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Posted by: admin | Posted on: July 30, 2024

Estrogen and Dementia: Challenging Conventional Wisdom

Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/07/29/estrogen-and-dementia.aspx

Analysis by Dr. Joseph Mercola July 29, 2024

STORY AT-A-GLANCE

A new study in JAMA Neurology challenges the long-held belief that estrogen protects against dementia in women. The research found that pure estrogen receptor antagonists and aromatase inhibitors were associated with a lower risk of dementia across women’s lifespans
This study contradicts previous research suggesting estrogen’s protective effects on the brain, particularly in post-menopausal women
The findings imply that other substances with anti-estrogenic effects, such as progesterone and certain vitamins, might also protect against dementia
The medical establishment’s response to this study has been mixed, with some attempts to misrepresent or downplay its implications
Natural anti-estrogenic approaches, including diet, exercise, and progesterone supplementation, may offer potential strategies for reducing dementia risk

For decades, mainstream medicine has promoted the idea that estrogen is protective for the brain, particularly in post-menopausal women. The conventional wisdom has been that the increased risk of dementia in older women is due to the “deficiency” of estrogen that occurs during menopause. However, a groundbreaking new study published in JAMA Neurology challenges this long-held belief, providing compelling evidence that blocking estrogen may lower the risk of dementia.¹

Research Causing a Paradigm Shift

This recent study is perhaps the most damaging piece of evidence I’ve encountered in the last five years that contradicts the claim that estrogen protects the brain. The research, published in one of the most prestigious medical journals, found that using pure estrogen receptor antagonists or aromatase inhibitors was associated with a lower risk of developing dementia across the entire expected female lifespan.

What makes this study particularly significant is its use of “pure” anti-estrogen drugs. Previous studies showing protective effects against dementia often used selective estrogen receptor modulators (SERMs) like clomiphene, tamoxifen, or raloxifene. These drugs have anti-estrogenic effects in some tissues but are potent estrogens in others.

This dual nature allowed the medical establishment to explain away the protective effects as actually confirming the “benefit” of estrogen for the brain, since SERMs can be estrogenic in brain tissue.

However, the current study leaves no room for such interpretations. It examined the effects of pure estrogen receptor antagonists like Faslodex (fulvestrant) and its nonsteroidal analog Elacestrant, as well as aromatase inhibitors like letrozole. These drugs are highly selective blockers of estrogen receptors with no other known major effects.

The fact that aromatase inhibitors, which reduce the body’s production of estrogen, also showed protective effects against dementia further solidifies the case against estrogen as a protective factor for brain health.

Rethinking Estrogen’s Role

These findings suggest that other substances with anti-estrogenic effects might also have protective effects against dementia. This includes:

Progesterone
Fat-soluble vitamins (A, D, E, K)
Aspirin
DHT (dihydrotestosterone)
Flavones and flavanones (apigenin, naringenin, chrysin, quercetin, luteolin)

The study’s results were particularly pronounced in patients under 75 years of age, indicating that anti-estrogenic interventions might be most effective when started earlier in life.

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The Medical Establishment’s Response

It will be interesting to see how the medical establishment responds to this study. Given its publication in JAMA, a highly respected journal, it will be difficult to dismiss outright. However, we’re already seeing some concerning trends in how the information is being presented and interpreted.

Nefarious Tactics in Reporting

1. Progesterone misrepresentation — Some popular press articles reporting on this study have attempted to implicate progesterone as a co-culprit with estrogen. They mention that the anti-estrogenic drugs in the study are used to treat breast cancers caused by “estrogen and progesterone.”

This misrepresentation could lead the public to believe that progesterone increases the risk of dementia or cancer, when in fact, the opposite is true. The drugs mentioned in the study target exclusively estrogen and estrogen-positive cancers, not progesterone-positive cancers. Moreover, progesterone itself acts as both an estrogen receptor antagonist and an aromatase inhibitor, potentially offering protection against dementia based on the study’s findings.

2. Misleading terminology — The study itself uses the term “hormone modulating therapy” (HMT) to describe the anti-estrogenic treatments. This vague terminology avoids stating that the therapy is purely estrogen-blocking in nature, unlike SERM drugs which have mixed effects. It also fails to clarify that the therapy targets solely estrogen, not progesterone.

These tactics appear to be attempts to twist the science to serve pharmaceutical interests and avoid stating the obvious conclusion based on the study’s findings: that estrogen may be a cause of dementia and Alzheimer’s, while anti-estrogenic therapy (including natural options like progesterone) may be protective and possibly even therapeutic for existing dementias.

A Critical Examination of the Estrogen Hypothesis

For years, the medical community has operated under the assumption that estrogen is beneficial for brain health, particularly in post-menopausal women. This belief has led to widespread use of hormone replacement therapy (HRT) and other estrogen-boosting interventions. However, this new study forces us to critically examine this hypothesis.

The idea that estrogen deficiency causes cognitive decline in older women has been based largely on observational studies and the timing of when women typically experience increased rates of dementia (post-menopause). However, correlation does not imply causation, and there are many other factors that change as women age that could contribute to cognitive decline.

Moreover, previous clinical trials of hormone replacement therapy have yielded mixed results regarding cognitive function and dementia risk. The Women’s Health Initiative Memory Study,² for instance, found that combined estrogen-progestin therapy actually increased the risk of dementia in postmenopausal women.

The current study provides strong evidence that blocking estrogen or reducing its production may be protective against dementia. This suggests that estrogen might actually be harmful to brain health, rather than protective. If this is the case, it would explain why rates of dementia increase after menopause — not because of estrogen deficiency, but because of the cumulative effects of lifelong estrogen exposure.

Natural Anti-Estrogenic Approaches

If blocking estrogen indeed proves protective against dementia, it opens up a range of potential preventive strategies beyond pharmaceutical interventions. Many natural compounds and lifestyle factors can have anti-estrogenic effects:

1. Cruciferous vegetables — Compounds in broccoli, cauliflower, and Brussels sprouts can help metabolize estrogen.

2. Green tea — Contains compounds that may inhibit aromatase, the enzyme that produces estrogen.

3. Exercise — Regular physical activity can help balance hormones and may have anti-estrogenic effects.

4. Sleep — Proper sleep hygiene is crucial for hormonal balance, including estrogen regulation.

5. Stress management — Chronic stress can disrupt hormone balance. Techniques like meditation, yoga, or deep breathing can help.

6. Vitamin D — This fat-soluble vitamin has been shown to have anti-estrogenic effects.

7. Progesterone — As mentioned earlier, natural progesterone can act as an estrogen antagonist.

The Role of Progesterone

It’s worth delving deeper into the role of progesterone, given its potential importance in light of this study’s findings. Progesterone is often overlooked in discussions about hormones and brain health, with most of the focus being on estrogen. However, progesterone has several properties that make it potentially neuroprotective:

1. Estrogen receptor antagonist — Progesterone can block the effects of estrogen in certain tissues.

2. Aromatase inhibitor — It can reduce the production of estrogen in the body.

3. Neuroprotective effects — Independent of its effects on estrogen, progesterone has been shown to have direct neuroprotective properties in animal studies.

4. Anti-inflammatory — Progesterone can reduce inflammation in the brain, which is thought to play a role in the development of dementia.

Given these properties, and the findings of the current study, it’s possible that progesterone supplementation could be a natural way to potentially reduce dementia risk. However, more research is needed to confirm this hypothesis.

How to Use Progesterone

Before you consider using progesterone it is important to understand that it is not a magic bullet, and that you get the most benefit by implementing a Bioenergetic diet approach that allows you to effectively burn glucose as your primary fuel without backing up electrons in your mitochondria that reduces your energy production. My new book, “Cellular Health: The Unified Theory of All Disease for Ultimate Longevity and Joy” comes out very soon and covers this process in great detail.

Once you have dialed in your diet, an effective strategy that can help counteract estrogen excess is to take transmucosal progesterone (i.e., applied to your gums, not oral or transdermal), which is a natural estrogen antagonist. Progesterone is one of only four hormones I believe many adults can benefit from. (The other three are thyroid hormone T3, DHEA and pregnenolone.)

I do not recommend transdermal progesterone, as your skin expresses high levels of 5-alpha reductase enzyme, which causes a significant portion of the progesterone you’re taking to be irreversibly converted primarily into allopregnanolone and cannot be converted back into progesterone.

Ideal Way to Administer Progesterone

Please note that when progesterone is used transmucosally on your gums as I advise, the FDA believes that somehow converts it into a drug and prohibits any company from advising that on its label. This is why companies like Health Natura promote their progesterone products as topical only.

However, please understand that it is perfectly legal for any physician to recommend an off-label indication for a drug to their patient. In this case progesterone is a natural hormone and not a drug and is very safe even in high doses. This is unlike synthetic progesterone called progestins that are used by drug companies, but frequently, and incorrectly, referred.

Dr. Ray Peat has done the seminal work in progesterone and probably was the world’s greatest expert on progesterone. He wrote his Ph.D. on estrogen in 1982 and spent most of his professional career documenting the need to counteract the dangers of excess estrogen with low LA diets and transmucosal progesterone supplementation.

He determined that most solvents do not dissolve progesterone well and discovered that vitamin E is the best solvent to optimally provide progesterone in your tissue. Vitamin E also protects you against damage from LA. You just need to be very careful about which vitamin E you use as most supplemental vitamin E on the market is worse than worthless and will cause you harm not benefit.

It is imperative to avoid using any synthetic vitamin E (alpha tocopherol acetate — the acetate indicates that it’s synthetic). Natural vitamin E will be labeled “d alpha tocopherol.” This is the pure D isomer, which is what your body can use. There are also other vitamin E isomers, and you want the complete spectrum of tocopherols and tocotrienols, specifically the beta, gamma, and delta types, in the effective D isomer.

There are also other vitamin E isomers, and you want the complete spectrum of tocopherols and tocotrienols, specifically the beta, gamma, and delta types, in the effective D isomer. As an example of an ideal vitamin E you can look at the label on our vitamin E in our store. You can use any brand that has a similar label.

You can purchase pharmaceutical grade bioidentical progesterone as Progesterone Powder, Bioidentical Micronized Powder, 10 Grams for about $40 on many online stores like Amazon. That is nearly a year’s supply, depending on the dose you choose.

However, you will need to purchase some small stainless steel measuring spoons as you will need a 1/64 tsp which is 25 mg and a 1/32 tsp which is 50 mg. A normal dose is typically 25 to 50 mg and is taken 30 minutes before bed, as it has an anti-cortisol function and will increase GABA levels for a good night’s sleep.

Unfortunately, this vendor frequently runs out of product, and if that’s the case, then you can use Simply Progesterone by Health Natura. It’s premixed with vitamin E and MCT oil. Again, while Health Natura states that its product is for “topical use only,” I recommend applying it transmucosally, by rubbing it on your gums.

If you are a menstruating woman, you should take the progesterone during the luteal phase or the last half of your cycle, which can be determined by starting 10 days after the first day of your period and stopping the progesterone when your period starts.

If you are a male or non-menstruating woman you can take the progesterone every day for four to six months and then cycle off for one week. The best time of day to take progesterone is 30 minutes before bed as it has an anti-cortisol function and will increase GABA levels for a good night’s sleep.

This is what I have personally doing for over a year with very good results. I am a physician so do not have any problems doing this. If you aren’t a physician you should consult one before using this therapy, as transmucosal progesterone therapy requires a doctor’s prescription.

Implications for Current Medical Practices

If the findings of this study are corroborated by further research, it could have significant implications for current medical practices:

1. Hormone replacement therapy — The use of estrogen-based HRT for menopausal symptoms and osteoporosis prevention may need to be reconsidered, especially in women with a family history of dementia.

2. Breast cancer treatment — The potential cognitive benefits of anti-estrogen therapies used in breast cancer treatment could be an additional factor to consider when weighing treatment options.

3. Preventive strategies — Healthcare providers may need to start considering anti-estrogenic approaches as part of dementia prevention strategies, particularly in high-risk individuals.

4. Research focus — This study may shift the focus of dementia research towards investigating the potential harmful effects of estrogen on the brain, rather than its presumed protective effects.

Challenges and Controversies

Despite the strength of this study’s findings, it’s likely to face significant pushback from certain sectors of the medical community. The estrogen hypothesis has been deeply ingrained in medical thinking for decades, and paradigm shifts often face resistance.

Moreover, there are powerful financial interests at stake. The hormone replacement therapy industry is worth billions of dollars globally. A shift away from estrogen-based therapies could have significant economic implications.

There’s also the challenge of reconciling these findings with other known effects of estrogen. For instance, estrogen is known to have protective effects against osteoporosis. How do we balance the potential cognitive risks with other health considerations? These challenges underscore the need for more research in this area.

So, while this study provides compelling evidence, it’s just one piece of the puzzle. We need large-scale, long-term studies to fully understand the relationship between estrogen, anti-estrogen therapies, and cognitive health.

A Call for Open-Minded Inquiry

The findings of this study challenge long-held beliefs about estrogen and brain health. They suggest that our understanding of hormones and cognitive function may be more complex than previously thought.

As a medical professional and health advocate, I believe it’s crucial that we approach these findings with an open mind. We must be willing to question our assumptions and follow the evidence where it leads, even if it contradicts established beliefs.

For individuals concerned about cognitive health, these findings offer new avenues to explore. While it’s too early to make definitive recommendations based on this single study, it may be worth discussing anti-estrogenic strategies with your healthcare provider, especially if you have a family history of dementia.

Remember, hormonal balance is complex and individualized. What works for one person may not work for another. Always consult with a qualified healthcare professional before making significant changes to your health regimen.

As we move forward, it’s my hope that this study will stimulate further research into the relationship between hormones and brain health. By continuing to ask questions and challenge our assumptions, we can work towards a better understanding of how to prevent and treat devastating conditions like dementia and Alzheimer’s disease.

In the meantime, focusing on overall brain health through a balanced diet, regular exercise, stress management, and cognitive stimulation remains a prudent approach for everyone. As we await further developments in this exciting area of research, these lifestyle factors continue to be our best defense against cognitive decline.

– Sources and References

Posted in Alzheimer's, Dementia, Estrogen, Hormones, Supplements, Vitamins | One Comment »

Posted by: admin | Posted on: July 5, 2024

Autopsies Link 73.9% of Post-Jab Deaths to the Shot

Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/07/05/post-covid-19-vaccination-deaths.aspx

Analysis by Dr. Joseph Mercola July 05, 2024

STORY AT-A-GLANCE

A peer-reviewed study in Forensic Science International found that 73.9% of post-COVID-19 vaccination deaths were directly caused by or significantly contributed to by the injections
The study, initially censored by The Lancet, analyzed 325 autopsy cases and found cardiovascular issues were the most common cause of death, followed by blood and respiratory problems
Researchers suggest the spike protein in COVID-19 vaccines may be responsible for side effects, potentially causing inflammation and clotting in various tissues and organs
Another study in South Korea found increased incidences of mild cognitive impairment and Alzheimer’s disease within three months of COVID-19 vaccination, particularly with mRNA vaccines
The article mentions censorship of research critical of COVID-19 vaccines and suggests seeking help from organizations like FLCCC for those experiencing post-vaccination injuries

A bombshell study that The Lancet¹ pulled within 24 hours is finally seeing the light of day. Now published in the peer-reviewed Forensic Science International journal, the systematic review of autopsy findings in deaths after COVID-19 shots revealed 73.9% “were directly due to or significantly contributed to” by the injections.² Canadian oncologist and cancer researcher Dr. William Makis posted on X:³

“This is a victory of SCIENCE over CENSORSHIP!! Incredible perseverance by first author Nicolas Hulscher who didn’t give up after LANCET pulled our paper within 24 hours after 100,000s of downloads for no legitimate reason. Big pharma put the squeeze on @TheLancet but has failed to stop us.

Our paper was delayed by one year, and those actions of CENSORSHIP and CANCELLATION led to many deaths that could have been prevented. This paper could be a game changer.”

High Likelihood of ‘Causal Link’ Between COVID-19 Shots and Death

Researchers including Makis, cardiologist, internist and epidemiologist Dr. Peter McCullough and Nicolas Hulscher, an epidemiologist with the University of Michigan School of Public Health, searched for all published autopsy and necropsy reports relating to COVID-19 shots through May 18, 2023.

Their systematic review included 44 papers with 325 autopsy cases and one necropsy case, which is an autopsy performed on an animal. The average age of the people in these reports was 70.4 years. Most often, the cardiovascular system was involved in the death, followed by hematological issues, or blood problems, and respiratory issues. In 21 of the cases, three or more organ systems were involved.

The mean time from vaccination to death was 14.3 days, but most deaths occurred within a week of the last shot. Three doctors who are experts in figuring out causes of death and studying diseases looked at each case separately.

They carefully examined all the information available for each person who died and concluded that in 73.9% of the cases, COVID-19 shots either directly caused or played a significant role in the person’s death. Among them, the primary causes of death were:⁴

Sudden cardiac death (35%)	Pulmonary embolism (12.5%)
Myocardial infarction (12%)	Vaccine-induced immune thrombotic thrombocytopenia (VITT) (7.9%)
Myocarditis (7.1%)	Multisystem inflammatory syndrome (4.6%)
Cerebral hemorrhage (3.8%)

“The consistency seen among cases in this review with known COVID-19 vaccine mechanisms of injury and death, coupled with autopsy confirmation by physician adjudication, suggests there is a high likelihood of a causal link between COVID-19 vaccines and death,” the researchers concluded.⁵

What Was The Lancet Trying to Hide? ‘Lots and Lots of Vaccine Deaths’

In the video above from The Jimmy Dore Show, they discuss why The Lancet almost immediately pulled the concerning study.⁶ The journal stated, “This preprint has been removed by Preprints with The Lancet because the study’s conclusions are not supported by the study methodology. Preprints with The Lancet reserves the right to remove a paper that has been posted if we determine that it has violated our screening criteria.”⁷ As noted by The Daily Sceptic on July 6, 2023:⁸

“Without further detail from the Preprints with the Lancet staff who removed the paper it is hard to know what substance the claim that the conclusions are not supported by the methodology really has. A number of the authors of the paper are at the top of their fields so it is hard to imagine that the methodology of their review was really so poor that it warranted removal at initial screening rather than being subject to full critical appraisal.

It smacks instead of raw censorship of a paper that failed to toe the official line. Keep in mind that the CDC has not yet acknowledged a single death being caused by the COVID mRNA vaccines. Autopsy evidence demonstrating otherwise is clearly not what the U.S. public health establishment wants to hear.”

The censored paper has now been peer-reviewed, however, and its findings add further support to those who have been sounding the alarm about COVID-19 shot dangers all along. The researchers explain, “We found by independent adjudication that 73.9% of deaths were attributable to fatal COVID-19 vaccine injury syndromes,” adding:⁹

“These results corroborate known COVID-19 vaccine-induced syndromes and show significant, temporal associations between COVID-19 vaccination and death involving multiple organ systems, with a predominant implication of the cardiovascular and hematological systems.

Criteria of causality from an epidemiological perspective have been met including biological plausibility, temporal association, internal and external validity, coherence, analogy, and reproducibility with each successive case report of death after COVID-19 vaccination combined with population-based studies describing mortality among the vaccinated.

Our findings amplify concerns regarding COVID-19 vaccine adverse events and their mechanisms.”

To answer the question of why The Lancet pulled the paper so quickly, The Vigilant Fox said:¹⁰

“Another COVID ‘conspiracy theory’ becomes reality as a bombshell study CENSORED by The Lancet has now been peer-reviewed. What were they trying to hide, you ask? Lots and lots of vaccine deaths.”

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What Makes COVID-19 Shots So Deadly?

Most of the COVID-19 injections are linked to deaths, which suggests they share a common factor causing side effects, most likely the spike protein, the study suggests.¹¹

Spike proteins can circulate in your body after infection or injection, causing damage to cells, tissues and organs. “Spike protein is a deadly protein,” McCullough said.¹² It may cause inflammation and clotting in any tissue in which it accumulates.¹³ In fact, some suggest that spike protein in COVID-19 shots was designed to cause severe disease.

In a study published in the journal Science, by researchers with the National Institutes of Health’s National Institute of Allergy and Infectious Diseases, it’s revealed that the S-2P spike protein used in several COVID-19 shots binds more strongly to the ACE2 receptors in the heart, lungs, kidneys and endothelial cells of blood vessels in the body compared to the spike protein of the original SARS-CoV-2 virus.¹⁴

“Given the average time (14.3 days) in which cases died after vaccination, a temporal association between COVID-19 vaccination and death among most cases is further supported by the finding that SARS-CoV-2 Spike mRNA vaccine sequences can circulate in the blood for at least 28 days after vaccination,” the featured study notes.¹⁵

Further, it’s been revealed that the spike protein on its own is enough to cause inflammation and damage to the vascular system, even independent of a virus.¹⁶ The spike protein is known to have deleterious effects on the heart, and COVID-19 vaccine-induced myocarditis and heart attack are well-described in peer-reviewed studies.¹⁷ Multisystem Inflammatory Syndrome (MIS) has also been reported after COVID-19 shots in both adults and children.

“A possible mechanism by which MIS occurs after vaccination could be the systemic distribution of the LNPs [lipid nanoparticles] containing mRNA after vaccine administration and the consequent systemic Spike protein expression and circulation resulting in system-wide inflammation,” the researchers explain.¹⁸ Given the study findings, they suggest that anyone who receives a COVID-19 shot should be monitored for at least one year:¹⁹

“The implications of our study apply to cases of unanticipated death without antecedent illness among COVID-19 vaccine recipients. We can infer that in such cases, death may have been caused by COVID-19 vaccination.

Further urgent investigation is required to build upon our results and further elucidate the pathophysiologic mechanisms of death with the goal of risk stratification and avoidance of death for the large numbers of individuals who have taken or will receive one or more COVID-19 vaccines in the future.

Autopsies should be performed on all diseased individuals that have received one or more COVID-19 vaccines. Clinical monitoring of COVID-19 vaccine recipients is indicated for a period of at least one year after vaccination to ensure the absence of serious adverse events that may lead to death.”

Potential Link Between COVID-19 Injections and Alzheimer’s Disease

In addition to deaths related to the cardiovascular system, McCullough and colleagues found COVID-19 shot-related deaths also involved the hematological system, pulmonary embolism and the respiratory system, while adverse events related to the gastrointestinal, immunological and neurological systems have also been reported after COVID-19 shots.²⁰

A separate study investigated the association between COVID-19 shots and the onset of Alzheimer’s Disease and mild cognitive impairment (MCI).²¹ The study involved 558,017 individuals in Seoul, South Korea, who were divided into two groups — those who received a COVID-19 shot and those who did not.

The findings showed an increased incidence of MCI and Alzheimer’s in those who received a COVID-19 injection, particularly in those who received mRNA shots, within three months post-injection. The mRNA vaccine group exhibited a significantly higher incidence of Alzheimer’s compared to the unvaccinated group.

The study suggests a potential link between COVID-19 shots, particularly mRNA injections, and increased incidences of Alzheimer’s disease and MCI. “This underscores the need for further research to elucidate the relationship between vaccine-induced immune responses and neurodegenerative processes, advocating for continuous monitoring and investigation into the vaccines’ long-term neurological impacts,” the researchers stated.

Rampant Censorship Downplays the Truth About COVID-19 Shot Dangers

In another example of the rampant censorship surrounding COVID-19 adverse effects, a now-retracted narrative review published in the journal Cureus called for a global moratorium on mRNA COVID-19 shots.²² The review cited significant increases in serious adverse events among those who received the injections, along with an “unacceptably high harm-to-reward ratio.”²³

When factoring in absolute risk and the “number needed to vaccinate” (NNV), a metric used to quantify how many people need to be vaccinated to prevent one additional case of a specific disease, the review found “for every life saved, there were nearly 14 times more deaths caused by the modified mRNA injections.”²⁴

As for the paper’s retraction, McCullough, one of the paper’s authors, called it a “stunning act of scientific censorship.”²⁵ In addition to calling for a global moratorium on mRNA COVID-19 shots, the authors of the paper said the shots should be immediately removed from the childhood vaccine schedule, while boosters should also be suspended.

“It is unethical and unconscionable to administer an experimental vaccine to a child who has a near-zero risk of dying from COVID-19 but a well-established 2.2% risk of permanent heart damage based on the best prospective data available,” the paper notes.²⁶

The moratorium is warranted based on the shots’ risks of serious adverse events, the mechanisms behind those adverse events, mortality data and issues with inefficacy, vaccine control and processing.²⁷ As with the featured Lancet study, the Cureus study was already incredibly popular, with more than 330,000 views/reads/downloads in one month compared to the average Cureus paper, which gets only 2,700 in an entire year.²⁸

With each unwarranted retraction, more people will begin to ask questions about why this crucial information is continuing to be censored and withheld from the public instead of openly debated and presented to the public.

Injured by a COVID-19 Shot? Here’s Help

If you’ve had a COVID-19 shot and developed any unusual symptoms, seek out help from an expert. The Front Line COVID-19 Critical Care Alliance (FLCCC) has a treatment protocol for post-jab injuries. It’s called I-RECOVER and can be downloaded from covid19criticalcare.com.²⁹

Dr. Pierre Kory, who cofounded the FLCCC, has transitioned to treating the vaccine injured more or less exclusively. For more information, visit DrPierreKory.com. McCullough is also investigating additional post-jab treatments, which you can find on PeterMcCulloughMD.com. Finally, if you’re suffering from long vax, be sure to review my strategies for boosting mitochondrial health to allow your body to heal.

– Sources and References

^1, ⁷ Preprints with The Lancet July 5, 2023 (Archived)
^2, ^4, ^5, ^9, ^11, ^15, ^17, ^18, ^19, ²⁰ Forensic Science International June 21, 2024
³ X, William Makis MD, June 21, 2024
⁶ YouTube, The Jimmy Dore Show July 26, 2023
⁸ The Daily Sceptic July 6, 2023
¹⁰ X, The Vigilant Fox June 21, 2024
¹² Rumble, Dr. Peter McCullough, Therapeutic Nihilism and Untested Novel Therapies, October 5, 2021, 6:00
¹³ World Council for Health, Spike Protein Detox Guide
¹⁴ Science. 2020 Mar 13; 367(6483): 1260–1263
¹⁶ Circulation Research March 31, 2021
²¹ QJM: An International Journal of Medicine May 28, 2024
²² Cureus January 24, 2024
²³ Cureus January 24, 2024, Abstract
²⁴ Cureus January 24, 2024, Review
^25, ²⁸ Substack, Courageous Discourse February 24, 2024
²⁶ World Tribune February 5, 2024
²⁷ Children’s Health Defense January 29, 2024
²⁹ Covid19criticalcare.com

Posted in Alzheimer's, Censorship, Coronavirus, Corruption, Mortality, Vaccinations | No Comments »

Posted by: admin | Posted on: May 11, 2024

How Light Exposure Plays a Role in Cognition

Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/05/11/light-exposure-cognition.aspx

Analysis by Dr. Joseph Mercola May 11, 2024

STORY AT-A-GLANCE

A preprint study conducted by researchers from the University of Liège in Belgium explored how different levels of light exposure influence your cognitive function
The researchers noted that higher levels of light exposure among participants led to better cognitive performance in executive tasks
To harness the power of light exposure, you can use photobiomodulation devices that emit red and near-infrared light
Photobiomodulation can help boost mitochondrial function, which may result in better cognitive function

Can bright light exposure lead to a sharper mind and heightened alertness? Researchers from the University of Liège in Belgium sought out the answer to this. In the 2024 preprint study titled “Regional Response to Light Illuminance Across the Human Hypothalamus,”¹ they investigated how light exposure affects cognitive function in humans.

According to Neuroscience News,² “The study … is described by the editors as of fundamental importance, and represents a key advancement to our understanding of how different levels of light affect human behavior.”

Light Affects the Emotional and Executive Areas of Your Brain

For context, prior research conducted on animals established that light exposure affects many subcortical structures,³ which are the parts of your brain that play “a pivotal role in cognitive, affective and social functions in humans.”⁴ Now, the researchers are investigating if the same effects are seen in humans, making the study a first of its kind.

Speaking to NeuroScience News,⁵ lead author Islay Campbell, Ph.D., from the University of Liège, Belgium, commented:

“Translating findings on how light exposure affects the brain in animal models to humans is a difficult process, as the later maturation of the cortex in human beings enables much more complex cognitive processing.

In particular, the question of whether hypothalamus nuclei contribute to the stimulating impact of light on cognition is not established.”

The Effects of Light on the Hypothalamus

Campbell and her team recruited 26 participants to complete two cognitive tasks designed to stimulate the emotional and executive areas of the hypothalamus while being subjected to varying levels of light intensity.⁶ They used seven Tesla MRI (magnetic resonance imaging) machines to monitor brain activity in real time and record the results.

The hypothalamus is responsible for managing the endocrine system. Essentially, it acts as a central station, receiving signals from other parts of your brain to release and inhibit hormones essential for maintaining life. These include the thyroid gland, adrenal gland and reproductive organs. The hypothalamus also helps regulate your appetite and temperature.⁷

Inside the hypothalamus, which all mammals have, lies the center master clock – the suprachiasmatic nuclei (SCN). The SCN cannot function on its own but requires environmental stimuli to synchronize the body clock. This allows you to follow a pattern of wakefulness and sleep.⁸

The hypothalamus is generally divided into two areas regions — anterior and posterior. The anterior region handles the production of hormones needed by the body, while the posterior region is where oxytocin and vasopressin are stored after being produced in the anterior region. Oxytocin and vasopressin are hormones that perform crucial functions such as maintaining mood and regulating temperature.⁹

For the study, the researchers subdivided the two parts of the hypothalamus into five. This approach helped them identify which specific areas of the hypothalamus experienced a reaction while under light exposure. Here’s an illustration from the study to help you visualize the intricacy of the divisions.

Image credit: eLife, “Regional Response to Light Illuminance Across the Human Hypothalamus,” Figure 2A¹⁰

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Light Intensities Can Have Varying Effects on Different Parts of the Hypothalamus

The participants were asked to get an MRI scan one week before the trials began. They were also required to get around seven hours of sleep, and were prohibited from consuming caffeine and alcohol, as well as undergoing strenuous exercise.¹¹

To create the test environment, the researchers used a lightbox that illuminated a cable on both ends, allowing them to vary the intensity while the participants performed the tasks.¹² The participants were then asked to complete two tests to identify the effects of light exposure on their cognition. Here’s a breakdown, summarized in a report by Sleep Review:¹³

1. Executive task — The participants were asked to determine if the current sound played to them was the same as one they heard two playbacks earlier, or if it contained the letter “K.”

2. Emotional task — They were asked to determine the gender of a voice that used either a neutral tone or angry tone.

Throughout the study, the participants were alternatively placed in darkness or exposed to bursts of light exposure through four levels of illumination. The researchers noted:¹⁴

“In the executive task, participants were exposed to 30s to 70s (median 30s) of light blocks separated by 10s of darkness (< 0.1 lux) and the light blocks were repeated 11 times for each light condition. For the emotional task, participants were exposed to 30 to 40s (median 35s) light blocks separated by 20s of darkness (< 0.1 lux) and the light blocks were repeated five times for each light condition.”

Once results were recorded, the researchers noticed that higher light intensity increased activity in the posterior hypothalamus among the participants.¹⁵ At the same time, higher light intensities resulted in decreased activity in the anterior and ventral sections of the hypothalamus. Furthermore, higher light intensities resulted in better performance in the executive task.¹⁶

The Role of the Hypothalamus in Your Cognitive Function

The response to this preprint study is positive, as it could not only help identify light’s effects on various brain structures but may also support further research into noninvasive treatments for sleep problems and cognitive fatigue.

According to Neuroscience News, “The strength of evidence is praised as compelling, supporting the authors’ analyses of the complex interplay between light exposure, hypothalamic activity, and cognitive function.”¹⁷

Previously published evidence also support the findings of this research. In a 2020 study¹⁸ published in Physiology & Behavior, researchers noted that sections of the brain such as the cortex, hippocampus and amygdala have been studied extensively in the role of cognition, but not the hypothalamus. Through the course of their research, they observed that the hypothalamus may play a role in cognition:¹⁹

“Such hypothalamic control of memory-related synaptic machinery may enable gating/thresholding/permissive/tagging operations within yet poorly defined logic gates for memory updating. Hypothalamic signals may thus facilitate cost-benefit analysis of learning and memory in real-world settings.”

In another study,²⁰ published in Frontiers in Neurology, authors noted that light exposure increases physiological arousal in the brain, leading to increased alertness.

The data from this preprint study clearly illustrate that light exposure can have a profound effect on your cognitive performance. So, how can you take advantage of it? Through a process called photobiomodulation (PBM), which is actually one of my favorite biohacks.

How Photobiomodulation Can Benefit Your Health

PBM refers to the process of using light therapy to benefit your health. Typically, this process involves using red and near-infrared wavelengths (with enough intensity) that your body can utilize.

One of the most notable benefits of near-infrared exposure is the increase in ATP (adenosine triphosphate) production in your mitochondria. Essentially, ATP is the energy currency used to power biological processes essential for life, such as muscle contractions, ion transport and chemical synthesis.²¹

As noted in a study published in Biology Letters, near-infrared exposure helped increase ATP in animal subjects and even reduced inflammation. Fruit flies exposed to near-infrared light also gained a significant increase in lifespan.²²

Another fantastic benefit of near-infrared exposure is melatonin production — 95% of melatonin is produced in your mitochondria in response to near-infrared light. The melatonin released by your pineal gland account for just 5% of the melatonin in your body.²³

Now, you might be wondering how mitochondria underscore these benefits. According to published research, your mitochondria play an important role in cognition. Here’s a succinct explanation, according to a study²⁴ published in Mitochondrion:

“Mitochondria have a crucial role in brain development and neurogenesis, both in embryonic and adult brains. Since the brain is the highest energy consuming organ, it is highly vulnerable to mitochondrial dysfunction. This has been implicated in a range of brain disorders including, neurodevelopmental conditions, psychiatric illnesses, and neurodegenerative diseases.”

In another study, published in the International Journal of Molecule Sciences,²⁵ mitochondrial dysfunction has been implied to be a common mechanism involved in the most recognizable features of Alzheimer’s disease.

Linking all points together, harnessing the power of PBM can help boost mitochondrial health. In turn, healthy mitochondria can help maintain optimal cognitive function.

Can Home Saunas Provide the Same Benefits as PBM?

Electric saunas designed for your home typically emit far-infrared light, which can still provide detoxing benefits. However, with some tinkering, they can be modified to function as a PBM device as well, which can save money since you won’t need a dedicated PBM device.

You can modify your sauna by using incandescent heat bulbs that emit the majority of their energy as near-infrared light. While it may take some work, the effort will be worth it.

If you want to save time and energy, consider near-infrared bulbs from SaunaSpace.²⁶ All their bulbs contain metal guards that prevent the glass from accidentally breaking and injuring you. Use the instructions to hang the new incandescent bulbs in your old sauna.

This simple trick can increase the benefits you experience in your sauna since you’re also getting the benefits of PBM from the new bulbs. Done correctly, eight incandescent red bulbs can heat up to 160 degrees Fahrenheit in about 20 minutes, which is far better than typical far-infrared saunas.

It’s also good to test your sauna for electromagnetic field (EMF) radiation. If it does have EMFs, I recommend shielding your sauna as best as you can to protect your health.

As for the actual sauna session, it’s always important to start out slowly. Listen to your body so you can decide how much heat stress you can tolerate. Ideally, sauna sessions should last anywhere between 15 and 30 minutes. Also, remember to stay hydrated before, during and after, since you’ll be sweating a lot.

Sunlight Is the Ideal Light Source

While a PBM device (or a modified sauna) can be a fantastic addition to your health routine, you shouldn’t shun proper sun exposure. Ideally, spend more time outdoors whenever possible. Only use PBM devices to get red and near-infrared light you need if you cannot get enough regular sun exposure.

Humans need direct sun exposure in order to optimally thrive, and while artificial lighting sources offering specific light spectrums may be helpful for various problems, ideally, we need the full spectrum of light that natural sunlight offers.

If you’re going out to get sunlight, I recommend doing it during solar noon. For those living in areas that implement Daylight Saving Time, it should be 12:30 to 1:30 PM. Scheduling your daily walk around this time allows you to maximize the benefits of ultraviolet B rays and near-infrared radiation from the sun.

Blocking Blue Light at Night Can Help Transform Your Sleep

Last but not least, light exposure during the day has a major impact on your sleep quality, which in turn affects health in countless ways. Getting bright light exposure first thing in the morning and mid-day helps properly “set” your circadian clock, while bright light from artificial lighting and screens in the evening prevents melatonin release, inhibiting sleep.

Normally, your brain starts progressively increasing the hormone melatonin around 9 or 10 pm, which makes you sleepy. Melatonin acts as a marker of your circadian phase or biological timing.

In a nutshell, this hormone influences what time of day or night your body thinks it is, regardless of what time the clock on the wall displays. Besides regulating your sleep cycle, it also provides other important health benefits, including helping to prevent cancer.

Somewhere between 50 and 1,000 lux is the activation range within which light will begin to suppress melatonin production. However, wavelength is also important. Red and amber lights will not suppress melatonin while blue, green, and white lights will.

The reason for this is because these are the wavelengths are the most common outdoors during daytime hours. So, you’ll want to avoid the blue light wavelength after sunset. This includes artificial light, and light emitted by electronics such as your TV, computer, and other electronic screens.

The blue light range (400–490 nm) can also induce photoreceptor damage in your eyes, so besides disrupting your sleep this is another potential problem with light emitting screens. As noted in one recent study,²⁷ “it is important to consider the spectral output of LED-based light sources to minimize the danger that may be associated with blue light exposure.”

Ways to Limit Blue Light Exposure at Night

There are several ways to avoid blue light in the evening depending on your lifestyle and personal preferences:

1.Turn off or dim all lights after sunset and avoid watching TV or using light emitting electronics for at least one hour before bedtime (ideally two hours or more). Research^28,²⁹ shows that using an electronic device within one hour of bedtime can delay falling asleep for more than an hour.

Another study³⁰ that compared melatonin profiles in individuals exposed to standard room light (<200 lux) vs. dim light (<3 lux) found that exposure to room light before bedtime shortened the time of elevated melatonin levels by about 90 minutes.

That means it may take you an extra hour and a half before you’re sleepy enough to fall asleep once you’re in bed. Combine room light and electronic displays right before bed and it’s easy to see how sleep may remain elusive for hours on end.

2.After sundown, shift to a low-wattage bulb with yellow, orange or red light if you need illumination. A salt lamp illuminated by a 5-watt bulb is an ideal solution that will not interfere with your melatonin production. If using a computer or smart phone, install blue light-blocking software like f.lux. The program automatically alters the color temperature of your screen as the day goes on, pulling out the blue wavelengths as it gets late.

3.One of the easiest solutions is to use amber colored glasses that block blue light. This way, you don’t have to worry about installing programs on all your devices, or buying special light bulbs for evening use. Once you have your glasses on, it doesn’t matter what light sources you have on in your house.

Studies^31,^32,³³ have confirmed that when using blue-blocking glasses, people produce as much melatonin as they do in dim light, even if they’re in a lit room or using light emitting technology. Other studies³⁴ have shown that people using blue-blocking glasses had major improvements in both sleep quality and mood. Shift workers who use them before bedtime (i.e. in the morning when it’s bright out) also report improved sleep.³⁵

– Sources and References

Posted in Alzheimer's, Brain, Hypothalamus, Sleep, Sunlight | No Comments »

Posted by: admin | Posted on: April 30, 2024

Doctors Predict Epidemic of Prion Brain Diseases

Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/04/29/prion-brain-diseases.aspx

Analysis by Dr. Joseph Mercola April 29, 2024

STORY AT-A-GLANCE

Mounting research suggests a serious side effect of the COVID mRNA jabs could be dementia, and the prions that cause it may be contagious
Frameshifting, as we now know occurs in the COVID shots, can induce prion production and lead to neurodegenerative diseases such as Alzheimer’s and Creutzfeldt-Jakob disease (CJD)
Sid Belzberg’s prions.rip website, which collected data on neurological side effects post-jab, found a notably high incidence of diagnosed CJD cases, suggesting an alarming trend
A series of articles highlight biases in clinical trials and observational studies, suggesting COVID-19 vaccines’ safety and effectiveness have been massively overstated
The Global COVID Vaccine Safety Project study — funded by the U.S. Centers for Disease Control and Prevention — reveals significant side effects, including myocarditis, pericarditis, and blood clots, underscoring the need for reevaluation of COVID vaccine risks and benefits

According to mounting data, one of the more serious side effects of the COVID mRNA jabs appears to be dementia, and worse yet, this previously untransmissible disease may now be “contagious,” transmissible by way of prions.

In my 2021 interview with Stephanie Seneff, Ph.D., she explained why she suspected the COVID shots may eventually result in an avalanche of neurological prion-based diseases such as Alzheimer’s. She also published a paper detailing those mechanisms in the May 10, 2021, issue of the International Journal of Vaccine Theory. As she explained in that paper:¹

“A paper published by J. Bart Classen (2021) proposed that the spike protein in the mRNA vaccines could cause prion-like diseases, in part through its ability to bind to many known proteins and induce their misfolding into potential prions.

Idrees and Kumar (2021) have proposed that the spike protein’s S1 component is prone to act as a functional amyloid and form toxic aggregates … and can ultimately lead to neurodegeneration.”

In summary, the take-home from Seneff’s paper is that the COVID shots, offered to hundreds of millions of people, are instruction sets for your body to make a toxic protein that will eventually wind up concentrated in your spleen, from where prion-like protein instructions will be sent out, leading to neurodegenerative diseases.

What Are Prions?

The term “prion” derives from “proteinaceous infectious particle.” Prions are known to cause a variety of neurodegenerative diseases in animals and humans, such as Creutzfeldt-Jakob disease (CJD) in humans, bovine spongiform encephalopathy (BSE or “mad cow disease”) in cattle, and chronic wasting disease in deer and elk.

These diseases are collectively referred to as transmissible spongiform encephalopathies (TSEs). They’re characterized by long incubation periods, brain damage, the formation of holes in the brain giving it a sponge-like appearance, and failure to induce an inflammatory response.

In short, prions are infectious agents composed entirely of a protein material that can fold in multiple, structurally distinct ways, at least one of which is transmissible to other prion proteins, leading to a disease that is similar to viral infections but without nucleic acids.

Unlike bacteria, viruses, and fungi, which contain nucleic acids (DNA or RNA) that instruct their replication, prions propagate by transmitting their misfolded protein state to normal variants of the same protein.

According to the prion disease model, the infectious properties of prions are due to the ability of the abnormal protein to convert the normal version of the protein into the misfolded form, thereby setting off a chain reaction that progressively damages the nervous system.

Prions are remarkably resistant to conventional methods of sterilization and can survive extreme conditions that would normally destroy nucleic acids or other pathogens, which is part of why prion diseases are so difficult to treat.

More Evidence mRNA Shots Can Trigger Dementia

Today, there’s even more evidence to support Seneff’s theory. In August 2022, tech entrepreneur Sid Belzberg wrote² about prions.rip, a website he’d set up to collect data on the neurological side effects of the jabs. (This site is no longer live.)

Within a few months, the site had received about 15,000 hits and gathered 60 reports from people who got the jab and suffered neurological deficits shortly thereafter, including six cases of diagnosed CJD.

“Normally this disease affects 1 in a 1,000,000 people,” Belzberg wrote.³ “To get 6 cases you would need 6,000,000 hits to the site assuming everyone reports. The chances of getting 1 case in 15,000 hits is 1 in 66. To see 6 cases in 1 group of 15,000 is 1/66^6 or 1 in 82,000,000,000, or 20 times more likely to win a Powerball lottery! …

To reiterate, CJD is an exceptionally rare disease that is now a known and established severe adverse reaction (SAE) from the DEATHVAX™. Injecting this slow kill bioweapon can cause ailments that are about as likely to develop in the real word as getting struck by lightning twice. The proof is now irrefutable.”

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Frameshifting Can Result in Prion Production

In mid-December 2023, researchers reported^4,^5,⁶ that the replacing of uracil with synthetic methylpseudouridine in the COVID shots — a process known as codon optimization — can cause frameshifting, a glitch in the decoding, thereby triggering the production of off-target aberrant proteins.

The antibodies that develop as a result may, in turn, trigger off-target immune reactions. According to the authors, off-target cellular immune responses occur in 25% to 30% of people who have received the COVID shot. But that’s not all.

According to British neuroscientist Dr. Kevin McCairn, this frameshifting phenomenon has also been linked to harmful prion production — and that frame shifted prions, specifically, are infectious and can be transmitted from one person to another. As reported in the Journal of Theoretical Biology in 2013:⁷

“A quantitatively consistent explanation for the titres of infectivity found in a variety of prion-containing preparations is provided on the basis that the etiological agents of transmissible spongiform encephalopathy comprise a very small population fraction of prion protein (PrP) variants, which contain frameshifted elements in their N-terminal octapeptide-repeat regions …

Frameshifting accounts quantitatively for the etiology of prion disease. One per million frameshifted prions may be enough to cause disease. The HIV TAR-like element in the PRNP mRNA is likely an effector of frameshifting.”

McCairn explained this mechanism in a February 19, 2023, interview with Health Alliance Australia (video above). In it, he noted:

“Mis-folded proteins caused by prions can impact every level organ and tissue system in the body … [They] bioaccumulate and are resistant to degradation, thereby building up …”

Prions may in fact be the primary molecule that is being “shed” by COVID jab recipients, and if those prions are due to frameshifting, that could be very bad news indeed, considering their implication in dementia.

Another doctor who believes we’ll be facing an “epidemic of prion disease” is Dr. David Cartland. In late February 2024, he posted⁸ 13 scientific papers linking the COVID jabs, prion diseases and CJD, noting that was just a “small selection” of what’s available in the medical literature.

Prions Implicated in Long COVID as Well

According to genomics expert Kevin McKernan, Ph.D., prions are also involved in long COVID (or as McKernan calls it, “long vax”).⁹ In one 2024 study,¹⁰ 96.7% of long COVID sufferers had received the jab. In an interview with the Front Line COVID-19 Critical Care Alliance (FLCCC), McKernan stated:¹¹

“If you frameshift over the stop codons, you’re going to be making proteins that are spike-mito proteins. When I talk to a lot of the long vax patients I hear of all these things that remind me of my time in the mitochondrial disease sequencing space …”

McKernan claims he tried to publish a paper on this in 2021 with Dr. Peter McCullough, but the editor of the journal “stepped in and torpedoed the paper.”¹²

World’s Largest Side Effect Analysis Has Been Published

In related news, the largest study¹³ to date on the side effects of the COVID jabs was published in the journal Vaccine in February 12, 2024, and it confirms what I and many other alternative news sources have been saying all along, namely that the mRNA jabs are the most dangerous medical products to ever hit the market.

The study — performed by the Global COVID Vaccine Safety (GCoVS) Project and funded by the U.S. Centers for Disease Control and Prevention, Public Health Ontario and the Canadian Health Research Institute — evaluated the risk of “adverse events of special interest” (AESI) following COVID-19 “vaccination.”

Data from 10 sites in eight countries (Argentina, Australia, Canada, Denmark, Finland, France, New Zealand and Scotland) were included, encompassing more than 99 million jabbed individuals.

Of the thousands of side effects Pfizer listed in its confidential report of post-authorization adverse events submitted to the U.S. Food and Drug Administration,¹⁴ the GCoVS focused on 13 AESIs that fall into three primary categories: Neurological, hematologic (blood-related) and cardiovascular conditions.

They calculated the AESI risk for each of the 13 AESIs based on the number of observed versus expected (OE) incidents occurring up to 42 days after injection. The “expected” number of side effects were based on vaccine adverse event data from 2015 to 2019. These rates were then compared to the adverse event rates observed in those who got one or more of the COVID jabs, either Pfizer’s BNT162b2, Moderna’s mRNA-1273, or AstraZeneca’s ChAdOx1.

Largest Study to Date Confirms COVID Jab Dangers

The analysis¹⁵ revealed several concerning side effects, including increased risks of myocarditis, pericarditis, blood clots in the brain, and various neurological conditions. Here’s a quick summary of the findings:

• Myocarditis and pericarditis:

◦ Pfizer vaccine — OE ratios for myocarditis were 2.78 and 2.86 after the first and second shots, with the risk remaining doubled after the third and fourth shots.

◦ Moderna vaccine — OE ratios for myocarditis were 3.48 and 6.10 after the first and second shots. Doses 1 and 4 also showed OE ratios of 1.74 and 2.64 for pericarditis.

◦ AstraZeneca vaccine — OE ratio for pericarditis was 6.91 after the third shot.

• Blood clots in the brain (cerebral venous sinus thrombosis, CVST):

◦ An OE of 3.23 for CVST was observed after the first AstraZeneca shot.

◦ A significant increase in CVST risk was also noted after the second Pfizer dose.

• Neurological conditions:

◦ Guillain-Barré syndrome — An OE ratio of 2.49 was observed following the AstraZeneca jab.

◦ Transverse myelitis — Risk nearly doubled with the AstraZeneca shot.

◦ Acute disseminated encephalomyelitis — OE ratios of 3.78 (Moderna) and 2.23 (AstraZeneca) were noted.

These findings really underscore the potential for serious side effects from the COVID shots, including conditions that may lead to other consequences in the longer term, such as stroke, heart attack, paralysis and death.

Effectiveness and Safety Was Wildly Exaggerated in Trials

Considering those findings, it’s no surprise to find that effectiveness and safety were exaggerated in clinical trials and observational studies. In a guest post on Dr. Robert Malone’s Substack, Raphael Lataster, Ph.D., writes:¹⁶

“An unofficial series of four crucially important medical journal articles, two by me, appearing in major academic publisher Wiley’s Journal of Evaluation in Clinical Practice reveals that claims made about COVID-19 vaccines’ effectiveness and safety were exaggerated in the clinical trials and observational studies, which significantly impacts risk-benefit analyses.

Also discussed are the concerning topics of myocarditis, with evidence indicating that this one adverse effect alone means that the risks outweigh the benefits in the young and healthy; and perceived negative effectiveness, which indicates that the vaccines increase the chance of COVID-19 infection/hospitalization/death, to say nothing about other adverse effects.”

Summary of Papers

The four papers in question include:

1. “Sources of Bias in Observational Studies of COVID-19 Vaccine Effectiveness” published in the Journal of Evaluation in Clinical Practice in March 2023, co-authored by BMJ editor Peter Doshi, Ph.D., statistician Kaiser Fung and biostatistician Mark Jones, which concluded that “case-counting window bias” had a significant effect on effectiveness estimates.¹⁷

As explained by Lataster, this “concerns the 7 days, 14 days, or even 21 days after the jab where we are meant to overlook jab-related issues, such as COVID infections, for some odd reason as ‘the vaccine has not had sufficient time to stimulate the immune system.’

This may strike you as quite bizarre since all of the ‘fully vaccinated’ must go through the process of being ‘partially vaccinated,’ sometimes even more than once. To make matters worse, the unvaccinated do not get such a ‘grace period,’ meaning that there is also a clear bias at play.

In an example using data from Pfizer’s clinical trial, the authors show that thanks to this bias, a vaccine with effectiveness of 0%, which is confirmed in the hypothetical clinical trial, could be seen in observational studies as having effectiveness of 48%.”

2. “Reply to Fung et. al. on COVID-19 Vaccine Case-Counting Window Biases Overstating Vaccine Effectiveness,” authored by Lataster, which discussed how the counting window bias not only affected effectiveness estimates in observational studies but also safety estimates, suggesting a need for reassessment of vaccine safety.¹⁸ The article also addresses “the mysterious rise in non-COVID excess deaths post-pandemic.”¹⁹

3. “How the Case Counting Window Affected Vaccine Efficacy Calculations in Randomized Trials of COVID-19 Vaccines,” again co-authored by Doshi and Fung, which detailed how case-counting window issues also overestimated effectiveness in Pfizer and Moderna clinical trials.²⁰

4. A second article by Lataster, in which he highlighted and summarized the evidence showing that clinical trials were affected by adverse effect counting window issues that led to exaggerated safety estimates.²¹

“Together, these four articles make clear that claims made about COVID-19 vaccines; effectiveness and safety were exaggerated in the clinical trials and observational studies, whilst also finding time to discuss myocarditis and perceived negative effectiveness, meaning that new analyses are very much needed,” Lataster writes.²²

Resources for Those Injured by the COVID Jab

Based on data from across the world, it’s beyond clear that the COVID shots are the most dangerous drugs ever deployed. If you already got one or more COVID jabs and are now reconsidering, you’d be wise to avoid all vaccines from here on, as you need to end the assault on your body. Even if you haven’t experienced any obvious side effects, your health may still be impacted long-term, so don’t take any more shots.

If you’re suffering from side effects, your first order of business is to eliminate the spike protein — and/or any aberrant off-target protein — that your body is producing. Two remedies shown to bind to and facilitate the removal of SARS-CoV-2 spike protein are hydroxychloroquine and ivermectin. I don’t know if these drugs will work on off-target proteins and nanolipid accumulation as well, but it probably wouldn’t hurt to try.

The Front Line COVID-19 Critical Care Alliance (FLCCC) has developed a post-vaccine treatment protocol called I-RECOVER. Since the protocol is continuously updated as more data become available, your best bet is to download the latest version straight from the FLCCC website at covid19criticalcare.com.²³

For additional suggestions, check out the World Council for Health’s spike protein detox guide,²⁴ which focuses on natural substances like herbs, supplements and teas. Sauna therapy can also help eliminate toxic and misfolded proteins by stimulating autophagy.

– Sources and References

Posted in Alzheimer's, Dementia, mRNA, Prion | No Comments »

Posted by: admin | Posted on: April 17, 2024

Shocking research links Alzheimer’s disease to common pathogens

Reproduced from original article:
https://www.naturalhealth365.com/shocking-research-links-alzheimers-disease-to-common-pathogens.html

by: Abby Campbell, staff writer | April 13, 2024

(NaturalHealth365) Western medicine often overlooks how pathogens may contribute to Alzheimer’s disease (AD) and other forms of dementia. In fact, a study published in the journal Medical Principles and Practice highlighted this issue, shedding light on how various pathogens, including bacteria and viruses, could play a role in the development and progression of these health issues.

Despite inflammation in the brain being recognized as a factor in Alzheimer’s disease, the specific involvement of pathogens like Helicobacter pylori, Chlamydia pneumoniae, Porphyromonas gingivalis, Borrelia burgdorferi, herpes simplex virus 1, cytomegalovirus, and Epstein-Barr virus is not commonly discussed in Western medical discourse. This omission might stem from the conventional focus on genetic and lifestyle factors in neurodegenerative diseases.

However, emerging research suggests that infections, particularly chronic ones, could significantly contribute to triggering and exacerbating the pathology of Alzheimer’s disease. In fact, studies are showing up to 95 percent of the American population has been infected by a disease that could eventually result in Alzheimer’s.

Could pathogens be responsible for the Alzheimer’s epidemic?

Cytomegalovirus (CMV) is one of the causes of mononucleosis, commonly known as the ‘kissing disease,’ alongside Epstein-Barr virus (EBV). While the symptoms of mononucleosis typically subside after a few weeks or months, research published in The Journal of Infectious Diseases suggests that both CMV and EBV may silently contribute to Alzheimer’s disease.

In a human study, CMV antibody levels showed a significantly higher association with neurofibrillary tangles, commonly known as the primary markers for the disease. According to the U.S. Centers for Disease Control and Prevention (CDC), CMV is in a person’s body for life once it is contracted. Among every 100 adults in the United States, 50 to 80 percent are infected by the age of 40.

Herpes simplex virus 1 and 2 proven to induce neurodegeneration

Several studies indicate that neuronal infection with herpes simplex virus types 1 (HSV-1) and 2 (HSV-2) causes biochemical alterations reminiscent of Alzheimer’s disease. HSV-1 is known for causing cold sores and fever blisters, while HSV-2 is known for genital herpes.

SHOCKING PROBIOTICS UPDATE: Discover the True Value of Probiotics and How to Dramatically Improve Your Physical, Mental and Emotional Wellbeing with ONE Easy Lifestyle Habit.

The Journal of Neurovirology reported data that demonstrated HSV-1 infection induces early upstream events in the neuronal cells that eventually lead to amyloid-ß deposition and tau hyperphosphorylation – suggesting it is a possible risk for Alzheimer’s. Oxidative damage is also one of the earliest problems associated with dementia, and evidence published in PLoS One suggested HSV-1 and oxidative damage interact to promote neurodegeneration events.

The Neurobiology of Aging journal also reported that HSV-2 infection leads to all major pathological hallmarks of Alzheimer’s disease. Scientists proved that HSV-2 strongly alters the tau phosphorylation state, amyloid-ß precursor protein, and autophagy process in human neuroblastoma cells, leading to the appearance of Alzheimer’s disease-like neurodegeneration markers.

The ‘chickenpox virus’ infects the central nervous system

The varicella-zoster virus (VZV) usually manifests itself as chickenpox (varicella) in children, which then becomes latent in most people’s cranial and spinal ganglia neurons. The elderly and those with a compromised immune system may reactivate the virus to produce shingles (zoster).

According to the Archives of Pathology & Laboratory Medicine, VZV can infect a wide variety of cell types in the central and peripheral nervous system, which explains the virus’ diversity of clinical disorders, including its contribution to Alzheimer’s.

Epstein-Barr is a risk factor for cognitive weakening and the progression of Alzheimer’s disease

The Epstein-Barr virus (EBV) is one of the most common viruses and is better known for mononucleosis than CMV. Symptoms include that of the common cold: sore throat, swollen lymph glands, headache, fatigue, and fever.

According to the CDC, 95 percent of adults are inflicted with the virus by the age of 40. And, while the virus does become dormant, the Neurobiology of Aging journal did detect a high percentage of Alzheimer’s patients with EBV.

Bottom line: With approximately 6.7 million Americans aged 65 and older living with Alzheimer’s dementia and numbers growing, annihilation of the condition is necessary and possible, with the help of an experienced holistic healthcare provider.

Clearly, data proves that viruses do contribute to the condition, with more evidence pointing to poor nutritional intake and deficiencies – which make matters worse. It’s important to include a healthy lifestyle, especially an organic and nutrient-dense diet that feeds the brain for protection And, of course, avoid as many environmental toxins as possible.

Sources for this article include:

NIH.gov
NIH.gov
NIH.gov
Journals.lww.com
NIH.gov
CDC.gov
NIH.gov
PLOS.org
NIH.gov
CDC.gov

Posted in Alzheimer's, Infection, Virus | No Comments »

Posted by: admin | Posted on: April 7, 2024

Alzheimer’s Is Now a Leading Cause of Death

Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/04/06/alzheimers-death-rate.aspx

Analysis by Dr. Joseph Mercola April 06, 2024

Story at-a-glance

Alzheimer’s disease, a severe form of dementia, affected an estimated 6.7 million Americans in 2023, and deaths from Alzheimer’s more than doubled between 2000 and 2019
Previous U.S. data placed the number dying from Alzheimer’s disease around 83,000 in 2010. By 2014, research suggested the true number was well over half a million per year — more than six times higher than previously thought. Today, 1 in 3 seniors dies with Alzheimer’s or some other dementia, and the death toll exceeds that of breast- and prostate cancer combined
Since there’s no conventional cure, prevention is crucial if you want to avoid becoming a statistic. Two key strategies are lowering your linoleic acid (LA) intake and avoiding estrogen and estrogenic compounds
Advances in diagnosis are being made. For example, researchers have created a blood test that predicts Alzheimer’s with great accuracy. There’s also a peanut butter smell test, and a free 15-minute at-home test called Self-Administered Gerocognitive Examination (SAGE) that can facilitate early diagnosis

Alzheimer’s disease, a severe form of dementia, affected an estimated 6.7 million Americans in 2023.¹ It is not pretty to lose your mind, as many of you know from firsthand experience with relatives or friends. This devastating degenerative brain disease develops slowly over time and tends to be lethal in its final stages.

As a general guideline, tell-tale symptoms of Alzheimer’s include a decline in memory along with a decline in at least one of the following cognitive abilities:

Speaking coherently or understanding spoken or written language
Recognizing or identifying objects
Ability to perform motor activities
Abstract thinking and ability to make sound judgments
Planning and carrying out complex tasks

Alzheimer’s Deaths Outpace Breast- and Prostate Cancer

Deaths from Alzheimer’s more than doubled between 2000 and 2019.² In 2014, research suggested the actual death toll may be well over half a million per year,³ which would put Alzheimer’s in the top three killer diseases in the U.S., right behind heart disease and cancer.

Officially, it’s the sixth-leading cause of death in the United States as of 2019,⁴ and with a total of 121,499 recorded deaths that year, Alzheimer’s claimed more lives than breast- and prostate cancer combined.⁵

However, it seems the 2014 study was onto something, because while Alzheimer’s was listed on 121,499 death certificates in 2019, underlying causes like AD are typically left off. As explained by Bryan James, an epidemiologist at the Rush Alzheimer’s Disease Center in Chicago and lead author of the 2014 study:⁶

“Death certificates are well known to underreport deaths from Alzheimer’s and other types of dementia. The more immediate causes of death, such as pneumonia or heart attack, are usually listed, and the underlying causes of death are usually left off.”

Alzheimer Death Toll May Be Six Times Higher Than Previously Thought

The 2014 study, published in the journal Neurology,⁷ followed 2,566 seniors aged 65 and over for eight years. In that time, close to one-quarter of them developed Alzheimer’s. Four hundred of them died from the disease.

Using statistic extrapolation, the researchers came up with an estimated annual Alzheimer’s death toll in excess of 503,000 — more than six times higher than previous estimates. According to Dallas Anderson,⁸ an overseer of population studies relating to Alzheimer’s and dementia at the National Institute on Aging (NIA):

“People who I think are knowledgeable about the death registration system in the U.S. would not be surprised that the official number is low, but it is somewhat of a surprise to see that kind of a difference … It’s just another reminder that Alzheimer’s is really an important public health problem, and we need to work on it.”

Indeed, and since there’s no conventional cure, the issue of prevention is crucial if you want to avoid becoming a statistic here. There are also few if any successful medical treatments available once Alzheimer’s sets in.

For example, memantine (sold under the brand name Namenda) is approved for moderate to severe cases of Alzheimer’s, but doctors also prescribe it off-label for mild cases. Unfortunately, the drug has been found to be useless for mild to moderate Alzheimer’s.

A 2011 analysis of data⁹ from three clinical trials showed that patients with mild Alzheimer’s who took Namenda had no improvement in mental function or their ability to perform everyday tasks when compared to placebo. Even among moderate to severe Alzheimer’s patients, for which the drug is approved to treat, the researchers found only “meager” improvements.

Other go-to drugs for the treatment of Alzheimer’s include cholinesterase inhibitor drugs such as Aricept, Exelon and Reminyl. These too may do more harm than good as they provoke slower heart rates, significantly increasing your chances of getting a permanent pacemaker. They also raise your risk of hip fracture.

So, what can you do? The good news is that two key prevention strategies (which virtually no one is talking about) are relatively easy to implement, namely minimizing your linoleic acid (LA) consumption and estrogen exposure.

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High Serotonin Levels Linked to Dementia

In September 2023, research^10,¹¹ linked high serotonin to dementia. Disturbingly, media outlets completely misrepresented the findings by confusing serotonin with serotonin transporter (SERT). What the researchers found was that having low levels of SERT is linked to problems with memory and thinking skills, which can eventually lead to dementia or Alzheimer’s disease.

Media, however, reported that “low serotonin” was linked to dementia, which is the converse of what they actually found. SERT is like a “clean-up crew” in the brain. It helps remove excess serotonin, which is a chemical messenger in the brain. When there’s not enough SERT around to do its job, serotonin levels outside of brain cells can rise too high. This excess serotonin floating around can cause trouble and contribute to problems with memory and thinking.

So, when the study talks about “low SERT” being associated with cognitive problems, it really means that having less of this clean-up crew leads to higher levels of serotonin outside brain cells. And higher levels of serotonin outside brain cells are linked to dementia. As noted by bioenergetic researcher Georgi Dinkov:¹²

“STUDY: high serotonin linked to dementia; MEDIA: low serotonin linked to dementia.^13,¹⁴ Once again, a level of misreporting that I am much more included to ascribe to malice than incompetence simply because most of the popular press outlets covering a specific scientific study get the study authors to proof-read the press article before publishing.

So, for patently false press articles like that to appear is most likely due to an attempt to preserve the status of serotonin as the ‘happy hormone,’ as well as to delay/prevent the avalanche of lawsuit for iatrogenic dementia from all people taking SSRI and other serotonergic drugs.

In summary, the actual study found that low levels of the serotonin transporter (SERT) — the sodium-dependent protein responsible for uptake and deactivation of serotonin — were associated with cognitive impairment (which usually develops into full-blown dementia/Alzheimer with age).

In other words, higher extracellular serotonin levels were associated with dementia. The press articles state the exact opposite — that lower levels of the ‘happiness’ hormone serotonin were associated with dementia …

[The] study also suggests the prevention of dementia/Alzheimer may be as simple as eating some extra salt (providing the required sodium co-factor of SERT), or using a serotonin antagonist.

Air ionizers, which also tend to decrease extracellular serotonin may be helpful too and can provide benefit 24×7 without any conscious effort on behalf of the person/people using them.”

How to Address Elevated Serotonin

Considering that high extracellular serotonin can contribute to dementia, you’d be wise to keep your serotonin level as low as possible. One way to do that is by increasing GABA, which is available as a supplement. GABA increases the degradation rate of serotonin, so you cannot have high levels of both.

People with high GABA/low serotonin are typically calm and gregarious, whereas GABA deficiency and elevated serotonin is associated with anxiety, fear, depression, short temper, phobias, impulsiveness and disorganization.

People who have high GABA levels usually have low serotonin, and vice-versa. People with high GABA/low serotonin are typically calm and gregarious, whereas GABA deficiency and elevated serotonin is associated with anxiety, fear, depression, short temper, phobias, impulsiveness and disorganization.

Another important strategy is to address your gut health. When complex carbs that aren’t digested in your stomach travel down to your intestine, they end up feeding gram-negative bacteria that produce endotoxin, also known as LPS (lipopolysaccharide).

Endotoxin catalyzes a series of metabolic reactions that converts tryptophan in your gut to serotonin. So, to inhibit serotonin production in your gut (which is where most of the serotonin in your body is produced), you want to prevent endotoxin production, which means you need to balance your gut microbiome. Here are a few strategies to do that:

Pre- and probiotics — Eat prebiotic foods such as onions, garlic, leeks, asparagus and bananas, and probiotic fermented foods like yogurt, kefir, kimchi and sauerkraut. Alternatively, take a probiotic supplement. Beneficial bacteria such as Bifidobacteria and Lactobacillus, and beneficial yeast like Saccharomyces boulardii, can all help rein in the endotoxin production through competitive inhibition.

Limit sugar and refined carbohydrates — High intake of sugar and refined carbohydrates can feed harmful bacteria in the gut and promote inflammation, potentially increasing endotoxin production.

Avoid resistant starches — Other carbs to avoid would be resistant starches from legumes, beans, lentils, most grains, green bananas, sushi rice and pasta. Oatmeal can also cause trouble for many. You’ll know it’s incompatible with you if you get gas and/or constipation, or if it slows your digestion. Oatmeal is also high in linoleic acid (LA), which is why I avoid it.

If you have small intestinal bacterial overgrowth (SIBO), you may also need to avoid starches like rice and cooked potatoes, as you have inhibited ability to break down the starch into glucose. As a result, these kinds of starches may impede your recovery.

Eat plenty of antioxidant-rich whole foods — Foods rich in antioxidants, such as berries, leafy greens, and other colorful fruits and vegetables, can help reduce oxidative stress and inflammation in the gut, thereby supporting gut health and reducing endotoxin production.

Choose healthy fats such as those found in avocados, coconut oil, organic grass fed butter and ghee to help reduce gut inflammation.

Optimize your omega-3 level — Consuming omega-3 fats from sources like fatty fish (salmon, mackerel, sardines) may help reduce gut inflammation and promote a healthy gut microbiome.

Prolonged Estrogen Exposure Linked to Alzheimer’s Severity

Other research,¹⁵ published in October 2021, linked prolonged estrogen exposure to Alzheimer’s severity in women. This is particularly notable considering nearly two-thirds of Alzheimer’s patients are women.¹⁶ Estrogen is also a known carcinogen.¹⁷ As reported by Dinkov:¹⁸

“The study is pretty straightforward in its claim that longer exposure to endogenous estrogen was associated with exacerbated/higher biomarkers of Alzheimer disease (AD), as well as lower glucose metabolism and smaller brain volume in women.

Another interesting link the study mentions, which is relevant for both sexes, is that lower testosterone levels are also associated with exacerbated/higher biomarkers of AD. The earlier puberty and earlier menopause associations also mean shorter exposure to progesterone. As such, the study can be summarized with the simple statement that estrogen is detrimental while progesterone and testosterone are protective against AD.”

There are two key ways to lower your estrogen:

1. Avoiding estrogen replacement therapy and minimizing exposure to estrogenic compounds found in hundreds of consumer products.¹⁹ Opt for natural and organic personal care products, including makeup, skin care, and hair care items, to reduce exposure to synthetic chemicals like parabens and phthalates, which have estrogenic properties.

Ditto for household cleaning products, laundry detergents and air fresheners, many of which contain chemicals with estrogenic properties. Swap them out for natural, nontoxic alternatives or make your own cleaning solutions using vinegar, baking soda and essential oils instead.

Also minimize your use of plastic containers and food packaging, which can leach estrogenic compounds into food and beverages. Instead, opt for glass or stainless steel containers for food storage and water bottles.

2. Taking natural progesterone. Most formulations are not effective as they are oral or transdermal. Ideally, pure progesterone powder should be dissolved in a high-quality vitamin E with MCT oil and rubbed on your gums. Typical doses are 25 to 50 mg once or twice a day.

In my view, what mature women really need are progesterone and pregnenolone, not estrogen. In practical terms, you’ll want to make sure your levels of progesterone and pregnenolone are within healthy limits (the levels you’d have in your 20s), which is around 30 mg a day.

Mitochondrial Dysfunction Is at the Heart of Alzheimer’s

Nearly a quarter century ago, the late Ray Peat, a biologist and “father” of bioenergetic medicine, argued that Alzheimer’s and aging are two examples of what happens when you have poor mitochondrial function, resulting in declining energy production. He presented this hypothesis in two extensive articles.^20,²¹

In the second article, he specifically addressed the role of estrogen and polyunsaturated fats (PUFAs) like LA, as well as the protective influence of progesterone. He wrote, in part:²²

“Estrogen stimulates cell division, but can also increase the rate of cell death. Unsaturated fatty acids can also stimulate or kill … Besides increasing the free fatty acid concentration, estrogen possibly depresses the level of cholesterol, both of which are changes seen in the senile brain.

Estrogen causes massive alterations of extracellular matrix, and seems to promote dissolution of microtubules (Nemetschek-Gannsler), as calcium does. Unsaturated fats increase calcium uptake by at least some brain cells (H. Katsuki and S. Okuda, 1995.)

Unsaturated fats, like estrogen, increase the permeability of blood vessels. The unsaturated fat causes edema of the brain, inhibits choline uptake, blocking acetylcholine production.

Progesterone is a nerve growth factor, produced by glial cells (oligodendrocytes). It promotes the production of myelin, protects against seizures, and protects cells against free radicals. It protects before conception, during gestation, during growth and puberty, and during aging. It promotes regeneration. Its production is blocked by stress, lipid peroxidation, and an excess of estrogen and iron …

A ‘deficiency’ of polyunsaturated fatty acids leads to altered rates of cellular regeneration and differentiation, a larger brain at birth, improved function of the immune system, decreased inflammation, decreased mortality from endotoxin poisoning, lower susceptibility to lipid peroxidation, increased basal metabolic rate and respiration, increased thyroid function, later puberty and decreases other signs of estrogen dominance.

When dietary PUFA are not available, the body produces a small amount of unsaturated fatty acid (Mead acids), but these do not activate cell systems in the same way that plant-derived PUFAs do, and they are the precursors for an entirely different group of prostaglandins.”

Interestingly, a near-identical argument was laid out in an October 2020 article by Vijay Pande, Ph.D., and Kristen Fortney, titled “The Cure for Aging Might be the Cure for Alzheimer’s:”²³

“What we are only now beginning to understand is that the diseases that ultimately kill us are inseparable from the aging process itself. Aging is the root cause. This means that studying these diseases without taking aging into account could be dangerously misleading … and worst of all, impede real progress …

The biggest risk factor for Alzheimer’s isn’t your APOE status; it’s your age. People in their twenties don’t get Alzheimer’s. But after you hit the age of 65, your risk of Alzheimer’s doubles every five years, with your risk reaching nearly one out of three by the time you’re 85.

What if going after this one biggest risk factor is the best vector of attack? Maybe even the only way to truly address it? This isn’t about the vanity of staying younger, about holding on to your good looks or your ability to run an 8 minute mile. It’s about the only concrete possibility we have to cure these diseases.”

How to Optimize Your Mitochondrial Function Through Diet

To optimize your mitochondrial function, you need to address your diet, as the foods you eat are the substrate from which cellular energy is produced. LA wreaks havoc with your cellular machinery and needs to be limited to 5 grams or less per day.

To reach that goal, you need to ditch all processed foods, fast foods and most restaurant foods, as they’re all loaded with or cooked in LA-rich seed oils. Focus on whole and minimally processed foods.

Your macronutrient ratios also matter. As explained in previous articles, including “A Surprising Reason Why You May Need More Carbs in Your Diet,” ideally, you want to burn glucose in the electron transport chain of your mitochondria, and to ensure that, you need to eat enough healthy carbs, and get no more than 35% or so of your daily calories from fat.

If your fat intake is too high, you’ll prevent glucose from being burned in the mitochondria and force it into glycolysis instead, which is a highly inefficient way to produce energy.

Advances Made in Alzheimer’s Diagnosis

While there are few options available once Alzheimer’s sets in, advances in diagnosis are being made. Early diagnosis may at least give you a chance to implement strategies that might slow down its progression, or in an ideal scenario perhaps even reverse it to some degree. Diagnostic tools include:

• A blood test that measures the patterns of 10 specific lipids associated with the plaques found in the brains of people with Alzheimer’s disease. These 10 lipids are highly predictive of whether or not you will suffer cognitive impairment.²⁴

• A blood test that measures “a molecular precursor in the blood that can cause proteins to irregularly fold and clump in the brain, ultimately forming amyloid beta plaques.”²⁵

• A peanut butter smell test — In tests, patients diagnosed with early stage Alzheimer’s experienced a significant difference in their ability to detect the smell of peanut butter between their right and left nostrils.

The left nostril tends to be impaired in those with Alzheimer’s, whereas those with other kinds of dementia experience either no differences in odor detection between the two nostrils, or the right nostril is worse for detecting the smell compared to the left one.

• A 15-minute at-home test called SAGE, which stands for Self-Administered Gerocognitive Examination, can help you assess your risk of Alzheimer’s and dementia.²⁶ If taken at intervals over time, it can also serve as an early warning, if your scores begin to decline. The test can also be used to monitor the condition in those already diagnosed with Alzheimer’s. You can download the SAGE test from the Ohio State University’s website.²⁷

Additional Alzheimer’s Prevention Guidelines

In addition to optimizing your mitochondrial function and avoiding things that raise your serotonin and estrogen, other helpful prevention strategies include:

Avoid gluten and casein (primarily wheat and pasteurized dairy, but not dairy fat, such as butter) — Research shows that your blood-brain barrier is negatively affected by gluten. Gluten also makes your gut more permeable, which allows proteins to get into your bloodstream, where they don’t belong. That then sensitizes your immune system and promotes inflammation and autoimmunity, both of which play a role in the development of Alzheimer’s.

Optimize your gut flora by regularly eating fermented foods or taking a high potency and high-quality probiotic supplement.

Make sure you’re getting enough animal-based omega-3 fats, such as krill oil. High intake of the omega-3 fats EPA and DHA help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression and lowering your risk of developing the disorder.

Optimize your vitamin D level with safe sun exposure — Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed. In one 2023 study, vitamin D reduced dementia risk by 40%.

Keep your fasting insulin levels below 3.

Eat a nutritious diet, rich in folate — Vegetables, without question, are your best form of folate, and we should all eat plenty of fresh raw veggies every day. Avoid supplements like folic acid, which is the inferior synthetic version of folate.

Avoid and eliminate mercury and aluminum from your body — Dental amalgam fillings, which are 50% mercury by weight, are one of the major sources of heavy metal toxicity. Make sure you use a biological dentist to have your amalgams removed. Sources of aluminum include antiperspirants, non-stick cookware and vaccine adjuvants.

Make sure your iron isn’t elevated and donate blood if it is — Studies show that iron accumulations in the brain tend to concentrate in areas most affected by Alzheimer’s, namely the frontal cortex and hippocampus. Magnetic resonance imaging tests have also revealed elevated iron in brains affected by Alzheimer’s.

Exercise regularly — It’s been suggested that exercise can trigger a change in the way the amyloid precursor protein is metabolized,²⁸ thus slowing down the onset and progression of Alzheimer’s. In one study, women with the highest cardiovascular fitness had an 88% lower risk of dementia than those with moderate fitness.

Eat blueberries and other antioxidant-rich foods — Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against neurological diseases.

Challenge your mind daily — Mental stimulation, especially learning something new, such as learning to play an instrument or a new language, is associated with a decreased risk of Alzheimer’s.

Avoid anticholinergics and statin drugs — Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence, and certain narcotic pain relievers.

Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of CoQ10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein.

– Sources and References

^1, ^2, ^5, ¹⁶ ALZ.org AD Facts and Figures
³ Time Magazine March 5, 2014
⁴ Alzheimer’s Association March 14, 2023; 19(4): 1598-1695
^6, ⁸ CNN Health March 5, 2014
⁷ Neurology March 5, 2014 [Epub ahead of print]
⁹ CNN Health April 12, 2011 (Archived)
¹⁰ Journal of Alzheimer’s Disease September 2023; 96(1): 215-227
¹¹ IosPress.com, Journal of Alzheimer’s Disease September 2023; 96(1): 215-227
¹² Haidut.me February 20, 2024 (Archived)
¹³ UPI.com December 11, 2023
¹⁴ Neuroscience News December 7, 2023
¹⁵ Menopause October 2021; 28(10): 1099-1107
¹⁷ Science Daily December 13, 2002
¹⁸ Haidut.me March 30, 2022 (Archived)
¹⁹ Environmental Health News January 10, 2024
²⁰ Ray Peat Alzheimer’s Part 1
^21, ²² Ray Peat Alzheimer’s Part 2
²³ A16z.com October 7, 2020
²⁴ NBC News March 9, 2014
²⁵ Science Alert December 22, 2022
²⁶ Journal of Neuropsychiatry and Clinical Neurosciences January 13, 2014 [Epub ahead of print]
²⁷ Ohio State University, SAGE Test
²⁸ Journal of Neuroscience, April 27, 2005: 25(17); 4217-4221

Posted in Alzheimer's, Brain, Cancer, Dementia, Hormones, Linoleic Acid, Mitochondria, Mortality | One Comment »

Posted by: admin | Posted on: March 31, 2024

The Subtle Early Signals of Dementia in Someone You Love

Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/03/26/early-dementia-sign.aspx

Analysis by Dr. Joseph Mercola March 26, 2024

STORY AT-A-GLANCE

Before memory and thinking problems become obvious, people with dementia may display changes in mood and behavior
In the early stages of the disease, irritability, anxiety or depression may occur
Apathy is another common sign, although some people may display more blatant changes like suddenly becoming sexually promiscuous or developing the habit of snatching food off other people’s plates
Alzheimer’s disease is the result of poor mitochondrial function; to optimize your mitochondrial function, you need to limit your intake linoleic acid (LA) to 5 grams a day or less
To achieve this, you’ll need to eliminate all processed foods, fast foods and the majority of restaurant meals, which are frequently loaded with or prepared using seed oils high in LA

Worldwide, more than 55 million people are living with dementia, and each year nearly 10 million new cases occur.¹ Dementia is not a disease in itself but rather a term used to describe a number of different brain illnesses that may affect your memory, thinking, behavior and ability to perform everyday activities. The most common type of dementia is Alzheimer’s disease, which accounts for up to 70% of cases.²

Many people associate dementia with memory loss — and this is a red flag — however, not all memory problems are due to Alzheimer’s (and some causes of dementia-like symptoms, including memory loss, can be reversed, such as those related to thyroid problems and vitamin deficiencies).³

If you’ve noticed yourself or a loved one becoming increasingly forgetful or experiencing changes in thinking abilities, you should see a health care provider right away. Oftentimes, however, the first symptoms are so subtle they may be easily missed — and they may manifest as changes in behavior and mood long before memory problems become apparent.

Fortunately, there are two crucial prevention strategies that remain largely underdiscussed yet are relatively simple to implement — reducing linoleic acid (LA) intake and limiting exposure to estrogen.

Pay Attention to Personality Changes — An Early Sign of Dementia

Before memory and thinking problems become obvious, people with dementia may display changes in mood and behavior, according to a team of neuropsychiatrists and Alzheimer’s experts, who say the latter symptoms may be among the earliest signs of dementia.

The team released a 34-question checklist they believe could help diagnosis a new condition called mild behavioral impairment (MBI).⁴ Similar to mild cognitive impairment (MCI), which is defined by a noticeable decline in cognitive abilities that does not yet interfere with most daily functions, MBI describes changes in behavior and mood that may occur prior to MCI and the cognitive changes associated with dementia.

The checklist is intended to identify patients at risk of dementia earlier, as according study author Dr. Zahinoor Ismail, a neuropsychiatrist at the University of Calgary, among people with MCI, those with mood and behavior changes will progress to full-blown dementia faster.⁵ Some have expressed concern that the checklist may lead to overdiagnosis or false diagnosis, putting some people through increased medical testing and worry unnecessarily.

In the case of MCI, for instance, not everyone diagnosed will go on to develop Alzheimer’s or other types of dementia. In fact, The New York Times reported, up to 20% of those with MCI later turn out to be cognitively normal.⁶

Still, others say keeping an eye out for unusual behavioral or personality changes can help people get help, at least symptom relief, faster. Sadly, there is currently no cure for Alzheimer’s disease and, as it progresses, the disease is devastating not only for those diagnosed but also their friends and family. Prevention remains the best option, and I detail steps that can help below.

Behavioral and Mood Changes to Watch Out For

Dementia manifests differently in everyone, which is why the most important changes to watch out for are those that are unusual for your loved one. A person may, for instance, stop doing something they’ve always loved to do, be it cooking a certain dish for your birthday or watching the evening news.

Apathy is another common sign, although some people may display more blatant changes like suddenly becoming sexually promiscuous or developing the habit of snatching food off other people’s plates.⁷ The Alzheimer’s Association noted:⁸

“Individuals living with Alzheimer’s or other dementia may experience mood and personality changes. They can become confused, suspicious, depressed, fearful or anxious. They may be easily upset at home, with friends or when out of their comfort zone.”

In the early stages of the disease, irritability, anxiety or depression may occur. In fact, a study published in the journal Neurology not only found that people who eventually developed dementia were twice as likely to develop depression earlier on in their lives, but they also tended to display mood changes in a consistent pattern.⁹ Time reported:¹⁰

“The symptoms appeared in consistent phases: first, irritability, depression and nighttime behavior changes; followed by anxiety, appetite changes, agitation and apathy. The final phase was elation, motor disturbances, hallucinations, delusions and disinhibition.”

In order for early mood and/or behavioral changes to be considered MBI, the change in behavior must persist for at least six months.

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Signs of Mild Cognitive Impairment

In some people, MCI may follow the earliest changes in mood and behavior. MCI is a slight decline in cognitive abilities that increases your risk of developing more serious dementia, including Alzheimer’s disease, although it is by no means a guarantee. It’s estimated that up to 18% of people aged 60 and older are living with MCI.¹¹

Simply misplacing your keys on occasion is not cause for alarm, however forgetting important information that you would have normally recalled, such as appointments, conversations or recent events, may be a sign. You may also have a harder time making sound decisions, figuring out the sequence of steps needed to complete a task or judging the time needed to do so.

If you’ve been diagnosed with MCI, be aware that some cases do not progress and may even improve. Regular exercise, proper diet — including reducing your intake of LA — and engaging in mentally and socially stimulating activities may help to boost your brainpower.

Dementia: When to Worry?

It can be difficult to gauge if a loved one is declining mentally. If you have suspicions but aren’t sure, try keeping a notebook to jot down instances that concern you. You may be able to identify a pattern of events that makes the picture clearer.

Agnes B. Juhasz, nurse, dementia care specialist and author of ‘The Dementia Whisperer: Scenes From the Frontline of Caring,’ suggested making note of anything out of ordinary for that particular person. She wrote in the [U.K.]’s Mirror news:¹²

“Naturally, there are a few typical signs and possible changes that are worth watching out for more closely. These include the level of forgetfulness; acute or permanent confusion about certain things; disorientation in time and place; significant changes in behavior and personality; decreased judgment; changes in speech or writing; and withdrawal from social interactions and activities.

But all these suggested signs ultimately lead us back to the essential, magical question we always have to ask before we can arrive at any further conclusions: ‘Is this abnormal for this individual, or is it part of who they have always been?’ When we notice that something is new and odd, that has never occurred in a person’s life before, as far as we have observed, that is the point when further help may be needed.”

Early Warning Signs of Alzheimer’s

While an absent-minded mistake, like putting a mug in the wrong cabinet, is not cause for alarm, feeling confused about day-to-day tasks is.

Losing interest in hobbies, repetitive behaviors (phrases, gestures or questions), mispronouncing words or stuttering can also be signs. And while occasional forgetfulness, like forgetting why you were walking into a room, is not typically reason to worry, more profound confusion, like the room itself feeling unfamiliar, may signal a problem.¹³

The Alzheimer’s Association also compiled differences between symptoms of dementia, including Alzheimer’s, and typical age-related changes:¹⁴

Signs of Alzheimer’s/dementia	Typical age-related changes
Poor judgment and decision-making	Making a bad decision once in a while
Inability to manage a budget	Missing a monthly payment
Losing track of the date or the season	Forgetting which day it is and remembering it later
Difficulty having a conversation	Sometimes forgetting which word to use
Misplacing things and being unable to retrace steps to find them	Losing things from time to time

Why Addressing Mitochondrial Dysfunction by Reducing LA Is Key

Work by the late Ray Peat, a biologist and “father” of bioenergetic medicine, suggests Alzheimer’s disease is the result of poor mitochondrial function, which results in reduced energy production.^15,¹⁶

To optimize your mitochondrial function, you need to address your diet, as the foods you eat are the substrate from which cellular energy is produced. LA wreaks havoc with your cellular machinery, which is why it should be limited to 5 grams or less per day.

To achieve this, you’ll need to eliminate all processed foods, fast foods and the majority of restaurant meals, which are frequently loaded with or prepared using seed oils high in LA. Instead, prioritize whole and minimally processed foods.

In addition to limiting LA in your diet, carnosine, a dipeptide composed of two amino acids — beta-alanine and histidine — is a crucial aid for LA detoxification, as it binds to advanced lipoxidation endproducts (ALEs) that form from oxidized seed oils in your diet.

While your body will slowly eliminate stored LA over time, provided you reduce your intake, carnosine can help reduce the oxidative damage caused by LA while your body is cleaning itself out. I take liposomal carnosine every day before meals to help detoxify LA.

LA is highly susceptible to oxidation, and as the fat oxidizes it breaks down into harmful sub-components such as ALEs and oxidized LA metabolites (OXLAMs). These ALEs and OXLAMs are what cause most of the damage.

Carnosine binds to ALEs like a magnet and acts as a sacrificial sink. It’s basically a substitute target for these profoundly damaging molecules. In this way, carnosine allows your body to excrete the ALEs from your body before they damage your mitochondria, DNA or proteins.

As an added benefit, carnosine is protective against Alzheimer’s,¹⁷ due to its ability to scavenge 4-hydroxynonenal (4HNE), a biomarker of oxidative stress that may increase the harm caused by free radicals.

Elevated Serotonin Linked to Dementia

High serotonin levels are also linked to dementia.¹⁸ While often described as the “happy hormone,” serotonin, a chemical messenger in the brain, acts as an antimetabolite, hindering energy production in your mitochondria. A September 2023 study found that having low levels of serotonin transporter (SERT) is linked to problems with memory and thinking skills, which can eventually lead to dementia or Alzheimer’s disease.

SERT is like a “cleanup crew” in the brain, helping to remove excess serotonin. When there’s not enough SERT around to do its job, serotonin levels outside of brain cells can rise too high. This excess serotonin floating around can cause trouble and contribute to problems with memory and thinking.

The Estrogen Connection

Alzheimer’s disease (AD) is more common in women than men,¹⁹ and prolonged estrogen exposure is also linked to Alzheimer’s severity in women.²⁰ As bioenergetic researcher Georgi Dinkov explained, “The study can be summarized with the simple statement that estrogen is detrimental while progesterone and testosterone are protective against AD.”²¹

Avoiding estrogen replacement therapy and minimizing your exposure to the estrogenic compounds found in hundreds of consumer products is therefore an important step to protecting your brain health.

Taking natural progesterone is also important, but be aware that most formulations are not effective as they are oral or transdermal. Ideally, pure progesterone powder should be dissolved in a high-quality vitamin E with MCT oil and rubbed on your gums. Typical doses are 25 to 50 milligrams once or twice a day.

More Tips to Prevent Alzheimer’s Disease

In addition to optimizing your mitochondrial function, lowering your intake of LA and avoiding things that raise your serotonin and estrogen, other helpful Alzheimer’s prevention strategies include:

Optimize your gut flora by regularly eating fermented foods or taking a high potency and high-quality probiotic supplement.

Keep your fasting insulin levels below 3.

Exercise regularly — It’s been suggested that exercise can trigger a change in the way the amyloid precursor protein is metabolized,²² thus slowing down the onset and progression of Alzheimer’s. In one study, women with the highest cardiovascular fitness had an 88% lower risk of dementia than those with moderate fitness.

Eat blueberries and other antioxidant-rich foods — Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against neurological diseases.

Challenge your mind daily — Mental stimulation, especially learning something new, such as how to play an instrument or speak a new language, is associated with a decreased risk of Alzheimer’s.

– Sources and References

^1, ² World Health Organization, Dementia March 15, 2023
³ Alzheimer’s Association, What Is Dementia?
⁴ J Alzheimers Dis. 2017; 56(3): 929–938
^5, ^6, ⁷ The New York Times July 26, 2016
^8, ¹⁴ Alzheimer’s Association, 10 Early Signs and Symptoms of Alzheimer’s and Dementia
⁹ Neurology February 10, 2015, 84(6) 617-622
¹⁰ Time January 14, 2015
¹¹ Alzheimer’s Association, Mild Cognitive Impairment
¹² Mirror November 9, 2016
¹³ Independent December 2015
¹⁵ Ray Peat Alzheimer’s Part 1
¹⁶ Ray Peat Alzheimer’s Part 2
¹⁷ Pharmaceuticals June 2023; 16(6): 778
¹⁸ Journal of Alzheimer’s Disease September 2023; 96(1): 215-227
¹⁹ ALZ.org AD Facts and Figures
²⁰ Menopause October 2021; 28(10): 1099-1107
²¹ Haidut.me March 30, 2022 (Archived)
²² Journal of Neuroscience, April 27, 2005: 25(17); 4217-4221

Posted in Alzheimer's, Brain, Dementia, Exercise, Linoleic Acid, Supplements | One Comment »

Posted by: admin | Posted on: March 23, 2024

6 Healthy Lifestyle Habits That May Help Slow Memory Decline

Analysis by Dr. Joseph Mercola March 23, 2024

STORY AT-A-GLANCE

Some people notice changes in memory as they get older, which one study suggests you can influence by making lifestyle changes in diet, exercise, smoking, alcohol consumption, cognitive activity and social contact
Each factor was categorized, and statistical analysis of the raw data demonstrated that each of the individual behaviors was associated with a slower decline in memory
The researchers also looked at individuals with the APOE4 genotype, linked to memory decline and Alzheimer’s disease, finding that those who made positive changes in at least two to three of the lifestyle factors had a slower memory decline than those who did not
Linoleic acid is a dietary factor that negatively influences overall health and brain health. This ubiquitous fat is the most destructive ingredient in your diet; a 2017 study found it was linked to worsening memory and learning ability in animals with Alzheimer’s-type disease
Several more steps you might consider making to protect brain health and slow memory decline include eating more mushrooms, gaining better balance, good oral health, walking backward and steering clear of statin medications to name just a few

Research¹ published in The BMJ has found links between a healthy lifestyle and memory decline in older adults using a 10-year, population based prospective cohort study. As people get older, some notice that they have changes in memory, like forgetting where they put their keys or having trouble remembering someone’s name.

For the most part, these changes don’t significantly impact a person’s daily life. Many people believe these are normal changes that occur with aging, and yet they don’t occur in everyone. It is normal for people of all ages to forget things occasionally, but progression to mild cognitive impairment, which is an early stage of loss of memory and other cognitive abilities, is not a normal part of aging.²

The prevalence of memory decline may be increasing. In a 1993 Spanish study³ of people aged 40 years and over, researchers found the prevalence of memory impairment was 3.6%, and in individuals 65 years and older it was 7.1%. According to the CDC, a more current measurement found that 1 in 10 U.S. adults aged 45 years and older reported having memory loss.⁴

While they are similar in nature, memory decline and dementia are two distinct conditions that affect how the brain functions. However, worsening memory loss is sometimes an early sign of Alzheimer’s disease,⁵ which affects an estimated 6 million Americans, 73% of which are 75 years and older. But there is hope, since data from the featured study indicates that making simple lifestyle choices can have a significant impact on your long-term brain health.

These Six Simple Steps Are Linked to Slower Memory Loss

A group of researchers from China were seeking to identify the types of lifestyle choices that might protect against memory loss as an individual ages.⁶ The researchers gathered participants aged 60 years or older from the northern, southern and western parts of China. In total, 29,072 people participated in the study. The researchers followed up with participants over a 10-year period, from 2009 to 2019.

Anyone who had a life-threatening disease, or hearing or vision loss, which are factors associated with cognitive decline, was excluded from the study. During the second phase, the people who were in Phase 1 who had available APOE genotyping, and who were not diagnosed with mild cognitive impairment or dementia, were included.

The researchers followed up with the participants four times over 10 years to look for links between memory in participants with normal cognitive function and lifestyle choices. Researchers used neuropsychological testing to identify cognitive performance at baseline, and at each follow-up during the 10-year period. Data for anyone who progressed to mild cognitive impairment or dementia was excluded in the main analysis.

The researchers analyzed six modifiable lifestyle factors, which included physical exercise, diet, alcohol, smoking, cognitive activity and social contact. In each category, individuals were ranked according to how much they participated in a particular factor. For example, people were categorized as currently smoking, never smoked or used to smoke.

After data collection, the researchers evaluated the association of each of these lifestyle factors against memory function. They found three distinct groups. Those who followed four to six of the lifestyle choices were in a favorable group, those who followed two to three were in an average group, and those who followed 0 to 1 were in the unfavorable group.

Statistical analysis of the raw data demonstrated that each of the individual behaviors was associated with a slower memory decline. After adjusting for health and socioeconomic factors, the individuals who had a healthy diet had the strongest protection against memory decline.⁷ This was followed by those who engaged in cognitive activity and then physical exercise.

The researchers began with the statement that “memory continuously declines as people age,” but the rate of that decline may be affected by lifestyle factors. Age-related memory decline is not always associated with Alzheimer’s disease or other types of dementia. Additionally, forgetfulness in old age may “be reversed or become stable rather than progress to a pathological state.”⁸

Results Were Also True for APOE4 Carriers

Factors that have been identified in past research that could affect memory include aging, chronic diseases, lifestyle patterns and the apolipoprotein (APOE) ε4 genotype.⁹ The researchers considered the APOE genotype because of its association with Alzheimer’s disease. APOE4 is a specific allele of the apolipoprotein E gene.

The APOE gene is involved in the production of a protein called apolipoprotein E, which plays a role in cholesterol metabolism and lipid transportation. The APOE gene has several alleles — or slight variations in the genetic sequencing — including APOE2, APOE3 and APOE4.

It is APOE4 that’s associated with an earlier and more rapid decline in memory and an increased risk of Alzheimer’s disease.¹⁰ People who inherit one copy of the APOE4 allele have an increased risk of developing Alzheimer’s disease and those who inherit two copies have an even higher risk.

However, the data from this study showed that while APOE4 genotype could increase your risk for developing dementia, those who carried APOE4 and had favorable or average lifestyles showed a slower memory decline as compared to those who had unfavorable lifestyles.¹¹ In other words, while the gene can increase your risk, you have some control over whether that risk is expressed by how you take care of yourself.

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Diet, Linoleic Acid and Memory Decline

I have long believed and talked about the difference that you can make in your health by making simple lifestyle choices in each of these same areas: nutrition, physical exercise, mental exercise, smoking, excessive alcohol and socialization. I would also suggest that there are other simple steps you can take to protect your memory and cognition, which I’ll discuss below.

But before moving further, I think we need to address one of the most destructive ingredients in your diet — linoleic acid. I take a more in-depth look at how linoleic acid destroys your health in “Linoleic Acid — The Most Destructive Ingredient in Your Diet.” But, if you don’t have time, let’s summarize the key points.

Fats are the primary building block of your cell membranes, which is why it’s important to eat the right type of fat for your health and longevity. Vegetable and seed oils are loaded with polyunsaturated fats (PUFAs), which are chemically unstable, making them highly susceptible to damage by oxygen species that are generated during energy production in the cells.

This damage causes them to form advanced lipoxidation end (ALE) products and free radicals that damage cell membranes, proteins, mitochondria and your DNA. Even worse, PUFAs are integrated into your cell membranes, where they can remain for five to seven years.

In the article linked above I explain why seed oils are far worse than sugar and how consuming LA can have a significant impact on your overall health, including increasing your risk of memory impairment and Alzheimer’s disease.

A 2017 study¹² published in Scientific Reports from Temple University concluded that replacing olive oil with canola oil (a seed oil) was not justified. However, in the press release,¹³ the researchers admitted that canola oil was linked to worsening memory and learning ability in animals with Alzheimer’s disease.

Other Strategies That Can Protect Your Memory and Cognitive Health

As the featured study demonstrated, protecting your cognitive health and memory is as much a function of what you should do as it is what you shouldn’t do. Let’s look at some other steps you can take to help protect your memory and cognitive health.

Mushrooms — As I discuss in “How Mushrooms Help Protect Your Brain,” these fungi contain ergothioneine and glutathione, also known as the “master antioxidant.” Both help protect against age-related diseases like heart disease, cancer and dementia. In countries with the highest levels of ergothioneine in the diet, individuals have the lowest risk of neurodegenerative diseases.

Data show that eating more than two portions of mushrooms in a week can reduce the risk of mild cognitive impairment by a significant percentage. Be sure to choose organic mushrooms or grow your own because fungi easily absorb air and soil contaminants.

10-second balance test — This quick 10-second test is independently linked to all-cause mortality. Data also shows that if you cannot stand on one leg for 20 seconds you may have an increased risk of reduced cognitive function.

If you don’t have an underlying health condition that causes vertigo or loss of balance, you can improve your balance and stability, reducing your risk of falling and taking a step toward taking care of your brain health. I share six ways to improve your balance and stability in “Can You Pass the 10-Second Balance Test?“

Address periodontal disease — Data show that periodontal disease may contribute to the development of Alzheimer’s. The risk of mild cognitive impairment and Alzheimer’s disease in those with periodontal disease is significantly higher than in those without periodontal disease. This underscores the importance of maintaining good oral health throughout your life.

Walking backward — A small study by researchers from London University has suggested that walking backward could boost your memory. Each time participants in the study walked backward consistently, they got more test answers correct, which suggested to researchers that there’s a link between time and space that is fundamental to the way our brain forms memory.

Walking backward is believed to have originated in ancient China. Today, it’s also used to build muscle, improve sports performance and promote balance.

Flavonol and choline — Nutrient deficiencies can impact memory function. A large-scale study of flavanol and epicatechin supplementation demonstrated that people with a baseline flavanol deficiency experienced improvements in memory. Choline is another essential nutrient that plays a role in memory, energy and metabolism.

Choline is necessary to make acetylcholine, which is a neurotransmitter involved in memory performance. Researchers have established a relationship between high dietary choline and better cognitive performance and low choline intake has been associated with an increase in anxiety.

Magnesium threonate — Researchers have found that some people’s brains shrink with age more than others, but now it’s believed that increasing synapses and their density could help prevent cognitive decline.

Scientists developed magnesium L-threonate in 2010, which is a patented compound with the ability to enhance working memory, short and long-term memory and learning. In 2016 they found that not only did it enhance performance, but it could reverse brain aging by more than nine years.

Avoid statins — Statins are promoted by Big Pharma to help protect against cardiovascular disease, yet they do not. People with early mild cognitive impairment and low to moderate cholesterol levels may more than double their risk of dementia when they use statin medications. The medication also contributes to a decline in metabolism in the brain’s posterior cingulate cortex, which is the region that declines significantly in early Alzheimer’s disease.

Shed excess body fat — Mounting evidence suggests that maintaining a healthy level of body fat and an increased level of muscle mass can affect your brain health and slow the rate of cognitive aging.

People with higher amounts of abdominal fat had lower levels of fluid intelligence with age while those with greater muscle mass were more protected against this decline. To fully understand your metabolism, and therefore the changes you can make to achieve a healthy weight see, “Crucial Facts About Your Metabolism.”

– Sources and References

Posted in Alzheimer's, Balance, Brain, Diet, Fat, Food, Linoleic Acid, Memory, Statins, Supplements, Teeth, Weight Loss | No Comments »

Posted by: admin | Posted on: March 22, 2024

Study Links Picking Your Nose to Alzheimer’s Disease

Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/03/21/nose-picking-alzheimers.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.

Analysis by Dr. Joseph Mercola March 21, 2024

STORY AT-A-GLANCE

Chronic neuroinflammation may trigger the development of amyloid plaques associated with Alzheimer’s disease, and neuroinflammation may be linked to nose picking
Other reasons to keep your finger out of your nose include avoiding spreading infection to others, such as asymptomatic colonization with Staphylococcus aureus that may lead to opportunistic infections. Changes in the nasal microbiome and damage to the inner tissues and structure of the nasal cavity can also occur when you pick your nose
Several strategies can lower your risk of Alzheimer’s disease including reducing or eliminating processed sugar, protecting your gut microbiome, ensuring you are not deficient in B vitamins, and protecting your lungs from air pollution, all of which are linked to a decline in memory and cognitive function
Strategies to stop picking your nose include keeping your nasal membranes hydrated by using a humidifier, drinking plenty of clean water and using coconut oil to moisten the membranes in your nose

The mechanism of chronic inflammation is at the root of many modern diseases, such as heart disease, cancer, auto-immune diseases and chronic hepatitis.¹ A review of the literature from Western Sydney University has suggested that chronic neuroinflammation triggered by chronic nose picking may contribute to the development of Alzheimer’s disease.²

Nose picking is a common practice. One 1995 study³ found that 91% of those asked admitted to picking their nose and 75% felt that “almost everyone does it.” In this first population survey, they found that “it is an almost universal practice in adults but one that should not be considered pathologic for most.”⁴

These results were confirmed in a sample of adolescents in which the researchers found that nearly the “entire sample admitted to nose picking, with a median frequency of four times per day.”⁵ There are a variety of reasons that people pick their noses, including removing dried nasal mucus, which also goes by the term “boogers,” and nervous habits that can become a compulsion falling under the mental health condition of body-focused repetitive behavior.

Like your gut, the nasal cavity has its own microbiome that provides your body with natural protection. The researchers of the featured study⁶ and other studies have theorized that altering that microbiome can influence pathogenic spread to the brain and contribute to chronic neuroinflammation.

A 2022 animal study⁷ found that chlamydia pneumoniae can infect the central nervous system by traveling along the olfactory and trigeminal nerves and thus contribute to an increased risk of Alzheimer’s disease.

Currently, data show⁸ that more than 6 million Americans live with Alzheimer’s disease and 1 in 3 seniors dies with dementia. In 2023, it was estimated that all forms of dementia cost the nation $345 billion, which experts estimate could rise to nearly $1 trillion by 2050.

In the midst of a nationwide health care workforce shortage, the Alzheimer’s Association estimates that by 2030 the country will need an additional 1.2 million direct care workers just to care for the growing number of individuals with dementia.⁹

Nose Picking Increases Inflammation and Risk of Alzheimer’s Disease

The paper published in Biomolecules¹⁰ reviewed data that associated pathogens with Alzheimer’s disease, including viruses, bacteria and fungi. After reviewing the data, the researchers proposed that neuroinflammation found in the brains of people with Alzheimer’s disease could be partially triggered by pathogens that entered through the nose and olfactory system.

It appeared to be a plausible route of entry because of the direct anatomical connection. Neuroinflammation is likely a major contributor to the development of amyloid plaques, which are the hallmark characteristic of Alzheimer’s disease. The researchers reviewed the different ways that this formation is thought to be linked to neuroinflammation and suggested that while the formation is complex, it’s also bi-directional.

The researchers also noted that periodontal infections, which typically triggered dysbiosis of the oral microbiome, are increasingly associated with an increased risk of Alzheimer’s disease.¹¹ Several studies that evaluated the oral microbiota of participants with Alzheimer’s disease found an altered composition including oral bacteria linked to amyloid beta plaque formation.

In addition to changes in the oral microbiota that may be associated with an increased risk of Alzheimer’s disease, the researchers noted that with age, the composition of the nasal microbiome changes to become more like that found in the oropharyngeal area. This influences the nasal microflora and could be a contributor to neurodegenerative diseases, considering the bi-directional association between the nasal microbiota and Alzheimer’s disease.

The researchers suggest¹² that pathogens could enter the brain through the olfactory system and contribute to neuroinflammation found in Alzheimer’s disease. However, they also state that one of the limitations of their review of the literature was the question of which came first.

Did individuals have a compromised immune system that led to neuroinflammation and Alzheimer’s disease, or did increasing age-related inflammation and subclinical Alzheimer’s disease trigger unhealthy habits or defects in the immune system that allowed the entry of olfactory pathogens?

The author suggested that this shift in the nasal microbiome may trigger mild brain infections without symptoms, but which also trigger chronic inflammation and protein plaques that contribute to the development of Alzheimer’s disease. The New York Post¹³ reports that some of the common pathogens found in the brains of people with Alzheimer’s disease include the cat-derived parasite Toxoplasma gondii, the herpes virus, and the bacteria that cause pneumonia.

The researchers suggest that until there’s a greater understanding of the role of olfactory pathogens in Alzheimer-associated neuroinflammation, improving hand hygiene could be an easy preventive step.

More Reasons to Keep Your Fingers Out of Your Nose

While data from the featured study suggest that nose picking may be associated with the development of Alzheimer’s disease, there are other reasons you should keep your fingers out of your nose. This is especially true for those who are sick or may have a weakened immune system.

The nasal cavity is a reservoir for pathogens that can potentially spread. Data have demonstrated that the nasal microbiome changes with age and after exposure to a range of infections and immunological conditions. Your nasal microbiome profile can influence your immune response. Data from 2018¹⁴ showed up to 30% of people are asymptomatically and permanently colonized with Staphylococcus aureus in their nasal cavity.

Individuals who pick their noses have a much higher risk of colonization,¹⁵ which may lead to opportunistic infections at surgical sites or other infections that increase morbidity, mortality and health care costs.¹⁶ For individuals whose noses are colonized, this can lead to serious infections if your fingernails leave tiny cuts within the nasal tissue, where the bacteria can find their way into the bloodstream.

Nose picking also changes the nasal microbiome as demonstrated in a 2023 study¹⁷ that revealed health care workers who pick their noses had an increased risk of contracting SARS-CoV-2. Other opportunistic infections can spread and lead to the development of pneumonia, otitis media, asthma and chronic rhinosinusitis.¹⁸

There’s a reason that a skin infection called impetigo is more commonly found around the nose and mouth. That’s because the bacteria that live in the nose can cause this type of infection. Nose picking can move that bacterium to other areas of the body where there’s broken skin and impetigo can develop.¹⁹

Nose picking also increases the risk of damaging the tissues and structures inside the nose²⁰ and triggering nosebleeds. Aggressive nose pickers may damage the septum, which is the bone and cartilage that divides the left and right sides of the nose.

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More Strategies to Help Reduce Your Risk of Alzheimer’s

The featured study and others have suggested that keeping your fingers out of your nose may help or reduce your potential risk of Alzheimer’s disease. However, as I discussed in a previous article on this topic, “Can Nose Picking Raise the Risk of Alzheimer’s and Dementia?” there are more steps you can take to help decrease your risk of Alzheimer’s disease and other types of dementia.

• Sugar — For many years I have warned about the dangers of processed sugars and high carbohydrate foods. Over the years, there have been several studies that found a significant relationship between a high carbohydrate diet and a significantly increased risk of dementia.

• Gut microbiome — Researchers have also found a link between Alzheimer’s disease and your gut microbiome, which appears to be related to lipopolysaccharides and two short-chain fatty acids — acetate and valerate — that increase amyloid deposits in the brain.²¹

• Cholesterol — While cholesterol has been vilified as something that should be as low as possible to prevent heart disease, it is a crucial component for good health, and levels that are too low can have serious repercussions. According to senior research scientist Stephanie Seneff, Ph.D., insufficient fat and cholesterol in the brain play a crucial role in the Alzheimer’s disease process.

She details the mechanism of this dysfunction in a 2009 paper.²² A 2018 study²³ found those with higher total cholesterol at midlife had a reduced risk for cognitive decline after age 85.

• Vitamin B deficiencies — B vitamin deficiencies are known to have an effect on the brain, including the development of depression. They play an important role in cognitive decline and dementia.

• Air pollution — Studies have linked exposure to air pollution in Europe and the U.S. with an increased risk of dementia. In “New Evidence Shows Link Between Air Pollution and Alzheimer’s” I discussed the results of a 10-year study presented at the Alzheimer’s Association International Conference 2021 that showed how women living in areas of lower air pollution had a slower decline f overall memory and cognitive function.

Tips to Help You Stop Picking Your Nose

Knowing you need to stop a behavior, or even deciding to stop, isn’t always enough to make you stop. When nose picking is not related to psychological factors, it’s commonly related to dry nasal passages that lead to the increased production of mucus and an urge to pick and clean.

Keeping your nasal passages moist can help reduce mucus production and therefore reduce the urge. You can improve hydration of the mucus membranes in your nasal passages by:

Using an indoor humidifier, especially during the winter months, to keep the humidity above 40%
Drink plenty of clean water and stay well-hydrated
Use a nasal saline spray sparingly, which helps to lubricate the nasal passages, but overuse can contribute to drying it as it tends to wash away the mucus that protects the membranes²⁴
Use coconut oil on the inside lining of the nostril to help hydrate the membranes and break the cycle of nose picking

Nose picking can also be associated with chronic stress and anxiety. When it becomes compulsive, it’s called rhinotillexomania²⁵ and may require the help of a mental health professional to address the stress and anxiety that leads to the compulsive behavior.

– Sources and References

¹ Chronic Inflammation, August 7, 2023, Differential Diagnosis 75% DTP
^2, ⁶ MDPI, 2023;13(11)
^3, ⁴ Journal of Clinical Psychiatry, 1995;56(2)
⁵ Journal of Clinical Psychiatry, 2001;62(6)
⁷ Scientific Reports, 2022; 12(2759)
^8, ⁹ Alzheimer’s Association, Alzheimer’s Disease Facts and Figures
¹⁰ MDPI, 2023;13(11) Section 2
¹¹ MDPI, 2023;13(11) Section 4
¹² MDPI, 2023;13(11) Section 9
¹³ The New York Post, February 4, 2024
^14, ¹⁶ Frontiers in Microbiology, 2018; 9
¹⁵ Infection Control and Hospital Epidemiology, 2006; 27(8)
¹⁷ Plos|One August 2, 2023
¹⁸ Therapeutic Advances in Allergy and Rhinology, 2020; doi: 10.1177/215265672091
¹⁹ Nationwide Children’s, January 13, 2021
^20, ²⁵ Cureus, 2018; 10(8)
²¹ Journal of Alzheimer’s Disease, 2020;78(2)
²² MIT.edu APOE-4: The Clue to Why Low Fat Diet and Statins May Cause Alzheimer’s by Stephanie Seneff
²³ The Conversation March 5, 2018
²⁴ The Ohio State University Wexner Medical Center, October 30, 2017

Posted in Alzheimer's, Brain, Inflammation | No Comments »

Posted by: admin | Posted on: March 9, 2024

What Do L-Carnitine Supplements Really Do?

Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/03/07/what-do-l-carnitine-supplements-really-do.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.

Analysis by Dr. Joseph Mercola March 07, 2024

STORY AT-A-GLANCE

Your body needs carnitine for energy production; it helps transport long-chain fatty acids into your mitochondria where they’re oxidized and turned into energy in the form of adenosine triphosphate (ATP)
Acetyl-L-carnitine has many beneficial effects on brain metabolism, protects against neurotoxic insults and has been shown to benefit certain forms of depression
Carnitine has been widely studied for autism as a treatment that targets mitochondria; one meta-analysis found low carnitine in 80% of children with autism
Carnitine may help moderate oxidative stress and decrease inflammation, benefiting heart health; it may also help prevent potentially fatal arrhythmias
Carnitine supplementation significantly improved ovulation and pregnancy rates, while reducing BMI and insulin resistance, in women with polycystic ovary syndrome (PCOS)

Carnitine is another important nutrient that’s abundant in animal foods. Your body produces L-carnitine from the amino acid lysine, and while healthy people are typically able to synthesize enough, certain conditions — like pregnancy — may cause your body’s need for carnitine to exceed its ability to produce it. For this reason, carnitine is considered a conditionally essential nutrient.¹

L-carnitine and acetyl-L-carnitine are forms of carnitine found in dietary supplements. While your body absorbs carnitine from animal foods such as grass fed beef better than carnitine in dietary supplements,² some research suggests L-carnitine supplements may benefit certain conditions.

Carnitine for Brain Health

Your body needs carnitine for energy production. It helps transport long-chain fatty acids into your mitochondria where they’re oxidized and turned into energy in the form of adenosine triphosphate (ATP),³ which is needed by your cells for life, repair and regeneration. Carnitine may also help remove toxins from the mitochondria.⁴

Acetyl-L-carnitine (ALCAR) is more easily absorbed in your gut than L-carnitine, and also crosses the blood-brain barrier.⁵ ALCAR has many beneficial effects on brain metabolism, protects against neurotoxic insults and has been shown to benefit certain forms of depression. In one study,⁶ healthy mice given ALCAR for 25 days at a dose of about half a gram per kilo were found to have increased levels of the neurotransmitters noradrenaline and serotonin.

According to the authors, this is “consistent with ALCAR’s potential efficacy for depressive symptoms.” In another study, ALCAR was found to improve the clinical condition of patients with degenerative cerebellar ataxia, a condition resulting in the loss of control of bodily movements.⁷ According to the authors, “statistically significant improvement of some symptoms and a slow progression of the disease in both groups of patients” were observed.

Carnitine for Alzheimer’s Disease and Autism

Carnitine is also being studied for use in Alzheimer’s disease. According to the National Institutes of Health:⁸

“Cholinergic neurons use the neurotransmitter acetylcholine, and Alzheimer’s disease is often treated by increasing acetylcholine levels or preventing its breakdown. Carnitine might be conditionally essential in individuals with Alzheimer’s disease because it may support acetylcholine synthesis and help remove toxic compounds to alleviate mitochondrial dysfunction associated with extensive degeneration of brain structures.

Therefore, researchers have examined whether acetyl-L-carnitine supplements benefit individuals with Alzheimer’s disease or other forms of dementia, but studies have had mixed results.”

In a meta-analysis of 21 studies, adults with mild cognitive impairment or Alzheimer’s disease took 1.5 grams to 3 grams of acetyl-L-carnitine or placebo daily for three to 12 months. Those taking acetyl-L-carnitine had greater improvements than those taking placebo.^9,¹⁰

It’s also been widely studied for autism as a treatment that targets mitochondria. One meta-analysis found low carnitine in 80% of children with autism.¹¹ As explained in Seminars in Pediatric Neurology:¹²

“Two medium sized (n = 30, 30) double-blind placebo-controlled studies using L-carnitine treatment (50 mg/kg/d for 3 months and 100 mg/kg/d for 6 months) found that scores on the Childhood Autism Rating Scale (CARS) improved with L-carnitine as compared to placebo with one study finding that greater symptomatic improvement was correlated with a greater increase in blood carnitine levels.

A small (n = 10) 8-week open-label trial of L-carnitine used particularly high doses (up to 400 mg/kg/d in 3 divided doses, maximum of 6000 mg/d) …

Several parental rated measures showed improvements in behavior and hyperactivity before correction for multiple comparisons and improvements in language correlated with post-treatment blood carnitine levels. Children with ASD and genetic mutations in the carnitine pathway also appear to response to L-carnitine.

… Thus, L-Carnitine is a promising treatment for children with ASD. For child neurologists, it is always important to remember that children with ASD could have an underlying defect in carnitine metabolism.”

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Carnitine for Heart Health

There’s some evidence that carnitine may help moderate oxidative stress and decrease inflammation, benefitting heart health. It may also help prevent potentially fatal arrhythmias, or irregular heart rhythms.¹³

One meta-analysis involving 3,629 adults found, “Compared with placebo or control, L-carnitine is associated with a 27% reduction in all-cause mortality, a 65% reduction in Vas [ventricular arrhythmias], and a 40% reduction in anginal symptoms in patients experiencing an acute myocardial infarction.”¹⁴

There’s some controversy over carnitine for cardiovascular disease, however, because it’s metabolized by gut microbiota into trimethylamine-N-oxide (TMAO), a substance associated with an increased risk of cardiovascular disease,¹⁵ although the evidence on that is mixed.

According to James DiNicolantonio, Pharm.D., who is also the coauthor of my book, “Superfuel: Ketogenic Keys to Unlock the Secrets of Good Fats, Bad Fats, and Great Health,” the likely true cause of elevated TMAO levels is hepatic insulin resistance.¹⁶ Because carnitine (and choline) raises TMAO, some recommend limiting dietary and supplementary intake of these nutrients.

However, DiNicolantonio and his coauthors point out there’s a significant flaw in this theory, stating, “… supplemental carnitine is known to be highly protective in patients with vascular disease; and fish, the richest dietary source of preformed TMAO, is also protective.”¹⁷ There’s little evidence to suggest that dietary intake of TMAO or its precursors actually promote CVD, provided your renal function is normal. DiNicolantonio explains:¹⁸

“With respect to carnitine and CV risk, a meta-analysis¹⁹ of prospective clinical trials in patients who had recently experienced a myocardial infarction concluded that carnitine supplementation is markedly protective with respect to total mortality, ventricular arrhythmias and new-onset angina …

Clinical trials^20,²¹ have also reported favorable effects of supplemental carnitine or carnitine esters on angina, intermittent claudication and heart failure.

Moreover, rodent atherogenesis studies, in which carnitine has been administered in doses reasonably proportional to the supplementation doses used clinically, have found that carnitine is anti-atherogenic, despite its propensity to raise TMAO …

It is therefore reasonable to suspect that moderately elevated TMAO, rather than being a mediator of the associated CV risk, is a marker for factors which both promote CV events and increase plasma TMAO.”

Carnitine for Weight Loss

Research suggests L-carnitine supplements, which are the least expensive form on the market with an absorption rate of 14% to 18%,²² may be useful for weight loss. In a systematic review and meta-analysis of 37 trials, L-carnitine supplementation significantly decreased body weight, body mass index and fat mass, particularly in adults who are overweight or obese.²³

“A nonlinear dose-response association was seen between L-carnitine supplementation and body weight reduction … suggesting that ingestion of 2000 mg L-carnitine per day provides the maximum effect in adults,” the team, from Shahid Sadoughi University of Medical Sciences in Iran, noted.²⁴

Carnitine May Improve Fertility

L-carnitine concentrates in the epididymis, a duct behind the testis where sperm mature. Concentrations of L-carnitine in semen have been linked to the number of sperm, suggesting it may play an important role in fertility in men. Some research also shows that L-carnitine supplementation for two months may improve sperm quality and motility.²⁵ According to the NIH:²⁶

“Carnitine might play a role in sperm maturation, sperm motility, and spermatogenesis. It might also reduce oxidative stress, which could improve oocyte growth and maturation. Therefore, researchers are examining whether supplemental carnitine improves sperm count, concentration, and motility as well as pregnancy rates.”

Women with polycystic ovary syndrome (PCOS), which can affect fertility, may also benefit from carnitine. A systematic review and meta-analysis involving women with PCOS revealed that carnitine supplementation ranging from 250 mg to 3,000 mg daily for 84 to 90 days significantly improved ovulation and pregnancy rates, while reducing BMI and insulin resistance.²⁷

Carnitine to Boost Athletic Performance

There’s interest in the use of carnitine to enhance athletic performance, in part because carnitine preserves muscle glycogen while boosting fat oxidation. “It also spares the use of amino acids as energy sources during exercise, making them potentially available for new protein synthesis, and decreases the accumulation of lactate,” NIH notes,²⁸ but research is mixed on its benefits.

In one study published in the Journal of Physiology, the data showed L-carnitine supplementation for six months raised levels of muscle carnitine by 21%.²⁹ Further, participants taking carnitine supplements raised their athletic performance and work output by 11% in a 30-minute performance trial.

The researchers explained this improvement “by the dual role of carnitine — glycogen sparing at low intensities and reduced muscle lactate accumulation at high intensities.”³⁰

Where carnitine further shines is for those with frailty. It’s been suggested that carnitine deficiency could cause frailty via mitochondrial dysfunction, with research showing pre-frail older adults had decreases in frailty and improvement in hand grip strength when they took 1.5 grams of carnitine daily for 10 weeks.³¹

Carnitine for Liver Health and More

Additional research is looking into the effects of carnitine supplementation on nonalcoholic fatty liver disease (NAFLD). A systematic review and meta-analysis revealed that L-carnitine supplementation may improve liver function and regulate triglyceride metabolism in those with NAFLD. Writing in Systematic Reviews, researchers explained:³²

“The main drivers in NAFLD are inflammation and accumulation of lipids, and L-carnitine has been shown to have anti-inflammatory effects by upregulating the peroxisome proliferator activator receptor-γ (PPAR-γ) in the liver. L-carnitine is also closely related to fat metabolism.”

Beyond the liver, carnitine also shows promise for a range of other health conditions, including:^33,34

Insulin resistance
Diabetes
Osteoarthritis
Muscle cramps

In another example, a systematic review and meta-analysis found men and women experienced improvements in waist circumference and blood pressure, two biomarkers of metabolic syndrome, when taking carnitine supplements.³⁵

The studies used carnitine doses between 0.75 grams (gm) and 3 gm per day for eight to 24 weeks, with researchers suggesting biomarkers of metabolic syndrome could improve with a carnitine dose of 1 gm to 3 gm per day, by reducing fasting blood sugar and triglycerides, while increasing high-density lipoprotein (HDL) cholesterol.

Are You Getting Enough Carnitine?

Most people can effectively synthesize between 11 mg and 34 mg of carnitine per day, which is typically enough to prevent deficiency.³⁶ Animal foods, including meat, seafood and dairy, are the richest sources of L-carnitine, so if you eat animal protein it will virtually assure you receive enough carnitine without having to take supplements.

However, if you eat a primarily plant-based diet or are targeting certain conditions, you may need to consider supplementation. Acetyl-L-carnitine (not regular L-carnitine), for instance, appears to be particularly beneficial for improving memory, but you need about 2,000 mg to 2,500 mg a day. Most notice a difference after a few weeks.

If you do choose to supplement, be sure to choose a reputable source. When NOW Foods tested seven largely unknown brands of acetyl-L-carnitine, none met label claims and most were labeled incorrectly.³⁷

– Sources and References

¹ Linus Pauling Institute, L-Carnitine
² NIH, Carnitine, Consumer
^3, ^4, ^8, ^9, ^13, ^15, ³³ NIH, Carnitine, Health Professional
^5, ²² Yahoo June 23, 2023
⁶ Neurochemistry International 2012 Jul;61(1):100-7
⁷ Clinical Neuropharmacology 2000 Mar-Apr;23(2):114-8
¹⁰ Int Clin Psychopharmacol. 2003 Mar;18(2):61-71. doi: 10.1097/00004850-200303000-00001
¹¹ Seminars in Pediatric Neurology October 2020, Volume 35, 100829, ASD Is Associated With Unique Disorders of Mitochondrial Metabolism
¹² Seminars in Pediatric Neurology October 2020, Volume 35, 100829
^14, ¹⁹ Mayo Clin Proc. 2013 Jun;88(6):544-51. doi: 10.1016/j.mayocp.2013.02.007. Epub 2013 Apr 15
^16, ^17, ¹⁸ Open Heart 2019; 6: e000890 (PDF)
²⁰ Int J Clin Pharmacol Ther Toxicol. 1985 Oct;23(10):569-72
²¹ Arzneimittelforschung. 1992 Sep;42(9):1101-4
^23, ²⁴ Clin Nutr ESPEN. 2020 Jun;37:9-23. doi: 10.1016/j.clnesp.2020.03.008. Epub 2020 Apr 18
²⁵ Linus Pauling Institute, L-Carnitine, Infertility
²⁶ NIH, Carnitine, Health Professional, Infertility
²⁷ Clin Endocrinol (Oxf). 2023 May;98(5):682-691. doi: 10.1111/cen.14885. Epub 2023 Feb 17
²⁸ NIH, Carnitine, Health Professional, Athletic performance enhancement
²⁹ Journal of Physiology, 2011;589(pt.4)
³⁰ Journal of Physiology, 2011;589(pt.7)
^31, ^34, ³⁶ Linus Pauling Institute, L-Carnitine, Frailty
³² Syst Rev. 2023; 12: 74
³⁵ Nutrients, 2020;12(9):2795
³⁷ NOW, All Acetyl-l-Carnitine Is Not Created Equal

Posted in Alzheimer's, Autism, Brain, Diabetes, Diet, Fertility, Food, Heart, Insulin, Liver, Mitochondria, Muscle, Supplements, Weight Loss | One Comment »

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