Day: November 19, 2022

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• In “Innate Immune Suppression by SARS-CoV-2 mRNA Vaccinations: The Role of G-quadruplexes, Exosomes and MicroRNAs,” Stephanie Seneff, Ph.D., and Drs. Peter McCullough, Greg Nigh and Anthony Kyriakopoulos explain how the COVID shots suppress your innate immune function, and how they may cause neurological diseases

• Their landmark paper was the source of major controversy in that the prominent journal in which it was published receive much negative feedback and the editor of the journal was forced to resign although the paper has not been retracted at this time

• G4s are genome-wide targets of transcriptional regulation. The “G” stands for guanine. G4 is DNA sequence of four consecutive guanines, which plays an important role in diseases such as cancers and neurological disorders. The COVID jab spike protein produces far more G-quadruplexes (G4) than the virus. The G4 causes prion protein to misfold, which can result in prion diseases such as Creutzfeldt-Jakob disease and Alzheimer’s

• Two specific microRNA have been found in people who got the jab, and these microRNA’s interfere with Type 1 interferon response, which is a key part of your immune system. When Type 1 interferon is suppressed, you become more prone to infection and chronic disease

• The COVID jab produces high levels of immunoglobulin (IgG) antibodies, which are associated with autoimmune disease. It does not produce mucosal antibodies

• Antibodies against the spike protein may be responsible for cases in which patients developed highly aggressive prion disease after their second jab

In this interview, return guest Stephanie Seneff, Ph.D., a senior research scientist at MIT for over five decades,1 discusses her paper,2 “Innate Immune Suppression by SARS-CoV-2 mRNA Vaccinations: The Role of G-quadruplexes, Exosomes and MicroRNAs,” published in the June 2022 issue of Food and Chemical Toxicology.

The paper was co-written with Drs. Peter McCullough, Greg Nigh and Anthony Kyriakopoulos. In May 2021, Nigh and Seneff published a paper3 detailing the differences between the spike protein and the COVID jab spike protein.

In the “Innate Immune Suppression” paper, they and their other co-authors delve deep into the mechanisms of the COVID shots, showing how they suppress your innate immune system.

The paper caused quite a stir when it was first posted, prior to publication. A campaign was launched to have it retracted on the premise that it would discourage people from getting these life-saving shots — regardless of whether the mechanisms described were true or not.

Ultimately, the controversy led to the resignation of the editor of the journal. Many have also tried to discredit Seneff, and McCullough has since been stripped of his medical credentials.4

G-quadruplexes (G4) are genomewide targets of transcriptional regulation, and as such as a novel target for drug design. The “G” in G4 stands for guanine, so G4 is DNA sequence of four consecutive guanines. It’s one of the four nucleotides — the basic code — in DNA, and it’s known to play an important role in diseases such as cancers and neurological disorders.5

As explained by Seneff, prions, when misfolded, build beta sheets and precipitate out of the cytoplasm, causing plaque to form. This plaque is a hallmark of several neurodegenerative diseases in animals and humans, such as Mad Cow disease, Creutzfeldt-Jakob disease, scrapie (which affects deer) and Alzheimer’s disease.

“So, there are all these debilitating neurodegenerative diseases that come out of the prion protein, and the prion protein actually binds to its own G4s, which are in its own RNA,” Seneff explains. “In so doing, it promotes [the prion protein] to misfold into the wrong shape … [which] causes prion disease.

The [COVID jabs] produce a version of the messenger RNA (mRNA) that codes for the spike protein. Their version is enriched in guanines — it produces a lot more G4s than the original mRNA that the virus produces — so, it’s a different form.

And there’s lots of mRNA in the [COVID jab]. It’s a big dose of this mRNA that is enriched in G4s … which then … causes the cell to produce the prion protein. So, the cell is producing the prion protein in the context of a situation with lots of G4s lying around from the mRNA from vaccine. That’s a really dangerous situation for causing the prion protein to misfold and causing prion disease.”

As explained by Seneff, the mRNA in the jab is taken into your lymph system and spleen, germinal centers where antibodies are produced, and in order to produce the antibodies, these germinal centers release exosomes. This can help explain the phenomenon of “shedding,” but it also helps explain the immune destruction we see occurring. Seneff explains:

“The exosomes are part of the process by which the cells communicate to induce the antibody production, which is the goal of the [COVID jab]. The [jab] does a fantastic job of producing high levels of IgG [immunoglobulin] antibodies, which are the ones that are associated with autoimmune disease.

It doesn’t make the mucosal antibodies. It makes IgG, which is actually much more dangerous if there are too many antibodies. They can cause autoimmune disease through molecular mimicry, and that’s another aspect that I think is going on.

That’s why you’re getting this platelet problem where platelet count goes down to zero, because you get antibodies to the platelets by molecular mimicry, or even because the spike protein is binding to the platelets. They’re getting antibodies to the complex and you’re wiping out the platelets.

Some people are getting thrombocytopenia and VITT [vaccine-induced immune thrombotic thrombocytopenia], conditions that can be life-threatening. And there’s a huge signal for thrombosis. The paper talks about thrombosis. We have … seven tables for different aspects of the symptoms of the vaccine.

There’s a table on the liver, there’s a table on thrombosis, there’s a table on cancer, there’s a table on the vagus nerve, and all of the inflammations of the nerves because those exosomes are traveling up the vagus nerve, making their way to the heart, brain and liver.

They’re causing disease in all of those organs, and you see that very clearly in the various databases — 98%, 99% of the [adverse event] reports in 2021 for these conditions were [from the] COVID shots and 1% was all the other vaccines combined.”

Swiss researchers recently reported finding elevated troponin levels in 100% of COVID jabbed individuals, indicating everyone is suffering some degree of heart damage, even if they’re asymptomatic.6 7 Seneff explains the mechanism by which the COVID shot damages your heart.

“I think the whole issue is the spike protein being released by the immune cells in the germinal centers — the lymph system and the spleen releasing these exosomes that then travel along their fibers and reach all these critical organs.

The spleen has a very good connectivity with the liver, heart, brain and gut via the nerve system, starting with the splanchnic nerve and then hooking up to the vagus nerve … So, these exosomes are migrating along the vagus nerve and they’re arriving at these organs and are getting taken up by cells there. And everywhere they go, they cause inflammation.

The spike protein is very good at causing inflammation. That’s been shown in multiple studies … It causes the immune cells to migrate to the heart, and that’s how you get myocarditis, this inflammation in the heart.

You also get inflammation in the muscles. I was looking at myositis, which is muscle inflammation, and that’s another issue. I’ve been in contact with multiple people who suffered severe muscle damage from the spike protein, even to the point of being debilitated because of [inflammation in the] muscles.

So, not just the heart, but the skeletal muscles are also affected in a really bad way. Inflammation in the brain also causes neurons to be damaged and that’s causing cognitive disorders.

So, I think the long COVID is caused by the spike protein reaching the brain. Many papers have talked about long COVID, and they think it’s the spike protein, not the virus, but the spike protein itself [that is causing it].”

Another piece of the puzzle is related to the role of microRNA, which are embedded in the exosomes that travel to the tissues. MicroRNA should not be confused with mRNA. They’re two different things. The microRNAs are short pieces of RNA, about 22 nucleotides long. Unlike mRNA, microRNA do not code for protein.

The mRNA in the jabs are designed to be extremely resilient. Normally, mRNA lasts a few hours, but the mRNA in the jabs stick around coding cells for several months, at minimum primarily because of the substitution of the nucleotide uridine with pseudouridine.

Because the mRNA is so resilient, spleen cells have to try to cope with all the spike protein that they cannot stop making, and one way they do that is by pushing the spike protein out in the form of exosomes. Those exosomes also contain microRNAs. Indian researchers found two specific microRNA in people who got the jab, and these microRNAs interfere with Type 1 interferon response.

“This is a big topic of our paper,” Seneff says. “We talk about innate immune suppression … due to the effect of these microRNAs that are packaged up with the spike protein.

Everywhere [the exosomes] go, they deliver these microRNAs, which disrupt the immune cell’s ability to respond to Type 1 interferon. These microRNAs actually have a very high-level controlling element in the regulatory process of biology. They control which genes are expressed.”

Seneff goes on to cite animal research from 2005, in which mice were exposed to a virus that causes myocarditis. They wanted to see what would happen if the mice were suffering from myocarditis and then got a shot of adrenaline. So, the mice were infected with the myocarditis-inducing virus, and then, 120 days later, they injected them with adrenaline.

The dose given killed 70% of them. Meanwhile, control mice that did not have myocarditis suffered no ill effect when injected with the same dose of adrenaline. The mice that died, died of heart failure. Basically, their hearts were too damaged to withstand the adrenaline rush. Today, we’re seeing a similar effect in athletes, who are dropping dead while exerting themselves.

Digging for other papers, Seneff found one that detailed the Type 1 interferon response in chromaffin cells, the cells that make adrenaline. Type 1 interferon inhibits and reduces their production of adrenaline.

Seneff’s theory is that the COVID jabs interferes with your body’s ability to respond to Type 1 interferon, thereby allowing too much adrenaline to be released. If your heart has been damaged by the spike protein, the outcome could be lethal, as we’ve seen.

“I think that could be what’s going on with the sudden death problem, because we certainly are seeing lots of young people dying of suddenly heart issues,” she says.

At the same time, microthrombi (micro blood clots) are activated by the spike protein, which could have lethal effects, and endothelial cells (the cells lining your blood vessels) are also inflamed. So, there’s not just one mechanism by which the jabs could kill you.

According to Seneff, blood clots are also connected to the prion aspect. Many different proteins are amyloidogenic and can misfold, causing them to precipitate out, including proteins in your blood. Blood clots are tough to break down, and when you add spike protein into them, they become even tougher.

Seneff suspects the spike protein binds to fibrin, causing it then to misfold in a way that makes it very resistant to breaking down. The same thing happens with prion proteins. When they misfold, they create a gel that becomes denser over time, eventually becoming completely inaccessible to the water base.

“It just precipitates out as this thing that just sits there for the rest of your life,” Seneff says. “Nothing can get at it. The immune cells can’t break it down. It just stays there. It can’t be cleared.”

This is why I recommend taking fibrinolytic enzymes like lumbrokinase (which is the most effective), serrapeptase and nattokinase, several times a day one hour before or two hours after a meal, if you’re struggling with long COVID, as they help break down the fibrin. To work, you have to take them between meals, on an empty stomach, or else they’ll just act as a digestive enzyme to break down food.

Another technique is to use a near-infrared sauna, which will help address the misfolding of proteins by encouraging autophagy, your body’s natural clean-out process.

Antibodies may also play a role in the devastating side effects from the COVID jab. We know that prion protein is upregulated in cells that produce it under stress, and the COVID jab spike protein has been shown to cause cells to make more prion protein. One possibility is that antibodies to a particular part of the spike protein end up binding to the prion protein through molecular mimicry.

As explained by Seneff, researchers have discovered that if you produce antibodies to the C-terminal end of the prion protein, it can cause disease that looks a lot like prion disease but develops much faster.

As it turns out, the antibodies to the C-terminal end of the prion protein prevent the prion protein from going into the endoplasmic reticulum (ER), where it needs to go in order to do its job. Instead, the antibodies keep the prion in the cytoplasm.

Subsequently, the cell gets sick because of these antibodies. The late Luc Montagnier posted a case study with 26 people who developed symptoms of prion disease within the first month after their second vaccine. All died, many within three months of their diagnosis. All were dead within a year, from what was basically an extremely aggressive form of Creutzfeldt-Jakob disease (the human Mad Cow disease equivalent).

Seneff believes antibodies against the spike protein are to blame, because it didn’t happen until they got their second dose. Antibodies developed after that first dose, which primed the cells. Then, after the second dose the cells started making loads of spike protein again, which the antibodies bound to.

This exosome package then traveled up the vagus nerve to the brain, where neurons took them up. Seneff suspects this explains the disease process on those 26 patients.

“It would be explained completely by this model of spike protein antibodies binding to the C-terminal domain and preventing the prion protein from going into the ER,” she says, “and then, it causes [the prion protein] to break down.

It gets broken down by the proteasome and disappears. So, it’s causing a loss of function problem for the prion protein in the neuron at a very accelerated rate, much faster than what goes on with the normal prion disease …

Montagnier and his team identified a segment of the spike protein that they thought had characteristic prion-like features. Within that segment is a piece that has five amino acids, YQRGS.

The prion protein has [the same] piece … Except for the middle one, the other four [amino acids] are all identical with this piece near the C-terminal end of the prion protein. So, it’s really perfect. It’s a place where, if you get antibodies to that, it’s basically a death sentence.”

Seneff, McCullough, Nigh and Kyriakopoulos recently posted yet another paper,8 “Potential Mechanisms for Human Genome Integration of Genetic Code from SARS-CoV-2 mRNA Vaccination,” describing how the mRNA in the COVID jab can change your genome.

According to Big Pharma, public health agencies and “fact checkers,” the mRNA in the jabs cannot integrate into human DNA. It’s impossible, they say. But science tells another story. In fact, there’s more than one way in which this can happen.

For example, LINE-1, the human version of a retrovirus, is a very common piece of DNA in the human genome, and it gets converted into RNA, which in turn codes for multiple proteins that can cause the RNA to copy itself into another place in the DNA. It can also copy and insert other RNA, such as the RNA in the COVID shot. This is a resource that your cells have naturally. Seneff continues:

“The Alzheimer’s brain has these neurons that have way too much DNA. It’s like their genome is too big, and what they found is they have lots of extra copies of the amyloid beta protein with different variations.

It’s a way for the cell to … try alternative forms of the protein that is not working. That’s what I think is going on. It’s really quite fascinating because I think that it provides the cell with the opportunity to fix a problem.

Let’s say that it has a protein like amyloid beta that it’s making and then that protein is misbehaving. It’s not working correctly. If … it needs to make a different version of [that protein], it can do that with LINE-1. Neurons express a lot of LINE-1, and any cell that expresses LINE-1 has the opportunity to put that spike protein RNA into the genome.”

In other words, the spike protein can hijack LINE-1, a system your body has that integrates viral DNA into your DNA by using it to copy and insert its mRNA into the cell’s DNA. There’s also another model. Nigh discovered research showing that double-stranded DNA viruses, such as the herpes virus, have a mechanism for incorporating human genes into its DNA.

It’s able to grab a hold of human RNA in the cytoplasm of the cell, convert it into DNA and then insert it into its own genome. What this means is that certain viruses (such as the herpes virus) could carry the genetic code for making spike protein, and it doesn’t involve entering the nucleus of your cells at all.

To circle back to where we began, it seems the reason so many jabbed individuals are now contracting COVID and other infections, and are dying from them, is because Type 1 interferon is suppressed. That suppresses your immune function, making you more prone to contracting infections.

In the interview, Seneff also reviews how chronic exposure to glyphosate is a predisposing condition for bad COVID-19 outcomes, as glyphosate disrupts the immune system. For more details on that, please listen to the interview in its entirety. We also review how glycine supplementation can help displace glyphosate in your body, thereby limiting its damaging influence.

To get a fuller, more in-depth grasp of the mechanisms by which the jabs injure your health, I also recommend reading through “Innate Immune Suppression by SARS-CoV-2 mRNA Vaccinations: The Role of G-quadruplexes, Exosomes and MicroRNAs,”9 and “Potential Mechanisms for Human Genome Integration of Genetic Code from SARS-CoV-2 mRNA Vaccination.”10

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• A case report of 100 patients diagnosed with cognitive decline using the ReCODE protocol showed both subjective and objective improvements in all participants

• The ReCODE protocol, which involves identifying the drivers of cognitive decline (such as pathogens, toxins and metabolic changes), then targeting those in a personalized program that includes dietary and lifestyle changes, allows your brain to create and maintain synapses again, thereby treating the root of the problem

• A hallmark of neurodegenerative diseases such as Alzheimer’s is that proteins are aggregated and are typically misfolded

• By inducing ketosis, improving insulin sensitivity and supporting the mitochondria, you can often regain the ability to refold or proteolyze misfolded proteins

• Electromagnetic field exposures, such as that from cellphones and Wi-Fi, may play an important role in Alzheimer’s, as it triggers high amounts of oxidative stress and damage to proteins and DNA

Alzheimer’s disease, which is the most common form of dementia, eventually leads to the inability to carry out even the most basic of bodily functions, such as swallowing or walking. It is ultimately fatal, as conventional treatment options are few and universally ineffective.

Like autism among children, Alzheimer’s among seniors has reached epidemic proportions, with no slowdown in sight. On the contrary, evidence suggests the trend is worsening.

In 2022, Alzheimer’s affects more than 6 million Americans,1 and 1 in 3 seniors dies with dementia or other demention. By 2050, Alzheimer’s diagnoses are projected to reach 13.8 million.23

Wile the U.S. Centers for Disease Control and Prevention lists the disease as the seventh leading cause of death in the U.S.,45 statistics published in the journal Neurology in 2014 revealed Alzheimer’s is vastly underreported on death certificates. In reality, the disease likely killed 503,400 American seniors in 2010,6 making it the third leading cause of death, right behind heart disease and cancer.7

The good news is that contrary to conventional claims, there are ways to prevent and even treat this tragic disease — not by drugs, but by diet and other lifestyle changes.

Dr. Dale Bredesen, professor of molecular and medical pharmacology at the University of California, Los Angeles School of Medicine, and author of “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline,” has identified a number of molecular mechanisms at work in Alzheimer’s, and created a novel program called ReCODE to treat and reverse it.8

One of Bredesen’s publications is a case report910 of 100 patients using the ReCODE protocol. He had previously published three case reports, each involving just 10 patients. This fourth case report contains 100 patients treated at 15 different clinics across the U.S., all of which have documented pre- and post-cognitive testing.

Not only did all show improvement in symptoms, some of them also showed improvement in their quantitative electroencephalographs (EEGs). Others who underwent magnetic resonance imaging (MRI) with volumetrics also showed objective improvement.

“By all the criteria, these people showed improvement, subjective and objective,” Bredesen says. This is no small thing, as there is no conventional treatment that can reverse Alzheimer’s. There have been many drug trials to date, but all have failed to reverse the disease. As noted by Bredesen:

“There are a couple of medications, Aricept, Namenda … but these have a very, very modest impact. The most important thing is their improvement is not sustained. They don’t change the outcome of the disease. You get a little bump in improvement, then you go right back to declining.

The most important part of the [ReCODE] protocol … is that the improvement is sustained. You’re actually going after the root cause of what is causing the cognitive decline. That’s a big difference.”

If one were to summarize Bredesen’s approach in one sentence, it would be “to improve the ratio between synaptoblastic and synaptoclastic activity, which is the brain’s ability to create new synapses versus destroying them.” In other words, the treatment allows your brain to create and maintain synapses again. Bredesen explains:

“The molecular biology of this disease shows that what we call Alzheimer’s disease is actually a protective response. It’s essentially a scorched-earth retreat.

You’re pulling back and saying, ‘We’re not going to let this insult kill us, so we’re going to scorch the earth so it (whether it’s bacteria or something else) cannot take advantage … of what’s there.’ You’re literally downsizing [your synapses]. As long as those insults are going on, you will be downsized.”

Beta-amyloid is a protein that is highly correlated with Alzheimer’s. However, all attempts at removing it have failed to improve the condition. Clearly, beta-amyloid in and of itself is not the primary cause, so simply getting rid of it is not the answer.

In Bredesen’s paper, he discusses the role of beta-amyloid as an antimicrobial peptide (AMP). Importantly, AMPs are critically important for host immunity. They target organisms such as bacteria, mycobacteria, viruses, fungi and protozoa. He explains:

“Here is the trick. It turns out amyloid beta is really part of the innate immune system. Its antimicrobial effect was first discovered and published by professor Robert Moir and professor Rudy Tanzi at Harvard.

This thing actually has, again, a protective response. Not only is it an AMP, but it also binds some toxins. For example, mercury, other divalent metals like iron and things like that. [Amyloid beta] has multiple effects. It is part of your response to insult.

When you take that into account, you realize it’s fine to remove amyloid, but please don’t do it before you remove all the insults. We’ve seen numerous people now who have had the amyloid reduced and gotten worse because the ongoing insults are still there.”

In 2019, the drug company Biogen halted its Phase II clinical trial for aducanumab, a drug designed to remove beta-amyloid, and this is the typical story for these kinds of drugs. And then a major trial of yet another approach to amyloid removal, the BACE inhibitor CNP520, was halted because the drug was associated with increased cognitive decline and brain atrophy.11

About one-third of the proteins your body makes on any given day are misfolded. Thankfully, your body has a mechanism by which those misfolded proteins are refolded. Heat-shock proteins play a central role in this process, and if the misfolding is too severe, the heat-shock proteins help remove them altogether.

In fact, heat-shock proteins are a corollary of autophagy, the process by which your body cleans out damaged organelles. This relates to Alzheimer’s, because the refolding process is one of several factors that need to work in order for your brain to function. As noted by Bredesen:

“In all of these different neurodegenerative diseases, whether you’re talking about Alzheimer’s, Huntington’s, Lou Gehrig’s disease, Parkinson’s disease or Lewy body, they all feature proteins that are aggregated and that are typically misfolded. They are not degraded appropriately.

You lose not only the ability to fold but the ability to degrade these proteins. That is a critical piece. In fact, just recently, an article came out on a common neurodegenerative condition, newly described, which is called LATE, which is limbic-predominant, age-related TDP-43 encephalopathy.

In other words, this is a little bit like Alzheimer’s … [LATE] features TDP-43, which is a protein that is involved in numerous things, including protein folding … We lose that [protein-folding] ability as we start to downsize [synapses], as you don’t have an appropriate energy, you don’t have the appropriate trophic support.

You don’t have the appropriate hormonal and nutritional support … When we target ketosis, when we target insulin sensitivity, when we target mitochondrial support, that typically allows you to generate the appropriate ability to refold misfolded proteins …

You can induce the heat-shock response … by doing this combination of sauna and then [going] into the cold and then back to the sauna and then back to the cold …

You are recurrently activating this critical response [by doing that]. There’s no question it is going to be important, especially in ALS, but likely in all of the neurodegenerative conditions.”

As noted by Bredesen, there are three kinds of autophagy: macro-autophagy, micro-autophagy and chaperone-mediated autophagy. Each offers a slightly different way to repair, remove or recycle damaged organelles within the cell.

Specific proteins, for example, can be targeted for chaperone-mediated autophagy. Bredesen recounts findings of research he did to ascertain the linkage between protein folding and programmed cell death (apoptosis, where the entire cell is killed off and removed):

“If you fail to reform these [misfolded proteins], you literally activate an entire system that initially stops producing more protein. It’s basically saying, ‘We’re not keeping up with this. We’re going to shut this down.’ It attempts to refold. Then it attempts to destroy the proteins if it can’t refold them.

Then ultimately, if it cannot … keep up … it literally activates programmed cell death through specific caspases … This is something where you want to intervene upstream; understand why this is happening. And then if you’re unable to keep up with this, now, at least increase your heat-shock proteins so that you can refold. In this case, you prevent the induction of programmed cell death.”

Unfortunately, a vast majority of people do not have well-functioning autophagy, for the simple reason that they’re insulin-resistant. If you’re insulin-resistant, you cannot increase your adenosine 5′ monophosphate-activated protein kinase (AMPK) level, which prevents the inhibition of mammalian target of rapamycin (mTOR), and mTOR inhibition is one of the primary drivers of autophagy.

While autophagy is clearly of critical importance, you don’t want to be in continuous autophagy. You also need to cycle through the rebuilding phase. One of the ways in which you can control this is through cyclical fasting. Bredesen typically recommends an intermittent fasting approach.

“You want to use appropriate fasting and an appropriate diet to activate this autophagy,” Bredesen says. “We recommend … 12 to 14 hours [of fasting] if you are apolipoprotein E4-negative (ApoE4-negative) … If you are ApoE4-positive, you’d want to go longer — 14 to 16 hours. There’s nothing wrong with doing a longer fast …

The reason we suggest longer for the ApoE4-positives [is because] if you are ApoE4-positive, you are better at absorbing fat. It tends to take longer to enter autophagy …

Typically, we recommend it about once a week. But again, a longer fast once a month is a good idea. It depends a lot on your body mass index (BMI). What we found is people who have higher BMIs respond better to this fasting early on. They’re able to generate the ketones.

If you lose both the carbohydrates and the ketones, you end up [feeling] completely out of energy … We are very careful when people are down below 20 on their BMI, especially the ones 18 or below. We want to be very careful to make sure to cycle them [in and out of ketosis] once or twice a week …

These are the ones where, often, exogenous ketones can be very helpful early on … Measure your ketones. It’s simple to do. We want to get you into, ultimately, the 1.5 to 4.0 millimolar [range for] betahydroxybutyrate. That is the goal.”

So, to recap, while dementia patients with excess weight tend to respond favorably to cyclical fasting, at least initially, underweight patients may experience cognitive decline, as they’re simply too underweight to produce ketones in response to the fasting. For those who are underweight, Bredesen recommends using a ketone supplement such as medium-chain triglycerides (MCT) oil.

If that doesn’t bring you into the desired ketone level (1.5 to 4.0 mmol), or if it’s adversely affecting your low-density lipoprotein (LDL) particle number, he might recommend exogenous ketones — either ketone esters or salts. “We’d like to look at your LDL particle number and use that to titrate, to make sure that your LDL particle number is not too high,” he says.

To test your ketones, I recommend KetoCoachX.12 It’s one of the least expensive testing devices on the market right now. Another good one is KetoMojo. KetoCoach, however, is less expensive, the strips are individually packed and the device is about half as thick as KetoMojo’s, making it easier to travel with.

Nutritional ketosis, in which your body produces endogenous ketones (water-soluble fats), is important for all neurodegenerative diseases, but it’s not a complete cure-all. Bredesen explains:

“What we’ve come to realize from the research over the years is that neurodegenerative diseases, whether Alzheimer’s … macular degeneration … Lewy body, Parkinson’s or ALS, they all have one thing in common. They are related to specific subdomains of the nervous system.

Each of these has a unique requirement for nutrients, hormones, trophic factors, et cetera … In each case, there is a mismatch between the supply and the demand. For most of your life, you’re keeping up with that demand. With all of these diseases, you have a repeated or a chronic mismatch between the support and the requirement.

In Parkinson’s disease, it’s quite clear. You can create Parkinson’s disease simply by inhibiting mitochondrial Complex I. That specific subdomain of motor modulation, which is what Parkinson’s is all about, is the thing that is the most sensitive to reductions in mitochondrial Complex I support.

Therefore, when people have this, you need to bring the supply back in line with the demand. A critical way to do that is to supply the appropriate ketosis — the appropriate energy.

Now, if the person is continuing to be exposed to whatever chemicals are inhibiting Complex I — and it’s typically … mold-related biotoxins or organic toxins such as paraquat or glyphosate — as long as these are ongoing, you’re going to get very temporary relief.

The goal here is both to get rid of what is inhibiting Complex I and to flood the system, to help the system by giving appropriate support for the energetics … With Alzheimer’s, we’re really talking about a mismatch in trophic support. You’ve got this ongoing need as you’re making neuroplasticity.”

Although I am not ApoE4-positive, I prefer fasting for 16 hours a day, essentially narrowing my eating window to just four to six hours. I also make sure to eat my last meal three to six hours before bedtime. One of the reasons for this advice is because avoiding late-night eating will increase your nicotinamide adenine dinucleotide (NAD+) levels, which are important for a variety of bodily functions.

Importantly, it will also reduce nicotinamide adenine dinucleotide phosphate (NADPH), which is essentially the true cellular battery of your cell and has the reductive potential to recharge your antioxidants. The largest consumer of NADPH is the creation of fatty acids.

If you’re eating close to bedtime, then you’re not going to be able to use the NADPH to burn those calories as energy. Instead, they must be stored some way. To store them, you have to create fat, so you’re basically radically lowering your NADPH levels when you eat late at night because they are being consumed to store your extra calories by creating fat.

Bredesen’s protocol includes this strategy as well. He calls his approach “KetoFlex 12/3,” because it generates mild ketosis and is flexible diet-wise. It can be done whether you’re a vegetarian or not. The 12/3 stands for a 12-hour minimum fast each day, and eating the last meal three hours before bedtime.

Certain supplements, including berberine, resveratrol, curcumin, quercetin and fisetin also boost autophagy, and can be used in addition to the nutritional timing. Bredesen explains:

“Sirtuin-1 (SIRT1) was identified as a critical molecule, both for longevity and has been studied extensively for its effects on longevity, but also for its effects on Alzheimer’s disease …

ApoE4 actually enters the nucleus and downregulates the production of this critical molecule, so you can see one of its many effects on Alzheimer’s disease. Well, when SIRT1 is made, it is actually made in an autoinhibitory fashion. It’s just like having a gun in a holster. It’s not active … NAD activates the SIRT1.

So does resveratrol. This is why people take resveratrol [or] nicotinamide riboside. These are both activating this program, which is moving you from … more of a pro-inflammatory approach to a longevity approach — a change in your metabolic pattern. That includes activating things like autophagy and also having an anti-Alzheimer’s and a pro-longevity effect …

[Q]uercetin also has an interesting impact on senescent cells … I think that that’s going to turn out to be an important way to impact a number of age-related conditions, including neurodegeneration.”

The drawback, and the reason you cannot rely on supplements alone, is that the bioabsorption of these polyphenols, like quercetin for example, is quite low. Oftentimes, you cannot absorb enough to get the full benefits.

There’s also convincing evidence showing electromagnetic field exposures (EMFs) such as that from cellphones and Wi-Fi play an important role. Bredesen agrees, and recommends his patients limit such exposures. In summary, EMFs activate your voltage-gated calcium channels, allowing the release of excess nitric oxide and superoxide in the cell, resulting in the creation of peroxynitrite.

Peroxynitrite causes similar damage to your DNA as ionizing radiation. It also damages your stem cells, mitochondria, proteins and cell membranes. Poly-ADP ribose polymerase helps repair DNA damage by extracting an adenosine diphosphate (ADP) molecule from NAD. Approximately 100 to 150 NAD are required to repair a single DNA break.

While this process works quite well, problems arise when continuous DNA damage requiring continuous PARP activation occurs, as this ends up decimating your NAD+ level. Bredesen adds:

“This is a critical area. The big problem we’ve had with this so far is that we can measure your NF-κB activation; we can measure your status of hormones, nutrients, magnesium, on and on and on. Typically, with our approach, we measure 150 different variables.

There is no simple way to measure the effect of EMF on a given person’s nervous system. I look forward to the day when we can do a test and say, ‘Aha. This person has 27.2 on their effects on their voltage-gated calcium channels because of EMFs.’ Because then we’ll really be able to alter that.

For now, the best we can say is — just as we go after biotoxins and chemotoxins — [EMF] is a physical toxin. The best we can say is, ‘Minimize that to the extent you can.’ You can certainly measure the exposure. We just don’t have a good way yet to measure its effect on your brain.”

There’s no decline in sight for Alzheimer’s, at least in the foreseeable future, so it would behoove most people to just assume you’re headed for it and take action now, regardless of your age, to prevent it. When it comes to Alzheimer’s, prevention is surely far easier than trying to treat it once it has set in. As noted by Bredesen:

“This is all about prevention and early reversal. Those are the people where we see virtually 100% response. This is why I think there needs to be a global effort to decrease the burden of dementia. We’re just now starting a clinical trial. We’ve been trying to get institutional review board (IRB) approval for years …

It has finally been approved, so we’re starting a trial with Dr. Ann Hathaway, Dr. Deborah Gordon and Dr. Kat Toups, who are all seeing patients. We’re very excited to see what the trial will show with this approach. Because certainly, anecdotally, we’re hearing it all the time.

As you mentioned, we just published a paper a few months ago on 100 patients who showed documented improvement … I’m convinced we could, today, if everyone got an appropriate prevention, make this a very rare disease.”

Bredesen’s case report13 is open access, so you can download and read the full study. His book, “The End of Alzheimer’s: The First Program to Prevent and Reverse Cognitive Decline,” also provides the details, and would be a valuable reference in anyone’s health library.

You can also learn more about Bredesen and his work by following him on Facebook, Twitter or visit his website, drbredesen.com. Last but not least, read his book, “The First Survivors of Alzheimer’s: How Patients Recovered Life and Hope in Their Own Words,” which features first-person accounts from patients diagnosed with Alzheimer’s who beat the odds and improved.

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