‘Transmissible’ Alzheimer’s theory gains traction


Mouse tests confirm that sticky proteins associated with degenerative brain diseases can be transferred — but researchers say risks for humans are likely to be minimal.

 

 

Alzheimer's disease

A normal brain of a 70-year-old (left slice), compared with the brain of a 70-year-old with Alzheimer’s disease.

Neuroscientists have amassed more evidence for the hypothesis that sticky proteins that are a hallmark of neurodegenerative diseases can be transferred between people under particular conditions — and cause new damage in a recipient’s brain.

They stress that their research does not suggest that disorders such as Alzheimer’s disease are contagious, but it does raise concern that certain medical and surgical procedures pose a risk of transmitting such proteins between humans, which might lead to brain disease decades later.

“The risk may turn out to be minor — but it needs to be investigated urgently,” says John Collinge, a neurologist at University College London who led the research, which is published in Nature1 on 13 December.

The work follows up on a provocative study published by Collinge’s team in 20152. The researchers discovered extensive deposits of a protein called amyloid-beta during post-mortem studies of the brains of four people in the United Kingdom. They had been treated for short stature during childhood with growth-hormone preparations derived from the pituitary glands of thousands of donors after death.

The recipients had died in middle-age of a rare but deadly neurodegenerative condition called Creutzfeldt-Jakob disease (CJD), caused by the presence in some of the growth-hormone preparations of an infectious, misfolded protein — or prion — that causes CJD. But pathologists hadn’t expected to see the amyloid build up at such an early age. Collinge and his colleagues suggested that small amounts of amyloid-beta had also been transferred from the growth-hormone samples, and had caused, or ‘seeded’, the characteristic amyloid plaques.

Seeds of trouble

Amyloid plaques in blood vessels in the brain are a hallmark of a disease called cerebral amyloid angiopathy (CAA) and they cause local bleeding. In Alzheimer’s disease, however, amyloid plaques are usually accompanied by another protein called tau — and the researchers worry that this might also be transmitted in the same way. But this was not the case in the brains of the four affected CJD patients, which instead had the hallmarks of CAA.

The team has now more directly tested the hypothesis that these proteins could be transmitted between humans through contaminated biological preparations. Britain stopped the cadaver-derived growth hormone treatment in 1985 and replaced it with a treatment that uses synthetic growth hormone. But Collinge’s team was able to locate old batches of the growth-hormone preparation stored as powder for decades at room temperature in laboratories at Porton Down, a national public-health research complex in southern England.

When the researchers analysed the samples, their suspicions were confirmed: they found that some of the batches contained substantial levels of amyloid-beta and tau proteins.

Mouse tests

To test whether the amyloid-beta in these batches could cause the amyloid pathology, they injected samples directly into the brains of young mice genetically engineered to be susceptible to amyloid pathology. By mid-life, the mice had developed extensive amyloid plaques and CAA. Control mice that received either no treatment or treatment with synthetic growth hormone didn’t have amyloid build up.

The scientists are now checking in separate mouse experiments whether the same is true for the tau protein.

“It’s an important study, though the results are very expected,” says Mathias Jucker at the Hertie Institute for Clinical Brain Research in Tubingen, Germany. Jucker demonstrated in 2006 that amyloid-beta extracted from human brain could initiate CAA and plaques in the brains of mice3. Many other mouse studies have also since confirmed this.

Surgical implications

That the transmissibility of the amyloid-beta could be preserved after so many decades underlines the need for caution, says Jucker. The sticky amyloid clings tightly to materials used in surgical instruments, resisting standard decontamination methods4. But Jucker also notes that, because degenerative diseases take a long time to develop, the danger of any transfer may be most relevant in the case of childhood surgery where instruments have also been used on old people.

So far, epidemiologists have not been able to assess whether a history of surgery increases the risk of developing a neurodegenerative disease in later life — because medical databases tend not to include this type of data.

But epidemiologist Roy Anderson at Imperial College London says researchers are taking the possibility seriously. Major population cohort studies, such as the US Framingham Heart Study, are starting to collect information about participants’ past surgical procedures, along with other medical data.

The 2015 revelation prompted pathologists around the world to reexamine their own cases of people who had been treated with similar growth-hormone preparations — as well as people who had acquired CJD after brain surgery that had involved the use of contaminated donor brain membranes as repair patches. Many of the archived brain specimens, they discovered, were full of aberrant amyloid plaques5,6,7. One study showed that some batches of growth-hormone preparation used in France in the 1970s and 1980s were contaminated with amyloid-beta and tau — and that tau was also present in three of their 24 patients.8

Collinge says he applied unsuccessfully for a grant to develop decontamination techniques for surgical instruments after his 2015 paper came out. “We raised an important public-health question, and it is frustrating that it has not yet been addressed.” But he notes that an actual risk from neurosurgery has not yet been established.

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Too Much Oxygen Is Harmful


A meta-analysis shows significantly higher mortality with liberal use of supplemental oxygen in acutely ill patients.

 

Supplemental oxygen can be a life-saving intervention for patients with hypoxemic respiratory failure; however, emerging evidence suggests that too much oxygen is harmful (NEJM JW Gen Med Dec 1 2016 and NEJM 2016; 316:1583). Small trials have shown excess cardiac arrhythmias, lung injuries, and other complications in hospitalized patients without demonstrated hypoxemia who receive oxygen or whose oxygen administration results in supra-normal partial pressures (i.e., hyperoxemia). Should we be doing more to turn down the oxygen when it’s not needed?

Investigators completed a meta-analysis of 25 randomized trials that included 16,000 acutely ill patients who were treated with either a liberal or a conservative oxygenation strategy. Oxygen targets and supplementation thresholds differed across studies. Median oxygen supplementation levels were fraction of inspired oxygen (FiO2) 0.52 vs. 0.21 (liberal vs. conservative).

Relative risk for death at 30 days was significantly higher in patients who received liberal oxygen (RR, 1.14), although no association was evident between mortality and either peripheral saturation or FiO2. Risk for disability, length of stay, and incidence of hospital-acquired infections, including pneumonia, were similar under both strategies.

Comment

All too often, a patient’s oxygen saturation is maintained at 100%. This is not only unnecessary but also probably harmful. It should become part of our practice to turn down the supplemental oxygen until we see oxygen saturations no higher than 95% for most patients and to stop oxygen use as soon as it is not needed. I suspect that we will learn that a target saturation lower than 95% is safe, but for now, avoiding hyperoxemia makes sense.

Whole-Fat or Nonfat Dairy? The Debate Continues


It’s been 40 years since the federal government first recommended that everyone except young children opt for low-fat or nonfat dairy products over high-fat dairy products as part of an overall goal of reducing saturated fat intake and calories.

Image description not available.

A decade later, US sales of low-fat and skim milk combined exceeded those of whole milk for the first time, according to the International Dairy Foods Association. And in 2010, the Healthy, Hunger-Free Kids Act required that schools follow dietary recommendations and replace whole milk with nonfat or low-fat unflavored milk or nonfat flavored milk.

But some recent studies have suggested that high-fat milk, cheese, and yogurt are at least as healthful as their low-fat or nonfat counterparts, and their authors are questioning the wisdom of advising people to avoid whole milk and products made with it.

“I don’t think there’s enough evidence to recommend low-fat dairy,” said cardiologist Dariush Mozaffarian, MD, dean of the Friedman School of Nutrition Science and Policy at Tufts University. However, Mozaffarian added, “I don’t think there’s enough evidence to recommend whole-fat dairy, either.”

Although dairy products account for about 10% of total fats in the average US diet, “we’ve been making recommendations on them based on theories,” he said.

Just as the evidence suggests that not all food sources of saturated fats—ie, animals, plants, and dairy—are the same, neither are all sources of dairy fats, Mozaffarian said. Because cheese is fermented and some yogurts contain probiotics, “they are probably better for you than milk,” he said. And yet, Mozaffarian said, scientists and dietary guidelines tend to lump all dairy products together.

“This is a very complicated area, because dairy is not a homogeneous food,” said Frank Hu, MD, PhD, MPH, chair of the nutrition department at Harvard University’s T. H. Chan School of Public Health. “Also, dietary patterns are very different among people who eat dairy products.”

For example, Hu said, while US consumers chow down on cheeseburgers and pizza, Europeans are more likely to eat cheese for cheese’s sake, not as a topping for foods that without it are already high in fat or sodium or both.

Teasing Out Dairy

Most of the evidence about the health effects of dairy products has come from observational studies. One of the largest to look at the association between dairy intake and cardiovascular disease (CVD) and mortality, the Prospective Urban Rural Epidemiology (PURE) study, involved 136 384 individuals aged 35 to 70 years in 21 countries on 5 continents. Participants recorded their intake of high-fat and low-fat milk, yogurt, and cheese on a food frequency questionnaire at the beginning of the study. During the 9.1-year follow-up, there were 6796 deaths and 5855 major cardiovascular events (death due to cardiovascular causes, nonfatal heart attack, stroke, or heart failure) among study participants.

A higher intake of total dairy, defined as more than 2 servings a day, was associated with a lower risk of death or a major cardiovascular event than no intake. However, the authors found no significant association between dairy intake and heart attack, and only consumption of milk and yogurt, not cheese or butter, was significantly associated with the studied outcomes.

Whole-fat dairy products appeared to be more protective than nonfat or low-fat products, which aren’t available in some PURE countries, including India and South Africa, noted coauthor Mahshid Dehghan, PhD, an investigator with the Population Health Research Institute at McMaster University. “In some countries,” Dehghan added, “daily [dairy] consumption is not part of the diet. In Malaysia, people do not drink milk or consume yogurt.”

Because of these variations in dairy consumption, Dehghan and her coauthors, who included Mozaffarian, conducted a subgroup analysis to determine whether the associations between dairy intake and outcomes were similar in each region. To minimize the possibility of reverse causality, they excluded people with known CVD, who might be more likely to choose lowfat or nonfat dairy.

“The consistency of results across regions with markedly different lifestyles makes it less likely that confounders, which are likely to vary in different regions, explain our observations,” the authors concluded.

However, the PURE study didn’t adjust for many socioeconomic variables that could influence individuals’ risk of CVD and death, Hu said. For example, he said, in poorer, developing countries, “if you have more money, you can afford to buy dairy, meats, eat more protein, less carbohydrates,” which leads to improved nutritional status compared with the poorest people in these countries. In other words, he said, dairy consumption alone might not deserve the credit for the better outcomes.

As John P. A. Ioannidis, MD, DSc, a professor at the Stanford Research Prevention Center, wrote in a recent JAMA Viewpoint, “extensive residual confounding and selective reporting” in nutritional epidemiologic research can lead to “implausible estimates of benefits or risks associated with diet.”

Another problem, Hu said, is that the highest category of dairy consumption in PURE was only 2 servings a day. “That’s not really generalizable to the United States,” he said. After all, the US dietary guidelines recommend 3 servings a day (although less than 20% of the population meets or exceeds that goal, according to the 2015-2020 guidelines report).

Looking at Biomarkers

The PURE study depended on participants’ recall of their average daily dairy consumption for the past year. However, “self-reported consumption may be limited by errors or reporting bias,” according to a recently published observational study that took a different approach. Besides, the authors continued, people might not be aware of how much dairy fat they’re consuming in a range of foods, including baked goods, sauces, fried foods, and coffee drinks.

So instead of depending on study participants to accurately report their dairy intake, the authors looked at the relationship between circulating biomarkers of fatty acids found in dairy products and total mortality, cause-specific mortality, and CVD risk among 2907 US adults aged 65 and older who did not have CVD when the study began. The researchers measured participants’ fatty acid concentrations at baseline and then 6 years and 13 years later.

During 22 years of follow-up, none of the fatty acids was significantly associated with total mortality. But high levels of one type of fatty acid, heptadecanoic acid, were inversely associated with CVD and stroke mortality. However, the authors note that other components of dairy products, such as protein, lactose, and minerals, could have confounded these findings.

Mozaffarian, a coauthor of the fatty acids and CVD risk study, and Hu were among the authors of a recent article examining the relationship of 3 fatty acids (that partly reflect dairy fat consumption) with type 2 diabetes risk. In their pooled analysis of 16 prospective cohort studies, totaling 63 682 adults who did not have diabetes at baseline, higher levels of the fatty acids were associated with a lower risk of type 2 diabetes.

While the biomarkers assessed are correlated with dairy intake, Hu said, he acknowledged that they have limitations. “This is a relatively crude estimate of the exact amount of intake,” he said. Some fatty acids are produced endogenously, Hu said. In addition, an individual who drank 3 glasses of low-fat milk could have higher levels of the dairy fatty acids than someone who drank 1 glass of full-fat milk.

Although biomarkers aren’t a perfect measure of dairy intake, “they’re a step in the right direction,” said Mario Kratz, PhD, a faculty member of the Nutritional Sciences Program at the University of Washington School of Public Health, who was not involved in either biomarker study.

Beyond Observational Studies

A randomized controlled trial would avoid the potential of confounding in observational studies that rely on biomarkers or food frequency questionnaires, Kratz said. But, he added, when he proposed seeking a National Institutes of Health grant to fund a randomized trial to study the health effects of dairy, a senior colleague advised him not to waste his time. That’s because it’s likely that at least 1 reviewer would think that the question had already been answered, according to his colleague.

“Our opinion is this was not fundable with public funds,” Kratz said. Reluctantly, he said, he decided to seek industry funding instead.

Kratz raised $1 million to fund his study from such organizations as the Dairy Research Institute, the Dairy Farmers of Canada, and Dairy Management Inc, all of whom took a risk, he said, because “it’s not guaranteed that dairy will look favorable. We may be just fine without any dairy.”

His trial has enrolled 75 men and women with metabolic syndrome; as of mid-October, 72 participants had completed a 4-week wash-in period—in which they were given the option of consuming 3 servings of skim milk per week but no more—and the first clinic visit. After the wash-in period, participants have been randomized to 1 of 3 groups for 12 weeks: up to 3 servings of skim milk per week, 3.3 daily servings of nonfat or low-fat dairy, or 3.3 daily servings of full-fat dairy. The dairy products were weighed, packaged, and distributed to study participants via the Fred Hutchinson Cancer Research Center’s Human Nutrition Laboratory (Fred Hutchinson provided approximately $500 000 to fund the study).

Besides their dairy assignment, participants have been told to eat what they normally eat except for no dairy besides what is provided. Because food diaries are unreliable, Kratz said, study participants received surprise phone calls from dietitians asking what they had eaten in the previous 24 hours.

Kratz and his collaborators want to see how different amounts and types of dairy products affect blood glucose regulation and cardiometabolic health. “All of us are excited about the study, because we really have no idea what the results [will be],” he said.

Weighty Matters

One reason people opt for low-fat or nonfat dairy products is because they think consuming whole-fat milk, yogurt, and cheese will make them gain weight and will elevate their blood lipids.

However, “these are really rich sources of important nutrients,” said Marcia de Oliveira Otto, PhD, assistant professor in the Department of Epidemiology, Human Genetics and Environmental Science at the UTHealth School of Public Health in Houston and a coauthor of the study that assessed dairy fat biomarkers and CVD risk.

In fact, Kratz said, “the data never overwhelmingly showed that full-fat dairy made you gain weight, contributed to heart disease, contributed to metabolic disease.” Actually, he added, “people who eat the most full-fat dairy products in observational studies are usually among the ones who gain the least amount of weight.”

That seems counterintuitive, but, Kratz said, “it’s very likely that there’s a type of compensation going on.” Low-fat or nonfat dairy isn’t as filling as whole-fat dairy, so people might end up craving unhealthy snacks if they opt for the former, he said. However, he added, “I would never recommend people consume large amounts of butter and cream.”

Time to Change Dietary Guidelines?

The US Department of Agriculture and the US Department of Health and Human Services publish Dietary Guidelines for Americans every 5 years. Development of the 2020-2025 guidelines is already under way, and de Oliveira Otto said that it might be time to revise the decades-old recommendation about choosing low-fat or nonfat dairy products over full-fat versions.

But Hu, who served on the panel that drew up the most recent US Dietary Guidelines, issued in 2015, continues to stand by that advice.

Members of the panel charged with writing the 2020-2025 Dietary Guidelines have not yet been selected, but, Hu said, he doesn’t expect them to change the recommendation that favors low-fat and nonfat dairy products over high-fat dairy products. “As far as I can tell, the evidence base hasn’t really changed substantially,” he said.

Hu recently coauthored a review of evidence about dairy products, dairy fatty acids, and the prevention of cardiometabolic disease. Although the more recent studies suggesting benefits of full-fat dairy were not included in his review, they would not have changed his conclusion that “more research is needed to examine health effects of different types of dairy products in diverse populations.”

Meanwhile, Hu advises, “don’t get overstressed about just one thing. Overall dietary pattern is very important, and dairy is only 1 of many food items on our plate.”

Reality is an illusion: The scientific proof everything is energy and reality isn’t real


Quantum physicists are discovering facts about the world that we would never have thought to be possible.

The scientific breakthroughs that have taken place in the last few years are as significant to our understanding of reality as Copernicus’s outline of the solar system.

The problem? Many of us simply do not understand quantum physics. And this all began roughly a hundred years ago, when physicists began challenging the assumption that the physical space and universe that we see around us is actually “real”.

Scientists decided that to prove that reality was not, in fact, simply an illusion, they had to discover the “point particle”, and this would be accomplished with innovations like the Large Hadron Collider.

This machine was initially built to smash particles into one another, and this is where they made the greatest discovery: the physical world is not as physical as we believe. Reality is an illusion as we see it.  Instead, everything around us is just energy.

How Reality Is Just Energy

We think of the atom as an organized group of electrons and protons zooming around a neutron, but this figure is completely wrong.

The particles that make up the atoms have no structure or size, no weight or physical presence.

They have no height, length, width, or weight, and are nothing more than events in time. They have zero dimensions.

Electrons also do not have a singular presence—they are both a particle and a wave simultaneously, depending on how they are observed.

They are never in a single location at a single moment, and instead exist in several moments at the same time.

Scientists also discovered what is known as the “superposition”, in which several particles aside from electrons can be proven to exist in multiple places at a single moment.



What does all this mean?

It means that the more we discover about the subatomic world, the more we discover that we know nothing about the true nature of reality at all.

The Copenhagen Interpretation

Many scientists have come to the Copenhagen Interpretation as their conclusion for understanding reality.

The Copenhagen Interpretation comes from the school of quantum mechanics, and it believes that reality does not exist without an observer to observe it.

As reality is nothing more than energy (what gives us physicality if the smallest parts of us have no physical characteristics?), then the energy is conscious when consciousness is observing it.

This may be difficult to understand.

Think of it this way: since particles exist in several areas at the same time, then it must respond to an observation by choosing to exist in a singular location, allowing the observer to have an image to observe.

A growing number of researchers in this field believe that reality exists only because human consciousness wills it to exist, by interacting with the energy that makes up the universe.



Understanding the Universe as Information

Another mind-blowing discovery in quantum physics is entanglement.

Entanglement is when a pair of particles have interacted and have affected the spin of the other particle.

What’s strange is that once these two particles have become tangled with one another, they can never become untangled.

No matter how far apart they may stretch from the other, the spin of one particle will always affect the spin of the other.

Researchers have observed this in living cells, communicating over far distances. In one famous experiment, researchers grew algae cells in a petri dish. They then separated these cells into two halves, taking one half to another laboratory.

What they found was that no matter how much they separated the two dishes, a low-voltage current applied on one dish would always affect the cells in the other dish in the exact same way at the exact same moment.

How Is this possible?

Understanding this requires shifting the way we think of the universe. We can no longer think of the universe as a physical realm in which the things we observe and sense are all that exists.

Instead, as famous physicist Sir Roger Penrose theorized, we must envision the universe as nothing but information.

We must believe that the physical universe is just a product of an abstract universe, in which we are all connected in an unobservable way.

Information is simply embedded into the physical constructs of the physical universe, but is transmitted to our physical states from the abstract realm, first theorized by Greek philosopher, Plato.

As Erwin Schrodinger famously stated, “What we observe as material bodies and forces are nothing but shapes and variations in the structure of space. Particles are just appearances.”

Simply put, everything is nothing but energy.

Coping With A Different Reality

There are certain questions and realizations you must come to terms with after learning this true state of reality. You could obsess over the implications indefinitely, but here are a few to start you off:

  • You have never touched anything, and you never will. The electrons that make up your atoms repulse against the electrons of other physical entities, making it impossible for you to interact with other material at the subatomic level.
  • If we are not touching anything, then what is it that we feel when we “touch”?
  • How is the world physical when the building blocks that make it have no dimensions?
  • How is anything real, and what does real mean?
  • Is reality determined by physicality?

Reality show idea: Make Flat-Earthers search for the world’s edge


The contestants would try to reach the end of the world, as they understand it.

Paul Ratner 25 September, 2018

  • According to Flat-Earthers, our planet is flat and space travel doesn’t happen.
  • People are calling for a reality show about Flat-Earthers.
  • Flat-Earthers say a 150-foot ice wall surrounds the world.

Amidst all the fake news, misinformation sponsored by governments, and the explosion of conspiracy theories that bombard us daily, it’s no surprise that there seems to be a growing number of Flat-Earthers. After all, once you start doubting reality and the solidity of the institutions around you, being unsure whether the Earth is flat or round seems almost warranted. This said, there is a strong demand (at least online) for a reality show about Flat-Earthers searching for the edge of the world.

Ah. And what else could better signify our times?

Your basic flat earth belief kit often stems from biblical references, such as one, apparently, that mentions a giant tree that’s supposedly visible from all corners of the Earth — at its “farthest bounds.” If the planet was spherical this would not be possible while a flat Earth allows for such a scenario. Other beliefs that go along with this include claiming that gravity isn’t real and that a Game of Thrones-like wall of ice surrounds the rim of the disc-like Earth. This wall is Antarctica while the Arctic Circle is the disc’s center. If you went over the wall, you would fall into outer space or end up on an infinite plane. But, as the Flat Earth Society site admits, “To our knowledge, no one has been very far past the ice wall and returned to tell of their journey.”

Notably, according to the Flat-Earthers, the 150-foot-tall wall is guarded by NASA. The agency’s real mission is to keep the truth away from regular citizens while being an embezzlement front and faking space travel.

Although these beliefs are certainly not supported by the ample evidence to the contrary, provided by people who have experienced the planet’s curvature from above — or those who have been to Antarctica — the number of Flat-Earthers is likely to grow. According to a 2018 survey, about a third of millennials are willing to entertain doubts about the Earth being round. Not all of these believe in the planet being flat, but it’s easy to envision their ranks expanding, as such memes tend to acquire new converts by their sheer scope and intellectual frivolity. One clear catalyst for the resurgence of this idea has certainly been the Internet.

An animation of the day/night cycle according to Flat Earth Theory over the course of 24 hours.

Credit: Flat Earth Society.

The net, in its infinite wisdom, keeps a strong meme alive. So it is in this case, as the desire to watch a reality show about Flat-Earthers searching for the edge of the world keeps popping up on popular Reddit threads time and time again, causing tends of thousands of upvotes and comments. Of course, the impetus behind this show stems, for many, from the hope Flat-Earthers will fail spectacularly.

One such thread proposes that it would be “funny” to “give them access to a helicopter, boats, transportation, and flights to try and find the end of the world.” And then, suggests user “Pilotavery,” the contestants or “Flerfers” should be made to tell the organizers where they plan to go. The poster thinks this would dampen their enthusiasm, adding “I wonder how long it will take before they give up?” On the other hand, the poster thinks it would be “funny to see how frustrated they get.”

We should fund a reality TV show, funding/following flat earthers in the search for the end of the earth. from r/flatearth

Another idea is to have a voting component to the show, with “the most trustworthy” Flat-Earthers being sent to the International Space Station to see the truth for themselves.

While it’s certainly amusing, there is clearly a danger of such a show being set up to make the contestants look ridiculous, especially if you believe that they will not find the edge of the world. The upside for Flat-Earthers could be an opportunity to share their beliefs to millions via television, all the while trying to prove their theory right. Maybe they can make everyone else looks silly by actually finding a wall of ice at the end of the world. Wouldn’t you want to watch that to find out?

In any case, no such show exists at the moment. But, Hollywood, if you’re reading this, the internet wants what the internet wants. Make it happen.

Facebook Isn’t Sorry


On Monday morning Facebook revealed a new gadget — a voice-activated video chat tablet with an always-listening microphone and camera for your living room or kitchen that can detect when you are in your own house. This in-home panopticon is called Facebook Portal, and its debut comes at what might seem like an inopportune time for the company — days after a Gizmodo report revealed it was harvesting two-factor authentication numbers; less than 10 days after it revealed that an attack on its computer network had exposed the personal information of nearly 50 million users (and left 40 million more vulnerable); and barely six months after CEO Mark Zuckerberg appeared before Congress to explain how it let Cambridge Analytica acquire the private information of up to 87 million users without consent to be used for psychographic profiling.

To call Facebook’s newest home surveillance device ill-timed is generous. It’s like Trump announcing a new resort and casino in Moscow or BP announcing a fleet of Deepwater Horizon oil tankers. It’s a flagrant flex of Facebook’s market share muscle and a yet another reminder that the company’s data collection ambitions supersede all else.

It’s also further confirmation that Facebook isn’t particularly sorry for its privacy failures — despite a recent apology tour that included an expensive “don’t worry, we got this” mini-documentary, full-page apology ads in major papers, and COO Sheryl Sandberg saying things like, “We have a responsibility to protect your information. If we can’t, we don’t deserve it.” Worse, it belies the idea that Facebook has any real desire to reckon with the structural issues that obviously undergird its continued privacy missteps.

But more troubling still is what a product like Portal says about us, Facebook’s users: We don’t care enough about our privacy to quit it.

Tone-deaf business decisions like Portal are nothing new for Facebook. Eleven years ago, before Facebook was even a full behemoth, it was rolling out invasive features only to issue awkward apologies. The company didn’t appear to have the foresight then, and it doesn’t appear to now.

Weeks after the Cambridge Analytica privacy scandal broke, Facebook announced at its annual conference that it would soon use its trove of user data to roll out a dating app to help pair users together in “long-term” romantic relationships. Later in the year, while Zuckerberg told Congress “I promise to do better for you” and pledged increased transparency in its handling of users’ data, the company admitted to secretly using a private tool to delete the old messages of its founder. This summer, just days after Zuckerberg assured “we have a responsibility to protect people,” reports surfaced that Facebook asked US banks for granular customer financial data (including card transactions and checking account balances) to use for a banking feature. Even the company’s good faith attempts to secure its platform feel ham-handed and oblivious, like last November when Facebook asked users in Australia to upload their nude photos to Facebook for employee review to combat revenge porn.

To observers, these might seem like easily avoidable errors, but to Facebook, whose very identity and foundational mandate is the instinctual drive to amass personal data, they make perfect sense.

Facebook’s unquenchable thirst for personal information is often interpreted as sinister or malicious in nature — a frame that feels a bit too convenient. Facebook is quite obviously interested in profit and power, but its problems seem to stem less from some inherent evil than a broader, foundational failure to see itself outside of this data-gathering, world-connecting prism.

Facebook is a company founded on the principle of collecting data, and virtually every part of its two core missions (“to bring the world closer together” and to deliver profit to shareholders) require amassing more data and finding creative new ways to parse and connect it. Almost every part of Facebook — from Messenger to News Feed advertisements — improves with every new morsel of personal information collected. For this reason, many of Facebook’s biggest problems are technological problems of scale — of amassing and processing so much data — and yet Facebook argues that amassing more data is the way to improve every experience, which includes fixing its myriad problems. Advertisements intrusive and clumsy? Collect more and more precise information with which to make them more relevant! Too much algorithmically tailored, low-quality content in News Feed? Ask people to rate and rank it! Collect more data! Feed it to the algorithms! Then collect even more data and use the algorithms to police it.

Facebook has seen enormous success with this strategy. Despite all of the bad press and fallout (which includes everything from disrupting the media business to election interference to ethnic cleansing in places like Myanmar), the company is vast, powerful, and profitable. You know what happened after the Cambridge Analytica scandal? After its first president, Sean Parker, expressed regret over its ruthless monetization of attention? After legislators trotted out examples of election interference in front of executives? Facebook reported earnings and monthly average users that exceeded expectations. The stock spiked.

For Facebook employees, there’s often a cognitive dissonance between their work and how they see it described beyond company walls. “If you could see what I see, a lot of this would make more sense,” one current employee told me in October of 2017. Only recently does that answer really begin to make sense: It’s about the data.

A former senior employee described this as part of the “deeply rational engineer’s view” that guides Facebook’s decisions. “They believe that to the extent that something flourishes or goes viral on Facebook — it’s not a reflection of the company’s role, but a reflection of what people want,” they said. Data informs how decisions get made; it also conveniently absolves Facebook of blame.

It is the crystal ball that allows the company to see ahead and do what might feel to us mere mortals (privacy advocates, the media, regular users) as reckless. This is why Facebook might feel confident rolling out an always-listening home camera a few weeks after a report revealing the company harvested two-factor authentication phone numbers to target users for advertising purposes. And it might be one reason — perhaps among many — that the founders of both WhatsApp and Instagram have left the company in recent months.

Facebook is intimidatingly large and deeply woven into our cultural fabric, largely because we have allowed it to become so, and we can’t consider a world without Facebook in it. It’s not that we aren’t worried about politics becoming a Facebook data acquisition and targeting game, or outsourcing the public square to a private technology company. It’s that it’s so mind-numbingly hard to imagine how to actually loosen the company’s grip on our discourse, ad ecosystem, and our personal information that we often focus only on superficial or temporary ways to relieve it.

And that’s a great substrate for apathy. We’ve already given it so much, why stop now? No one else is going to delete Facebook, so why should I? Facebook understands this — the data tells them so. It also tells them that slickly produced videos and contrite congressional testimony are small ways to ameliorate lingering public concern.

But the real truth lies in the company’s innovations and ambitions, products like Portal. Facebook doesn’t really care. And maybe we don’t either.

Think You Don’t Need A Flu Shot? Here Are 5 Reasons To Change Your Mind


Alex Schwartzman, a law student at George Washington University in Washington, D.C., is one of only 8 to 39 percent of college students who get the flu shot in a given year.

 

There are a lot of misconceptions out there about the flu shot.

But following a winter in which more than 80,000 people died from flu-related illnesses in the U.S. — the highest death toll in more than 40 years — infectious disease experts are ramping up efforts to get the word out.

“Flu vaccinations save lives,” Surgeon General Jerome Adams told the crowd at an event to kick off flu vaccine awareness last week at the National Press Club in Washington, D.C. “That’s why it’s so important for everyone 6 months and older to get a flu vaccine every year.”

But many Americans ignore this advice. The U.S. vaccination rate hovers at about 47 percent a year. This is far below the 70 percent target. And college students are among the least vaccinated.


“We have long known that college students are at a particularly high risk of getting and spreading flu viruses,” says Lisa Ipp, an adolescent medicine specialist at Weill Cornell Medicine. “Yet, on U.S. college campuses, flu vaccination rates remain strikingly low,” she writes in a 2017 post published by the National Foundation for Infectious Disease. The group sponsored a survey of college students and found that only between 8 and 39 percent of students get the vaccine.

So why aren’t people getting the vaccine? The college survey data point to a mix of misperception and fear.

For instance, among students who don’t get the vaccine, 36 percent say that they are healthy and don’t need it, and 30 percent say they don’t think the vaccine is effective. Then, there’s the fear: 31 percent say they don’t like needles.

So, let’s do a reality check. If you’re on the fence about a flu shot, here are five arguments to twist your arm.

1. You are vulnerable.

People 65 and older are at higher risk of flu-related complications, but the flu can knock young, healthy people off their feet, too. It does every year.

“The flu can, on occasion, take a young, healthy person and put them in the intensive care unit,” says William Schaffner, medical director at the NFID.

And, even when it’s not that severe, it’s still bad. “If you get the flu, you’re [down] for the count for about a week,” Ipp tells her college-age patients.

Here’s a sobering thought: Healthy children die from flu, too. According to the CDC, 172 American children and teens (under the age of 18) died from the flu last winter. Eighty percent of them had not received a flu vaccine. And about half had no underlying illnesses before getting the flu. In other words, they’d been healthy children.

And there’s this: The flu doesn’t just make you feel lousy. It can increase the risk of having a heart attack, according to a study published this year.

2. Getting a flu shot is your civic duty.

“Nobody wants to be the dreaded spreader,” says Schaffner. But everybody gets the flu from somebody else. According to the Centers for Disease Control and Prevention, people who have caught the flu virus are contagious one day before they start to feel sick and for up to seven days after. (Check out our video on flu contagion if you really need to be convinced!)

So getting the flu shot will help protect your family, friends and co-workers. “It’s the socially correct thing to do,” Schaffner says.

3. You can still get the flu, but you won’t be as sick.

After last winter’s severe season, some people are skeptical. They say: “I got the flu shot, but I still caught the flu.”

In fact, the 2017-18 season was the deadliest in more than 40 years. “We had a very vicious virus, the so-called H3N2 influenza strain,” says Schaffner.

And yes, it’s true that the vaccine does not offer complete protection. The CDC estimates that flu vaccination reduces the risk of the virus by about 40 to 60 percent. Think of it this way: If you catch the flu, the vaccine does still offer some protection. It cushions the blow. “Your illness is likely to be milder” if you’ve had a flu shot, says Schaffner. You’re less likely to get pneumonia, which is a major complication of the flu, and less likely to be hospitalized.

4. Pregnant women who get the flu shot protect their babies from flu.

Women who are pregnant should be vaccinated to protect themselves. The vaccine also offers protection after babies are born. “[Women] can pass the protection on, across the placenta,” Schaffner explains. And this will protect their baby during the first six months of life, until the baby is old enough to be vaccinated.

5. You cannot get flu from the flu vaccine.

It’s still a common misperception: the idea that you can get the flu from the flu shot.

The NFID-sponsored survey of college students found that close to 60 percent of students seem to think that the flu vaccine can cause flu. “That’s, of course, incorrect,” says Schaffner.

The most common side effects are a sore arm, and perhaps a little swelling. “A very small proportion of people, 1 to 2 percent, get a degree of fever,” Schaffner says. That’s not the flu, he explains. “That’s the body reacting to the vaccine.”

Because the flu is unpredictable, it’s too soon to know what to expect this winter. But Schaffner has this advice: Don’t wait. “The time to get vaccinated is right now,” he says.

If that doesn’t move you, maybe a little reward will. The survey data of college students found that incentives are a good idea. Think: free food, free entertainment or a gift card for a free coffee. Ipp found about 60 percent of students said these types of incentives would increase the likelihood of their getting the flu vaccine.

Another way to nudge people? Make it super convenient. On the campus of George Washington University, the medical director of the student health center has organized flu-clinic pop-ups in venues where students hang out, such as the library. “We don’t wait for them to come to us,” Isabel Goldenberg told us.

For workers in offices, flu clinics at the workplace can be an effective way to encourage vaccination, too.

What about the use of social media to motivate people? “I’ve had the flu, which was horrible,” Max Webb, a student at George Washington University, told me. He thinks if people shared their flu stories, it could help nudge people in their social networks to get the flu shot.

And what would you name this campaign, I asked Webb? “Say boo to the flu,” Webb replied. Or simply, #boo2flu.

Kinda catchy.

Brain Activity Has Been Recorded as Much as 10 Minutes After Death


main article image

 

Doctors in a Canadian intensive care unit stumbled on a very strange case last year – when life support was turned off for four terminal patients, one of them showed persistent brain activity even after they were declared clinically dead.

For more than 10 minutes after doctors confirmed death through a range of observations, including the absence of a pulse and unreactive pupils, the patient appeared to experience the same kind of brain waves (delta wave bursts) we get during deep sleep.

And it’s an entirely different phenomenon to the sudden ‘death wave’ that’s been observed in rats following decapitation.

“In one patient, single delta wave bursts persisted following the cessation of both the cardiac rhythm and arterial blood pressure (ABP),” the team from the University of Western Ontario in Canada reported in March 2017.

They also found that death could be a unique experience for each individual, noting that across the four patients, the frontal electroencephalographic (EEG) recordings of their brain activity displayed few similarities both before and after they were declared dead.

“There was a significant difference in EEG amplitude between the 30-minute period before and the 5-minute period following ABP cessation for the group,” the researchers explained.

Before we get into the actual findings, the researchers are being very cautious about the implications, saying it’s far too early to be talking about what this could mean for our post-death experience, especially considering their sample size is one.

In the absence of any biological explanation for how brain activity could possibly continue several minutes after the heart has stopped beating, the researchers said the scan could be the result of some kind of error at the time of recording.

But they were at a loss to explain what that error could be, as the medical equipment showed no signs of malfunction, meaning the source of the anomaly cannot be confirmed – biologically or otherwise.

“It is difficult to posit a physiological basis for this EEG activity given that it occurs after a prolonged loss of circulation,” the researchers wrote.

“These waveform bursts could, therefore, be artefactual [human error] in nature, although an artefactual source could not be identified.”

You can see the brain scans of the four terminal patients below, showing the moment of clinical death at Time 0, or when the heart had stopped a few minutes after life support had been turned off:

brain-waves-deathsNorton et al. (2017)

The yellow brain activity is what we’re looking for in these scans (view a larger version here), and you can see in three of the four patients, this activity faded away before the heart stopped beating – as much as 10 minutes before clinical death, in the case of patient #2.

But for some reason, patient #4 shows evidence of delta wave bursts for 10 minutes and 38 seconds after their heart had stopped.

The researchers also investigated if a phenomenon known as ‘death waves’ occurred in the patients – in 2011, a separate team observed a burst of brain activity in rat brains about 1 minute after decapitation, suggesting that the brain and the heart have different moments of expiration.

“It seems that the massive wave which can be recorded approximately 1 minute after decapitation reflects the ultimate border between life and death,” researchers from Radboud University in the Netherlands reported at the time.

death-wave

When the Canadian team looked for this phenomenon in their human patients, they came up empty.

“We did not observe a delta wave within 1 minute following cardiac arrest in any of our four patients,” they reported.

If all of this feels frustratingly inconsequential, welcome to the strange and incredibly niche field of necroneuroscience, where no one really knows what’s actually going on.

But what we do know is that very strange things can happen at the moment of death – and afterwards – with a pair of studies from 2016 finding that more than 1,000 genes were still functioning several days after death in human cadavers.

And it wasn’t like they were taking longer than everything else to sputter out – they actually increased their activity following the moment of clinical death.

The big takeaway from studies like these isn’t that we understand more about the post-death experience now than we did before, because the observations remain inconclusive and without biological explanation.

But what they do show is that we’ve got so much to figure out when it comes to the process of death, and how we – and other animals – actually experience it, from our bodies to our brains.

Can Exercise Worsen Dementia?


Could exercise worsen dementia? The idea runs against one of the fondest hopes of patients with Alzheimer disease, their caregivers, and physicians. It contradicts some early research and tentative recommendations. But it is a key finding of one of the largest studies yet to examine the question.

In the Dementia And Physical Activity (DAPA) trial, the mean score on the Alzheimer’s Disease Assessment Scale-Cognitive Subscale (ADAS-cog) worsened more for people with dementia who were assigned to a year of vigorous exercise than for people who kept to their usual routines.[1]

The difference was small but statistically significant, says Bart Sheehan MRCPsych, MD, consultant liaison psychiatrist at the Coventry and Warwickshire Partnership Trust in Coventry, United Kingdom. “It does raise the possibility that, at this point, vigorous exercise might be damaging for people.”

The finding has experts in the field taking a harder look at what they thought they knew about the way physical activity affects a declining brain. It comes as a particular blow because no one has found a way to halt Alzheimer disease. “People are desperate for a treatment,” Sheehan said.

Until the DAPA results came out, exercise was looking like one of the most promising possibilities—if not to stop dementia, then at least to slow its progression. “Among patients with dementia or mild cognitive impairment, randomized controlled trials (RCTs) documented better cognitive scores after 6 to 12 months of exercise compared with sedentary controls,” wrote the authors of a 2011 meta-analysis.[2]

Such results were enough to prompt the Mayo Clinic website, a health information website for consumers, to advise that “Exercising several times a week for 30 to 60 minutes may… improve memory, reasoning, judgment and thinking skills (cognitive function) for people with mild Alzheimer’s disease or mild cognitive impairment.”[3]

But these findings were from relatively small trials. And negative results have also cropped up in the literature for years, including in other reviews of the literature.[1] Funded by the British government, Sheehan and his colleagues set out to settle the question with the most authoritative trial possible.

They recruited 494 people with mild to moderate dementia according to the criteria in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV). All lived in the community and were able to sit on a chair and walk 10 feet without assistance. The average age was 77. Sixty-one percent were men.

The researchers randomly assigned 329 to exercise and 165 to make no change in their physical activity. The exercisers attended group sessions in a gym twice a week for 4 months under the guidance of physical therapists. Each session lasted 60-90 minutes. The researchers asked them to work out for an additional hour each week at home during this period. The sessions included cycling in place for 25 minutes of moderate to hard intensity, as well as weight training such as biceps curls, shoulder forward raise, lateral raise, and sit-to-stand using a weighted vest or waist belt.

After the 4 months, the researchers prescribed a home-based program of unsupervised exercise of 150 minutes each week. They encouraged the participants to choose activities at home that they preferred and followed up with phone calls to encourage them. Eighty-eight percent reported continuing the exercises at home. Less than 1% of the participants reported doing structured exercise outside of the trial.

The people who evaluated the patients didn’t know which ones participated in the exercise programs and which ones did not.

After 12 months, the patients improved their fitness compared with the usual-care group. But when it came to cognitive function, the researchers recorded abysmal results. On the ADAS-cog, where a higher score means worsening function, the usual-care group went from 21.4 to 23.8, a worsening of 2.4 points, as might be expected with the progressive diseases that cause dementia.

But the exercisers fared even worse, going from a mean score of 21.2 to 25.2, a worsening of 4.0. For perspective, a normal score for someone who does not have dementia is 5, while the average score of someone diagnosed with probable Alzheimer’s or mild cognitive impairment is 31.2.

The difference was statistically significant (P =.03). It’s not clear whether it has clinical significance, Sheehan says. Still, it startled the researchers.

Despite their improved physical fitness, the exercisers did not improve in activities of daily living, behavior, or health-related quality of life.

“It didn’t come as a surprise that physical exercise was not effective as a treatment for dementia, because dementia is notoriously difficult to treat,” he said. “I think what was a surprise is the very strong signal that it may make dementia worse.” They ran the statistics again and again but found no mistake.

And the finding held up regardless of the patients’ sex or mobility and regardless of whether they were diagnosed with Alzheimer’s versus other kinds of dementia, or whether they had mild versus severe cognitive impairment.

Despite their improved physical fitness, the exercisers did not improve in activities of daily living, behavior, or health-related quality of life.

The finding should influence what clinicians say to people with dementia and their caregivers, said Sheehan, who has treated many such patients. He now tells them that exercise won’t help with such core features of dementia as memory or the ability to organize oneself, and that it might actually do damage.

People who are already exercising and enjoying it shouldn’t necessarily stop, he added. But they must weigh the enjoyment and other health benefits—which are many—against the risk for harm.

Not everyone interprets the results of the DAPA trial as pessimistically as Sheehan. “We don’t have the evidence yet to be able to say that exercise is going to improve cognitive function,” said J. Carson Smith, PhD, an associate professor of public health at the University of Maryland. “But there is more evidence of a benefit in mild cognitive impairment and in people at increased risk for dementia.”

He is among the researchers whose small studies have suggested that exercise can improve cognitive ability in people with mild cognitive impairment. Epidemiologic studies measuring the benefits of long-term exercise for preventing dementia are even more impressive.

This includes a recent sample of 191 Swedish women who were 38-60 years of age in 1968 when they underwent an ergometer cycling test. Examinations of dementia were done six times up to 2010 and supplemented with information from medical records. Women with high physical fitness at middle age were nearly 90% less likely to develop dementia decades later, compared with women who were moderately fit.[4]

Smith and others have found biological differences between more and less fit people that could explain a difference in dementia risk. Lower cardiovascular fitness is associated with a smaller brain volume two decades later, for example.[5]

It’s hard to explain why exercise in healthy people might protect against cognitive decline, but exercise in people with dementia might make it worse. Sheehan theorized that already weakened brains might be too fragile to withstand the temporary loss of oxygen that comes with vigorous exercise. But there isn’t much information yet to support or refute such ideas.

Such studies can’t prove cause and effect. Not only physical activity but also genes affect physical fitness. And people who exercise may have other healthy behaviors.

But even Sheehan has not given up on the idea that physical activity can help people in their declining years. Some kinds of exercise can improve balance, for example. “People say, ‘I wish my father could recognize me,’ but they also say, ‘I wish my father didn’t fall over,'” he points out.

Why BMI is a Big Fat Scam


Story at-a-glance

  • Body mass index (BMI), a formula that divides your weight by the square of your height, is one of the most commonly used measures of overweight, obesity, and overall health
  • Initially, BMI was primarily a tool used by insurance companies to set premiums (people with BMIs in the “obese” category may pay 22 percent more for their insurance compared to those in the “normal” category
  • BMI is a flawed measurement tool, in part because it uses weight as a measure of risk, when it is actually a high percentage of body fat that increases your disease risk
  • BMI also tells you nothing about where fat is located in your body, and the location of the fat, particularly if it’s around your stomach (visceral fat), is more important than the absolute amount of fat when it comes to measuring certain health risks
  • Your waist-to-hip ratio is a more reliable indicator of your future disease risk because a higher ratio suggests you have more visceral fat.

 

BY DR. MERCOLA

In 1832, a Belgian mathematician named Adolphe Quetelet developed what is today known as the body mass index (BMI).1The formula divides a person’s weight by the square of his height, and is one of the most commonly used measures of excess weight, obesity, and overall health.

Initially, BMI was primarily a tool used by insurance companies to set premiums (people with BMIs in the “obese” category may pay 22 percent more for their insurance compared to those in the “normal” category2).

Today, however, BMI is an accepted tool used in medical research and in clinical practice. When you have your height and weight recorded at your doctor’s office, it will give him or her an automatic calculation of your BMI, classifying you as underweight if your BMI is below 18.5, normal if it’s 18.5-24.9, overweight if it’s 25-29.9, and obese if it’s 30 or over.

Your doctor may use this number to advise you on your weight, as well as your risk of related conditions like heart disease, high blood pressure, and type 2 diabetes. Unfortunately, BMI is an incredibly flawed tool, and a high BMI doesn’t automatically mean you’re unhealthy, the way many physicians and health insurance companies imply that it does.

The Obesity Paradox: Sometimes Higher BMI Is Healthier

Research involving data from nearly 3 million adults suggests that a having an overweight BMI may be linked to a longer life than one that puts you within a “normal” weight range.

The research, which analyzed 97 studies in all, found that people with BMIs under 30 but above normal (the overweight range) had a 6 percent lower risk of dying from all causes than those who were normal weight, while those whose BMIs fell into the obese range were 18 percent more likely to die of any cause.3

Separate research published in the Journal of the American College of Cardiology, also found that a high BMI was associated with a lower risk of death, a phenomenon known as the “obesity paradox.”4

Indeed, it is quite possible to be overweight and healthy, just as it’s possible to be normal weight and unhealthy. And in some cases, it may, in fact, be healthier to carry a few extra pounds. In a Journal of the American Medical Association (JAMA)editorial, Steven Heymsfield, M.D. and William Cefalu, M.D. explained:5

“The presence of a wasting disease, heart disease, diabetes, renal dialysis, or older age are all associated with an inverse relationship between BMI and mortality rate, an observation termed the obesity paradox or reverse epidemiology. 

The optimal BMI linked with lowest mortality in patients with chronic disease may be within the overweight and obesity range. 

Even in the absence of chronic disease, small excess amounts of adipose tissue may provide needed energy reserves during acute catabolic illnesses, have beneficial mechanical effects with some types of traumatic injuries, and convey other salutary effects that need to be investigated in light of the studies…” 

However, for the vast majority of those who carry around extra pounds, health problems will often result. So why would these studies suggest otherwise? They are likely examples of why BMI is such a flawed tool for measuring your health.

Makers of Weight Loss Drugs Altered BMI Categories, Making 29 Million Americans ‘Overweight’

BMI is used as the measure of national obesity rates, which currently stand at close to 35 percent for adults and 18 percent for kids. However, the cut-off for classifying a person as normal or overweight seems to be quite arbitrary – and at one point was significantly modified by a task force funded, primarily, by companies making weight loss drugs. Mother Jones reported:6

“In 1998, the National Institutes of Health lowered the overweight threshold from 27.8 to 25—branding roughly 29 million Americans as fat overnight—to match international guidelines. 

But critics noted that those guidelines were drafted in part by the International Obesity Task Force, whose two principal funders were companies making weight loss drugs. 

In his recent book ‘Fat Politics: The Real Story Behind America’s Obesity Epidemic,’ political scientist Eric Oliver reports that the chairman of the NIH committee that made the decision, Columbia University professor of medicine Xavier Pi-Sunyer, was consulting for several diet drug manufacturers and Weight Watchers International.”

BMI Uses Weight, Not Body Fat, to Measure Risk

Branding yourself as unhealthy or overweight simply based on your BMI is not recommended (unfortunately, your insurance company probably won’t see it this way). On the other hand, assuming you’re healthy just because your BMI is normal isn’t advised either.

Research suggests BMI may underestimate obesity rates and misclassify up to one-quarter of men and nearly half of women.7 According to researcher Dr. Eric Braverman, president of the nonprofit Path Foundation in New York City:8

“Based on BMI, about one-third of Americans are considered obese, but when other methods of measuring obesity are used, that number may be closer to 60%.”

One of the primary reasons why BMI is such a flawed measurement tool is that it uses weight as a measure of risk, when it is actually a high percentage of body fat that increases your disease risk. Your weight varies according to the density of your bone structure, for instance, so a big-boned person may weigh more, but that certainly doesn’t mean they have more body fat or make them more prone to heart disease, for example.

Athletes and completely out-of-shape people can also have similar BMI scores, or a very muscular person could be classified as “obese” using BMI, when in reality it is mostly lean muscle accounting for their higher-than-average weight. BMI also tells you nothing about where fat is located in your body, and it appears that the location of the fat, particularly if it’s around your stomach, is more important than the absolute amount of fat when it comes to measuring certain health risks, especially heart disease.

Waist-to-Hip Measurement Is Superior to BMI, But Only 10 Percent of Physicians Use It

Your waist-to-hip ratio is a more reliable indicator of your future disease risk because a higher ratio suggests you have more visceral fat. Excess visceral fat—the fat that accumulates around your internal organs — is far more hazardous to your health than subcutaneous fat (the more noticeable fat found just under your skin) – a measure that BMI tells you nothing about. The danger of visceral fat is related to the release of proteins and hormones that can cause inflammation, which in turn can damage arteries and enter your liver, and affect how your body breaks down sugars and fats.

Unfortunately, according to Donna Ryan, a physician who has trained thousands of primary-care doctors in obesity screening, only about 10 percent use waist circumference as a health indicator. She told Mother Jones:9 “Doctors are so pressed for time… And it’s intrusive. You have to put your arms around the patient.” To determine your waist-to-hip ratio, get a tape measure and record your waist and hip circumference. Then divide your waist circumference by your hip circumference. For a more thorough demonstration, please review the video above.

Waist to Hip Ratio Men Women
Ideal 0.8 0.7
Low Risk <0.95 <0.8
Moderate Risk 0.96-0.99 0.81 – 0.84
High Risk >1.0 >0.85

How Much You Exercise Also Predicts Your Disease Risk

Your fitness level is also a far better predictor of mortality than your BMI. One study found that people who rarely exercised had a 70 percent higher risk of premature death than those who exercised regularly, independent of their BMI.10 If you want a simple test to gauge your fitness level, try the abdominal plank test (for a demonstration of how to do a plank, see the video below. If you can hold an abdominal plank position for at least two minutes, you’re off to a good start. If you cannot, you’re likely lacking in core strength, which is important for overall movement stability and strength.

A strong core will also help prevent back pain. Being unable to hold a plank for two minutes may also indicate that you’re carrying too much weight and would benefit from shedding a few pounds. Unfortunately, over 50 percent of American men, and 60 percent of American women, never engage in any vigorous physical activity lasting more than 10 minutes per week.11 This despite a growing body of research clearly showing that “exercise deficiency” threatens your overall health and mental well-being, and shortens your lifespan.

In fact, according to research published in the American Journal of Physiology, the best way to stay young is to simply start exercising, as it triggers mitochondrial biogenesis, a decline of which is common in aging.12 Researchers have also suggested that exercise is “the best preventive drug” for many common ailments, from psychiatric disorders to heart disease, diabetes, and cancer.13 According to Jordan Metzl, a sports-medicine physician at New York City’s Hospital for Special Surgery and author of The Exercise Cure: “Exercise is the best preventive drug we have, and everybody needs to take that medicine.”

So rather than stressing over an arbitrary number like your BMI, you’d be better served by coming up with a comprehensive fitness plan. I recommend incorporating high-intensity interval training (HIIT)strength training (including super slow), core exercises, stretching, and non-exercise activity into your routine. The key is to simply get moving, and work at a high enough intensity with enough variance to keep your muscles adequately challenged.

Every person is different, so there’s not just one “correct” way to exercise. Equally, if not more, important is incorporating regular intermittent movement into your day, as this will help to counteract some of the effects excess sitting has on your body. If you exercise correctly and keep moving throughout your day, and combine it with a healthy eating program, you will optimize your body-fat percentage naturally, and with it gain a predisposition for optimal health.