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By Cecilia Munoz Federal Parity Task Force Takes Steps to Strengthen Insurance Coverage for Mental Health and Substance Use Disorders From the national opioid epidemic to disturbing rates of suicid…
Source: Report to the President on Mental Health and Substance Use Disorder Parity
From the national opioid epidemic to disturbing rates of suicide, we see the consequences every day of untreated mental health and substance use disorders. Access to effective mental health and substance use disorder services can mean the difference between graduating from school and falling behind; between keeping a good job and becoming involved with the criminal justice system; between living a full life in recovery and dying by overdose or suicide. But if those services are needed, will your health insurance cover them in the same way it covers other medical treatment?
The Mental Health and Substance Use Disorder Parity Task Force was led by the Domestic Policy Council and consisted of the Departments of Labor, the Treasury, Defense, Justice, Health and Human Services, and Veterans Affairs, as well as the Office of Personnel Management and the Office of National Drug Control Policy. Our Task Force met with consumers, providers, employers, health plans, and State regulators, and read more than 1,100 public comments.
Today, we are presenting the President our final report, which includes a series of new actions and recommendations to ensure that insurance coverage for mental health and substance use disorder services is comparable to—or at parity with—general medical care.
Parity laws and regulations aim to eliminate restrictions on mental health and substance use disorder coverage – like annual visit limits, higher copayments, separate deductibles for mental health and substance use disorder services, and rules on how care is managed (such as pre-authorizations or medical necessity reviews) – if comparable restrictions are not placed on medical and surgical benefits. Comprehensive insurance coverage that meets parity requirements can provide access to treatment and services, which in turn can reduce the difficulties faced by people with mental health and substance use disorders, help their loved ones, and increase their independence.
However, parity is only meaningful if health plans are implementing it well, consumers and providers understand how it works, and the government provides clear guidance and appropriate oversight.
During its tenure, Task Force agencies produced a user-friendly “Know Your Rights” brochure to increase knowledge about parity; released guidance outlining plans’ obligations for disclosing information to assess their compliance with parity; and issued a best practices report based on a series of interviews with State regulators on parity implementation and enforcement.
In conjunction with the final report, the Task Force announced an additional series of immediate action steps to advance parity. Examples of these steps include:
Examples of the longer-term recommendations included in the Task Force final report include:
These and the other actions and recommendations in the Task Force report build on the ongoing work of the Administration to ensure that people with mental health and substance use disorders receive the care they need.
For example, the Affordable Care Act ended insurance company discrimination based on pre-existing conditions, including mental health and substance use disorders; required coverage of mental health and substance use disorder services in the individual and small group insurance markets; ensured that recommended preventive screenings, including for depression and alcohol misuse, are available with no co-pays; and, expanded Medicaid to millions of additional Americans, significantly improving coverage for mental health care and substance use disorder treatment.
The work of the Task Force provides a road map for moving forward so that our country will continue to make significant progress in expanding mental health and substance use disorder coverage for millions of Americans.
The final report is available here: http://www.hhs.gov/parity
About
The Mental Health Parity Act (MHPA) is legislation signed into United States law on September 26, 1996 that requires annual or lifetime dollar limits on mental health benefits to be no lower than any such dollar limits for medical and surgical benefits offered by a group health plan or health insurance issuer offering coverage in connection with a group health plan.[1] It was largely superseded by the Paul Wellstone and Pete Domenici Mental Health Parity and Addiction Equity Act (MHPAEA), which the 110th United States Congress passed as rider legislation on the Troubled Asset Relief Program (TARP), signed into law by President George W. Bush in October 2008. Prior to MHPA and similar legislation, insurers were not required to cover mental health care and so access to treatment was limited, underscoring the importance of the act.
By Carol Torgan, Ph.D. The age of many human tissues and cells is reflected in chemical changes to DNA. The finding provides insights for cancer, aging, and stem cell research. We may gauge how we’…
Source: Epigenetic Clock Marks Age of Human Tissues and Cells
By Carol Torgan, Ph.D.
The age of many human tissues and cells is reflected in chemical changes to DNA. The finding provides insights for cancer, aging, and stem cell research.
We may gauge how we’re aging based on visible changes, such as wrinkles. For years, scientists have been trying to gauge aging based on changes inside our cells.
Many alterations occur to our DNA as we age. Some of these changes are epigenetic — they modify DNA without altering the genetic sequence itself. These changes affect how cells in different parts of the body use the same genetic code. By controlling when specific genes are turned on and off, or “expressed,” they tell cells what to do, where to do it, and when to do it.
One such type of modification occurs when chemical tags known as methyl groups attach to DNA in specific places. This process, known as methylation, affects interactions between DNA and protein-making machinery. Changes in DNA methylation — both increases and decreases — occur with aging.
Dr. Steve Horvath from the University of California, Los Angeles, examined the relationship between DNA methylation and aging. He took advantage of publicly available methylation datasets, including ones from The Cancer Genome Atlas, a joint effort of NIH’s National Cancer Institute (NCI) and National Human Genome Research Institute (NHGRI). The datasets were developed by hundreds of researchers and comprised almost 8,000 samples of 51 healthy tissues and cell types. Samples came from people ranging in age from newborns to 101 years. They included tissues from throughout the body, including the brain, breast, skin, colon, kidney, liver, lung, and heart.
Horvath first developed an age predictor using 39 datasets. The tool was based on 353 specific DNA sites where methyl groups increased or decreased with age. He then tested the predictor in 32 additional datasets. Results appeared in the October 21, 2013, issue of Genome Biology.
Horvath found that the computed biological age based on DNA methylation closely predicted the chronological age of numerous tissues and cells to within just a few years. There were some tissues, however, where the biological age did not match the chronological age. These included skeletal muscle, heart tissue, and breast tissue. The clock also worked well in chimpanzees.
In both embryonic and induced pluripotent stem cells — genetically altered adult cells with characteristics of embryonic stem cells — the DNA methylation age proved to be near zero.
Horvath also analyzed nearly 6,000 samples from 20 different cancers and found that cancer greatly affected DNA methylation age. However, in most cancers the age acceleration didn’t reflect the tumor grade and stage.
The rate of ticking of the biological clock, as measured by the rates of change in DNA methylation, wasn’t constant. It was faster from birth to adulthood, and then slowed to a constant rate around the age of 20.
Horvath didn’t find evidence of a relationship with DNA methylation age in B cells (a type of white blood cell) from people with a premature aging disease (progeria).
“Pinpointing a set of biomarkers that keeps time throughout the body has been a 4-year challenge,” Horvath says. “My goal in inventing this age-predictive tool is to help scientists improve their understanding of what speeds up and slows down the human aging process.”
UCLA has filed a provisional patent on the age-predictive tool, which is freely available to scientists online. Horvath plans to examine whether DNA methylation is only a marker of aging or itself affects aging.
By Harrison Wein, Ph.D. Certain DNA changes can better predict a person’s life expectancy than traditional risk factors such as age. The findings could lead to novel insights into the molecular mec…
Source: DNA changes predict longevity
By Harrison Wein, Ph.D.
Our DNA changes as we age. Some of these changes are epigenetic—they modify DNA without altering the genetic sequence itself. Epigenetic changes affect how genes are turned on and off, or expressed, and thus help regulate how cells in different parts of the body use the same genetic code. Previous studies have shown that levels of one type of epigenetic modification, called DNA methylation, roughly reflect a person’s age.
Recent work suggests that epigenetic age might also be associated with health outcomes independent of chronological age. Dr. Steve Horvath from the University of California, Los Angeles, and his colleagues set out to investigate the relationship between epigenetic age and mortality.
The researchers analyzed DNA in blood samples from more than 13,000 people, including non-Hispanic whites, Hispanics, and African Americans. Many of the samples came from large NIH-funded studies, including the Framingham Heart Study and the Women’s Health Initiative. The researchers were funded in part by NIH’s National Institute on Aging (NIA). The team also included scientists from NIA and NIH’s National Heart, Lung, and Blood Institute (NHLBI). The study appeared on September 28, 2016, in Aging.
The researchers tested different models of epigenetic age. Different cell types—even similar ones like various blood cell types—have different epigenetic patterns. As people get older, the mix of immune cells in their blood shifts. When these age-related changes to blood cell composition were factored in, the researchers’ epigenetic age model predicted mortality from all causes better than previous measures of epigenetic age. The relationship between epigenetic age and mortality was significant within both sexes and across all the ethnic groups in the study.
“Our findings show that the epigenetic clock was able to predict the lifespans of Caucasians, Hispanics, and African-Americans in these cohorts, even after adjusting for traditional risk factors like age, gender, smoking, body-mass index, and disease history,” says NIA’s Dr. Brian Chen, the study’s first author.
These results support the notion that epigenetic age captures some aspect of biological aging over and above chronological age and other risk factors. “Our research reveals valuable clues into what causes human aging, marking a first step toward developing targeted methods to slow the process,” Horvath says.
The precise roles that epigenetic factors play in aging and death remain unknown and require further study.
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Description: The study of human genetic disorders and mutant mouse models has provided evidence that genome maintenance mechanisms, DNA damage signaling and metabolic regulation cooperate to drive the ageing process. In particular, age-associated telomere damage, diminution of telomere ‘capping’ function and associated p53 activation have emerged as prime instigators of a functional decline of tissue stem cells and of mitochondrial dysfunction that adversely affect renewal and bioenergetic support in diverse tissues. Constructing a model of how telomeres, stem cells and mitochondria interact with key molecules governing genome integrity, ‘stemness’ and metabolism provides a framework for how diverse factors contribute to ageing and age-related disorders. Exploiting the experimental merits of the mouse, we have shown that telomere dysfunction activates p53-mediated cellular growth arrest, senescence and apoptosis to drive progressive atrophy and functional decline in high-turnover tissues.
The broader adverse impact of telomere dysfunction across many tissues including more quiescent systems prompted transcriptomic network analyses to identify common mechanisms operative in haematopoietic stem cells, heart and liver. These unbiased studies revealed profound repression of PGC-1α and PGC-1β and the downstream network in mice null for either telomerase reverse transcriptase (Tert) or telomerase RNA component (Terc) genes. Consistent with PGCs as master regulators of mitochondrial physiology and metabolism, telomere dysfunction is associated with impaired mitochondrial biogenesis and function, decreased gluconeogenesis, cardiomyopathy, and increased reactive oxygen species. We demonstrate that telomere dysfunction activates p53 which in turn binds and represses PGC-1α and PGC-1β promoters, thereby forging a direct link between telomere and mitochondrial biology. This telomere-p53-PGC axis contributes to organ and metabolic failure and to diminishing organismal fitness in the setting of telomere dysfunction.
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It has been a long standing goal to develop molecular biomarkers of biological age. Recent studies demonstrate that powerful epigenetic biomarkers of aging can be defined based on DNA methylation l…
Source: Contributing factors to aging
It has been a long standing goal to develop molecular biomarkers of biological age. Recent studies demonstrate that powerful epigenetic biomarkers of aging can be defined based on DNA methylation levels. For example, the epigenetic clock (PMID: 24138928) is a multivariate age estimation method that applies to sorted cell types (CD4T cells or neurons), complex tissues, and organs and even prenatal brain samples. The epigenetic clock is an attractive biomarker of aging because a) it applies to most human and chimpanzee tissues, b) its accurate measurement of chronological age is unprecedented, c) it is predictive of all-cause mortality even after adjusting for a variety of known risk factors, d) it correlates with measures of cognitive and physical fitness in the elderly, and e) it has been found useful for detecting accelerated aging effects due to obesity, Down syndrome, and HIV infection. Recent genomewide association studies shed light on the underlying biological mechanisms.
For more information go to https://oir.nih.gov/wals
Author: Steve Horvath, Sc.D., Ph.D., University of California, Los Angeles
Permanent link: http://videocast.nih.gov/launch.asp?1…
A study published in Genome Biology in August 2016 supplies the first analysis of the epigenetic clock across different racial groups. By analyzing blood, saliva, and brain samples, epigenetic agin…
Source: Epigenetic Clock Predicts Aging Rates of Racial Groups and Gender
By Samantha Blady
A study published in Genome Biology in August 2016 supplies the first analysis of the epigenetic clock across different racial groups. By analyzing blood, saliva, and brain samples, epigenetic aging rates were compared among seven different racial groups and in men and women. As discovered in the study, rates of epigenetic aging are significantly associated with race and gender.
This study was based on paradoxical tendencies among gender and race. Women tend to have lower mortality rates yet show higher rates of developing disease when compared to men. After adjusting for socioeconomic disadvantage, racial groups show different mortality rates. In the United States, Hispanics have a higher cardio-metabolic risk than Caucasians, yet they also have a higher life expectancy.
The epigenetic clock is based on 353 epigenetic markers and measures the epigenetic age of a certain cell, tissue, or organ. The unprecedented accuracy of the epigenetic clock in measuring chronological age has shown to predict mortality. In a past study, offspring of people who lived over 105 had epigenetically younger blood than others of the same age. The epigenetic clock has been used in research on obesity, HIV, Down’s syndrome, Parkinson’s disease, Alzheimer’s, lung cancer, and lifetime stress. In this study, researchers use the epigenetic clock to analyze relationships between epigenetic age, life expectancy, and cardio-metabolic risk among gender and race.
Blood, saliva, and brain samples were taken from Caucasians, Hispanics, East Asians, Tsimane Amerindians, and people of African ancestry. Epigenetic age was measured using the Ilumina Infinitum 450K. A “universal measure” of epigenetic age acceleration was defined as the difference between epigenetic age values of samples and values predicted from a model for Caucasians. This measure can be defined in most cells and tissues other than sperm.
IEAA (Intrinsic Epigenetic Age Acceleration) is a measure of epigenetic aging that measures intrinsic changes and does not include extracellular changes in blood cell counts. EEAA (Extrinsic Epigenetic Age Acceleration) measures epigenetic aging effects including extracellular changes in blood cell counts and immune-related aging, and is thus a better measure.
After analyzing samples, researchers found that
The Hispanic paradox is echoed in this study as Hispanics have a lower IEAA than Caucasians despite their higher cardio-metabolic risk. As is currently being studied, this contradiction may be due to differences in the Hispanic immune system.
The black-white mortality crossover is echoed in this study as well. Mortality rates are higher in blacks than in whites in younger age but are lower in black men and women aged 85 and older. This observation is paralleled by the finding of a lower EEAA in older African-Americans when compared to Caucasians in this study.
The Tsimane inflammation paradox states that high levels of inflammation in Tsimane are not associated with cardiovascular aging. This finding is consistent with the lower rate of IEAA in Tsimane found in this study. However, a low life expectancy is still reported. A higher EEAA is consistent with the observation that elevated inflammation ultimately depletes T cells and deteriorates the immune system, leading to the low life expectancy of Tsimane.
The sex morbidity-mortality paradox holds that despite higher rates of comorbidity in women, mortality rates are lower in women than in men. Consistent with this paradox, epigenetic aging rates are faster in men than in women. Epigenetic markers of blood, saliva, and brain tissue show higher vulnerability in males of all racial groups.
Overall, this study provides data that shows how epigenetic aging rates differ among racial groups as well as between men and women. This study is the first to directly compare and contrast epigenetic rates of aging among races and ethnicities.
And, although, much of the science of epigenetics still remains to be revealed, this study does provide interesting insight into epidemiological paradoxes.
By Adam B. Dorfman Epigenetic mechanisms is the study of how environmental information is translated into gene expression, which genes are read or not, has been especially crucial to learning how e…
Source: Exercise and gene expression
By Adam B. Dorfman
Epigenetic mechanisms is the study of how environmental information is translated into gene expression, which genes are read or not, has been especially crucial to learning how environmental signals influence the living cell.
There are two important epigenetic mechanism’ that plays critical roles in genetic expression: DNA Methylation and the other is Histone Modification. Both alter the genes expression without changing the gene sequence, and these changes can be inherited. DNA methylation occurs when certain methyl molecules bind to the DNA to switch on or off a particular gene.
Histone modifications is the other epigenetic mechanism and it occurs when an environmental signals, binds to the histone, that covers the DNA, and causes in to detach; enabling sections of your genetic code to be read or not. Again these modifications enable certain regions of DNA to be exposed and over expressed or under expressed.
We know that eating certain diets or being exposed to pollutants and toxins, for instance, can change the expression of our genes. However, surprisingly, until recently, very little research had been pursued on the epigenetic mechanisms from endurance training.
We have all been told we should perform moderate exercise five days a week to maintain and improve our physical conditions and immune systems to reduce the risk of various diseases including obesity and stroke. A new study in epigenetics has found that endurance training can actually change the way genes are read and consequently lead to improvements in metabolism and control over inflammation. The principal investigator of the study was Carl Johan Sundberg of the Karolinska Institutet in Sweden. The paper about the new study was published in Epigenetics.
In a press release, Sundberg said, “It is well-established that being inactive is perilous, and that regular physical activity improves health, quality of life and life expectancy. However, exactly how the positive effects of training are induced in the body has been unclear. This study indicates that epigenetics is an important part in skeletal muscle adaptation to endurance training.” One of the biggest obstacles to accurately study epigenetic changes is to distinguish epigenetic-specific changes from other factors such as behaviors and diet.
To tackle the issue, researchers in Karolinska Institute recruited 23 young men and women for a series of clinical test including muscle biopsy; every one of them engaged in 45 minutes of endurance for four times a week during three months study. Each was required to cycle using only one leg, so everyone was actually a group study. This research helped scientists to analyze DNA methylation process in both legs as an effect of endurance training.
After three months of moderate training, the exercised leg of every volunteer became stronger than the other, confirming that endurance training did give physical improvement, but this was not the objective of the study. Using sophisticated genomic analysis, researchers found that changes within muscle cells’ DNA were a bit more interesting. The exercised legs featured new gene expressions in more than 5,000 sites on the genome of muscle cells. Some of them showed more changes, while others showed less.
These changes were significant, but the unexercised legs did not show the same thing. Many portions of the genome, which can amplify expression of proteins by genes known as enhancers, showed positive effects.
Malene Lindholm, a graduate student at Karolinska Institute who also led the study said, “Many mysteries still remain, though.” There are at least two big questions yet to answer. First is whether or not the genetic changes triggered by endurance training linger if the person quits exercising. The second question is the possibility that different types or intensity of exercise affect gene expression. Despite those unanswered questions, the study did bring new understanding about epigenetics. Ms. Lindholm added, “Through endurance training — a lifestyle change that is easily available for most people and doesn’t cost much money, we can induce changes that affect how we use our genes and, through that, get healthier and more functional muscles that ultimately improve our quality of life.”
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