Lose Them Pounds

Aside from being vital pollinators, bees produce a number of products that benefit human health. Honey1 is an obvious one, but there are others as well, such as royal jelly, a nutritious substance secreted by nurse bees as exclusive nourishment for the queen of the hive.
Recent research2,3,4,5 by Stanford University scientists found royalactin (also known as major royal jelly protein 1, or MRJP1), a protein found in royal jelly responsible for the queen’s massive growth, has the ability to keep embryonic stem cells pluripotent.
This initial finding could eventually lead to the development of drugs to boost stem cells in the human body, allowing for the regeneration of healthy tissue in damaged organs, be it your heart, eyes, skin or spinal cord.
They also identified a protein with similar qualities found in mammals, which they dubbed Regina — a nod to the queen bee for which royalactin is made — which like royalactin allows embryonic stem cells to maintain their naïve state. According to the authors:

“This reveals an important innate program for stem cell self-renewal with broad implications in understanding the molecular regulation of stem cell fate across species.”

Researchers Discover Innate Program for Stem Cell Self-Renewal

Embryonic stem cells are the product of the initial meeting of egg and sperm. Three days after fertilization of the egg, an inner cell mass can be isolated, and these are the embryonic stem cells that, if left alone, will grow into a fetus.
Stem cells are pluripotential, meaning that they have the ability to turn into any and every type of tissue to form an entire being, be it animal or human. Adult stem cells, in contrast, are multipotential, meaning they only have the ability to form subsets of tissue.
The problem researchers have is that embryonic stem cells have a tendency to differentiate into mature tissue cells of various kinds when grown in the lab, and in order to use the stem cells for research and/or therapies, they must be kept in their “naïve” state long enough. As explained by New Atlas:6

“With the ability to differentiate into all kinds of cells that serve specialized functions, like muscle cells, red blood cells or brain cells, embryonic stem cells have incredible potential. But growing them in the laboratory is difficult, because their natural inclination is to quickly outgrow their pluripotent state and become something else.

To preserve that pluripotency, scientists must add special molecules to the culture that inhibit that behavior. Wang and his team found that by adding royalactin instead, they could stop the embryonic stem cells from differentiating just as well.

In fact, they found that they were able to maintain the cells in their embryonic state for up to 20 generations in culture without the need for inhibitors.”

This was a complete surprise. Normally, scientists must use leukemia inhibitor factor to prevent the embryonic stem cells from differentiating when grown in culture. What they discovered is that royalactin performed the same function. The question is: How?
Royalactin-Like Protein in Mammals Inhibit Embryonic Stem Cell Differentiation

Mammals do not produce the royalactin protein, yet the royalactin activated a network of genes known to code proteins that allow the embryonic stem cells to maintain their pluripotency. To find the answer, the researchers searched scientific databases to identify human proteins with structures similar to that of royalactin.
What they found was a protein known as NHL repeat-containing-3 protein or NHLRC3, produced during the development of the mammalian (including human) embryo. They then duplicated the mouse experiment using NHLRC3, which was found to trigger a similar gene network as royalactin.
The end result was the same — the embryonic stem cells maintained their pluripotency in culture. Kevin Wang, assistant professor of dermatology and lead author of the study, commented on the results, saying:7

“It’s fascinating. Our experiments imply Regina is an important molecule governing pluripotency and the production of progenitor cells that give rise to the tissues of the embryo. We’ve connected something mythical to something real.”

Next, Wang and his team will investigate whether Regina — the mammalian equivalent of royalactin — has the ability to affect cell regeneration and wound healing in adult animals. And, as reported by New Atlas:8

“It could be used as another way to keep embryonic stem cells pluripotent in the lab, and could one day lead to the development of synthetic versions that deliver stocks of stem cells in the human body.

[T]hose kinds of drugs could be used for all kinds of things, from generating healthy tissue for damaged hearts, degenerating eyes, injured spinal cords and severe burns.”

What Is Royal Jelly and How Is It Made?

Royal jelly is a gelatinous, milky substance secreted by the hypopharyngeal and mandibular glands of worker honeybees between the sixth and twelfth days of their life,9 and is an essential food for the development of the queen bee. It’s a complex substance containing proteins (12 to 15 percent), sugars (10 to 12 percent), fat lipids (3 to 7 percent), along with a variety of amino acids, vitamins and minerals.10
Compared with the short-lived and infertile worker bees, the queen bee, which is exclusively fed royal jelly, is characterized by her extended lifespan and her well-developed gonads. Therefore, royal jelly has been long-used as a supplement for nutrition, antiaging or infertility.
The larva selected to become queen is fed royal jelly exclusively, while the rest of the larva receive royal jelly along with pollen and honey. Research11,12 reveals this exclusive royal jelly diet activates certain genes in the queen bee, allowing her to grow much larger and become such a prolific egg layer. The honey and beebread fed to worker bee larvae contains p-coumaric acid, and it’s the presence or absence of p-coumaric acid that determines the caste of the bee.
Larvae fed royal jelly to which p-coumaric acid had been added produced adults with reduced ovary development. “Thus, consuming royal jelly exclusively not only enriches the diet of the queen-destined larvae, but also may protect them from inhibitory effects of phytochemicals present in the honey and beebread fed to worker-destined larvae,” the researchers explain.13
Health Benefits of Royal Jelly

Folklore in Europe and Asia has it that royal jelly is a powerful rejuvenator capable of boosting longevity and fertility. It’s also been used to promote hair growth and minimize wrinkles. In Chinese medicine, royal jelly is revered as a substance that helps increase life expectancy, prevent disease and restore youth.
The fact that the protein Regina in mammals and humans appears to work like royalactin in royal jelly could possibly account for some of these benefits. Royal jelly also has antimicrobial benefits, courtesy of bee defensin-1, an antimicrobial peptide found in it. Because of components such as these, it’s fair to assume that royal jelly is in fact beneficial for humans.
That said, the idea that consuming royal jelly might somehow affect your stem cells is probably taking things too far. There’s no evidence of that — only that royalactin allows mammalian embryonic stem cells in an undifferentiated state in a lab environment.
Also keep in mind that it’s difficult to ensure potency and quality of royal jelly products on the market. Toxicology tests suggest most if not all honeys, for example, are tainted with the herbicide glyphosate, and the bee population has taken a hit around the world due to various pesticide exposures. If the bees have toxins in them, it’s feasible their royal jelly might be contaminated as well.
Still, the research was conducted by a very prestigious institution and published in a respectable journal, and they seem to believe there are possibilities here. Just realize that the focus is on Regina, the mammalian protein equivalent of royalactin, and not on royal jelly itself.
Health Benefits of Bee Propolis

Propolis is yet another bee product with health benefits, including immune-boosting properties and strengthening your body’s defenses against bacteria, viruses and other disease-causing organisms.
Propolis is used by bees to close openings in their beehives, which is why it is also referred to as “bee glue.” The materials are usually taken from leaves, bark, flower buds and other plant parts. These are then combined with bee saliva, wax and pollen, which are then adhered to the hive holes.
Studies suggest propolis also protects the bees from bacterial infections and possible external elements that may endanger the whole colony. In some cases, propolis may also be used to encase the carcasses of hive intruders to stop bacteria from spreading.14
Propolis has been used for years in folk medicine because of its proposed effect on various body systems, dating back to the time of the ancient Greeks, Romans and Egyptians.
In fact, Hippocrates notes that propolis is beneficial for promoting wound healing, both internal and external, while Pliny the Elder documents that propolis may be used to treat tumors, muscle pain and ulcers. This bee product was also documented in the Persian manuscripts as a remedy for various conditions, including eczema and rheumatism.15
Today, propolis is used in a wide variety of skin care products, including creams and extracts to promote wound healing and ease various types of infections. It is also available as a supplement, with people taking it on a regular basis to boost their immune system function.16
Another Bee Product, Propolis Has Flavonol With Health Benefits

Research also suggests a flavanol in propolis called galangin has anticancer effects on several cancers, including melanoma, hepatoma, leukemia and colon cancer.
In one such study,17 galangin was found to induce apoptosis (programmed cell death) in two types of colon cancer cells (HCT-15 and HT-29 specifically), and that the effect killed the cancer cells in a dose-dependent manner. According to the authors:

“We also determined that galangin increased the activation of caspase-3 and -9, and release of apoptosis inducing factor from the mitochondria into the cytoplasm by Western blot analysis.

In addition, galangin induced human colon cancer cell death through the alteration of mitochondria membrane potential and dysfunction. These results suggest that galangin induces apoptosis of HCT-15 and HT-29 human colon cancer cells and may prove useful in the development of therapeutic agents for human colon cancer.”

Galangin has also been shown to inhibit inflammation by regulating the nuclear factor-kappa B (NF-?B), PI3K/Akt and peroxisome proliferator activated receptor-? (PPAR ?) signaling in activated microglia in the brain and thus should improve or prevent Alzheimer’s.18 Additionally, galangin reduces insulin resistance by increasing the activity of hexokinase and pyruvate kinase, promoting glucose consumption and glycogen synthesis.19
Royal Jelly May Be Beneficial for Health, But Don’t Expect Miracles

In summary, while royal jelly has a number of health benefits, it’s premature to assume it can affect your stem cells directly. A number of studies done on royal jelly have focused on its potential effects on cancer, fertility and its role in testosterone production.
In one study,20 infertile men were given different dosages of royal jelly and honey to increase the production of testosterone. After three months, those given royal jelly had higher testosterone levels, improved sperm active motility and luteinizing hormone levels, thus showing the potential impact royal jelly can have on infertility in men.
In another study,21 royal jelly was found to reduce symptoms of mucositis in patients suffering from neck and head cancer. Mucositis refers to the inflammation of the digestive tract brought on by chemotherapy and radiotherapy. Patients who were given royal jelly thrice a day showed a decreased occurrence of mucositis.
A recent study22 published in an obscure Chinese journal also suggests royal jelly has an antisenescence effect on human lung fibroblasts in cell cultures. Other studies have found royal jelly supplementation can improve menopausal symptoms23 and Type 2 diabetes outcomes.24,25
How to Identify a Quality Product
So, provided you can find a high-quality product (which can be expensive), it could be a valuable supplement in some instances. In terms of what to look for when shopping for a royal jelly product, here are a few pointers:

Fresh royal jelly is ideal if you can find it, but lyophilized royal jelly is also a good and more convenient option

To assess quality, look for 10-hydroxydecanoic acid (10-HDA) content. Most companies that care about quality will test their royal jelly for this. For fresh royal jelly the typical range is ~1.5 to 2.3 percent. For lyophilized royal jelly, it is ~4.5 to 6.6 percent

Look for organic royal jelly as it is less likely to contain antibiotics or be adulterated

http://articles.mercola.com/sites/articles/archive/2018/12/17/royal-jelly-benefits.aspx

The older you get, the more important your muscle mass becomes. Not only are strong muscles a requirement for mobility, balance and the ability to live independently, but having reserve muscle mass will also increase your chances of survival1 when sick or hospitalized.

Muscle is lost far more easily and quicker than it’s built, so finding ways to continuously promote and maintain your muscle mass is really crucial, especially as you get older.
Age-related loss of muscle mass is known as sarcopenia, and if you don’t do anything to stop it you can expect to lose about 15% of your muscle mass between your 30s and your 80s.2 An estimated 10% to 25% of seniors under the age of 70 have sarcopenia and as many as half those over the age of 80 are impaired with it.3

In the lecture above, Brendan Egan, Ph.D., associate professor of sport and exercise physiology at the School of Health and Human Performance and the National Institute for Cellular Biotechnology at Dublin City University in Ireland, reviews the latest research on exercise training for aging adults, which places a significant focus on building and maintaining muscle, and the nutritional components that can help optimize training results.
Muscle Strength and Function in Relation to Muscle Size
While it’s true that larger muscle is indicative of stronger, more functional muscle, it’s not a true 1-to-1 relationship. As noted by Egan, “you can have situations where you can gain back function without necessarily gaining muscle size.” To illustrate this point, Egan presents data from the Baltimore Longitudinal Study of Aging, which looked at leg strength and lean muscle mass.

While declines in muscle mass and strength are relatively well-synchronized in the 35- to 40-year-old group, strength dramatically drops off as you get into the 75-year-old and over groups, with 85-year-olds seeing dramatic declines in strength and function relative to the decline in muscles size.
Speed as a Measure of Functional Muscle Capacity
One way to measure functional capacity in older adults is gait (walking) speed, which is a strong predictor of life expectancy. Data suggest that if you have a walking speed of 1.6 meters (about 5.2 feet) per second (approximately 3.5 mph) at the age of 65, your life expectancy is another 32 years, meaning you may live into your late 90s.

Having a walking speed at or below the cutoff for sarcopenia, which is 0.8 meters (about 2.6 feet) per second, your life expectancy would be another 15 years, which means you’d be predicted to live to 80. At this speed, you would not be able to make it safely across a typical pedestrian crossing before the light changes to red.
Strength as a Predictor of Survival
Strength can also tell us a lot about an individual’s chances of survival. Egan presents data from a study in which people’s chest and leg press strength were measured to arrive at a composite score of whole body strength. The pattern is quite revealing, showing the strongest one-third of the population over 60 had a 50% lower death rate than the weakest.

Exercise guidelines recommend getting 150 minutes of aerobics exercise and two strength training sessions per week. As noted by Egan, you need both. It’s not just one or the other.

Research shows aerobic exercise in isolation reduces your all-cause mortality by 16% and strength training-only reduces it by 21%, whereas if you do both, you reduce your all-cause mortality by 29%.4 Disturbingly, U.K. data suggest only 36.2% of adults over the age of 30 meet aerobic guidelines, and a minuscule 3.4% meet strength training guidelines.

Part of the problem may be that many don’t want to go to the gym. But there’s little difference between doing gym-based strength training and doing bodyweight resistance training at home.
The Danger of Bedrest and Disuse Atrophy
As noted by Egan, enforced bedrest, such as acute hospitalization, can have a dramatic impact on your muscle mass. For example, a 2015 review5 in Extreme Physiology & Medicine notes you can lose 2.5% of your muscle mass in the first two weeks of bedrest. By Day 23, you can have lost up to 10% of your quadriceps muscle mass. As explained in this review:6

“Skeletal muscle mass is regulated by a balance between MPS [muscle protein synthesis] and MPB [muscle protein breakdown]. In a 70-kg human, approximately 280 g of protein is synthesized and degraded each day.
The two processes are linked … as facilitative or adaptive processes, whereby MPS facilitates (allows modulation of muscle mass) and MPB adapts (limiting said modulation).
When exposed to an anabolic stimulus, MPS rises. MPB rises too, but to a lesser amount, resulting in a net synthetic balance. In response to an anti-anabolic stimulus, MPS decreases and MPB decreases to a lesser degree, resulting in a net breakdown.
The interaction between critical illness and bed rest may result in greater muscle loss compared to bed rest alone. The musculoskeletal system is a highly plastic and adaptive system, responding quickly to changing demands. Relatively short periods of immobilization decrease MPS, with no effect on MPB.
Furthermore, this altered balance is relatively resistant to high dose amino acid delivery … Immobilization has significant effects on peripheral muscle aerobic capacity, contractility, insulin resistance and architecture.
Microvascular dysfunction occurring in severe sepsis is associated with immobilization and may have an additive effect on reducing MPS. In critically ill patients, MPS is reduced even with nutritional delivery, with increased MPB seen, leading to a net catabolic state and thus muscle wasting.”

Research7 has shown even healthy young subjects in their 20s can lose 3.1 pounds of muscle mass in a single week of bedrest. This is why it is so important to have a reserve in case you wind up in the hospital and lose this much muscle mass. It may take you the better part of a year to regain that muscle, as gaining muscle mass is hard work and many elderly fail to do so.
The loss of muscle mass also significantly decreases your insulin sensitivity. One of the reasons for this has to do with the fact that muscle tissue is a significant reservoir for the disposal of glucose. Your muscle tissue also produces cytokines and anti-inflammatory myokines that play an important role in health.
Concurrent Exercise Training

While three to five sessions of aerobic exercise and two or more strength sessions per week may sound like a lot, for many, the lack of time is a restricting factor. However, some of these sessions can be done together. “That’s called concurrent exercise training,” Egan says.
He goes on to cite research looking at time matched concurrent exercise in the elderly, 65 and older, where an aerobic training group and a strength training group were compared to a group that spent half of their session doing aerobic exercise and the other half doing resistance training. All groups spent the same overall time exercising (30 minutes, three times a week for 12 weeks).
In terms of leg strength, the concurrent training group had better responses to training than aerobic or strength training alone. There was little difference in lean body mass, meaning they didn’t necessarily bulk up, but they had a 50% increase in strength nonetheless. They also lost more body fat around the trunk area. In short, concurrent training appears to give you more bang for your buck.
Blood Flow Restriction Training

One of the reasons I’m so passionate about blood flow restriction (BFR) training is because it has the ability to prevent and widely treat sarcopenia like no other type of training.
There are several reasons why BFR is far superior to conventional types of resistance training in the elderly. Importantly, it allows you to use very light weights, which makes it suitable for the elderly and those who are already frail or recovering from an injury. And, since you’re using very light weights, you don’t damage the muscle and therefore don’t need to recover as long.

While most elderly cannot engage in high-intensity exercise or heavy weightlifting, even extraordinarily fit individuals in their 60s, 70s and 80s who can do conventional training will be limited in terms of the benefits they can achieve, thanks to decreased microcirculation. This is because your microcirculation tends to decrease with age.
With age, your capillary growth diminishes, and capillary blood flow is essential to supply blood to your muscle stem cells, specifically the fast twitch Type II muscle fiber stem cells. If they don’t have enough blood flow — even though they’re getting the signal from the conventional strength training — they’re not going to grow and you’re not going to get muscle hypertrophy and strength.
BFR, because of the local hypoxia that is created, stimulates hypoxia-inducible factor-1 alpha (HIF1a) and, secondarily, vascular endothelial growth factor (VEGF), which acts as “fertilizer” for your blood vessels. VEGF allows your stem cells to function the way they were designed to when they were younger.
What’s more, the hypoxia also triggers vascular endothelial growth factor, which enhances the capillarization of the muscle and likely the veins in the arteries as well. Building muscle and improving blood vessel function are related, which is why BFR offers such powerful stimulus for reversing sarcopenia.
In short, BFR has a systemic or crossover training effect. While you’re only restricting blood flow to your extremities, once you release the bands, the metabolic variables created by the hypoxia flow into your blood — lactate and VEGF being two of them — thereby spreading this “metabolic magic” throughout your entire system. To learn more, please see my special report, “What You Need to Know About BFR,” and “BFR Training for Muscle Mass Maintenance.”
Nutrition for Muscle Maintenance

It should come as no surprise that there is an important synergy between nutrition and exercise. When it comes to muscle building and maintenance, amino acids, the building blocks of protein, are of particular importance.
In the podcast above, Megan Hall, scientific director at Nourish Balance Thrive delves into this topic at greater depth and reviews the current recommended daily allowances of protein compared to the optimal levels needed to support muscle mass and strength in at various life stages.8
Research9 looking at post-prandial protein handling and amino acid absorption shows 55.3% of the dietary protein of a given meal is in circulation within five hours after eating, which significantly increases muscle protein synthesis.
Research10 suggests healthy young adult men “max out the protein synthesis signal from a given meal” at a dose of 0.24 grams of protein per kilogram of total bodyweight, or 0.25 grams of protein per kilogram of lean body mass.
The current U.S.-Canadian recommended dietary protein allowance is 0.8 g/kg/d (0,36/grams/pound/day), but healthy older adults may actually require about 1.20 g/kg/d or .55 grams/pound/day. According to this study:11

“Our data suggest that healthy older men are less sensitive to low protein intakes and require a greater relative protein intake, in a single meal, than young men to maximally stimulate postprandial rates of MPS [myofibrillar protein synthesis].
These results should be considered when developing nutritional solutions to maximize MPS for the maintenance or enhancement of muscle mass with advancing age.”

Amino acids also act as signaling molecules that trigger muscle growth. Leucine is a particularly potent signaling agent, although all of the amino acids are required to actually build the muscle. The richest source of leucine (which helps regulate the turnover of protein in your muscle), by far, is whey protein. In fact, it can be difficult to obtain sufficient amounts of leucine from other sources.

The typical requirement for leucine to maintain body protein is 1 to 3 grams daily. However, to optimize its anabolic pathway, research shows12 you need somewhere between 8 and 16 grams of leucine per day, in divided doses.13,14

To reach the 8-gram minimum, you’d have to eat nearly 15 eggs.15 Whey, on the other hand, contains about 10% leucine (10 grams of leucine per 100 grams of protein).16 So, 80 grams of whey protein will give you 8 grams of leucine.
Time-Restricted Eating Adds Benefits
One of the problems with Egan is that he’s not very literate on time-restricted eating. During the question and answer portion, an audience member asks him about it and he admits he hasn’t studied it.
This is important because restricting your eating window to six to eight hours, which means you’re fasting 14 to 18 hours each day, would make it far easier for each of the meals to be over the leucine threshold. It will also activate autophagy, which is another factor essential for optimal muscle growth.
Autophagy is a self-cleaning process in which your body digests damaged cells, which in turn encourages the proliferation of new, healthy cells. The harder your workout, the more autophagy you will activate.
So, I recommend fasting for as long as you can before your morning workout, and then, shortly thereafter, have your largest meal of the day with plenty of high-quality protein, making sure you get several grams of leucine and arginine, both of which are potent mTOR stimulators.
The mTOR pathway is an important key for protein synthesis and muscle building. As explained in David Sabatini’s excellent review paper “mTOR at the Nexus of Nutrition, Growth, Ageing and Disease,” published in Nature Reviews Molecular Cell Biology:17

“Over the past two and a half decades, mapping of the mTOR signaling landscape has revealed that mTOR controls biomass accumulation and metabolism by modulating key cellular processes, including protein synthesis and autophagy.
Given the pathway’s central role in maintaining cellular and physiological homeostasis, dysregulation of mTOR signaling has been implicated in metabolic disorders, neurodegeneration, cancer and ageing.”

In summary, fasting activates autophagy, allowing your body to clean out damaged subcellular parts. Exercising while fasted maximizes autophagy even further. In fact, exercising while you are fasting for more than 14 to 18 hours likely activates as much autophagy as if you were fasting for two to three days. It does this by increasing AMPK, increasing NAD+ and inhibiting mTOR.

Refeeding with protein after your fasted workout then activates mTOR, thus shutting down autophagy and starting the rebuilding process. These two processes need to be cyclically activated to optimize your health and avoid problems.
Muscle Health Is Central to an Active Lifestyle

As noted by Egan, “Hopefully I’ve convinced you that muscle health is central to active lifestyles. There’s been this increased awareness of muscle size, but I think we need to emphasize the idea about strength and function. These are the things that are easiest to change with the right type of training.”
In short, if you want to increase muscle size and strength, then there’s no getting around resistance training. It simply must be part of your exercise prescription, and concurrent training, where you’re combining aerobic and strength training in a given session is a time-efficient model.
BFR is also a particularly excellent way to ensure you’re getting effective strength training without the risks of conventional strength training using heavy weights, and is easy to combine with exercises such as walking and swimming. You simply wear the BFR bands while walking or exercising as normal.

Defy Aging by Improving Your Muscle Mass
In my February 2020 interview with Ben Greenfield, author of “Boundless: Upgrade Your Brain, Optimize Your Body & Defy Aging,” we discuss the importance of strength training and getting the appropriate amount of protein to build and maintain your muscle mass and optimize mitochondrial density and biogenesis.
In summary, Greenfield recommends a fitness program that includes the following types of exercise in order to target the main pathways involved in health and aging:

• High-intensity interval training once a week to boost mitochondrial density and biogenesis — Brief spurts of exercise followed by longer rest periods. Greenfield recommends a 3-to-1 or 4-to-1 rest-to-work ratio.

• Muscle endurance training two to three times a week to improve lactic acid tolerance — An example is the classic Tabata set, which has a 2-to-1 work-to-rest ratio.

• Longer training sessions twice a week to improve your VO2 max — To target and improve your VO2 max, you’ll want your training sessions to be longer, about four to six minutes in duration with four to six minutes of recovery in between, for a 1-to-1 work-to-rest ratio.

Examples include The New York Times’ seven-minute workout18 and bodyweight training done in a fast explosive manner or with a very light medicine ball, sandbag or kettle bells.

• Long walk once a week to improve your stamina — Greenfield recommends taking a 1.5- to three-hourlong walk, bike ride or paddle session — anything where your body is engaged in chronic repetitive motion for a long period of time — preferably in a fasted state. Alternatively, do 20 to 30 minutes of fasted cardio followed by a cold shower.

• Super-slow weight training once or twice a week to improve muscle strength — Alternatives include elastic band training systems and blood flow restriction (BFR) training. You can also combine BFR with super-slow training.

http://articles.mercola.com/sites/articles/archive/2020/03/14/skeletal-muscle-aging.aspx

I’ve previously discussed the synergy between magnesium and vitamin D, and the importance of vitamin D for optimal immune function and overall health — especially as it pertains to lowering your risk of COVID-19. Previous studies have also highlighted the role this duo plays in cognitive function among older adults, as well as overall mortality.
Vitamin D and Magnesium Protect Cognitive Health
One such study,1 “Association of Vitamin D and Magnesium Status with Cognitive Function in Older Adults: Results from the National Health and Nutrition Examination Survey (NHANES) 2011 to 2014,” points out that vitamin D not only protects neuronal structures and plays a role in neuronal calcium regulation, but also appears to impact your risk for neurodegeneration as you grow older.
Magnesium, meanwhile, aside from being required for converting vitamin D to its active form,2,3,4 also plays a role in cognitive health, and magnesium deficiency has been implicated in several neurological disorders.
Higher serum 25(OH)D levels were associated with reduced risk of low cognitive function in older adults, and this association appeared to be modified by the intake level of magnesium.
Using NHANES data from 2,984 participants over the age of 60, the researchers compared serum vitamin D status and dietary magnesium intake against cognitive function scores.
After adjusting for confounding factors, including total calorie consumption and magnesium intake, higher blood levels of vitamin D positively correlated with decreased odds of having a low cognitive function score on the Digit Symbol Substitution Test.
The same trend was found when they looked at vitamin D intake, rather than blood level. The correlation of higher vitamin D levels and better cognitive function was particularly strong among those whose magnesium intake was equal to or greater than 375 mg per day. According to the authors:5

“We found that higher serum 25(OH)D levels were associated with reduced risk of low cognitive function in older adults, and this association appeared to be modified by the intake level of magnesium.”

Magnesium Improves Brain Plasticity

While magnesium intake by itself did not appear to have an impact on cognitive function in the study above, other research has highlighted its role in healthy cognition.
Memory impairment occurs when the connections (synapses) between brain cells diminish. While many factors can come into play, magnesium is an important one. As noted by Dr. David Perlmutter, a neurologist and fellow of the American College of Nutrition:6

“It has now been discovered that magnesium is a critical player in the activation of nerve channels that are involved in synaptic plasticity. That means that magnesium is critical for the physiological events that are fundamental to the processes of learning and memory.”

A specific form of magnesium called magnesium threonate was in 2010 found to enhance “learning abilities, working memory, and short- and long-term memory in rats.”7 According to the authors, “Our findings suggest that an increase in brain magnesium enhances both short-term synaptic facilitation and long-term potentiation and improves learning and memory functions.”
COVID-19 Can Deprive Brain of Oxygen

While we’re on the topic of the brain, a July 1, 2020, article8 in The Washington Post reviewed findings from autopsies of COVID-19 patients. Surprisingly, Chinese researchers have reported9 that COVID-19 patients can exhibit a range of neurological manifestations.
A June 12, 2020, letter to the editor10 published in The New England Journal of Medicine also discusses the neuropathological features of COVID-19. As reported by The Washington Post:11

“Patients have reported a host of neurological impairments, including reduced ability to smell or taste, altered mental status, stroke, seizures — even delirium … In June, researchers in France reported that 84% of patients in intensive care had neurological problems, and a third were confused or disoriented at discharge.
… Also this month, those in the United Kingdom found that 57 of 125 coronavirus patients with a new neurological or psychiatric diagnosis had experienced a stroke due to a blood clot in the brain, and 39 had an altered mental state.
Based on such data and anecdotal reports, Isaac Solomon, a neuropathologist at Brigham and Women’s Hospital in Boston, set out to systematically investigate where the virus might be embedding itself in the brain.
He conducted autopsies of 18 consecutive deaths, taking slices of key areas: the cerebral cortex (the gray matter responsible for information processing), thalamus (modulates sensory inputs), basal ganglia (responsible for motor control) and others …”

Interestingly, while doctors and researchers initially suspected that brain inflammation was causing the neurological problems seen in some patients, Solomon’s autopsies found very little inflammation. Instead, these neurological manifestations appear to be the result of brain damage caused by oxygen deprivation.
Signs of oxygen deprivation were present both in patients who had spent a significant amount of time in intensive care, and those who died suddenly after a short but severe bout of illness. I believe this is likely due to increases in clotting in the brain microvasculature.
Solomon told The Washington Post he was “very surprised,” by the finding. It makes sense, though, considering COVID-19 patients have been found to be starved for oxygen. As reported by The Washington Post:12

“When the brain does not get enough oxygen, individual neurons die … To a certain extent, people’s brains can compensate, but at some point, the damage is so extensive that different functions start to degrade … The findings underscore the importance of getting people on supplementary oxygen quickly to prevent irreversible damage.”

Magnesium and Vitamin D Impact Mortality
Getting back to magnesium and vitamin D, previous research13 using NHANES data from 2001 through 2006 found the duo has a positive impact on overall mortality rates. This study also pointed out that magnesium “substantially reversed the resistance to vitamin D treatment in patients with magnesium-dependent vitamin-D-resistant rickets.”
The researchers hypothesized that magnesium supplementation increases your vitamin D level by activating more of it, and that your mortality risk might therefore be lowered by increasing magnesium intake. That is indeed what they found. According to the authors:

“High intake of total, dietary or supplemental magnesium was independently associated with significantly reduced risks of vitamin D deficiency and insufficiency respectively. Intake of magnesium significantly interacted with intake of vitamin D in relation to risk of both vitamin D deficiency and insufficiency.
Additionally, the inverse association between total magnesium intake and vitamin D insufficiency primarily appeared among populations at high risk of vitamin insufficiency.
Furthermore, the associations of serum 25(OH)D with mortality, particularly due to cardiovascular disease (CVD) and colorectal cancer, were modified by magnesium intake, and the inverse associations were primarily present among those with magnesium intake above the median.
Our preliminary findings indicate it is possible that magnesium intake alone or its interaction with vitamin D intake may contribute to vitamin D status. The associations between serum 25(OH)D and risk of mortality may be modified by the intake level of magnesium.”

Magnesium Lowers Vitamin D Requirement by 146%
According to a scientific review14,15 published in 2018, as many as 50% of Americans taking vitamin D supplements may not get significant benefit as the vitamin D simply gets stored in its inactive form, and the reason for this is because they have insufficient magnesium levels.

Research published in 2013 also highlighted this issue, concluding that higher magnesium intake helps reduce your risk of vitamin D deficiency by activating more of it. As noted by the authors:16

“High intake of total, dietary or supplemental magnesium was independently associated with significantly reduced risks of vitamin D deficiency and insufficiency respectively.
Intake of magnesium significantly interacted with intake of vitamin D in relation to risk of both vitamin D deficiency and insufficiency … Our preliminary findings indicate it is possible that magnesium intake alone or its interaction with vitamin D intake may contribute to vitamin D status.”

More recently, GrassrootsHealth concluded17 you need 146% more vitamin D to achieve a blood level of 40 ng/ml (100 nmol/L) if you do not take supplemental magnesium, compared to taking your vitamin D with at least 400 mg of magnesium per day.

The interplay between magnesium and vitamin D isn’t a one-way street, though. It goes both ways. Interestingly, while vitamin D improves magnesium absorption,18 taking large doses of vitamin D can also deplete magnesium.19 Again, the reason for that is because magnesium is required in the conversion of vitamin D into its active form.
Magnesium + Vitamin K Lowers Vitamin D Requirement Even More
Magnesium isn’t the only nutrient that can have a significant impact on your vitamin D status. GrassrootsHealth data further reveal you can lower your oral vitamin D requirement by a whopping 244% simply by adding magnesium and vitamin K2. As reported by GrassrootsHealth:20

“… 244% more supplemental vitamin D was needed for 50% of the population to achieve 40 ng/ml (100 nmol/L) for those not taking supplemental magnesium or vitamin K2 compared to those who usually took both supplemental magnesium and vitamin K2.”

How to Boost Your Magnesium Level
The recommended daily allowance for magnesium is around 310 mg to 420 mg per day depending on your age and sex,21 but many experts believe you may need anywhere from 600 mg to 900 mg per day.22

Personally, I believe many may benefit from amounts as high as 1 to 2 grams (1,000 to 2,000 mg) of elemental magnesium per day, as most of us have EMF exposures that simply cannot be mitigated, and the extra magnesium may help lower the damage from that exposure.

My personal recommendation is that unless you have kidney disease and are on dialysis, continually increase your magnesium dose until you have loose stools and then cut it back. You want the highest dose you can tolerate and still have normal bowel movements.

When it comes to oral supplementation, my personal preference is magnesium threonate, as it appears to be the most efficient at penetrating cell membranes, including your mitochondria and blood-brain barrier. But I am also fond of magnesium malate, magnesium citrate, and ionic magnesium from molecular hydrogen as each tablet has 80 mg of elemental magnesium.
Eat More Magnesium-Rich Foods
Last but not least, while you may still need magnesium supplementation (due to denatured soils), it would certainly be wise to try to get as much magnesium from your diet as possible. Dark-green leafy vegetables lead the pack when it comes to magnesium content, and juicing your greens is an excellent way to boost your intake. Foods with high magnesium levels include:23

Avocados
Swiss chard

Turnip greens

Beet greens

Herbs and spices such as coriander, chives, cumin seed, parsley, mustard seeds, fennel, basil and cloves

Broccoli

Brussel sprouts
Organic, raw grass fed yogurt and natto

Bok Choy
Romaine lettuce

http://articles.mercola.com/sites/articles/archive/2020/07/16/magnesium-cognitive-function.aspx

Vitamin K is a fat-soluble vitamin that can be found in some foods. The body uses it for certain functions, such as those required for bone metabolism, blood clotting and a variety of other cellular functions.1
Your body has a limited ability to store vitamin K, so it must be absorbed from your food or a supplement on a daily basis. It’s also recycled within your system, optimizing its benefits.2 Several different medications, such as antibiotics, weight loss drugs, cholesterol medications and the blood thinner warfarin, may interfere with its absorption, and therefore affect blood clotting.
Vitamin K is distributed throughout the body, including in your brain, heart, bones and liver.3 Since it’s broken down and excreted quickly it rarely reaches toxic levels in a way that happens with other fat-soluble vitamins.
Since the vitamin is crucial to several bodily functions, it’s not surprising to learn that if you don’t get enough every day, on a daily basis, you could be at risk for an earlier death.
Vitamin K Lowers Risk of Death in Older Adults

Recently, a paper was published in the American Journal of Clinical Nutrition by a team that investigated the vitamin K-dependent proteins that may affect atherosclerosis, which is the stiffness and calcification of the arterial vessels.4
The aim of the investigation was to determine if there was an association between circulating vitamin K, cardiovascular disease and all-cause mortality. The study was carried out at Tufts University and led by Kyla Shea, who commented:5

“The possibility that vitamin K is linked to heart disease and mortality is based on our knowledge about proteins in vascular tissue that require vitamin K to function. These proteins help prevent calcium from building up in artery walls, and without enough vitamin K, they are less functional.”

The researchers gathered data from three science databases, including the Framingham Offspring Study. The participants had circulating vitamin K1 (phylloquinone) measured, and each person either had some type of heart event or they died. There were 3,891 men and women with 858 heart events and 1,209 deaths over 13 years.
Interestingly, although vitamin K is associated with vascular health, the data did not show an association between low vitamin K and cardiovascular disease (CVD). However, there was a link between low levels and all-cause mortality. They found a 19% increased risk of all-cause mortality in those with the lowest serum levels of vitamin K.6
Since the study was observational, the scientists could not establish a causal link, yet the data fit with what we know about the function of vitamin K in the body. One-third of the participants in the study were not white, which allowed the researchers to theorize that the association is multi-ethnic.7 Dr. Daniel Weiner, nephrologist from Tufts Medical center, explained the association between stiff arteries and CVD:8

“Similar to when a rubber band dries out and loses its elasticity, when veins and arteries are calcified, blood pumps less efficiently, causing a variety of complications. That is why measuring risk of death, in a study such as this, may better capture the spectrum of events associated with worsening vascular health.”

Vitamin K: The Basics

There are two basic types of vitamin K.9 Vitamin K1 is found in green leafy vegetables and works through the liver to help maintain a healthy clotting system. This is the type researchers measured in the study. Vitamin K1 also helps reduce calcification in the blood vessels and assists your bones in retaining calcium.
Vitamin K2 (menaquinone) is produced by bacteria in your gut and can be found in some animal products and fermented foods, particularly cheese and natto. This is the one that helps activate vitamin D and move calcium out of the arterial system and into your bones and teeth.10
There are also several different forms of vitamin K2. They are named for the length of the chemical chain, beginning with the letter M for menaquinone. The two most important types are found in animal products and fermented foods. Most Western diets are deficient in both forms of vitamin K2.11
In one study, researchers sought to compare the effectiveness of giving supplements of these two types, MK-4 and MK-7, to healthy women. They “demonstrated that a nutritional dose of MK-7 is well absorbed in humans, and significantly increases serum MK-7 levels, whereas MK-4 had no effect on serum MK-4 levels.”12
More Benefits of Vitamin K

Vitamin K is integral to the body’s ability to coagulate, or clot, blood. These clotting factors are involved in a cascade of events that stop bleeding and are produced in the liver. Therefore, individuals with severe liver disease can have difficulty with vitamin K-dependent clotting and are at an increased risk for hemorrhage.13
As discussed previously, Vitamin K is also integral to moving calcium out of the arterial system and to preventing soft tissue calcification. This function is central to preventing osteoporosis and maintaining strong bone health.
Another benefit is a vitamin K-dependent protein, growth arrest specific gene 6 protein (Gas6), which was identified in 1993 and is found in the heart, kidneys, lungs and cartilage. It contributes to many cellular functions that may play a role in protecting an aging nervous system, and it appears to regulate vascular homeostasis.
Separate studies using vitamin K2 on cancer cells in the lab have demonstrated an apoptotic effect. In one study, researchers found vitamin K2 induced apoptosis in bladder cancer cells and in another, against triple negative breast cancer.14,15
Vitamin K2 and Magnesium Optimize Vitamin D Supplementation

The evidence that your serum vitamin D level is protective against COVID-19 and reduces the severity of the disease continues to grow. While your body produces vitamin D from the reaction to sunlight, many don’t get enough sun to raise their vitamin D levels above 30 ng/mL.
To reach this minimal goal, you may need a supplement. Yet, taking vitamin D3 supplements without magnesium and vitamin K2 may offer little effective protection and could increase your risk of atherosclerosis. Before you can determine how much supplementation is needed, you’ll want to test your current level. You can do this using a home kit through GrassrootsHealth.16
The kit is delivered to your home where you use a finger stick and send the kit back to the lab. Only you get the results of the test, which you can then input into the GrassrootsHealth calculator to determine the amount of supplement you’ll need to achieve your desired result.17
Vitamin D is important in the absorption and utilization of vitamin K2. In fact, a vitamin K deficiency may contribute to symptoms of “vitamin D toxicity.” In my interview with Dr. Kate Rheaume-Bleue, natural health physician and author of Vitamin K2 and the Calcium Paradox, she talked about this challenge:18

“We don’t see symptoms of D toxicity very often but when we do those symptoms are inappropriate calcification. That’s a symptom of D toxicity and that is actually a lack of vitamin K2 that will cause that. K2 protects you against that toxicity quite simply.”

Added to this, I’ve written about the importance of vitamin K2 when you’re taking supplemental vitamin D3 to avoid excessive calcification in your arteries. Magnesium is also a crucial part of raising your vitamin D level as it is necessary for the activation of the vitamin.
Without sufficient amounts your body can’t properly use the vitamin you’re taking. Mohammed Razzaque is a professor of pathology at Lake Erie College of Osteopathic Medicine in Pennsylvania. He notes that without magnesium, vitamin D supplements may not be useful.19
To lower the risk of vitamin D deficiency it’s necessary to have optimal amounts of magnesium.20 According to one scientific review, as many as 50% of Americans who are taking vitamin D supplementation may not benefit, as it’s stored in the inactive form without sufficient levels of magnesium.21,22
The relationship is a two-way street. While vitamin D improves the absorption of magnesium, large doses of vitamin D may deplete magnesium.23,24 This is because large doses of vitamin D will require large doses of magnesium to convert it to the active form.
GrassrootsHealth published research that was based on data from nearly 3,000 people showing you must take 244% more vitamin D if you aren’t also taking a magnesium and vitamin K2 supplement.25 Practically speaking, this means when you take all three in combination you’ll need far less vitamin D to achieve a healthy level.
According to researchers, “those taking both supplemental magnesium and vitamin K2 have a higher vitamin D level for any given vitamin D intake amount than those taking either supplemental magnesium or vitamin K2 or neither.”26
Consider Supplementing With Magnesium and Vitamin K2

There are several forms of magnesium. In each form, the magnesium is bound to another molecule. Some forms have compounds that serve other functions in the body, as you’ll find in “NYC Doctor Highlights Importance of Vitamin D Optimization”:

Magnesium glycinate,27 a powder with low solubility. Glycine is an important amino acid and precursor for glutathione.
Ionic magnesium found in molecular hydrogen tablets. Each water-soluble tablet has about 80 mg of highly bioavailable unbound magnesium ions, which is about 20% of the recommended daily allowance.
Magnesium threonate28 is another excellent choice as it seems it can efficiently penetrate the blood-brain barrier.
Magnesium malate,29 which dissolves well in water. Malate is an intermediary in the Krebs cycle, so it likely contributes to ATP production.
Magnesium citrate30 also dissolves well and has a pleasant citric acid taste.

Since most people eating a Western diet are deficient in vitamin K2 and the vitamin is quickly used and excreted, it’s important to either change the foods you eat, or consider supplementation. As noted in the featured study, those with higher levels of vitamin K have a lower risk of death.
It can be difficult to tell if you’re getting enough vitamin K, as there’s no easy way to screen or test for vitamin K2 sufficiency. For more information about getting enough vitamin K, see “Spinach, Eggs and Gouda Cheese to Combat COVID?”
http://articles.mercola.com/sites/articles/archive/2020/09/02/vitamin-k-and-elderly.aspx

Dr. Chris Knobbe, an ophthalmologist, is the founder and president of the Cure AMD Foundation, a nonprofit dedicated to the prevention of age-related macular degeneration (AMD).
AMD, a leading cause of blindness in the U.S. — and the third leading cause of blindness globally (after cataracts and glaucoma)1 — is said to be a disease associated with aging, but, in the presentation above, Knobbe asks, “Could age-related macular degeneration be a disease of processed food consumption?”
Nine years of research and investigation have led Knobbe to conclude that AMD is, indeed, being driven by nutrient deficiencies and toxicity caused by processed foods. This common denominator isn’t linked only to AMD, however — it’s also linked to chronic diseases of all kinds, including Type 2 diabetes, heart disease and cancer.
The root of the problem lies in mitochondrial dysfunction, which is caused by the excessive consumption of a Westernized diet, including toxic industrially processed seed oils (incorrectly called “vegetable oils”), refined flour, refined added sugars and trans fats.
Chronic Metabolic and Degenerative Disease ‘Didn’t Exist’
According to Knobbe, chronic metabolic and degenerative disease “clearly didn’t exist 125 years ago,” at least not nearly to the extent they do today, citing a study by Dr. David Jones and colleagues, published in the New England Journal of Medicine in 2012.2 The study looked at the history of disease over the past 200 years, comparing the top 10 causes of death in the U.S. from 1900 to 2010.
In 1900, the top four causes of death were infectious in nature: pneumonia/influenza, tuberculosis, gastrointestinal infections and cardiac valvular disease. The latter is classified as heart disease, but, Knobbe says, “This wasn’t coronary artery type heart disease. This was cardiac valvular disease driven by syphilis, endocarditis and rheumatic fever … It was infectious still.”
By 2010, this had all changed, with chronic diseases replacing infectious diseases as the top killers. “Today, heart disease, cancer, stroke, COPD, Alzheimer’s disease, Type 2 diabetes, kidney disease, all chronic diseases account for seven of the top 10 causes of death.” In reviewing the data, Knobbe found that diabetes of any type was rare in the 19th century, but it increased 25-fold in a period of 80 years.
He also cites data that found the obesity rate in the 19th century was 1.2%. By 1960, it had already risen to 13% — an 11-fold increase — and continued to climb steadily to this day. “Obesity is on target to be 50% of adults obese in the United States by 2030, half obese,” Knobbe says. “So the increase looks something like … a 33-fold increase already in 115 years.” He continues:

“Again, you have to ask, you know, what accounts for this … All right, well, let’s go back to the dietary history now. So you’re going to see Westernized disease correlate to modernized diets. That’s the theme of this, essentially …
And I will submit to you that this has really been a global human experiment that began in 1866, it didn’t begin in 1980, you know, with our low-fat, low saturated-fat dietary guidelines, it began in the 19th century and nobody gave informed consent of us. Not one of us knew what we were getting into and most of us still don’t.”

Four Primary Processed Food Culprits

The four primary components that make up processed foods that are, in turn, contributing to chronic diseases like AMD are sugar, industrially processed seed oils, refined flour and trans fats. Knobbe says:

“ … Sugar has been in the food supply for hundreds of years, but between 1822 and 1999 sugar increased 17-fold … Cotton seed oil, the world’s first, highly polyunsaturated vegetable oil introduced right here in the good old US of A in 1866, the entire world, or at least 99.9-plus% of it had never seen a polyunsaturated vegetable oil, ever. All right, 1880 roller mill technology was introduced.
And in the United States, it was introduced in Minneapolis … roller mill gives us refined white, wheat flour, which is a nutrient deficient food. And then fourth, 1911, Proctor and gamble introduced Crisco. That’s trans fats, they’re hydrogenated and partially hydrogenated vegetable oils … by 2009, our own USDA reports that those four foods make up 63% of the American diet, 63%. That’s the recipe for disaster.”

As the consumption of processed foods rose, so too did chronic diseases. According to Knobbe, AMD was rare from 1851 to about 1930, but had reached epidemic proportions by the 1970s. As of 2020, 196 million people worldwide suffer from AMD.
“And what we always see is that the processed foods come first and then the AMD hits later,” Knobbe says. “It’s always this way. There’s a temporal relationship. It’s at least 30 years of this consumption, probably closer to 50. You know, these are chronic … diseases that take a long time to develop, right? There’s a dose response relationship … I believe if you look at all of our data, this becomes nearly a mathematical certainty that this relationship between food and macular degeneration exists.”

Knobbe also cites the work of Weston A. Price, the dentist who wrote the classic book “Nutrition and Physical Degeneration.” In the 1900s, Price did extensive research on the link between oral health and physical diseases.

He was one of the major nutritional pioneers of all time, and his research revealed native tribes that still ate their traditional diet had nearly perfect teeth and were almost 100% free of tooth decay. But when these tribal populations were introduced to refined sugar and white flour, their health, and their perfect teeth, rapidly deteriorated. In many ways, Knobbe is the 21st century equivalent of Price.
Diet-Related Macular Degeneration

Download Interview Transcript

Knobbe believes “age-related” macular degeneration should be called diet-related macular degeneration instead, and states that out of all the components in processed foods, polyunsaturated vegetable oils are the greatest contributor. Comparing them to “biological poisons,” Knobbe notes that industrially processed seed oils are not only nutrient deficient but also pro-oxidative and proinflammatory:

“ … When vegetable oils are produced … oil seeds are crushed, heated, pressed. They go through about four or five heatings … then they go to a petroleum drive, hexane, solvent bath, right? And then it’s steamed, degummed … then they go through a chemical process of being alkalinized, bleached and deodorized before they go into this bottle and we think they’re healthy.
They’re extraordinarily oxidized. They’re toxic. Aldehydes in these, these are literally poison. These are extremely noxious agents, and … vegetable oils replaced animal fats.”

He cites the work of nutrition pioneer Elmer V. McCollum, who, in the early 20th century, fed rats diets enriched with either 5% cotton seed oil or 1.5% butterfat — “this is good butter,” Knobbe points out. “It’s coming from pasture-raised cattle grazing on grass, right? That’s all they had back then.”
Stark differences were observed among the rats, with the cottonseed oil group experiencing stunted growth, illness and shorter survival. The rats fed butterfat fared much better, growing to about twice the size of the other rats and living about twice as long. The fat-soluble vitamins A, D and K2 in the pastured butterfat were a likely factor in the marked health differences.
“We need them to maintain our health and prevent degenerative disease,” Knobbe says. “There’s absolutely no question in my mind — all the data supports this — that macular degeneration patients are vitamin A-, D- and K2-deficient.”
Knobbe cites data from native populations around the globe, including the Maasai tribe in Eastern Africa, inhabitants of Papua New Guinea and Tokelau in the South Pacific, which had very different diets with one major similarity: “In general … they have no refined sugar, no refined wheat, no processed foods, no vegetable oils.” They also have little or no macular degeneration.
Vegetable Oils Cause Mitochondrial Failure, Insulin Resistance

AMD is ultimately a disease process rooted in mitochondrial dysfunction and insulin resistance, and the catastrophic cascade of health declines are triggered by the long-term consumption of vegetable oils (omega-6) and other processed foods, Knobbe explains the complex process in his presentation:

“Here’s what excess omega-6 does in a Westernized diet: induces nutrient deficiencies, causes a catastrophic lipid peroxidation cascade, is what this does … This damages … a phospholipid called cardio lipid in the mitochondrial membranes. And this leads to electron transport chain failure … which causes mitochondrial failure and dysfunction.
And this leads first to reactive oxygen species, which feeds back into this peroxidation cascades. So, you’re filling up your fat cells and your mitochondrial membranes with omega-6, and these are going to peroxidize because of the fact that they are polyunsaturated.
All right, the next thing that happens is insulin resistance, which leads to metabolic syndrome, Type 2 diabetes, nonalcoholic fatty liver disease. When the mitochondria fail, you get reduced fatty acid, beta oxidation, meaning you can’t burn these fats properly for fuel.
So now you’re … carb dependent and you’re heading for obesity. So, you’re feeling tired. You’re gaining weight. Your mitochondria are failing to burn fat for fuel … this is a powerful mechanism for obesity.
So, the energy failure at the cellular level leads to nuclear mitochondrial DNA mutations, and this leads to cancers. Three weeks on a high-PUFA diet causes heart failure in rats — three weeks. And this also leads to apoptosis and necrosis. And of course, that’s how you get disorders like AMD and Alzheimer’s.”

Knobbe has also been studying the toxic aldehydes that result from omega-6 fats. When you consume an omega-6 fat, it first reacts with a hydroxyl radical or peroxide radical, producing a lipid hydroperoxide.
This lipid hydroperoxide then rapidly degenerates into toxic aldehydes, of which there are hundreds, which in turn lead to cytotoxicity, genotoxicity, mutagenicity carcinogenicity and more, along with being obesogenic, at very low doses.
Ancestral Diet Key to AMD Prevention
According to Knobbe, there were only 50 cases of dietary blindness described across the globe between 1851 and 1930, some of which were likely other diseases. This skyrocketed to an estimated 196 million cases in 2020.3 Knobbe believes that by following an ancestral diet, rich in grass fed meat and poultry, pastured dairy, wild-caught fish, vegetables, nuts and seeds, the majority of AMD cases would disappear.

“Could modernized processed foods drive this disease? That’s the question. I mean, is it as simple as this, you know, could this difference be due to diet and diet alone?” Knobbe asked. “I will submit to you that everything I have found so far indicates that it is, and I can’t find anything that doesn’t support this concept.”
For more details, Knobbe discusses more of this eye-opening information in his book, “Ancestral Dietary Strategy to Prevent and Treat Macular Degeneration,” as well as via his website, on CureAMD.org. As Knobbe says:

“Today, about 534 people will go blind due to AMD. They’ve already lost vision in their first eye. They’ll lose vision in their second eye. And I think this is a travesty because I believe it’s all preventable. So, our mission at Cure AMD foundation is to prevent and treat AMD through ancestral dietary strategy advocacy. And we need more scientific research in order to convince all of us and our peers.”

Single Most Important Strategy You Can Implement

It is vital that you reduce your intake of industrially processed seed oils as much as you can. This means eliminating all of the following oils:

SoyCorn

CanolaSafflower

SunflowerPeanut

Olive and avocado oil should also be on the list as over 80% of these are adulterated. But even if they weren’t it simply isn’t worth it to have high levels of olive oil as it is loaded with the omega-6 fat called linoleic acid.
It will also be important to avoid nearly all processed foods as it is the rare processed food that does not include these toxic oils. Nearly every fast food restaurant is also guilty of using high levels of these toxic fats. This is why it is so important to prepare as much of your food as you can in your home so you can know what you are eating.
Most health “experts,” including many I have previously interviewed, simply do not understand how much more dangerous these oils are than sugar. These fats become embedded in your cell membranes and stay there for years wreaking havoc on your health.
This is one of the reasons why a high fat diet can be harmful. If it is loaded with these dangerous omega-6 fats it will make you metabolically unhealthy and radically increase your risk for nearly every chronic degenerative disease, like heart disease, cancer, diabetes and blindness.
http://articles.mercola.com/sites/articles/archive/2020/11/07/dr-chris-knobbe-macular-degeneration.aspx

Iron is an essential nutrient, integral to hundreds of biological functions including oxygen transport, DNA synthesis and energy metabolism. Almost every cell in your body contains iron.1 Plants, bacteria, animals and even cancer cells cannot survive without it.2,3
Plants use iron to make chlorophyll, while animals and humans need it to make hemoglobin, a protein in your red blood cells used to transport oxygen. Approximately 6% of the iron in your body is bound as a component to proteins and 25% is stored as ferritin.4
Having too much or too little can have serious consequences. Yet, what many people and physicians do not realize is that an excessive amount of iron is more common than having a deficiency.
Doctors may check for iron deficiency as it relates to anemia, but iron overload is a far more common problem. Adult men and non-menstruating women are at risk of having dangerously high levels of iron. When left untreated, excess iron can damage your organs and contribute to the development of heart disease, diabetes, neurodegenerative diseases and cancer.5
High Levels of Iron Linked to Shorter Life Span

Researchers have linked iron overload to several medical conditions, and now find that people age at different rates when they have excess amounts in the body. European scientists gathered data from an international database to test this theory.6
The set of data was equivalent to about 1.75 million lifespans.7 They looked at the total number of years lived (life span), the total number of years marked by good health (health span) and living to an old age (longevity).8 The researchers identified 10 loci in the genetic sample that appear to influence aging.
The majority of the loci were associated with cardiovascular disease. Based on statistical analysis, the data suggested “that genes involved in metabolizing iron in the blood are partly responsible for a healthy long life.”9
The new information is exciting as it suggests a modifiable pathway to explain biological aging and chronic disease rate differences among people. The researchers noted that high iron levels can reduce “the body’s ability to fight infection in older age,”10 which may be yet another reason that age is a factor in infectious disease severity.
As Paul Timmers from the University of Edinburgh says, the data also offer a reasonable explanation for the association between red meat and heart disease. While cholesterol has been blamed in the past, in a growing number of studies, no association has been found between cholesterol and heart disease.11 Timmers commented:12

“We are very excited by these findings as they strongly suggest that high levels of iron in the blood reduces our healthy years of life, and keeping these levels in check could prevent age-related damage. We speculate that our findings on iron metabolism might also start to explain why very high levels of iron-rich red meat in the diet has been linked to age-related conditions such as heart disease.”

Excess Iron Impairs Mitochondrial Function

Researchers have known since the mid-1990s that when iron is bound to a protein such as hemoglobin, it plays a part in cell metabolism and growth.13 But when it is free, it kicks off a reaction producing hydroxyl free radicals from hydrogen peroxide. This is one of the most damaging free radicals in the body and can cause severe mitochondrial dysfunction.
Hydroxyl free radicals damage cell membranes, protein and DNA. Other research has shown excessive iron promotes apoptosis and ferroptosis in cardiomyocytes.14 Apoptosis is the programmed cell death of diseased and worn-out cells and, as the name implies, ferroptosis refers to cell death that is specifically dependent on and regulated by iron.15
Your cardiomyocytes are the muscle cells in the heart that generate and control contractions.16 In short, this tells us that excess iron can impair heart function. These are two ways iron overload can lead to cardiomyopathy, which is a leading cause of death in patients with hemochromatosis.
Excess iron also affects blood pressure and other markers of cardiovascular disease, and glycemic control in individuals with metabolic syndrome. One study was done with 64 participants who had a diagnosis of metabolic syndrome.17 The participants were randomly assigned to two groups. In the first, they gave blood at the beginning of the study and again after 4 weeks.
Researchers regulated the amount of blood given and each person’s iron level. They measured systolic blood pressure, insulin sensitivity, plasma glucose and hemoglobin A1c. The group who gave blood showed a significant reduction in systolic blood pressure and had lower blood glucose levels, hemoglobin A1c and heart rate. There was no effect on insulin sensitivity.
In an earlier study, scientists removed blood in individuals who had chronic gout.18 Twelve participants with hyperuricemia gave blood over the course of 28 months to maintain their body at the lowest amount of iron stores possible, without inducing anemia. The data showed a marked reduction in the number and severity of gout attacks. Removing blood was also found to be safe and beneficial.
How Do High Iron Levels Build Up?

Men and non-menstruating women have a higher potential for iron buildup since the body has limited ways of excreting excess iron.19 With the genetic disorder hemochromatosis, the body accumulates excessive and damaging levels of iron.20 When this is left untreated it contributes to many of the disorders discussed above.
Hemochromatosis is a prevalent genetic condition in Americans. It takes two inherited genetic mutations, one from your mother and one from your father, to cause the disease. In one study, researchers estimated 40% to 70% of people with the defective genes will eventually have iron overload.21
It is also easy to get too much iron from your food, particularly when it’s “fortified” with iron. Iron is a common nutritional supplement found in many multivitamin and mineral supplements. Many processed foods are also fortified with iron.
For example, two servings of fortified breakfast cereal may give you as much as 44 milligrams (mg) of iron, rising dangerously close to the upper tolerance limit of 45 mg for adults.22 However, the upper tolerance limit is well over the recommended daily allowance, which is 8 mg for men and 18 mg for premenopausal women.23 It’s easy to see how you might consistently eat too much iron.
Another common cause for iron excess is the regular consumption of alcohol.24 Alcohol increases the amount of iron you absorb from your food. In other words, by drinking alcohol with foods that are high in iron, you will likely absorb more than you need.
Other contributing factors include using iron pots and pans, drinking well water high in iron, using multivitamins and mineral supplements together or eating processed foods.
You Can Help Severe Blood Shortages and Help Yourself

Routine blood donation may be one of the simplest and quickest ways to reduce your ferritin and iron overload. Blood donation may also save the life of someone else. The American Red Cross collects blood at both permanent and mobile locations. According to the organization, more than 80% of what they collect comes from blood drives on college campuses and at workplaces.
Unfortunately, one of the consequences of COVID-19 has been a reduction in the number of blood drives and blood donations across the U.S. This has led to a severe shortage.25 Chris Hrouda, who serves as president of the Red Cross Biomedical Services, expressed his concerns to a reporter from the Press Herald:26

“In our experience, the American public comes together to support those in need during times of shortage and that support is needed now more than ever during this unprecedented public health crisis. Unfortunately, when people stop donating blood, it forces doctors to make hard choices about patient care, which is why we need those who are healthy and well to roll up a sleeve and give the gift of life.

We know that people want to help, but they may be hesitant to visit a blood drive during this time. We want to assure the public that blood donation is a safe process, and we have put additional precautions in place at our blood drives and donation centers to protect all who come out.”

Blood donation is a safe and effective way of managing your iron stores and helping someone else. The Red Cross answers questions about your eligibility requirement on their website.27 They recommend that you wait at least eight weeks between donations so your body can completely restore your blood volume.
If you are unable to donate blood because of a health condition, consider therapeutic phlebotomy. While your blood won’t be used for a donation, they may do the procedure and then dispose of the blood.
If you can’t find a place in your community for the services, your insurance policy may pay for routine therapeutic phlebotomies with a doctor’s prescription.28 In either case, whether you donate the blood or it’s thrown out, the amount they take is the same.
To donate, you only need a blood donor card, a driver’s license or two forms of identification. People who are at least 17, weigh at least 110 pounds and are in generally good health are eligible.
Yearly GGT and Iron Screening Tests Advisable

Another way to measure the impact of iron toxicity and the effect on mortality is the gamma glutamyl transpeptidase test, sometimes called gamma-glutamyl transferase (GGT). GGT is a liver enzyme that is involved in the metabolism of glutathione and the transport of amino acids and peptides.
It can be used as a marker for excess free iron, and as an indicator of your risk of chronic kidney disease.29 Low levels of GGT tend to be protective against high levels of ferritin.
When both ferritin and GGT are high, you have a higher chance of having chronic health problems and/or early death. As with many lab tests, the normal references vary among the labs. Normal laboratory ranges are often far from ideal and those used for GGT may not be adequate for preventing disease.
As I’ve shared before, the range of ideal to “normal” GGT can be wide. To fully understand your risks, you’ll need both the ferritin and GGT levels tested. For more information on ferritin and GGT, including healthy ranges, see “Donate Blood: You May Be Saving Your Own Life.”
http://articles.mercola.com/sites/articles/archive/2020/08/01/benefits-of-good-iron-levels.aspx

Youthfulness, vitality and a long, prosperous life have been sought after throughout human history. And now, it seems scientists may have discovered one of the keys to turning back the hands of time.

Researchers from Arizona State University and Texas A&M University have made a breakthrough discovery in plant DNA that could lead to stopping cancer cold and slowing the aging process, ABC affiliate News 15 Arizona reports.1

The research involves telomerase, an enzyme that produces the DNA of telomeres, which have been shown to play a role in the aging process. As your telomeres lengthen, they protect your cells from aging.
Take It From the Experts: Centenarians Share Their Secrets
While direct applications from the study to human health are distant, there are a number of things you can do now to improve your health span, according to one of the co-authors. In interviews and surveys with centenarians, certain themes came up time and time again when they explained why they’ve lived so long. The 10 most common reasons they gave for their long lives were:

Keeping a positive attitude
Eating good food

Participating in moderate exercise like walking, gardening swimming, etc.Living clean (not smoking or drinking excessively)

Living independentlyHaving family to interact with

Having a circle of friendsBeing born with “good” genes

Having faith/spiritualityStaying mentally active and continually learning

Centenarians are the fastest growing segment of the U.S population, with numbers doubling every decade; by the year 2050, the number of people who will have reached the century mark is expected to pass 1 million.

Centenarians have 60% lower rates of heart disease, stroke and high blood pressure, yet scientific explanations for their health and longevity remain elusive. As a group, they are happy and optimistic and have extremely low rates of depression and other psychiatric problems, suggesting you may live longer by maintaining the right attitude.
Hopefulness and Positivity Affect the Heart
There are compelling links between cardiac health and mental health. For example, having untreated depression or anxiety disorder increases your odds of having a heart attack or developing heart disease. Stress hormones are again a primary culprit.

According to Julia Boehm, author of earlier Harvard studies looking at optimism and cardiovascular disease (CVD):2

“The absence of the negative is not the same thing as the presence of the positive. We found that factors such as optimism, life satisfaction and happiness are associated with reduced risk of CVD regardless of such factors as a person’s age, socioeconomic status, smoking status or body weight.”

With a later study,3 author Eric Kim told The Harvard Gazette:

“While most medical and public health efforts today focus on reducing risk factors for diseases, evidence has been mounting that enhancing psychological resilience may also make a difference.
Our new findings suggest that we should make efforts to boost optimism, which has been shown to be associated with healthier behaviors and healthier ways of coping with life challenges.”

The Significance of Sound Sleep
Getting adequate sleep is an important part of both mental and physical health. Too much or too little can lead to metabolic issues, as well as changes in mood and your ability to focus. Your circadian rhythm, which affects your sleep/wake cycle, holds implications for your brain, body temperature, hormones and cell regeneration among other things.4

“Irregular rhythms have been linked to various chronic health conditions, such as sleep disorders, obesity, diabetes, depression, bipolar disorder and seasonal affective disorder,” say scientists from the National Institute of General Medical Sciences.5

Italian researchers found that deletion of a specific gene related to aging also affects glucose homeostasis. According to their article, published in the journal Glia, “Disruption of the circadian cycle is strongly associated with metabolic imbalance and reduced longevity in humans.”6

Telomeres and telomerase activity are also controlled by your circadian rhythm,7 making proper sleep an important part of longevity. In a 2007 study involving 21,268 adult twins, Finnish researchers found that adults who slept more than eight hours per night, or less than seven, showed increased risk of death.8

Of course, the quality of your sleep is also important, not just the quantity. Good quality sleep, in the appropriate amount, can improve how you think and adapt to the demands on your time and changes throughout your day. There is evidence suggesting that a calm mind and active body are two important ingredients for longevity.

The meditative technique known as “mindfulness” has even been shown to have a beneficial effect on genetic expression. According to a 2018 article in Brain, Behavior, and Immunity,9 meditation has also been found to affect the enzyme telomerase, which some researchers believe is actively involved with the process of aging.
After Resting, Be Sure to Refuel
Additionally, there are many other strategies you can implement to improve your health and extend your life span. To live longer, you need to counteract the progressive loss of muscle mass by increasing your protein intake as you age. The elderly, bodybuilders and endurance athletes typically have higher than normal protein requirements for their age group.

It’s also important to cycle high and low protein intake. Ideally, combine protein restriction with time-restricted eating, followed by increased protein intake on strength training days.

Fasting 16 to 20 hours each day is likely ideal, as this allows your body to more thoroughly deplete the glycogen stores in your liver. Benefits of fasting include the suppression of mammalian target of rapamycin (mTOR) and the activation of autophagy, both of which play decisive roles in disease prevention and longevity.

You’d also be wise to avoid eating two to three hours before bed, as late-night eating will decrease your nicotinamide adenine dinucleotide (NAD+) level, which is crucial for health and longevity. Late-night eating will also make you pack on unwanted pounds, as the excess calories will not be burned but stored as fat.
Preventing Cognitive Decline
Naturally, if you’re going to live longer, you’ll want to be healthy for the remainder, and that includes maintaining your cognitive function. Specific nutrients that can help prevent dementia and cognitive decline include vitamin D, DHA, folate and magnesium. Additional nutrients of notable interest, which are readily available in supplement form, include:

Astaxanthin — Commonly called “king of the carotenoids,” is a potent anti-inflammatory from specific types of microalgae and may be useful for treating joint and muscle pain. It also supports healthy vision and can be used as an “internal sunscreen.”
Ergothioneine — Found in porcini mushrooms, ergothioneine appears to play a specific role in protecting your DNA from oxidative damage. Along with glutathione, it may offer protection against age-related conditions such as Alzheimer’s disease, cancer and heart disease.
PQQ — Particularly important for the health and protection of your mitochondria, PQQ has been shown to help protect against Alzheimer’s and Parkinson’s disease. It also works synergistically with CoQ10, producing better results than when either one is used alone. Celery, parsley and kiwi are dietary sources of PQQ.

Kick the Chemicals to the Curb
Naturally, there’s also the issue of toxic exposures, which can take a toll on your health, so avoiding toxins is a given, right along with eating a wholesome diet of organic, unprocessed foods.

This includes tossing out your toxic household cleaners, soaps, personal hygiene products, air fresheners, bug sprays, lawn pesticides and insecticides, just to name a few, and replacing them with nontoxic alternatives.

A group of scientists from Southeast University and Changzhou No. 7 People’s Hospital in China recently published a study10 about the role of plastics in our environment and how long-term exposure affects our health. They found that high concentrations of nanoplastic particles reduced the life span of roundworms.

They believe that different levels of exposure may have effects on locomotion and immune response, indicating that nanopolystyrene is likely toxic to all types of organisms.

“Our results highlight the potential of long-term nanopolystyrene exposure in reducing longevity and in affecting health state during the aging process in environmental organisms,” they wrote. Next week I will post my interview with leading researcher James Clement on his book, “The Switch,” that will go into far more fascinating details on this topic.
http://articles.mercola.com/sites/articles/archive/2019/12/24/10-ways-to-live-longer.aspx

The hope of living longer and healthier lives has been a focus of attention for centuries. In 1513, Juan Ponce de Leon left Puerto Rico and landed in Florida. He was said to be searching for the fabled Fountain of Youth, which people thought would confer everlasting life.1
While history would eventually tell a different story, with some now thinking his trek was more about politics than philanthropy, what hasn’t changed is our fascination with living longer, healthier lives.
Today, researchers and skin experts are in search of products that give the appearance of youth and vitality — qualities which are highly valued in society. In 2019, Forbes reported that the beauty industry, built on helping women look younger and more attractive, was worth $532 billion across the globe.2
Reducing Blood Plasma Reverses Aging in Mice

Fifteen years ago, researchers from the west coast of the U.S. discovered that old mice that shared blood with younger mice performed as if they were younger.3 The University of California-Berkeley team decided to pursue the matter and have recently published details of their new study in the journal Aging.4 They were determined to find the factor involved in the results from their first study, so they designed a follow-up to see if plasma had an influence on aging.
Using a process to exchange blood in small animals, the team removed half of the plasma in mice and replaced it with a saline solution and albumin. They called this intervention neutral aged blood exchange (NBE). The process essentially diluted plasma factors and replenished albumin.
Just one round of this was enough to assist with muscle repair, lower liver adiposity and fibrosis, and help with brain functioning in older mice. An analysis of the blood after transfusion showed elevated levels of proteins that would be present with tissue maintenance and repair.
Researchers did not believe albumin added to the saline solution was the sole reason for the outcomes. They concluded that the process helps to forward understanding of rejuvenation and suggests a new approach for therapeutic plasma exchange in humans that may improve the health of older individuals.
Importantly, the data from this experiment moves the needle away from investigating young blood for antiaging effects and toward the potential for removing harmful factors in blood that could contribute to antiaging.
Young Blood May Not Be the Answer

The researchers on the 2005 study, led by a husband and wife team, found that blood from younger mice could reverse signs of aging in older animals.5 They created conjoined mice using one old and one young animal. The animals shared blood and certain organs.
Their findings sparked interest in the scientific community and generated other research into whether transfusing young blood could reduce the signs of aging and essentially serve as a “fountain of youth.” As told by the lead scientist,6

“There are two main interpretations of our original experiments: The first is that, in the mouse joining experiments, rejuvenation was due to young blood and young proteins or factors that become diminished with aging, but an equally possible alternative is that, with age, you have an elevation of certain proteins in the blood that become detrimental, and these were removed or neutralized by the young partners.

As our science shows, the second interpretation turns out to be correct. Young blood or factors are not needed for the rejuvenating effect; dilution of old blood is sufficient.”

A therapeutic plasma exchange has been approved in the U.S. for the treatment of some autoimmune diseases. The process is also called plasmapheresis. Currently, the research team is finalizing plans for the next step, which is a clinical trial to explore modified plasma exchange in humans to improve the health of older adults.
In a separate study, scientists compared the actions and performance of older animals on tests of spatial memory. Special attention was paid to the hippocampus, an area of the brain crucial for forming memory and recognizing spatial patterns. The researchers concluded:7 “Our data indicate that exposure of aged mice to young blood late in life is capable of rejuvenating synaptic plasticity and improving cognitive function.” This was published in the journal Nature Medicine.
They are also evaluating the potential this intervention may be used to treat muscle wasting, immune deregulation and Type 2 diabetes.8 Another scientist on the team said this study may divert attention away from using plasma and other blood products from young people:9

“I think it will take some time for people to really give up the idea that young plasma contains rejuvenation molecules, or silver bullets, for aging. I hope our results open the door for further research into using plasma exchange — not just for aging, but also for immunomodulation.”

The point is that while positive effects from transfusing blood products from younger animals is possible, the practice is not necessary.
Chronic Disease Is Not Necessarily a Normal Part of Aging

The aging process is associated with changes in physiological, biological and psychological processes. Some changes are innocuous, while others result in declining function or disability.10 The leading causes of death in the U.S. related to disease or illness include:11

Heart disease
Cancer

Alzheimer’s disease
Diabetes

Influenza and pneumonia
Stroke (cerebrovascular diseases)

Chronic lower respiratory diseases
Nephritis, nephrotic syndrome, and nephrosis

Many of these conditions are highly influenced by nutrition and lifestyle choices. In other words, while you could possibly develop heart disease or cancer as an older adult, you may delay or entirely prevent the disease through smart life choices.
After a lifetime of smoking, metabolic dysfunction or lack of physical activity you may be discouraged, but it is still possible to make an impact on your health. Even small changes made later in life can change overall health.12
A moderate amount of activity may help older adults retain independence, reduce blood pressure, improve pain from arthritis and improve mental health.13 Addressing potential health issues before they are overwhelming eases the challenges even further.
Intermittent Fasting One Key to Longevity

Geneticist and author David Sinclair, Ph.D., is a thought leader in how to improve health span. One important strategy that helps to slow your biological clock is calorie restriction and intermittent fasting. You’ll find more information in “Revolutionary Science of Aging and Longevity.”
Results from animal studies have suggested that the younger a person is when they start intermittent fasting, the better the results. Of course, it would be foolhardy to put an infant or young child on a fasting regimen. Teens and young adults are also not good candidates, as Sinclair says, “… there’s still a lot going on in their bodies and their brains.”14
However, after the age of 30, regular fasting is likely to lengthen life, based on the research. Time-restricted eating or intermittent fasting generally involves fasting for 12 to 16 hours each day. Typically, you either eliminate breakfast or dinner. If you choose to eat dinner, be sure it’s at least three hours before bedtime.
As Sinclair and I talk about in the video above, this is because late-night eating increases your nicotinamide adenine dinucleotide (NAD+) levels which are important in a variety of bodily functions. It also reduces nicotinamide adenine dinucleotide phosphate (NADPH), an essential energy component for your cells.
If you’re eating too close to bedtime, your body cannot use the NADPH to burn calories and instead they are stored as fat. Additionally, you may try exercising while fasting. This means you’ll workout just before your first meal, after a 16 or 18 hour fast. This raises your growth hormone levels to reach maximum benefit for mitochondrial biogenesis.
Sinclair’s goal is to identify ways to reprogram cells in the body, so they don’t just act younger, but literally are younger on a molecular level. To learn more about Sinclair’s research, the science behind aging and the potential for reversing its effects, be sure to pick up a copy of his book, “Lifespan: Why We Age — and Why We Don’t Have To.”
More Antiaging Strategies You Can Use at Home

The foundations to good health and a long life are good nutrition, exercise, sensible sun exposure, quality sleep and hydration. Of course, there are other factors as well, but these are a good place to start.
Your body needs quality nutrition to deliver optimal health. Practicing intermittent fasting while eating junk food or processed foods will not accomplish your goal. Your body has micro- and macronutrient requirements for health that you must meet in order to thrive at the cellular level.
Since you can’t out-exercise the amount of food you’re eating, you have to make sure you’re eating highly nutritious foods. Shop around the perimeters of the grocery store aisles to find whole foods you can cook at home. You’ll find more information about the sun and vitamin D, the importance of quality sleep to mitochondrial health and how to stay well-hydrated in the articles listed below:

Your Vitamin D Level Must Reach 60ng/mL Before the Second Wave
Nutrients and Supplements That Can Improve Your Sleep Quality
Average Sleep Time Drops, Increasing Health Risk
This Could Prevent 3 Million Cases of Degenerative Disease
The Science Behind Molecular Hydrogen Tablets

http://articles.mercola.com/sites/articles/archive/2020/07/10/can-aging-be-slowed-by-diluting-blood.aspx

The fabled “fountain of youth” wasn’t just an intriguing physical location sought after by ancient explorers, but a concept that has captured the imaginations of ordinary mortals since the dawn of time. Some have pursued every avenue they could think of to help them live longer.
But like so many things in life, scientists found that a little healthy competition is all that’s needed — cell competition, that is. Scientists in Japan recently discovered a protein called COL17A1 that encourages cell competition by driving out weak cells and revitalizing stronger cells toward replication and, in the process, maintaining tissue fitness.
Aging and other stressors, such as excess ultraviolet radiation and damaging free radicals, take a toll on your skin, and so does steadily depleting COL17A1, as it replicates weaker cells, not stronger ones. The inevitable results: skin that is thinner, more prone to damage and takes longer to heal.
The research involved the use of mice tails because of their similarity to human skin.1 Emi Nishimura, a professor at the Tokyo Medical and Dental University’s stem cell biology department and leader of the featured study, noted that “Damaged or stressed stem cells can be selectively eliminated by intact stem cells every day in our skin.”
How COL17A1 ‘Rescues’ Aging Skin

When the researchers learned how important COL17A1 is in maintaining skin resilience, they set about investigating the possibility of stimulating it once it was depleted. They looked for compounds with the ability to “kick-start” the antiaging process and identified two chemical compounds: Both Y27632 and apocynin proved to produce positive results on skin cells, pointing to ways of “facilitating skin regeneration and reducing skin aging.” 
The two compounds “significantly promoted” repair and regeneration even to deep-tissue skin wounds, and it was done two ways, according to the study, published in the journal Nature.2 As the study authors observed:

“Stem cells with higher potential or quality are thus selected for homeostasis, but their eventual loss of COL17A1 limits their competition, thereby causing ageing. The resultant hemidesmosome fragility and stem cell delamination deplete adjacent melanocytes and fibroblasts to promote skin ageing.

Conversely, the forced maintenance of COL17A1 rescues skin organ ageing, thereby indicating potential angles for anti-ageing therapeutic intervention.”3

How Y27632 and Apocynin ‘Kick-Start’ Antiaging

When two professors from the University of Colorado reviewed the Tokyo study, they reported that fruit flies had been the only subjects ever closely scrutinized in regard to cell competition.
Ganna Bilousova and James DeGregori wrote that the research conducted by Nishimura and her colleagues could be considered “proof of principle” in regard to the ability of Y27632 and apocynin to fight aging. They also noted that the research “Provides evidence that healthy cells in mammals can also efficiently repopulate adult tissues, replacing unfit or damaged cells.”4
While conceding that more studies would be required to nail down the mechanisms responsible for cell competition in other tissues, Nishimura told news agency AFP5 they also hoped to identify compounds capable of performing the same antiaging functions in other organs.
She added, “We are working on other epithelial organs as well to find out (whether) similar competition may underlie long-term tissue maintenance as well as organ ageing.”6
She also noted the study team’s hope that the research would lead to the development of tablets, creams and other products that could halt the deterioration of and promote the repair of skin cells, and that they could “collaborate with pharmaceutical or cosmetic companies for the clinical use of the chemicals.”7 According to a Mediators of Inflammation study published in 2008:

“Apocynin is a naturally occurring methoxy-substituted catechol, experimentally used as an inhibitor of NADPH-oxidase. It can decrease the production of superoxide from activated neutrophils and macrophages while the ability of phagocytosis remains unaffected.”8

In explanation, neutrophils are the most common type of white blood cells that help your body respond to infection and heal damaged tissue.9 Macrophages “act as antimicrobial warriors” that “play critical roles in immune regulation and wound healing.”10 Phagocytosis is described as a complex process for the ingestion and elimination of pathogens, and fundamental for tissue homeostasis.11
Apocynin: What It Is and What It Does

Perhaps a simpler way of characterizing apocynin is to explore where it’s found. The 2008 inflammation study12 notes that it was first described in an investigation conducted in 1883 when the compound was isolated from the roots of Canadian hemp (Apocynum cannabinum) and used to treat dropsy and heart problems.
It was also found in the root of Picrorhiza kurroa, a plant with the faint odor of vanilla, native to India, Nepal, Tibet and Pakistan and common in Ayurvedic treatments. In India and Sri Lanka, extracts were used “for the treatment of ailments of liver, heart, joints, and lungs.”13
A 2014 study14 shows that the “small phenolic antioxidant” known as apocynin and extracted from the Jatropha multifida plant, also known as Guatemala rhubarb or coral plant, grown from Mexico to Central America to Brazil, was shown to have potential for treating neurodegenerative diseases.
Researchers also found apocynin to be one of five volatile vanilla flavor compounds in the vanilla bean, aka Vanilla planifolia.15 Another study suggested its cancer-fighting potential:

“The spread of cancer cells to distant organs, in a process called metastasis, is the main factor that contributes to most death in cancer patients. Vanillin, the vanilla flavoring agent, has been shown to suppress metastasis in a mouse model … (and) their structurally related compounds, apocynin and diapocynin, in hepatocellular carcinoma cells.”16

Besides its advantageous effects on fighting inflammation and free radical scavenging, apocynin has a history of successful treatment of a long list of ailments, including:

Ischemia-reperfusion, characterized by damaged lung tissue due to a lack of oxygen and subsequent returned supply,17 with apocynin also showing potential in treating several other respiratory diseases
Possible neuroprotective abilities, particularly in brain injury following an eschemic stroke,18 as well as reduced cerebral and vascular injury in experimental stroke models19
Potential in the treatment of atherosclerosis due to reduced blood pressure,20 and preventing endothelial dysfunction21

Chronic inflammatory joint diseases such as osteoarthritis and rheumatoid arthritis22

Inhibiting tumor migration in breast cancer cells23

A 2014 study notes that “the perspectives for apocynin in chronic neurodegenerative disorders,” suggests a “potentially beneficial role” in amyotrophic lateral sclerosis (ALS) or Lou Gehrig’s disease,24 Alzheimer’s25 and Parkinson’s disease.26 Although mouse models were the usual subjects in experimentation, the researchers are hopeful that apocynin will prove just as effective in human patients.
Other Beneficial Functions of Apocynin

Arguably the most important aspect of apocynin is its role in fighting inflammation, and the above study notes that it’s been demonstrated in a variety of cell and animal models. Apocynin also “inhibits the assembly of NADPH-oxidase that is responsible for reactive oxygen species (ROS) production.”27
The 2008 study explains NADPH-oxidase as the enzyme responsible for ROS production, so suppressing it is often the goal in disease prevention therapies. When antioxidants are in place or introduced, oxidative stress is diminished. Your body produces an “armory of antioxidants to defend itself,” which nonetheless are sometimes insufficient to effectively defend against ROS.
ROS damages your cells as well as your DNA, which is part of the reason your body begins showing signs of aging. To a large degree, how well your mitochondria work is determined by your diet, optimally a ketogenic diet (in which you replace carbs with moderate amounts of high-quality protein and high amounts of beneficial fat).
However, the featured study notes that it’s the excessive production of ROS that becomes damaging, and that’s how it’s been implicated in the progression of many diseases. It’s also why apocynin is noted as a potential treatment for many of them.
A Mediators of Inflammation review concluded that apocynin, besides its lack of known side effects, deserves further attention in the development of “safe and selective anti-inflammatory drugs which lack the often serious side effects of steroids.”28
http://articles.mercola.com/sites/articles/archive/2019/04/15/why-apocynin-regenerates-skin.aspx

By Dr. Mercola

Scientists in Norway have released results from experimental feeding studies carried out over a 10-year period, and the verdict is in: If you want to avoid obesity, then avoid eating genetically engineered (GE) corn, corn-based products, and animals that are fed a diet of GE grain.
As reported by Cornucopia.org1, the project also looked at the effects on organ changes, and researchers found significant changes that affected weight gain, eating behaviors, and immune function.

How Genetically Engineered Corn and Soy Can Wreak Havoc on Your Health

According to the featured article2:

“The results show a positive link between GE corn and obesity. Animals fed a GE corn diet got fatter quicker and retained the weight compared to animals fed a non-GE grain diet. The studies were performed on rats, mice, pigs and salmon, achieving the same results.
… Researchers found distinct changes to the intestines of animals fed GMOs compared to those fed non-GMOs. This confirms other studies done by US researchers. Significant changes occurred in the digestive systems of the test animals’ major organs including the liver, kidneys, pancreas, genitals and more.”

Their findings (which were published July 11, 2012 in Norway by Forskning.no, an online news source devoted to Norwegian and international research3) showed that animals fed genetically engineered Bt corn ate more, got fatter, and were less able to digest proteins due to alterations in the micro-structure of their intestines.
They also suffered immune system alterations. The impaired ability to digest proteins may be of particular concern as this can have far-reaching implications for your health. If your body cannot digest proteins, your body will be less able to produce amino acids, which are necessary building blocks for proper cell growth and function.
As noted by Cornucopia.org:

“This not only may relate to a rise in obesity, but to increases in many modern diseases. These diseases include diabetes, digestive disorders, inflammatory bowel disease, colitis, autism spectrum disorders (ASD) (ADD), autoimmune diseases, sexual dysfunction, sterility, asthma, COPD and many more.
…[Lead author] Professor Krogdahl explains: “It has often been claimed that the new genes in genetically modified foods can’t do any damage because all genes are broken down beyond recognition in the gut. Our results show the contrary; that genes can be taken up across the intestinal wall, is transferred to the blood and is left in the blood, muscle and liver in large chunks so that they can be easily recognized… The biological impact of this gene transfer is unknown.”

Bt Toxin Found in Blood of Women and Fetuses

This is not the first time scientists have revealed significant biological impacts and related health problems as a result of eating a diet of genetically engineered foods. More often than not, unless the research is tainted by industry ties, studies into the effects of genetically engineered foods demonstrate that it is anything but safe. This isn’t so surprising when you consider that simple logic will tell you it’s probably not wise to consume a plant designed to produce its own pesticide, for example.
So-called “Bt corn” is equipped with a gene from the soil bacteria Bacillus thuringiensis (Bt), which produces Bt-toxin—a pesticide that breaks open the stomach of certain insects and kills them. This pesticide-producing corn entered the food supply in the late 1990’s, and over the past decade, the horror stories have started piling up.
Monsanto and the US Environmental Protection Agency (EPA) swore that the toxin would only affect insects munching on the crop. The Bt-toxin, they claimed, would be completely destroyed in the human digestive system and would not have any impact on animals and humans. The biotech companies have doggedly insisted that Bt-toxin doesn’t bind or interact with the intestinal walls of mammals, and therefore humans.
The featured research proves all such claims false.
Prior findings have already shown that Bt corn is anything but innocuous to the human system. Just last year, doctors at Sherbrooke University Hospital in Quebec found Bt-toxin in the blood4 of:

93 percent of pregnant women tested
80 percent of umbilical blood in their babies, and
67 percent of non-pregnant women

Bt-toxin breaks open the stomach of insects. Could it similarly be damaging the integrity of your digestive tract? If Bt-toxins can damage the intestinal walls of newborns and young children, the passage of undigested foods and toxins into the blood from the digestive tract could be devastating to their future health. Scientists speculate that it may lead to autoimmune diseases and food allergies. Furthermore, since the blood-brain barrier is not developed in newborns, toxins may enter the brain causing serious cognitive problems. Some healthcare practitioners and scientists are convinced that this one mechanism for autism.
If Bt genes are colonizing the bacteria living in the digestive tract of North Americans, we might expect to see an increase in gastrointestinal problems, autoimmune diseases, food allergies, and childhood learning disorders since the advent of Bt crops in 1996, and that’s exactly what’s being reported. For example, between 1997 and 2002 the number of hospitalizations related to allergic reactions to food increased by a whopping 265 percent. One out of 17 children now has some form of food allergy and allergy rates are rising.

Genetically Engineered Foods Trigger Adverse Immune System Responses

There’s plenty of evidence showing that the Bt-toxin produced in genetically modified Bt crops like corn and cotton plants is toxic to humans and mammals andtriggers immune system responses. For example, in government-sponsored research in Italy5, mice fed Monsanto’s Bt corn showed a wide range of immune responses, such as:

Elevated IgE and IgG antibodies, which are typically associated with allergies and infections
An increase in cytokines, which are associated with allergic and inflammatory responses. The specific cytokines (interleukins) that were found to be elevated are also higher in humans who suffer from a wide range of disorders, from arthritis and inflammatory bowel disease, to MS and cancer
Elevated T cells (gamma delta), which are increased in people with asthma, and in children with food allergies, juvenile arthritis, and connective tissue diseases.

Rats fed another of Monsanto’s Bt corn varieties called MON 863, also experienced an activation of their immune systems, showing higher numbers of basophils, lymphocytes, and white blood cells6. These can indicate possible allergies, infections, toxins, and various disease states including cancer. There were also signs of liver and kidney toxicity.

USDA Clears Roundup Ready Sugar Beets

So-called “Roundup Ready” crops are another type of genetically engineered crops. While Bt crops contain a gene that produces a pesticide inside the plant itself, Roundup Ready crops are designed to withstand otherwise lethal topical doses of glyphosate—a broad spectrum herbicide, and the active ingredient in Monsanto’s herbicide Roundup as well as hundreds of other products.
This way, the crop survives while all weeds are theoretically eliminated from the field. I say ‘theoretically’ because the overuse of the herbicide has led to the rapid development of glyphosate-resistant superweeds. It’s estimated that more than 130 types of weeds spanning 40 U.S. states are now herbicide-resistant, and the superweeds are showing no signs of stopping.
Roundup Ready crops have also been linked to serious health problems—particularly relating to fertility and birth defects—as has glyphosate itself, which is why the latest news regarding the deregulation of Roundup Ready sugar beets is all the more disappointing.
A number of organizations challenged the USDA approval of Roundup Ready (RR) sugar beets in 2008, arguing that the beets would contaminate related organic and non-GE crops such as table beets and chard. Further, they said that the pesticide-resistant beets would increase pesticide impacts on the environment and worsen the current epidemic of pesticide-resistant superweeds.
A lawsuit was filed against the USDA in 2009 for failure to complete an Environmental Impact Study. A federal judge agreed, temporarily suspending all planting of RR sugar beets. The suspension was later overridden by the USDA, ostensibly to prevent a sugar shortage. After a number of additional legal twists and turns, the USDA has now announced its decision to deregulate Monsanto’s Roundup Ready genetically modified sugar beets7. According to a July 19 press release by the U.S. Department of Agriculture’s Animal and Plant Health Inspection Service (APHIS)8:

“After completing both a thorough environmental impact statement and plant pest risk assessment, holding three public meetings and considering and analyzing thousands of comments regarding its analyses, APHIS has determined that, from the standpoint of plant pest risk, Roundup Ready sugarbeets are as safe as traditionally bred sugarbeets.”

GM Companies Threaten Food Security and Sovereignty

A landmark speech delivered during the 2011 SEMEAR conference in Sao Paulo, Brazil, on how genetically modified (GM) seed companies threaten food security and food sovereignty has resulted in a call to action by an unlikely source who is a key player in the soy industry. Pierre Patriat, President of APROSMAT, the association of seed producers of Mato Grosso, Brazil, does not oppose genetically engineered (GE) crops, but he does recognize the unprecedented threat to food security that GM seeds pose.
Saying that the GM industry is rapidly taking away Brazilian farmers’ freedom of choice, he asked for “immediate mobilization and action on the part of concerned industry members, government, lawmakers, farmers, and civil society to avert the threat to food sovereignty posed by the GM industry’s control of markets through their patented seeds,” according to a recent report by GM Watch9.
In his speech, which I recommend reading in its entirety to learn more, Patriat wisely says:

“… [T]oday, people think everything can be resolved through the seed. If soybean rust occurs they say, “Just wait, this can be resolved with genetic engineering!” A problem with nematodes? – “We’ll change the seed directly!” They want to solve all problems that way… But as long as we have alternative solutions we don’t need genetic engineering to get rid of all problems.
Today we have a big problem with nematodes for a simple reason, not least because of the lack of a medium-term agricultural policy. There is a solution known to every agronomist: Crop rotation! That is how weeds and pests are weakened. It is so simple! Another way is soil management and measures to correct the soil – fundamental things nobody pays attention to anymore because everything has to be resolved through the seed.
No one does rotation any more – everyone does succession [planting same crop in succession]. These are problems that are not resolved by biotechnology. The man who is going to spend 150-200 Brazilian dollars per hectare would do much better to invest it in the [quality of the] land. The profitability in the medium term will be much better for sure. This does not mean that constant seed improvement will not bring solutions. But we ought to cooperate and define the base for new regulations, so that everyone may collaborate harmoniously without abusing their economic power.
Because today there are no brakes on the abuse of economic power over seed, and even worse, this affects the sovereignty of a country, because it is a matter of food security and food security is national security.”

The issue of food sovereignty is certainly not restricted to Brazil. It’s becoming a serious threat to every nation on this planet as genetically engineered crops spread. These seeds are owned by private companies, and it’s imperative to understand that once a country allows GE crops to monopolize their agricultural sector, it becomes completely beholden to and dependent upon a corporation for the ability to grow food and feed its citizens!

http://articles.mercola.com/sites/articles/archive/2012/08/07/genetically-engineered-foods-hazards.aspx