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Do you feel like doing something out of the ordinary today? It might be because on Leap Day interesting things have happened throughout history. Everyone knows you have 365 days on the calendar, but nearly every four years you get an extra day.
This happens since nearly every four years the dates on the calendar don’t line up with the true year, or the amount of time it takes the Earth to orbit the sun. In other words, leap year is the year an extra day is added to the month of February to synchronize the seasons with the calendar.
If you think having a leap year is confusing, wait until we talk about the "leap second."1 In both cases, with the Leap Day and leap second, scientists adjust the calendar and time to bring the solar day into alignment with Universal Time used in sensitive applications, aviation and the internet.
A leap second accounts for a difference in the gravitational pull on the Earth from the sun and moon. As the Earth rotates it slows imperceptibly so one second of time is added intermittently to the clock.
The last one happened at midnight December 31, 2016, and the next is scheduled for June 30, 2020. The extra second has been added 27 times since 1972. While a leap second may be fascinating, it is unnoticeable in your day. But, an extra day every 4 years may be something to celebrate.
The addition of one day every four years is due to the sun. It takes the Earth 365.242189 days to rotate around the sun one time. Expressed another way, circling the sun takes 365 days, 5 hours, 48 minutes and 45 seconds. When calendars to mark the year were first created, they were based on 365 days in a year without any additional hours or minutes.
The change began in 46 BC2 when Julius Caesar asked the Greek astronomer Sosigenes to adjust the Roman calendar with the seasons.3 One of the adjustments called for an extra day to keep the calendar, Earth and sun in sync. But too many leap years created another problem.
By 1577 the difference between the number of days in the Julian calendar base — 365.25 days — and the actual number of days — 365.24219 — resulted in the calendar being 10 days out of alignment with the Earth's position relative to the sun.
To correct for the 11-minute discrepancy, Pope Gregory XIII created the Gregorian calendar.4 At the same time, 10 days were dropped from October that year and February 29 became the official additional day.
The point was to make sure the spring and autumn equinoxes fell on the same days each year.5 The equinox describes the tilt of the Earth's equator in relation to the sun over the course of one year.6 The word is from Latin, meaning aequus (equal) and nox (night) since on the spring and autumn equinox the length of day and night are each 12 hours at all points except at the North and South Poles.
Although leap year happens on your calendar every four years, it doesn't happen exactly every four years. During Leap Year the extra day is added to the end of February making that year 366 days. If the solar year, sometimes called the tropical year,7 was precisely six hours longer than the calendar year, then adding one day every four years would make up for the 24 hours lost.8
Instead, the time difference is 11 minutes short of six hours. Without the addition of a leap year the calendar would be off 24 days every 100 years, which would quickly put Christmas during summer in the Northern Hemisphere. However, if a leap year happens exactly every four years, the calendar would also shift, albeit more slowly, by 11 minutes each year.
So, a Gregorian calendar has a slightly more complex set of guidelines. The criteria that helps identify which years are leap years begins with the rule of division. If the year is divisible by four then it is a leap year. However, years that mark centuries are different. These must be divisible by 400. This meant 2000 and 2400 are leap years but 2200 will not be.
The idea of adding an extra day to the calendar every four years seemed silly to some. One British play poked fun at it with the inclusion of a joke that on that day, women could act like men.9 The play was meant to be ridiculous but by the 1700s a tradition was born.
Now it's known as Bachelor's Day in the U.K. or Sadie Hawkins Day in the U.S., a day when it's acceptable for women to ask men for their "hand in marriage." The tradition continues to be popular in the U.K., inspiring some stores to offer discount wedding packages to those who said yes on Leap Day.
One legend has it that women proposing on Leap Day dates back to when English law didn't recognize February 29.10 The idea was if a day has no legal status it was acceptable to break tradition. In other cultures, a man would be fined if he said "no" to a woman's proposal of marriage on Leap Day. In Denmark he was bound to give her 12 pairs of gloves and in Finland, cloth for a skirt.
Traditions attached to marriages in Leap Year don't stop there. In Greece, 20% of couples don't get married in Leap Year as they believe it's bad luck. Engaged couples aren't the only ones who think there may be some bad luck in the leap year.
In Scotland they say, "Leap Year was ne'er a good sheep year." as they thought livestock didn't thrive in those years. Mother Nature Network reports the Italians go a bit further:11
"In Italy, where they say ‘anno bisesto, anno funesto’ (which means leap year, doom year), there are warnings against planning special activities such as weddings. The reason? ‘Anno bisesto tutte le donne senza sesto’ which means ‘In a leap year, women are erratic.’"
The twin cities Anthony, Texas, and Anthony, New Mexico, took the concept of Leap Year to heart and declared themselves the leap year capitals of the world. Each year they throw a Worldwide Leap Year Festival that goes on for four days, including a birthday party for those who were born on the day.12
The festival was proposed in 1988 when two women born on Leap Day, one in each city, proposed the event that includes parades, dancing and tours. The gala has attracted people from around the world.13
Most of the 4.1 million "leaplings" or "leapers" don't wait four years to celebrate.14 Birthdays are either commemorated on February 28 or March 1 — until February 29 rolls around again. The chance of being born on that day is 1 in 1,461, according to History.com.15
If the chances of being born on Leap Day are that low, then what are the odds that one family might have three children born on consecutive leap days? History.com reports that the Henriksens of Norway made the Guinness Book of World Records when Heidi, Olav and Leif-Martin were born in 1960, 1964 and 1968, respectively.
Others who claim Leap Day as the day of their birth include singer actress Dinah Shore, motivational speaker Tony Robbins and big band leader Jimmy Dorsey.
Those born on Leap Day have access to a special club launched in 1997.16 The mission of the Honor Society of Leap Year Day Babies (HSLYDB) is to promote awareness and the challenges people born on Leap Day face with insurance companies and governmental documents. The website says:17
"Membership in the society is free but is restricted to people born on Leap Year Day. We think we are the world's largest birthday club, and we hope it offers all people born on Leap Year Day even more pleasure in celebrating their birthday."
Corporations also have had some difficulty with people born on a day happening only once every four years. In 2008 Toys R Us had a computer glitch that caused Leap Year babies to miss out on their personalized birthday cards from Geoffrey the Giraffe, the Toys R Us mascot.18 The problem was fixed after the co-founder of the HSLYDB wrote:
“How do you explain to a five-year-old that they won’t receive a birthday card from Geoffrey over at Toys "R" Us this year, because the Toys "R" Us computer has no way to recognize their birthday?”
More than a few interesting events have happened on February 29. One quirky item is February 30. This rare date happened in 1712 in Sweden and Finland when they added the day as they switched from the Julian to the Gregorian calendar.19 Here are several more happenings on a day that happens just once every four years:
• Salem Witch Trials — The first arrest warrants were issued on February 29, 1692, for Sarah Good, Sarah Osborne and Tituba. Good hung after refusing to confess, Osborne perished in prison and Tituba admitted to being a witch, earning her release a year later.20
• La Bougie du Sapeur — You can purchase this French newspaper published once every four years for €4 at a newsstand.21 The publication, The Sapper's Candle, is a spoof that takes its lead from a "Sapper," the name for a military engineer known for digging trenches and tunnels.22
• Buddy Holly's Glasses — The lost was found on February 29, 1980, when county Sheriff Jerry Allen found the famed singer’s trademark glasses buried in an envelope in old court records.23 The glasses were initially recovered in the spring after the plane crash that killed Holly and the Big Bopper in the winter of 1959. They were then sealed in a manila envelope. It was over 20 years later when the frames were returned to Holly's widow.
• Hank Aaron — February 29, 1972, Hank Aaron became the highest paid major league baseball player in history, earning a $200,000 contract to play in Atlanta.
I was recently interviewed by Siim Land about my new book, "EMF*D," described by Siim as "the most comprehensive guide … to everything you need to know about EMF."
In it, I explain what electromagnetic fields (EMFs) are, the different types of EMFs you're exposed to, the harms associated with exposure, the concerns surrounding 5G and, ultimately, how to protect yourself and limit your exposure.
As I explain in the interview, the thing that catalyzed me to write "EMF*D" was my deep appreciation of the impact of mitochondrial function in health and disease. Once I realized how EMFs impact mitochondrial function — because it's very clear that EMF causes massive mitochondrial dysfunction — the danger our wireless society poses became very clear to me.
Just recently, I read a study1 stressing the importance of mitochondrial numbers for improving senescent cells — cells that are, in a manner of speaking, "senile" and have stopped reproducing properly. Instead, senescent cells produce inflammation, contributing to old age and, ultimately, death.
The fewer mitochondria you have, and the more dysfunctional they are, the faster you'll age and the more prone you'll be to chronic degenerative disease. By inducing mitochondrial dysfunction, our wireless world may well be driving us all into an early grave.
Considering the research data now available, you'd think everyone would understand and accept the fact that EMF is a serious health danger, yet many are still completely in the dark. With "EMF*D," I hope to help more people understand this biological threat.
In 2011, the World Health Organization's International Agency for Research on Cancer (IARC) classified radiofrequency EMFs as "possibly carcinogenic to humans."2 Then, in 2018, the U.S. National Toxicology Program published two lifetime exposure studies conclusively showing cellphone exposure causes cancer.
The NTP's findings were also duplicated by the Italian Ramazzini Institute just a couple of months later. In the wake of these studies, Fiorella Belpoggi, principal investigator and director of the Ramazzini Institute, urged the IARC to upgrade RF-EMF to "probably carcinogenic" or higher.3
Now, just like smoking cigarettes, EMF exposure takes decades before its effects become evident (and even then, the health problem might not be directly linkable to EMF exposure), and this is a significant part of the problem as it allows the telecom industry to — just like the tobacco industry before it — whitewash concerns, manipulate research and prevent proper safety studies from being done.
There's no doubt cellphone manufacturers are aware that EMFs from cellphones contribute to health problems, though. The evidence has been published for decades, and new research is constantly being added.
However, by downplaying positive findings and saying that findings of harm are inconclusive — in other words, by creating doubt and controversy — they effectively prevent the public from knowing the truth and demanding safer products.
Another wireless industry strategy that prevents the problem from becoming public knowledge is the capturing of our federal regulatory agencies, which the tobacco industry wasn't even capable of.
The U.S. Environmental Protection Agency, the Surgeon General and the Centers for Disease Control and Prevention all warned people about smoking, yet the tobacco industry continued successfully selling cigarettes for another 20 or 30 years. The wireless industry, on the other hand, has captured the federal regulatory agencies, which prevents those warnings from being issued in the first place.
For example, the chief lobbyist for the wireless industry, Tom Wheeler, was appointed by President Obama to be the head of the Federal Communications Commission, which is a most egregious example of the fox guarding the hen house. Not surprisingly, then, in December 2019 the FCC announced they're going to fund rural 5G deployment to the tune of $9 billion!4
As detailed in my February 1, 2020, article, "The War Against 5G Heats Up," the telecom industry has engaged in a vast and illegal fraud where, for decades, basic telephone rate payers — wire line customers — have funded the deployment of wireless in general, and now 5G in particular, through their phone bills.
This illegal redirection of funds amounts to about $1 trillion over the past 15 years, and without this money, 5G would not have been possible in the first place. Were the wireless industry forced to pay its fair share of infrastructure costs, 5G simply wouldn't be economically feasible as a consumer product.
What exactly is 5G and why do some people want it? In short, it's all about improving speed. Compared to 4G, 5G is 100 times faster. On a side note, you can determine what your bandwidth is by pulling up fast.com on your cellphone's browser. If you're on 4G, your bandwidth is probably not going to exceed 10 megabytes per second (mb/s). If you're on 5G, it's going to be between 500 and 800 mb/s.
So, the primary benefit of 5G is noticeably faster speed. The vast majority of people simply don't need this kind of bandwidth, but it has great applications for commercial uses such as self-driving cars.
The problem is, 5G may end up making the earth uninhabitable for many who are already struggling with electrosensitivity, and the countless others for whom 5G may prove to be the thing that tips them over the edge into electrohypersensitivity syndrome.
Elon Musk's Starlink project, which is slated to deploy up to 42,000 satellites into low earth orbit, will blanket the entire planet with 5G internet. You won't be able to escape it, no matter how far into the wilderness you go.
Then there are the long-term dangers of 5G, which we still do not have a complete picture of. There has not been a single safety study done on 5G. Studies using 2G, 3G and 4G, however, including the NTP and Ramazzini studies, clearly show there's cause for concern.
5G is more complex, as it uses a variety of frequencies, which makes it a potentially greater threat. The frequency of 4G is typically around 2 to 5 gigahertz (GHz), while 5G will be around 20 to 30 GHz, initially.
Eventually, it may go as high as 80 GHz, which will cause problems for people trying to remediate exposures because there are currently no inexpensive meters that can measure frequencies that high.
Based on the studies already done on previous generations of wireless, we know it's harmful, and 5G is only going to make matters worse, as it will dramatically increase our exposures. 5G requires what essentially amounts to a mini cellphone tower outside every fifth or sixth house on every block.
We also have studies showing the impact of millimeter waves, which is what 5G is using, on insects, animals and plants, and those hazards are well-documented. So, it doesn't just pose a problem for human health, but for the ecosystem as a whole.
Martin Pall, Ph.D., wrote an excellent paper explaining how EMFs affect your voltage gated calcium channels (VGCCs) — channels in the outer plasma membrane of your cells. Each VGCC has a voltage sensor, a structure that detects electrical changes across the plasma membrane and opens the channel. EMFs work through the voltage sensor to activate the channel and radically increase intracellular calcium levels into dangerous ranges.
Similar channels are found in most biological life, including animals, insects, plants and trees. So, flooding the planet with these frequencies will undoubtedly have serious biological consequences across the ecosystem. As such, it's an existential threat to humanity.
One biological consequence is arrhythmia (irregular heartbeat). Other potential consequences include autism and Alzheimer's. Heart and neurological problems top the list because your heart and brain have the greatest density of VGCCs. Men's testes also have a very high density of VGCCs and, indeed, we have evidence showing EMFs increase men's risk of infertility.
Everything points to these frequencies being a prescription for biological disaster, and between skyrocketing autism, Alzheimer's and infertility rates, how can a society be sustained? It can't. It will be extinguished.
In reality, we can still get the bandwidth of 5G without 5G wireless. The alternative would be to deploy fiber optic cable. It's faster, safer and less expensive.
Unfortunately, the money originally set aside to implement nationwide fiber optics was rerouted and illegally used to build the wireless infrastructure instead. This is why a group called The Irregulators5 are now suing the FCC to put a stop to the illegal subsidy to the wireless industry.
Wireline customers paid for an upgrade to fast and safe fiber optic wiring across the nation, but now we're getting harmful 5G wireless instead. As explained in "The War Against 5G Heats Up" (hyperlinked above), this lawsuit has the potential to alter the telecommunications industry from the ground up, and may be the "weapon" we need to halt to the 5G rollout in the U.S.
Along with practical remediation strategies, "EMF*D" also covers things you can do to protect yourself on a biochemical level. A perfect storm of DNA and cellular protein and membrane destruction is created when you aren't burning fat for fuel (which creates excess superoxide) and then get exposed to EMFs.
This causes a radical increase in nitric oxide release that nearly instantaneously combines with superoxide to create enormous levels of peroxynitrate, which triggers a cascade of destructive events to your cellular and mitochondrial DNA, membranes and proteins.
Although all biologic damage is of concern, it is the DNA strand breaks that are most concerning as they will lead to a radical increase in inflammation and virtually all degenerative diseases.
The good news is your body has the ability to repair this damaged DNA with a family of enzymes called poly ADP ribose polymerase or PARP It is a very effective repair system and works wonderfully to repair the damage as long as it has enough fuel in the form of NAD+.
The bad news is many of us are running low on this fuel. When excess peroxynitrate activates PARP to repair the DNA damage, it consumes NAD+, and if you run out, you can't repair the damage. This appears to be a central cause for most of the diseases we now see in the modern world.
Optimizing your NAD+ levels may be the single most important strategy for improving your mitochondrial health. The first step is to reduce NAD+ consumption by the correct diet (low in processed foods and net carbohydrates and higher in healthy fats), along with EMF avoidance, as recent research shows NAD+ levels dramatically drop when exposed to EMFs.
Time restricted eating is also very helpful, as is exercise, both of which are powerful, inexpensive and safe ways to boost your NAD+ level.
In "EMF*D" I also cover the Nrf2 pathway and the importance of minerals such as magnesium to limit the biological damage caused by EMFs. As explained in this interview, upregulating your Nrf2 pathway activates genes that have powerful antioxidant effects, thus helping protect against EMF damage, while magnesium — which is a natural calcium channel blocker — helps reduce the effects of EMF on your VGCCs.
On a side note, molecular hydrogen tablets are an excellent source of ionic elemental magnesium. Each tablet provides about 80 milligrams of ionic elemental magnesium.
There's no doubt in my mind that EMF exposure is an important lifestyle component that needs to be addressed if you're concerned about your health, which is why I spent three years writing "EMF*D."
My aim was to create a comprehensive and informative guide, detailing not only the risks, but also what you can do to mitigate unavoidable exposures. To get you started, see the tips listed in my previous article, "Top 19 Tips to Reduce Your EMF Exposure."
If you know or suspect you might already be developing a sensitivity to EMFs (full-blown hypersensitivity can often strike seemingly overnight), mitigating your exposures will be particularly paramount. Many sufferers become obsessed with finding solutions, as the effects can be severely crippling. My book can be a valuable resource in your quest for relief.
The EMF Experts website6 also lists EMF groups worldwide, to which you can turn with questions, concerns and support, and EMFsafehome.com7 lists a number of publications where you can learn more about the dangers of EMFs.
Should you need help remediating your home, consider hiring a trained building biologist to get it done right. A listing can be found on the International Institute for Building-Biology & Ecology's website.8
Brian Hoyer, a leading EMF expert9 and a primary consultant for "EMF*D" also has a company called Shielded Healing that can provide a thorough analysis of the EMF exposure in your home, and help you devise a remediation plan. You can listen to our excellent three-hour interview for more information, featured in "Your EMF Questions Answered Part 1" and "Your EMF Questions Answered Part 2."
A few years ago, my grandmother suffered a fall and broke her hip. She has never fully recovered and is now constantly fearful of falling, and has significantly limited her activities to prevent a fall from ever happening again. As a scientist focused on translational research in mobility and falls in older adults, of course I asked her how she fell. She stated that she was standing in the kitchen and reading a recipe when the phone rang. When she turned and started to walk over to the phone, her feet “weren’t in the right spot.” She fell sideways and unfortunately, her hip was unable to absorb the impact without breaking.
For older adults, falls are a leading cause of hip and wrist fractures, concussions, mobility disability, loss of independence, and even death. As it turns out, the circumstances leading up to my grandmother’s fall were typical. In fact, the majority of falls occur when an individual is “dual-tasking;” that is, standing or walking while at the same time performing a separate cognitive task (such as reading), a motor task (carrying groceries), or both (walking while talking and carrying a cup of coffee).
It turns out that the seemingly simple acts of standing upright, or walking down an empty, well-lit hallway, are quite complex. To complete these tasks, we must continuously stabilize our body’s center of mass — a point located just behind our sternum — over the relatively small base of support that we create by positioning our feet on the ground. This control requires quick reflexes, as well as strong muscles of the trunk, hips, legs, ankles, and toes. However, to avoid falling we also need to pay attention to our body and environment, predict and perceive unsafe movements of our body, and adjust accordingly. Our brains need to quickly make sense of information coming from our eyes, ears, and bodies to produce patterns of muscle activity that appropriately adjust our body’s position within the environment.
Therefore, tasks of standing and walking are in fact cognitive tasks, and these tasks require more and more cognitive effort as we grow older and our senses and muscles no longer work as well as they once did. For my grandmother and many others, dual-tasking led to a fall because it diverted shared cognitive resources away from the critical job of controlling her body’s center of mass over her feet on the ground.
Older adults who are cognitively impaired are more than two times as likely to fall compared to those who are cognitively intact. A recent study by researchers at the Albert Einstein College of Medicine has shown that even subtle differences in the brain’s ability to dual-task when walking are predictive of future falls in healthy older adults. Specifically, the researchers asked their volunteers to walk while completing a word-generation task in their laboratory, and used a technology called functional near-infrared spectroscopy to measure brain activity. Those volunteers who required more brain activity (mental effort) to complete these tasks were more likely to fall during a four-year follow-up period.
Thankfully, these startling studies have a silver lining: they suggest that cognitive function is a promising — and largely untapped — target for the prevention and rehabilitation of falls. In fact, there are several large-scale clinical trials currently underway that are testing the effects of computer-based cognitive training on balance, mobility, and falls in older adults (see here and here). There is also strong evidence that a physical therapy program that asks patients to balance while completing cognitive tasks like counting backwards significantly reduces the incidence of falls in stroke survivors.
It seems like only a matter of time before cognitive and dual-task training become mainstays of fall prevention programming in older adults. In the meantime, if you are worried about falling, or feel like your balance is slipping, you might consider the following:
The post The role of our minds in the avoidance of falls appeared first on Harvard Health Blog.
The Nutrition Labeling and Education Act of 1990 (NLEA) mandated nutrition labeling on most packaged foods. These include canned and frozen foods, breads, cereals, desserts, snacks, beverages, and a variety of other foods that line the aisles of grocery stores. Food labels — officially called Nutrition Facts labels — are intended to help consumers choose healthy foods. It is the FDA’s responsibility to make sure that foods are properly labeled.
Over the years there have been many changes to the initial law, and to the label. The newest version of the food label rolled out on January 1, 2020 for larger food manufacturers; smaller manufacturers have until January 1, 2021 to introduce the new labels.
Here’s a rundown of features you’ll encounter on the new food labels.
The new food label shows “servings per container” and “serving size” in a larger font size and a bolder type. Per the NLEA, serving sizes must be based on the Reference Amounts Customarily Consumed (RACCs) — that is, the amounts that people are actually eating, not what recommendations suggest they should be eating. The amounts that people eat and drink have changed since 1993, when the previous serving size requirements were published. For example, in 1993 the reference amount used for a serving of soda was 8 ounces; it will now be 12 ounces. A serving of ice cream has also increased, from 1/2 cup to 2/3 cup.
For packages that are between one and two servings, such as a 15-ounce can of soup, the label will now treat the package as a single serving, since people usually consume it at one time.
Certain foods and beverages that are larger than a single serving but could be eaten in one sitting will now display two columns: one showing calories and other nutrients per serving, the other showing the same information for the entire package.
Calories will now be displayed much more prominently on the label. But you’ll no longer see “calories from fat” on the food label, since research has shown that the type of fat in a food is more important than the amount of fat.
One of the biggest changes is that the new food labels will specify the amount of added sugar — sugars that are added during food processing. Added sugars are a bigger concern than natural sugars, which occur naturally in all foods that contain carbohydrates, including fruits and vegetables, grains, and dairy products.
Research shows that it is difficult to meet nutritional needs while staying within calorie limits if you consume more than 10% of your total daily calories from added sugar (added sugars will appear on the label in both grams and percent daily value). Too much added sugar can also lead to weight gain and other health problems, including diabetes and heart disease.
The FDA definition of fiber, which is used as a guideline for what appears on food labels, includes both naturally occurring fibers and fibers added to foods that show a physiological health benefit. Fiber is naturally present in vegetables, whole grains, fruits, cereal bran, flaked cereal, and flours. In addition, some nondigestible carbohydrates that are added to food also meet the FDA’s definition of dietary fiber, and are accounted for in the dietary fiber value on the new food label.
The list of nutrients that appear on the food label has been updated. Vitamin D and potassium will now be required; vitamins A and C will no longer be required, since deficiencies of these vitamins are rare today. Calcium and iron will continue to be required. Manufacturers must declare the actual amount, in addition to percent daily value, of vitamin D, calcium, iron, and potassium. In the old food label, manufacturers only needed to include percent daily value of these nutrients.
Daily values are reference amount of nutrients to consume or not to exceed, and are used to calculate the daily value percentages on the label. This can help the consumer use the nutrition information in the context of a total daily diet. They are based on 2,000 calories, which is a reference number of calories for general advice. Individuals may need less or more than 2,000 calories per day depending upon their specific needs.
The daily values for nutrients like fiber, sodium, vitamin D, and potassium have all been updated based on the most recent research from the Institute of Medicine, and the 2015 Dietary Guidelines Advisory Committee Report used in the development of the 2015–2020 Dietary Guidelines for Americans.
With its more realistic measure of serving size and emphasis on calories and added sugars, the new food label has the potential to help consumers make healthier food choices.
Source: FDA
The post What’s new with the Nutrition Facts label? appeared first on Harvard Health Blog.
According to the U.S. Centers for Disease Control and Prevention,1 nearly 805,000 Americans have a heart attack each year, and 605,000 are first heart attacks. Knowing the risk factors, symptoms and how to take early action will increase your chances of survival.
However, what may look and feel like an apparent heart attack may actually be a panic attack, and according to researchers, the cost of misdiagnosing noncardiac chest pain is high.2 "It is important for physicians to be able to recognize panic attacks and to distinguish them from cardiac disease, thus avoiding unnecessary use of health care resources," one report states.3
An investigation4 published in 1996 found that 25% of emergency room patients presenting with chest pain met the DSM-III-R criteria for panic disorder, yet attending emergency department cardiologists failed to recognize patients having a panic attack 98% of the time. As noted by the authors:5
"Panic disorder is a significantly distressful condition highly prevalent in ED [emergency department] chest pain patients that is rarely recognized by physicians. Nonrecognition may lead to mismanagement of a significant group of distressed patients with or without coronary artery disease."
So, just how do you tell the two apart? Before we get into those details, let's take a look at the common signs and symptoms associated with each.
When a heart attack starts, blood flow to your heart has suddenly become blocked and the muscle can't get oxygen. If not treated quickly, the muscle fails to pump and begins to die. While often a result of coronary heart disease, a heart attack can also be caused by a blood clot blocking an artery. Some of the most common symptoms of a heart attack include:6
Chest pain or discomfort |
Upper body discomfort |
Shortness of breath |
Breaking out in a cold sweat |
Nausea |
Sudden dizziness |
Feeling unusually tired |
Lightheadedness |
A panic attack typically comes on abruptly, producing intense fear and a sense of impending doom or even death that is typically severely disproportionate to the situation at hand. Common symptoms include:
Hyperventilation |
Chest pain |
Heart palpitations |
Trembling |
Sweating; hot or cold flashes |
Nausea |
Dizziness or lightheadedness |
Numbness and/or tingling sensations |
Panic attacks tend to peak within 10 minutes, and most subside within 30 minutes. Few last more than one hour. It's not uncommon for people to seek medical help, thinking they're having a heart attack or are dying, when panic attacks first set in and they're unfamiliar with the symptoms.7
While it can be very difficult to tell a panic attack from a heart attack, some generalizations can be made that can help tell them apart.8
When in doubt, seek immediate medical attention. It's better to be safe than sorry, as sudden death is the most common symptom of a heart attack. As noted by Dr. Sam Torbati, medical director of the Ruth and Harry Roman Emergency Department in an interview for Cedars-Sinai Medical Center:9
"Unfortunately, there is great crossover between the symptoms of panic attack and heart attack, making it very challenging to discern between the two without a physician assessment and testing, such as an EKG.
Common symptoms that may affect patients with either a panic or heart attack include chest pain, shortness of breath, dizziness, sweating, passing out, tingling, or a sensation of impending doom.
These shared symptoms of heart and panic attack may also be caused by other serious conditions such as blood clots, lung infection or collapse, or tear in the large vessels of the chest for patients with certain pre-existing risk factors. So when in doubt, seek immediate medical attention …
The best predictor as to whether symptoms are due to panic versus heart attack is the patient's age and previous history of panic attacks … Patients should immediately go to the ER if they have new onset chest pain (tightness, squeezing, heaviness), shortness of breath, sweating, lightheadedness, pain that radiates to the jaw or arm, or a ripping sensation in their chest or back.
Heart attacks tend to occur in middle-aged people and older age groups, so the older the person is, the lower a threshold they should have for coming to the ER right away.
Patients with pre-existing coronary artery disease and those with risk factors associated with coronary artery disease should also be evaluated immediately, including those with hypertension, diabetes, obesity, high cholesterol, or a history of smoking."
It's also worth getting your symptoms checked out even if you're certain they're due to a panic attack. Some research suggests there may in fact be a connection between panic disorder and coronary artery disease, although the exact relationship is still unclear. According to a 2008 review in The Primary Care Companion to the Journal of Clinical Psychiatry:10
"There are several reasons to consider that a relationship between panic disorder and coronary artery disease (CAD) might exist. First, panic disorder has been linked to other forms of cardiac disease.
Second, the most likely source of the chest pain during panic attacks is ischemia. Finally, there is evidence that panic disorder may be associated with cardiovascular risk factors, such as hypertension, hyperlipidemia, and smoking.
Panic disorder is associated with several cardiac abnormalities. In addition to patients with panic disorder having elevated standing heart rates, 10% have an arrhythmia.
Panic disorder is associated with increased left ventricular mass and diameter, and patients with panic disorder have poorer cardiovascular fitness as demonstrated by lower maximum oxygen consumption and decreased exercise tolerance …
Case reports have linked panic disorder to a descending aortic aneurysm and pulmonary hypertension secondary to an atrial septal defect with pulmonic valve disease. However, the strongest association is between panic disorder and mitral valve prolapse (MVP) … but MVP is not likely to be the source of chest pain.
In addition, the significance of the panic-MVP relationship is unclear … Indirect linkages via autonomic vulnerability or dysfunction have … been proposed. However, the most likely explanation is that the decreased left ventricular volume due to the tachycardia seen in panic disorder produces the MVP."
The review11 cites evidence suggesting ischemia is the cause of the chest pain felt during a panic attack, and researchers have found there's an association between panic attacks and ischemic and nonischemic chest pain alike. According to the authors, "Myocardial ischemia could cause panic attacks via increased catecholamines or cerebral carbon dioxide levels secondary to lactate."
What's more, when looking at a large managed care database, researchers found an association between panic disorder and coronary heart disease and this association remained even after controlling for covariates.12
Overall, patients with panic disorder were between 80% and 91% more likely to also have coronary heart disease. Patients diagnosed with both panic disorder and depression were, on average, 260% more likely to develop coronary heart disease than patients without those mental health problems.13
On the flip side, research14 published in 2017 also points out that "Anxiety and its associated disorders are common in patients with cardiovascular disease and may significantly influence cardiac health." According to this paper:
"Both physiologic (autonomic dysfunction, inflammation, endothelial dysfunction, changes in platelet aggregation) and health behavior mechanisms may help to explain the relationships between anxiety disorders and cardiovascular disease."
It's also important to realize that the symptoms of heart attack can vary from person to person and some may have very few symptoms, especially women.15 Importantly, research16,17 shows women are less likely to report chest pain when having a heart attack.
They're also less likely to suspect their discomfort is related to a heart problem. Compared to just 11.8% of men, 20.9% of women attributed their chest pain to stress or anxiety. Women also tend to describe their pain differently. They're more likely to use terms such as "pressure," "tightness" or "discomfort" in the chest rather than referring to it as "chest pain."
Doctors are also more likely to dismiss women's complaints of chest pain as being noncardiac in nature. Overall, 53% of female heart attack patients reported that their doctor did not think their symptoms were heart-related, compared to 37% of male heart attack patients.
Approximately 29.5% of women had actually sought medical help before being hospitalized with a heart attack, compared to just 22.1% of men. What these findings suggest is that women and their doctors tend to misdiagnose or dismiss symptoms of heart attack, placing women at a higher risk of death than men. As noted by the authors:18
"The presentation of AMI [acute myocardial infarction] symptoms was similar for young women and men, with chest pain as the predominant symptom for both sexes.
Women presented with a greater number of additional non-chest pain symptoms regardless of the presence of chest pain, and both women and their health care providers were less likely to attribute their prodromal symptoms to heart disease in comparison with men."
Unfortunately, the absence of chest discomfort is a strong predictor of diagnosis and treatment delays.19 For this reason, it's important to remember there are many other symptoms that might indicate a heart attack in progress, including the following:20
Anxiety attack |
|
Hot flashes |
|
Extreme fatigue |
Feeling electric shocks down on the left side of your body |
Numbness and stiffness in the left arm and neck |
Feeling like you have a large pill stuck in your throat |
When it comes to panic attacks, familiarizing yourself with the function of your fight-or-flight response can be helpful to guide you toward self-help strategies that work for your unique situation.
For example, contrary to popular belief, taking deep breaths can actually worsen a panic attack, as explained by Buteyko Breathing expert Patrick McKeown. A breathing exercise that can help quell anxiety and panic attacks is summarized below.
This sequence helps retain and gently accumulate carbon dioxide (CO2), leading to calmer breathing and reduced anxiety. In other words, the urge to breathe will decline as you go into a more relaxed state.
McKeown has also written a book specifically aimed at the treatment of anxiety through optimal breathing, called "Anxiety Free: Stop Worrying and Quieten Your Mind — Featuring the Buteyko Breathing Method and Mindfulness," which can be found on Amazon.com.21
In addition to the book, ButeykoClinic.com also offers a one-hour online course and an audio version of the book, along with several free chapters22 and accompanying videos.23
Energy psychology techniques such as the Emotional Freedom Techniques (EFT) can also be very effective for anxiety and panic attacks.24,25,26 EFT is akin to acupuncture, which is based on the concept that a vital energy flows through your body along invisible pathways known as meridians.
EFT stimulates different energy meridian points in your body by tapping them with your fingertips, while simultaneously using custom-made verbal affirmations. This can be done alone or under the supervision of a qualified therapist. By doing so, you reprogram the way your body responds to emotional stressors.
EFT is particularly powerful for treating stress and anxiety because it specifically targets your amygdala and hippocampus, which are the parts of your brain that help you decide whether or not something is a threat.27 EFT has also been scientifically shown to lower cortisol levels,28 which are elevated when you're stressed or anxious.
In the video above, EFT therapist Julie Schiffman demonstrates how to tap for panic attacks. Please keep in mind that while anyone can learn to do EFT at home, self-treatment for serious issues like persistent anxiety is not recommended. For serious or complex issues, you need someone to guide you through the process. That said, the more you tap, the more skilled you'll become.
As for heart attacks, your best course of action is to take proactive measures to prevent them. According to a 2015 study, more than 70% of heart attacks could be prevented by implementing:29
To this I would add maintaining a healthy iron level is important for your heart, as various studies show that both iron deficiency and iron overload30 can be a significant risk factor for heart attack.
For example, a Scandinavian study31 found elevated ferritin levels raised men's risk of heart attack two- to threefold. Another32 found elevated ferritin raised the risk of a fatal heart attack by 218% in men, while women with high levels were 5.53 times more likely to have a fatal heart attack.
As discussed in "Why Hard Water Decreases Heart Attacks," magnesium insufficiency has also been implicated in heart attacks, so you want to make sure you're getting enough magnesium from your diet and/or supplements. In "Could You Have a Heart Attack and Not Know It?" I also review some of the underlying issues that cause heart attacks, and additional steps you can take to lower your risk.
Alzheimer’s disease, a condition characterized by an accumulation of beta-amyloid plaques and neurofibrillary tangles in the brain, affects an estimated 5 million Americans; this number is expected to reach 14 million by 2060.1 With no known cure, researchers are scrambling to find treatments, often with a misguided focus on drugs designed to remove excess beta-amyloid in the brain.
Drug development for Alzheimer’s has so far been a dismal failure, with 300 failed trials to date.2 Despite the history of letdowns, the latest failed drug trial is still making waves in the research community because there were high hopes that it would provide a breakthrough treatment for people with gene mutations known to cause Alzheimer’s.
Now, with the experimental drugs failing to lead to improvements, researchers are asking if the focus on drugs to target and neutralize beta-amyloid in the brain is all wrong, and if other potential targets should become the focus of future research.3
The study, which was a collaboration between Washington University in St. Louis, drug companies Eli Lilly and Roche, the National Institutes of Health and others, involved 194 participants, of which 52 took Roche’s drug gantenerumab and 52 took Eli Lilly’s solanezumab.
The drugs were intended to remove beta-amyloid from the brain, and while the researchers are still evaluating this outcome, they failed to achieve the primary outcome of the study, which was slowed cognitive decline, as measured by tests on thinking and memory.
The study, Dominantly Inherited Alzheimer Network-Trials Unit (DIAN-TU), involved people with an inherited form of early-onset Alzheimer’s known as dominantly inherited Alzheimer’s disease or autosomal dominant Alzheimer’s disease, which account for less than 1% of Alzheimer’s cases.4
While in most cases Alzheimer’s symptoms begin after the age of 60, and risk increases with increasing age, people with this early-onset Alzheimer’s may begin to experience memory decline in their 30s, 40s or 50s. However, the brain changes that occur are similar in both those with inherited Alzheimer’s and the more common sporadic Alzheimer’s, so a treatment that works in one will likely work in the other.
According to a Washington University School of Medicine in St. Louis news release, a silent phase of Alzheimer’s occurs up to 20 years before symptoms develop. Study participants were expected to develop symptoms within 15 years of enrolling in the study or had very mild symptoms at the beginning of the study. Most also had early signs of the disease in their brains. Researchers explained:5
“People who inherit the mutation are all but guaranteed to develop symptoms at about the same age their parents did. While devastating for families, such mutations allow researchers to identify people in the early stages of the disease before their behavior and memory begin to change.”
The news that the drugs had failed came after an average of five years of follow-up and was a shock even to the researchers. “It was really crushing,” lead study author Dr. Randall Bateman of Washington University St. Louis told The New York Times.6 However, should it have been so shocking, considering both drugs have failed previously?
Researchers with the featured study are still wondering whether the experimental drugs could work at different doses or if they would work better if they were started even earlier. However, past studies suggest the drugs are useless for Alzheimer’s.
In one study of solanezumab, published in The New England Journal of Medicine in 2018, patients with mild dementia due to Alzheimer’s disease received solanezumab or placebo intravenously every four weeks for 76 weeks.7 The drug did not significantly affect cognitive decline, and the researchers even suggested this could be because the target is all wrong:8
“ … [S]olanezumab was designed to increase the clearance of soluble Aβ [amyloid-beta] from the brain, predicated on the Aβ hypothesis of Alzheimer’s disease — that the disease results from the overproduction of or reduced clearance of Aβ (or both).
Although the amyloid hypothesis is based on considerable genetic and biomarker data, if amyloid is not the cause of the disease, solanezumab would not be expected to slow disease progression.”
A study comparing gantenerumab at different doses with placebo came up with similarly disappointing results. A futility analysis was conducted when 50% of the patients had completed two years of treatment, and it found no differences between the drug or placebo, prompting researchers to stop the study early.9
A subsequent study that significantly increased the dose of the drug found it did reduce amyloid-beta plaques in Alzheimer’s patients,10 but how this translates to affecting cognitive decline remains to be seen.
The reason why beta-amyloid drugs continue to fail to improve Alzheimer’s disease is because beta-amyloid is a symptom of Alzheimer’s — not the cause.
Alzheimer’s has many causes, as discussed eloquently by Dr. Dale Bredesen, professor of molecular and medical pharmacology at the University of California, Los Angeles School of Medicine, and author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline.”11
Bredesen’s ReCODE protocol evaluates 150 factors — including biochemistry, genetics and historical imaging — known to contribute to Alzheimer’s disease. This identifies your disease subtype or combination of subtypes so an effective treatment protocol can be devised.
For instance, Bredesen states that type 1 Alzheimer’s is “inflammatory” or “hot,” and patients present predominantly inflammatory symptoms. Type 2 is atrophic or “cold,” with patients presenting an atrophic response. In type 3, or toxic “vile” Alzheimer’s, patients have toxic exposures.
There’s also a mixed type, type 1.5, which is referred to as “sweet” and is a subtype that involves both inflammation and atrophy processes, due to insulin resistance and glucose-induced inflammation. An algorithm is used to determine a percentage for each subtype based on the variables evaluated, and an individualized treatment protocol is created.
Bredesen’s most recent publication is a case report of 100 patients using the ReCODE protocol.12,13 He has previously published three case reports, each involving just 10 patients. The fourth case report contains 100 patients treated at 15 different clinics across the U.S., all of which have documented pre- and post-cognitive testing.
Not only did all show improvement in symptoms, some of them also showed improvement in their quantitative electroencephalographs (EEGs). Others who underwent magnetic resonance imaging (MRI) with volumetrics also showed objective improvement.
The results are impressive, to put it mildly. Here’s an example of just one patient’s outcome — a 73-year-old woman with cognitive decline who could not remember recent conversations, mixed up the names of people and pets and forgot the names of books she had read. Her significant other described her memory as “disastrous,” but this changed remarkably for the better:14
“She was treated with the programmatic approach described previously, and over 12 months, her on-line cognitive assessment improved from the 9th percentile to the 97th percentile. Her significant other noted that her memory had improved from “disastrous” to “just plain lousy” and finally to “normal.” She remains on the therapeutic program, and has sustained her improvement.”
A hallmark of neurodegenerative diseases such as Alzheimer’s is that proteins are aggregated and typically misfolded. By inducing ketosis, improving insulin sensitivity and supporting the mitochondria, you can often regain the ability to refold or proteolyze misfolded proteins.
Likewise, researchers wrote in the International Journal of Neuropsychopharmacology, “Research teams have reported some success in ameliorating the severity of symptoms in neurodegenerative diseases, most notably in patients with mild cognitive impairment or early Alzheimer’s disease [via diet-induced ketosis and/or ingestion of ketone bodies] … ”15
Bredesen's ReCODE protocol makes use of nutritional ketosis, in which your body produces endogenous ketones (water-soluble fats), but that’s not all. Your body has a mechanism by which misfolded proteins are refolded. Heat-shock proteins play a central role in this process, and if the misfolding is too severe, the heat-shock proteins help remove them altogether.
Heat-shock proteins are a corollary of autophagy, the process by which your body cleans out damaged organelles, which relates to Alzheimer’s because the refolding process is one of several factors that need to work in order for your brain to function. In Medicinal Research Reviews, researchers explained:16
“There are few more neurodegenerative diseases, like amyotrophic lateral sclerosis (ALS), Alzheimer's, and other dementias that have been investigated for their autophagy interconnection in the last two decades …
Autophagy also clears the aggregates formed by Alzheimer's and dementia associated proteins tau, β‐secretase, and presenilin 1 for neuronal cells and provide cytoprotection against proteotoxicity caused by these mutant proteins aggregates.
The autophagy pathway participates in amyloid‐beta (Aβ) protein secretion and further clearance of accumulated aggregates of this protein in Alzheimer's disease.”
Unfortunately, a vast majority of people do not have well-functioning autophagy, for the simple reason that they’re insulin-resistant. If you’re insulin-resistant, you cannot increase your adenosine 5’ monophosphate-activated protein kinase (AMPK) level, which prevents the inhibition of mammalian target of rapamycin (mTOR), and mTOR inhibition is one of the primary drivers of autophagy.
Ultimately, Bredesen typically recommends an intermittent fasting approach, which helps your body to cycle through autophagy and the rebuilding phase:
“You want to use appropriate fasting and an appropriate diet to activate this autophagy,” Bredesen says. “We recommend … 12 to 14 hours [of fasting] if you are apolipoprotein E4-negative (ApoE4-negative) … If you are ApoE4-positive, you’d want to go longer — 14 to 16 hours. There’s nothing wrong with doing a longer fast …
The reason we suggest longer for the ApoE4-positives [is because] if you are ApoE4-positive, you are better at absorbing fat. It tends to take longer to enter autophagy …
Typically, we recommend it about once a week. But again, a longer fast once a month is a good idea. It depends a lot on your body mass index (BMI). What we found is people who have higher BMIs respond better to this fasting early on. They’re able to generate the ketones.
If you lose both the carbohydrates and the ketones, you end up [feeling] completely out of energy … We are very careful when people are down below 20 on their BMI, especially the ones 18 or below. We want to be very careful to make sure to cycle them [in and out of ketosis] once or twice a week …
These are the ones where, often, exogenous ketones can be very helpful early on … Measure your ketones. It’s simple to do. We want to get you into, ultimately, the 1.5 to 4.0 millimolar [range for] betahydroxybutyrate. That is the goal.”
To test your ketones, I recommend KetoCoachX.17 It’s one of the least expensive testing devices on the market right now. Another good one is KetoMojo. KetoCoach, however, is less expensive, the strips are individually packed and the device is about half as thick as KetoMojo’s, making it easier to travel with.
While drug trials for Alzheimer’s continue to fail, Bredesen’s latest book, “The First Survivors of Alzheimer’s,” contains exciting first-person accounts from patients diagnosed with Alzheimer’s who beat the odds and improved. You can learn more about Bredesen and his work by visiting his website, drbredesen.com.
The dopamine fast, created by California psychiatrist Dr. Cameron Sepah, has very little to do with either fasting or dopamine. As Sepah told the New York Times, “Dopamine is just a mechanism that explains how addictions can become reinforced, and makes for a catchy title. The title’s not to be taken literally.” Unfortunately, with such a snazzy name, who could resist? This is where the misconceptions begin.
What Sepah intended with his dopamine fast was a method, based on cognitive behavioral therapy, by which we can become less dominated by the unhealthy stimuli — the texts, the notifications, the beeps, the rings — that accompany living in a modern, technology-centric society. Instead of automatically responding to these reward-inducing cues, which provide us with an immediate but short-lived charge, we ought to allow our brains to take breaks and reset from this potentially addictive bombardment. The idea is that by allowing ourselves to feel lonely or bored, or to find pleasures in doing simpler and more natural activities, we will regain control over our lives and be better able to address compulsive behaviors that may be interfering with our happiness.
The six compulsive behaviors he cites as behaviors that may respond to a dopamine fast are: emotional eating, excessive internet usage and gaming, gambling and shopping, porn and masturbation, thrill and novelty seeking, and recreational drugs. But he emphasizes that dopamine fasting can be used to help control any behaviors that are causing you distress or negatively affecting your life.
Dopamine is one of the body’s neurotransmitters, and is involved in our body’s system for reward, motivation, learning, and pleasure. While dopamine does rise in response to rewards or pleasurable activities, it doesn’t actually decrease when you avoid overstimulating activities, so a dopamine “fast” doesn’t actually lower your dopamine levels.
Unfortunately, legions of people have misinterpreted the science, as well as the entire concept of a dopamine fast. People are viewing dopamine as if it was heroin or cocaine, and are fasting in the sense of giving themselves a “tolerance break” so that the pleasures of whatever they are depriving themselves of — food, sex, human contact — will be more intense or vivid when consumed again, believing that depleted dopamine stores will have replenished themselves. Sadly, it doesn’t work that way at all.
Sepah recommends that we start a fast in a way that is minimally disruptive to our lifestyles. For example, we could practice dopamine fasting from one to four hours at the end of the day (depending on work and family demands), for one weekend day (spend it outside on a Saturday or Sunday), one weekend per quarter (go on a local trip), and one week per year (go on vacation).
This all sounds sensible, if not necessarily new or groundbreaking. In fact, it sounds a lot like many mindfulness practices and good sleep hygiene, in the suggestion of no screen time before bed.
However, people are adopting ever more extreme, ascetic, and unhealthy versions of this fasting, based on misconceptions about how dopamine works in our brains. They are not eating, exercising, listening to music, socializing, talking more than necessary, and not allowing themselves to be photographed if there’s a flash (not sure if this applies to selfies).
When you think that none of this is actually lowering dopamine, it’s kind of funny! Especially since avoiding interacting with people, looking at people, and communicating with people was never part of Sepah’s original idea. Human interaction (unless it is somehow compulsive and destructive) is in the category of healthy activities that are supposed to supplant the unhealthy ones, such as surfing social media for hours each day. In essence, the dopamine fasters are depriving themselves of healthy things, for no reason, based on faulty science and a misinterpretation of a catchy title.
The original intent behind the dopamine fast was to provide a rationale and suggestions for disconnecting from days of technology-driven frenzy and substituting more simple activities to help us reconnect us with ourselves and others. This idea is noble, healthy, and worthwhile, but it’s certainly not a new concept. Most religions also suggest a rest day (for example, the Jewish Sabbath) or holidays without technological distractions, so that you can reflect and reconnect with family and community, Thousands of years of meditation also suggests that a mindful approach to living reaps many health benefits.
Unfortunately, the modern wellness industry has become so lucrative that people are creating snappy titles for age-old concepts. Perhaps that is how to best categorize this fad, if only we can get its proponents to look at us or speak to us, without disturbing their dopamine levels, in order to explain this to them.
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