiber (more fiber than any other berry). Like most berries, raspberries are a low-glycemic index food. Raspberries contain phytochemicals, such as ellagic acid, quercetin, gallic acid, cyanidins, pelargonidins, catechins, kaempferol and salicylic acid.
Animal and cellular studies examining how phytochemicals may work at the molecular level suggest that certain phytochemicals may help slow age-related declines. Age is the number one risk factor for many chronic diseases. Likewise, obesity is a major risk factor for chronic disease. These latest animal studies examine two important areas of health where raspberry products may play a role in weight management and also support motor function.
An animal study conducted by researchers at Oregon State University found that when added to a high-fat, high-sucrose diet, raspberry products and raspberry phytochemicals were found to significantly decrease weight gain associated with a high-fat, high calorie diet. Raspberry juice and raspberry puree concentrates were provided at 10% of total energy (the equivalent of 200 calories in a 2,000 calorie diet), and a combination of ellagic acid and raspberry ketone were provided at 0.2% weight/weight.
In the study, 76 male mice were divided into the following diets: a low-fat control group (10% calories from fat), a high-fat control group (45% calories from fat) and seven “high-fat treatment” groups that included a high-fat diet plus either raspberry juice concentrate, raspberry puree concentrate, raspberry fruit powder, raspberry seed extract, raspberry ketone and a combination of equal parts of ellagic acid and raspberry ketone.
“The addition of raspberry juice concentrate, raspberry puree concentrate and the combination of ellagic acid plus raspberry ketones to the high fat diet significantly reduced weight gain observed in the high-fat fed mice,” said Dr. Neil Shay, Principal Investigator. “In the case of the high-fat and raspberry juice concentrate diet, weight gain was reduced to a level that was statistically equivalent to the weight gain of the low-fat fed mice, despite the fact that all high-fat fed groups consumed the same amount of calories and more energy than the low-fat control group throughout the study.”
The researchers concluded that the intake of a reasonable level of some raspberry food products may influence some of the metabolic consequences of consuming a high-fat, high-calorie diet in the development of obesity in male mice.
“We hope that the findings from this study can help guide the design of future clinical trials,” said Dr. Shay.
Researchers from the Human Nutrition Research Center on Aging at Tufts University evaluated the effectiveness of a red raspberry-supplemented diet on age-sensitive measures of learning, memory and motor performance in older rats.
In this 10-week study, red raspberry supplementation was found to significantly improve motor skills. Specifically, compared to rats fed a standard well-balanced diet, rats fed a diet supplemented with freeze-dried raspberry extract performed better on tests which measured psychomotor coordination and balance, as well as tests that measure muscle tone, strength, and stamina.
“These results may have important implications for healthy aging,” said lead researcher Barbara Shukitt-Hale, PhD. “While further research in humans is necessary, animal model studies are helpful in identifying deficits associated with normal aging.”
Public Release: 5-Oct-2016
Vitamin E may prevent pneumonia in nonsmoking elderly men
University of Helsinki
Dr. Harri Hemila, University of Helsinki, Finland, studied whether vitamin E supplementation might influence the risk of community-acquired pneumonia. He analyzed the data of the randomized trial (Alpha-Tocopherol Beta-Carotene Cancer Prevention [ATBC] Study) which was conducted in Finland between 1985-1993 and included male smokers aged from 50 to 69 years. The age when the participant had started to smoke significantly modified the effect of vitamin E on pneumonia.
Vitamin E decreased the risk of pneumonia by 35% in 7,469 participants who had started smoking at a later age, at 21 years or older, whereas the vitamin had no apparent effect on pneumonia for those who had started to smoke at a younger age.
Among the 7,469 participants who started to smoke at a later age, vitamin E supplementation reduced the incidence of pneumonia by 69% in a subgroup of 2,216 light smokers who exercised in their leisure time. In this subgroup, vitamin E prevented pneumonia in 12.9% of the participants by the time they reached the age of 74 years, which corresponds to one in eight getting a benefit from the vitamin. The vitamin did not have a significant effect on participants who smoked heavily or had not been taking exercise.
One-third of the 7,469 participants quit smoking for a period and 27 of them got pneumonia. These 27 cases of pneumonia can be used to estimate the effect of vitamin E on currently nonsmoking males. The incidence of pneumonia was 72% lower in the vitamin E participants who had quit smoking, and this benefit from vitamin E was also seen among those who smoked heavily or did not exercise.
Although the evidence of benefit from vitamin E against community-acquired pneumonia in elderly males is strong in this analysis, the overall findings about vitamin E have been complex. Furthermore, the participants of the ATBC Study had mostly been born in the 1920s and 1930s, and lived through the World War II years. “Thus, even though the 72% decrease in pneumonia risk with vitamin E in ATBC participants who quit smoking may be a real effect, it should not be generalized to current elderly males in Western countries. Further research on vitamin E in nonsmoking elderly males is warranted”, Dr. Hemilä states.
Public Release: 7-Oct-2016
Antibacterial and antiinflammatory properties of bovine colostrum
This research article by Dr. Ramesh Yadav et al. is published in Recent Patents on Inflammation & Allergy Drug Discovery, Volume 10, Issue 1, 2016
Bentham Science Publishers
Colostrum is a thick, sticky, yellowish mammary secretion that all mammals provide to their newborns during the first 24-48 hours after delivery. Human newborns receive colostrum from their mothers during the first few hours after birth, and this ‘Elixir of Life’ not only provides naturally produced nutrients and antibodies in a highly concentrated low volume form but also creates the foundation of lifelong immunity. Bovine colostrum (BC) is rich in immunoglobulins and lactoferrin, growth and antimicrobial factors, which promote tissue growth and maturation of digestive tract and immune function in neonatal animals and humans. It has been reported that constituents from BC are 100-fold to 1,000-fold more potent than human colostrum. This means that even human infants can rely on cow or buffalo colostrum to gain health benefits. The immunoglobulins present in BC show antimicrobial activity by forming a chelated complex with bacterial and viral antigens. BC also has high antiinflaamtory activity and antioxidant properties. The oxidative stress and microbial infections lead to an inflammatory response and generate free radicals such as reactive oxygen species (ROS) and reactive nitrogen intermediates (RNI), which in the absence of antioxidants can cause DNA damage. High levels of antioxidants and growth factors present in colostrum have proven beneficial in wound healing and to reduce oxidative stress in athletes due to heavy exercise. The goal of the present study was to determine the antimicrobial and antiinflammatory activities of BC using standardized tests.
At 100 μg/ml, BC depicted strong antimicrobial activity against both Gram -ve and +ve strains of bacteria (E. coli, S. aureus, P. vulgaris, E. aerogenes and Salmonella typhi). The carrageenan-induced rat paw edema was moderately reduced in BC treated animals. It was found that the combination of BC with diclofenac, produce greater antiinflammatory effects than that of BC alone, which suggests that combination treatment may reduce or minimize the side effects of this antiinflammatory synthetic drug. Our findings suggest that BC could be used as an alternative remedy for treating the microbial infections and inflammation-related disorders.
Public Release: 7-Oct-2016
Fewer indications of ADHD in children whose mothers took vitamin D during pregnancy
Children of mothers who took vitamin D during pregnancy with resultant high levels of the vitamin in the umbilical blood have fewer symptoms of ADHD at the age of 2.5 years
University of Southern Denmark Faculty of Health Sciences
Children of mothers who took vitamin D during pregnancy with resultant high levels of the vitamin in the umbilical blood have fewer symptoms of ADHD at the age of 2½ years.
These were the findings in a new study from the Odense Child Cohort just published in The Australia & New Zealand Journal of Psychiatry.
– “And for every 10 nmol/L increase in the vitamin D concentration in umbilical blood, the risk of a being among the 10% highest score on the ADHD symptom scale fell by 11%,” explains one of the study’s initiators, Professor Niels Bilenberg.
1,233 children from Odense Municipality were monitored in the study. Vitamin D was measured in umbilical blood, and mothers completed the Child Behavior Checklist (CBCL) when their child was 2½ years old. The CBCL questionnaire can be used to identify early symptoms of ADHD, even though an ADHD diagnosis cannot be made at that age.
– “And the trend was clear: those mothers who had taken vitamin D, and had a vitamin D level (25OHD) in their umbilical blood over 25 nmol/L, had children with lower ADHD scores,” continues Bilenberg. “This was after we had corrected for other factors that could explain the link, such as the mother’s age, smoking, alcohol, obesity, education, number of children, psychiatric disease in the parents, child’s sex, age and seasonal variation.”
The link between vitamin D and early ADHD symptoms has not been described before, and has therefore attracted attention.
– “We were very surprised that the link was so clear,” say two of the study’s other authors, medical students Jens Bull Aaby and Mats Mossin, “as there was no previous awareness that this link could be identified at such an early age. It’s impossible to say with which children will develop ADHD later on, but it will be interesting to further follow up those children who were at the highest end versus the normal range of the ADHD scale.”
The study offers no explanation as to how vitamin D can protect against ADHD, but other studies have shown that vitamin D plays an important role in the early development of the brain.
“We had an idea about it,” says Aaby, “but we cannot say with certainty that vitamin D protects against early symptoms of ADHD. Our study only indicates that there is a link that we cannot explain in any other way.”
Facts: Odense Børnekohorte is a joint study between Odense University Hospital, the Psychiatric Service of the Region of Southern Denmark, Odense Municipality, and the University of Southern Denmark. In the study, 2,500 mothers and their children are being monitored from early pregnancy to the child’s 18th birthday. The children are now 3-5 years old and a number of follow-up studies are planned.
Public Release: 11-Oct-2016
DHA supplementation improves cognition in older adults with mild cognitive impairment
Chinese study shows improved IQ with omega-3 supplementation
Results from a recent study published in the Journal of Alzheimer’s Disease support the cognitive benefits of DHA, which have been consistently demonstrated with doses of 900 mg/day or greater. The study, which took place in Tianjin, China, was a randomized, double-blind, placebo-controlled trial in 240 (219 completed) Chinese individuals aged 65 and older with mild cognitive impairment. The participants received either 2g/day of DHA or a corn oil placebo for 12 months and specific measures of cognitive function were measured at baseline, six months and 12 months.
The study results showed that there was a significant difference in the Full-Scale Intelligence Quotient (IQ) in the DHA group versus placebo, with IQ in the DHA group measuring 10% higher than the placebo group. Additionally, there were statistically significant increases in two IQ sub-tests (Information and Digit Span). The Information and Digit Span Subdomains are considered indicators of long-term and short-term memory, respectively. The findings suggest that DHA supplementation of 2g/day for 12 months in MCI subjects can significantly improve cognitive function.
While additional larger longer-term studies are needed to confirm the results, this paper adds to the body of science supporting DHA omega-3s and their role in supporting cognitive function.
Public Release: 11-Oct-2016
Running triggers production of a molecule that repairs the brain in animal models
Ottawa Hospital Research Institute
Credit: The Ottawa Hospital
Researchers at The Ottawa Hospital and the University of Ottawa have discovered that a molecule triggered by running can help repair certain kinds of brain damage in animal models. They found that this molecule, called VGF nerve growth factor, helps to heal the protective coating that surrounds and insulates nerve fibres. Their study, published in Cell Reports, could pave the way for new treatments for multiple sclerosis and other neurodegenerative disorders that involve damaged nerve insulation.
“We are excited by this discovery and now plan to uncover the molecular pathway that is responsible for the observed benefits of VGF,” said Dr. Picketts, senior author of the paper and a senior scientist at The Ottawa Hospital and professor at the University of Ottawa. “What is clear is that VGF is important to kick-start healing in damaged areas of the brain.”
The team made this discovery while studying mice genetically modified to have a small cerebellum, the part of the brain that controls balance and movement. These mice had trouble walking and lived only 25 to 40 days.
However, if these mice were given the opportunity to run freely on a wheel, they lived over 12 months, a more typical mouse lifespan. The running mice also gained more weight and acquired a better sense of balance compared to their sedentary siblings. However, they needed to keep exercising to maintain these benefits. If the running wheel was removed, their symptoms came back and they did not live as long.
Looking at their brains, the researchers found that the running mice gained significantly more insulation in their cerebellum compared to their sedentary siblings.
To find out why running was causing this insulation, the team looked for differences in gene expression between the running and sedentary mice and identified VGF as a prime candidate. VGF is one of the hundreds of molecules that muscles and the brain release into the body during exercise. It also has an anti-depressant effect that helps make exercise feel good.
When the research team used a non-replicating virus to introduce the VGF protein into the bloodstream of a sedentary mutant mouse, the effects were similar to having the mouse run – more insulation in the damaged area of the cerebellum, and fewer disease symptoms.
“We saw that the existing neurons became better insulated and more stable,” said Dr. Matías Alvarez-Saavedra, the lead author on the paper. “This means that the unhealthy neurons worked better and the previously damaged circuits in the brain became stronger and more functional.”
Dr. Alvarez-Saavedra obtained his PhD in Dr. Picketts’ research group, and is currently a postdoctoral fellow at the New York University School of Medicine and the Howard Hughes Medical Institute.
“We need to do broader research to see whether this molecule can also be helpful in treating multiple sclerosis and other neurodegenerative diseases,” said Dr. Picketts.
Public Release: 14-Oct-2016
Researchers find 2 distinct genetic subtypes in Crohn’s disease patients
The UNC School of Medicine discovery could lead to more effective, personalized treatments for the debilitating gastrointestinal condition
University of North Carolina Health Care
CHAPEL HILL, NC – Crohn’s disease, a common inflammatory disorder of the intestinal tract, can have devastating consequences for a patient’s quality of life and is notoriously hard to treat successfully, in part because its course and severity vary so much from one case to the next. Now, UNC School of Medicine scientists have made a discovery that could explain why Crohn’s is so variable: the disease appears to have at least two distinct subtypes, each with its own pattern of gene expression and mix of clinical features.
The discovery, published in the journal Gut, could lead to more effective strategies for treating Crohn’s, which affects close to one million people in the United States. Although people with the disease typically are treated with powerful immune-suppressing drugs, roughly 70 percent eventually require surgery to remove portions of the intestinal tract that have developed blockages or other problems caused by severe inflammation. Even after surgery, the disease often recurs and is therefore not curative.
A deeper understanding of the biology of Crohn’s disease should enable doctors to target it more effectively.
“The one-treatment-fits-all approach doesn’t seem to be working for Crohn’s patients,” said Shehzad Z. Sheikh, MD, PhD, assistant professor in UNC’s departments of medicine and genetics and co-senior author of the study. “It’s plausible that this is because only a subset of patients has the type of disease that responds to standard therapy, whereas, for the rest of the patients, we’re really not hitting the right targets.”
For the new study, published online today, Sheikh teamed up with Terry Furey, PhD, associate professor in UNC’s departments of genetics and biology and study co-senior author, to map the levels of gene expression in non-inflamed, healthy-looking colon tissue samples taken from 21 Crohn’s patients. When they began looking at the gene expression patterns in these patients, two clear groupings dominated.
“Although we saw a difference between the Crohn’s samples and samples from people without Crohn’s, we saw an even greater difference at the molecular level between these two subsets of the Crohn’s samples,” Furey said.
How the two disease subtypes differed was unexpected.
“It was surprising,” said Jeremy Simon, PhD, a research assistant professor in UNC’s department of genetics and co-first author of the study with former graduate student Matthew Weiser, PhD. “Many of the genes that were different between the two Crohn’s subtypes are markers that distinguish the colon from the ileum, despite these being colon biopsies.”
The team described how in one disease subtype, the pattern of gene expression mostly resembled that of normal colon tissue. In the other, gene expression shifted towards the pattern normally seen in the ileum – the part of the small intestine that empties (via a structure called the cecum) into the colon, and is often the first area affected in Crohn’s.
The team looked not only at specific gene expression products in the sampled tissue, but also at indicators of the “epigenetic” state of the tissue DNA – the pattern of molecular switches on chromosomes that effectively permit or repress nearby gene activity. Here, too, there was a distinction between the two Crohn’s subtypes, suggesting that their differences in gene expression stemmed from differences in the basic programming of the affected cells.
The colon samples were from adults with Crohn’s that had all undergone surgery, leaving open the possibility that their treatment and disease histories may have played a role in the observed gene expression patterns. So the team then looked at a recently published gene expression dataset from 201 children with newly diagnosed, never-treated Crohn’s, and although the tissue samples this time were from the ileum, the researchers again observed the same two colon-like and ileum-like disease classes.
“This suggests that these molecular programs or baseline genomic signatures of Crohn’s subtypes exist independently of patients’ ages or treatment histories,” said Sheikh.
Importantly, these two signatures were linked to different patterns of clinical illness. The “colon-like” cases, for example, were more likely to have gut inflammation visible during colonoscopy, rectal disease (notoriously difficult to manage from a clinical standpoint), and severe enough colon inflammation to require surgical removal of the colon (colectomy).
Sheikh, Furey, and their colleagues now hope to translate these results into a diagnostic test on tissue samples from routine colonoscopies, or perhaps even on blood samples. Such tests could help doctors classify Crohn’s patients and choose the best therapies.
As an initial follow-up, they plan a broadened study to confirm their findings in a much larger set of patient samples, a project for which they recently received funding from the National Institutes of Health. They also hope to undertake a long-term study, in which they would test patients for their Crohn’s subtype when they are initially diagnosed with the disease, and then follow them for several years to see whether the assigned subtype predicts the disease course.
“We hope one day to be able to test Crohn’s patients for the subtype of the disease they have, and thus determine which treatment should work best,” Sheikh said. “The idea is to find the best therapeutic course for each patient as quickly and efficiently as possible.”