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Siim Land Interviews Dr. Mercola About ‘EMF*D’

Reproduced from original article:

Analysis by Dr. Joseph Mercola     


  • Electromagnetic fields (EMFs) cause massive mitochondrial dysfunction, thus raising the risk for, and worsening, chronic and degenerative diseases
  • A perfect storm of DNA and cellular protein and membrane destruction is created when you aren’t burning fat for fuel (which creates excess superoxide) and then get exposed to EMFs
  • By creating doubt and controversy, the wireless industry effectively prevents the public from knowing the truth and demanding safer products. Another wireless industry strategy that prevents the problem from becoming public knowledge is the capturing of our federal regulatory agencies
  • Elon Musk’s Starlink project, which is slated to deploy up to 42,000 satellites into orbit around the earth, will blanket the entire planet with 5G internet frequencies. You won’t be able to escape it
  • Based on the studies already done on previous generations of wireless, we know it’s harmful, and 5G is only going to make matters worse, as it will dramatically increase our exposures

I was recently interviewed by Siim Land about my new book, “EMF*D,” described by Siim as “the most comprehensive guide … to everything you need to know about EMF.”

In it, I explain what electromagnetic fields (EMFs) are, the different types of EMFs you’re exposed to, the harms associated with exposure, the concerns surrounding 5G and, ultimately, how to protect yourself and limit your exposure.

As I explain in the interview, the thing that catalyzed me to write “EMF*D” was my deep appreciation of the impact of mitochondrial function in health and disease. Once I realized how EMFs impact mitochondrial function — because it’s very clear that EMF causes massive mitochondrial dysfunction — the danger our wireless society poses became very clear to me.

Just recently, I read a study1 stressing the importance of mitochondrial numbers for improving senescent cells — cells that are, in a manner of speaking, “senile” and have stopped reproducing properly. Instead, senescent cells produce inflammation, contributing to old age and, ultimately, death.

The fewer mitochondria you have, and the more dysfunctional they are, the faster you’ll age and the more prone you’ll be to chronic degenerative disease. By inducing mitochondrial dysfunction, our wireless world may well be driving us all into an early grave.

Cellphone Industry Hides Truth by Manufacturing Doubt

Considering the research data now available, you’d think everyone would understand and accept the fact that EMF is a serious health danger, yet many are still completely in the dark. With “EMF*D,” I hope to help more people understand this biological threat.

In 2011, the World Health Organization’s International Agency for Research on Cancer (IARC) classified radiofrequency EMFs as “possibly carcinogenic to humans.”2 Then, in 2018, the U.S. National Toxicology Program published two lifetime exposure studies conclusively showing cellphone exposure causes cancer.

The NTP’s findings were also duplicated by the Italian Ramazzini Institute just a couple of months later. In the wake of these studies, Fiorella Belpoggi, principal investigator and director of the Ramazzini Institute, urged the IARC to upgrade RF-EMF to “probably carcinogenic” or higher.3

Now, just like smoking cigarettes, EMF exposure takes decades before its effects become evident (and even then, the health problem might not be directly linkable to EMF exposure), and this is a significant part of the problem as it allows the telecom industry to — just like the tobacco industry before it — whitewash concerns, manipulate research and prevent proper safety studies from being done.

There’s no doubt cellphone manufacturers are aware that EMFs from cellphones contribute to health problems, though. The evidence has been published for decades, and new research is constantly being added.

However, by downplaying positive findings and saying that findings of harm are inconclusive — in other words, by creating doubt and controversy — they effectively prevent the public from knowing the truth and demanding safer products.

Wireless Industry Is Even Worse Than the Tobacco Industry

Another wireless industry strategy that prevents the problem from becoming public knowledge is the capturing of our federal regulatory agencies, which the tobacco industry wasn’t even capable of.

The U.S. Environmental Protection Agency, the Surgeon General and the Centers for Disease Control and Prevention all warned people about smoking, yet the tobacco industry continued successfully selling cigarettes for another 20 or 30 years. The wireless industry, on the other hand, has captured the federal regulatory agencies, which prevents those warnings from being issued in the first place.

For example, the chief lobbyist for the wireless industry, Tom Wheeler, was appointed by President Obama to be the head of the Federal Communications Commission, which is a most egregious example of the fox guarding the hen house. Not surprisingly, then, in December 2019 the FCC announced they’re going to fund rural 5G deployment to the tune of $9 billion!4

As detailed in my February 1, 2020, article, “The War Against 5G Heats Up,” the telecom industry has engaged in a vast and illegal fraud where, for decades, basic telephone rate payers — wire line customers — have funded the deployment of wireless in general, and now 5G in particular, through their phone bills.

This illegal redirection of funds amounts to about $1 trillion over the past 15 years, and without this money, 5G would not have been possible in the first place. Were the wireless industry forced to pay its fair share of infrastructure costs, 5G simply wouldn’t be economically feasible as a consumer product.

What’s so Great About 5G?

What exactly is 5G and why do some people want it? In short, it’s all about improving speed. Compared to 4G, 5G is 100 times faster. On a side note, you can determine what your bandwidth is by pulling up fast.com on your cellphone’s browser. If you’re on 4G, your bandwidth is probably not going to exceed 10 megabytes per second (mb/s). If you’re on 5G, it’s going to be between 500 and 800 mb/s.

So, the primary benefit of 5G is noticeably faster speed. The vast majority of people simply don’t need this kind of bandwidth, but it has great applications for commercial uses such as self-driving cars.

The problem is, 5G may end up making the earth uninhabitable for many who are already struggling with electrosensitivity, and the countless others for whom 5G may prove to be the thing that tips them over the edge into electrohypersensitivity syndrome.

Elon Musk’s Starlink project, which is slated to deploy up to 42,000 satellites into low earth orbit, will blanket the entire planet with 5G internet. You won’t be able to escape it, no matter how far into the wilderness you go.

5G Is a Prescription for Biological Disaster

Then there are the long-term dangers of 5G, which we still do not have a complete picture of. There has not been a single safety study done on 5G. Studies using 2G, 3G and 4G, however, including the NTP and Ramazzini studies, clearly show there’s cause for concern.

5G is more complex, as it uses a variety of frequencies, which makes it a potentially greater threat. The frequency of 4G is typically around 2 to 5 gigahertz (GHz), while 5G will be around 20 to 30 GHz, initially.

Eventually, it may go as high as 80 GHz, which will cause problems for people trying to remediate exposures because there are currently no inexpensive meters that can measure frequencies that high.

Based on the studies already done on previous generations of wireless, we know it’s harmful, and 5G is only going to make matters worse, as it will dramatically increase our exposures. 5G requires what essentially amounts to a mini cellphone tower outside every fifth or sixth house on every block.

We also have studies showing the impact of millimeter waves, which is what 5G is using, on insects, animals and plants, and those hazards are well-documented. So, it doesn’t just pose a problem for human health, but for the ecosystem as a whole.

Martin Pall, Ph.D., wrote an excellent paper explaining how EMFs affect your voltage gated calcium channels (VGCCs) — channels in the outer plasma membrane of your cells. Each VGCC has a voltage sensor, a structure that detects electrical changes across the plasma membrane and opens the channel. EMFs work through the voltage sensor to activate the channel and radically increase intracellular calcium levels into dangerous ranges.

Similar channels are found in most biological life, including animals, insects, plants and trees. So, flooding the planet with these frequencies will undoubtedly have serious biological consequences across the ecosystem. As such, it’s an existential threat to humanity.

One biological consequence is arrhythmia (irregular heartbeat). Other potential consequences include autism and Alzheimer’s. Heart and neurological problems top the list because your heart and brain have the greatest density of VGCCs. Men’s testes also have a very high density of VGCCs and, indeed, we have evidence showing EMFs increase men’s risk of infertility.

Everything points to these frequencies being a prescription for biological disaster, and between skyrocketing autism, Alzheimer’s and infertility rates, how can a society be sustained? It can’t. It will be extinguished.

We Don’t Need Wireless 5G

In reality, we can still get the bandwidth of 5G without 5G wireless. The alternative would be to deploy fiber optic cable. It’s faster, safer and less expensive.

Unfortunately, the money originally set aside to implement nationwide fiber optics was rerouted and illegally used to build the wireless infrastructure instead. This is why a group called The Irregulators5 are now suing the FCC to put a stop to the illegal subsidy to the wireless industry.

Wireline customers paid for an upgrade to fast and safe fiber optic wiring across the nation, but now we’re getting harmful 5G wireless instead. As explained in “The War Against 5G Heats Up” (hyperlinked above), this lawsuit has the potential to alter the telecommunications industry from the ground up, and may be the “weapon” we need to halt to the 5G rollout in the U.S.

The Importance of EMF Avoidance to Protect Your NAD+ Level

Along with practical remediation strategies, “EMF*D” also covers things you can do to protect yourself on a biochemical level. A perfect storm of DNA and cellular protein and membrane destruction is created when you aren’t burning fat for fuel (which creates excess superoxide) and then get exposed to EMFs.

This causes a radical increase in nitric oxide release that nearly instantaneously combines with superoxide to create enormous levels of peroxynitrate, which triggers a cascade of destructive events to your cellular and mitochondrial DNA, membranes and proteins.

Although all biologic damage is of concern, it is the DNA strand breaks that are most concerning as they will lead to a radical increase in inflammation and virtually all degenerative diseases.

The good news is your body has the ability to repair this damaged DNA with a family of enzymes called poly ADP ribose polymerase or PARP It is a very effective repair system and works wonderfully to repair the damage as long as it has enough fuel in the form of NAD+.

The bad news is many of us are running low on this fuel. When excess peroxynitrate activates PARP to repair the DNA damage, it consumes NAD+, and if you run out, you can’t repair the damage. This appears to be a central cause for most of the diseases we now see in the modern world.

Optimizing your NAD+ levels may be the single most important strategy for improving your mitochondrial health. The first step is to reduce NAD+ consumption by the correct diet (low in processed foods and net carbohydrates and higher in healthy fats), along with EMF avoidance, as recent research shows NAD+ levels dramatically drop when exposed to EMFs.

Time restricted eating is also very helpful, as is exercise, both of which are powerful, inexpensive and safe ways to boost your NAD+ level.

Helpful Strategies to Limit EMF Damage

In “EMF*D” I also cover the Nrf2 pathway and the importance of minerals such as magnesium to limit the biological damage caused by EMFs. As explained in this interview, upregulating your Nrf2 pathway activates genes that have powerful antioxidant effects, thus helping protect against EMF damage, while magnesium — which is a natural calcium channel blocker — helps reduce the effects of EMF on your VGCCs.

On a side note, molecular hydrogen tablets are an excellent source of ionic elemental magnesium. Each tablet provides about 80 milligrams of ionic elemental magnesium.

Addressing EMF Pollution — A 21st Century Health Imperative

There’s no doubt in my mind that EMF exposure is an important lifestyle component that needs to be addressed if you’re concerned about your health, which is why I spent three years writing “EMF*D.”

My aim was to create a comprehensive and informative guide, detailing not only the risks, but also what you can do to mitigate unavoidable exposures. To get you started, see the tips listed in my previous article, “Top 19 Tips to Reduce Your EMF Exposure.”

If you know or suspect you might already be developing a sensitivity to EMFs (full-blown hypersensitivity can often strike seemingly overnight), mitigating your exposures will be particularly paramount. Many sufferers become obsessed with finding solutions, as the effects can be severely crippling. My book can be a valuable resource in your quest for relief.

The EMF Experts website6 also lists EMF groups worldwide, to which you can turn with questions, concerns and support, and EMFsafehome.com7 lists a number of publications where you can learn more about the dangers of EMFs.

Should you need help remediating your home, consider hiring a trained building biologist to get it done right. A listing can be found on the International Institute for Building-Biology & Ecology’s website.8

Brian Hoyer, a leading EMF expert9 and a primary consultant for “EMF*D” also has a company called Shielded Healing that can provide a thorough analysis of the EMF exposure in your home, and help you devise a remediation plan. You can listen to our excellent three-hour interview for more information, featured in “Your EMF Questions Answered Part 1” and “Your EMF Questions Answered Part 2.”

3 superfood greens that are more nutritious than kale

Reproduced from original article:
Posted by Jonathan Landsman on 24th January 2020

For a long time now, we’ve all thought kale was the super food in terms of nutrient density – and it wasn’t that easy for a lot of us to make it past that bitter taste, unfortunately.

But did you know that kale actually ranks 15th in terms of nutrient density in a study recently published by the CDC titled Defining Powerhouse Fruits and Vegetables (PFV): A Nutrient Density Approach?  You can find a link to that report below, so that you can read all about the 41 fruits and vegetables that the CDC found to be nutrient powerhouses.

Let’s look at the top 3 “super food” greens that rank higher than kale.

Watercress (nutrient density score of 100) 

 Watercress might look like a more delicate smallish leaves, but watercress is actually a relative of horseradish and mustard greens and it tastes very peppery, indeed.

 Watercress is a member of the cruciferous vegetable family, alongside nutritious vegetables like Brussel’s sprouts, kale, arugula, and broccoli. Plus, it’s packed with so much nutrition it might just qualify as the super food of the decade.

Ranking at 100 in terms of nutrient-density, just one cup of watercress gives you 106% of your vitamin K requirement, and around a fourth of your RDA for vitamins A and C.

Watercress is also a great source of fiber, potassium, protein, calcium, and magnesium and it’s jam-packed with antioxidants and phytonutrients that can protect you against oxidative damage in the form of free radicals, which are associated with aging, cancer, and many other debilitating diseases like Alzhiemer’s.

Scientists have also found that eating watercress daily can reduce DNA damage to blood cells, which is considered to be the hallmark event that triggers the development of cancer. The same study revealed that eating watercress daily improved blood levels of lutein (by 100%) and beta-carotene (by 33%) – 2 phytonutrients which are very protective of the eyes, preventing macular degeneration and cataracts.

 Try adding watercress to your salads, pairing it with mild but equally nutritious greens like green leaf lettuce or Bibb lettuce!

Chinese or Napa cabbage (nutrient density score of 91.99)

Napa cabbage is another cruciferous vegetable that is jam-packed with nutrition. Napa cabbage provides 85% of your RDA for vitamin K and over half your RDA for vitamin C.

It’s also rich in nutrients like folate, hard-to-get manganese, and vitamin B6 as well. Cabbage was voted one of two vegetables which can help prevent diabetes (the other being root vegetables). Being a cruciferous vegetable, it’s also proven to help reduce blood markers for inflammation.

Like watercress, Chinese or Napa cabbage is packed with antioxidants and phytonutrients and is currently being researched for its cancer-fighting benefits. One study of Chinese women found that consumption of brassica vegetables like Chinese cabbage helped to significantly reduce breast cancer risk.

Swiss chard (nutrient density score of 89.27) 

 A nutrient-dense powerhouse, Swiss chard contains 44% of your RDA for vitamin A, 18% of your RDA or vitamin C, and a whopping 374% of your RDA for vitamin K.

Swiss chard is loaded with antioxidants and phytonutrients, including a potent flavonoid called syringic acid, which aids the liver in detoxifying the body, and which helps lower liver enzymes and prevent liver degeneration as well.

Swiss chard is also rich in powerful antioxidants called betalains, which have powerful antioxidant and detoxification properties by supporting the phase II pathways of the liver.

Because it’s so packed with vitamin K, yielding over 3 times your RDA for this nutrient, Swiss chard can help lower blood cytokines, which raise your risk for inflammation and inflammation-based diseases, especially type 2 diabetes.

Editor’s note: The NaturalHealth365 Store offers the finest quality nutritional supplements to support a healthy lifestyle.  Click here to shop today!

Sources for this article include:







The Importance of Lutein for Eye and Brain Health

Reproduced from original article:
Analysis by Dr. Joseph Mercola     

February 10, 2020


  • Lutein is well-known for its vision-enhancing properties. Research also suggests it has neuroprotective qualities, improving memory and boosting intelligence
  • There’s an inverse association between lutein levels in the eyes and age-related macular degeneration (AMD), the primary cause of blindness in the elderly, as well as cataracts
  • Lutein has also been shown to prevent cell death caused by retinal detachment when administered in a timely manner, and can help improve night vision
  • Lutein may help prevent neurodegenerative diseases by preventing DNA damage, the depletion of BDNF and the degradation of a synaptic vesicle protein involved in Alzheimer’s and Parkinson’s. It’s also been shown to help maintain the integrity of your brain’s white matter
  • Your body cannot manufacture lutein, so you need to get it from your diet. Lutein is a carotenoid found in egg yolks, avocados, cruciferous vegetables and dark, leafy greens, especially kale and spinach

Lutein — a carotenoid found in egg yolks, avocados, cruciferous vegetables and dark, leafy greens — is well-known for its vision-enhancing properties.1 Research also suggests it has neuroprotective qualities,2 improving memory3 and boosting intelligence.4 As reported in the Senior Resource Guide:5

“Lutein belongs in the subclass of xanthophylls, which have polar molecular structures that possess unique membrane properties, such as fluidity, communication between brain cells, ion exchange, diffusion of oxygen, membrane stability, and the prevention of oxidation and inflammation.

Like other xanthophylls, lutein accumulates in neural tissue. In fact, lutein accounts for most of the carotenoid accumulation in the human brain, and this high concentration of lutein in the brain may indicate its neuroprotective value.

Lutein accumulates in the brain and embeds in cell membranes. There, lutein protects the neuronal structure and function of brain cells. While lutein is distributed in the gray matter of the brain, researchers have detected its presence in the temporal cortex, the prefrontal cortex, and the hippocampus. Lutein accumulates in the brain over a person’s lifespan and may therefore provide lifelong benefits to brain health.”

Your body cannot manufacture lutein, so you need to get it from your diet. Unfortunately, many do not get enough lutein simply because they don’t eat enough vegetables and/or eggs.

How Lutein Protects Your Vision

As its name implies, lutein is found in high concentrations in your macula lutea,6 the small central part of your retina responsible for detailed central vision. It’s also found in your macular pigment (it’s responsible for the yellow hue of the macula7) and the lens of your eye.

Epidemiological research has found an inverse association between lutein and zeaxanthin levels in the eyes and age-related macular degeneration (AMD), the primary cause of blindness in the elderly, and cataracts.8,9

As explained in the 2013 paper,10 “The Role of Lutein in Eye-Related Disease,” lutein and zeaxanthin (another carotenoid present in high concentration in the eyes) help prevent age-related eye degeneration by ameliorating the damage caused by blue light and oxygen free radicals. Blue light is responsible for a majority of the damage to the eye, and lutein selectively absorbs blue light.

According to this paper, “Dietary concentrations between 6 and 20 mg per day of lutein have been associated with a reduced risk of ocular disorders such as cataracts and age-related macular degeneration.”

A more recent scientific review,11 published in 2019 in PLOS ONE, found people who took 10 mg or 20 mg of lutein per day had greater macular pigment optical density (MPOD), and better visual acuity and contrast sensitivity than those who did not supplement.

Macular pigment, the yellow pigmented area found in the center of your retina, acts as “internal sunglasses,” protecting your macula from harmful blue light. The denser your macular pigment, the lower your risk of developing AMD. Greater MPOD is also associated with better visual performance overall.12

According to the authors of the 2019 PLOS ONE review, “The available evidence suggests that dietary lutein may be beneficial to AMD patients and the higher dose could make MPOD increase in a shorter time.” Lutein has also been shown to prevent cell death caused by retinal detachment, when administered in a timely manner,13 and can help improve night vision.14,15


Click here to find out why 5G wireless is NOT harmless

Lutein’s Role in Brain Health and Cognition

More recent research has also found lutein plays an important role in brain health, and may even help prevent neurodegenerative diseases.16 As noted in the 2012 paper,17 “Neuroprotective Effects of Lutein in the Retina,” lutein benefits your brain and cognition by preventing:

  • DNA damage
  • Depletion of brain-derived neurotrophic factor (BDNF), which is important for brain health
  • Degradation of synaptophysin, a synaptic vesicle protein involved in neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease

Lutein and zeaxanthin have also been shown to help maintain the integrity of your brain’s white matter,18 and this too can lower your risk of age-related decline.

Lutein Benefits Both the Old and the Young

In one 2017 study,19,20,21 which involved 60 adults between the ages of 25 and 45, those with higher levels of lutein in middle-age had more youthful neural responses than those with lower levels.

Carotenoid status was assessed by measuring MPOD, which is also highly correlated with the lutein status in your brain. Most studies have focused on the effects of diet after cognitive decline has already set in.

Here, they wanted to evaluate whether lutein might have a preventive effect, as the process of cognitive decline has been shown to begin far earlier than typically expected. According to the researchers, you can start seeing cognitive deterioration as early as your 30s.

Indeed, the results suggest your diet, and in this case lutein-rich foods, does help keep your brain young. As noted by co-author Naiman Khan, professor of kinesiology and community health at the University of Illinois:22

“Now there’s an additional reason to eat nutrient-rich foods such as green leafy vegetables, eggs and avocados. We know these foods are related to other health benefits, but these data indicate that there may be cognitive benefits as well.”

Lutein has also been shown to benefit younger people. In one such study,23 healthy 18- to 30-year-olds exhibited better brain function after taking lutein and zeaxanthin supplements for a year. Significant improvements were seen spatial memory, reasoning ability and complex attention.

Cognitive Benefits Associated With Higher Lutein Levels

Several other studies support these findings. For example, in one University of Georgia study,24 older adults (mean age 72) taking 10 mg of lutein and 2 mg of zeaxanthin daily for one year were able to maintain their brain function, whereas the placebo group’s verbal learning ability and word recall deteriorated over the course of the study.

The mechanism thought to be responsible for this protective effect was enhanced blood flow through the brain. A number of other studies looking at lutein’s influence on cognition have shown that higher lutein and zeaxanthin levels in the macula are associated with improved:25,26,27

Verbal learning and fluency

Word recall

Executive function such as sorting and prioritizing information and the ability to take action

“Crystallized intelligence”28 — the ability to use learned knowledge and experience (opposed to the ability to logically reason your way through a new situation or problem, which is known as “fluid intelligence”29)

Relational memory performance30,31 — the ability to remember a person’s name when seeing their face, or to retell a story

Other Health Benefits of Lutein

Lutein has also been found to promote health in other ways, beside optimizing vision and cognition. For example, studies have found:

Diets rich in the carotenoids beta-carotene, lutein and lycopene resulted in greater resistance against oxidation of low-density lipoprotein (LDL) cholesterol. Higher plasma concentration of carotenoids was also associated with lower DNA damage.32
Lutein and zeaxanthin in combination with vitamin E appears to improve lung function and respiratory health.33
Plasma levels of antioxidants such as lutein, zeaxanthin, vitamin E, beta-cryptoxanthin, lycopene, alpha-carotene and beta-carotene are inversely correlated with congestive heart failure severity.34
Plasma carotenoid levels are also inversely correlated with prostate cancer.35
Lutein and lycopene enhance eye health by reducing your risk for oxidative stress-induced loss of retinal pigment epithelial (RPE) cells, and inhibiting the cell growth in undifferentiated RPE cells.36
Lutein has been shown to induce autophagy and may help shield your body against certain stresses.37
Lutein and zeaxanthin have also been shown to increase bone density in young, healthy adults.38 Lutein appears to stimulate bone mineralization and formation by suppressing bone resorption.

Lutein-Rich Foods

Lutein is primarily found in green leafy vegetables, with kale and spinach topping the list of lutein-rich foods. You’ll also find it in orange- and yellow-colored fruits and vegetables. The word lutein actually comes from the Latin word “luteus,” which means “yellow.”

As a general rule, anywhere from 15% 47% of the total carotenoid content in dark green leafy vegetables is lutein.39 Following is a list of foods that are particularly rich in lutein.40,41,42 Most of these also contain zeaxanthin, albeit in lesser quantities than lutein.

  • Egg yolks
  • Kale and spinach
  • Avocado
  • Broccoli
  • Green, red and yellow peppers

Ideally, you’ll want to buy the whole food and consume these foods as close to raw as possible, as the lutein (and other carotenoids such as zeaxanthin) are easily damaged by heat. Accessory micronutrients in the foods that enhance their action also tend to get easily damaged.

While there’s no recommended daily intake for lutein or zeaxanthin, studies have found health benefits for lutein at a dose of 10 milligrams (mg) per day and at 2 mg/day for zeaxanthin.

How to Optimize Lutein Absorption

Lutein and other carotenoids are fat-soluble, so to optimize absorption, be sure to add a little bit of healthy fat to your meal. For example, research43,44 shows that adding a couple of eggs — which contain both lutein and healthy fats — to your salad can increase the carotenoid absorption from the whole meal as much as ninefold.

Ideally, opt for organically-raised, free-range pastured eggs. Not only do they tend to have a better nutritional profile, by opting for pastured eggs you’ll also avoid pesticide exposure and genetically modified organisms. I raise six chickens and typically eat five eggs a day — the yolks raw in my smoothie and the whites cooked with my meat.

The vast majority of commercially available eggs come from concentrated animal feeding operations (CAFOs), where the hens are not permitted to forage on pasture. Instead, they’re typically fed a diet of corn and soy, the vast majority of which are genetically engineered. CAFO eggs are also far more prone to cause foodborne illness caused by salmonella contamination

If you live in an urban area, visiting a local health food store is typically the quickest route to finding high-quality local egg sources. Your local farmers market is another source for fresh free-range eggs. Cornucopia.org also offers a helpful organic egg scorecard45 that rates egg manufacturers based on 22 criteria that are important for organic consumers.

You can often tell the eggs are free-range by the color of the egg yolk. Foraged hens produce eggs with bright orange yolks, indicative of higher amounts of lutein and zeaxanthin. Another way to boost absorption of lutein from your vegetables is to add some raw organic butter or healthy oil such as olive or coconut oil to your salad.

Eat Right to Avoid AMD

To protect your vision over the long haul, aside from making sure you’re eating plenty of lutein-rich foods, you’ll also want to avoid a high-glycemic diet. As reported by Tufts University in 2017:46

“Sheldon Rowan, a scientist in the Laboratory for Nutrition and Vision Research at the Human Nutrition Research Center on Aging at Tufts, said there are plenty of indications that the types of carbohydrates we eat play a role in the development of AMD.

People who eat lots of simple carbohydrates, like those in white bread and sweetened beverages, are more likely to get the disease. This could be because simple carbs break down rapidly during digestion, creating a spike in blood sugar that can lead to widespread inflammation, a condition linked to AMD … If … blood glucose stays low over a long period of time, Rowan said, it can lower incidence of AMD.

To understand why, Rowan tested the two diets on laboratory mice. Over the course of a year, he fed one group of mice ‘high-glycemic’ foods — ones with lots of simple starches. A second group got a ‘low-glycemic’ diet, rich in complex carbs, but otherwise identical in calories and nutrients. In a third group, Rowan switched the mice’s diet from high- to low-glycemic foods halfway through the study.

Sure enough, mice with the low-glycemic diet did not develop AMD, while mice fed the high-glycemic diet almost all came down with the disease … In the mice that switched diets, though, Rowan saw something completely unexpected. Not only did they avoid AMD, but the existing damage to their retinas was reversed.

‘No one had ever seen that before,’ Rowan said of the findings, which were reported in Proceedings of the National Academy of Sciences.47 ‘The most common form of AMD doesn’t really have a treatment right now — but this suggests that just changing to a healthier eating pattern could have a huge impact.’”

Further exploration revealed that high-glycemic diets led to higher levels of advanced glycation end products (AGEs), which Rowan points out are “toxic end products of sugars” that “can damage the proteins and lipids that a cell needs to function.”

In the retina, the damaged proteins accumulate forming drusen, yellow deposits that damage your retinal cells.48 Elevated insulin levels also affect the development of your eyeball, making it abnormally long, thereby causing near-sightedness.49

Following my nutrition plan will help normalize your insulin level by reducing, or eliminating, excess sugar and processed grains from your diet. To learn more about which foods can help safeguard your vision, please see my previous articles, “Eat Right to Protect Your Eyesight,” and “The Best Foods for Healthy Eyes.”

– Sources and References

More Health Benefits of Quercetin Revealed

Reproduced from original article:
Analysis by Dr. Joseph Mercola     Fact Checked image

January 27, 2020
quercetin benefits


  • Quercetin has been shown to combat inflammation and acts as a natural antihistamine. Several studies have highlighted quercetin’s ability to prevent and treat both the common cold and influenza
  • Another, less known benefit and use for quercetin includes the prevention and/or treatment of high blood pressure, cardiovascular disease, metabolic syndrome, certain cancers, gout, arthritis and mood disorders
  • A review of quercetin’s effect on metabolic syndrome found it significantly reduced fasting plasma glucose when taken for at least eight weeks at a dosage of 500 milligrams per day or more
  • Other recent research found quercetin has a beneficial impact on nonalcoholic fatty liver disease by ameliorating inflammation, oxidative stress and lipid metabolism
  • Quercetin also has the ability to trigger tumor regression by interacting with your DNA and activating the mitochondrial pathway of apoptosis (the programmed cell death of damaged cells)

Quercetin1 is an antioxidant flavonol found naturally in foods such as apples, plums, red grapes, green tea, elder flower and onions, just to name a few.2 According to a 2019 Market Watch report,3 the quercetin market is growing rapidly as its health benefits are becoming more widely known.

Quercetin has been shown to combat inflammation and acts as a natural antihistamine. In fact, its antiviral capacity appears to be the primary focus of many studies looking at quercetin’s benefits, and a number of studies have highlighted quercetin’s ability to prevent and treat both the common cold and influenza.4,5,6,7

But there are also other, less known benefits and uses for this supplement, including the prevention and/or treatment of:8

High blood pressure9 Cardiovascular disease10
Metabolic syndrome11 Certain kinds of cancer12
Nonalcoholic fatty liver disease (NAFLD)13 Gout14
Arthritis15 Mood disorders16
Longevity, thanks to its senolytic benefits (clearing out damaged and worn-out cells)17,18

Additionally, quercetin is also helpful for aluminum-induced neurodegenerative changes, such as those seen in Alzheimer’s, Parkinson’s and amyotrophic lateral sclerosis (ALS). As noted in a 2016 study:19

“Administration of quercetin (10 mg/kg body wt/day) reduced aluminum (10 mg/kg body wt/day)-induced oxidative stress (decreased ROS production, increased mitochondrial superoxide dismutase (MnSOD) activity).

In addition, quercetin also prevents aluminum-induced translocation of cyt-c, and up-regulates Bcl-2, down-regulates Bax, p53, caspase-3 activation and reduces DNA fragmentation …

Further electron microscopic studies revealed that quercetin attenuates aluminum-induced mitochondrial swelling, loss of cristae and chromatin condensation. These results indicate that treatment with quercetin may represent a therapeutic strategy to attenuate the neuronal death against aluminum-induced neurodegeneration.”

Quercetin Improves Metabolic Syndrome Traits

Among the most recent papers on this powerful antioxidant is a review20 published in the March 2019 issue of Phytotherapy Research, which looked at nine randomized controlled trials investigating quercetin’s effect on metabolic syndrome.

Metabolic syndrome refers to a cluster of conditions (including high blood pressure, high blood sugar, high triglyceride levels and fat accumulation around the waist) that raise your risk for Type 2 diabetes, heart disease and stroke.

While pooled findings found no effect on fasting plasma glucose, insulin resistance or hemoglobin A1c levels, further subgroup analyses revealed quercetin supplementation “significantly reduced” fasting plasma glucose in studies lasting at least eight weeks and in which dosages of at least 500 milligrams (mg) per day were used.

In studies that included people over the age of 45, “significant” reductions in insulin were also found when using a dosage of 500 mg per day or more. An earlier study,21 published in 2011, looked at quercetin’s effects on certain traits of metabolic syndrome.

This study focused specifically atherosclerosis and inflammation in men with the APOE genotype 3/3, 3/4 and 4/4, and found quercetin significantly decreased waist circumference, postprandial systolic blood pressure, postprandial triacylglycerol, and increased HDL-cholesterol compared to placebo. Here, participants were given 150 mg of quercetin per day for eight weeks.

Research22 on obese rats published in 2008 also found that quercetin supplementation at doses of 2 mg per kilo or 10 mg/kg of body weight for 10 weeks improved systolic blood pressure, triglyceride, total cholesterol and free fatty acid levels. The 10 mg/kg dose also improved the animals’ inflammation status. As noted by the authors:

“In conclusion, both doses of quercetin improved dyslipidemia, hypertension, and hyperinsulinemia in obese Zucker rats, but only the high dose produced antiinflammatory effects in VAT together with a reduction in body weight gain.”

One of the first studies23 to demonstrate quercetin’s beneficial effects on blood pressure was published in 2007. As reported by the authors:

“Epidemiological studies report that quercetin … is associated with reduced risk of coronary heart disease and stroke … Men and women with prehypertension and stage 1 hypertension were enrolled in a randomized, double-blind, placebo-controlled, crossover study to test the efficacy of 730 mg quercetin/d for 28 d[ays] vs. placebo.

Blood pressure at enrollment was … 148 +/- 2/96 +/- 1 in stage 1 hypertensive subjects … Reductions in systolic (-7 +/- 2 mm Hg), diastolic (-5 +/- 2 mm Hg), and mean arterial pressures (-5 +/- 2 mm Hg) were observed in stage 1 hypertensive patients after quercetin treatment … These data are the first to our knowledge to show that quercetin supplementation reduces blood pressure in hypertensive subjects.”

Similarly, a January 2020 systematic review24 of 17 studies concluded quercetin “significantly decreased” blood pressure in human subjects. Those who took it for eight weeks or more also had “significantly” improved high-density lipoprotein cholesterol and triglycerides.


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Quercetin Improves Diabetes-Induced NAFLD

Other recent research25 published in the August 2019 issue of Phytotherapy Research concluded quercetin has a beneficial impact on NAFLD “by ameliorating inflammation, oxidative stress and lipid metabolism.”

Diabetes can play a role in NAFLD as well, showing just how influential insulin resistance is in the development of chronic diseases of all kinds. As explained in the abstract:

“Multiphase pathological processes involve in Type 2 diabetes (T2DM)‐induced nonalcoholic fatty liver disease (NAFLD). However, the therapies are quite limited. In the present study, the hepatoprotective effects and underlying mechanisms of quercetin in T2DM‐induced NAFLD were investigated …

The results revealed that quercetin alleviated serum transaminase levels and markedly reduced T2DM‐induced histological alterations of livers. Additionally, quercetin restored superoxide dismutase, catalase, and glutathione content in livers.

Not only that, quercetin markedly attenuated T2DM‐induced production of interleukin 1 beta, interleukin 6, and TNF‐α. Accompanied by the restoration of the increased serum total bile acid and the decreased liver total bile acid, quercetin could reduce lipid accumulation in the liver … These findings suggested that quercetin might be a potentially effective drug for the treatment of T2DM‐induced NAFLD.”

Quercetin Helps Modulate Gene Expression

According to research26 published in 2016, quercetin even has the ability to trigger tumor regression by interacting with your DNA and activating the mitochondrial pathway of apoptosis (the programmed cell death of damaged cells).

Quercetin was found to induce cytotoxicity in leukemic cells, and the effect was dose-dependent. Limited cytotoxic effects were also found in breast cancer cells. Overall, quercetin increased the life span in cancer-ridden mice fivefold compared to untreated controls.

The authors attributed these effects to quercetin’s direct interaction with DNA and its activation of the mitochondrial pathway of apoptosis, and suggested quercetin’s potential use as a cancer therapy adjunct deserves further exploration.

More recent research27 in the journal Molecules also highlights quercetin’s epigenetic influence and ability to:

  • Interact with cell-signaling pathways
  • Modulate gene expression
  • Influence the activity of transcription factors
  • Modulate microRNAs

MicroRNAs used to be considered “junk” DNA. Far from being useless, research has now revealed that “junk” DNA is actually microRNA and plays a crucial role in regulating genes that make the proteins that build your body.

The microRNA function as “on/off” switches for the genes. Depending on the microRNA input, a single gene can code for any of more than 200 protein products. Quercetin’s ability to module microRNA may also help explain its cytotoxic effects, and why it appears to improve cancer survival (at least in mice).

Quercetin Is a Powerful Antiviral

As mentioned, one of the most well-studied attributes of quercetin is its antiviral capacity, which have been attributed to three main mechanisms of action:

  1. Inhibiting the virus’ ability to infect cells
  2. Inhibiting replication of already infected cells
  3. Reducing infected cells’ resistance to treatment with antiviral medication

For example, research28 funded by the U.S. Department of Defense, published in 2007, found it lowers your risk of viral illness and boosts mental performance following extreme physical stress, which might otherwise undermine your immune function and render you more susceptible to infections.

Here, cyclists who received a daily dose of 1,000 mg of quercetin in combination with vitamin C (which enhances plasma quercetin levels29,30) and niacin (to improve absorption) for five weeks were significantly less likely to contract a viral illness after bicycling three hours a day for three consecutive days, compared to untreated controls. While 45% of the placebo group got sick, only 5% of the treatment group did.

In another study31 funded by the U.S. Defense Advanced Research Projects Agency (DARPA), published in 2008, animals treated with quercetin were challenged with a highly pathogenic H1N1 influenza virus. Again, the treatment group had significantly lower morbidity and mortality than the placebo group. A number of other studies have also confirmed quercetin’s effectiveness against a variety of viruses, including the following:

A 1985 study found quercetin inhibits infectivity and replication of herpes simplex virus type 1, polio-virus type 1, parainfluenza virus type 3 and respiratory syncytial virus.32
A 2010 animal study found that quercetin inhibits both influenza A and B viruses. Two other important discoveries were made. Firstly, the viruses were unable to develop resistance to quercetin, and secondly, when used concomitant with antiviral drugs (amantadine or oseltamivir), the effect was significantly amplified — and it prevented drug-resistance from developing.33
A 2004 animal study investigating quercetin’s effect on influenza used a strain of the H3N2 virus. According to the authors:34

“During influenza virus infection, there is ‘oxidative stress.’ Because quercetin restored the concentrations of many antioxidants, it is proposed that it may be useful as a drug in protecting the lung from the deleterious effects of oxygen derived free radicals released during influenza virus infection.”

Another 2016 study found quercetin offered protection against influenza A virus H1N1 by modulating protein expression. More specifically, the regulation of heat shock proteins, fibronectin 1 and prohibitin was instrumental in reducing viral replication.35
A third study published in 2016 found quercetin inhibited a wide spectrum of influenza strains, including H1N1, H3N2 and H5N1. According to the authors, “This study indicates that quercetin showing inhibitory activity in the early stage of influenza infection provides a future therapeutic option to develop effective, safe and affordable natural products for the treatment and prophylaxis of [influenza A viruses] infections.”36
In 2014, researchers noted that quercetin appears to be “a promising treatment for the common cold,” caused by the rhinovirus, adding that “Quercetin has been shown to reduce viral internalization and replication in vitro, and viral load, lung inflammation and airways hyper-responsiveness in vivo.”37

By attenuating oxidative damage, it also lowers your risk of secondary bacterial infections, which is actually the primary cause of influenza-related deaths. Importantly, quercetin increases mitochondrial biogenesis in skeletal muscle, which suggests part of its antiviral effects are due to enhanced mitochondrial antiviral signaling.

A 2016 animal study38 found quercetin inhibited mouse dengue virus and hepatitis virus. Other studies have confirmed quercetin’s power to inhibit both hepatitis B39 and C40 infection.
Most recently, a March 2020 study41 in the Microbial Pathogenesis journal found quercetin “provides comprehensive protection against Streptococcus pneumoniae infection,” both in vitro and in vivo, primarily by neutralizing pneumolysin (PLY),42 one of the toxins released from pneumococci that encourages S. pneumoniae infection to blossom in the first place. As reported by the authors in Microbial Pathogenesis:

“The results indicated that quercetin significantly reduced PLY-induced hemolytic activity and cytotoxicity via repressing the formation of oligomers.

In addition, treatment with quercetin can reduce PLY-mediated cell injury, improve the survival rate of mice infected with a lethal dose of S. pneumoniae, alleviate the pathological damage of lung tissue and inhibit the release of cytokines (IL-1β and TNF-α) in bronchoalveolar lavage fluid.

Considering the importance of these events in antimicrobial resistant S. pneumoniae pathogenesis, our results indicated that quercetin may be a novel potential drug candidate for the treatment of clinical pneumococcal infections.”

Quercetin Combats Inflammation and Boosts Immunity

Aside from its antiviral activity, quercetin is also known for boosting immunity and combating inflammation. As noted in a 2016 study43 in the journal Nutrients, mechanisms of action include (but is not limited to) the inhibition of:44

Lipopolysaccharide (LPS)-induced tumor necrosis factor α (TNF-α) production in macrophages. TNF-α is a cytokine involved in systemic inflammation, secreted by activated macrophages, a type of immune cell that digests foreign substances, microbes and other harmful or damaged components

LPS-induced mRNA levels of TNF-α and interleukin (IL)-1α in glial cells, which results in “diminished apoptotic neuronal cell death”

The production of inflammation-producing enzymes

Calcium influx into the cell, which in turn inhibits:

Pro-inflammatory cytokine release

Histamine and serotonin release from intestinal mast cells release45

According to this paper, quercetin also stabilizes mast cells, has cytoprotective activity in the gastrointestinal tract, and “a direct regulatory effect on basic functional properties of immune cells,” which allows it to inhibit “a huge panoply of molecular targets in the micromolar concentration range, either by down-regulating or suppressing many inflammatory pathways and functions.”46

Quercetin May Be a Useful Supplement for Many

Considering its wide-ranging benefits, quercetin may be a useful supplement for many, either acutely or more long-term. It’s one of the supplements I recommend keeping in your medicine chest for times when you feel you’re “coming down” with something, be it the common cold or influenza.

If you’re prone to colds and flu, you could consider taking it for a couple of months before cold and flu season hits to boost your immune system. More long-term, it appears useful for those with metabolic syndrome, although it would be foolish to rely on any given supplement without also addressing more fundamental strategies such as diet and exercise.

As explained in my 2015 interview with Dr. Robert Lustig, sugar has been shown to be a causative factor in insulin resistance, which is a hallmark of metabolic syndrome and a risk factor for virtually all chronic disease.

If you have one or more of the conditions that make up metabolic syndrome, you’d be wise to limit your total sugar consumption to 15 grams per day. If you’re healthy, and want to stay that way, your daily sugar limit would be around 25 grams. You can learn more about this and related treatment strategies in “Vitamin D Can Significantly Lower Your Risk of Metabolic Syndrome.”

– Sources and References

Why Your Brain Craves PQQ

Reproduced from original article:

Analysis by Dr. Joseph MercolaFact Checked
December 02, 2019
pqq for brain health


  • Pyrroloquinoline quinone (PQQ) is particularly important for the health and protection of your mitochondria. It also helps regenerate new mitochondria
  • PQQ has been shown to improve the function of beta amyloid-damaged brain cells — a hallmark of Alzheimer’s disease — and prevent the formation of alpha-synclein proteins associated with Parkinson’s disease. It can even help prevent neuronal cell death in cases of traumatic brain injury
  • Studies show PQQ improves mental processing and memory. It also works synergistically with CoQ10, producing better results than either of these nutrients alone
  • PQQ lowers C-reactive protein and interleukin-6, which are inflammatory biomarkers, and upregulates Nrf2 expression — a biological hormetic that upregulates beneficial intercellular antioxidants
  • PQQ has also been shown to boost the activity of primary life span extension transcriptional factors, which led the researchers to surmise that PQQ may play a role in longevity

While your diet is one of the most important tools you can use to take control of your health, certain supplements can be helpful, especially when it comes to improving your mitochondrial function. One particularly powerful supplement in this regard is pyrroloquinoline quinone (PQQ),1 which has been shown to promote the growth of new mitochondria (mitochondrial biogenesis).

Your mitochondria also require PQQ to catalyze energy producing reactions, and it’s critical in protecting your mitochondria from damage. Your mitochondria are the tiny energy producers inside your cells, which is why mitochondrial dysfunction is at the heart of just about all chronic diseases, old age and death.

In order for your body to function properly, it needs sufficient energy and, for that, you need well-nourished, well-functioning mitochondria. PQQ is an important player in this regard.2 As noted by Dave Asprey, founder of Bulletproof and author of books on energy, life span and brain power:3

“Anti-aging starts at the cellular level and PQQ is an easy way to protect your cells, all while helping to improve the most mitochondrial-dense parts of your body like your brain and heart.”

PQQ Enhances Mitochondrial Density and Function

PQQ is relatively unique in its ability to enhance mitochondrial biogenesis, i.e., the creation of new, healthy mitochondria in aging cells, which is the basis of so many of its health benefits. As reported by Better Nutrition magazine:4

“In addition to improving energy production, this characteristic of PQQ shifts some of the aging process into reverse gear. In a study5 at the University of California, Davis, researchers gave a small group of men and women PQQ supplements and tested the effects 76 hours later.

Using blood and urine tests, researchers found that PQQ improved mitochondrial performance and reduced chronic inflammation. The effective dose was 0.3 mg of PQQ per kilogram of body weight — 20 mg of PQQ for a 150-pound person, as an example.”

One mechanism by which PQQ lowers inflammation, improves mitochondrial function and stimulates mitochondrial biogenesis is by upregulating Nrf2 expression — a biological hormetic that upregulates intercellular antioxidants such as superoxide dismutase and catalase.

PQQ has also been shown to boost the activity of primary life span extension transcriptional factors, which led the researchers to surmise that PQQ may play a “novel role” in longevity.6 Indeed, it modulates a variety of signaling pathways, including mTOR, which plays a role in aging and cancer,7 and helps repair DNA,8 all of which suggests it may help you live longer.

PQQ also enhances NADH,9 which is converted to NAD+ as food is broken down into energy.10 When DNA damage is repaired, NAD+ is used up, and if you run out you can’t repair the damage, which is likely the central cause for most of the diseases we are seeing in the modern world now.

How PQQ Protects and Benefits Your Brain

PQQ’s ability to shield your brain cells and their DNA from harm also suggests it can be a powerful preventive aid against neurodegenerative diseases. Mitochondrial DNA is quite prone to damage from free radicals and pro-oxidants. Most of the free radicals in the body are produced within the mitochondria themselves, which is why they’re so susceptible.

Free radicals are an unavoidable artifact of converting food into cellular fuel, and your food is ultimately metabolized in your mitochondria. PQQ has been shown to protect against this kind of damage. It also activates your mitochondria’s built-in repair and replication mechanisms.

In your brain, the practical end result is an overall improvement of neurologic function,11 including improved cognition, learning and memory,12 and a reduced risk of neurodegenerative diseases. Research13 has shown PQQ protects and improves the survival of neurons by stimulating the synthesis of nerve growth factor (NGF) in certain glial cells found in your central nervous system.

It’s also been shown to improve the function of beta amyloid-damaged brain cells14 — a hallmark of Alzheimer’s disease — and prevent the formation of alpha-synclein proteins associated with Parkinson’s disease.15

According to a 2012 study,16 PQQ can even help prevent neuronal cell death in cases of traumatic brain injury. According to the authors of this study, “PQQ may play an important role in recovery post-TBI.”

Adding CoQ10 Provides Synergistic Benefits

Both animal and human studies using doses between 10 and 20 milligrams (mg) of PQQ have demonstrated improvement in mental processing and memory on its own, but combining it with Coenzyme Q10 could potentially be even more beneficial.

One study found PQQ in combination with CoQ10 produced better results than either of these nutrients alone, so there appears to be some synergistic effects. I recommend using the reduced form of CoQ10, called ubiquinol, as it is more readily available for your body.

Both CoQ10 and PQQ are fat-soluble, so they’re best taken with a small amount of fat in your meal rather on an empty stomach. In addition to being a powerful antioxidant in its own right, CoQ10/ubiquinol also facilitates the recycling (catalytic conversion) of other antioxidants, so when taken in combination with PQQ, you’re really turbocharging your body’s antioxidant capacity.

PQQ Is a Powerful Antioxidant and Immune Booster

Another reason why PQQ is so beneficial has to do with its powerful antioxidant activity. It’s capable of undergoing upward of 20,000 catalytic conversions. A catalytic conversion is when an antioxidant neutralizes a free radical. In other words, PQQ is a remarkably efficient antioxidant. For comparison, vitamin C can only go through four catalytic conversions before it’s used up.17,18

Research has shown PQQ lowers the inflammatory biomarkers C-reactive protein and interleukin-6 in humans at doses between 0.2 mg and 0.3 mg per kg.19

PQQ also supports your immune function and PQQ deficiency has been linked to immune dysfunction.20 In one study,21 PQQ supplementation increased the responsiveness of B- and T-cells (white blood cells that play central roles in your immune response) to mitogens (proteins that induces cell division or mitosis).

PQQ Activates Metabolic Master Switch

The list of potential applications for PQQ is extremely long, as its metabolic effects go well beyond improving mitochondrial function. For example, it helps activate adenosine monophosphate-activated protein kinase (AMPK), which is an important molecular target for metabolic health.

AMPK is an enzyme inside your body’s cells. It’s sometimes called a “metabolic master switch” because it plays an important role in regulating metabolism. As noted in the Natural Medicine Journal:22

“AMPK induces a cascade of events within cells that are all involved in maintaining energy homeostasis … AMPK regulates an array of biological activities that normalize lipid, glucose, and energy imbalances.

Metabolic syndrome (MetS) occurs when these AMPK-regulated pathways are turned off, triggering a syndrome that includes hyperglycemia, diabetes, lipid abnormalities, and energy imbalances …

AMPK helps coordinate the response to these stressors, shifting energy toward cellular repair, maintenance, or a return to homeostasis and improved likelihood of survival.

The hormones leptin and adiponectin activate AMPK. In other words, activating AMPK can produce the same benefits as exercise, dieting, and weight loss — the lifestyle modifications considered beneficial for a range of maladies.”

With age, your AMPK level drops naturally, but poor diet can reduce AMPK activity at any age. This enzyme plays a major role in body fat composition, inflammation and blood lipids, so boosting its activity can go a long way toward improving blood sugar control, reducing visceral fat and lowering LDL cholesterol.

AMPK also stimulates mitochondrial autophagy (mitophagy) and mitochondrial biogenesis, as well as five other critically important pathways: insulin, leptin, mTOR, insulin-like growth factor 1 (IGF-1) and proliferator-activated receptor gamma co-activator 1-alpha (PGC-1α).

It is important to note that PQQ will not likely work well, if at all, if you are eating around the clock, as elevated insulin levels will activate mTOR and inhibit AMPK, thus limiting PQQ’s ability to increase it.

Other Benefits of PQQ

PQQ has also been linked to several other health benefits, including:

  • Improved reproductive outcomes in animals23 (PQQ deficiency has been linked to abnormal reproductive performance24)
  • Reduced risk of nonalcoholic fatty liver disease in offspring when given to obese mouse mothers during pregnancy and lactation25
  • Improved sleep (by modulating the cortisol awakening response)26

As you can see, the list of PQQ’s health benefits is quite long. And, while PQQ is found in foods such as natto, parsleygreen pepperspinachpapaya, kiwi and green tea,27 the amounts you get from your diet are likely to be insufficient if you want to reap all of its beneficial health effects.

When taking a PQQ supplement, you’ll know within a few weeks whether the brand and dosage is working for you. Overall, you should feel better, with greater energy and clearer thinking.

– Sources and References

Gene-Editing Unintentionally Adds Bovine DNA, Goat DNA, and Bacterial DNA, Mouse Researchers Find

© 6th November 2019 GreenMedInfo LLC. This work is reproduced and distributed with the permission of GreenMedInfo LLC. Want to learn more from GreenMedInfo? Sign up for the newsletter here www.greenmedinfo.com/greenmed/newsletter
Reproduced from original article:

Originally published on www.independentsciencenews.org

The gene-editing of DNA inside living cells is considered by many to be the preeminent technological breakthrough of the new millennium. Researchers in medicine and agriculture have rapidly adopted it as a technique for discovering cell and organism functions. But its commercial prospects are much more complicated.

Gene-editing has many potential uses. These include altering cells to treat human disease, altering crops and livestock for breeding and agriculture. Furthermore, in a move that has been widely criticised, Chinese researcher He Jiankui claims to have edited human babies to resist HIV by altering a gene called CCR5.

For most commercial applications gene-editing’s appeal is simplicity and precision: it alters genomes at precise sites and without inserting foreign DNA. This why, in popular articles, gene-editing is often referred to as ‘tweaking’.

The tweaking narrative, however, is an assumption and not an established fact. And it recently suffered a large dent. In late July researchers from the US Food and Drug Administration (FDA) analysed the whole genomes of two calves originally born in 2016. The calves were edited by the biotech startup Recombinetics using a gene-editing method called TALENS (Norris et al., 2019). The two Recombinetics animals had become biotech celebrities for having a genetic change that removed their horns. Cattle without horns are known as ‘polled’. The calves are well-known because Recombinetics has insisted that its two edited animals were extremely precisely altered to possess only the polled trait.

However, what the FDA researchers found was not precision. Each of Recombinetics’ calves possessed two antibiotic resistance genes, along with other segments of superfluous bacterial DNA. Thus, apparently unbeknownst to Recombinetics, adjacent to its edited site were 4,000 base pairs of DNA that originated from the plasmid vector used to introduce the DNA required for the hornless trait.

The FDA finding has attracted some media attention; mainly focussed on the incompetence of Recombinetics. The startup failed to find (or perhaps look for) DNA it had itself added as part of the editing process. Following the FDA findings, Brazil terminated a breeding program begun with the Recombinetics animals.

An animal research facility

But FDA’s findings are potentially trivial besides another recent discovery about gene-editing: that foreign DNA from surprising sources can routinely find its way into the genome of edited animals. This genetic material is not DNA that was put there on purpose, but rather, is a contaminant of standard editing procedures.

These findings have not been reported in the scientific or popular media. But they are of great consequence from a biosafety perspective and therefore for the commercial and regulatory landscape of gene-editing. They imply, at the very least, the need for strong measures to prevent contamination by stray DNA, along with thorough scrutiny of gene-edited cells and gene-edited organisms. And, as the Recombinetics case suggests, these are needs that developers themselves may not meet.

Understanding sources of stray DNA

As far back as 2010 researchers working with human cells showed that a form of gene-editing called Zinc Finger Nuclease (ZFN) could result in the insertion of foreign DNA at the editing target site (Olsen et al., 2010). The origin of this foreign DNA, as with Recombinetics’ calves, was the plasmid vector used in the editing process.

Understanding the presence of plasmid vectors requires an appreciation of the basics of gene-editing, which, confusingly, are considerably distinct from what the word ‘editing’ means in ordinary English.

Ultimately, all DNA ‘editing’ is really the cutting of DNA by enzymes, called nucleases, that are supposed to act only at chosen sites in the genome of a living cell. This cut creates a double-stranded break that severs (and therefore severely damages) a chromosome. The enzymes most commonly used by researchers for this cutting are the Fok I enzyme (for TALENS type editing), Cas9 (for CRISPR), or Zinc Finger Nucleases (for ZFN).

Subsequent to this cutting event the cell effects a repair. In practice, this DNA repair is usually inaccurate because the natural repair mechanism in most cells is somewhat random. The result is called the ‘edit’. Researchers typically must select from many ‘edits’ to obtain the one they desire.

Like virtually all enzymes these nucleases are proteins. And like most proteins they are somewhat tricky to produce and relatively unstable once made. Typically, therefore, rather than produce the DNA cutting enzymes directly, researchers introduce vector plasmids into target cells. These vector plasmids are circular DNA molecules that code for the desired enzyme(s). (vector plasmid DNA may also code for the guide RNA that CRISPR editing techniques require). What this means, in practice, is that TALENS, Cas9 and the other cutting enzymes end up being produced by the target cell itself.

Introducing DNA rather than proteins is thus much easier, research-wise, but it has a downside: non-host (i.e. transgenic) DNA must be introduced into the cell that is to be edited and this DNA may end up in the genome.

Plasmid vectors are not simple. As well as specifying the nucleases, the vector plasmid used by Recombinetics contained antibiotic resistance genes, plus the lac Z gene, plus promoter and termination sequences for each of them, plus two bacterial origins of replication. Each of these DNA components comes from widely diverse microbes.

As Olsen et al. and the FDA showed, using both TALENS and ZFN types of DNA cutters can result in plasmid vector integration at the target site. In 2015 Japanese researchers showed that DNA edits made to mouse zygotes using the CRISPR method of gene editing are also vulnerable to unintended insertion of non-host DNA (Ono et al., 2015).

Since then, similar integrations of foreign DNA at the target site have been observed in many species: fruitflies (Drosophila melanogaster), medaka fish (Oryzias latipes), mice, yeast, Aspergillus (a fungus), the nematode C. elegans, Daphnia magna, and various plants (e.g. Jacobs et al., 2015Li et al., 2015Gutierrez-Triana et al., 2018).

Other sources of stray DNA

The vector plasmids themselves are not the only source of potential foreign DNA contamination in standard gene-editing methodologies.

Earlier this year the same Japanese group showed that DNA from the E. coli genome can integrate in the target organisms’ genome (Ono et al. 2019). Acquisition of E. coli DNA was found to be quite frequent. Insertion of long unintended DNA sequences occurred at 4% of the total number of edited sites and 21% of these were of DNA from the E. coli genome. The source of the E. coli DNA was traced back to the E. coli cells that were used to produce the vector plasmid. The vector plasmid, which is DNA, was contaminated with E. coli genome DNA. Importantly, the Japanese researchers were using standard methods of vector plasmid preparation.

Even more intriguing was the finding, in the same paper, that edited mouse genomes can acquire bovine DNA or goat DNA (Ono et al., 2019). This was traced to the use, in standard culture medium for mouse cells, of foetal calf serum; that is, body fluids usually extracted from cows. This serum contains DNA from whichever animal species it happened to have been extracted from, hence the insertion in some experiments of goat DNA (which occurred when goat serum was used instead of calf serum).

Even more worrisome, amongst the DNA sequences inserted into the mouse genome were bovine and goat retrotransposons (jumping genes) and mouse retrovirus DNA (HIV is a retrovirus). Thus gene-editing is a potential mechanism for horizontal gene transfer of unwanted pathogens, including, but not limited to, viruses.

Other potential sources of unwanted DNA also exist in cell cultures used for gene editing. In 2004 researchers observed that when cells from a hepatoma cell line were caused to have DNA breaks, some of these breaks were filled by hepatitis B virus sequences (Bill and Summers, 2004). In other words, pathogens contaminating the foetal serum, such as DNA viruses, should also be a source of concern.

Furthermore, the insertion of superfluous DNA from other species is likely not restricted to the intended target site. As is becoming appreciated, gene-editing enzymes can act at unwanted locations in the genome (e.g. Kosicki et al., 2018). Accidentally introduced DNA can also end up at such sites. This has been shown for human cells and also plants using CRISPR (Kim and Kim 2014; Li et al., 2017; Jacobs et al., 2015). There is every reason to suppose that the more exotic DNAs mentioned above can integrate there as well, but this has not been specifically tested for.

Implications of superfluous DNA in edited cells

In summary, the new findings are very simple: cutting DNA inside cells, regardless of the precise type of gene editing, predisposes genomes to acquire unwanted DNA. The unwanted DNA may come from inside the edited cell, or it may come from the culture medium, or it may come from any biological material added to the culture medium, whether accidentally or on purpose. Therefore, it is not hard to imagine, for instance, gene-edited animals becoming the breeding stock that leads to the development or spread of novel or unwelcome viruses or mycoplasmas.

Stuart Newman of New York Medical College is a cell biologist, a founding member of the Council for Responsible Genetics, and Editor-In-Chief of the journal Biological Theory. According to him, the addition of DNA originating from cell culture “is something that has not been broached in the discourse around safety of CRISPR and other gene modification techniques.”

In the case of gene-editing intended to generate altered living organisms, cell culture media “contain genes that could cause developmental problems if reincorporated by CRISPR/Cas9 into the zygote genome in extra numbers and uncontrolled chromosomal sites.” says Newman.

“I have little doubt E. coli DNA has been inadvertently incorporated into many CRISPR targets, and it is likely to cause problems, as it has in the horned cattle.”

Similar concerns apply to human applications. The incorporation of DNA from other species has not publicly been raised in connection with the gene-edited human babies of researcher He Jiankui. Clearly, it should be. From what cell types, for example, did He Jiankui purify the proteins he presumably used to edit the CCR5 gene? Rabbit cells? Insect cells? Those, at least, are the standard methods.

The second important conclusion, and what the Recombinetics case exemplifies, is that researchers are often not looking for stray DNA. If they were to look, many more examples would likely be reported. We can conclude this because the research cited above used standard methods of gene-editing. The only untypical aspect was the extra effort put towards detecting superfluous DNA.

Gene-editing versus GMOs

What these recent findings also highlight is a more general, but little-discussed, aspect of gene-editing. Although the goals of gene-editors and genetic engineers are assumed to be very different, their standard methods are, in practice, virtually indistinguishable.

Consider crop plants, which are where much of the immediate commercial interest in gene-editing resides. To edit plants, DNA, in the form of vector plasmid, is introduced into plant cells. In contrast to methods of animal gene-editing, this vector plasmid is necessary (and not optional) since proteins cannot penetrate plant cell walls. This vector plasmid must access the cell interior, which requires either a gene gun or infection with the DNA-transferring bacterium Agrobacterium tumefaciens. Lastly, in-vitro cell culture is used to regenerate the edited cells into whole plants.

Gene guns, tissue culture, and A. tumefaciens are all standard genetic engineering methods for crops. They also all create mutations. That is, they damage DNA. Depending on the specifics of the method used, such as the length of time in tissue culture, the collective result can be ten thousand mutations per genome (Wilson et al., 2006Latham et al., 2006). For gene-editing of crops this means that one on-target mutation may be dwarfed by thousands of off-target ones.

The other necessary comparison with GMOs is their track record of being found, long after commercialisation, to have unintended foreign DNA present in their genomes. Cornell’s virus-resistant papaya, released in Hawai’i, turned out to contain at least five (and possibly six) separate fragments of transgenic DNA. Cornell had previously told regulators its papaya contained two transgenes (Ming et al., 2008). Monsanto’s Roundup Ready Soybean, by then grown on 96% of US soybean acres, was found by independent researchers to have substantially more foreign DNA than Monsanto had claimed (Windels et al., 2001).

So, if one only listened to the rhetoric contrasting ‘precise’ ‘tweaks’ of gene-editing with ‘messy’, ‘random’ genetic engineering one would hardly suspect that, when it comes to plants, and often to animals as well, there is little difference between the reality of gene-editing and that of genetic engineering.

Are there solutions to the presence of superfluous DNA?

Solutions to the presence of superfluous DNA (at or distant from the editing site) come in two basic forms: prevention or detection followed by removal.

An obvious preventive step is to avoid the use of vector plasmids and undefined culture media (undefined media are those containing fluids or extracts from living organisms). Another is to explicitly breed (backcross) gene-edited animals and plants to remove superfluous DNAs. A third is to sequence their whole genome, compare it to the parent genome, and select only unaltered lines, if they can be found (Ahmad et al., 2019).

However, these remedies are effortful. They are time-consuming and costly, or not yet fully developed, or only available for some species. These are also solutions that nullify the advantages of speed and ease that are often the stated reasons for editing in the first place.

The requirements for expertise and effort do much to explain the second major problem, which is that the industry, and not just Recombinetics, is not showing much interest in self-examination. Far greater even than the GMO industry before it, there is a cowboy zeitgeist: blow off problems and rush to market. Thus most gene-editing companies are reluctant to share information and consequently very little is known about how, in practice, many of these companies derive their ‘gene-edited’ products.

Many countries are at present formulating regulations that will go a long way to determining who benefits and who loses from any potential benefits that gene-editing may have. But in any event, these results provide a compelling case for active government oversight.

It is not just regulators who need to step up, however. Investors, insurers, journalists, everyone, in fact, should be asking far more questions of the scientists and companies active in gene-editing. Otherwise, boom is likely to stray into bane.


Ahmad, Niaz Mehboob-ur Rahman, Zahid Mukhtar, Yusuf Zafar, Baohong Zhang (2019) A critical look on CRISPR-based genome editing in plants. J. Cellular Physiology.

Bill, Colin A. and Jesse Summers (2004) Genomic DNA double-strand breaks are targets for hepadnaviral DNA integration. PNAS: 101 (30) 11135-11140.

Gutierrez-Triana, Jose Arturo, Tinatini Tavhelidse, Thomas Thumberger , Isabelle Thomas, Beate Wittbrodt, Tanja Kellner, Kerim Anlas, Erika Tsingos, Joachim Wittbrodt (2018) Efficient single-copy HDR by 5′ modified long dsDNA donors. eLife 2018;7:e39468.

Thomas B Jacobs, Peter R LaFayette, Robert J Schmitz & Wayne A Parrott (2015) Targeted genome modifications in soybean with CRISPR/Cas9. BMC Biotechnology 15: 16.

Kim, J. & Jin-Soo Kim (2016) Bypassing GMO regulations with CRISPR gene editing. Nature Biotechnology 34: 1014-1015.

Kosicki, M , K. Tomberg and A. Bradley (2018) Repair of double-strand breaks induced by CRISPR-Cas9 leads to large deletions and complex rearrangements. Nature Biotechnology 36: 765-771.

Norris, Alexis. L., Stella S. Lee, Kevin J. Greenlees, Daniel A. Tadesse, Mayumi F. Miller, Heather Lombardi (2019) Template plasmid integration in germline genome-edited cattle. doi: https://doi.org/10.1101/715482

Olsen, P.A., Gelazauskaite, M., Randol, M. & Krauss, S. (2010) Analysis of illegitimate genomic integration mediated by zinc-finger nucleases: implications for specificity of targeted gene correction. BMC Mol Biol 11, 35.

Latham, Jonathan R., Allison K. Wilson and Ricarda A. Steinbrecher (2006) The Mutational Consequences of Plant Transformation. The Journal of Biomedicine and Biotechnology (2006) 7 pages doi:10.1155/JBB/2006/25376

Li, Zhongsen, Zhan-Bin Liu, Aiqiu Xing, Bryan P. Moon, Jessica P. Koellhoffer, Lingxia Huang, R. Timothy Ward, Elizabeth Clifton, S. Carl Falco, A. Mark Cigan (2015) Cas9-Guide RNA Directed Genome Editing in Soybean. Plant Physiol. 169: 960-970.

Li, Rong Sheng Quan, Xiaofang Yan, Sukumar Biswas, Dabing Zhang, Jianxin Shi (2017) Molecular characterization of genetically-modified crops: Challenges and strategies. Biotechnology Advances 35:s 302-309.

Ming, R., S Hou, Y Feng, Q Yu, A Dionne-Laporte (2008) The draft genome of the transgenic tropical fruit tree papaya (Carica papaya Linnaeus). Nature 452: 991-996.

Windels, Pieter, Isabel Taverniers, Ann Depicker, Erik Van Bockstaele and Marc De Loose (2001) Characterisation of the Roundup Ready soybean insert. Eur. Food Res. Technol. 213:107-11.

Ono, Ryuichi, Masayuki Ishii, Yoshitaka Fujihara, Moe Kitazawa, Takako Usami, Tomoko Kaneko-Ishino, Jun Kanno, Masahito Ikawa & Fumitoshi Ishino (2015) Double strand break repair by capture of retrotransposon sequenc es and reverse-transcribed spliced mRNA sequences in mouse zygotes. Scientific Reports 5: 12281.

Ryuichi Ono, Yukuto Yasuhiko, Ken-ichi Aisaki, Satoshi Kitajima, Jun Kanno & Yoko Hirabayashi (2019) Exosome-mediated horizontal gene transfer occurs in double-strand break repair during genome editing. Communications Biology 2: 57 https://www.nature.com/articles/s42003-019-0300-2.pdf?origin=ppub

Wilson, Allison K., Jonathan R. Latham, and Ricarda A. Steinbrecher (2006) Transformation-induced mutations in transgenic plants: analysis and biosafety implications. Biotechnology and Genetic Engineering Reviews 23.1 : 209-238.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.

How Functional Genetics Can Help You Take Control of Your Health

Analysis by Dr. Joseph Mercola  – Fact Checked – May 12, 2019

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Story at-a-glance

  • Functional genetics looks at the single nucleotide polymorphisms (SNPs, pronounced “snips”) of genes
  • When you have SNPs (genetic variants or defects on the genes), enzymes may not be working effectively, or the gene may be upregulated or downregulated
  • While traditional genetics often looks for potential disease states, functional genetics looks for potential impairment of function and helps find the best nutritional intervention to bring your body back into balance
  • People with genetic weaknesses that hamper detoxification who are exposed to high amounts of environmental toxins can be struggling with health due to their limited ability to detoxify
  • NutriGenetic Research Institute is devoted to functional genomic testing, training health professionals to help people understand the results and how to apply it to improve their health

Functional genomics is a gene testing modality with enormous value that many are completely unaware of. Bob Miller1 is a certified traditional naturopath specializing in genetic-specific nutrition. He’s the founder of the NutriGenetic Research Institute,2 devoted to testing and helping people understand the results of their functional genetic testing and how to apply it to improve their health.

“As a traditional naturopath, we’re not licensed medical doctors, so we don’t diagnose, treat or prescribe,” Miller explains. “We look at the functional approach of, ‘How is the terrain off in the body?’ … [W]hen the body is toxic or inflamed, that’s when pathogens have a better opportunity to thrive.

Many years ago, I learned about how homocysteine has pathways that clear it that may be impaired by genetic variants. I became very fascinated by it. I started looking at the enzymes that clear it, and then the genetics behind it.

My whole naturopathic and holistic practice is [now] dedicated to helping clients measure their functional genomics, which is quite a bit different than traditional genetics that looks for disease patterns, and trying to find out how we can make interventions to bring the body back into balance …

Our goal is to be able to make a contribution to functional practitioners, so they can do their job a lot better and improve the lives of those who are suffering with some of those things that nobody can seem to figure out …

To sum up what we’re finding is that those with genetic weakness in detox pathways are exposed to environmental factors we weren’t dealing with 50 to 75 years ago; their ability to detox is overwhelmed. I think this is a whole new paradigm that we have to look at in wellness.

Those who don’t have a specific disease, so to speak, but are just totally overwhelmed by all of the epigenetic factors, such as pesticides, electromagnetic fields (EMFs) … excess iron … plastics … mold … [and] sometimes even oversupplementation with things like folate and glutamine … that no matter what they try, it doesn’t work …

That’s why we need to move to personalized care, based upon the individual. Fortunately, we now have tools to do that.”

What Is Functional Genetics?

Certain genes are known to predispose you to, or raise your risk of, certain diseases. That’s not what we’re talking about here. Functional genetics looks at the single nucleotide polymorphisms (SNPs, pronounced “snips”) of genes related to function.

You’ve probably seen representations of the DNA ladder. On the end of each rung is a molecule from each of your parents. These molecules can either make your DNA optimal or, if you have a SNP, meaning a defect, that gene will not work at optimal efficiency. Miller explains:

“To make this simple, we eat fats, carbohydrates and proteins. We drink water, breathe air and are exposed to sunlight. What an absolute miracle it is that all of that turns into us: our blood, our skin, our nails, our organs and our thought processes. All of that is one enzymatic process after another.

So, an enzyme takes substance A; pulls in what we call cofactors and makes substance B. That continually happens throughout your body — one process after another. It’s your genetic makeup that [provides] the instructions on how to make these enzymes.

When we have genetic variants, SNPs, on the genes, sometimes those enzymes either aren’t as effective … or might be upregulated or downregulated. Therefore, that substance A to substance B [conversion] may not occur as it should.

Now, people get all excited about whether they have genetic variants or not, but there’s something else just as important. That’s the cofactor. Remember, substance A plus cofactors turns into substance B. You could have absolutely perfect genetics, that enzyme is made perfectly, but if you’re missing the cofactors, that A to B [conversion] is not going to work …

Where people really get hit hard is when they’ve got genetic weakness and cofactor weakness. Then there’s a third piece. Sometimes there are things that interfere. For example, lead, mercury and other things may suppress that enzymatic function …

Now, interestingly, we have all kinds of backups. One pathway may not be working, but another one might kick in. But what we’re observing … is that those who are struggling usually have multiple pathways blocked. Plus, they get multiple epigenetic exposures … When you get those epigenetic and genetic factors going together, that’s when things really start going awry.”


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The Relationship Between mTOR Pathway and Autophagy

Autophagy means “self-eating” and refers to your body’s process of eliminating damaged and defective cellular parts that are targeted for lysosome, which then digests them. The mammalian target of rapamycin (mTOR) is a molecular signaling pathway responsible for either growth or repair, depending on whether it is stimulated or inhibited.

I’ve often stated that to upregulate maintenance and repair (which will boost longevity and reduce your risk for cancer), you need to suppress the mTOR pathway. One of the most efficient ways to do this is to limit your protein intake, but it’s not the only way. Autophagy and mTOR are two processes that work together, but are inverse to each other. Miller likens mTOR to a construction crew, whereas autophagy refers to the cleanup crew.

“One of the ways you can tell if your autophagy is not working is when you get those age spots, sun spots, liver spots, whatever you’d like to call them,” Miller says. “That’s when the old cell is not cleared away and it becomes oxidized, it becomes senescent. It actually becomes a free radical-giving reactive oxygen species.

Now, we need a balance between [mTOR and autophagy]. We need a time to build and we need a time to clean. One of the things our research institute [found] in some of our studies on those with chronic Lyme disease [is] that we are being exposed to more epigenetic environmental factors that stimulate mTOR … ”

Factors That Activate mTOR Versus Those That Support Autophagy

Examples of environmental factors that activate mTOR include:

Xenoestrogens (chemicals in plastic) EMFs
Insulin Excess protein
Excess iron Excess folic acid, folate or methyl folate
Excess glutamate Amino acids such as leucine, isoleucine and valine

When mTOR is activated, it inhibits autophagy and, according to Miller, many of the health challenges people face these days appear to be related to excess mTOR activation.

This is also one way by which a cyclical ketogenic diet helps improve your health, as it inhibits mTOR and activates autophagy. When mTOR is chronically activated, it will not only inhibit autophagy but also impair apoptosis (cell death), and if that’s impaired, your risk for cancer will significantly increase as well.

“We have identified the genes that are involved with autophagy,” Miller says. “They’re called Unc-51 like autophagy activating kinase 1 (ULK1), serine/threonine-protein kinase (ULK2), 5’ AMP-activated protein kinase (AMPK) and AuTophaGy related 1 (ATG1).

Those all stimulate autophagy. We’re finding that when people have a lot of genetic variants, especially when they inherit it from both parents, this is where their autophagy’s weakened. They’re 45 years old and covered with age spots. They can’t detox.

Ketogenic diet, intermittent fasting and nutrients [such as] lithium and berberine support autophagy. Resveratrol and curcumin slow down mTOR.

When you put the three together — the caloric restriction mimetics (CRM) [editor’s note: supplements that mimic the antiaging effects of calorie restriction] … along with the keto diet, along with some form of intermittent fasting — you’re able to bring balance to mTOR and autophagy.”

If Ketogenic Diet or Intermittent Fasting Fails for You, This Could Be Why

While intermittent fasting is an excellent strategy for a majority of people, it doesn’t work as expected for everyone. As explained by Miller, members of his research team have discovered having a functional heme pathway is extremely important when you’re on a ketogenic diet and/or intermittently fasting.

Heme protein is created through an eight-step process beginning with succinyl coenzyme A (succinyl CoA), glycine and amino acids. Heme protein in turn is a component of hemoglobin, but it’s also involved in the making of nitric oxide, catalase, superoxide dismutase (SOD) and sulfite oxidase (SUOX), which is your sulfide to sulfate conversion.

“It’s involved in so many processes that I didn’t even realize until we started to research,” Miller says. “This [heme] pathway may be impaired by … glyphosate [which impacts glycine] … lead … and genetic variants in the heme pathway.

If any of those happen, you don’t make adequate heme, so you’re going to be a very poor detoxer. Now, what’s interesting … [is that] if porphyrins [glycoproteins responsible for pore formation in cell membranes] are not transferred one to another, they will block the gamma-aminobutyric acid (GABA) receptor sites. GABA is the ‘Don’t worry. Be happy. Sleep. Relax’ [neurotransmitter]. Clearly, there are problems with anxiety in the world today.

If this heme pathway gets disturbed, people oftentimes crave carbohydrates. If they try to go keto, it doesn’t work. If they try to do intermittent fasting, it doesn’t work … It’s a small amount of people, but for some individuals who just crave carbohydrates, they’ll get hangry if they don’t have their carbohydrates. They’re actually feeding that heme pathway.

If someone’s ever tried keto and is like, ‘This just does not work for me,’ there’s a potential that the heme pathway could be impaired. You have to keep those carbohydrates coming in on a regular basis to feed it, or else you feel horrible. I remember in the past people telling me, ‘Whenever I try to eat healthy, I feel horrible. When I eat junk, I feel better.’

I used to think, ‘Yeah. I’m not sure I buy that.’ But now that you understand this heme pathway and how carbohydrates and simple sugars can feed it, it starts to make sense that that is a potential scenario for some people.”

Even if You’re Anemic, You May Be Overabsorbing Iron

As mentioned earlier, iron stimulates mTOR. Clearly, iron is crucial for optimal health. Without sufficient amounts of iron, you cannot make sufficient amounts of hemoglobin, which carries oxygen through your body. However, in excess, iron is incredibly destructive.

“Here’s one of the interesting things we found through our research. There are many people who have genetic predisposition to overabsorbing iron, yet they’re told all their life they’re anemic. It just seems like such a dichotomy; how can you be anemic if you’re overabsorbing iron?

One of the things that we … find in many who are struggling and can’t get answers anywhere else is that they overabsorb iron. There’s an enzyme called ferroportin, [which] is what takes iron out of the cells. SNPs there, or genetic defects, inhibit the removal of the iron. Through something called the Fenton reaction … iron may combine with hydrogen peroxide to make hydroxyl radicals.

This can then go on to make another nasty free radical called peroxynitrite. Consequently, the person is anemic because they are measuring what’s in the blood, but the iron can be in excess and inside the cells, causing massive inflammation.

As that iron bangs around inside the cell, it creates fatigue, because the mitochondria are having a hard time making energy. These are the people who if someone gives them iron, many times, they feel considerably worse, because they’ve just fed the fire.

In our consulting, one of the things we probably do the most is identifying the Fenton reaction going on and taking remedial action to, for example, help turn the hydrogen peroxide into water through an enzyme called catalase; supporting enzymes and antioxidants called glutathione and thioredoxin that turn the hydrogen peroxide into water, [and] using homeopathics to make the iron behave itself.”

Hydrogen water can be helpful here, Miller notes, because it helps decrease the excess hydroxyl radicals. “Quite simply, H2O2 plus iron equals hydroxyl free radical (OH-), which is one of the most highly reactive and damaging free radicals,” Miller explains.

I’ve previously interviewed Tyler LeBaron, one of the leading experts on molecular hydrogen, and he believes the benefits may be related more to the upregulation of antioxidant pathways, such as the nuclear factor erythroid 2-related factor 2 (Nrf2). Either way, whatever the mechanism, it seems clear hydrogen water has the ability to neutralize free radicals.

Situations in Which NAC or Methyl Folate May Backfire

I’ve previously written about the benefits of N-acetyl cysteine (NAC), the rate-limiting factor for glutathione, which is a master antioxidant made by your body. However, in order for this to work, you must have the required enzymes. What’s more, if you have an iron problem, the cysteine you take can combine with the iron to create hydroxyl radicals — essentially worsening your situation.

“It goes back to the fact that we’ve got to get away from the cookie cutter, ‘Oh, you’re inflamed. Take NAC.’ NAC can be the perfect thing for you, or it can make you worse, depending on your genomic make up,” Miller says.

Miller has developed a hierarchical pyramid of different variables and his approach to treating them. Interestingly, many who superficially look at functional genomics think that the methylation defect is one of the most important. It is important, but according to Miller there are many others that supersede it in terms of importance.

nutrigenetic hierarchical pyramid

“[Methylation] is about how we take folic acid or folate from our diet and turn it into methyl folate, which is a very important molecule. For a woman who’s pregnant, you’ve got to have it for a good pregnancy. We’re not saying it’s not a good thing … Now, one of the interesting things about methyl folate is you need it for pregnancy because it supports mTOR.

If someone’s already in mTOR dominance and they take methyl folate, they’re going to get more anxious and more inflamed. I’ve talked to so many people who’ve said, ‘Oh, yeah. I have MTHFR. Somebody put me on methyl B12, methyl folate. I felt great for two weeks, and then I crashed.’

The reason they may have crashed is because they started to stimulate mTOR, weakening their autophagy even more, driving more inflammation … As we dug deeper, we realized that methyl folate is important, but it has to be done at the right time. That’s why I developed my pyramid.

At the very bottom we have things we have to address first, such as, is iron becoming a free radical? Is hydrogen peroxide not being cleared? Is there nitric oxide synthase (NOS) uncoupling? — where rather than making nitric oxide, we make more peroxynitrite.

And then we look at how we’re making antioxidants. How’s our glutathione pathways? How’s our superoxide dismutase? How are we making NADPH? … For the most part, I believe that when people are massively inflamed, you need to address that first.

If someone is massively inflamed, if their iron is creating hydroxyl radicals, if they have weakness in their antioxidants … and you throw methyl folate in there … there’s a very good chance it will make the situation worse.

By and large, if someone’s massively inflamed, I’d like to think about methyl folate six to eight months down the road, two to three days a week. We tend to think, ‘If a little’s good for us, a lot must be good for us.’ I’m now thinking need to be pulsing things.”

I totally agree pulsing is a key component that should not be overlooked, whether you’re taking supplements, fasting or doing a ketogenic diet. It’s important to go through cycles of buildup and tear-down.

For example, during a partial fast, you’re stimulating autophagy through caloric restriction. At that time, you would not want to take anything that stimulates mTOR (such as methyl folate or any of the other items listed above), as by stimulating mTOR you effectively interrupt the autophagy process.

Mast Cells Could Be Wreaking Havoc With Your Health

Glutathione rapidly loses electrons, making it useless unless recharged by nicotinamide adenine dinucleotide phosphate hydrogen (NADPH). As explained by Miller, the “NADPH steal,” a term he coined, may also be at play in many of the health issues people face today.

It’s becoming more widely known that you can have excess mast cells. Miller estimates about 80 percent of his clients have excess mast cell activation triggering histamine reactions. One of the signs of this is redness of the face due to heat intolerance. Sensitivity to touch is another, as are frequent, red, raised rashes.

Mast cells are white blood cells that come to the rescue when there’s a pathogen or a foreign invader that needs to be eliminated. While overfiring mast cells can cause problems, they’re not inherently bad, and strategies that inhibit them can backfire. Instead, Miller recommends determining why your mast cells are overactive.

His team presented research at the International Lyme and Associated Diseases Society’s 19th Annual Conference in November last year, identifying epigenetic factors that stimulate mast cells. He explains the relationships between mast cells, NADPH, NOX and glutathione:

“In simple terms, glutathione … has one chance to give a free radical an electron. Once it does that, it becomes oxidized. Then we need to donate that electron back. There’s this substance called NADPH that donates that electron back.3 It takes that oxidized glutathione and turns it back into reduced. That’s a good thing.

Now, NADPH has a dual role. There’s also an enzyme called NOX (NADPH oxidase). Its only purpose is to take this NADPH and turn it into a free radical … Now, they’ve done studies on animals. When they knock out that NOX enzyme, the animal dies from infection because it doesn’t have the ability to kill the pathogen.

Again, NOX and free radicals are not bad. But there are multiple factors that are now overstimulating NOX. One of them is sulfite. Sulfite needs to turn into sulfates. If we have deficiency of heme, we may not turn sulfites in sulfates … If sulfites don’t turn into sulfates, the sulfites may tell the NOX enzyme, ‘You need to make inflammation.’

Dopamine stimulates it [NOX], so stress will cause it. Glutamate stimulates it. Iron stimulates the NOX enzyme, and so does excessive mTOR … The NADPH steal is when NADPH gets stolen away from recycling glutathione, recycling thriodoxine, making nitric oxide, and potentially making excess mast cells.

There are a lot of people struggling with excess mast cells firing. They’re really sick. They don’t know what to do … Mold will also stimulate mast cells …

To sum it up, NADPH is critical for recycling your antioxidants. I believe the nicotinamide adenine dinucleotide (NAD+) and the NADPH are some of the most important things we can have adequate levels of for longevity and good health. We’re using up a lot of it because we’re exposed to so many toxic substances. Then, if another set of substances are stealing it to stimulate NOX to make mast cells, then we’ve just doubled the problem.”

Molecular hydrogen serves a role here as well, as studies have shown molecular hydrogen is an effective inhibitor of NOX,4 and can increase your concentration of NADPH. Curcumin also inhibits NOX, as does luteolin, apigenin and olive leaf. Aldosterone, on the other hand, stimulates NOX, Miller says.

More Information

This interview is quite loaded with information, not all of which has been covered in this article. For even more side notes and fascinating tangents, I recommend listening to the interview in its entirety.

Health practitioners interested in learning more about functional genomic analysis and how to apply it in your own practice, see the NutriGenetic Research Institute’s website, where you can sign up for their 30-hour, 14-module online certification course to become a nutritional genetic consultant.

Webinars for health practitioners are held every other Thursday. They also hold an annual conference in Hershey, Pennsylvania. The next one is scheduled for November 2019. In September, they’re also holding a seminar on environmental toxicity, detoxification and methylation mapping.

Patients interested in more information are directed to the yourgenomicresource.com which includes a listing of doctors who have completed the training and are qualified to provide nutritional guidance based on your SNPs. Up until last year, Miller could guide patients based on the genetic data provided by companies such as 23andMe. Now, he has developed his own DNA testing, which is capable of identifying some 300,000 SNPs.

Importantly, NutriGenetic Research Institute will never sell your private DNA or health data to anyone, which is one of the reasons why 23andMe is so inexpensive — they make their money by selling your DNA results to drug companies.

“I have pledged to everyone in writing that this data will never be sold to anyone. The other thing people can do, if they’re still worried, you can just change your name. Just come up with a fake name. It doesn’t matter. We don’t care. You just have to remember what it is,” Miller says.

“The [DNA] data from Brooks at Rutgers gets loaded into my software, which is in Chambersburg, Pennsylvania — a huge database. Then it crunches the data and gives a report, including the pyramid …

If you’re sick, you’ve been everywhere and you’re not getting better, this is certainly an option … Our whole goal is to help people get well. And to make a little bit of a dent in functional medicine — to help functional practitioners have tools that they can help, because functional medicine doctors see the tough cases. We want to give them some tools so that they can do a better job …

One of my favorite sayings is, ‘Genetics is never a diagnosis, but it tells you where to start looking.’ It’s like shining a light. ‘Think about looking here. Investigate whether this is a problem.’ Sometimes the SNPs show a problem, sometimes they don’t, but it can really give you clues to look where you may never have thought to look before.”

Sources and References