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It’s Not Just What You Eat, It’s What’s Eating You

It’s Not Just What You Eat, It’s What’s Eating You

Source: Florida Atlantic University.

New study provides clues for a longer lifespan.

Restricting how much you eat without starving has been shown to robustly extend lifespan in more than 20 species of animals including primates. How this works is still unclear.

In a new study published in PLOS Genetics, neuroscientists from Florida Atlantic University show that it’s not just what or how much you eat that matters.

Smelling food in addition to consuming calories could influence the aging process.

And, what’s “eating” you or more specifically your cells may provide clues to healthy aging.

Using a tiny worm called C. elegans, these researchers are the first to demonstrate how autophagy, a garbage disposal-like process where cells “eat” debris they produce through basic metabolism, combined with food absorption through the gastrointestinal (GI) tract and food smell through olfactory neurons impact the aging process mainly by diet restriction.

This study reveals that autophagy is an essential component in a neuroendocrine pathway that allows sensory neurons and nutrient levels to work together to influence lifespan.

It also reduces the insulin growth factor signaling pathway, part of a complex system that cells use to communicate with their physiologic environment.

These new findings could help to better understand the human aging process, extend lifespan as well as develop treatments for diseases like obesity.

“We found that autophagy works in both the brain and the intestine to mediate communication between the GI tract and the brain and in turn to the GI tract. We were specifically looking for how this interaction influences aging,” said Kailiang Jia, Ph.D., corresponding author of the study, associate professor of biological sciences in FAU’s Charles E. Schmidt College of Science, and a member of FAU’s Brain Institute.

Jia and the study’s first author Justin Minnerly, Ph.D., who graduated from FAU in 2017, suspect that both the calorie of food or perhaps the combination of the food together with the smell of the food influences the aging process through diet restriction. Olfaction is simply how a neuron detects the smell of a food.

“When people are on a diet they might say something like ‘I didn’t eat a lot of food,’” said Jia. “Except it’s not only the calories that count, but also the smell of food that can influence the function of the brain and the GI tract.”

Prior research on fruit flies confirms this notion. When they were on restricted diets, the fruit flies lived longer. But when they were allowed to smell the food while on this restricted diet their life expectancy was not as dramatic as it was without smelling the food.

“If you want to extend the lifespan of any animal, after limiting their diet, you have to have functional autophagy in this animal otherwise you won’t see this lifespan extending effect,” said Jia. “This is especially true for autophagy in the olfactory neuron since it appears that it mediates this effect for the smell of food. Autophagy in the GI tract also is required for this lifespan extension mechanism, which indicates that the nutrients we absorb into the GI tract also regulates autophagy and in turn controls the aging process.”

Image shows 2 green worms.

There are a number of hypotheses as to why restricting calories extends lifespan and most physicians and scientists today believe that diet or caloric restrictions adjust the metabolism and physiology of the human body on a cellular level.

“We now know which molecules are responsible for the aging process and autophagy is one of these processes,” said Jia. “So potentially, autophagy in the olfactory neuron, at least in the worm, can sense the food smell and then secrete neuron signals, which in turn influence the aging process.”

Now that Jia and the research team know that autophagy is involved in the aging process they have to figure out which proteins regulate this process. They also plan to establish a protocol to screen a compound library to look for autophagy inhibitors and activators.

They hope ultimately to develop treatments for obesity and other diseases like cancer and neurodegenerative diseases.

“Autophagy can be activated and enhanced when you restrict calories and we can actually see the autophagy process activated through caloric restriction,” said Jia. “With disease, when you decrease autophagy the disease process is exacerbated and when you increase it you get the opposite effect.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The study is supported by the National Institutes of Health (NIH) (grant number 1R15HD080497-01) and the Ellison Medical Foundation Aging Scholarship awarded to Jia.

Source: Gisele Galoustian – Florida Atlantic University
Image Source: NeuroscienceNews.com image is credited to Florida Atlantic University.
Original Research: Full open access research for “The cell non-autonomous function of ATG-18 is essential for neuroendocrine regulation of Caenorhabditis elegans lifespan” by Justin Minnerly, Jiuli Zhang, Thomas Parker, Tiffany Kaul, and Kailiang Jia in PLOS Genetics. Published online May 30 2017 doi:10.1371/journal.pgen.1006764

Florida Atlantic University “It’s Not Just What You Eat, It’s What’s Eating You.” NeuroscienceNews. NeuroscienceNews, 2 August 2017.
<http://neurosciencenews.com/worm-longevity-eating-7228/&gt;.

Abstract

The cell non-autonomous function of ATG-18 is essential for neuroendocrine regulation of Caenorhabditis elegans lifespan

Dietary restriction (DR) and reduced insulin growth factor (IGF) signaling extend lifespan in Caenorhabditis elegans and other eukaryotic organisms. Autophagy, an evolutionarily conserved lysosomal degradation pathway, has emerged as a central pathway regulated by various longevity signals including DR and IGF signaling in promoting longevity in a variety of eukaryotic organisms.

However, the mechanism remains unclear. Here we show that the autophagy protein ATG-18 acts cell non-autonomously in neuronal and intestinal tissues to maintain C. elegans wildtype lifespan and to respond to DR and IGF-mediated longevity signaling.

Moreover, ATG-18 activity in chemosensory neurons that are involved in food detection sufficiently mediates the effect of these longevity pathways. Additionally, ATG-18-mediated cell non-autonomous signaling depends on the release of neurotransmitters and neuropeptides.

Interestingly, our data suggest that neuronal and intestinal ATG-18 acts in parallel and converges on unidentified neurons that secrete neuropeptides to regulate C. elegans lifespan through the transcription factor DAF-16/FOXO in response to reduced IGF signaling.

“The cell non-autonomous function of ATG-18 is essential for neuroendocrine regulation of Caenorhabditis elegans lifespan” by Justin Minnerly, Jiuli Zhang, Thomas Parker, Tiffany Kaul, and Kailiang Jia in PLOS Genetics. Published online May 30 2017 doi:10.1371/journal.pgen.1006764

How to end the obesity epidemic?

  • Fed Up,” narrated by Katie Couric, investigates the misinformation touted by the processed food industry, and how these fallacies have created (and continue to drive) the global obesity epidemic
  • One widely held belief is that all you have to do to normalize your weight is to eat less and exercise more. But just as the fitness craze exploded across the U.S., so did our waistlines. Between 1980 and 2000, memberships to fitness clubs doubled, and so did the national obesity rate
  • The conventional low-fat, high-carb recommendation created the obesity epidemic. If you struggle with excess weight, stop counting calories, eat real food, increase your dietary fat intake and reduce your net carbs

By Dr. Mercola

“Fed Up,” narrated by Katie Couric, investigates the misinformation touted by the processed food industry, and how these fallacies have created (and continue to drive) the global obesity epidemic. This includes the lies you’ve been told about calories and diet versus exercise, government subsidies that support the junk food industry, and government policies that prop up the processed food industry even though they’re harming public health.

As noted by Couric, obesity has been a topic of discussion for the last 30 years. Entire industries have grown around it. All sorts of diets and exercise programs have promised lasting results. Yet the problem has continued to balloon, seemingly out of control. In 2014, the obesity rate among American adults hit 38 percent — a 3 percent increase from 2012.1 Researchers looking at obesity rates around the world note that for the first time in history, obese people now outnumber those who are underweight.2,3,4,5

One in 5 American deaths is now associated with obesity,6 and the younger you are, the greater obesity’s influence on your mortality. Considering one-third of American children between the ages of 2 and 19 are now overweight or obese, chronic disease and mortality rates will likely climb dramatically in coming decades.

The Energy Balance Myth

While the struggles of obesity were initially featured mostly in magazines and on talk shows, today, obesity has become a genre of entertainment, with reality TV programs detailing the lives and weight loss struggles of the obese. “We get new solutions every day,” Couric says. “Everything in the grocery store is made with less fat and fewer calories, yet our kids keep getting bigger and sicker.”

Could there be a link between the ever-growing obesity problem and the governments dietary guidelines? the film asks. “That got me thinking. What if the solutions weren’t really solutions at all?”Couric says. “What if they were actually making things worse? What if our approach toward this epidemic has been dead wrong?”

One of the most widely held beliefs is that all you have to do to normalize your weight is to eat less and exercise more. This energy balance, “calories in, calories out” theory, originated with a simple observation involving mice, in 1953. Up until that point, exercise was strongly discouraged. Doctors warned it would cause heart attacks and lower sex drive.

In his laboratory, the late nutritionist Jean Mayer noticed that fat mice ate the same amount of food as skinny mice. The difference was their activity level. The fat mice were not nearly as active as the thin ones. The logical conclusion Mayer drew from this observation was that lack of physical activity must be the cause of weight gain. “His finding sparked a fitness revolution,” Couric notes.

Ironically, just as the fitness craze exploded across the U.S., so did our waistlines! Between 1980 and 2000, memberships to fitness clubs doubled. In that same span of time, the national obesity rate also doubled. One decade later, 2 in 3 Americans were either overweight or obese. The same parallel trend is seen in other parts of the world.

So, how is it that the more people exercise, the worse the obesity rates get? In recent years, we’ve also seen a trend of obese toddlers. Seeing how a 6-month-old child cannot exercise (or diet, for that matter), how does one explain this phenomenon? Clearly, something doesn’t add up.

Why Calorie Counting Doesn’t Work

As noted by several obesity experts in this film, calorie counting does not work. The entire premise that losing weight is a matter of expending more calories than you put in is flawed in more than one way. First of all, the average person simply cannot exercise long and hard enough to burn up the calories they eat in a given day.

To offset a single 20-ounce soda, a child would have to bike ride for an hour and 15 minutes. To burn off a single chocolate chip cookie, you’re looking at a 20-minute jog; a medium french fry would require just over an hour and 10 minutes of swimming.

There’s simply not enough time in the day to burn off the calories consumed, let alone burn more than you’re putting in. Modern research has also shown that all calories are not made equal. Some calories are burned far easier than others, and some will stubbornly lodge themselves on your frame in the form of fat. A crucial point that must be understood is that the metabolic effects of nutrients (fats, carbs and proteins) differ.

As an example, when you eat 160 calories’ worth of almonds, the fiber in the nuts slows down absorption, resulting in a slower blood sugar rise and lower insulin release. Contrast that to a glass of soda. Because it has no fiber and contains processed fructose, your liver gets a large, sudden hit of sugar, causing a dramatic rise in blood sugar and insulin, which is a very potent fat regulator.

Moreover, because fructose is metabolized entirely by your liver, nearly all of those calories are turned directly into body fat, opposed to being used up as fuel for energy. After fructose, other sugars and grains are among the most excessively consumed foods that promote weight gain and chronic disease.

Yet the food industry, and especially the soda industry, keeps telling us that “all calories count, no matter where they come from.” This simply isn’t true, and the science is quite clear on this.

Yet another part of the problem is a fundamental error in the understanding of the law of thermodynamics. Energy is actually used up in making nutrients available in your body. In addition to that, your body also self-regulates the amount of activity you engage in, based on the available energy. Zoe Harcombe’s book, “The Obesity Epidemic,” explains this beautifully.

Food Industry Lies

Obesity is rooted in inappropriate food choices, not lack of exercise. Unfortunately, the food industry has been permitted to confuse the issue by shifting the focus and discussion to exercise, completely omitting the importance of your specific food choices.

As you can clearly see in this film, every single family struggling with obesity is eating precisely what they shouldn’t — lots of cereal, for example, and low-fat or “diet” foods — thinking they’re doing the right thing. Despite following conventional advice, they just keep getting fatter and, no wonder, because conventional advice is in fact dead wrong.

Whole grains are supposed to help you lose weight. They don’t. Whole grains are just as fattening as other grains. Grains and starches are rapidly converted into glucose (sugar) in your digestive tract, and are among the foods you should eat as little of as possible if you’re struggling with excess weight. Low-fat foods are also supposed to help you lose weight.

They don’t. Low-fat foods are typically very high in sugar, and sugar is what makes you pack on excess weight, and prevents your body from burning body fat. Additionally, nearly all grains, especially whole grains, are high in lectins, which can have very serious adverse metabolic consequences by increasing inflammation and autoimmune conditions.

The ramifications of this high-sugar, low-fat trend are dire. We are now seeing heart attacks and strokes in children as young as 8. We’re seeing 30-year-olds on kidney dialysis after suffering kidney failure. According to the film, the number of cases of type 2 diabetesamong American adolescents in 1980 was zero. Indeed, type 2 diabetes was referred to as adult-onset diabetes and was historically unheard of in children and young adults. In 2010, nearly 57,640 American adolescents were diagnosed with type 2 diabetes.

Why Low-Fat ‘Diet’ Foods Make You Gain Weight

What happened in the 1980s, food-wise to precipitate this rapid increase in type 2 diabetes and obesity? As detailed in the film, the 1977 McGovern Report,7 which warned the U.S. was facing an avalanche of obesity and ill health thanks to excessive consumption of animal fats, cholesterol and sugar, was firmly rejected by food industry lobbyists. And, while the first-ever dietary goals for the U.S. were published, the recommendation to reduce consumption of specific foods were omitted.

Instead, Americans were encouraged to buy leaner meats and foods lower in saturated fats and cholesterol. This spawned a whole new industry of low-fat, “diet” foods. Alas, as fat was removed, sugar was added in. Between 1977 and 2000, Americans doubled their daily sugar intake, and sugar — not saturated fat and cholesterol — is the primary culprit causing weight gain. Eating fat does not make you fat. Eating sugar does.

According to Dr. Robert Lustig, who is featured in the film, sugar is a chronic, dose-dependent liver toxin. Today, of the 600,000 food items sold in grocery stores, 80 percent of them contain added sugar. So, far from being relegated to sweet desserts, most everything you eat is loaded with sugar if you’re eating processed foods. A jar of spaghetti sauce, for example, contains 5.5 teaspoons more sugar than a snack-sized pack of M&Ms.

Most all commercial yogurts are also notoriously high in sugar, with some containing upward of 35 grams of sugar in a single-serving — 10 grams over the daily recommended limit for good health.

Sugar also hides under several dozen different names. Some food manufacturers will hide their sugar content even more by listing several different kinds of sugar separately on the list of ingredients. Since ingredients are listed in order of its ratio to the total amount of a serving, this little trick makes it look as though there’s far less sugar in it. Were they to lump all the different sugars together, it might have had to be listed as the No. 1 ingredient.

Many also make the mistake of switching to artificially sweetened “diet” foods and drinks to avoid unnecessary calories. Alas, research has conclusively shown artificial sweeteners add to the obesity problem, and perhaps more so than regular sugar.

Food Addiction Is Real

The film also addresses the very real issue of food addiction, and sugar addiction in particular. Studies have demonstrated that sugar is eight times more addictive than cocaine. The biological mechanisms behind food addiction were clearly spelled out in a previous interview with Dr. Pamela Peeke, author of “The Hunger Fix.”

When babies are fed high-sugar foods from day one, they rapidly grow addicted to sugar. Few parents would consider doing this on purpose. They simply fail to realize that many infant formulas are absolutely loaded with sugar. They’re basically feeding their infant the equivalent of soda, several times a day.

Many also give their children fruit juice rather than water, thinking it’s a healthy drink loaded with vitamins, again failing to realize a glass of fruit juice has as much sugar as a glass of soda. And, as noted in the film, the notion that all you need is the willpower to resist simply doesn’t work when you’re addicted.

The other variable that is rarely if ever addressed in these discussions is the timing of your food. You can eat the same amount of calories but if you eat them in a time-restricted window, as one does in intermittent fasting, then you can help your body to burn fat for fuel and not suffer the metabolic consequences. I have recently increased my daily fast up to 18 to 20 hours and exercise fasting, as I believe that provides me with superior metabolic results.

I’ve found intermittent fasting to be a highly effective tool that helps your body to shift from burning sugar to burning fat as its primary fuel, and with that change, food cravings tend to simply vanish. While intermittent fasting has not been tested specifically for people meeting the criteria of food addiction, if you’re struggling with sugar cravings, I believe it would be worthwhile to give it a try.

Interestingly, I just interviewed Dr. Dale Bredesen for his new book “The End of Alzheimer’s,” coming out August 22, and he shared that the dreaded ApoE 4 allele that is highly predictive of Alzheimer’s is actually designed to give us metabolic flexibility to use fat for fuel and be able to go for long periods without food. So, if you have this gene, it means you MUST intermittently fast unless you want to lose your brain function as you age.

Sugar Industry Recommendations Are a Recipe for Heart Disease and Early Death

In 2002, the World Health Organization (WHO) published a technical report on diet and nutrition for the prevention of chronic disease, in which they specifically recommend limiting daily sugar consumption to a maximum of 10 percent of calories to prevent obesity and metabolic dysfunction. Not surprisingly, the report was strongly rejected by the sugar industry, which recommends getting 25 percent of your daily calories from sugar.

Two U.S. Senators, Larry Craig (R-Idaho) and John Breaux (D-La.), asked then Secretary of Health and Human Services, Tommy Thompson, to stop the publication of the report as it would devastate the sugar industry. Thompson complied. He flew to Geneva and told WHO that if this report was published, the U.S. would withhold $406 million of funding. The extortion had the desired effect. Moving forward, the sugar recommendation was not included in WHO dietary reports.

What happens when you follow the sugar industry’s recommendation to get 25 percent of your daily calories from sugar? A 2014 study8gave us the answer. It found that 10 percent of Americans consume 25 percent or more of their daily calories in the form of added sugars, as recommended by the sugar industry.

Those who got 21 percent or more of their daily calories from sugar were TWICE as likely to die from heart disease compared to those who got 7 percent or less of their daily calories from added sugar. The risk was nearly TRIPLED among those who consumed 25 percent or more of their calories from sugar.

How First Lady’s Organic Garden Became a Junk Food Campaign

When Barrack Obama became president, first lady Michelle Obama took a strong stance against the food industry, urging them to reformulate foods to reduce sugar and rethink their advertising toward children. The food industry quickly took control of the situation by offering to partner with her, thereby steering her entire wellness program away from concrete change toward a focus on physical exercise and teaching kids about the phony theory known as energy balance.

Her “Let’s Move” campaign was a failure, in terms of making a dent in childhood obesity and related disease. In fact, research shows childhood obesity continued to worsen after the launch of this nationwide program in 2010,9 with severe obesity rising the most. This was entirely predictable, since the campaign didn’t focus on the source of the problem (toxic, high-sugar, processed foods) and recommended solutions that don’t work (just exercise more).

As noted in the film, the food industry has become expert at switching the conversation from talk about real food and cooking, to talk about reengineered processed foods that are lower in calories, and the need for more exercise — both of which obscure the real solution and perpetuate the problem.

Even the name of the campaign, “Let’s Move,” was co-opted and twisted to serve the processed food industry. Originally, the first lady said the name represented a call to action — we need to get moving on this issue of children’s diets — but by the end, it became all about physical activity, and the issue of getting back to real food was lost altogether.

How to Reverse the Obesity Epidemic

The conventional low-fat, high-carb recommendation has without a doubt contributed to the obesity epidemic. If you or your child is struggling with excess weight, some key facts you need to realize are:

  1. Calorie counting does not work because the source of the calories is far more important than the amount, as they are not all metabolized equally. Calories from carbohydrates (think sugars and grains) raise your insulin level and turn to body fat, whereas dietary fats and protein have very little impact on your insulin, and dietary fats are a far more efficient fuel for your body than sugar
  2. You cannot exercise your way out of a poor diet
  3. A poor diet is one that is high in processed foods, added sugars (especially processed fructose), harmful fats (vegetable oils and trans fats, not saturated fats or cholesterol found in whole foods) and artificial ingredients

I am firmly convinced we can turn the obesity epidemic around, but it requires a new base of knowledge. First, we need to return to a diet of real, minimally processed foods. Second, we need to educate people about the importance of eating healthy fats and avoid consistently eating large amounts of net carbs (carbohydrates minus the fiber). Once we are burning fat for fuel we need to cycle healthy carbs back in to feed our gut microbes.

As a general rule, if the fat is found in a whole food, it’s going to be good for you. This includes the fat found in meat, eggs, raw dairy, avocados, nuts, coconuts and more. It’s the fats found in processed foods you need to be leery of, along with vegetable oils for cooking, margarines and vegetable oil spreads.

Last but not least, it would be wise to limit your consumption of protein to just what your body needs, as excess protein also has health implications. Not so much in terms of obesity per se, but certainly in terms of heart disease and cancer. Most people eat far more protein than their body requires, and most of it is low-quality CAFO beef, the nutritional composition of which is compromised by the unnatural way these animals are raised and fed.

In my view, the single most important driver of obesity is consuming over 50 grams of net carbs a day and excessive protein. Once you get net carbs below 50 grams, moderate your protein intake to 0.5 gram per pound of lean body weight, along with higher amounts of high quality fat, your body will start to regain its ability to burn fat as its primary fuel. Once you become an efficient fat burner, it will become virtually impossible to be overweight.

Regaining Your Health, One Meal at a Time

Many end up throwing their hands up in disgust when trying to clean up their diet, complaining that once they start to read labels, they realize there’s “nothing safe to eat.” If this sounds like you, you’re probably still looking at processed foods, trying to figure out which ones are “good” for you, and that’s the problem. If you’re serious about losing weight, you really need to avoid all processed foods and cook from scratch using whole ingredients.

The list of ingredients to avoid is just about endless, starting with all sorts of added sugars, and keeping track of it can be really discouraging. The answer is to create a list of healthy options instead, which is far shorter and easier to remember. The following short list of super-simple, easy-to-remember guidelines will not only improve your nutrition, it will also help you avoid countless chemical exposures that can affect your weight:

Eat REAL FOOD. Buy whole, ideally organic, foods and cook from scratch. First of all, this will automatically reduce your added sugar consumption, which is the root cause of insulin resistance and weight gain.

If you buy organic produce, you’ll also cut your exposure to pesticides and genetically engineered ingredients, and in ditching processed foods, you’ll automatically avoid artificial sweeteners and harmful processed fats. For more detailed dietary advice, please see my free Optimized Nutrition Plan and/or my new book, “Fat for Fuel

Opt for AGA certified grass fed meats to avoid genetically engineered ingredients, pesticides, hormones, antibiotics and other growth promoting drugs

Opt for glass packaging and storage containers to avoid endocrine disrupting chemicals

Reduce net carbs to under 50 grams a day and restrict protein to 0.5 gram/pound of lean body mass. The remaining calories come from high-quality fat sources like avocados, butter, coconut oil, macadamia and pecans

Once you’ve cleaned up your diet, if you’re still struggling you may want to seriously reconsider the timing of your meals. Intermittently fasting can be very effective for helping your body shift from sugar- to fat-burning mode. Also consider increasing your daily physical activity.

Ideally, aim for 7,000 to 10,000 steps a day or even double that if you have the time. Later you can add on a more regimented workout routine, which will really help maximize all the other healthy lifestyle changes you’ve implemented. But for general health and longevity, staying active throughout each day and avoiding sitting takes precedence.

How Putin Got Trump – And America – Wrong

Secretary of State Rex Tillerson delivered remarks at the State Department yesterday ahead of his trip to Asia. Source: Getty
Can Tillerson Ease Tensions With North Korea?
“We are not your enemy.” That’s the message U.S. Secretary of State Rex Tillerson wants North Korea to hear as he heads to Asia this week for a security meeting. It could be a sign that the White House wants to dial down tensions between Washington and Pyongyang, but it’s unclear whether Tillerson can effectively speak for a president who’s rattled his saber after North Korea’s launch of two ICBMs within a month. Either way, he’s made it clear dialogue is impossible unless Pyongyang gives up its nuclear goals.
SOURCES: WASHINGTON POST,REUTERS,CNN
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Trump Chides Maduro Amid Venezuela Crisis
He’s talking tough. President Donald Trump on Tuesday warned his Venezuelan counterpart, Nicolas Maduro, that he’s “personally responsible” for the safety of two opposition leaders arrested during the strongman’s escalating crackdown on dissent. As Venezuela descends further into political turmoil — exacerbated by a recent vote establishing a new, Maduro-friendly legislative body — its currency is sinking alongside prospects for a peaceful settlement of the conflict. In fact, the bolivar is now worth about half as much as the virtual gold featured in the popular computer game, World of Warcraft.
SOURCES: FORTUNE,BBC,AP
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Feds Go After University Admissions ‘Discrimination’
But not the way you might expect. Officials say Attorney General Jeff Sessions’ Justice Department will refocus its civil rights resources on investigating possible discrimination against white university applicants, potentially fueling lawsuits that could dismantle longstanding affirmative action policies. Just last year, the Supreme Court reaffirmed universities’ rights to consider race as a factor in admissions in order to ensure diversity in the classroom. The new investigations represent the latest Justice Department challenge to longstanding civil rights enforcement, part of a campaign that’s also targeted employment discrimination policies and voting rights.
SOURCES: WASHINGTON POST,NYT
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Apple Shares Soar as CEO Defends China Policy
Everybody’s picking up the phone. Apple’s stock rose 6 percent to an all-time high above $159 in after-hours trading Tuesday following reports of strengthening iPhone and iPad sales. The company is predicting revenue of as much as $52 billion for the current quarter, which could push the Dow Jones above the 22,000 mark today. Meanwhile, Apple CEO Tim Cook defended the removal of VPNs from its Chinese app store, widely seen as abetting internet freedom crackdowns, saying the company must follow existing laws even if he’s hopeful restrictions will loosen.
SOURCES: REUTERS,QUARTZ,FT (SUB),FORTUNE
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BRIEFLY
Know This: The Trump administration is reportedly considering a major trade action against China over intellectual property rules. Sweden is seeking to beef up its data security after a massive leak of private information prompted two ministers to resign. And 12 inmates who escaped an Alabama prison Sunday after tricking a guard using peanut butter have been recaptured.

Listen to This: The Girls Connect project in Nigeria is using stories of fictionalized women, performed by professional radio actors, to get young women to call in and talk to counselors. Though it’s currently only available in the Hausa language, a monthlong test period saw 42,000 calls from young women seeking mentorship and empowerment.

Answer This: Tell us how you really feel. OZY’s next TV show, Third Rail With OZY, is launching on PBS this fall! To kick things off, we’re shelving the PC and launching debates. Each Wednesday, we’ll post a provocative question, focusing on topics that might make it onto the show. This week: Should all Americans be entitled to healthcare? Go deep. Email thirdrail@ozy.com with your thoughts or a personal story, and we might feature your answer next week.

INTRIGUING
How Putin Got Trump – And America – Wrong
Nothing gold can stay. Russian President Vladimir Putin has a history of trying to smooth relations with Western countries by befriending incoming leaders, but it’s never truly worked. Exhibit A is the Trump administration, consumed by chaos and investigations. Kremlin officials may be watching with dismay as checks and balances inherent in working democracies override the promise of unbridled cooperation. Even as new sanctions kick in, Putin may not be ready to give up on working with Trump: He understands that seriously souring relations with Washington could hurt Moscow, too.
SOURCES: TIME,FOREIGN POLICY
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Upgrade Rift Divides Bitcoin
Who’ll be right on the money? A widely anticipated “hard fork” has split Bitcoin in two. Alternative cryptocurrency Bitcoin Cash will allow for more transactions at any moment, as opposed to the seven-per-second limit built into the original system. Some users of Bitcoin, collectively valued at $47 billion, say the Bitcoin Cash upgrade, with each software block growing from one to eight megabytes, will allow the currency to make a greater impact on the financial world. But traditionalists say the fork could sow confusion — and possibly hacking — keeping Bitcoin from penetrating mainstream markets.
SOURCES: WIRED,THE VERGE,BI
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Eating Alone Could Be Bad for Your Health
Solitude leaves a bad taste in your mouth. New research suggests food tastes worse if you’re eating alone, which in turn may have a negative impact on our well-being. Yet fixing that skewed perception may be as simple as looking into a mirror. When the study’s participants were faced with their own reflection, or even just a photo of themselves eating, researchers recorded an increase in declared tastiness and volume consumed. The results are provisional, but they nonetheless underscore our need to commune with others, especially at dinner.
SOURCES: OZY
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New TV Shows Imagine Post-Secession America
Did the war ever end? That’s what television producers seem to be wondering these days, with two different shows attempting to explore alternative, post-Civil War narratives. Amazon’s Black America will envision an American South founded by freed slaves, while HBO’s Confederate, from the creators of Game of Thrones, will imagine what modern slaverywould’ve looked like if the war had ended differently. While many were outraged over the latter, Amazon may find its tale of empowerment boosted by viewers looking for an alternative that won’t attract white nationalist fans.
SOURCES: THE GUARDIAN,DEADLINE
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Jordan: LaVar Ball Needs to ‘Shut Up’
“I don’t think he could beat me if I was one-legged.” That was Michael Jordan’s long-awaited response to LaVar Ball — father of Los Angeles Lakers rookie Lonzo — who infamously claimed he could’ve beaten Jordan in a one-on-one during Ball’s 1980s Washington State “heyday.” Jordan’s probably right: During the 1987-88 season, Ball averaged 2.2 points per game, while the Greatest Player of All Time was putting away 35 for the Chicago Bulls. His advice for the loud-mouthed father? “Shut up and let the kid play.”

Calif. law requires identifying family caregivers for patients

Calif. law requires identifying family caregivers for patients

A new California law that requires hospitals to identify and engage a family caregiver for discharged patients is raising concerns about its practicality.As of Jan. 1, California hospitals are required to identify a caregiver during a patient’s hospitalization and inform that caregiver of the individual’s discharge date and instructions, such as medication schedules.
Hospitals are still required to maintain privacy requirements and cannot release information without the patient’s consent.
About a dozen states have passed similar laws.Supporters such as the AARP say it will improve the quality of the transition to the home setting and reduce readmissions.
The law will stimulate conversations about individual preferences and capabilities to help loved ones remain independent, said Suzanne.
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Health care financial news

TODAY’S TOP HEALTHCARE FINANCIAL NEWS

CMS gives hospitals $2 billion raise, finalizes unpopular uncompensated care plan 

The new inpatient pay rule for hospitals is a mixed bag for industry as CMS is planning to give hospitals a major raise, but will move forward with a controversial plan to change the way it hands out uncompensated care funds.  READ MORE

CHS to sell additional hospitals worth $1.5 billion in revenue

Buyer interest in more Community Health Systems hospitals has the chain unloading another $1.5 billion in annualized hospital revenue to reduce debt and focus resources in core markets.  READ MORE

Appeals court rules states can fight to preserve ACA subsidies

The appellate court order allowing state attorneys general to intervene in a lawsuit over the ACA’s cost-sharing subsidies means the Trump administration cannot unilaterally stop the CSR payments and dismiss the appeal.  READ MORE
MARKETS/FINANCIALS

Humana doubles second-quarter profit on higher Medicare Advantage revenue 

Improved earnings in its Medicare Advantage business and individual commerical plans helped boost Humana’s bottom line despite lower revenue in the second quarter.  READ MORE

Cardinal Health profit declines as generic drug prices deflate

The Dublin, Ohio-based pharmaceutical and medical products distributor saw its pharmaceutical segment profit drop 7% to $505 million as companies along the pharmaceutical supply chain have taken a financial hit resulting from the increasing scrutiny surrounding surging drug prices.  READ MORE
MERGERS AND ACQUISITIONS

Christus turns to national operator to run home health businesses

Catholic-sponsored Christus Health has agreed to contribute 21 home health, hospice and long-term hospitals to a joint venture with LHC Group, joining other hospitals in offloading those businesses.  READ MORE
HEALTHCARE ECONOMICS

Health insurer files for rate decrease for Alaska market

If approved, the lone insurer’s proposed double-digit rate decrease would be the first time the average rate has decreased under the current federal healthcare law in Alaska.  READ MORE

Medical board certification fees are excessive, according to JAMA research letter

A new research letter in JAMA finds that medical boards have nearly tripled their net assets over the past decade, bolstered by fees charged to physicians to get and maintain their board certification status.  READ MORE

BCBS of North Carolina asks for lower ACA rate increase

The insurer chose to lower its initital individual rate increase request, saying the insurance market is less “volatile” now and marketplace members are using fewer healthcare services. READ MORE
POLITICS AND POLICY

Senate OKs bills to address VA budget crisis, claims backlog

The Senate unanimously approved a pair of bills taking aim at urgent problems at the Department of Veterans Affairs, clearing a $3.9 billion emergency spending package to fix a looming budget crisis and adopting new measures to pare down a rapidly growing backlog of veterans’ disability claims.  READ MORE
SPOTLIGHT

This week’s poll: Should the CMS mandate participation in bundled payment initiatives, or should it be voluntary?

Share your opinion in the latest edition of our bi-weekly reader poll. Should the CMS mandate participation in bundled payment initiatives, or should it be voluntary?  READ MORE

The new age of healthcare marketing: Are you ready?

Registration is now open for Modern Healthcare’s Strategic Marketing Conference. Discover the best— and next— practices being used to keep pace with emerging trends in healthcare marketing. Nov. 7 in Chicago. Co-located with the Healthcare Marketing IMPACT Awards dinner.  READ MORE

Leading through Disruption, Complexity and Uncertainty: The Roadmap to a Transformed Healthcare System

CEO of Kaiser Permanente, Bernard J. Tyson, will serve as the closing keynote for Modern Healthcare’s second annual, invitation-only Leadership Symposium. Sign up for this exclusive event to learn from and network with the nation’s top healthcare C-Suite executives.  READ MORE
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WHITE PAPERS, RESEARCH AND OTHER CONTENT

Addressing Medicare’s Appeals Backlog

The Medicare appeals backlog is significant and has been increasing in recent years, but relief – or at least improvement – appears to be on the horizon.  READ MORE

Turning challenges into opportunities: 5 ways to improve the hospital supply chain

Given the critical role that supply chain plays in hospital operations, it is essential to understand how hospital stakeholders gauge its importance and how it impacts them on a daily basis.  READ MORE

Reducing Door to Needle Times and Expediting Transfer for Endovascular Care for Acute Ischemic Stroke Patients

Learn how a hospital reduced delays in stroke care by embracing teleneurology.  READ MORE

Genetic Factors in Depression

Genetic factors involved in depression have been difficult to identify. In 2003 Science published an influential[1] study of Avshalom Caspi et al. who found that a gene-environment interaction (GxE) may explain why life stress is a predictor for depressive episodes in some individuals, but not in others, depending on an allelic variation of the serotonin-transporter-linked promoter region (5-HTTLPR).[2] Soon after, the results were replicated by Kenneth Kendler‘s group, raising hopes in the psychiatric genetics community.[3] By 2007 there were 11 replications, 3 partial replication and 3 non-replications of this proposed GxE. However, two of the largest studies[4][5]were negative.[6] Two 2009 meta-analyses were also negative; one included 14 studies,[7] and the other five, owing to different study selection criteria.[8]

A 2010 review found 17 replications, 8 partial replications (interaction only in females or only with one of several types of adversity), and 9 non-replications (no interaction or an interaction in the opposite direction). It also found that all studies using objective indicators or structured interviews to assess stress replicated the gene–environment interaction fully or partially, whereas all non-replications relied on self-reported measures of adversity. This review also argued that both 2009 meta-analyses were significantly biased toward negative studies.[9]

BDNF polymorphisms have also been hypothesized to have a genetic influence, but replication results have been mixed and, as of 2005, were insufficient for a meta-analysis.[10] Studies also indicate an association of decreased BDNF production with suicidal behavior.[11] However, findings from gene-environment interactions studies suggest that the current BDNF models of depression are too simplistic.[12]

A 2008 study found interactions (biological epistasis) in the signaling pathways of the BDNF and the serotonin transporter; the BDNF Val66Met allele, which was predicted to have reduced responsitivity to serotonin, was found to exercise protective effects in individuals with the short 5-HTTLPR allele that is otherwise believed to predispose individuals to depressive episodes after stressful events.[13] Thus, the BDNF-mediated signalling involved in neuroplastic responses to stress and antidepressants is influenced by other genetic and environmental modifiers.[12]

The largest genome-wide study to date failed to identify variants with genome-wide significance in over 9000 cases.[14]

Recently, a genetics study positively identified two variants with genome-wide association with major depressive disorder (MDD).[15] This study, conducted in Chinese Han women, identified two variants in intronic regions near SIRT1 and LHPP.[16]

Attempts to find a correlation between norepinephrine transporter polymorphisms and depression have yielded negative results.[17]

One review identified multiple frequently studied candidate genes. The 5-HTT SLC6A4 and 5-HTR2A gene’s yielded inconsistent results, however they may predict treatment results. Mixed results were found for BDNF Val66Met polymorphisms. Polymorphisms in tryptophan hydroxylase genes were found to be associated with suicidal behavior.[18]

A meta analysis of 182 case controlled genetic studies published in 2008 found Apolipoprotein verepsilon 2 to be protective, and found GNB3 825T, MTHFR 677T, SLC6A4 44bp insertion or deletions, and SLC6A3 40 bpVNTR 9/10 genotype conferred risk.[


MTHFR 677T

Methylene tetrahydrofolate reductase (MTHFR) is the rate-limiting enzyme in the methyl cycle, and it is encoded by the MTHFR gene.[3] Methylenetetrahydrofolate reductase catalyzes the conversion of 5,10-methylenetetrahydrofolate to 5-methyltetrahydrofolate, a cosubstrate for homocysteine remethylation to methionine. Natural variation in this gene is common in healthy people. Although some variants have been reported to influence susceptibility to occlusive vascular disease, neural tube defects, Alzheimer’s disease and other forms of dementia, colon cancer, and acute leukemia, findings from small early studies have not been reproduced. Some mutations in this gene are associated with methylenetetrahydrofolate reductase deficiency.


 

GNB3 825T GENE

gnas.JPG


LHPP

LHPP (Phospholysine Phosphohistidine Inorganic Pyrophosphate Phosphatase) is a Protein Coding gene. Among its related pathways are Purine metabolism (REACTOME) and Respiratory electron transport, ATP synthesis by chemiosmotic coupling, and heat production by uncoupling proteins.. GO annotations related to this gene include protein homodimerization activity and inorganic diphosphatase activity. An important paralog of this gene is HDHD2.

Leptin and other pro inflammatory biomakers for chronic fatigue syndrome

Researchers identify biomarkers associated with chronic fatigue syndrome severity

Stanford investigators used high-throughput analysis to link inflammation to chronic fatigue syndrome, a difficult-to-diagnose disease with no known cure.

Man in a lab coat sitting near a microscope with a woman in a lab coat in the background

Jose Montoya and his colleagues have found evidence inflammation may be the culprit behind chronic fatigue syndrome, a disease with no known cure.
Steve Fisch

Researchers at the Stanford University School of Medicine have linked chronic fatigue syndrome to variations in 17 immune-system signaling proteins, or cytokines, whose concentrations in the blood correlate with the disease’s severity.

The findings provide evidence that inflammation is a powerful driver of this mysterious condition, whose underpinnings have eluded researchers for 35 years.

The findings, described in a study published online July 31 in the Proceedings of the National Academy of Sciences, could lead to further understanding of this condition and be used to improve the diagnosis and treatment of the disorder, which has been notably difficult.

More than 1 million people in the United States suffer from chronic fatigue syndrome, also known as myalgic encephomyelitis and designated by the acronym ME/CFS. It is a disease with no known cure or even reliably effective treatments. Three of every four ME/CFS patients are women, for reasons that are not understood. It characteristically arises in two major waves: among adolescents between the ages of 15 and 20, and in adults between 30 and 35. The condition typically persists for decades.

“Chronic fatigue syndrome can turn a life of productive activity into one of dependency and desolation,” said Jose Montoya, MD, professor of infectious diseases, who is the study’s lead author. Some spontaneous recoveries occur during the first year, he said, but rarely after the condition has persisted more than five years.

The study’s senior author is Mark Davis, PhD, professor of immunology and microbiology and director of Stanford’s Institute for Immunity, Transplantation and Infection.

‘Solid basis for a diagnostic blood test’

“There’s been a great deal of controversy and confusion surrounding ME/CFS — even whether it is an actual disease,” said Davis. “Our findings show clearly that it’s an inflammatory disease and provide a solid basis for a diagnostic blood test.”

Many, but not all, ME/CFS patients experience flulike symptoms common in inflammation-driven diseases, Montoya said. But because its symptoms are so diffuse —sometimes manifesting as heart problems, sometimes as mental impairment nicknamed “brain fog,” other times as indigestion, diarrhea, constipation, muscle pain, tender lymph nodes and so forth — it often goes undiagnosed, even among patients who’ve visited a half-dozen or more different specialists in an effort to determine what’s wrong with them.

Mark Davis

Mark Davis

Montoya, who oversees the Stanford ME/CFS Initiative, came across his first ME/CFS patient in 2004, an experience he said he’s never forgotten.

“I have seen the horrors of this disease, multiplied by hundreds of patients,” he said. “It’s been observed and talked about for 35 years now, sometimes with the onus of being described as a psychological condition. But chronic fatigue syndrome is by no means a figment of the imagination. This is real.”

Antivirals, anti-inflammatories and immune-modulating drugs have led to symptomatic improvement in some cases, Montoya said. But no single pathogenic agent that can be fingered as the ultimate ME/CFS trigger has yet been isolated, while previous efforts to identify immunological abnormalities behind the disease have met with conflicting and confusing results.

Still, the sporadic effectiveness of antiviral and anti-inflammatory drugs has spurred Montoya to undertake a systematic study to see if the inflammation that’s been a will-o’-the-wisp in those previous searches could be definitively pinned down.

To attack this problem, he called on Davis, who helped create the Human Immune Monitoring Center. Since its inception a decade ago, the center has served as an engine for large-scale, data-intensive immunological analysis of human blood and tissue samples. Directed by study co-author Holden Maecker, PhD, a professor of microbiology and immunology, the center is equipped to rapidly assess gene variations and activity levels, frequencies of numerous immune cell types, blood concentrations of scores of immune proteins, activation states of intercellular signaling models, and more on a massive scale.

Finding patterns

This approach is akin to being able to look for and find larger patterns — analogous to whole words or sentences — in order to locate a desired paragraph in a lengthy manuscript, rather than just try to locate it by counting the number of times in which the letter A appears in every paragraph.

The scientists analyzed blood samples from 192 of Montoya’s patients, as well as from 392 healthy control subjects. The average age of patients and controls was about 50. Patients’ average duration of symptoms was somewhat more than 10 years.

Importantly, the study design took into account patients’ disease severity and duration. The scientists found that some cytokine levels were lower in patients with mild forms of ME/CFS than in the control subjects, but elevated in ME/CFS patients with relatively severe manifestations. Averaging the results for patients versus controls with respect to these measures would have obscured this phenomenon, which Montoya said he thinks may reflect different genetic predispositions, among patients, to progress to mild versus severe disease.

I have seen the horrors of this disease, multiplied by hundreds of patients.

When comparing patients versus control subjects, the researchers found that only two of the 51 cytokines they measured were different. Tumor growth factor beta was higher and resistin was lower in ME/CFS patients. However, the investigators found that the concentrations of 17 of the cytokines tracked disease severity. Thirteen of those 17 cytokines are pro-inflammatory.

TGF-beta is often thought of as an anti-inflammatory rather than a pro-inflammatory cytokine. But it’s known to take on a pro-inflammatory character in some cases, including certain cancers. ME/CFS patients have a higher than normal incidence of lymphoma, and Montoya speculated that TGF-beta’s elevation in ME/CFS patients could turn out to be a link.

One of the cytokines whose levels corresponded to disease severity, leptin, is secreted by fat tissue. Best known as a satiety reporter that tells the brain when somebody’s stomach is full, leptin is also an active pro-inflammatory substance. Generally, leptin is more abundant in women’s blood than in men’s, which could throw light on why more women than men have ME/CFS.

More generally speaking, the study’s results hold implications for the design of future studies of disease, including clinical trials testing immunomodulatory drugs’ potential as ME/CFS therapies.

“For decades, the ‘case vs. healthy controls’ study design has served well to advance our understanding of many diseases,” Montoya said. “However, it’s possible that for certain pathologies in humans, analysis by disease severity or duration would be likely to provide further insights.”

Other Stanford co-authors of the study are clinical research coordinator Jill Anderson; Tyson Holmes, PhD, senior research engineer at the Institute for Immunity, Transplantation and Infection; Yael Rosenberg-Hasson, PhD, immunoassay and technical director at the institute; Cristina Tato, PhD, MPH, research and science analyst at the institute; former study coordinator Ian Valencia; and Lily Chu, MSHS, a board member of the Stanford University ME/CFS Initiative.

The study was funded by the National Institutes of Health (grant U19AI057229), the Stanford ME/CFS Initiative Fund and an anonymous donor.

Stanford’s departments of Medicine and of Microbiology and Immunology also supported the work.

Answer these 5 questions to match a bay area caregiver

For a 30-min response when looking for a bay area caregiver for home health for your seniors with Alzheimer’s, Parkinson, Stroke, Hospice care or other health issues, please complete this form (5 questions) that will help you decide on choosing the right match of caregiver for your needs:

https://conniedellobuono.typeform.com/to/gPWK4E

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