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Vote if you pay taxes

In the 1860s, suffragette Sarah E. Wall of Worcester, Massachusetts invoked the principle of “no taxation without representation”, initiating an anti-tax protest in which she encouraged women not to pay taxes until they were granted the right to vote.

Soon after she began this movement, the Worcester city tax collector sued Wall for refusing to pay taxes, and the case reached the Massachusetts Supreme Court in 1863. In “Wheeler v. Wall,” the court ruled against Wall and held that despite not having the right to vote, women are still obligated to meet their tax burden. Even still, Wall refused to cooperate with the collector, and as a result, officers seized and sold her property in order to raise the money necessary to meet her tax obligation.

After several years, Wall’s inexorability eventually prevailed, as the collector began to ignore Wall and allow her to abstain from paying taxes.[88] In 1884, Susan B. Anthony cited Wall’s audacity and willingness to stand up for women’s suffrage, stating, “for the last twenty-five years, [she] has resisted the tax gatherer when he came around. I want you to look at her. She looks very harmless, but she will not pay a dollar of tax.

She says when the Commonwealth of Massachusetts will give her the right of representation she will pay her taxes.”[89]

Shimer College student holds “No tuition without representation” sign during protest over school governance in 2010.

The phrase is also used by other groups in America who pay various types of taxes (sales, income, property) but lack the ability to vote, such as felons (who are, in many states, barred from voting), people who work in one state and live in another (thus having to pay income tax to a state they don’t live in), or people under 18.[90]

To become citizens of the United States, immigrants most often must be permanent residents for a period of time (usually 5 years).[91]

Permanent residents must pay taxes on their worldwide income and, in most cases, cannot vote. However, throughout the 19th century, many states did allow immigrants to vote after they had declared their intention to become citizens. This was primarily because these new states were populated in large part by immigrants who had not yet attained citizenship.

Throughout U.S. history, non-citizens have been allowed to vote in 40 U.S. states and territories.[92] As of 2005, non-citizens are allowed to vote in seven jurisdictions in the United States: Chicago and six towns in Montgomery County, Maryland.[93]

In 2009, the phrase “taxation without representation” was also used in the Tea Party protests, where protesters were upset over increased government spending and taxes, and specifically regarding a growing concern amongst the group that the U.S. government is increasingly relying upon a form of taxation without representation through increased regulatory levies and fees which are allegedly passed via unelected government employees who have no direct responsibility to voters and cannot be held accountable by the public through elections.[94]

A modified version of the phrase, “no tuition without representation”, is sometimes used in disputes over governance in higher education in the United States to emphasize student’s rights to a voice in institutional decisions. The term first emerged in a 1977 dispute at Union County College in New Jersey.[95] It has been used more recently in disputes at Dartmouth College,[96]UC Berkeley School of Law,[97] and elsewhere.

Two different payment pathways for physicians, proposed rule

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2016-10032

Two Payment Pathways for Physicians

See link above for the proposed rule.

Consistent with the law, the proposed rule creates 2 different payment pathways for physicians—alternative payment models (APMs) and the Merit-Based Incentive Payment System (MIPS).

Inside Medicare’s New Payment System

Listen to industry experts and physician leaders discuss topics such as new payment models and quality reporting in this interview series from ReachMD™ and the AMA. Recent interviews include the following podcasts:


CMS Finalizes Historic Medicare Reform Law

A final rule released on Oct. 14, 2016 by the Centers for Medicare and Medicaid Services (CMS) details the final regulations for implementation of the Medicare Access and CHIP Reauthorization Act (MACRA), the historic Medicare reform law that repealed the Sustainable Growth Rate (SGR) formula last year. Read the AMA summary or view the key changes in the QPP final rule.

While the AMA is in the process of fully analyzing the regulations, a first review reveals that CMS responded to many of the concerns expressed by physicians about the proposed rule issued last spring. Read more about the details on AMA Wire®. Summaries, fact sheets and other CMS resources are available on the agency’s website.

The AMA will host educational webinar sessions to help physicians prepare and understand what the final rule means for their practice. Physicians and medical society staff are welcome. Both sessions will cover the same material. Register for Nov. 21st or register for Dec. 6th.


MACRA Resources

Women are more vulnerable to eating disorders, brain study suggests

By Honor Whiteman

Lead author Dr. Catherine Preston, of the Department of Psychology at York University in the United Kingdom, and colleagues publish their findings in the journal Cerebral Cortex.

According to the National Eating Disorders Association (NEDA), around 30 million peoplein the United States have some form of eating disorder, and around 20 million of these are women.

Popular notion has long held that women are more concerned with body image than men, and previous studies have shown that women are more likely than men to have body dissatisfaction.

When it comes to negative perceptions of physical appearance, social pressures are believed to play a key role. Since women tend to be more susceptible to such pressures, this may explain in part why eating disorders affect women more than men.

However, previous studies have shown that in some eating disorders, particularly anorexia, patients overestimate their body size – that is, they perceive themselves to be larger in size than they actually are.

“In today’s Western society, concerns regarding body size and negative feelings towards one’s body are all too common,” says Dr. Preston. “However, little is known about the neural mechanisms underlying negative feelings towards the body and how they relate to body perception and eating-disorder pathology.”

For their study, Dr. Preston and team aimed to pinpoint the brain activity that might underlie negative body perceptions.

Using virtual reality to assess the brain’s response to body appearance

The team enrolled 32 healthy individuals – 16 men and 16 women – to the study. None of the participants had a history of eating disorders, and their height and weight were measured upon enrollment.

Each participant was required to wear a virtual reality headset that, when they looked down, showed them a first-person video of a “slim” or “obese” body. In other words, it looked like the body belonged to them.

In order to enhance this illusion, the researchers poked the subjects’ torso with a stick, in synchronization with the video.

During this experiment, each participant had their brain activity monitored through magnetic resonance imaging (MRI).

When participants looked at their “obese” bodies, the team identified a direct link between activity in the area of the brain associated with body perception – the parietal lobe – and activity in the anterior cingulate cortex, the brain region related to the processing of subjective emotions, such as fear and anger.

What is more, the researchers found that such brain activity was more prominent in women than men, suggesting that “owning” an obese body is likely to lead to higher body dissatisfaction in women.

The researchers say their findings may help shed light on why women are more affected by eating disorders than men.

“This research is vital in revealing the link between body perception and our emotional responses regarding body satisfaction, and may help explain the neurobiological underpinnings of eating-disorder vulnerability in women.”

Dr. Catherine Preston

In future research, the team plans to further investigate how emotions influence body perceptions.

Fitness, not physical activity, mitigates negative effects of prolonged sitting

By Hannah Nichols Living a sedentary lifestyle – such as sitting for prolonged periods – has been shown to be a risk factor for cardiovascular disease and other conditions. Physical ina…

Source: Fitness, not physical activity, mitigates negative effects of prolonged sitting

Fitness, not physical activity, mitigates negative effects of prolonged sitting

By Hannah Nichols

cardio

Living a sedentary lifestyle – such as sitting for prolonged periods – has been shown to be a risk factor for cardiovascular disease and other conditions. Physical inactivity raises the risk of developing high blood pressure and coronary heart disease and has been found to increase the risk of certain cancers.

Studies have linked excessive sitting to being overweight and obese, type 2 diabetes, and early death. Lack of physical activity can also lead to feelings of anxiety and depression.

Sitting for long periods has been suggested to slow the metabolism, which affects the body’s ability to regulate blood sugar, blood pressure, and break down body fat.

Regular physical activity is essential for healthy aging, and adults aged 65 years and over gain substantial health benefits from regular exercise. Physical activity guidelines recommend older adults do at least 150 minutes of moderate-intensity aerobic activity per week, such as brisk walking, and muscle-strengthening activities on 2 or more days per week to work all major muscle groups.

Among individuals who meet physical activity recommendations, the risk of cardiovascular disease with high sedentary time remains. However, high levels of cardiorespiratory fitness are associated with reduced levels of cardiovascular risk factors, including high blood pressure, obesity, type 2 diabetes, and dyslipidemia.

Most active participants still spent 12-13 hours per day sedentary

Researchers from the Norwegian University of Science and Technology (NTNU) aimed to determine whether meeting physical activity guidelines or having high age-specific cardiorespiratory fitness would reduce the adverse effect of prolonged sitting on cardiovascular risk factors for seniors.

Cardiorespiratory fitness is the ability of the heart and lungs to provide the working muscles with oxygenated blood for a prolonged period and determine the level of fitness, which goes downhill with age. Cardiorespiratory fitness is an important health indicator that can predict cardiovascular disease mortality and can be improved by increasing both the intensity and amount of exercise.

While the average American adult sits for between 9-11 hours a day, the NTNU research found that the participants who were in the least sedentary third of the study still spent between 12-13 hours per day in sedentary behavior. The most sedentary of all participants were sedentary for up to 15 hours a day.

The NTNU study was part of a randomized controlled clinical trial with the primary objective of investigating the effect of exercise training on morbidity and mortality in the older adult population.

The team conducted a cross-sectional study of 495 women and 379 men from Norway aged between 70-77 years. Sedentary time and physical activity were assessed by accelerometers, while cardiorespiratory fitness was determined by peak oxygen uptake (VO2 peak) – the measurement of the volume of oxygen that the body can utilize during physical exertion.

Researchers compared different levels of activity with fitness levels and cardiovascular risk factor clusters. A cardiovascular risk factor cluster was defined as the presence of three to five risk factors for heart disease.

These risk factors included: elevated waist circumference, elevated blood triglycerides or reduced “good” cholesterol levels, high blood pressure or treatment for hypertension, and elevated fasting blood sugar levels – combined symptoms commonly referred to as metabolic syndrome.

High cardiorespiratory fitness reduced risk of heart disease

Findings – published in Mayo Clinic Proceedings – showed that when compared with women and men who were the least sedentary, women and men from the most sedentary group were 83 percent and 63 percent more likely to have cardiovascular risk factors from extended time sitting, respectively.

However, when the team took participants’ level of fitness into consideration – measured by having high age-specific cardio respiratory fitness – they found that the fittest 40 percent had a decreased likelihood of cardiovascular risk factors from prolonged sitting.

This finding held true even though the fittest participants spent between 12-13 hours per day sedentary and did not meet current moderate to vigorous physical activity guidelines.

No decreased risk was observed in older adults who were physically active without being fit. Therefore, say the researchers, meeting physical activity guidelines alone does not eliminate the cardiovascular risks of sedentary behavior if individuals do not have a certain level of cardiorespiratory fitness.

“Our Western lifestyles necessarily involve a lot of sitting, and we spend more and more time sitting on average as we age. But our findings show that being fit plays an important part in successful aging and may lend protection against the negative health effects of being sedentary.”

First author Silvana Sandbakk

Regular physical exercise, even below the recommended guidelines, is beneficial to health and longevity. “However, it seems that fitness makes a difference for this age group and while we wait for more evidence, some physical activity in elders that improves fitness will go a long way,” Sandbakk concludes.

Your endocrine organ and the mechanism that triggers fat formation uncovered

By Hannah Nichols Fat depots – sites where large quantities of mature fat cells are stored along with small amounts of stem cells – are distributed in various locations around the body.…

Source: Your endocrine organ and the mechanism that triggers fat formation uncovered

Your endocrine organ and the mechanism that triggers fat formation uncovered

By Hannah Nichols

hormone

Fat depots – sites where large quantities of mature fat cells are stored along with small amounts of stem cells – are distributed in various locations around the body. The findings – published in Science Signaling – piece together the puzzle of how the stem cells in these areas are triggered to change and develop into more fat cells.

Senior study author Dr. Brian Feldman, Ph.D., assistant professor of pediatrics, and colleagues found that stored mature fat cells secrete the hormone ADAMTS1, which subsequently toggles a “switch” that controls whether the surrounding stem cells differentiate into more fat cells ready to also store fat.

The research indicates that the production of ADAMTS1 hormone may increase fat formation as a result of a high-fat diet and taking glucocorticoid medications.

“Intuitively, people understand that when you eat more, you get fatter,” says Dr. Feldman. “You’re ingesting food, and some signal has to tell your body to make more fat. We didn’t know what was gating or triggering that process in vivo. This new research goes a long way to fill in the in-between steps.”

Previous studies have shown that while mature fat cells have a primary storage function, they also send and receive many hormone signals to help regulate metabolism.

The Stanford team conducted experiments using fat cells and fat stem cells in a lab, followed by mice and human studies to investigate the function of ADAMTS1.

Initially, the scientists aimed to identify genes that change activity in response to glucocorticoid medications. While glucocorticoid medications – such as prednisone and dexamethasone – are widely used to treat inflammatory conditions, they have adverse side effects of promoting obesity and type 2 diabetes.

The researchers set an objective to understand how obesity risk is increased through glucocorticoid medications.

High-fat diet decreased ADAMTS1 hormone, increased fat cells

Mice experiments showed that mature fat cells usually produce and secrete ADAMTS1. However, when mice were given glucocorticoids, the levels of the hormone dropped. When mice were genetically engineered to produce more ADAMTS1 than average, they were found to have smaller fat depots and fewer mature fat cells.

Laboratory experiments revealed that when purified ADAMTS1 was added to fat stem cells in a dish, the hormone blocked the glucocorticoid-induced differentiation from fat stem cells to mature fat cells, which suggests that ADAMTS1 typically acts as a signal outside of fat cells.

Upon reaching the fat stem cell, the researchers say that the hormone transmits instructions through signals inside the cell that overlap with the cells’ glucocorticoid response pathway. The team also points out that a cell-signaling molecule, called pleiotrophin, plays a crucial role in the pathway. Blocking the molecule’s signal appears to block the stem cells’ entire response to ADAMTS1.

Mice were provided with a high-fat diet to examine the effect of the diet on ADAMTS1 signal. As a result of the high-fat diet, the mice became fatter, and new fat cells matured in visceral fat tissue – the fatty tissue that surrounds the internal organs – with decreased ADAMTS1.

However, in contrast, increased ADAMTS1 and less fat cell maturation were seen in subcutaneous fat tissue – the fat under the skin.

These results are consistent with earlier studies that show that more visceral, but not more subcutaneous fat cells, mature when a high-fat diet is consumed. These findings suggest that the hormone is a significant regulator of the difference in mature fat cells between the two types of fat.

Finally, in humans who gained weight from a high-fat diet, the same responses were observed as in the mice experiments.

Fat formed during childhood affects lifelong obesity risk

The research provides an overview of how high-fat diets and both synthetic and natural stresshormones are linked to obesity. Stress hormones transmit a message via ADAMTS1 to mature more fat cells. “We think it is a signal that there may be hard times ahead, a trigger to store as much available energy as you can,” says Dr. Feldman.

Dr. Feldman notes that the same signals and processes take place when people consume a high-fat diet without being stressed or taking glucocorticoid medications. “We’ve basically seen that the glucocorticoid signal is embedded in the high-fat feeding pathway. Connecting those dots together was really exciting,” he adds.

While there may be other undiscovered hormones that influence maturation of fat cells, the potency of ADAMTS1 indicates that the hormone is a dominant signal and a major player, Dr. Feldman continues.

The findings may help understand how fat formation during childhood affects the risk of lifelong obesity.

Exercise transforms bad fat to good fat

Researchers have found that exercise helps “bad” fat transform into a form of “good” fat that is more metabolically active.

The findings were presented at the American Diabetes Association’s 73rd Scientific Sessions.

Humans have two types of fat:

  • Brown fat (the good fat) – this type of fat burns through calories to generate body heat.
  • White fat (the bad fat) – this fat develops as a result of storing excess calories, it is just an energy reserve.

People with more brown fat are generally slimmer and better able to stay warm when it is cold, whereas individuals who have high levels of white fat tend to live more sedentary lifestyles.

In this study, the researchers found that mice and men who underwent an intense exercise regime experienced a browning of their subcutaneous white adipose tissue (SCWAT).

The exercise regime had the men training on an exercise bicycle for 12 weeks and the mice running on an exercise wheel for 11 days.

Compared to the original white fat caused by sedentary behavior, the new, browner fat, was much more metabolically active.

The researchers transplanted this trained browner fat into sedentary fat mice to see how the browner fat might affect the way their bodies use glucose. They found that after the transplant the mice had increased glucose tolerance and insulin sensitivity for at least 3 months.

Kristin Stanford, PhD, a postdoctoral fellow at Joslin Diabetes Center in Boston, said:

“Our results showed that exercise doesn’t just have beneficial effects on muscle, it also affects fat. It’s clear that when fat gets trained, it becomes browner and more metabolically active. We think there are factors being released into the bloodstream from the healthier fat that are working on other tissues.”

It is still uncertain whether browner fat is having the same impact on humans as there is currently no way to try out fat transplantation on human beings.

Senior investigator of one of the studies, Laurie Goodyear, PhD, and associate professor at Harvard Medical School, said:

“We know that exercise is good for us. But what we’re showing here is that fat changes dramatically in response to exercise training and is having good metabolic effects.

This is not the fat that’s around your middle, which is bad fat and can lead to diabetes and other insulin resistant conditions. It’s the fat that’s under the skin, the subcutaneous fat that adapts in a way that appears to be having important metabolic effects.”

In conclusion the study reveals that browner fat is associated with a better body composition, lower fat mass and increased glucose uptake and insulin sensitivity in mice.

Stanford says the findings provide even more motivation to go out and start exercising. Even if you don’t lost weight, the study suggests that exercising will still train your fat to be more metabolically active and improve overall metabolism and health.

Dr. Jim Lyons, author of The Brown Fat Revolution, explains why brown fat is healthy.

Epigenetics in Adipose Tissue, Obesity, Weight Loss, and Diabetes

Epigenetic Changes in Diabetes and Cardiovascular Risk

Cardiovascular complications remain the leading causes of morbidity and premature mortality in patients with diabetes mellitus. Studies in humans and preclinical models demonstrate lasting gene expression changes in the vasculopathies initiated by previous exposure to high glucose concentrations and the associated overproduction of reactive oxygen species.

The molecular signatures of chromatin architectures that sensitize the genome to these and other cardiometabolic risk factors of the diabetic milieu are increasingly implicated in the biological memory underlying cardiovascular complications and now widely considered as promising therapeutic targets. Atherosclerosis is a complex heterocellular disease where the contributing cell types possess distinct epigenomes shaping diverse gene expression.

Although the extent that pathological chromatin changes can be manipulated in human cardiovascular disease remains to be established, the clinical applicability of epigenetic interventions will be greatly advanced by a deeper understanding of the cell type–specific roles played by writers, erasers, and readers of chromatin modifications in the diabetic vasculature. This review details a current perspective of epigenetic mechanisms of macrovascular disease in diabetes mellitus and highlights recent key descriptions of chromatinized changes associated with persistent gene expression in endothelial, smooth muscle, and circulating immune cells relevant to atherosclerosis. Furthermore, we discuss the challenges associated with pharmacological targeting of epigenetic networks to correct abnormal or deregulated gene expression as a strategy to alleviate the clinical burden of diabetic cardiovascular disease.

http://circres.ahajournals.org/content/118/11/1706/tab-figures-data


Given the role that diet and other environmental factors play in the development of obesity and type 2 diabetes, the implication of different epigenetic processes is being investigated. Although it is well known that external factors can cause cell type-dependent epigenetic changes, including DNA methylation, histone tail modifications, and chromatin remodeling, the regulation of these processes, the magnitude of the changes and the cell types in which they occur, the individuals more predisposed, and the more crucial stages of life remain to be elucidated. There is evidence that obese and diabetic people have a pattern of epigenetic marks different from nonobese and nondiabetic individuals.

The main long-term goals in this field are the identification and understanding of the role of epigenetic marks that could be used as early predictors of metabolic risk and the development of drugs or diet-related treatments able to delay these epigenetic changes and even reverse them. But weight gain and insulin resistance/diabetes are influenced not only by epigenetic factors; different epigenetic biomarkers have also been identified as early predictors of weight loss and the maintenance of body weight after weight loss. The characterization of all the factors that are able to modify the epigenetic signatures and the determination of their real importance are hindered by the following factors: the magnitude of change produced by dietary and environmental factors is small and cumulative; there are great differences among cell types; and there are many factors involved, including age, with multiple interactions between them.

Introduction

Epigenetics can be defined as inheritable and reversible phenomena that affect gene expression without altering the underlying base pair sequence (1). Epigenomics is the study of genome-wide epigenetic modifications. Epigenetics was introduced as a theoretical framework seeking to understand putative undisclosed relations between genes and environmental settings (diet, inactivity, smoking, etc.) to generate a phenotype (2). Epigenetics can provide some insights to help understand genetic fetal programming, monozygotic twin differences, and chronic disease onset in adults, which interact with dietary intake and nutritional processes.

Some epigenetic information might be inherited from one generation to the next. Although DNA methylation status is currently the most-studied epigenetic marker, there is increasing recognition that other modifications such as those of the histone code can modify the chromatin organization and folding (euchromatin vs. herochromatin) in such a way as to affect gene expression patterns (3).

These mechanisms, together with other transcriptional regulatory events, ultimately regulate gene activity and expression during development and differentiation or in response to nutritional and environmental stimuli.

Important recent investigations have highlighted that chromatin modifications/accessibility mark important disease-relevant regulatory regions in the genome (46, 8). Some of these studies suggest that common phenotypically associated single nucleotide polymorphisms (SNPs)7, which are enriched for expression quantitative trait loci, might act by altering gene regulatory regions (4).

Whereas many expression quantitative trait loci and regulatory variants act universally, some of the most relevant to disease might have tissue-specific activity (9). In this sense, chromatin state differences between cell types are related to cell type-specific gene functions (5).

The Encyclopedia of DNA Elements project (6) has systematically mapped regions of transcription, transcription factor association, chromatin structure, and histone modification within different cell types (including up to 12 histone modifications), which are allowing researchers to assign functional attributes to genomic regions.

The study of Ernst et al. (5) also revealed that the levels of DNA methylation usually correlate with chromatin accessibility and that, because most of the disease-associated SNPs are either intronic or intergenic and show consistently higher overlap with Encyclopedia of DNA Elements annotations, it seems like the genome-wide association study-identified regions are the ideal place to look for such epigenetic signatures.

The National Human Genome Research Institute Catalogue of Published genome-wide association study provides a quality-controlled, manually curated, literature-derived collection of all published GWA studies, which, as of 1 October 2013, included 1724 publications and 11,680 SNPs (7).

One proposed mechanism of action of the SNPs is that they would affect the activity of enhancer elements regulating critical target genes.

Thus, Maurano et al. (8) demonstrated that disease-associated variants systematically perturb transcription factor recognition sequences, frequently alter allelic chromatin states, and form regulatory networks in a tissue-specific way.

For example, of the 67 SNPs for type 2 diabetes (implicating a total of 2776 H3K4me3 peaks) analyzed in this study (8), 14 (20.1%) were either highly specific for chromatin marks within the liver or pancreatic islets, 2 tissues having a key role in mediating glucose metabolism and insulin secretion.

http://advances.nutrition.org/content/5/1/71.full