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Shared genetic influence on frailty and chronic widespread pain: a study from Twins UK 

Shared genetic influence on frailty and chronic widespread pain: a study from Twins UK 

DOI:
https://doi.org/10.1093/ageing/afx122

Abstract

Introduction

frailty is an increased vulnerability to adverse health outcomes, across multiple physiological systems, with both environmental and genetic drivers. The two most commonly used measures are Rockwood’s frailty index (FI) and Fried’s frailty phenotype (FP).

 

Material and methods

The present study included 3626 individuals from the TwinsUK Adult Twin Registry. We used the classical twin model to determine whether FI and FP share the same latent aetiological factors. We also investigated the relationship between frailty and chronic widespread musculoskeletal pain (CWP), another holistic age-related condition with significant clinical impact.

 

Results

 

FP and FI shared underlying genetic and environmental aetiology. CWP was associated with both frailty measures, and health deficits appeared to mediate the relationship between phenotypic frailty and pain. Latent genetic factors underpinning CWP were shared with frailty. While frailty was increased in the twins reporting pain, co-twin regression analysis indicated that the relationship between CWP and frailty is reduced after accounting for shared genetic and environmental factors.

 

Conclusions

 

Both measures of frailty tap the same root causes, thus this work helps unify frailty research. We confirmed a strong association between CWP and frailty, and showed a large and significant shared genetic aetiology of both phenomena. Our findings argue against pain being a significant causative factor in the development of frailty, favouring common causation. This study highlights the need to manage CWP in frail individuals and undertake a Comprehensive Geriatric Assessment in individuals presenting with CWP. Finally, the search for genetic factors underpinning CWP and frailty could be aided by integrating measures of pain and frailty.

Chronic widespread muscoloskeletal pain

Chronic widespread muscoloskeletal pain (CWP) is prevalent in the general population and associated with high health care costs, so understanding the risk factors for chronic pain is important for both those affected and for society. In the present study we investigated the underlying etiological structure of CWP to understand better the association between the major clinical features of fatigue, depression and dihydroepiandrosterone sulphate (DHEAS) using a multivariate twin design.

Methodology/Principle Findings

Data were available in 463 UK female twin pairs including CWP status and information on depression, chronic fatigue and serum DHEAS levels. High to moderate heritabilities for all phenotypes were obtained (42.58% to 74.24%). The highest phenotypic correlation was observed between fatigue and CWP (r = 0.45), and the highest genetic correlation between CWP and fatigue (rg = 0.78). Structural equation modeling revealed the AE Cholesky model to provide the best model of the observed data. In this model, two additive genetic factors could be detected loading heavily on CWP—A2 explaining 40% of the variance and A3 20%. The factor loading heaviest on DHEAS showed only a small loading on the other phenotypes and none on fatigue at all. Furthermore, one distinct non-shared environmental factor loading specifically on CWP—but not on any of the other phenotypes—could be detected suggesting that the association between CWP and the other phenotypes is due only to genetic factors.

Conclusions/Significance

Our results suggest that CWP and its associated features share a genetic predisposition but that they are relatively distinct in their environmental determinants.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0140289

 

Long-term use of proton pump inhibitors is associated with increased microbial product translocation, innate immune activation, and reduced immunologic recovery in patients with chronic HIV-1 infection

Source: Long-term use of proton pump inhibitors is associated with increased microbial product translocation, innate immune activation, and reduced immunologic recovery in patients with chronic HIV-1 infection

Long-term use of proton pump inhibitors is associated with increased microbial product translocation, innate immune activation, and reduced immunologic recovery in patients with chronic HIV-1 infection

ppi.JPG

ppi 2Long-term use of proton pump inhibitors is associated with increased microbial product translocation, innate immune activation, and reduced immunologic recovery in patients with chronic HIV-1 infection

DOI:
https://doi.org/10.1093/cid/cix609

Abstract

Background:

Translocation of microbial products from the damaged gut causes increased immune activation in HIV. Proton pump inhibitors (PPIs) predispose to bacterial overgrowth in the gut. We hypothesized that long-term use of PPIs is associated with greater microbial translocation and immune activation in HIV.

 

Methods:

HIV-infected persons on suppressive antiretroviral therapy (ART), including those receiving long-term PPIs (PPI+ group) or not (PPI–group), were enrolled. We determined CD38+HLA-DR+CD8+(activated) T-cell frequency, and plasma levels of lipopolysaccharide (LPS), LPS binding protein (LBP), soluble CD14 (sCD14), and intestinal fatty acid binding protein (I-FABP).

 

Results:

We recruited 77 HIV-infected participants (37 PPI+ and 40 PPI–), and 20 HIV-uninfected volunteers. PPI+ subjects were older and more likely to have hypertension and receive statins than PPI–. Nadir and enrollment CD4 counts, activated T-cells, and time on ART were similar in both groups. PPI+ group had higher sCD14 (2.15 vs. 1.50 mcg/mL, P <0.01), and LBP (21.78 vs. 18.28 mcg/mL, P=0.02), but lower I-FABP levels (608.5 vs. 2281.7 pg/mL, P=0.05) than PPI–. In multivariate analysis, sCD14 levels remained associated with PPIs. In the year prior to enrollment, PPI+ group lost more CD4 cells than PPI– (-18 vs. 54 cells/mm3, P = 0.03). HIV-infected subjects had higher immune activation and microbial translocation biomarkers than uninfected volunteers.

 

Conclusion:

In HIV, long-term use of PPIs was associated with increased microbial translocation, innate immune activation, and reduced immune reconstitution. Further studies are needed to evaluate the clinical implications of our findings. In the meantime, cautious use of PPIs is advised.

 

https://academic.oup.com/cid/article-abstract/doi/10.1093/cid/cix609/3933542/Long-term-use-of-proton-pump-inhibitors-is?redirectedFrom=fulltext

Prevacid (lansoprazole) is a proton pump inhibitor (PPI) used to treat GERD, heartburn, gastric ulcer, and duodenal ulcer. It works by reducing acid in the stomach. … Esomeprazole is more popular than other proton pump inhibitors. It is available in brand and generic versions.

More Reasons Why Reducing Your Stomach Acid is a Risky Bet

When you take PPIs, which significantly reduce the amount of acid in your stomach, it impairs your ability to properly digest food.

Reduction of acid in your stomach also diminishes your primary defense mechanism for food-borne infections, thereby increasing your risk of food poisoning.

Additionally, if you fail to digest and absorb your food properly, you will not only increase your risk of stomach atrophy but also nearly every other chronic degenerative disease.

These drugs have also been linked to an increased risk of pneumonia, and result in an elevated risk of bone loss. The risk of a bone fracture has been estimated to be over 40 percent higher in patients who use these drugs long-term.

If You’re Already Taking These Drugs, Avoid Stopping Cold Turkey

You should NEVER stop taking proton pump inhibitors cold turkey. You have to wean yourself off them gradually or else you’ll experience a severe rebound of your symptoms, and the problem may end up being worse than before you started taking the medication.

Ideally, you’ll want to get a lower dose than you’re on now, and then gradually decrease your dose. Once you get down to the lowest dose of the proton pump inhibitor, you can start substituting with an over-the-counter H2 blocker like Tagamet, Cimetidine, Zantac, or Raniditine. Then gradually wean off the H2 blocker over the next several weeks.

Natural Treatment Options for Heartburn, GERD and Acid Reflux

As I explained in my recent Acid Reflux video,while you wean yourself off these drugs (if you’re already on one), you’ll want to start implementing a lifestyle modification program that can eliminate this condition once and for all.

These strategies include:

  • Eliminating food triggers — Food allergies can be a problem, so you’ll want to completely eliminate items such as caffeine, alcohol, and all nicotine products.
  • Increasing your body’s natural production of stomach acid — Like I said earlier, acid reflux is not caused by too much acid in your stomach — it’s usually a problem with too little acid. One of the simplest strategies to encourage your body to make sufficient amounts of hydrochloric acid (stomach acid) is to consume enough of the raw material.

One of the simplest, most basic food items that many people neglect is a high quality sea salt (unprocessed salt).

I recommend eliminating processed, regular table salt for a lot of different reasons, all of which I’ve reviewed before. But an unprocessed salt like Himalayan salt — one of the best salts on the planet – will not only provide you with the chloride your body needs to make hydrochloric acid, it also contains over 80 trace minerals your body needs to perform optimally, biochemically.

  • Taking a hydrochloric acid supplement — Another option is to take a betaine hydrochloric supplement, which is available in health food stores without prescription. You’ll want to take as many as you need to get the slightest burning sensation and then decrease by one capsule. This will help your body to better digest your food, and will also help kill the helicobacter and normalize your symptoms.
  • Modifying your diet – Eating large amounts of processed foods and sugars is a surefire way to exacerbate acid reflux as it will upset the bacterial balance in your stomach and intestine.

Instead, you’ll want to eat a lot of vegetables, and high quality, organic, biodynamic, and locally grown foods. You can also supplement with a high quality probiotic or make sure you include fermented foods in your diet. This will help balance your bowel flora, which can help eliminate helicobacter naturally.

  • Optimizing your vitamin D levels — As I’ve mentioned many times in the past, vitamin D is essential, and it’s essential for this condition as well because there’s likely an infectious component causing the problem. Once your vitamin D levels are optimized, you’re also going to optimize your production of 200 antimicrobial peptides that will help your body eradicate any infections that shouldn’t be there.

You’ll want to make sure your vitamin D level is about 60 ng/ml, and I strongly recommend you use LabCorp, which is a high quality testing facility.

As I’ve discussed in many previous articles, you can increase your vitamin D levels through appropriate amounts of sun exposure, or through the use of a safe tanning bed.

If neither of those are available, you can take an oral vitamin D3 supplement. However, whenever you use oral vitamin D, it’s imperative you get tested regularly to make sure you’re not reaching toxic levels.

  • Implementing an exercise routine — Exercise is yet another way to improve your body’s immune system, which is imperative to fight off all kinds of infections.

The New Yorker

Oral sex spreading unstoppable bacteria

Oral sex spreading unstoppable bacteria

By James Gallagher 
KissingImage copyrightGETTY IMAGES

Oral sex is producing dangerous gonorrhoea and a decline in condom use is helping it to spread, the World Health Organization has said.

It warns that if someone contracts gonorrhoea, it is now much harder to treat, and in some cases impossible.

The sexually transmitted infection is rapidly developing resistance to antibiotics.

Experts said the situation was “fairly grim” with few new drugs on the horizon.

About 78 million people pick up the STI each year and it can cause infertility.

The World Health Organization analysed data from 77 countries which showed gonorrhoea’s resistance to antibiotics was widespread.

Dr Teodora Wi, from the WHO, said there had even been three cases – in Japan, France and Spain – where the infection was completely untreatable.

She said: “Gonorrhoea is a very smart bug, every time you introduce a new class of antibiotics to treat gonorrhoea, the bug becomes resistant.”

Worryingly, the vast majority of gonorrhoea infections are in poor countries where resistance is harder to detect.

“These cases may just be the tip of the iceberg,” she added.

Throat infection

Gonorrhoea can infect the genitals, rectum and throat, but it is the last that is most concerning health officials.

Dr Wi said antibiotics could lead to bacteria in the back of the throat, including relatives of gonorrhoea, developing resistance.

She said: “When you use antibiotics to treat infections like a normal sore throat, this mixes with the Neisseria species in your throat and this results in resistance.”

Thrusting gonorrhoea bacteria into this environment through oral sex can lead to super-gonorrhoea.

“In the US, resistance [to an antibiotic] came from men having sex with men because of pharyngeal infection,” she added.

A decline in condom use, which had soared because of fears of HIV/Aids, is thought to help the infection spread.

What is gonorrhoea?

GonorrhoeaImage copyrightCAVALLINI JAMES/SCIENCE PHOTO LIBRARY

The disease is caused by the bacterium called Neisseria gonorrhoea.

The infection is spread by unprotected vaginal, oral and anal sex.

Symptoms can include a thick green or yellow discharge from sexual organs, pain when urinating and bleeding between periods.

However, of those infected, about one in 10 heterosexual men and more than three-quarters of women, and gay men, have no easily recognisable symptoms.

Untreated infection can lead to infertility, pelvic inflammatory disease and can be passed on to a child during pregnancy.

The World Health Organization is calling on countries to monitor the spread of resistant gonorrhoea and to invest in new drugs.

Dr Manica Balasegaram, from the Global Antibiotic Research and Development Partnership, said: “The situation is fairly grim.

“There are only three drug candidates in the entire drug [development] pipeline and no guarantee any will make it out.”

But ultimately, the WHO said vaccines would be needed to stop gonorrhoea.

Prof Richard Stabler, from the London School of Hygiene & Tropical Medicine, said: “Ever since the introduction of penicillin, hailed as a reliable and quick cure, gonorrhoea has developed resistance to all therapeutic antibiotics.

“In the past 15 years therapy has had to change three times following increasing rates of resistance worldwide.

“We are now at a point where we are using the drugs of last resort, but there are worrying signs as treatment failure due to resistant strains has been documented.”

Follow James on Twitter.

Is oral sex more common now? By BBC World online

It’s hard to say if more people around the world are having more oral sex than they used to, as there isn’t much reliable global data available.

Data from the UK and US show it’s very common, and has been for years, including among teenagers.

The UK’s first National Survey of Sexual Attitudes and Lifestyles, carried out in 1990-1991, found 69.7% of men and 65.6% of women had given oral sex to, or received it from, a partner of the opposite sex in the previous year.

By the time of the second survey during 1999-2001, this had increased to 77.9% for men and 76.8% for women, but hasn’t changed much since.

A national survey in the US, meanwhile, has found about two-thirds of 15-24 year olds have ever had oral sex.

Dr Mark Lawton from the British Association for Sexual Health and HIV said people with gonorrhoea in the throat would be unlikely to realise it and thus be more likely to pass it on via oral sex.

He recognises that while condoms would reduce the risk of transmission, many people wouldn’t want to use them.

“My message would be to get tested so at least if you’ve got it you know about it,” Dr Lawton said.

http://www.bbc.com/news/health-40520125

They said it’s esophageal cancer, inoperable and we’re calling hospice

Does the fact that someone has a fast or slow metabolism contribute to thyroid hormones?

Does the fact that someone has a fast or slow metabolism contribute to thyroid hormones?

Connie b. Dellobuono
Connie b. Dellobuono, Bay area Senior Care at Motherhealth (2000-present)

Hypothyroidism and slow metabolism are related. The pituitary gland in the brain is responsible for sleep, food cravings, stress and sex/thyroid hormones. It regulates thyroid hormones.

From:

https://www.ncbi.nlm.nih.gov/pmc…

Thyroid hormone (TH) is required for normal development as well as regulating metabolism in the adult. The thyroid hormone receptor (TR) isoforms, α and β, are differentially expressed in tissues and have distinct roles in TH signaling. Local activation of thyroxine (T4), to the active form, triiodothyronine (T3), by 5′-deiodinase type 2 (D2) is a key mechanism of TH regulation of metabolism. D2 is expressed in the hypothalamus, white fat, brown adipose tissue (BAT), and skeletal muscle and is required for adaptive thermogenesis. The thyroid gland is regulated by thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH). In addition to TRH/TSH regulation by TH feedback, there is central modulation by nutritional signals, such as leptin, as well as peptides regulating appetite. The nutrient status of the cell provides feedback on TH signaling pathways through epigentic modification of histones. Integration of TH signaling with the adrenergic nervous system occurs peripherally, in liver, white fat, and BAT, but also centrally, in the hypothalamus. TR regulates cholesterol and carbohydrate metabolism through direct actions on gene expression as well as cross-talk with other nuclear receptors, including peroxisome proliferator-activated receptor (PPAR), liver X receptor (LXR), and bile acid signaling pathways. TH modulates hepatic insulin sensitivity, especially important for the suppression of hepatic gluconeogenesis.

A. Hypothalamic-Pituitary-Thyroid Axis

TH is secreted from the thyroid gland under the regulation of the hypothalamic-pituitary axis (Figure 1). TRH, secreted from the hypothalamus, acts upon the pituitary gland, binding to G protein-coupled TRH receptors on the thyrotrope, resulting in an increase in intracellular cAMP, and subsequent thyrotropin (TSH) release (113). Hormone signals that have modulatory effects on TSH secretion include dopamine (219), somatostatin (250), and leptin (223), which function as a point of central regulation of thyroid hormone release (93). TSH secretion, and its sensitivity to TRH stimulation, is affected by renal failure, starvation, sleep deprivation, depression, and hormones, including cortisol, growth hormone, and sex steroids (89, 128).

The importance of the adrenergic nervous system in central TRH/TSH regulation is being increasingly recognized (163). The combination of central nutritional and hormonal signals, including leptin, adrenergic signaling, and cortisol, integrate information regarding overall nutritional status, circadian rhythms, as well as acute stress, to modulate thyroid hormone production (93, 117). A central regulator of circadian rhythms, the RevErbAα/RevErbAβ nuclear receptors, are activated by BMAL-1, which then suppresses BMAL-1 transcription (74). RevErbAα is transcribed from the strand opposite the TRα gene and binds heme.

TSH binds to a G protein-coupled TSH receptor on the thyroid follicular cell, stimulating the production and release of TH. T4, a prohormone, is the primary secretory product of the thyroid gland, which utilizes MCT8 for secretion (59). Local conversion of T4 to T3

, by D2, provides negative feedback at the level of both thyrotrophs in the pituitary and tanycytes in the hypothalamus (79, 90, 149). This results in reduction in TRH and TSH secretion in response to adequate tissue levels of TH. Polymorphisms in the D2 gene have been associated with interindividual variation in the TSH-free T4 “set point” (116).

. Ashwaganda: This supplement may increase both thyroxine (T4) and its more potent counterpart, active thyroid hormone (T3). Ashwaganda appears to boost thyroid function without influencing the release of the TSH, indicating that it works directly on the thyroid gland and other body tissues. This is good news, since thyroid problems most often occur within the thyroid gland itself, or in the conversion of T4 into T3 in tissues outside the thyroid gland. Take 750-1,000 mg twice a day. Ashwaganda is my favourite choice for supporting the thyroid when stress is also a concern.

2. L-Tyrosine: The amino acid tyrosine is necessary for the production of thyroid hormone in the body. It takes four weeks to reach full effectiveness, so starting this at the beginning of a weight-loss program is a good idea. Seeing as tyrosine increases the production of both dopamine and thyroid hormone, it could give you just the boost you need to push past your plateau. The recommended dose is 1,000 mg on rising, before breakfast. Do not take this supplement if you have high blood pressure.

3. Coconut oil: Not all fats are created equal and by the same token, not all fats are unhealthy. One way to boost a sluggish thyroid is to consume non-hydrogenated coconut oil. This is a medium-chain saturated fat that promotes healthy weight loss and is thought to naturally stimulate the thyroid. Unlike olive oil, it has a high heat tolerance so you can actually use it to cook your food, or include a tablespoon in your morning smoothies for a summer-fresh taste.

High HDL less heart attacks

Why Is Cholesterol Important?

Your blood cholesterol level has a lot to do with your chances of getting heart disease. High blood cholesterol is one of the major risk factors for heart disease. A risk factor is a condition that increases your chance of getting a disease. In fact, the higher your blood cholesterol level, the greater your risk for developing heart disease or having a heart attack. Heart disease is the number one killer of women and men in the United States. Each year, more than a million Americans have heart attacks, and about a half million people die from heart disease.

How Does Cholesterol Cause Heart Disease?

When there is too much cholesterol (a fat-like substance) in your blood, it builds up in the walls of your arteries. Over time, this buildup causes “hardening of the arteries” so that arteries become narrowed and blood flow to the heart is slowed down or blocked. The blood carries oxygen to the heart, and if enough blood and oxygen cannot reach your heart, you may suffer chest pain. If the blood supply to a portion of the heart is completely cut off by a blockage, the result is a heart attack.

High blood cholesterol itself does not cause symptoms, so many people are unaware that their cholesterol level is too high. It is important to find out what your cholesterol numbers are because lowering cholesterol levels that are too high lessens the risk for developing heart disease and reduces the chance of a heart attack or dying of heart disease, even if you already have it. Cholesterol lowering is important for everyone–younger, middle age, and older adults; women and men; and people with or without heart disease.

What Do Your Cholesterol Numbers Mean?

Everyone age 20 and older should have their cholesterol measured at least once every 5 years. It is best to have a blood test called a “lipoprotein profile” to find out your cholesterol numbers. This blood test is done after a 9- to 12-hour fast and gives information about your:

  • Total cholesterol
  • LDL (bad) cholesterol–the main source of cholesterol buildup and blockage in the arteries
  • HDL (good) cholesterol–helps keep cholesterol from building up in the arteries
  • Triglycerides–another form of fat in your blood

If it is not possible to get a lipoprotein profile done, knowing your total cholesterol and HDL cholesterol can give you a general idea about your cholesterol levels. If your total cholesterol is 200 mg/dL* or more or if your HDL is less than 40 mg/dL, you will need to have a lipoprotein profile done. See how your cholesterol numbers compare to the tables below.

Total Cholesterol Level Category
Less than 200 mg/dL Desirable
200-239 mg/dL Borderline High
240 mg/dL and above High

* Cholesterol levels are measured in milligrams (mg) of cholesterol per deciliter (dL) of blood.

LDL Cholesterol Level LDL-Cholesterol Category
Less than 100 mg/dL Optimal
100-129 mg/dL Near optimal/above optimal
130-159 mg/dL Borderline high
160-189 mg/dL High
190 mg/dL and above Very high

HDL (good) cholesterol protects against heart disease, so for HDL, higher numbers are better. A level less than 40 mg/dL is low and is considered a major risk factor because it increases your risk for developing heart disease. HDL levels of 60 mg/dL or more help to lower your risk for heart disease.

Triglycerides can also raise heart disease risk. Levels that are borderline high (150-199 mg/dL) or high (200 mg/dL or more) may need treatment in some people.

What Affects Cholesterol Levels?

A variety of things can affect cholesterol levels. These are things you can do something about:

  • Diet. Saturated fat and cholesterol in the food you eat make your blood cholesterol level go up. Saturated fat is the main culprit, but cholesterol in foods also matters. Reducing the amount of saturated fat and cholesterol in your diet helps lower your blood cholesterol level.
  • Weight. Being overweight is a risk factor for heart disease. It also tends to increase your cholesterol. Losing weight can help lower your LDL and total cholesterol levels, as well as raise your HDL and lower your triglyceride levels.
  • Physical Activity. Not being physically active is a risk factor for heart disease. Regular physical activity can help lower LDL (bad) cholesterol and raise HDL (good) cholesterol levels. It also helps you lose weight. You should try to be physically active for 30 minutes on most, if not all, days.

Things you cannot do anything about also can affect cholesterol levels. These include:

  • Age and Gender. As women and men get older, their cholesterol levels rise. Before the age of menopause, women have lower total cholesterol levels than men of the same age. After the age of menopause, women’s LDL levels tend to rise.
  • Heredity. Your genes partly determine how much cholesterol your body makes. High blood cholesterol can run in families.

What Is Your Risk of Developing Heart Disease or Having a Heart Attack?

In general, the higher your LDL level and the more risk factors you have (other than LDL), the greater your chances of developing heart disease or having a heart attack. Some people are at high risk for a heart attack because they already have heart disease. Other people are at high risk for developing heart disease because they have diabetes (which is a strong risk factor) or a combination of risk factors for heart disease. Follow these steps to find out your risk for developing heart disease.

Step 1: Check the table below to see how many of the listed risk factors you have; these are the risk factors that affect your LDL goal.

Major Risk Factors That Affect Your LDL Goal

  • Cigarette smoking
  • High blood pressure (140/90 mmHg or higher or on blood pressure medication)
  • Low HDL cholesterol (less than 40 mg/dL)*
  • Family history of early heart disease (heart disease in father or brother before age 55; heart disease in mother or sister before age 65)
  • Age (men 45 years or older; women 55 years or older)

* If your HDL cholesterol is 60 mg/dL or higher, subtract 1 from your total count.

Even though obesity and physical inactivity are not counted in this list, they are conditions that need to be corrected.

Step 2: How many major risk factors do you have? If you have 2 or more risk factors in the table above, use the attached risk scoring tables (which include your cholesterol levels) to find your risk score. Risk score refers to the chance of having a heart attack in the next 10 years, given as a percentage. My risk score is ________%.

Step 3: Use your medical history, number of risk factors, and risk score to find your risk of developing heart disease or having a heart attack in the table below.

If You Have You Are in Category
Heart disease, diabetes, or risk score more than 20%* I. High Risk
2 or more risk factors and risk score 10-20% II. Next Highest Risk
2 or more risk factors and risk score less than 10% III. Moderate Risk
0 or 1 risk factor IV. Low-to-Moderate Risk

* Means that more than 20 of 100 people in this category will have a heart attack within 10 years.

My risk category is ______________________.

Health Care News 7-7-2017

Price appoints Georgia health commissioner Fitzgerald to head CDC 

HHS Secretary Tom Price on Friday named Georgia’s top public health official, Dr. Brenda Fitzgerald, the next director of the Centers for Disease Control and Prevention.  READ MORE

Healthcare hiring soars in June with 36,500 new jobs

The healthcare industry added 36,500 jobs in June, marking the strongest month so far in 2017 for job creation in the sector. The healthcare hiring machine continued to churn even as Senate Republicans mull over plans to repeal and replace the Affordable Care Act.  READ MORE
MEDICAL DEVICES & EQUIPMENT

Houston to Goop: We’ve got a problem

Gwyneth Paltrow, whose Goop website has a blog post rhapsodizing about a line of “wearable stickers thar promote healing,” got fact-checked by NASA.  READ MORE
PHARMACEUTICALS

Wide variation in opioid prescribing among U.S. counties, report finds

Despite an overall decline in recent years in the amount of opioids prescribed nationally, large disparities have been found among counties due largely to inconsistencies in prescribing practices, a new government report found.  READ MORE

Painkiller maker stops sales at FDA request because of abuse

The maker of opioid painkiller Opana ER is pulling the drug off the market at the request of federal regulators because it’s being abused.  READ MORE
CLINICAL PRACTICE

S.C. hospital to pay $1.3 million for not properly treating emergency psych patients

AnMed Health has agreed to pay the largest-ever settlement in a case brought under the federal law requiring hospitals to stabilize and treat patients in emergency situations.  READ MORE

NQF launches opioid stewardship initiative

Looking to play a larger role the fight against opioid abuse, the National Quality Forum on Wednesdaylaunched a new stewardship program to lower rates of overprescribing among healthcare providers and curb patient addiction risks.  READ MORE
SPOTLIGHT

News from other sources…

The VA and Air Force team up for telehealth, generic drug manufacturers challenge a price-gouging law, and scientists modulate sleep brainwaves to control memory.  READ MORE
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How eClinicalWorks’ comprehensive EHR system provided more efficient and streamlined workflows to this urgent care center, from enrollment to the point of care and beyond.  READ MORE

Controlling Costs in a New Age of Workforce Management

Learn how traditional scheduling software is being replaced with mobile real-time solutions that prepare hospitals for a new age in workforce management.  READ MORE

Turnover to Triumph 

Like most providers, you recognize turnover as a growing problem. Read how B.E. Smith researched and developed strategies to combat turnover in today’s healthcare industry.  READ MORE

Schizophrenia Meta-Analysis Reveals Role for Rare, Damaging Variants

Schizophrenia Meta-Analysis Reveals Role for Rare, Damaging Variants

NEW YORK (GenomeWeb) – A new meta-analysis suggests that rare, damaging mutations may contribute to schizophrenia, both alongside and in the absence of intellectual disability.

As they reported in Nature Genetics today, researchers from the Wellcome Trust Sanger Institute, Cardiff University, the Royal Edinburgh Hospital, and elsewhere brought together exome sequences, de novo mutation profiles, and copy number variant patterns for thousands of cases and controls from three existing cohorts. Together, these data led them to nearly 3,500 genes that are typically intolerant to change, but prone to rare loss-of-function mutations in schizophrenia.

“While the identification of individual genes remains difficult at current sample sizes, we show that the burden of damaging de novo mutations and rare [single nucleotide variants] and CNVs in schizophrenia is not scattered across the genome but is primarily concentrated in 3,488 genes intolerant of loss-of-function variants,” first author Tarjinder Singh and his co-authors wrote.

Singh was a graduate student in Jeffrey Barrett’s lab at the Sanger Institute when the study was done and is currently a postdoctoral researcher with Mark Daly’s group at the Broad Institute.

When the team looked at the types of rare variants identified in schizophrenia in relation to those described in autism spectrum disorder (ASD) and other neurodevelopmental conditions, it found that many of the same genes were affected by loss-of-function mutations across the conditions. In individuals affected by both schizophrenia and intellectual disability, the rare, damaging variants tended to cluster in genes with neurodevelopmental roles, though rare variants also marked other schizophrenia cases.

“Our study supports the observation that genetic risk factors for psychiatric and neurodevelopmental disorders do not follow clear diagnostic boundaries,” the authors explained. “Coding variants disrupting the same genes and, quite possibly, the same biological processes increase risk for a range of phenotypic manifestations.”

Prior research has uncovered some of the pathway changes associated with schizophrenia, the team noted, along with some of the genes that tend to be affected by mutations ranging from common to rare. But the contribution of rare variants across schizophrenia cases — and potential ties between these rare variants and those involved in other conditions — are less fully delineated.

For their analyses, the researchers focused on rare variants identified in exome sequences for 4,133 individuals with schizophrenia and almost 9,300 population-matched controls, along with de novo mutations detected in 1,077 trios of children with schizophrenia and their parents. To that, they added array-based CNV profiles for another 6,882 individuals with schizophrenia and 11,255 individuals without.

After identifying 3,488 genes that appeared to be intolerant to loss-of-function mutations in psychiatric disease-free cases in the ExAC database, the team found an over-representation of rare, damaging changes to this gene set in the schizophrenia cases.

“Although this result is consistent with observations in ASD and severe developmental disorders,” the authors noted, “the absolute effect size is smaller.”

In 279 schizophrenia cases that also involved intellectual disability — found from a subset of 2,971 individuals with schizophrenia who had documented cognitive phenotypes — the researchers saw an apparent uptick in rare, damaging mutations in the loss-of-function intolerant gene set. That was particularly true for rare, damaging variants falling in genes previously implicated in developmental conditions, they reported.

Nevertheless, rare, damaging variants in the genes that are normally adverse to loss-of-function alterations also turned up in individuals with schizophrenia who did not have intellectual disability or those with indeterminate cognitive status.

“Together, these results demonstrate that rare variants have different contributions to schizophrenia risk depending on the degree of cognitive impairment,” the authors wrote. “Notably, these variants do not simply confer risk for a small subset of patients but contribute to disease pathogenesis more broadly.”

https://www.genomeweb.com/sequencing/schizophrenia-meta-analysis-reveals-role-rare-damaging-variants?utm_source=Sailthru&utm_medium=email&utm_campaign=Scan%20Fri%202017-07-07&utm_term=The%20Scan%20Bulletin

Are dog size and intelligence linked?

dog size.JPG

Classification Obey Heavy Weight Avg Low Weight Avg
Lowest Degree of Working/Obedience Intelligence 71 56
Fair Working/Obedience Intelligence 0.30 43 30
Average Working/Obedience Intelligence 0.50 60 44
Above Average Working Dogs 0.70 55 40
Excellent Working Dogs 0.85 53 41
Brightest Dogs 0.95 66 49

https://data.world/sharon/what-is-the-correlation-between-dog-size-and-intelligence/insights

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