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American College of Healthcare Sciences Announces Opening of Community Focused Satellite Campus in Kona, Hawaii

Metabolic syndrome: Toxicology's next patient

UAB Study Shows Link Between Microbiome in the Gut and Parkinson’s




Released: 03/16/17


American College of Healthcare Sciences Announces Opening of Community Focused Satellite Campus in Kona, Hawaii

Accredited holistic health college opens satellite campus in Hawaii to provide on-site wellness workshops and classes serving Pacific Rim students, ACHS students and graduates, and the public.

Portland, Ore.—March 9, 2017American College of Healthcare Sciences (ACHS) announces the opening of its new satellite campus in the Central Kona Center Building in Kealakekua, Hawaii. Initially, the college’s new campus will offer on-site wellness workshops and classes to the local community, training to its Pacific Rim students who want to study aromatherapy with industry experts in a face-to-face environment, and additional on-site learning opportunities for current ACHS students and graduates.

Community members, students, and graduates in the Kona area can tour the satellite campus at the college’s Open House event on Saturday, March 18 from 11 a.m. – 2 p.m., 81-958 Halekii St., Suite 5C, Kealakekua, HI 96750. Also, meet College President and Health and Wellness Expert Dorene Petersen, learn about upcoming holistic health classes and workshops (aromatherapy, holistic nutrition, and more!), and enter to win a free door prize.

“It’s exciting to see how much the ACHS community has grown since founding the college nearly 40 years ago. Our community of students, alumni, and faculty—who are committed to the advancement of the holistic health and wellness industry—is truly amazing,” says ACHS President and Founder Dorene Petersen. “Our goal is always to provide an outstanding academic experience, and our new Kona campus will be integral to that mission. There is a lot of opportunity for community outreach and enrichment, and expanded student support. Dean of Students Heather Baley will manage the new campus and has more than 15 years’ experience in Student Services.”

ACHS has nearly 40 years’ experience providing accredited complementary alternative medicine and holistic health and wellness education. Programs vary from full-length graduate and undergraduate degrees to professional certificates to one-hour webinars. Areas of specialty include aromatherapy, herbal medicine, holistic nutrition, holistic spa management, wellness coaching, and sports nutrition, among others.

ACHS is committed to professionalism, integrity, and ethical and social responsibility, and was one of the first accredited higher education institutions specializing in holistic health and wellness to come a Certified B Corporation®. ACHS is one of only approximately 1,800 other companies to earn this designation through a verifiable commitment to higher standards of social and environmental performance, transparency, accountability, and to maintaining a clear mission to benefit the communities served.

The ACHS satellite campus in Kona plans to offer extensive community service through free and low-cost clinics for wellness and nutrition coaching provided by students and graduates. 

“Hawaii has always been top of my list for a satellite campus,” says ACHS Chief Strategy Officer Erika Yigzaw. “As a New Zealander, Hawaii feels like home, and the rich history of botanical medicine and the amazing native plants offer much inspiration for health and wellness advocates. In fact, island life should inspire us all to reduce stress and live more simply. There’s a reason that so many of the world’s Blue Zones are on islands! The Hawaii satellite campus creates more opportunities for our students and graduates to experience transformational learning and lets ACHS give back to Kama’aina through community education and health coaching clinics with students and graduates from programs like the Master of Science in Holistic Nutrition and Diploma in Aromatherapy. It’s a win-win for a B CorpTM like ACHS.”

 

For more information about ACHS and its current programs, visit www.achs.edu, call 800.487.8839 or email admissions@achs.edu.

Released: 03/07/17


Metabolic syndrome: Toxicology's next patient

Metabolic syndrome: Toxicology's next patient

A rise in caloric consumption combined with a decrease in physical activity has contributed to a boom of metabolic diseases, such as type 2 diabetes mellitus and cardiovascular diseases (e.g., heart failure and stroke). Over the last couple of decades, studies exploring these diseases have uncovered some of the complex pathophysiological mechanisms involved, resulting in the identification of a plethora of interconnected physiological, pathophysiological, biochemical, and clinical factors that play a role in their development. These factors include obesity/abdominal adiposity, insulin resistance, dyslipidemia, a low-grade state of chronic inflammation, hypoxia, oxidative stress, fasting hyperglycemia, high blood pressure (hypertension), endothelial dysfunction, a hypercoagulable state, genetics, and more. This constellation of interconnected risk factors that play a role in the development of metabolic and cardiovascular diseases has been dubbed metabolic syndrome.

The concept of this complex syndrome was first introduced by Gerald M. Raven during the Banting Medal Address during the 1988 American Diabetes Association meeting. He proposed that cardiovascular risk was high among insulin-resistant, hyperinsulinemic individuals who were glucose intolerant and who exhibited a collection of other risk factors, such as increased levels of plasma triglyceride, low HDL-cholesterol, and essential hypertension. He called the collection of these factors Syndrome X, as the significance of these abnormalities and their precise role in cardiovascular diseases was not fully understood at the time. While the condition has been given several definitions over the years based on improved understanding, a harmonized definition for metabolic syndrome was the result of a 2009 joint meeting of the American Heart Association, the National Heart Lung and Blood Institute, the International Diabetes Foundation, the World Heart Federation and the International Association for the Study of Obesity. Accordingly, metabolic syndrome is diagnosed based on the presence of any three of five criteria:

• Increased waist circumference (as a measure of abdominal obesity that is specific to populations and ethnic groups);

• Triglycerides levels at 150mg/dl or higher;

• HDL-c levels at 40 mg/dL or lower in men and 50 mg/dL or lower in women;

• Blood pressure at 130/85 or higher; and

• Fasting plasma glucose (glycemia) at 100mg/dL or higher.

Diagnosed with these criteria, metabolic syndrome confers a five-fold increased risk for type 2 diabetes and a three-fold increased risk for cardiovascular disease, including an up to four-fold increased risk for stroke or heart failure. Metabolic syndrome also is associated with several other diseases, including many cancers, polycystic ovarian syndrome, and neurological disorders.

Metabolic Percentages.pngWith approximately 35% of all adults and 50% of individuals aged 60 years or older estimated to have metabolic syndrome, it is a major public health issue and is changing what was thought of as a "normal" individual. The presence of metabolic syndrome in an increasing percentage of individuals suggests an altered metabolic, physiological, and pathophysiological state that may change or exacerbate the toxic responses to drugs and/or environmental toxicants. And this syndrome is not limited to the adult population. It increasingly is diagnosed in the pediatric population with a prevalence rate of about 11.9% in overweight children and 29% in obese children.

While several intricate pathways and mechanisms are at play in metabolic syndrome, obesity (abdominal obesity in particular) and insulin resistance are considered to be at the core of this syndrome. For example, a positive energy balance leads to adipose tissue expansion and obesity resulting in consequences, which include the following:

• Infiltration of macrophages and other immune cells into the adipose tissue, giving rise to an inflamed adipose tissue with an increased secretion of proinflammatory cytokines and adipokines and a concomitant decrease in the anti-inflammatory adipokine, adiponectin.

• Ectopic deposition of fat in key organs such as the liver, heart, skeletal muscle, and pancreas due to spill over from expanded adipose tissue, resulting in tissue lipotoxicity and consequent inhibition of insulin signaling.

• Binding of circulating free fatty acids to toll receptors on various organs, augmenting inflammatory signaling via the downstream activation of NFκB and JNK pathways resulting in a vicious cycle of inflammation, which further inhibits insulin signaling in these tissues.

• Free fatty acid accumulation in tissues and in its breakdown to intracellular diacylglycerol and ceramide, which interferes with insulin signaling and insulin-stimulated glucose uptake. This accumulation of free fatty acids and its incomplete oxidation mediates mitochondrial dysfunction, which triggers formation of reactive oxygen species that induce oxidative stress, which further impairs mitochondrial function. Increased reactive oxygen species levels also hinder insulin signaling and impair GLUT4 translocation.

A failure of cells to respond to insulin results in the pathological condition of insulin resistance. Insulin, by activating complex signaling pathways involving pI3K/AKT, MAPK, and clb and by binding to transcriptions factors such as FOXO and PPARg, regulates glucose uptake and glucose and lipid metabolism in peripheral tissues. Insulin resistance disrupts these pathways, resulting in hyperglycemia and dyslipidemia. Dyslipidemia also results from the accumulation of free fatty acids in the liver along with insulin-augmented lipogenesis, increasing triglyceride production and release, together with an increased hepatic uptake and renal clearance of HDL-c resulting in a dysregulated lipid profile of low levels of HDL-c and high triglyceride seen in metabolic syndrome. Glucotoxicity and lipotoxicity mediate pancreatic β-cell dysfunction in insulin resistance and hyperinsulinemia. This combination of insulin resistance and hyperinsulinemia, additionally, plays a role in the development of hypertension by tipping the balance between endothelial cell secretion of the vasodilator, NO, and the vasoconstrictor, ET-1.

Although obesity and IR are at the core of the pathophysiological mechanisms of metabolic syndrome, several other factors also are implicated, including dysregulation of the hypothalamic-pituitary-adrenal axis, the renin-angiotensin-aldosterone system, the autonomic nervous system, impact of gut microbiome on metabolism, the cellular and metabolic alterations in response to drugs, alcohol, and environmental toxicants. Both genetic and epigenetic mechanisms are thought to play a role besides environmental and lifestyle causes of MS.

An examination of the metabolic disturbances associated with metabolic syndrome reveals that many of the pathways and mechanisms involved overlap with those affected by drugs and environmental toxicants and can result in similar types of cellular and organ toxicities. It also is conceivable that drug responses and toxicities may be altered in subjects with metabolic syndrome in whom several metabolic and signaling pathways have gone awry.

To help further understanding and expand your knowledge of the complex and multidimensional condition of metabolic syndrome, SOT is hosting a Contemporary Concepts in Toxicology (CCT) meeting titled "Metabolic Syndrome and Associated Diseases: From the Bench to the Clinic" on March 11, in Baltimore, Maryland. Scheduled for the day before the start of the SOT Annual Meeting and ToxExpo, the CCT meeting aims to explore several aspects of metabolic syndrome, including the risk factors, causes, and the manifestations of diseases associated with it; the various cellular and pathophysiological mechanisms that may play a role; and the current and potential therapeutic strategies and risk assessment, which together will enable the development of safer drugs and potential new therapeutics.

The CCT organizers hope that a "focus on understanding the pathways and risk factors leading to disease and on how these pathways can be perturbed to develop drugs for disease interventions will create a unique combination that is likely to lead to new thought processes and scientific collaborations in addition to defining knowledge gaps, identifying research needs, protecting public health, and empowering product development."


Story Source:  Materials provided by Society of Toxicology

 

 

Released: 03/06/17


UAB Study Shows Link Between Microbiome in the Gut and Parkinson’s

UAB Study Shows Link Between Microbiome in the Gut and Parkinson’s

 

There is growing evidence showing a connection between Parkinson’s disease — a neurodegenerative condition — and the composition of the microbiome of the gut. A new study from researchers at the University of Alabama at Birmingham shows that Parkinson’s disease, and medications to treat Parkinson’s, have distinct effects on the composition of the trillions of bacteria that make up the gut microbiome.

The findings were published in February in Movement Disorders, the journal of the International Parkinson and Movement Disorder Society.

“Our study showed major disruption of the normal microbiome ¬— the organisms in the gut — in individuals with Parkinson’s,” said Haydeh Payami, Ph.D., professor in the Department of Neurology, in the UAB School of Medicine.

Payami says, at this point, researchers do not know which comes first. Does having Parkinson’s cause changes in an individual’s gut microbiome, or are changes in the microbiome a predictor or early warning sign of Parkinson’s? What is known is that the first signs of Parkinson’s often arise as gastrointestinal symptoms such as inflammation or constipation.

“The human gut hosts tens of trillions of microorganisms, including more than 1,000 species of bacteria,” she said. “The collective genomes of the microorganisms in the gut is more than 100 times larger than the number of genes in the human genome. We know that a well-balanced gut microbiota is critical for maintaining general health, and alterations in the composition of gut microbiota have been linked to a range of disorders.”

Payami’s team studied 197 patients with Parkinson’s and 130 controls. Subjects came from Seattle, New York and Atlanta.

The study indicated that Parkinson’s is accompanied by imbalance in the gut microbiome. Some species of bacteria were present in larger numbers than in healthy individuals; other species were diminished. Different medications used to treat Parkinson’s also appear to affect the composition of the microbiome in different ways.

“It could be that, in some people, a drug alters the microbiome so that it causes additional health problems in the form of side effects,” Payami said. “Another consideration is that the natural variability in the microbiome could be a reason some people benefit from a given drug and others are unresponsive. The growing field of pharmacogenomics — tailoring drugs based on an individual’s genetic makeup — may need to take the microbiome into consideration.”

The study subjects came from three regions, the Northeast, Northwest and South. Payami says the research team detected an unexpected difference in gut imbalance as a function of geographic site, which may reflect the environmental, lifestyle and diet differences between the three regions.

Another function of the microbiome is to help the body rid itself of xenobiotics — chemicals not naturally found in the body often arising from environmental pollutants. The study found evidence that the composition of bacteria responsible for removing those chemicals was different in individuals with Parkinson’s. This may be relevant because exposure to pesticides and herbicides in agricultural settings is known to increase the risk of developing Parkinson’s.

Payami says the study of the microbiome is a relatively new field, and a better understanding of macrobiotics may provide unexpected answers for Parkinson’s disease and potentially other disorders.

“This opens up new horizons, a totally new frontier,” she said. “There are implications here for both research and treatment of Parkinson’s disease. Therapies that regulate the imbalance in the microbiome may prove to be helpful in treating or preventing the disease before it affects neurologic function.” However, Payami cautions against grand conclusions until more data are available.

Payami says another study is underway at UAB with individuals with Parkinson’s and healthy individuals in Alabama in an effort to replicate and confirm the results.

“The present findings lend support to the notion that the composition of the gut microbiome may hold new information for assessing efficacy and toxicity of Parkinson’s medications,” Payami said. “Additional studies are needed to assess the effects of those drugs, with larger numbers of treated and untreated patients as well as individuals who do not have Parkinson’s.”

The study was supported by funding from the National Institute of Neurological Disorders and Stroke, one of the National Institutes of Health.

About UAB
Known for its innovative and interdisciplinary approach to education at both the graduate and undergraduate levels, the University of Alabama at Birmingham is an internationally renowned research university and academic medical center.

Link for highlight:  http://www.newswise.com/institutions/newsroom/625/

 

 

 

 

 

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