Archive for the ‘Alzheimer’s’ Category

CoQ10: What is It & Do You Need It?

CoQ10: What is it & Do You Need It?

By Holtdorf Medical Group

Do You Need CoQ10?

As the body ages, many systems and functions begin to decline and deteriorate. Common problems associated with aging include reduced energy, cognitive troubles, fertility issues, and of course greater risk of cardiovascular and neurodegenerative disease. Many assume that these difficulties are an unavoidable part of getting older. However, this may not be the case.

Is CoQ10 the Answer?

CoQ10 is a substance that naturally occurs in the body and is an important part of healthy bodily function. As we get older, levels of CoQ10 decline, which can contribute to various difficulties and health issues associated with aging. By maintaining or restoring appropriate levels of CoQ10 through effective supplementation, you may be able to significantly reduce the risk of age-related issues and support long-term wellness. CoQ10 influences many bodily functions but perhaps its greatest impact is on energy production. CoQ10 is stored in mitochondria, which are responsible for producing cellular energy in the form of adenosine triphosphate (ATP). ATP is the most widely utilized form of energy throughout the body. CoQ10 is necessary for ATP production. Therefore, without an adequate supply of CoQ10, cells can experience a cellular energy deficit resulting in widespread dysfunction. Issues associated with poor CoQ10 levels include heart disease, fibromyalgia, neurological and neurodegenerative disorders, diabetes, muscle conditions, cancer, and others.

Getting the CoQ10 Your Body Needs

Most individuals are able to acquire enough CoQ10 to maintain healthy bodily functions. However, tissue levels of CoQ10 decline with age. Other factors including nutrient deficiencies, genetic issues, mitochondrial disease, medications such as statins, and oxidative stress can further contribute to CoQ10 deficiency. Despite CoQ10 being found in common foods including beef, chicken, fish, and whole grains, there are many individuals who suffer from a deficiency. Part of the reason may be that CoQ10 has a low absorption rate when acquired from food sources. Because of this, an individual may have poor CoQ10 levels even if they consume a high volume of foods containing CoQ10. An effective and safe solution to poor CoQ10 acquisition is supplementing with a product such as HoltraCeuticals’ CoQ10 Plus. CoQ10 Plus is a supplement that provides high-quality and easily absorbed CoQ10.

HoltraCeuticals developed the supplement with the goal of improving individual wellness and longevity. To achieve this goal, specific elements have been included in CoQ10 Plus. CoQ10 Plus utilizes soft gel capsules that improve absorption, meaning that the CoQ10 contained within is more easily utilized by the body. CoQ10 Plus also contains Vitamin E, which has been shown to work synergistically with CoQ10. Studies show that the combination of these two substances provides better absorption and greater antioxidant action than if they were to be taken separately. Greater absorption and quality ingredients make CoQ10 Plus an exceptional supplement that can be used to support long-term wellness.

Benefits of Supplementing with CoQ10

Supplementing with CoQ10 provides a wide range of benefits that support sustained wellness and longevity. Its influence can be seen in areas including metabolic activity, antioxidant action, and safeguarding heart health. Below are several areas that are benefited by supplementing with CoQ10.

Combatting Free Radical Damage

Free radicals cause oxidative damage, which is a primary contributor to issues and disorders commonly associated with aging. An excess of free radicals can cause oxidative damage, which weakens cell membranes, damages DNA, and disrupts cell function. When maintained at the appropriate volume, CoQ10 within mitochondria protects against free radicals and other agents of oxidation. Therefore, supplementing with CoQ10 may provide protection against age-related illness and dysfunction.

Protecting Against Neurological Disorders

Neurodegenerative diseases such as Alzheimer’s and Parkinson’s are triggered by a lack of energy in brain cells. As mentioned above, mitochondria are the primary producers of cellular energy. Mitochondrial function declines with age due in part to oxidation. In addition to cellular damage, oxidation triggers the production of harmful substances that disrupt neurological function. Such disruption can cause a reduction in memory, motor skills, and cognitive ability. Supplementing with CoQ10 helps protect mitochondrial function and may reduce the production of neurological-disrupting substances, thereby limiting the progression of neurodegenerative disease.

Reducing Risk of Heart Disease

A major contributor to heart disease is oxidative damage and inflammation in veins and arteries. Once these elements reach a certain threshold, they can inhibit the heart’s ability to contract and relax. This results in heart failure or stroke. There is a notable concentration of CoQ10 in the cardiovascular muscle that helps prevent oxidation and inflammation that can lead to cardiovascular episodes. Supplementing with CoQ10 can help protect heart health by combating oxidative and inflammatory agents in veins, arteries, and heart muscles.

Combatting Infertility

Supplementing with CoQ10 may be able to resolve infertility issues in both men and women. In men, sperm count and quality declines with age, due primarily to oxidative damage. Similarly, women experience a decline in egg production and quality as oxidative damage accrues. Regardless of gender, the antioxidant properties of CoQ10 help protect against oxidation that contributes to infertility.

Reducing Headaches & Migraines

Those who are deficient in CoQ10 frequently experience headaches and migraines. Poor mitochondrial activity can increase cellular uptake of calcium resulting in greater production of free radicals and reduced antioxidant activity. When the mitochondria in brain cells become damaged or disrupted due to increased oxidation, the brain becomes starved for energy. An energy deficit in the brain can trigger headaches and migraines. As a guardian of mitochondrial activity, CoQ10 safeguards cellular activity, limits inflammation, and supports energy production in the brain. The protective action of CoQ10 may help limit cognitive difficulties and reduce the occurrence of migraines or other head pains.

Support Sustained Wellness with CoQ10 Plus

Aging is a major concern for many people. Fortunately, it is possible to combat the oxidative damage that causes the many troubles associated with growing older. CoQ10 is a critical precursor enzyme produced by the body that supports and protects many systems including the heart and brain. Ensuring that the body has an adequate supply of this important substance protects against incremental oxidative damage and promotes long term wellness. Safeguard your future health by supplementing with a high-quality CoQ10 supplement such as HoltraCeuticals’ CoQ10 Plus

Holtorf Medical GroupThe Holtorf Medical Group specializes in optimizing quality of life and being medical detectives to uncover the underlying cause of symptoms, rather than just prescribing medications to cover-up the symptoms. We are experts in natural, prescription bioidentical hormone replacement and optimization, complex endocrine dysfunction, fibromyalgia, chronic fatigue syndrome and Lyme disease. We’ve dedicated our practice to providing you the best in evidenced-based, integrative medicine that’s not only safe and effective, but provides measurable results.

Chlamydia & Alzheimer’s

Circulating Chlamydia Trachomatis Antigens in Subjects With Alzheimer’s Disease



Background/Aim: Chlamydia pneumoniae (C. pneumoniae) is implicated in the pathogenesis of Alzheimer’s disease (AD). Chlamydial elementary and reticulate bodies have been identified in tissues from afflicted AD brain regions by electron and immunoelectron microscopy, whereas similar tests of non-AD brains were negative for the bacterium. Studies in mice have shown that C. pneumoniae can rapidly penetrate the central nervous system by entering glia and causing beta amyloid deposition via the nerves between the nasal cavity and the brain, which serve as invasion pathways.

Materials and Methods: We used data from the UK Biobank (UKBB) to assess the relationship of chlamydia and AD. Circulating C. pneumoniae antigen measurements were not available, but UKBB data field 23037 held measurements of PorB antigen for Chlamydia trachomatis (C. trachomatis). We used C. trachomatis as a surrogate for C. pneumoniae since serum cross-reactivity to C. trachomatis and C. pneumoniae antigens occurs in patients with documented infection and in healthy children as revealed by microimmunofluorescence and immunoblotting techniques. Single nucleotide polymorphism (SNP) data for rs429358 and rs7412 were used to impute ApoE genotypes.

Results: PorB antigen levels for C. trachomatis were significantly higher in subjects with AD (p=0.007). PorB antigen levels were not related to ApoE genotype (e3e3, e3e4, e4e4) p=0.783. To control for the effects of age, sex, educational level, and apoE genotype, logistic regression analysis was performed. AD was the dependent variable. Independent variables were sqrt PorB antigen for C. trachomatis, age, sex, educational level, apoE genotype. AD odds ratio (OR) increased 1.156 for each unit increase of sqrt PorB antigen for C. trachomatis and the effect was significant (p=0.004).

Conclusion: PorB antigens for C. trachomatis being significantly higher in subjects with AD, corroborates previous studies demonstrating that C. pneumoniae inflammation appears to play a role in AD development. AD may result from the reactivation of embryologic processes and pathways silenced at birth. A trigger for the reactivation may be bacterial or viral infections. Further studies are warranted.


Chlamydia pneumoniae can infect the central nervous system via the olfactory and trigeminal nerves and contributes to Alzheimer’s disease risk


Chlamydia pneumoniae is a respiratory tract pathogen but can also infect the central nervous system (CNS). Recently, the link between C. pneumoniae CNS infection and late-onset dementia has become increasingly evident. In mice, CNS infection has been shown to occur weeks to months after intranasal inoculation. By isolating live C. pneumoniae from tissues and using immunohistochemistry, we show that C. pneumoniae can infect the olfactory and trigeminal nerves, olfactory bulb and brain within 72 h in mice. C. pneumoniae infection also resulted in dysregulation of key pathways involved in Alzheimer’s disease pathogenesis at 7 and 28 days after inoculation. Interestingly, amyloid beta accumulations were also detected adjacent to the C. pneumoniae inclusions in the olfactory system. Furthermore, injury to the nasal epithelium resulted in increased peripheral nerve and olfactory bulb infection, but did not alter general CNS infection. In vitro, C. pneumoniae was able to infect peripheral nerve and CNS glia.

In summary, the nerves extending between the nasal cavity and the brain constitute invasion paths by which C. pneumoniae can rapidly invade the CNS likely by surviving in glia and leading to Aβ deposition.


For more:

Some Scientists Now Say Alzheimer’s is an Autoimmune Disease But Ignore the Root Cause to Market New Drugs & One Doctor’s Program to Reverse Cognitive Decline

Scientists Say Alzheimer’s Is an Autoimmune Disease, Not Result of Amyloid Plaque

Nov 16 2022

Not long ago, some Canadian scientists clearly put forward a different explanation for the cause of Alzheimer’s disease—they suggested that Alzheimer’s may be an autoimmune disease.

Alzheimer’s May Be an Autoimmune Disease

According to statistics from the World Health Organization (WHO), there are about 50 million dementia patients in the world, with 10 million new cases every year; it means that about one person is diagnosed every three seconds.

Over the years, the “amyloid hypothesis” has been widely accepted among various theories of the cause of Alzheimer’s disease, but it has also been controversial as some phenomena in patients with Alzheimer’s do not fit the hypothesis. For example, people with amyloid plaques in their brains may not have Alzheimer’s. Besides, there are still many uncertainties about the clinical benefit of drugs targeting the elimination of amyloid beta.

Recently, Canadian scientists published a post saying that the amyloid beta found in the brains of Alzheimer’s patients is actually a substance released by the body’s immune response. They further speculate that Alzheimer’s is an autoimmune disease centered on the brain.  (See link for article)



Lyme/MSIDS patients should already be familiar with this refrain because it’s exactly what they say causes chronic/persistent Lyme disease – that old, wonky immune system strikes again.

The problem with this is it completely bypasses the root cause that can be treated, thereby helping that wonky immune system and perhaps even preventing the wonkiness from happening. In my opinion, which has plenty of research to back it up, infections are to blame for both diseases which means all the immune modulating drugs on the planet are not going to fix it. Don’t get me wrong, immunomodulators have their place and can really help with symptoms, but again, won’t deal with the root issue: infections.

You would think researchers would learn from past mistakes, but alas, the same drivers of error (money and power) are still at play.

Rather than researching diseases for true answers to alleviate patient misery, diseases are studied as potential income earners with Big Pharma to create the next hot drug or lucrative “vaccine.”  The same tune continues to be played on the same harp.

So rather than deal with the root of these diseases (infections) in which cheap, already existing antimicrobials can be repurposed, scientists carefully craft it to “autoimmune” diseases where sexier, more expensive, new drugs can be created – of which they will patent and profit from.  Sound familiar?

While I’m glad they finally quit blaming amyloid beta as the culprit, they are still far from real answers that will help real people.


Case Study Reveals How Cognitive Decline Can Be Reversed

Analysis by Dr. Joseph Mercola
Nov. 20, 2022


  • 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.2,3

While the U.S. Centers for Disease Control and Prevention lists the disease as the seventh leading cause of death in the U.S.,4,5 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

100-Patient Case Report Sheds Light on Treatment Options

One of Bredesen’s publications is a case report9,10 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.”

Alzheimer’s Is a Protective Response to Inflammation

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

The Protein Refolding Process Is Impaired in Alzheimer’s

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.”

The Link Between Protein Folding and Cell Death

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.

The Case for Cyclical Fasting

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.”

Test Your Ketones

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.

Energy Demands Are Not Met in Neurodegenerative Diseases

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.”

Why Late-Night Eating Is Ill Advised

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.

Limit Electromagnetic Field Exposures

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.”

More Information

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 FacebookTwitter or visit his website, 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.

Sources and References

Ahead of the Curve Interview With Dr. Alan McDonald  Interview Here (Approx. 2 hours 13 min)

Episode 300: Ahead of the Curve – an interview with Dr. Alan McDonald

Audio Player

Dr. Alan MacDonald is an Ivy League educated Medical Doctor who worked as a hospital pathologist in the eastern Long Island, New York area at the outset of the modern Lyme disease pandemic. He and his pioneering work were first featured on episode 171 of the Tick Boot Camp Podcast.

In this comprehensive interview, Dr. MacDonald discusses his groundbreaking and yet to be published research findings on topics such as the Lyme disease connection to suicide, brain cancer, Leukemia, dementia, Alzheimer’s disease, and Parkinson’s disease, in addition to how acute Lyme disease disrupts liver function and why and how Lyme disease testing is flawed.

PS you can also view an exclusive Tick Boot Camp presentation created by Dr. MacDonald with photos of Lyme under a microscope and descriptions highlighting the various topics discussed in this interview

Check out his GoFundMe page  to help him continue his groundbreaking work.

McDonald has truly done ground-breaking work but has been vilified by many of his own colleagues who seemingly can’t think outside the box or accept new information. Go here to watch other videos where he shows parasitosis (Neural Larval Migrans) within MS patients as he discovered nematode worms, eggs and both larval forms and mating adult pairs present in the brain and spinal fluid of MS patients.  These videos are circa 2016 and are revolutionary yet are quietly collecting dust and simply ignored in mainstream research.

At 5 min and 51 sec into the 2016 London lecture, you will see the discovery of worms in the brain and spinal fluid of EVERY MS patient tested.  He also explains the difficulty in finding these worms as they move from one area to another.

These worms cause inflammation and damage in the CNS on their own but also infect us with Lyme and other infections. 

CLICK HERE to view the research poster of Dr. MacDonald’s discovery of filarial (small roundworms) in the central nervous system of MS patients at their time of death.

CLICK HERE to view the research poster of Dr. MacDonald’s discovery of tapeworm larva and developing juvenile tapeworms in the central nervous system of MS patients at their time of death.

What this means regarding treatment, is that if you are one of those patients with these worms, you need to disable/kill the worms to get to the borrelia/MSIDS inside them.  Anthelminitics such as ivermectin and Albenza are used to kill worms as well as natural medicines; however, this must be done under the supervision of a doctor as the inflammation and herxheimer reactions can be very great. 

For some patients, addressing worms is a game-changer.  Consider talking to your LLMD about it.

For more:

Bb Brain Infection & Lewy Body Dementia

Borrelia burgdorferi spirochetal brain infection and Lewy Body Dementia

Carl Tuttle

Hudson, NH, United States

Aug 2, 2022 — 

Latest email to the Federal Tick-Borne Disease Working Group…

———- Original Message ———-
To: “” <>
Cc: (All members of the TBDWG)
Date: 08/02/2022 9:40 AM
Subject: Borrelia burgdorferi spirochetal brain infection and Lewy Body Dementia

To the Tick-Borne Disease Working Group,

Please see the attached publication from Pathologist Alan MacDonald who has discovered borrelia burgdorferi spirochetal brain infection and Lewy Body Dementia.

Microbial DNA globular liquid crystal like deposits inside Lewy bodies in four Lewy dementia patients

Alan B MacDonald


Four autopsy brains demonstrated concurrent evidence of Diffuse Cortical Lewy Body Dementia and active Lyme neuroborreliosis in adjacent brain sites. Lewy bodies In DCLBD contain microbial DNA. Alpha Synuclein proteins, which intrinsically bind to human nuclear DNA also bind to microbial DNA deposits inside Lewy bodies in the cytoplasmic compartment of diseased neurons. This is the first report of an association between spirochetal brain infection and Lewy Body Dementia.

This is just one additional piece of evidence as identified in my Verbal Public Comment that there has been a 30yr deliberate mishandling/avoidance of Lyme disease while refusing to recognize its severity.

Now would be a good time to review how the deception was pulled off using taxpayer dollars through a grant issued by the CDC; an open checkbook handed to Gary Wormser to produce his junk science focusing on the acute stage of disease with bulls-eye rash and early treatment under Grant# RO1 CK 000152

2019 Communication Sent to the TBDWG:

———- Original Message ———-
Cc:,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,,, Alex.Azar@HHS.GOV,,,,,,,,,,,,,,,,,
Date: February 9, 2019 at 9:42 AM

Subject: Efficacy of a 14-day course of amoxicillin for patients with erythema migrans


Diagnostic Microbiology and Infectious Disease

Efficacy of a 14-day course of amoxicillin for patients with erythema migrans.

Wormser GP1, Brady KC2, Cho MS2, Scavarda CA2, McKenna D2.


“….findings provide additional evidence that a 14-day course of 500 mg amoxicillin given 3 times per day is highly effective therapy for patients with early Lyme disease.”

Feb 9, 2019

Division of Infectious Diseases,
New York Medical College,
Valhalla, NY 10595
Attn: Gary P. Wormser, MD

Dr. Wormser,

Once again, as previously stated in the email below; “Your fixation on the acute stage of disease [with bulls-eye rash] after early treatment has done nothing to advance our understanding of how Lyme disease disables its victim.”

Early treatment of strep throat prevents patients from advancing to rheumatic fever which as you know causes irreversible heart damage. If we focused on the acute stage of strep we would never have realized that missed early treatment caused serious life-altering/life-threatening health consequences.

-Ignoring the late stage horribly disabled Lyme population which could total in the millions worldwide.

I noticed that your manuscript did not include the following reference:

July 2017- In Vitro Susceptibility of the Relapsing-Fever Spirochete Borrelia miyamotoi to Antimicrobial Agents.


“We were able to show that both B. miyamotoi strains and B. hermsii demonstrated greater susceptibility to doxycycline and azithromycin, equal susceptibility to ceftriaxone and proved to be resistant to amoxicillin in vitro as compared to the B. burgdorferi s.l. isolates.” 

Your retirement Dr. Wormser is highy, highly anticipated.

Carl Tuttle
Lyme Endemic Hudson, NH

NOTE: Wormser’s study was funded directly from the US Centers for Disease Control

Funding: RO1 CK 000152 which appears to be an open checkbook for his junk science.

(Wasteful taxpayer spending)

Cc: Tick Borne Disease Working Group

Assistant Secretary for Health, ADM Brett P. Giroir, M.D.

On January 4, 2019 at 10:48 AM CARL TUTTLE <> wrote:


Shapiro ED, Wormser GP. Lyme disease in 2018: what is new (and what is not).

Jan 4, 2019

Division of Infectious Diseases,
New York Medical College,
Valhalla, NY 10595
Attn: Gary P. Wormser, MD

Dr. Wormser,

In reference to your response to my letter to the Editor published in the December 18th issue of JAMA, it would appear that you and your coauthor Dr. Shapiro conveniently ignored my question highlighted below:

Excerpt from my letter to the editor:

Controversies About Lyme Disease

-Carl Tuttle

“It is well known that untreated streptococcal pharyngitis can progress to rheumatic fever, causing irreversible heart damage. Untreated syphilis leads to progressive disability and dementia, and untreated HIV infection progresses to AIDS with significant disability and death. What happens to the patient with Lyme disease who goes months, years or decades before diagnosis because of a false negative serological test?”

Untreated Lyme is destroying lives, ending careers while leaving the patient in financial ruin as reported by the disabled Lyme community for the past three decades. The absence of a bulls-eye rash after tick bite allows patients to progress to severe neurological disease instead of obtaining a prompt diagnosis and early treatment.

I would like to call attention to the following quote taken from an interview with Professor Willy Burgdorfer, the discoverer of the Lyme disease spirochete:

“The controversy in Lyme disease research is a shameful affair. I say that because the whole thing is politically tainted. Money goes to people that have for the past thirty years produced the same thing. Nothing.  – Willy Burgdorfer

Source: (Live interview)

Prof. Willy Burgdorfer Talks About Lyme Disease

Your fixation on the acute stage of disease after early treatment Dr. Wormser has done nothing to advance our understanding of how Lyme disease disables its victim.

For example:

Subjective symptoms after treatment of early Lyme disease.

Gary Wormser, New York Medical College

(Financed by the U.S. Centers for Disease Control)


“At 12 months after enrollment, only 5 (2.2%) of 230 evaluable patients reported new or increased symptoms, and in none of the patients were these symptoms of sufficient severity to be functionally disabling”


Summary of Wormser’s study: Anyone experiencing symptoms after the one-size-fits-all treatment approach is just experiencing nothing more than the “aches and pains of daily living.”

So basically Wormser’s results are then assumed to apply to the entire patient population; in other words, Lyme is no big deal which has wrongly influenced our nation’s response to this serious life-altering health threat. The research into how Lyme disables should have been completed by now but the misclassification of Lyme as a simple nuisance disease (hard to catch and easily treated) has paralyzed the response to this runaway plague.

Many infections as I continue to point out evolve into an entirely different and serious life-altering/life-threatening disease when left untreated.

Post Treatment Lyme Disease Syndrome (PTLDS) after early treatment and untreated Lyme of months, years or decades are two entirely different disease states; the latter being ignored for three decades. Patients who have had a prolonged exposure to the pathogen are almost always incapacitated.

Purposely avoiding the advanced stage of disease hides the horribly disabled and anyone unable to see this is somewhat naive.

So I ask the question Dr. Wormser, What is the motivation for downplaying the severity of Lyme disease while ignoring patient outcry for thirty years?

A prompt response to this inquiry is requested.

Please hit Reply-All as I have carbon copied the Tick Borne Disease Working Group and Assistant Secretary for Health, ADM Brett P. Giroir, M.D.

Carl Tuttle
Lyme Endemic Hudson, NH


For more: