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In vitro study finds digested formula, but not breast milk, is toxic to cells

In vitro study finds digested formula, but not breast milk, is toxic to cells Findings may help explain development of fatal condition in premature infants IMAGE:This microscopic image of cells shows the effects of breast milk vs. infant formula digestion. Cells are alive and healthy after the digestion of breast milk (top row) with only... Click here for more information. Free fatty acids created during the digestion of infant formula cause cellular death that may contribute to necrotizing enterocolitis, a severe intestinal condition that is often fatal and occurs most commonly in premature infants, according to a study by University of California, San Diego bioengineers. Their report, which was based on in vitro tests comparing the digestion of fresh human breast milk and nine different infant formulas, was published online in the journal Pediatric Research. Scientists have long known that premature infants fed formula are more likely to develop necrotizing enterocolitis than those fed breast milk. The condition is the leading cause of death from gastrointestinal diseases in premature infants, but the underlying mechanism has not been understood. Alexander Penn, a research scientist working in the Microcirculation Laboratory of bioengineering Professor Geert Schmid-Schönbein from the UC San Diego Jacobs School of Engineering, believes they have come closer to an answer. Penn and others had previously determined that the partially digested food in a mature, adult intestine is capable of killing cells, due to the presence of free fatty acids which have a "detergent" capacity that damages cell membranes. The intestines of healthy adults and older children have a mature mucosal barrier that may prevent damage due to free fatty acids. However, the intestine is leakier at birth, particularly for preterm infants, which could be why they are more susceptible to necrotizing enterocolitis. Therefore, the researchers wanted to know what happens to breast milk as compared to infant formula when they are exposed to digestive enzymes. They "digested," in vitro, infant formulas marketed for full term and preterm infants as well as fresh human breast milk using pancreatic enzymes or fluid from an intestine. They then tested the formula and milk for levels of free fatty acids. They also tested whether these fatty acids killed off three types of cells involved in necrotizing enterocolitis: epithelial cells that line the intestine, endothelial cells that line blood vessels, and neutrophils, a type of white blood cell that is a kind of "first responder" to inflammation caused by trauma in the body. IMAGE:This chart shows the high concentration of unbound (cytotoxic) free fatty acids (FFAs) (shown in white) created by the digestion of infant formula compared to the relatively small presence of... Click here for more information. Overwhelmingly, the digestion of formula led to cellular death, or cytotoxicity – in less than 5 minutes in some cases – while breast milk did not. For example, digestion of formula caused death in 47 percent to 99 percent of neutrophils while only 6 percent of them died as a result of milk digestion. The study found that breast milk appears to have a built-in mechanism to prevent cytotoxicity. The research team believes most food, like formula, releases high levels of free fatty acids during digestion, but that breast milk is digested in a slower, more controlled, process. Currently, many neonatal intensive care units are moving towards formula-free environments, but breastfeeding a premature infant can be challenging or physically impossible and supplies of donor breast milk are limited. To meet the demand if insufficient breast milk is available, less cytotoxic milk replacements will need to be designed in the future that pose less risk for cell damage and for necrotizing enterocolitis, the researchers concluded. This may be of benefit not only to premature infants, but also to full-term infants at higher risk for disorders that are associated with gastrointestinal problems and more leaky intestines, such as autism spectrum disorder. Dr. Sharon Taylor, a professor of pediatric medicine at UC San Diego School of Medicine and a pediatric gastroenterologist at Rady Children's Hospital, San Diego, said the study offers more support to an already ongoing push by hospitals, including neonatal intensive care units, to encourage breastfeeding even in more challenging circumstances in the NICU. For patients who are too premature or frail to nurse, Dr. Taylor said hospital staff should provide consultation and resources to help mothers pump breast milk that can be fed to the baby through a tube. The research was carried out in collaboration with Dr. Taylor, Karen Dobkins of the Department of Psychology, and Angelina Altshuler and James Small of the Department of Bioengineering at UC San Diego and was funded by the National Institutes of Health (NS071580 and GM85072). The researchers conclude that breast milk has a significant ability to reduce cytotoxicity that formula does not have. One next step is to determine whether these results are replicated in animal studies and whether intervention can prevent free fatty acids from causing intestinal damage or death from necrotizing enterocolitis. ###

New evidence for epigenetic effects of diet in healthy ageing

6 December, 2012

New research in human volunteers has shown that molecular changes to our genes, known as epigenetic marks, are driven mainly by ageing but are also affected by what we eat.

The study showed that whilst age had the biggest effects on these molecular changes, selenium and vitamin D status reduced the accumulation of epigenetic changes, and high blood folate and obesity increased them. These findings support the idea that healthy ageing is affected by what we eat.

Dr Nigel Belshaw

Researchers from the Institute of Food Research led by Dr Nigel Belshaw, working with Prof John Mathers and colleagues from Newcastle University, examined the cells lining the gut wall from volunteers attending colonoscopy clinic. The Institute of Food Research is strategically funded the Biotechnology and Biological Sciences Research Council and this study was also funded by the Food Standards Agency.

The study volunteers were free from cancer or inflammatory bowel disease and consumed their usual diet without any supplements. The researchers looked for specific epigenetic modifications of the volunteers’ genes that have been associated with the earliest signs of the onset of bowel cancer – an age-related disease. These epigenetic marks, known as DNA methylation, do not alter the genetic code but affect whether the genes are turned on or off. These methylation marks are transmitted when cells divide, and some have been associated with the development of cancer.

The investigators studied the relationship between the occurrence of these epigenetic marks at genes known to be affected in cancer, and factors including the volunteers’ age, sex, body size and the levels of some nutrients in the volunteers’ blood. The biggest influence on gene methylation was age. This fits with the fact that the biggest risk factor for bowel cancer is age, with risk increasing exponentially over 50 years old.

The findings, published in the journal Aging Cell, showed that men tended to have a higher frequency of these epigenetic changes than women, which is consistent with men being at a greater risk of bowel cancer. Volunteers with higher vitamin D status tended to show lower levels of methylation, and a similar effect was observed for selenium status. Again, this is consistent with the known links between higher vitamin D and selenium and reduced bowel cancer risk.

The B vitamin folate is essential for health, but in this study, high folate status was associated with increased levels of epigenetic changes linked with bowel cancer.   These findings are consistent with some epidemiological studies suggesting that excessive folate intakes may increase risk in some people.  The results of this study showing an association between folate status and epigenetic changes linked to cancer, together with those from another recent study by Nigel Belshaw’s group showing that, in cells grown in the laboratory, they could be induced by exposure to high levels of folic acid, emphasise the need for further research on optimal folate status in humans.  The researchers intend to investigate the mechanism for the effect of folate on DNA methylation in a follow-up study.

Obesity is also a risk factor for bowel cancer. This study found relationships between body size (height, weight and waist circumference) and epigenetic changes. How excess body weight induces these epigenetic changes, and the consequences for gut health, are currently being investigated at IFR and in Newcastle University.

In summary, the results of this study support the hypothesis that ageing affects the epigenetic status of some genes and that these effects can be modulated by diet and body fatness.

Reference:

Nutritional factors and gender influence age-related DNA methylation in the human rectal mucosa, Aging Cell, doi: 10.1111/acel.12030

For more information on this, please see the article written by Nigel Belshaw and Ian Johnson on the Gut Health and Food Safety blog.

For more information on cancer and epigenetics, see:

Johnson IT, Belshaw NJ  (2008) Environment, diet and CpG island methylation: epigenetic signals in gastrointestinal neoplasia. Food Chem Toxicol. 2008 Apr;46(4):1346-59. Epub 2007 PMID:17976883

Baylin SB, Jones PA: (2011) A decade of exploring the cancer epigenome – biological and translational implications. Nat Rev Cancer 11, 726-34

Contacts:

IFR Press Office:

Andrew Chapple, 01603 251490, andrew.chapple@ifr.ac.uk

My microbes Our gut bacteria’s collection of genomes is unique, and remains stable over time

My microbes

• PR_05Dec12_My_microbes
• PR05Dec12_Mikroben_ganz_persönlich

In a nutshell :

• The gut metagenome is the collection of all the genomes of all the microbes in the
  human intestinal tract : it is specific to each human, like a second genetic
  signature
• At least in healthy humans, this personal metagenome is stable over time
• The gut metagenome is very large and complex: scientists developed innovative,
  state-of-the-art, computational tools to analyse it with a high resolution

We all have E.coli
bacteria in our gut but each of us carries a version that is genetically
slightly different. The same can be said of most gut microbes: our own gut
metagenome, that is the sum of all the genomes of all our gut microbes, appears
to be really specific to each of us, and to remain stable over time. For the
first time, researchers from the European Molecular Biology Laboratory (EMBL)
have studied this metagenome at such a high resolution that individual
mutations in the various strains could be analysed. Their findings, published
today in Nature, could have widespread consequences in medicine: gut
microbes are known to be essential for functions as vital as digesting food or
providing vitamins, but can also be involved in diseases if they carry certain
mutations.

The scientists analysed the gut metagenome
of 207 individuals from Europe and the USA, matching more than 7 billion
pieces of DNA (of 100 lettres each) to the genomes of our most abundant gut
microbial species. “This large scale analysis showed that, at least when
healthy, we carry a unique set of bacterial strains and their mutations in our
gut, over a long time,” explains Peer Bork who led the study at EMBL. “It is
like a second genetic signature, but one that probably does not come from our
parents but that we acquire from the environment in early childhood.”

When comparing the specific
mutations from the same individual over time, the researchers found that the
metagenome remains stable for at least one year, and probably much longer when
the individuals are healthy. Results also show that there is only little
geographic difference when comparing metagenomes of European with
North-American individuals. This indicates that gradual adaptation is possible.

For each individual,
approximately 6 billion DNA letters of their gut metagenome have been analysed,
many more than the 3.3 billion DNA letters of human DNA that we inherit from
each of our parents. These 6 billion DNA letters belong to hundreds of
microbes, each with thousands of different strains or variants: mapping each
DNA fragment of the metagenome to its right place, in the right bacterial
genome, is extremely complex. To achieve this breakthrough and carry the
analysis down to the single DNA letter, scientists had to develop various new
computational methods. In the current study more than 10 million mutations have
been detected in the 207 individuals.

All these detailed data is now
stored in public databases, such as dbSNP, freely available to the scientific
community. These findings could lead to the development of new approaches in
the identification of gut diseases, pathogens, or antibiotic resistance. On the
longer term, they may also open new avenues for personalised therapies.

Further information:

More
information on the research projects of the Bork group

Previous research on the gut microbiome by Peer Bork

My Microbes project - discover your gut type

Source Article

Genomic variation landscape of
the human gut microbiome

Siegfried Schloissnig,
Manimozhiyan Arumugam, Shinichi Sunagawa, Makedonka Mitreva, Julien Tap, Ana
Zhu, Alison Waller, Daniel R. Mende, Jens Roat Kultima, John Martin, Karthik
Kota, Shamil R. Sunyaev, George M. Weinstock and Peer Bork. Nature, Advanced online Publication: 5 December, 2012

Article Abstract

While large-scale efforts have
rapidly advanced the understanding and practical impact of human genomic
variation, the latter is largely unexplored in the human microbiome. We
therefore developed a framework for metagenomic variation analysis and applied
it to 252 fecal metagenomes of 207 individuals from Europe and North America. Using 7.4 billion reads aligned to 101
reference species, we detected 10.3 million single nucleotide polymorphisms
(SNPs), 107,991 short indels, and 1,051 structural variants. The average ratio
of non-synonymous to synonymous polymorphism rates of 0.11 was more variable
between gut microbial species than across human hosts. Subjects sampled at
varying time intervals exhibited individuality and temporal stability of SNP
variation patterns, despite considerable composition changes of their gut
microbiota. This implies that individual-specific strains are not easily
replaced and that an individual might have a unique metagenomic genotype, which
may be exploitable for personalized diet or drug intake.

Press Contact

Isabelle Kling,
Communications Officer

EMBL Heidelberg, Meyerhofstraße 1, 69117 Heidelberg, Germany

Tel:	+49 6221 387-8355
E-mail:	isabelle.kling@embl.de

Lena Raditsch, Head of Communications

EMBL Heidelberg, Meyerhofstraße 1, 69117 Heidelberg, Germany

Tel:	+49 6221 387-8125
E-mail:	lena.raditsch@embl.de

http://www.embl.de/aboutus/communication_outreach/media_relations/2012/121205_Heidelberg/

Modified Citrus Pectin Protects Against Vascular Hardening

Cardiovascular disease will kill nearly 2.5 million people in the United States this year, according to the Centers for Disease Control. Over time, inflammation, collagen deposition and scar tissue formation can cause blood vessels to stiffen, a process called vascular fibrosis. Though researchers have known that the hormone aldosterone (Aldo) plays a role in this process, the precise mechanisms have been poorly understood.

Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association

http://www.newswise.com/articles/view/596282/?sc=dwhn

Cardiovascular disease will kill nearly 2.5 million people in the United States this year, according to the Centers for Disease Control. Over time, inflammation, collagen deposition and scar tissue formation can cause blood vessels to stiffen, a process called vascular fibrosis. Though researchers have known that the hormone aldosterone (Aldo) plays a role in this process, the precise mechanisms have been poorly understood.

Now, an international study published in Arteriosclerosis, Thrombosis, and Vascular Biology: Journal of the American Heart Association is providing new insights into cardiovascular disease. Particularly significant, the study illuminates how Aldo and the protein galectin-3 jointly contribute to vascular remodeling and congestive heart failure by fueling the processes of inflammation, fibrosis and collagen deposition.

The findings indicate that galectin-3 is required for inflammatory and fibrotic responses to Aldo, suggesting a key role for galectin-3 in vascular fibrosis.  Equally important, the study proves that modified citrus pectin (MCP), a preparation derived from the pith of citrus peels, prevents these effects by binding to galectin-3 and controlling Aldo induced elevated galectin-3 levels.

MCP is a form of citrus pectin modified to a specific molecular weight and structure for enhanced absorption and bioactivity. Regular pectin goes through the gastrointestinal tract unabsorbed, whereas MCP is readily absorbed and has been demonstrated in published research to perform multiple beneficial functions. MCP’s small molecular weight and unique structure allow it to bind and block excess galectin-3 throughout the body. Elevated serum galectin-3 has been linked to high mortality rates in heart failure and metastatic cancer. MCP slows cancer progression and metastasis, blocks inflammation, helps prevent fibrosis, and offers other critical benefits related to the inhibition of galectin-3. It also supports immunity and safely chelates heavy metals.

Aldo and Galectin-3
The researchers in this study sought to understand exactly how Aldo and galectin-3 work together to affect vascular remodeling. In small quantities, Aldo and galectin-3 perform necessary biological functions. Aldo regulates blood pressure and electrolyte balance; galectin-3 facilitates cell-to-cell communication and cell growth. However, high levels of Aldo are linked to arterial stiffness and heart failure. Similarly, high levels of galectin-3 play a direct role in chronic inflammation, fibrosis and subsequent tissue remodeling in the kidneys, liver, heart and other organs; as well as cancer formation and metastasis.

In 2011, the Food and Drug Administration approved a serum galectin-3 test to assess the risk and progression of congestive heart failure and heart disease. This test is widely available and covered by most health insurances for cardiovascular screening. Practitioners also use this test to assess the risk and progression of cancer and other galectin-3 related diseases.

Dr. Isaac Eliaz, a recognized expert in the field of galectin-3 and the use of modified citrus pectin states, “The results of this study have enormous implications for the prevention and treatment of heart disease and fibrosis related conditions. Because it functions as an active, culprit biomarker, galectin-3 serves as a therapeutic target in multiple life-threatening conditions. According to the scientific literature, this is achievable with the oral application of MCP, a galectin-3 inhibitor without side effects. This approach offers a new solution to numerous chronic conditions related to inflammation, fibrosis and metastatic cancer for which there are limited conventional treatments.”

Study Details
In the study, rats were given Aldo and sodium chloride salt, which increased blood pressure, inflammation, fibrosis and galectin-3 levels. Using MCP, the research team blocked excess galectin-3 with significant results. Collagen type 1 deposition, blood pressure, inflammation, fibrosis and aortic wall thickness were all reduced. Spironolactone, a pharmaceutical Aldo inhibitor, achieved similar results.

However, the side effects of spironolactone are significant while MCP is proven to achieve greater results without toxicity or side effects. Specifically, the MCP was shown to outperform spironolactone in a few key areas related to inflammation and fibrosis. MCP achieved better suppression of fibrotic markers. Importantly, MCP completely inhibited the cytokine interleukin-6 (IL-6) which plays a key role in inflammation, fibrosis, immune response and cancer/metastasis. Spironolactone only partially blocked the Aldo induced IL-6.

The team went on to test the impact of increasing Aldo in regular mice as well as in galectin-3 knockout mice unable to produce the protein. When given Aldo, the normal mice experienced the inflammation and overabundant collagen formation associated with vascular remodeling. However, the knock-out mice experienced no ill effects, supporting the conclusion that Aldo requires galectin-3 to induce the collagen type 1 synthesis and deposition associated with vascular fibrosis.

Beyond Heart Disease
This new research confirms a number of earlier studies which implicate galectin-3 in numerous conditions related to inflammation and fibrosis. In particular, it substantiates research published in the journal PLoS One in 2011 demonstrating the role that galectin-3 plays in acute fibrosis-related kidney injuries. That study also shows that MCP blocks the harmful effects of excess galectin-3 and helps to reverse related damages.

This recent study marks a critical step toward understanding the mechanisms behind vascular fibrosis, and the role MCP can play in inhibiting these and other factors associated with heart failure and organ fibrosis. More research must be done to further illuminate the role of galectin-3 in cardiovascular and chronic diseases. Further research including clinical trials are being planned to explore MCP as a safe and natural preventative and treatment for congestive heart failure and metastatic cancer.

For more information on modified citrus pectin call (707) 583-8619, or visit www.mcprecommends.org

Source: Galectin-3 mediates aldosterone-induced vascular fibrosis. Laurent C, Maria M, Pascal R, Victoria C, Ernesto MM, de Boer RA, Françoise P, Patrick L, Faiez Z, Patrick R, Natalia LA. Arterioscler Thromb Vasc Biol. 2012 Nov 1.

 

Diabetes is reversable in 8 weeks on low caloric diet or what doctors don't want you to know

100 % success rate !!  Remarkable

What doctors don't want you to know.....

Low calorie diet may reverse diabetes in 8 weeks: Study

A new study has transformed thinking on type 2 diabetes by reporting that an extreme low
calorie diet could reverse the condition in just eight weeks.

The research, published in the journal Diabetologia, reports that a low calorie diet of 600 calories a day for two months can remove excess fat clogging up the pancreas, thus allowing normal insulin secretion to be restored – overturning the long held belief that type 2 diabetes is a lifelong condition.

The early stage clinical trail in eleven people reported a 100 per cent reversal of diabetes symptoms
during the two month diet period, with 64 per cent of the participants remaining diabetes free three months after the diet had finished.

“To have people free of diabetes after years with the condition is remarkable - and all because of an eight week diet,” said Professor Roy Taylor of Newcastle University, UK, who led the study.



“This is a radical change in understanding Type 2 diabetes. It will change how we can explain it to people newly diagnosed with the condition.

“It has long been believed that someone with Type 2 diabetes will always have the disease, and that it will steadily get worse … we have shown that we can reverse the condition,” said Taylor

Study details

Under close supervision of a medical team, 11 people who had developed diabetes later in life were put on an extreme diet of just 600 calories a day, consisting of liquid diet drinks and non-starchy vegetables.

They were matched to a control group of people without diabetes and then monitored over eight weeks to measure the production of insulin from their pancreas and fat content in the liver and pancreas.



After just one week, the research team found that pre-breakfast blood sugar levels had returned to normal, whilst scans revealed that fat levels in the pancreas had lowered from an elevated level of eight per cent to the healthy, normal level of six per cent.

 

In combination with the reduction of fat levels, the pancreas was found to regain its normal ability to produce insulin. As a result, blood sugar after meals was reported to steadily improve.

“We believe this shows that Type 2 diabetes is all about energy balance in the body,” explained Taylor, “if you are eating more than you burn, then the excess is stored in the liver and pancreas as fat which can lead to Type 2 diabetes in some people.”

The researchers said that the new insight “allows an understanding of the causality of type 2 diabetes in individuals as well as in populations.”

“It carries major implications for information to be given to newly diagnosed patients, who should know that they have a potentially reversible condition and not one that is inevitably progressive,” they concluded.

Source: Diabetologia

Published online ahead of print, doi: 10.1007/s00125-011-2204-7

“Reversal of type 2 diabetes: normalisation of beta cell function in
association with decreased pancreas and liver triacylglycerol”

Authors: E. L. Lim, K. G. Hollingsworth, B. S. Aribisala, M. J. Chen, J. C.
Mathers, R. Taylor

http://www.foodnavigator-usa.com/Science/Low-calorie-diet-may-reverse-diabetes-Study

News from Ukraine about fullerenes in nanomedicine!!!

Science, Research & Technology
News from Ukraine about fullerenes in nanomedicine!!!

Grigoriy Andrievsky
Director of Science, PhD. at "Institute of Physiological Active Compounds" LLC
To:Walter Derzko, […]

Dear sir/madam,
Dear colleagues,

After many years of scientific research and extended preclinical and clinical trials, at the end of 2010 in Ukraine, for the first time in the world, the following products “Concentrated solutions of hydrated С60 fullerene” (C60FWS), “Water with hydrated С60 fullerene” and fully highly purified С60 fullerene were approved by the Ministry of Health of Ukraine for use as a component in food products and cosmetics. This includes their administration as a multifunctional dietary supplement, which has unique medicinal and preventive properties while, at the same time, being absolutely safe for humans.

You may find this same information upon visiting our site http://www.ipacom.com, in particular via the following links: http://www.ipacom.com/index.php/ru/products-left/68 and
http://www.ipacom.com/index.php/ru/products
http://ipacom.com/index.php/en/fullerenes-and-water-left/74
http://ipacom.com/index.php/en/publications-about-c60hyfn/70
http://ipacom.com/images/Articles/annotation_en.pdf

In addition, you may see our News and obtain the file of presentation: “About the most important physical, chemical and biological properties of hydrated С60 fullerene (С60HyFn) and its water solutions (С60FWS)” on our site:
http://ipacom.com/index.php/en/publications-about-c60hyfn/92

Thus, the water solutions of hydrated fullerene С60 have already become available commercially and they can now be purchased for your own research and applications in many areas of human activity and, especially, as optimum means for preventive medicine of the future.

Thank you very much in advance.

On behalf of my colleagues,

Grigoriy Andrievsky

Director of Science, PhD.
Institute of Physiological Active Compounds, LLC.
58, Lenin ave.,
61072, Kharkov,
Ukraine
Phone: +38 057 763 0521 (Phone/Fax, Office)
+38 057 763 0336 (Lab.)
E-mail: yard@kharkov.ua or
science@ipacom.com
http://www.ipacom.com (russ./engl.)

A 'nutty' solution to type 2 diabetes management

Eating nuts daily could help control type 2 diabetes and prevent complications

TORONTO, Ont., July 12, 2001--Eating nuts every day could help control Type 2 diabetes and prevent its complications, according to new research from St. Michael's Hospital and the University of Toronto.

In the research, published online by the journal Diabetes Care, a team of researchers led by Dr. David Jenkins (University of Toronto Department of Nutritional Sciences; St. Michael's Hospital Risk Factor Modification Centre) reports that consuming two ounces of nuts daily as a replacement for carbohydrates proved effective at glycemic and serum lipid control for people with Type 2 diabetes. The article, entitled "Nuts as a Replacement for Carbohydrates in the Diabetic Diet," is available here: http://care.diabetesjournals.org/content/early/2011/06/02/dc11-0338.abstract

"Mixed, unsalted, raw, or dry-roasted nuts have benefits for both blood glucose control and blood lipids and may be used as part of a strategy to improve diabetes control without weight gain," said Dr. Jenkins, who also has appointments with St. Michael's Division of Endocrinology and Metabolism and the U of T's Department of Medicine. He also serves as Canada Research Chair in Nutrition and Metabolism.

Jenkins and his colleagues provided three different diet supplements to subjects with Type 2 diabetes. One group was given muffins, one was provided with a mixture of nuts including raw almonds, pistachios, walnuts, pecans, hazelnuts, peanuts, cashews, and macadamias, and one group was given a mixture of muffins and nuts.

Subjects receiving the nut-only supplement reported the greatest improvement in blood glucose control using the glycosylated hemoglobin (HbA1c) test. The nut diet subjects also experienced a reduction in low-density lipoprotein cholesterol (known as LDL, or "bad cholesterol"). The subjects provided the muffin supplement or mixed muffin-and-nut supplement experienced no significant improvement in gylcemic control but those receiving the muffin-nut mixture also significantly lowered their serum LDL levels.

"Those receiving the full dose of nuts reduced their HbA1c [the long-term marker of glycemic control] by two-thirds of what the U.S. Food and Drug Administration recognizes as being clinically meaningful for therapeutic agents. Furthermore, neither in the current study nor in previous reports has nut consumption been associated with weight gain. If anything, nuts appear to be well suited as part of weight-reducing diets," Dr. Jenkins said.

"The study indicates that nuts can provide a specific food option for people with Type 2 diabetes wishing to reduce their carbohydrate intake."

###
Acknowledgments—This work was supported by the Canada Research Chair Endowment of the Federal Government of Canada, the International Tree Nut Council Nutrition Research & Education Foundation (representing almonds, Brazils, cashews, hazelnuts, macadamias, pecans, pine nuts, pistachios, and walnuts), and the Peanut Institute. None of the funding organizations or sponsors played any role in the design and conduct of the study; in the collection, management, analysis, and interpretation of the data; or in the preparation, review, or approval of the manuscript. Dr. Jenkins has also received honorariums for consultation from the International Tree Nut Council and the Almond Board of California.

For more information, contact:

Leslie Shepherd
Manager, Media Strategy,
Phone: 416-864-6094 or 647-300-1753
shepherdl@smh.ca
St. Michael's Hospital
Inspired Care. Inspiring Science.
www.stmichaelshospital.com
Follow us on Twitter: http://www.twitter.com/stmikeshospital

or

Paul Cantin,
Associate Director, Strategic Communications,
Phone: 416-978-2890
Email: paul.cantin@utoronto.ca
Twitter: @uoftmedicine
www.facmed.utoronto.ca

 

--------------------------------------------------------------------------------

Effects of exercise on meal-related gut hormone signals

Effects of exercise on meal-related gut hormone signals

New animal research demonstrates mechanisms that are involved in suppressing food intake and preventing obesity with exercise

07/07/11, Clearwater Beach, FL.  Research to be presented at the upcoming annual meeting of the Society for the Study of Ingestive Behavior (SSIB), the foremost society for research into all aspects of eating and drinking behavior, finds that alterations of meal-related gut hormone signals may contribute to the overall effects of exercise to help manage body weight.

Regular exercise is important in maintaining low body weight and also is known to facilitate weight loss in obese subjects. Running exercise is known to increase sensitivity to leptin, a hormone released from fat cells that inhibits food intake.  The authors’ new study reveals additional mechanisms that contribute the beneficial effects of exercise.

Gut hormones are released before and after a meal to initiate and terminate food intake. The authors measured gut hormone release after a palatable tasty meal before and after rats exercised in running wheels. In rats with a lot of running wheel experience, consuming a tasty meal led to increased blood levels of an inhibitory feeding hormone, amylin.  After the meal, the same rats showed a more rapid rebound of a stimulatory feeding hormone, ghrelin.  The authors also demonstrated that compared to sedentary control rats, exercise-experienced rats decrease their food intake more robustly after treatment with CCK, a gut hormone that limits meal size.

Dr. Nu-Chu Liang reports, “Our new results indicate that the beneficial effects of exercise to control body weight might occur by altering the way in which meals release gut hormones that regulate food intake, and also by changing the sensitivity of individuals to these gut hormone signals. Furthermore, these findings suggest that both body and brain mechanisms are involved in the effects of exercise to modulate food intake.” 

 

Research funded by National Institutes of Health grant DK19302

Lead author: M.E. Smith (Johns Hopkins University, Baltimore, MD, USA)

 Co-authors: N.-C. Liang and T.H. Moran (Johns Hopkins University, Baltimore, MD, USA)

Contact author:  Dr. Nu-Chu Liang, postdoctoral fellow

Email:  nliang2@jhmi.edu

Higher-protein diets can improve appetite control and satiety

Research demonstrates dietary protein reduces hunger and increases fullness in overweight and obese men during weight loss

Park Ridge, Ill. (July 11, 2011) – A new study demonstrates that higher-protein meals improve perceived appetite and satiety in overweight and obese men during weight loss.(1) According to the research, published in Obesity, higher-protein intake led to greater satiety throughout the day as well as reductions in both late-night and morning appetite compared to a normal protein diet.

"Research has shown that higher-protein diets, those containing 18 to 35 percent of daily calorie intake from dietary protein, are associated with reductions in hunger and increased fullness throughout the day and into the evening hours," said Heather Leidy, Ph.D., study author and professor in the Department of Nutrition and Exercise Physiology at the University of Missouri. "In our study, the two groups ate either 25 or 14 percent of calories from protein, while the total calories and percent of calories from fat stayed the same between the higher-protein and normal-protein diet patterns. "

During the study, Dr. Leidy and associates also conducted an eating frequency substudy in which the 27 participants on both normal- and higher-protein diets consumed either three meals or six meals per day. The researchers found that eating frequency had no effect on appetite and satiety on the normal-protein diet. However, subjects on the higher-protein diet who ate three meals per day experienced greater evening and late-night fullness than those who ate six meals per day.

Dietary Protein and Reduced Calorie Consumption

This study supports previous research that demonstrates higher-protein diets, including egg breakfasts, are associated with decreased calorie consumption. A study published last year in Nutrition Research showed that men ate roughly 112 fewer calories at a buffet lunch and 400 fewer calories in the 24-hour period following a protein-rich egg breakfast compared to a bagel breakfast. (2) Another study demonstrated that overweight dieters who ate eggs for breakfast lost 65 percent more weight and felt more energetic than those who ate a bagel breakfast of equal calories and volume. (3)

Protein: A Component of a Healthy Meal Pattern

Protein not only plays a role in weight management but is also important in muscle maintenance and the prevention of sarcopenia which is age-related muscle loss. The 2010 Dietary Guidelines for Americans highlight that healthy Americans can have an egg a day to help meet dietary protein needs, and eggs are included in the protein foods section of MyPlate.

"Americans should include dietary protein sources at every meal," says Serena Ball, MS, RD, registered dietitian, nutrition consultant and advisor to the Egg Nutrition Center. "The 2010 Dietary Guidelines and MyPlate education series highlight that protein is an important component of a healthy diet."

Give Eggs the Company They Deserve

Serena Ball suggests pairing protein-rich eggs with whole grains, fruits, vegetables and dairy for a complete, healthy breakfast. Some meal and recipe ideas include:

• Cherry Tomato & Portobello Omelet with whole-grain toast, an orange and low-fat or fat-free milk

• Mini Breakfast Pizzas on a whole wheat English muffin with sliced apples and yogurt

• Basic Scrambled Eggs with low-fat mozzarella cheese and veggies along with fresh strawberries and a bowl of oatmeal made with low-fat or fat-free milk

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References

(1)Leidy HJ, Tang M, Armstrong CLH, Martin CB, Cambell WW.The effects of consuming frequent, higher protein meals on appetite and satiety during weight loss in overweight/obese men. Obesity. 2011;19:818-824.

(2) Ratliff J, Leite JO, de Ogburn R, Puglisi MJ, VanHeest J, Fernandez ML. Consuming eggs for breakfast influences plasma glucose and ghrelin, while reducing energy intake during the next 24 hours in adult men. Nutrition Research 2010;30:96-103.

(3)Vander Wal JS, Gupta A, Khosla P, Dhurandhar NV. Egg breakfast enhances weight loss. International Journal of Obesity. 2008;32:1545-1551.

About the American Egg Board (AEB)

AEB is the U.S. egg producer's link to the consumer in communicating the value of The incredible edible egg™ and is funded from a national legislative checkoff on all egg production from companies with greater than 75,000 layers, in the continental United States. The board consists of 18 members and 18 alternates from all regions of the country who are appointed by the Secretary of Agriculture. The AEB staff carries out the programs under the board direction. AEB is located in Park Ridge, Ill. Visit www.IncredibleEgg.org for more information.

About the Egg Nutrition Center (ENC)

The Egg Nutrition Center (ENC) is the health education and research center of the American Egg Board. Established in 1979, ENC provides science-based information to health promotion agencies, physicians, dietitians, nutritional scientists, media and consumers on issues related to egg nutrition and the role of eggs in the American diet. ENC is located in Park Ridge, IL. Visit www.eggnutritioncenter.org or www.nutritionunscrambled.com for more information.

When will the Recession End? Part 191 US 1930s dust bowl a repeat in this decade?

Conventional agriculture is a lot like conventional medicine (or conventional debt spending) -- it's not sustainable!

Much of the farming taking place today in Oklahoma, Nebraska, Colorado, Kansas and Texas is entirely dependent on fossil water stored in the Ogallala Aquifer.

 

Never heard of the Ogallala Aquifer? Most people haven't. But if you eat food in North America, a significant portion of the food on your plate comes from farms that only exist because of water from the Ogallala.

The Ogallala Aquifer is running dry. It is not being "recharged." The plummeting water levels are already turning some former farm hubs into dust towns.

Learn why this is happening and why the availability of cheap food is coming to an end:

Walter Derzko