Is Organic Meat Truly Better for You?

Without a doubt, organic produce is the superior choice compared to GMO and other conventional varieties, but do organic meats share the same benefits? The answer may surprise you.

In the past few decades, the negative effects of pesticides have been receiving more and more attention in the media. As a result, the organic movement has experienced an exponential increase in popularity, with many of us aiming to eat organic produce whenever possible. While the studies are mixed on whether organic produce contain more nutrients than their conventionally-grown counterparts, they are presumably lower in pesticides, insecticides, and herbicides.

While there is much research lauding the benefits of organic fruit and vegetables, there are very few studies comparing organic meats to non-organic meats. Recently, a 2015 study dove into this topic, with surprising results.

In this study, Spanish researchers examined 76 samples of organic and conventional beef, chicken, and lamb for 33 carcinogenic pollutants that are commonly found in non-organic meat. As expected, pesticides were found in the non-organic samples.

The surprising finding came from the organic samples – not only were none of the samples free from contaminants, but the difference in levels of pollutants between the organic and conventional samples was very minimal.

Of the samples, they found that lamb – both non-organic and organic – had the highest level of pesticides of all the samples. In fact, the organic samples actually containing more pollutants than the non-organic!

In short, the organic meat was far from being devoid of persistent organic pollutants.

It appears that none of the researchers in this study were founded by the large meat industry, which makes the findings even more powerful.

Although studies on organic meat are rare (only 35 studies appear in Medline when “organic meat” is searched), a meta-analysis published in March 2016 showed that the nutrient quality was different between conventional and organic meat, with organic meat having more unsaturated fat, including the anti-inflammatory omega-3s.

Similarly, another group of researchers found that people who ate grass-fed beef had higher levels of omega-3s compared with those who ate conventional meat.

What does this mean? Should you stop eating organic meat altogether?

Deciding whether to eat meat, whether it’s organic or conventional, is a charged topic in and of itself. What we do know is that a significant portion of environmental toxins are stored in fat tissue, and animal products may have different types of fat, but they still have fat nonetheless. So, you will probably not be able to avoid fat-soluble toxins regardless of the type of meat you choose, but you may be able to get more omega-3s from organic or grass-fed beef.

Furthermore, organic practices support the health and welfare of animals and aren’t continually confined. They have access to grazing and to a pasture.

While this study might be discouraging if you are a meat eater, there are still many benefits of eating organically – including reduced pesticide consumption from many types of food. However, be a smart shopper! It’s important to stay informed, and not blindly purchase everything marked as organic without knowing what you’re actually getting.

How Artificial Sweeteners May Cause Us to Eat More

Like a freshly cracked diet soda, suspicions have been fizzing away for years that artificial sweeteners may not be the best way to slim down.

A vast body of research suggests that sugar substitutes, despite having far fewer calories than sugar itself, can wreak various forms of metabolic havoc such as upping diabetes risk and—perhaps paradoxically—causing weight gain in the long term. A new study published Tuesday in Cell Metabolism suggests that artificial sweeteners mimic a starvation state in the brain, causing some organisms to seek energy by eating more food.

In the study—a collaboration between researchers from the University of Sydney’s Charles Perkins Center and the Garvan Institute of Medical Research—fruit flies were fed either a diet of yeast and sucrose or one with the synthetic sweetener sucralose, used in a variety of low-calorie foods. Flies fed the sugar-free diet for five or more days consumed 30 percent more calories than those on sugar. When sucralose was removed from their diet, calorie consumption in the formerly sugar-free group fell back to normal.

Using a technique called the proboscis extension response (PER) assay—essentially a taste test that can determine a fly’s interest in ingesting a certain food—the authors also found that sucralose consumption resulted in an increased motivation to eat real sugar. What’s more, by recording electrical activity in a fly’s sensillas—structures that house their taste receptors—it also appeared that a prolonged sucralose diet actually increased the insects’ sensitivity to sugar, meaning they presumably grew to find it more pleasurable. “After sustained consumption of artificial sweetener, the animals could detect much smaller concentrations of real sugar, would eat more of it and respond to it physiologically with much more intensity,” associate professor of genomics and study lead author Greg Neely explained in an e-mail.

By monitoring the expression and effects of compounds involved in appetite and energy regulation—including various enzymes and neurotransmitters—Neely and his colleagues were able to identify a neural network in the brain that appears responsible for the hunger-inducing effects of artificial sweeteners. In short, the compounds interfere with an evolutionarily ancient interplay between insulin, taste neurons and the brain’s reward circuitry that normally drives us to seek out life-sustaining food when nutrients are scarce. “We found that inside the brain’s reward centers sweet sensation is integrated with energy content,” Neely was quoted as saying separately in a press release. “When sweetness versus energy is out of balance for a period of time, the brain recalibrates and increases total calories consumed.” In other words, when the brain detects sweetness in the absence of actual caloric energy, it compensates by increasing the palatability of sugar, driving increased food consumption. “The pathway we discovered is part of a starvation response that actually makes nutritious food taste better when you are starving,” Neely said in the press release.

It appears that Neely’s findings may not be limited to fruit flies. His team was able to replicate the findings in mice: After seven days on a sucralose diet the rodents showed a 50 percent increase in food consumption, partly due to the activity of a neurotransmitter called neuropeptide Y that drives hunger during fasting. Yet it is too early to fully extrapolate these results to humans. Whereas a number of past studies suggest that artificial sweeteners can prompt us to eat more, the literature is inconsistent when it comes to people. And sweetener research, like other dietary investigations, is an easy target for the sort of embellished science and science reporting so expertly eviscerated by Last Week Tonight host John Oliver back in May.

Still, the evidence that synthetic “sugars” are in some way metabolically detrimental via a variety of mechanisms is getting stronger. Researchpublished in Nature in 2014 reported that some artificial sweeteners can alter the gut microbe population in both mice and humans to promote calorie absorption. Another recent study found that sucralose ingestion impairs the body’s ability to process regular sugar. As Scientific Americancontributing writer Ferris Jabr reported earlier this year, overindulging in sweet and fatty foods alters brain chemistry in the reward system, driving us to overeat.

If artificial sweeteners render these foods even more palatable than usual, we could be setting ourselves up for a losing battle between Whoppers and willpower. But none of this is to say doctors should start recommending that people give up artificially sweetened food in favor of sugary alternatives; excess sugar intake comes with its own set of ills.

As Neely puts it, “I think the basic message here is that we know the artificial sweetener sucralose is not totally inert—at least in animals. This justifies more research into how these compounds affect people as well.”

Pharma and Feds Hide Opioid Report

Increasing numbers of middle-aged Americans are becoming hooked on painkillers, often after using the drugs for back pain. Seeking ever-stronger highs, more potent drugs are now reaching the black market.

opioid report

Story at-a-glance

  • In 2012, Max Baucus (D-Mont.) and Chuck Grassley (R-Iowa) began an investigation into financial ties between opioid drug makers and the medical organizations setting guidelines on opioid use
  • Senate staffers spent a year working on the investigation and subsequent report, but its results have not been made public
  • In 2015, public health advocates asked that the findings of the opioid investigation be released, noting that many of those targeted by the report continue to “promote aggressive opioid use and continue to block federal and state interventions that could reduce overprescribing”

There’s W-18, a synthetic opioid that’s said to be 100 times more potent than the opioid pain reliever fentanyl and 10,000 times stronger than morphine. Fentanyl is also being picked up by drug traffickers, who are selling it mixed with (or instead of) heroin.

It’s cheaper to make and far more potent than heroin, making it extremely easy to overdose. In New Orleans, deaths caused by Fentanyl are now higher than the murder rate.1

Meanwhile, more than 28,000 Americans died from opioid overdoses in 2014 — more deaths than any other year on record according to data from the U.S. Centers for Disease Control and Prevention (CDC).

The number includes deaths from both heroin and prescription opioid pain relievers, but the latter accounted for at least half.2,3 The United Nations World Drug Report 2016 also revealed a three-fold increase in U.S. heroin users from 2003, reaching about 1 million in 2014. That’s the most reported in 20 years.

The CDC states that addiction to prescription opioid painkillers is the strongest risk factor for heroin addiction, and among heroin users, 45 percent are also addicted to opioid painkillers.4

Clearly, Americans’ excessive use of opioid painkillers has created a nation of drug addicts, which leaves the burning question: how did this excessive opioid use begin?

Sealed Opioid Report May Hold Clues to the Opioid Overdose Epidemic

In 2012, as opioid overdoses continued to rise, two senators — Max Baucus (D-Mont.) and Chuck Grassley (R-Iowa) — began an investigation into financial ties between the drugs’ makers and the medical organizations setting guidelines on opioid use.

The targets of the investigation were Purdue Pharma (maker of Oxycontin), Endo International plc (Percocet) and Johnson & Johnson (Duragesic) along with five organizations, including the Center for Practical Bioethics and the American Pain Foundation (APF).

Senate staffers spent a year working on the investigation and subsequent report, but its results have not been made public (the report is sealed in the Senate Committee on Finance’s office).5

Financial Ties Between Drug Makers, Nonprofits and Policy Makers

There are many reasons to question the relationships between opioid makers and some leading non-profits, as well as their influence on the now out-of-control opioid epidemic. STAT reported some of the most concerning examples in an op-ed article:6

  • The APF, billed as the largest U.S. organization for pain patients, was at one point receiving 90 percent of its funding from pharmaceutical and medical device companies (the foundation shut down days after the investigation began)
  • The Center for Practical Bioethics, which is a supposedly independent nonprofit that helps policymakers and corporate leaders make health care decisions, received ample funding from Purdue Pharma, including seed money to create a $1.5-million chair in pain management

Myra Christopher, who co-founded the Center for Practical Bioethics and holds the chair in pain management, has authored studies in support of opioid use. STAT reported:7

“In 2008, Christopher coauthored a study to calm physicians’ fears that they might be criminally prosecuted or disciplined for inappropriately prescribing opioids.8

In 2011, as money from pharmaceutical companies continued to pour into the center, she wrote a commentary titled ‘It’s Time for Bioethics to See Chronic Pain as an Ethical Issue’ for the American Journal of Bioethics,9 which was then housed at the Center for Practical Bioethics.

The commentary failed to disclose that the center had received funding from the pharmaceutical industry and was one of many articles promoting opioid use the journal published.”

Due to changes in position, it’s now Senator Orrin Hatch (R-Utah), current chair of the Senate Committee on Finance, and Senator Ron Wyden (D-Ore.), who stand to get the opioid report released.

In 2015, public health advocates asked the senators that the findings of the opioid prescribing investigation be released, noting that many of those targeted by the report continue to “promote aggressive opioid use and continue to block federal and state interventions that could reduce overprescribing.”10 Still, the report remains sealed.

New Haven, Connecticut, Declares Public Health Emergency Due to Overdoses

In late June, New Haven, Connecticut — a city known for its New England charm and Yale University — declared a public health emergency after 16 people overdosed on tainted heroin or cocaine in a one-week period.11

Police were investigating whether fentanyl was involved. The surge in overdoses highlights the fact that drug overdoses have reached virtually the entire U.S. In Connecticut alone, more than 200 people had already died from accidental drug overdoses.

Unfortunately, stats like these are not unique. In Utah, 24 people die each month from prescription drug overdoses, and such deaths have outpaced deaths due to firearms, falls and motor vehicle crashes. In Utah, the majority of prescription drug overdoses are due to oxycodone.12

Connecticut Senator Richard Blumenthal told The New York Times, “an increase in ‘treatment services, law enforcement support, opioid overprescription prevention and other steps’ was ‘urgent and critical,’” and this sentiment applies not only to his home state but all of the U.S.13

Overdose Deaths Are Overwhelming Coroner Offices

In Connecticut, the chief medical examiner has considered renting a refrigerated truck to store bodies because the storage space at the medical examiner’s office is often maxed out.

The space shortage is attributed to rising drug overdose deaths, including opioid overdoses, which are pushing many U.S. medical examiner and coroner offices to their limits.

In areas like Cincinnati, Ohio, forensic pathologists responsible for conducting autopsies on many such victims may conduct more than 325 autopsies this year alone. The National Association of Medical Examiners’ (NAME) accrediting program puts the limit at 325 a year, and offices that conduct more risk losing accreditation.

Some coroner’s offices are also facing backlogs of DNA testing for drug investigations, again in large part due to overdose deaths.

Dr. David Fowler, Maryland’s chief medical examiner and president of the NAME, again highlighted the fact that this problem isn’t confined to one area; it stretches across the U.S. He told STAT:14

“There are many, many parts of the country that have substantial problems … I think the drug overdoses have substantially increased the problems.”

Painkiller Deaths Drop in Medical Marijuana States

If you’re in severe pain, there are times when opioid drugs have a place, and they can be of great benefit when used cautiously and correctly. It’s quite clear however, that prescription opioid painkillers are being overprescribed and can easily lead you into addiction and other, more illicit, drug use.

If you’re in severe pain, you need a knowledgeable practitioner who can help you attack the pain from multiple angles, giving you both relief and healing. One option that is receiving increasing attention in the U.S. is medical marijuana.

It’s the cannabidiol (CBD) in marijuana that has medicinal properties. CBD is an excellent painkiller and has been used successfully to treat a variety of pain disorders.

In states where medical marijuana is legal, overdose deaths from opioids like morphine, oxycodone and heroin decreased by an average of 20 percent after one year, 25 percent after two years and up to 33 percent by years five and six.15 For those with severe chronic pain, medical marijuana can be life changing, allowing for a far safer form of treatment than opioids.

There is a wealth of research linking marijuana with pain relief. In one study, just three puffs of marijuana a day for five days helped those with chronic nerve pain to relieve pain and sleep better.16 I do, however, still recommend working with a health care practitioner who can guide you on the most effective dosage and form of use (marijuana may be inhaled, smoked, vaporized, taken orally or even applied topically in oil form).

Non-Drug Solutions for Pain Relief

Not everyone who takes a prescription opioid will wind up an addict, but the risk is real. This is why I strongly recommend exhausting other options before you resort to an opioid pain reliever. The health risks associated with these drugs are great, and addiction and overdose happen far more often than you might think.

Many people find themselves addicted to painkillers before they even realize what’s happened, often after taking the drugs to recover from surgery or treat chronic back, or other pain. The drugs work by binding to receptors in your brain to decrease the perception of pain. But they also create a temporary feeling of euphoria, followed by dysphoria, which can easily lead to physical dependence and addiction.

This may drive some people to take larger doses in order to regain the euphoric effect or escape the unhappiness caused by withdrawal. Others find they need to continue taking the drugs not only to reduce withdrawal symptoms but also to simply feelnormal. Large doses of the painkillers can cause sedation and slowed breathing to the point that your breathing stops altogether, resulting in death.

If you have chronic pain of any kind, please understand that there are many safe and effective alternatives to prescription and even over-the-counter painkillers. The pain remedies that follow are natural, providing excellent pain relief without any of the health hazards that pain medications often carry.

Astaxanthin: one of the most effective oil-soluble antioxidants known, astaxanthin has very potent anti-inflammatory properties. Higher doses are typically required and one may need 8 milligrams or more per day to achieve this benefit.

Ginger: this herb is anti-inflammatory and offers pain relief and stomach-settling properties. Fresh ginger works well steeped in boiling water as a tea or grated into vegetable juice.

Curcumin: curcumin is the primary therapeutic compound identified in the spice turmeric. In a study of osteoarthritis patients, those who added only 200 milligrams of curcumin a day to their treatment plan had reduced pain and increased mobility. In fact, curcumin has been shown in over 50 clinical studies to have potent anti-inflammatory activity, as well as demonstrating the ability in four studies to reduce Tylenol-associated adverse health effects.

Boswellia: also known as boswellin or “Indian frankincense,” this herb contains powerful anti-inflammatory properties, which have been prized for thousands of years. This is one of my personal favorites, as I have seen it work well with many rheumatoid arthritis patients.

Bromelain: this protein-digesting enzyme found in pineapples is a natural anti-inflammatory. It can be taken in supplement form, but eating fresh pineapple may also be helpful. Keep in mind that most of the bromelain is found within the core of the pineapple, so consider leaving a little of the pulpy core intact when you consume the fruit.

Cetyl Myristoleate (CMO): this oil, found in fish and dairy butter, acts as a “joint lubricant” and an anti-inflammatory. I have used a topical preparation for myself to relieve ganglion cysts and a mild annoying carpal tunnel syndrome that pops up when I type too much on non-ergonomic keyboards.

Evening Primrose, Black Currant and Borage Oils: these contain the fatty acid gamma-linolenic acid (GLA), which is useful for treating arthritic pain.

Cayenne Cream: also called capsaicin cream, this spice comes from dried hot peppers. It alleviates pain by depleting the body’s supply of substance P, a chemical component of nerve cells that transmit pain signals to your brain.

Dietary Changes and Additional Pain Relief Options

When physicians don’t know how to effectively treat chronic pain, they resort to the only treatment they know: prescription drugs, which will do nothing to solve the underlying reasons why you’re in pain. Toward that end, if you suffer from chronic pain, there’s a good chance you need to tweak your diet as follows:

  1. Start taking a high-quality, animal-based omega-3 fat like krill oil. Omega-3 fats are precursors to mediators of inflammation called prostaglandins. (In fact, that is how anti-inflammatory painkillers work, they positively influence prostaglandins.) The omega-3 fats EPA and DHA contained in krill oil have been found in many animal and clinical studies to have anti-inflammatory properties, which are beneficial for pain relief.
  2. Reduce your intake of most processed foods as not only do they contain sugar and additives, but also most are loaded with omega-6 fats that upset your delicate omega-3 to omega-6 ratio. This, in turn, will contribute to inflammation, a key factor in most pain.
  3. Eliminate or radically reduce most grains and sugars (especially fructose) from your diet. Avoiding grains and sugars will lower your insulin and leptin levels. Elevated insulin and leptin levels are one of the most profound stimulators of inflammatory prostaglandin production. That is why eliminating sugar and grains is so important to controlling your pain.
  4. Optimize your production of vitamin D by getting regular, appropriate sun exposure, which will work through a variety of different mechanisms to reduce your pain. This satisfies your body’s appetite for regular sun exposure.

Finally, the natural pain relief methods that follow are useful for ongoing and lasting pain relief and management:

  • Chiropractic adjustments: according to a study published in the Annals of Internal Medicine and funded by the National Institutes of Health (NIH), patients with neck pain who used a chiropractor and/or exercise were more than twice as likely to be pain-free in 12 weeks compared to those who took medication.17
  • Massage: massage releases endorphins, which help induce relaxation, relieve pain and reduce levels of stress chemicals such as cortisol and noradrenaline.
  • Acupuncture: researchers concluded that acupuncture has a definite effect in reducing chronic pain such as back pain and headaches — more so than standard pain treatment.

Antibiotic Resistance — What Promotes It, and How Can We Beat It?

The featured Catalyst documentary, “Antibiotic Resistance,” offers a 30-minute-long review of some of the many factors contributing to this man-made scourge.

Story at-a-glance

  • Prior to antibiotics, half of the world’s population died from infections. This is the reality we now face yet again, unless we somehow manage to get antibiotic resistance under control
  • Bacteria are incredibly adaptable, capable of sharing genetic material through proximity alone. If they’re close enough, gene packages can rapidly transfer between different bacteria
  • Bacteriophages, a type of virus, are a natural predator of bacteria, capable of killing bacteria that antibiotics cannot. Phage therapy is now being explored as a potential alternative to conventional antibiotics

Today, people are so used to the idea that an antibiotic can cure just about any infection; few can even consider the possibility that someday this remedy may no longer be an option.

Indeed, antibiotics have increased the human lifespan by about a decade, and certain conditions simply could not be treated without them. Take organ transplants for example. Without antibiotics, such procedures become tremendously risky, with a low rate of success.

According to Catalyst, about half of all emergency room admissions are also related to bacterial infections, and they too would have a poor rate of recovery without antibiotics.

Even minor surgeries become risky propositions without these infection-busting drugs. Ditto for everyday infections resulting from cuts, scrapes or bites.

In many ways, modern medicine as we know it is built around a foundation of antibiotics, and that foundation is now severely threatened by the emergence of microbes that are resistant to even our harshest, last-resort antibiotics.

Prior to antibiotics, half of the world’s population died from infections, and many died during early childhood. This is the reality we now face yet again, unless we somehow manage to get antibiotic resistance under control.

Animals and Humans Are Part of a Bacterial Ecosystem

In recent years, researchers have discovered that bacteria and other microorganisms are far from mere adversaries to be carpet-bombed into oblivion. Instead, microorganisms are part and parcel of us — we exist as part of a bacterial ecosystem and, in fact, many of our biological processes rely on them.

Even pathogenic bacteria that can cause severe disease only really become a threat to health when they’re allowed to crowd out other, more beneficial bacteria that naturally help keep the pathogens in check. Even certain viruses play an important and supportive role in human health.

Part of the drug resistance problem we’re now facing as a result of decades’ worth ofantibiotic misuse is the fact that bacteria are incredibly adaptable. Unless they’re completely wiped out, the surviving stragglers pass on their resistance to other bacteria.

Another piece of the puzzle is bacteria’s ability to share genetic material outside of the procreative process. Scientists recently discovered a bacterial gene (called mcr-1) that can spread among different bacteria with remarkable ease, conferring resistance to the strongest antibiotics in our medical arsenal.

This is a scenario that many have feared might happen, and now there’s no escaping its reality. Less than a year after the mcr-1 gene was first discovered in pigs and people in China,1,2,3 it has now been identified in the U.S., both in pork samples and a patient being treated for E.coli infection.4,5

How Bacteria Share Genetic Material

All that’s required for bacteria to share genetic material, delivered in little packages called plasmids, is proximity. If they’re close enough, the plasmid can rapidly transfer between the various bacteria bumping against each other.

As explained in the film, if humans had this kind of gene-sharing ability, you’d be able to change the color of your eyes from blue to brown simply by standing next to a brown-eyed person. For bacteria, this ability means they can spread drug resistance to other bacteria at “astonishing speeds.”

Unfortunately, scientists drastically underestimated the speed at which resistance can spread, and now we’re faced with a far shorter deadline, in terms of “the end of antibiotics” in medicine, than previously expected.

To give you an idea of just how quickly resistance is now spreading, consider this: a brand new antibiotic was introduced in 2010. The very next year, resistant bacteria were detected.

Antibiotics Are Overused in Human Medicine

Overuse of antibiotics in human medicine is one contributing factor to rising drug resistance among bacteria. In Australia, antibiotics are prescribed at a rate of more than one prescription for every man, woman and child each year. The situation is similar in many other developed nations.

According to Dr. Arjun Srinivasan, associate director of the U.S. Centers for Disease Control and Prevention (CDC), as much as half of all antibiotics used in American clinics and hospitals “are either unneeded or patients are getting the wrong drugs to treat their infections.”6

Lack of education is part of the problem. More than 40 percent of Americans and an astonishing 65 percent of Australians still believe antibiotics can treat viral infections.7Many patients also insist on taking an antibiotic “just in case” — a strategy that is highly inadvisable.

Antibiotics have both short- and long-term effects on the composition and health of the microbes in your gut, and your microbiome plays a crucial role in your overall immune function and general health. You really don’t want to decimate yourmicrobiome with an antibiotic unless absolutely necessary.

Children treated with antibiotics also raise their risk of developing health problems in adulthood, including making them more susceptible to infectious diseases, allergies, obesity and autoimmune disorders as they grow older.8,9

Doctors are not without blame though. Forty-five percent of British doctors admit prescribing antibiotics even when they know it won’t do any good.10

Antibiotic Use in Food Production Must Be Curbed

According to the CDC,11 there are 12 antibiotic-resistant pathogens that pose a “serious” threat to public health, and one-third of them are found in food. The four drug-resistant pathogens in question are:

  • Campylobacter
  • Salmonella
  • E. coli
  • Shigella

While livestock sometimes need antibiotics to cure an infection, concentrated animal feeding operations (CAFOs) routinely use antibiotics to speed up growth and counteract poor hygiene and crowded living conditions.

In the U.S., an estimated 80 percent of antibiotics sold end up in livestock. In Australia, approximately 70 percent of all antibiotics are used in agriculture.

As noted in the film, industrialized factory farming owes its success to the routine use of antibiotics. However, we’re now paying an unexpectedly heavy price for this convenient way of raising cheap food, as agricultural use of antibiotics is feeding and speeding up the spread of drug-resistant bacteria that kill an estimated 23,000 Americans each year.

Antibiotic Resistance Spreads Via Multiple Routes

Drug-resistant bacteria also accumulate in CAFO manure that is then spread on fields and enters waterways, allowing the drug-resistant bacteria to spread far and wide and ultimately back up the food chain to your dinner plate. You can see how easily antibiotic resistance spreads, via the food you eat and community contact, in the CDC’s infographic below.

Phage Therapy Explored as an Alternative to Antibiotics

A type of virus called a bacteriophage, or simply “phage,” is a natural predator of bacteria, capable of killing bacteria that antibiotics cannot. In fact for every bacteria in your intestine there are about 10 phages. Wherever bacteria reside, you will also find phages, because phages depend on bacteria for their survival. Evidence suggests that phages partner with animals and humans to stave off bacterial infections and control the composition of friendly microbes in your body.

So-called phage therapy is now being explored as a potential alternative to conventional antibiotics. As noted in the film, if a patient can be safely infected with the right phage, it could be a therapy to beat antibiotic resistance.

Phages specialize in breaking open and killing certain kinds of bacteria, hijacking them in order to replicate. Most phages have hollow heads, which store their DNA and RNA, and tunnel tails designed for binding to the surface of their bacterial targets. Once a phage has attached itself to a bacterium, the viral DNA is injected through the tail into the host cell.

Progeny are rapidly produced inside the host, until these little phages burst from the host cell, killing it in the process. These phages then go on to infect and kill more target bacteria until all bacteria have been consumed. What makes phages unique is that they cannot affect any cell other than bacteria, so they offer great hope as a targeted therapy against bacterial infections.

Another experimental type of treatment involves removing the drug-resistant gene package (the plasmid) from the bacteria, using a genetically engineered bacterium. Animal studies show that mice infected with drug-resistant bacteria that are given this treatment end up responding to the conventional antibiotics again. Scientists believe this kind of tool may allow them to develop treatments against bacterial infections that won’t promote resistance in the process.

How You Can Help Stop the Spread of Antibiotic-Resistant Disease

In light of the growing problem of antibiotic-resistant disease, it would be wise to employ techniques and strategies that will not only reduce your own risk of falling victim, but also help curtail the spread of antibiotic resistance in general. While the problem of antibiotic resistance really needs to be stemmed through public policy on a nationwide level, the more people who get involved on a personal level, the better. Such strategies include:

Using antibiotics only when absolutely necessary

For example, antibiotics are typically unnecessary for most ear infections, and they do NOT work on viruses. They only work on bacterial infections, and even then, they’re best reserved for more serious infections.

Taking an antibiotic unnecessarily will kill off your beneficial gut bacteria for no reason at all, which could actually make it more difficult for you to recover from your illness. If you do take a course of antibiotics, be sure to reseed your gut with healthy bacteria, either by eating fermented foods or taking a high-quality probiotic.

As an all-around preventive measure, make sure your vitamin D level is optimized year-round, especially during pregnancy, along with vitamin K2. A number of other natural compounds can also help boost your immune system function to help rid you of an infection, including vitamin C, oil of oregano, garlic, Echinacea and tea tree oil.

High-quality colloidal silver may be a valuable addition to your medicine cabinet to treat cuts and scrapes in lieu of antibacterial creams. Colloidal silver has been regarded as an effective natural antibiotic for centuries, and research shows it can even be helpful against some antibiotic-resistant pathogens.12,13,14

Manuka honey can also be used for topical applications. Clinical trials have found that Manuka honey can effectively eradicate more than 250 clinical strains of bacteria, including some resistant varieties, such as MRSA.

Avoiding antibacterial household products

This includes items such as antibacterial soaps, hand sanitizers and wipes, as these too promote antibiotic resistance.

Properly washing your hands with warm water and plain soap, to prevent the spreading of bacteria

Be particularly mindful of washing your hands and kitchen surfaces after handling raw meats, as about half of all meat sold in grocery stores around the U.S. is likely to be contaminated with potentially dangerous bacteria.

Purchasing organic, antibiotic-free meats and other foods

Reducing the spread of antibiotic-resistant bacteria is a significant reason for making sure you’re only eating grass-fed, organically raised meats and animal products. Besides growing and raising your own, buying your food from responsible, high-quality, and sustainable sources is your best bet, and I strongly encourage you to support the small family farms in your area.

How Good Fats Prevent Heart Disease

Omega-3 fats — specifically EPA and DHA — are essential to your overall health, including your heart health.

Omega-3 Fats

Story at-a-glance

  • A recent analysis found regular consumption of fish and other omega-3- rich foods may lower your risk of a fatal heart attack (myocardial infarction) by about 10 percent
  • Omega-3s EPA and DHA from marine animal and plant sources are NOT interchangeable
  • Plant sources that contain omega-3 ALA do not provide the same benefits as theomega-3s you find in marine sources

A recent analysis of 19 studies confirms that regular consumption of fish and other omega-3 rich foods, including certain plant-based sources, may lower your risk of a fatal heart attack (myocardial infarction) by about 10 percent.1,2,3

This effect held true even after accounting for confounding factors like age, sex, ethnicity, diabetes and use of aspirin or cholesterol-lowering drugs.

According to senior study author Dr. Dariush Mozaffarian, “Our results lend support to the importance of fish and omega-3 consumption as part of a healthy diet.” Other studies have found even more significant effects.

One large Italian trial found that heart attack survivors who took 1 gram of omega-3 fat each day for three years had a 50 percent reduced chance of sudden cardiac death.4

Health Benefits of Omega-3 Fat

Omega-3 fats benefit your cardiovascular health in several ways. In addition to lowering your blood pressure and triglyceride concentrations and improving endothelial function (a major factor in promoting the growth of new blood vessels), research has demonstrated omega-3s are:

  • Antiarrhythmic: counteracting or preventing cardiac arrhythmia
  • Antithrombotic: tending to prevent thrombosis (a blood clot within a blood vessel)
  • Antiatherosclerotic: preventing fatty deposits and fibrosis of the inner layer of your arteries from forming
  • Anti-inflammatory: counteracting inflammation (heat, pain, swelling, etc.)

Researchers are also attributing a number of other health benefits to omega-3 fat, including:


Healthier, stronger bones Improved mood regulation Reduced risk of Parkinson’s disease
Reduced risk of death from ALL causes Protecting your tissues and organs from inflammation Brain and eye development in babies, and preventing premature delivery
Reduced risk of Alzheimer’s disease Delayed progression to psychosis among patients at high risk forschizophrenia Protection againstosteoarthritis and rheumatoid arthritis(RA)5,6, 7
Protection against metabolic syndrome,8including obesity, fatty liver9 and type 2 diabetes (by reducing inflammation and blood sugar) Improvements in premenstrual syndrome (PMS) and dysmenorrhea10 Lowered risk for other neurological/cognitive dysfunction, including: memory loss, brain aging, learning disorders and ADHD,11 autism and dyslexia12
Reduced risk of Crohn’s disease Reduced risk of colon cancer13 Reduced risk of kidney disease14
Reduced risk of autoimmune disorders, such as lupus and nephropathy

Not All Omega-3s Are Made the Same

It’s crucial to understand that not all omega-3 fats are created equal. There are two areas of confusion about omega-3s that I will attempt to clarify here:

  • Marine animal- versus plant-based omega-3 (docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) versus alpha-linolenic acid (ALA))
  • The difference between fish- and krill-based omega-3 (triglyceride-bound omega-3s versus phospholipid-bound omega-3s)

For starters, omega-3 fats can be obtained from both marine animal and plant sources, but contrary to popular belief, they are simply NOT interchangeable.

In recent years, a “myth” of sorts has sprung up, where people who avoid animal foods believe they can simply consume plant-based omega-3 ALA to meet their needs. But this isn’t true and the science doesn’t support this assertion.

Omega-3s EPA/DHA are essential polyunsaturated fats your body needs for a variety of functions, including digestion, muscle activity, blood clotting, visual acuity, memory and learning, and basic cell division and function of cell receptors.

Omega-3s EPA/DHA are considered “essential” fats as your body cannot make them and, hence, you must get them from your diet. Omega-3 ALA on the other hand is quite ubiquitous in the diet and therefore there is no real need to supplement.

Plant-based omega-3 has 18 carbons whereas marine-based omega-3s have between 20 and 22. They all have their first double-bond in the third position — hence the name “omega-3.” However, as you will see below, the difference in the length of the carbon chain makes a significant difference.

This is where the distinction between long-chain and short-chain omega-3s comes from. EPA and DHA are long-chain fatty acids and ALA is a short-chain fatty acid.

Although your body can convert some of the ALA found in plants to the DHA found in marine oils, it is very rare for it to be more than 5 percent and typically found to be 1 to 3 percent, or even less. This is an insufficient amount to have any significant benefit.

Animal- Versus Plant-Based Omega-3

Here’s a rundown of the core differences between marine-animal and plant-based omega-3s:15,16,17,18,19

Marine animal-based omega-3

Sources: Fatty fish (such as salmon, anchovies, sardines and herring), fish and krill oils.

Primary omega-3 content: DHA: a long-chain polyunsaturated fatty acid (PUFA) consisting of 22 carbons, and EPA: a long-chain polyunsaturated fatty acid consisting of 20 carbons.

Long-chain fatty acids EPA and DHA are more readily available to your body.

Your body also seems to have a significant capacity to synthesize another omega-3 fat, docosapentaenoic acid (DPA), most likely by elongating  EPA.

Biological effects: DHA and EPA are structural elements with many biological effects, most notably anti-inflammatory activity and communication within the cell and between cells.

More than 90 percent of the omega-3 fat found in brain tissue is DHA; as much as 30 percent of the fatty mass of the prefrontal cortex is DHA and the development of a normal brain in a fetus is absolutely dependent on the availability of DHA.

All other omega-3 fats are found only in trace amounts, including ALA, regardless of how much ALA you consume.20

Plant-based omega-3

Sources: Certain plants, such as flaxseed, flaxseed oil, chia seeds, nuts (especially walnuts) and leafy greens.

Primary omega-3 content: ALA is a short-chain fatty acid consisting of 18 carbons; it’s conversion to long-chain fatty acids is very poor, around 1 to 3 percent.

ALA is a precursor to EPA and DHA. However, enzymes are required to elongate and de-saturate the shorter 18 carbon ALA into long-chained omega-3. In most people,  this doesn’t work very well and hence the conversion rate is very small.

Typically, less than 1 percent of ALA is converted to EPA/DHA. Some studies have found the conversion rate to be as low as 0.1 to 0.5 percent.21 Your conversion is also dependent on having adequate levels of other vitamins and minerals.

So, while a tiny amount of the ALA you consume can be converted by your body into long-chain omega-3, it’s a highly inefficient strategy and nowhere near as helpful as supplying EPA/DHA directly from marine sources.

Biological effects: Source of energy (fat).

Key Difference: ALA Is a Source of Energy Whereas EPA and DHA Are Structural Elements

According to Nils Hoem, Ph.D., a leading scientist in omega-3 phospholipids whom I recently interviewed, when you look at the uptake and distribution of EPA and DHA you see something rather strange.

After eating a meal of salmon or taking a krill or fish oil, the fatty acid level in your plasma (blood) will remain elevated for more than three days afterward. “Your body works on its distribution, redistribution and re-redistribution for three days. That’s hardly consistent with being “just food,” he says.

On the other hand, the short-chain omega-3s (ALA) are rapidly absorbed, peaking a couple of hours after ingestion. Within 10 hours, they’re gone. This suggests your body is using them very differently.

According to Hoem, the short-chain fatty acids are simply food — they’re a source of energy — while the long-chain fatty acids, those with 20 and more carbons, especially EPA and DHA, are structural elements. So EPA and DHA are not just “food;” they’re elements that actually make up your cells, and those are two completely different functions. To learn more about this, please keep your eye out for Hoem’s interview, which is scheduled to run shortly.

EPA and DHA are extensively distributed throughout your body, including your heart and brain. In fact, research shows there are specific transporters in your blood-brain barrier, the placenta (in pregnant women), and likely also in your liver, which transport these molecules in a very precise way into the cell membranes where they belong.

The Difference Between Fish- and Krill-Based Omega-3

The next area of confusion relates to the different types of marine-based omega-3. Fish and krill are two sources that provide both EPA and DHA. However, there are important differences between these two marine sources of omega-3s. One of the most important differences between fish and krill oil is the fact that krill oil is bound to phospholipids.

Fatty acids are water insoluble, so they cannot be transported directly in their free form in your blood — they require “packaging” into lipoprotein vehicles. Most fatty acids are typically bound to esters, which do not travel efficiently in your bloodstream. The phospholipids in krill oil seem to be partially different in this regard.

  • Fish oil is bound to triglycerides and methyl esters
  • Krill oil is bound to triglycerides and phospholipids

Phospholipids are also one of the principal compounds in high-density lipoproteins (HDL), which you want more of, and by allowing your cells to maintain structural integrity, phospholipids help your cells function properly. (You can learn more about this in the video above.)

There’s also a synthetic form of marine omega-3, which is bound to ethyl esters. This is simply a fatty acid that has been sliced off from its triglyceride source and then ethylated with ethanol. Pharmaceutical omega-3 supplements are typically made this way, and research shows ethyl esters, unless taken in conjunction with a meal, may simply pass through your body without being absorbed whatsoever.

Other Advantages of Krill Oil Over Fish Oil

Research also shows krill oil has a number of other advantages over fish oil, including the following:

Higher potency

Studies have shown that krill oil is more potent than fish oil. This means you need far less of it than fish oil, as confirmed by a 2011 study published in the journal Lipids.22 Researchers gave subjects less than 63 percent as much krill-based EPA/DHA as the fish oil group, yet both groups showed equivalent blood levels — meaning the krill was more potent.

Contains phosphatidylcholine

When you consume fish oil, your liver has to attach it to phosphatidylcholine in order for it to be utilized by your body. Krill oil already contains phosphatidylcholine, which is another reason for its more efficient cellular uptake. Phosphatidylcholine is composed partly of choline, the precursor for the vital neurotransmitter acetylcholine, which sends nerve signals to your brain, and for trimethylglycine, which protects your liver.

Choline is important to brain development, learning and memory. In fact, choline plays a vital role in fetal and infant brain development, so it is particularly important if you are pregnant or nursing.

Resists oxidation

Fish oil is quite prone to oxidation, and oxidation leads to the formation of free radicals. Consuming free radicals further increases your need for antioxidants. Fish oil is very low in antioxidants whereas krill oil contains astaxanthin — probably the most potent antioxidant in nature — which is why krill oil is so stable and resistant to oxidation.


Fish are very prone to mercury and other heavy metal contamination, courtesy of widespread water pollution. Antarctic krill is not prone to this contamination. Not only are they fished from cleaner waters, but since krill is at the bottom of the food chain, it feeds on phytoplankton and not other contaminated fish.

Although processed fish oil can be purified, it requires extensive additional damaging processing to do so, unlike krill, which is not contaminated from the start and requires no additional processing to achieve high purity levels.

Environmentally sustainable

Krill is far more sustainable than fish because it’s the largest marine biomass in the world, making krill fishing one of the most sustainable practices on the planet. Krill fishing is also carefully regulated, and only less than 1 percent of the total krill biomass in the areas where the fishery is allowed (designated as “Area 48” in the Southern Ocean) is caught each year.

The krill population is monitored by the Commission for the Conservation of Antarctic Marine Living Resources (CCAMLR). The Marine Stewardship Council (MSC) certifies that krill fishing is carried out in compliance with strict sustainability criteria to avoid overfishing. For more information, please read my 2009 article that goes into the sustainability aspects of krill harvesting in greater depth.

Superior metabolic influence

Researchers have found that krill oil is vastly superior to fish oil when it comes to having a beneficial influence on your genetic expression and metabolism. Genes have “switches” that can be flipped on and off, which control virtually every biochemical process in your body, and nutrients like omega-3 fats control those switches.

Fatty acids help to direct metabolic processes such as glucose production, lipid synthesis, cellular energy, oxidation and dozens of others. We now know that various types and sources of omega-3 fat affect liver tissue differently, which is what a 2011 study23  in Frontiers in Genetics was designed to examine.

It compared the livers of mice fed krill oil to those fed fish oil by looking at the gene expression triggered by each. Although both fish oil and krill oil contain omega-3s, they differ greatly in how they affect the genes controlling your metabolism. Krill oil:

  • Enhances glucose metabolism in your liver, whereas fish oil does not
  • Promotes lipid metabolism; fish oil does not
  • Helps regulate the mitochondrial respiratory chain; fish oil does not
  • Decreases cholesterol synthesis, whereas fish oil increases it

So krill will help lower your triglyceride and cholesterol levels and increase your energy production, whereas fish oil does neither. Last year, an Italian study24,25 confirmed that krill oil helps improve lipid and glucose metabolism and mitochondrial function, which may help protect against hepatic steatosis (fatty liver disease) caused by an unhealthy diet (such as diets high in unhealthy fats).

By stimulating certain mitochondrial metabolic pathways, including fatty acid oxidation, respiratory chain complexes and the Krebs cycle, krill oil helps restore healthy mitochondrial energy metabolism.

Can Melatonin and 5-HTP Improve Your Sleep?

An estimated 40 percent of Americans are sleep deprived, according to the documentary “Sleepless in America,” with many getting less than five hours of sleep per night.

Melatonin Levels

Story at-a-glance

  • Melatonin significantly reduced or prevented jet lag when taken close to the target bedtime at the destination
  • Melatonin may decrease the time it takes to fall asleep and improve total sleep time and quality
  • Your body produces 5-HTP (5-hydroxytryptophan) from the amino acid tryptophan
  • 5-HTP works in your brain and central nervous system by promoting the production of the neurotransmitter serotonin, and thereby may help boost mood and enhance sleep

There are many reasons for this, from intentionally staying up late to watch TV or surf the web to health problems (like pain) that keep you awake.

Millions of Americans struggle to fall asleep each night, including about 10 percent who suffer from chronic insomnia. This latter condition involves difficulty falling asleep and staying asleep, as well as waking up too early in the morning.

In many cases, making changes to your sleep-hygiene routine and lifestyle, such as exercising more and avoiding exposure to blue light at night, can significantly improve your sleep.

However, if you feel like you’ve tried virtually everything and you’re still struggling to get a restful night’s sleep, it might be time to consider two natural supplements, melatonin and 5-hydroxytryptophan (5-HTP).

Why Melatonin Is Important for Sound Sleep

Your brain typically starts secreting the hormone melatonin around 9 or 10 p.m., which makes you sleepy. These regularly occurring secretions help regulate your sleep cycle as well as provide other important health benefits, including helping to prevent cancer.

Melatonin acts as a marker of your circadian phase or biological timing. In a nutshell, this hormone influences what time of day or night your body thinks it is, regardless of what time the clock on the wall displays.

Melatonin is produced by a pea-sized gland in the middle of your brain called the pineal gland.

In a normal night’s sleep, your melatonin levels stay elevated for about 12 hours. Then, as the sun rises, your pineal gland reduces your production of melatonin, and the levels in your blood decrease until they’re hardly measurable at all.

When your circadian rhythms are disrupted, such as from shift work, jet lag or nighttime light exposure, your body produces less melatonin.

Melatonin deficiency may come with some profound biological disadvantages, such as higher levels of inflammation, a weakened immune system, and an increased risk of cancer.

Who May Benefit From Melatonin Supplements?

It is best to encourage your body to produce its own melatonin. Your pineal gland produces melatonin roughly in approximation to the contrast of bright sun exposure in the day and complete darkness at night.

If you are in darkness all day long, it can’t appreciate the difference and will not optimize your melatonin production.

So one of the best ways to increase your melatonin production naturally is to get exposure to bright sunlight during the day and sleep in complete blackness at night. Supplementation may be beneficial in some cases, particularly if your circadian rhythm is off (such as from jet lag).

In a Cochrane review that analyzed 10 randomized trials, melatonin significantly reduced or prevented jet lag when taken close to the target bedtime at the destination.

The researchers recommended melatonin for adult travelers flying across five or more time zones, particularly in the eastern direction, and, if necessary, for those flying across two to four time zones.1

A recent review published in the French journal Annales Pharmaceutiques Françaises further revealed the importance of melatonin in regulating the body’s internal clock for optimal sleep:2

“The internal or biological clock which is located in the suprachiasmatic nuclei of the anterior hypothalamus is controlled by clock genes and environmental factors which are able to synchronize the clock to 24h.

Rhythm desynchronization (shiftwork and nightwork, transmeridian flights, aging, some psychiatric diseases, blindness, intake of some drugs … ) occurs when the internal clock does no longer work in harmony with the astronomical time i.e. our watch.

The circadian system consists of three major elements, which are the clock, the retinohypothalamic tract and melatonin which is secreted by the pineal gland and considered as the arrow of the clock.

Both light and melatonin present a phase response curve useful for the treatment of sleep circadian disorders.”

More Is Not Typically Better With Melatonin Supplementation

As for dosage, the researchers noted, “Daily doses of melatonin between 0.5 and 5 mg [milligrams] are similarly effective, except that people fall asleep faster and sleep better after 5 mg than 0.5 mg. Doses above 5 mg appear to be no more effective.”

In a study looking into the use of melatonin for primary sleep disorders, the supplement also appeared safe and effective, working to decrease the time it takes to fall asleep and improve total sleep time and quality.3

Keep in mind that only a very small dose is required — typically 0.25 mg or 0.5 mg to start with, and you can adjust it up from there.

Taking higher doses, such as 3 mg, can sometimes make you more wakeful instead of sleepier, so adjust your dose carefully and, ideally, under the guidance of a holistic health care practitioner.

In addition, melatonin supplementation may be most effective in people with low melatonin levels. If your levels are optimized, you may not experience additional sleep benefits from added supplementation.

Melatonin’s Link to Diabetes Risk

About one-third of people are thought to carry a gene variant to melatonin receptor 1B (MTNR1B), which increases the risk of developing type 2 diabetes.

A new study from researchers at Lund University in Sweden has now revealed that the effect of melatonin is stronger in carriers of this genetic variant, and this may be responsible for the increased diabetes risk.4

The study involved 23 carriers of the genetic variant and 22 non-carriers. Both groups received 4 mg of melatonin at bedtime for three months. The variant carriers had lowered insulin secretion and significantly higher blood sugar levels after melatonin supplementation.

Similar results were first demonstrated in lab-cultured beta cells and mice, which showed melatonin causes insulin-producing cells to reduce insulin release via signaling from MTNR1B melatonin receptor proteins.

Mice with disrupted MTNR1B receptors produced more insulin, but in people with the aforementioned genetic variant, the amount of MTNR1B protein on insulin-producing cells is increased.

Since the cells then become more sensitive to melatonin, they produce less insulin, leading to higher blood sugar levels. As reported by Medical News Today:5

“Senior investigator Dr. Hindrik Mulder, a professor specializing in molecular metabolism at Lund’s Diabetes Center, says their findings could explain why the risk of developing type 2 diabetes is higher in people who work overnight or who have sleeping disorders.”

What Is 5-HTP and How Does It Affect Sleep?

Your body produces 5-HTP (5-hydroxytryptophan) from the amino acid tryptophan (found in foods like poultry, eggs and cheese).

However, eating tryptophan-rich foods is not likely to significantly increase your 5-HTP levels, so 5-HTP supplements (which are made from extracts of the seeds of the African tree Griffonia simplicifolia) are sometimes used.

The chemical 5-HTP works in your brain and central nervous system by promoting the production of the neurotransmitter serotonin, and thereby may help boost mood and enhance sleep.

In one study, an amino acid preparation containing both GABA (a calming neurotransmitter) and 5-HTP reduced time to fall asleep, increased the duration of sleep and improved sleep quality.6 Further, as noted by the University of Maryland Medical Center:7

“In one study, people who took 5-HTP went to sleep quicker and slept more deeply than those who took a placebo. Researchers recommend 200 to 400 mg at night to stimulate serotonin, but it may take six to 12 weeks to be fully effective.”

There may be some beneficial “side effects” to 5-HTP as well. Research suggests the supplement naturally reduces appetite and food intake (including reduced carbohydrate consumption) and is associated with significant weight loss.8

Another study found 5-HTP led to significant improvements in symptoms of fibromyalgia as well, with only mild and transient side effects reported.9 The anti-depressant properties of 5-HTP are also of interest, and preliminary research suggests it may work as well as certain antidepressants in people with mild to moderate depression.10

Try Natural Sleep Aids Before Sleeping Pills

Natural sleep aids work with your body’s natural circadian rhythm to help you get truly restful sleep. This is not the case with prescription sleeping pills. A study in 2012 revealed that people who take sleeping pills are not only at higher risk (by 35 percent) for certain cancers, but they are also nearly four times as likely to die as people who don’t take them. The list of health risks from sleeping pills includes:

  • Higher risk of death, including from accidents
  • Increased risk of cancer
  • Increased insulin resistance, food cravings, weight gain and diabetes
  • Complete amnesia, even from events that occurred during the day
  • Depression, confusion, disorientation, and hallucinations

Research involving data from more than 10,500 people who received drugs for poor sleep (including benzodiazepines) also showed that “as predicted, patients prescribed any hypnotic had substantially elevated hazards of dying compared to those prescribed no hypnotics.”

The association held true even when patients with poor health were taken into account — and even if the patients took fewer than 18 pills in a year.11 In “The Dark Side of Sleeping Pills,” an e-book by one of the study’s researchers, Dr. Daniel Kripke, it’s explained:12

“The patients who took sleeping pills died 4.6 times as often during follow-ups averaging 2.5 years. Patients who took higher doses (averaging over 132 pills per year) died 5.3 times as often. It seems quite likely that the sleeping pills were causing early death for many of the patients …

Theoretically, there could be confounding factors or biases in the selection of patients which caused these deaths without involving sleeping pills. We can only say that we found almost no evidence of such biases … If sleeping pills cause even a small portion of the excess deaths and cancers associated with their use, they are too dangerous to use.”

Try This First for Better Sleep Starting Tonight

If you need more sleep, I suggest you read through my full set of 33 healthy sleep guidelines for details on proper sleep hygiene, but to start, consider implementing the following changes. If you’ve tried these steps and are still having trouble sleeping, you may want to consider melatonin or 5-HTP.

Avoid watching TV or using your computer in the evening, at least an hour or so before going to bed. These devices emit blue light, which tricks your brain into thinking it’s still daytime. Normally, your brain starts secreting melatonin between 9 and 10 p.m., and these devices emit light that may stifle that process. Even the American Medical Association (AMA) now states:13

” … [N]ighttime electric light can disrupt circadian rhythms in humans and documents the rapidly advancing understanding from basic science of how disruption of circadian rhythmicity affects aspects of physiology with direct links to human health, such as cell cycle regulation, DNA damage response, and metabolism.”

Make sure you get BRIGHT sun exposure regularly. Your pineal gland produces melatonin roughly in approximation to the contrast of bright sun exposure in the day and complete darkness at night. If you are in darkness all day long, it can’t appreciate the difference and will not optimize your melatonin production.

Sleep in complete darkness, or as close to it as possible. The slightest bit of light in your bedroom can disrupt your body’s clock and your pineal gland’s melatonin production. Even the tiniest glow from your clock radio could be interfering with your sleep, so cover your radio up at night or get rid of it altogether.

Move all electrical devices at least 3 feet away from your bed. You may want to cover your windows with drapes or blackout shades. If this isn’t possible, wear an eye mask.

Install a low-wattage yellow, orange, or red light bulb if you need a source of light for navigation at night. Light in these bandwidths does not shut down melatonin production in the way that white and blue bandwidth light does. Salt lamps are handy for this purpose. You can also download a free application called f.lux that automatically dims your monitor or screens14 or use blue-light-blocking glasses.

Keep the temperature in your bedroom no higher than 70 degrees F. Many people keep their homes too warm (particularly their upstairs bedrooms). Studies show that the optimal room temperature for sleep is between 60 to 68 degrees F.

Take a hot bath 90 to 120 minutes before bedtime. This increases your core body temperature, and when you get out of the bath it abruptly drops, signaling your body that you are ready to sleep.

Avoid using loud alarm clocks. Being jolted awake each morning can be very stressful. If you are regularly getting enough sleep, you might not even need an alarm.

Get some sun in the morning, if possible. Your circadian system needs bright light to reset itself. Ten to 15 minutes of morning sunlight will send a strong message to your internal clock that day has arrived, making it less likely to be confused by weaker light signals during the night. More sunlight exposure is required as you age.

Be mindful of electromagnetic fields (EMFs) in your bedroom. EMFs can disrupt your pineal gland and its melatonin production, and may have other negative biological effects as well. A gauss meter is required if you want to measure EMF levels in various areas of your home. Ideally, you should turn off any wireless router while you are sleeping. You don’t need the Internet on when you are asleep.

Supplements Proven Beneficial for Depression

One in 20 Americans over the age of 12 struggles with depression1 and 11 percent of the U.S. population over the age of 12 is on antidepressant medication.2 This, despite overwhelming evidence showing that antidepressants are no better than placebo in terms of effectiveness.

Story at-a-glance

  • Antidepressants work no better than placebo in terms of effectiveness. Studies now suggest their effectiveness can be boosted by adding certain supplements, but other studies suggest the supplements alone may do the trick
  • Fish oil, vitamin D, methylfolate (a form of folic acid/vitamin B9), and S-Adenosylmethionine (SAMe) were found to boost the impact of the antidepressants when compared to medication only
  • Other studies have shown that omega-3, vitamin D, and SAMe can help combat depression all on their own. In fact, both omega-3 and vitamin D are very important for mental health

As noted in a 2014 paper on antidepressants and the placebo effect, published in the journal Zeitschrift Fur Psychologie:3

“Antidepressants are supposed to work by fixing a chemical imbalance, specifically, a lack of serotonin in the brain. Indeed, their supposed effectiveness is the primary evidence for the chemical imbalance theory.

But analyses of the published data and the unpublished data that were hidden by drug companies reveals that most (if not all) of the benefits are due to the placebo effect …

Even the small statistical difference between antidepressants and placebos may be an enhanced placebo effect, due to the fact that most patients and doctors in clinical trials successfully break blind.”

Serotonin Theory Has Been Proven Wrong

Research4,5 published in 2009 added further evidence to the pile indicating the low serotonin idea was incorrect, as they found strong indications that depression actually begins further up in the chain of events in the brain. Essentially, the medications have been focusing on the effect, not the cause.

More recent research into the mechanisms driving anxiety and social phobias has also turned conventional drug treatment with serotonin reuptake inhibitors (SSRIs) on its ear.

As it turns out, these mental health problems are actually linked to elevated levels of serotonin in the amygdala, not low levels.6,7,8,9 Your amygdala is the seat of primitive emotions such as fear. And the more serotonin produced in this area, the more anxious you feel.

This helps explain why some depressed patients end up feeling more anxious than before when taking a serotonin-boosting antidepressant. As noted in the paper above:

The serotonin theory is as close as any theory in the history of science to having been proved wrong. Instead of curing depression, popular antidepressants may induce a biological vulnerability making people more likely to become depressed in the future.”

Vitamins and Supplements Boost Effectiveness of Antidepressants

A recent study10 raises even more questions about the effectiveness of antidepressants.

The meta-analysis, published in the American Journal of Psychiatry, found that certain nutritional supplements boosted the effectiveness of several classes of antidepressants, including SSRIs, serotonin-norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants.

A total of 40 clinical trials were included in the review, and four supplements — fish oil, vitamin D, methylfolate (an effective form of folic acid), and S-Adenosylmethionine (SAMe) — were found to boost the impact of the medication when compared to medication only.

Fish oil — specifically the fat EPA — produced the most significant improvement. Studies investigating the use of creatine, zinc, vitamin C, tryptophan (an amino acid), and folic acid (B9) produced mixed results. As reported by Scientific American:11

“By some estimates, two-thirds don’t respond to the first antidepressant they try and a third fail to get better after several treatment attempts.

‘The implications are that clinicians and the public can consider [adding] therapeutic doses of nutrients such as omega-3s as a potential low-cost approach to reducing depression in people who are non-responsive to antidepressants,’ (lead author Jerome Sarris) says.”

Could Supplements Alone Be Responsible for Improvements?

According to the authors, “more patients in the studies showed an improvement in mood when prescribed omega-3 fish oil, methylfolate, vitamin D and SAMe supplements in combination with antidepressant medication, compared to those who took medication only.”12

What’s really missing here is a comparison between supplements only, medication only, and a combination of both.

Considering the fact that antidepressants have been proven to be no better than placebo, and can worsen depression in some people, perhaps patients would experience the same or even better results just by taking the supplement, without the drug.

If that’s indeed the case, then why risk your health by taking an antidepressant? In fact, other studies have shown that bothomega-3 and vitamin D can help improve mental health all on their own.

One likely theory as to why they work is because these supplements help combat inflammation and oxidative stress, not only in your brain but also in your gut.

Depression is often found alongside gastrointestinal inflammation, autoimmune diseases, cardiovascular diseases, neurodegenerative diseases, type 2 diabetes, and cancer.

Chronic low-grade inflammation is a significant contributing factor to all of these, leading researchers to suggest that “depression may be a neuropsychiatric manifestation of a chronic inflammatory syndrome,” and that the primary cause of inflammation may be dysfunction of the gut-brain axis.13

An increasing number of clinical studies have indeed confirmed that treating gastrointestinal inflammation with probiotics, omega-3, and vitamins B and D can improve symptoms of depression by attenuating pro-inflammatory stimuli to your brain that originate in your gut.14

The Importance of Omega-3

Many Americans’ diets are lacking in healthy fats, including the animal-based omega-3 fats EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid). Although omega-3s are most well known for their role in heart health, they also play an integral role in brain health and mental health.

The 2001 book, “The Omega-3 Connection,” written by Harvard psychiatrist Dr. Andrew Stoll, was among the first works to bring attention to, and support the use of, omega-3 fats for depression.

There is no set recommended standard dose of omega-3 fats, but some health organizations recommend a daily dose of 250 to 500 milligrams (mg) of EPA and DHA for healthy adults. If you suffer from depression, higher doses may be called for.

In one study,15 an omega-3 supplement with a dose range of 200 to 2,200 mg of EPA per day was effective against primary depression. Omega-3 has also been shown to improve more serious mental disorders, including schizophrenia, psychosis, and bipolar disorder.16

Making sure you’re getting enough omega-3 in your diet, either from wild Alaskan salmon, sardines and anchovies, or a high-quality omega-3 supplement like krill oil is, I believe, absolutely crucial for optimal health, including brain health, so it doesn’t surprise me in the least that it was found to be the most effective addition against depression.

Low Vitamin D Repeatedly Linked to Depression

Vitamin D receptors appear in a wide variety of brain tissue early in the fetal development, and activated vitamin D receptors increase nerve growth in your brain. Researchers believe that optimal vitamin D levels may enhance the amount of important chemicals in your brain and protect brain cells by increasing the effectiveness of the glial cells in nursing damaged neurons back to health. As noted by the Vitamin D Council:17

“Exactly how vitamin D works in the brain isn’t fully understood. One theory is that vitamin D affects the amount of chemicals called monoamines, such as serotonin, and how they work in the brain. Many anti-depressant medications work by increasing the amount of monoamines in the brain. Therefore, researchers have suggested that vitamin D may also increase the amount of monoamines, which may help treat depression.”18

Regardless of the exact mechanism, a number of studies have linked low vitamin D to depression, including the following:

  • Seniors with the lowest levels of vitamin D have been found to be 11 times more prone to be depressed than those who had normal levels.
  • A study19 conducted by VU University Medical Center in Amsterdam found that people with minor and major depression had on average 14 percent lower vitamin D levels than non-depressed participants.
  • In another study,20 people with vitamin D levels below 20 ng/mL had an 85 percent increased risk of depression compared to those with vitamin D levels greater than 30 ng/mL.
  • Vitamin D deficiency has long been associated with Seasonal Affective Disorder (SAD)21 and, in 2007, researchers noted that vitamin D deficiency is associated with depression and fibromyalgia.22
  • A double-blind randomized trial23 published in 2008 also concluded that: “It appears to be a relation between serum levels of 25(OH)D and symptoms of depression. Supplementation with high doses of vitamin D seems to ameliorate these symptoms indicating a possible causal relationship.”

Other Supplements and Habits Shown to Lessen Depressive Symptoms

SAMe is an amino acid derivative that occurs naturally in all cells. It plays a role in many biological reactions by transferring its methyl group to DNA, proteins, phospholipids and biogenic amines. Several scientific studies indicate that SAMe may be useful in the treatment of depression.

5-Hydroxytryptophan (5-HTP) is another natural alternative to traditional antidepressants. When your body sets about manufacturing serotonin, it first makes 5-HTP. Taking 5-HTP as a supplement may raise serotonin levels.

The evidence suggests 5-HTP outperforms a placebo when it comes to alleviating depression24 — more than can be said about antidepressants! However, keep in mind that anxiety and social phobias can worsen with higher levels of serotonin, so it may be contraindicated if your anxiety is already high. St. John’s Wort has also been shown to provide relief from mild depressive symptoms.

While the featured study found some benefit from methylfolate, vitamin B12 deficiency can also contribute to depression, and affects about 1 in 4 people. If you’re curious about methylfolate read through this quick summary of its side effects.25 Vitamin B12, on the other hand, is sorely needed by many, and if you’re deficient, may help lessen symptoms of depression. Additionally to the best of my knowledge there have never been any overdoses of vitamin B12. It’s incredibly safe.

Many also suffer from “exercise deficiency,” and exercise is one of the most potent anti-depressants at your disposal. Research has confirmed it actually outperforms drug treatment. It’s also a key treatment strategy for anxiety disorders.

Exercise primarily works by helping to normalize your insulin levels while simultaneously boosting “feel good” hormones in your brain. But researchers have also recently discovered that exercise helps your body eliminate kynurenine, a harmful protein associated with depression.26

And, confirming the link between inflammation and depression, your body metabolizes kynurenine in the first place via a process that is activated by stress and inflammatory factors. Additionally, exercise increases BDNF (brain-derived neurotropic factor) and is a powerful activator of mitochondrial biogenesis.

Key Factors to Overcoming Depression and Anxiety Without Drugs

It’s important to realize that your diet and general lifestyle are foundational factors that must be optimized if you want to resolve mental health problems such as depression or anxiety, because your body and mind are so closely interrelated. For example, while many think of their brain as the organ in charge of their mental health, your gut may actually play a far more significant role.

The drug treatments available today for depression fail miserably in addressing people’s mental health problems. While adding one or more supplements to the treatment protocol is a step in the right direction, it still falls short, as the side effects of these drugs can be worse than the original complaint, running the gamut from sexual side effects to lack of emotions or “emotional flatness,” restlessness, sleep disturbances, brain damage, and even to suicide and homicide.

Antidepressants can also result in chronic, long-term, and worsening depression, so ideally, you’ll want to avoid them unless absolutely necessary.

Since antidepressants are on par with placebo in terms of effectiveness, wouldn’t it make sense to try something else first? Your diet is an obvious place to start. Research tells us that the composition of your gut flora not only affects your physical health, but also has a significant impact on your brain function and mental state, and your gut microbiome can be quickly impacted by dietary changes — for better or worse.

Research has also revealed there are a number of other safe effective ways to address depression that do not involve hazardous drugs. So, if you suffer from an anxiety or depression-related disorder, please consider addressing the following diet and lifestyle factors before you resort to drugs:

Eat real food, and avoid all processed foods, sugar (particularly fructose), grains and GMOs

High sugar and starchy carbohydrates lead to excessive insulin release, which can result in falling blood sugar levels, or hypoglycemia. In turn, hypoglycemia causes your brain to secrete glutamate in levels that can cause agitation, depression, anger, anxiety, and panic attacks.

Sugar also fans the flames of inflammation in your body. In addition to being high in sugar and grains, processed foods also contain a variety of additives that can affect your brain function and mental state, especially MSG, and artificial sweeteners such as aspartame.

Gluten sensitivity is also a common, hidden cause of depression, so going on a gluten-free diet can be part of the answer. Recent research also shows that glyphosate, used in large quantities on genetically engineered crops like corn, soy, and sugar beets, limits your body’s ability to detoxify foreign chemical compounds.

As a result, the damaging effects of those toxins are magnified, potentially resulting in a wide variety of diseases, including brain disorders that have both psychological and behavioral effects.

Increase consumption of traditionally fermented and cultured foods

Reducing gut inflammation is imperative when addressing mental health issues,27 so optimizing your gut flora is a critical piece. To promote healthy gut flora, increase your consumption of probiotic foods, such as fermented vegetables, kimchee, natto and kefir.

Get adequate vitamin B12

Vitamin B12 deficiency can contribute to depression and affects one in four people.

Optimize your vitamin D levels

Vitamin D is very important for your mood. Remember, Seasonal Affective Disorder is a type of depression related to sunshine deficiency, so it would make sense that the perfect way to optimize your vitamin D is through UV exposure. Be sure to check your levels (via blood test) at least once or twice a year. You’ll want to be within the therapeutic range of 40 to 60 ng/ml year-round.

If you cannot get sufficient sun exposure to maintain this level, taking an oral vitamin D3 supplement would be advisable. Just remember to also increase your vitamin K2 when taking oral vitamin D.

Get plenty of high-quality animal-based omega-3 fats

Your brain is 60 percent fat, and DHA, an animal-based omega-3 fat, along with EPA, is crucial for good brain function and mental health28,29 Unfortunately, most people don’t get enough from diet alone, so make sure you take a high-quality omega-3 fat, such as krill oil.

Evaluate your salt intake

Sodium deficiency actually creates symptoms that are very much like those of depression. Make sure you do NOT use processed salt (regular table salt), however. You’ll want to use an all natural, unprocessed salt like Himalayan salt, which contains more than 80 different micronutrients.

Get adequate daily exercise

Studies have shown there is a strong correlation between improved mood and aerobic capacity. There’s also a growing acceptance that the mind-body connection is very real, and that maintaining good physical health can significantly lower your risk of developing depression in the first place.

Exercising creates new GABA-producing neurons that help induce a natural state of calm. It also boosts your levels of serotonin, dopamine, and norepinephrine, which help buffer the effects of stress.

Get enough sleep

You can have the best diet and exercise program possible but if you aren’t sleeping well you can easily become depressed. Sleep and depression are so intimately linked that a sleep disorder is actually part of the definition of the symptom complex that gives the label depression.

Energy psychology

Energy psychology techniques such as the Emotional Freedom Techniques (EFT) can also be very effective for reducing symptoms of depression or anxiety by correcting the bioelectrical short-circuiting that causes your body’s reactions — without adverse effects.

Recent research has shown that EFT significantly increases positive emotions, such as hope and enjoyment, and decreases negative emotional states. 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.30,21

For serious or complex issues, seek out a qualified health care professional that is trained in EFT32 to help guide you through the process.

Metastatic Prostate Cancer Needs Genetic Testing; Here’s Why

Germline genetic testing should be offered to men with metastatic prostate cancer, regardless of age or family history, say the authors of a new study.

The incidence of germline mutations in genes that mediate the DNA-repair processes in patients with metastatic prostate cancer was found to be significantly higher than that in men with localized disease (11.8% vs 4.6%).

Almost three quarters of these men also had a first-degree relative with cancers other than prostate cancer.

These cancers include breast, ovarian, pancreatic, and other gastrointestinal malignancies, as well as leukemia and lymphoma.

The findings were published online July 6 in the New England Journal of Medicine.

“This information is important, not only for the patient but for other family members as well, as they too may be predisposed to cancer,” said Michael F. Walsh, MD, co-lead author of the study and a geneticist and pediatric oncologist at Memorial Sloan Kettering Cancer Center in New York, New York.

Dr Walsh recommended that family members should also be offered testing, in addition to the patients. “There are preventative and risk reduction options that may be relevant for family members which they should consider if also carrying the same pathogenic germline mutation,” he said.

These findings also can potentially change clinical practice. “We are now at a point where we have specific therapies that we can offer people with heritable DNA repair mutations,” Dr. Walsh told Medscape Medical News.

These include agents such as poly adenosine phosphate ribose polymerase inhibitors, for which there has been a precedent to try these therapies in women with breast and ovarian cancer. “These are emerging therapies and only available in clinical trials at this time,” he said. “And these trials are ongoing now.”

Higher Rates in Metastatic Disease

Previously, as part of other research, the authors sequenced germline DNA exomes from a population of men with metastatic prostate cancer. That is when they unexpectedly found that 8% of these men carried pathogenic germline mutations in DNA-repair genes.
Now, Dr Walsh and colleagues have assessed mutations in 20 DNA-repair genes that are associated with autosomal dominant cancer-predisposition syndromes in 692 men with metastatic prostate cancer.

The objective was to confirm the earlier findings and further ascertain the spectrum and prevalence of these mutations in this population.

They identified a total of 84 germline DNA-repair gene mutations that were presumed to be deleterious in 82 men in the cohort (11.8%).

Mutations were identified in 16 genes; these included BRCA2 (37 men [5.3%]), ATM (11 [1.6%]), CHEK2 (10 [1.9% of 534 men with data]), BRCA1 (6 [0.9%]), RAD51D (3 [0.4%]), and PALB2 (3 [0.4%]).

The frequency of mutations did not seem to be affected by a family history of prostate cancer or the patient’s age at diagnosis.

However, it was significantly more prevalent than the 4.6% frequency observed in the 499 men with localized prostate cancer (P < .001). This included patients with high-risk disease.

A family history was available for 72 of 82 men (88%) with mutations in DNA-repair genes and for 537 of 610 men (88%) without them.

In both groups of men, 22% (16 of 72 men with DNA-repair gene mutations and 117 of 537 men without them) had a first-degree relative with prostate cancer (P = 1.0).

But 51 patients with DNA-repair gene mutations (71%) had a first-degree relative with another cancer type compared with 270 patients (50%) without the mutations (odds ratio, 2.4; P = .001).

The authors point out that the 11.8% overall frequency of germline mutations seen in this study is substantially higher than the 1.2% to 1.8% incidence of BRCA2 mutations detected in localized prostate cancer or the 7.3% incidence of mutations in 22 tumor-suppressor genes identified in familial prostate cancer.

Even though testing for gene mutations is becoming increasingly available, Dr Walsh recommends that patients be tested in a comprehensive cancer center, where they will have access to genetic counselors.

“In addition to coming across mutations in the genes that we know are harmful, variants of uncertain significance may also be detected in these genes,” Dr Walsh said. “So we need to make sure that patients are being counseled appropriately by an experienced team.”

At the current time, it is unknown whether these mutations are prognostic, and that needs to be studied, he added. “This research is ongoing.”

NIH’s Fauci on Combating Zika: ‘You Have to Have the Resources to Act Quickly’

Every day there are headlines about the Zika virus.

The number of travel-related cases is growing, and public health officials — especially in states such as Florida, which could be among the hardest hit — predict it is only a matter of time until the first locally transmitted case is confirmed. They are scrambling to prepare strategies to combat Zika’s spread. On the research front, at least one private pharmaceutical company is slated to begin human trials on a Zika vaccine in the fall, and National Institutes of Health researchers hope to bring their version to clinical trials as soon as summer’s end. But on Capitol Hill, efforts to approve emergency funding to support all of these initiatives are being held up by partisan disputes.

At the center is Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases. He oversees federal Zika vaccine research and development activities and has been the leading government spokesman on the overall anti-Zika effort. It’s also been his job to find resources within NIH to support vaccine development while fighting for Congress to provide the additional funding. If it doesn’t happen soon, he warns, the progress made so far will stall. And, in the interim, he has been applying the lessons learned from the past outbreaks with which he has dealt — illnesses such as the West Nile virus and Ebola. “Outbreaks occur,” he said. “And if you find out you’re behind it as opposed to ahead of it, things are worse than they could’ve been.”
Dr Anthony Fauci
Fauci recently spoke with Kaiser Health News’ Carmen Heredia Rodriguez about the safety considerations that go into developing a vaccine and the ongoing funding fight. The conversation was edited for space and clarity.

Where do the resources to support federal vaccine research efforts come from — especially without congressional action to provide emergency funding?

In the early stages, we just diverted people, money, resources, activity away from the standard things that we were doing to start working on a Zika vaccine. We said, okay, we’re going to be asking for new resources. But, let’s get started on a full-blown, multi-component vaccine program. I mean not just one vaccine, but a series of four or five vaccines that are in various stages of development. And we did that.
Then it became very clear, very quickly, that in order to really mount this effort including vaccine [and] other things, we would need additional resources. That was when President Barack Obama asked us, together with the Centers for Disease Control and Prevention and the U.S. Agency for International Development, to put together what we would need. The president added it all up and it came to the $1.9 billion that he asked [Congress] for — of which ultimately, over a two-year period — $277 million would have been for NIH.

Then, when it became clear that we were not going to get that money expeditiously because of the back and forth between the Senate and the House and the administration, we needed some money pretty quickly. I started taking funds from malaria, from universal flu, from tuberculosis [programs]. And this is what people need to understand — it’s not that we were slowing down [that] work. The money that we were spending in February, March, April and May [on Zika] was money that we would be spending in July and August [on the other research]. We were borrowing money. We were mortgaging our resources.

So, that’s when the administration said, okay. In lieu of getting our appropriations and emergency supplement, we’re going to use some of the Ebola money that had not be spent by USAID and by the CDC. … That is what we are spending now.

Very soon — and when I say soon, I’m talking July, August — we’re going to run out of that money. And then, the effort that we’ve mounted on a vaccine and all other things, will come to a very, very — I wouldn’t say screeching halt — but, it would slow down.

What about testing the vaccine and conducting trials? Does the fact that pregnant women are likely the most vulnerable population complicate this part of the process?

Well, I think there’s a misunderstanding. It is likely — even though people don’t seem to understand that — that you would not be vaccinating pregnant women. You would be vaccinating women of child-bearing age. Because, once women are pregnant, the most vulnerable period is in the first trimester. Most women in those countries [Latin American countries which have already experienced outbreaks of Zika] don’t even know that they’re pregnant until they’re well into their first trimester. So, the horse is already out of the barn. That doesn’t mean that we won’t ever be vaccinating pregnant women. But the fundamental target is women of child-bearing age before they’re pregnant to protect them during pregnancy.

The Zika virus has been linked to Guillain–Barré syndrome in adults and deemed to cause microcephaly. What are the implications of these links for vaccine development?

You know, vaccine development is a very difficult issue because of the fact that you’re going to be vaccinating normal people. Before you do anything else, you have to make sure it’s safe. Guillain-Barré is associated with the disease. … Is that a risk? Yes. Is it a big risk? No, very likely a small risk.

But, that’s the reason why when you do vaccine trials, you’ve got to do a well-controlled trial that pays attention to safety.

Has work done on other viruses given researchers a leg up on finding a vaccine?

More than a leg up. Many of the things that we’re doing now are derivatives of things we had done with other vaccines. The leading candidate from the Vaccine Research Center [here at the National Institutes of Health] is one that will go into Phase I clinical trials likely in the beginning of September, or the end of August. It was [derived from] the same class of a vaccine that we [worked on] for West Nile several years ago. The live, attenuated vaccine that we’ll be testing in Brazil, in Colombia and likely in other areas in Central and South America and the Caribbean, is a vaccine that’s exactly the same broad class of a vaccine that we [work with] for dengue. So, already, work with West Nile and work with dengue has given us a very important head start on our vaccine work with Zika.

Are there lessons that can be learned from the recent Ebola experience that can be applied to this outbreak?

You know, there are so many lessons. One is that outbreaks occur. And if you find out you’re behind it as opposed to ahead of it, things are worse than they could’ve been.

Now, [an] Ebola outbreak is very different than a Zika outbreak because it’s a totally different disease. You have a vector instead of person-to-person contact. … It’s a mosquito-borne disease. Even though there’s some sexual transmission, the overwhelmingly major way of transmission is by mosquitoes. So, there are certain public health issues that are important and mosquito control that are different than the kind of ways you prevent the spread of Ebola. So, although they are very, very different, the common denominator is that if you are dealing with an emerging outbreak, in order to get control over it, you have to have the resources to act quickly and not wait around for them.

UK Rise in Bisphosphonate Use Dovetails With Fracture Decline

Publication of the National Institute for Health and Care Excellence (NICE) guidelines on use of antiosteoporosis agents for the secondary prevention of osteoporotic fractures in 2005, coupled with the release of generic alendronate shortly thereafter, led to a spike in use of bisphosphonates in England and Wales and a clinically meaningful reduction in subsequent fractures among hip-fracture patients, a new large-scale observational study indicates.

“It is clear that the guidance, coupled with the availability of a low-cost bisphosphonate, drove a major change in prescribing by general practitioners,” senior author of the work, Andrew Judge, MD, University of Oxford, United Kingdom, says in a statement.

“It is unclear how much this was due to the new guidance and how much due to generic alendronic acid arriving on the market, but it is notable that prescriptions for alendronic acid clearly outstrip those for other treatments, suggesting that it had a part to play,” he adds.

The study results were published online July 6 in the Journal of Bone and Mineral Research.

Lead author Samuel Hawley, DPhil candidate, University of Oxford, United Kingdom, and colleagues conducted the REFReSH study by identifying 10,873 individuals who had sustained a hip fracture in England or Wales anywhere between April 1999 and September 2012.

The prescribing patterns of physicians for osteoporosis treatments among hip-fracture patients in England and Wales were then tracked following publication of the NICE guidelines in January 2005 and for the first three years following the introduction of generic alendronate, which came shortly thereafter.

The publication of the guidelines and the release of generic alendronate were considered the “intervention,” and prescribing and fracture rates were documented before and after the start of the intervention period.
Overall, Mr Hawley and colleagues estimate there was a 17.2% absolute increase in the use of antiosteoporosis agents within a year of patients sustaining their initial hip fracture across the 3-year observational interlude.

This increase represented a relative increase of 79% compared to the “preintervention” period.

The incidence of subsequent major refracture, defined as fractures of the hip, pelvis, proximal-humerus, rib, spine, or wrist/forearm, prior to the intervention was stable at 6.3%.

Following the intervention, “there was a significant (P = .001) downward trend by -0.19% per 6 months,” Mr Hawley notes.

This downward trend translated into an approximate 14% relative decrease in the risk of major refracture rates over a period of 3 years after the start of the intervention period.

The same trend was seen for subsequent hip fracture.

Initially, hip refracture rates were stable at a rate of 3.8% prior to the introduction of the intervention. Following the intervention, there was again a downward trend in hip refracture rates of -0.17% for every 6 months (P = .001), which translated into a 22% reduction in hip fractures over a period of 3 years.

Mr Hawley and colleagues caution that while the observed decrease in the incidence of refracture rates did dovetail with an increase in prescriptions for bisphosphonates, “we have not been able to establish whether increased prescribing caused the reduction in subsequent fracture.”

However, as they also note, evidence from randomized controlled trials suggests that alendronate does reduce the risk of hip fracture relative to placebo.

Other changes in the UK healthcare system, including initiation of the Fracture Liaison Service model of care, may also have contributed to the decline in fractures over the study interval, they suggest.

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