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Heart attack survivors face a hidden nightmare: Two-thirds develop brain damage
Reproduced from original article:
https://www.naturalhealth365.com/heart-attack-survivors-face-a-hidden-nightmare-two-thirds-develop-brain-damage.html
by: June 28, 2025</span
(NaturalHealth365) You beat the odds. You survived a massive heart attack when your heart literally stopped doing its job. The doctors called you lucky. Your family threw a celebration. You thought the worst was behind you.
Then you tried to go back to your normal life and realized something was wrong.
You can’t remember where you put your keys. Simple conversations leave you confused. Tasks you’ve done a thousand times suddenly feel impossible. Your brain feels like it’s wrapped in thick fog that never lifts.
Welcome to the nightmare that doctors don’t warn you about – and a shocking new study reveals it’s happening to almost everyone who survives cardiogenic shock.
Two-thirds of survivors get their brains scrambled
Researchers from UT Southwestern Medical Center just released a bombshell report that should wake up every person dealing with heart disease.
They tracked 141 people who survived cardiogenic shock – a life-threatening condition where your heart literally can’t pump enough blood to keep your organs alive – and discovered that 65% developed new brain damage by the time they left the hospital. Even worse, 53% were still mentally impaired three months later.
Dr. James de Lemos, who led this research, didn’t mince words: “Nearly two-thirds of cardiogenic shock survivors experienced cognitive impairment within three months of hospital discharge, underscoring a critical but overlooked aspect of recovery.”
Think about those numbers for a second. If you survive one of the most catastrophic heart events possible, you’ve got better than a coin flip’s chance of walking out of that hospital with a damaged brain. And nobody, not your cardiologist, not your nurses, not your discharge team, is going to warn you about it.
What cardiogenic shock does to you
Here’s what happens when your heart goes into cardiogenic shock: it basically gives up. Whether from a massive heart attack, severe heart failure, or surgical complications, your heart just stops pumping enough blood to keep you alive.
About 100,000 Americans go through this hell every year. Until recently, most people died. Period. However, medical technology has advanced to the point where up to 70% of patients now survive the initial event.
The problem? While doctors are patting themselves on the back for keeping you breathing, your brain is slowly starving to death.
Your brain needs about 20% of all the blood in your body to function properly. When your heart can’t pump enough blood, your brain cells start dying from oxygen starvation. Even if the medical team manages to get your heart working again, the damage to your brain tissue might already be permanent.
The medical cover-up that’s destroying lives
The medical establishment has known for years that heart problems cause brain damage, but they have not paid much attention to what kind of life they’re sending people back to.
Dr. Eric Hall, who led the study, admits: “We found that cardiogenic shock is associated with cognitive impairment, which is an under-recognized consequence strongly linked to patients’ overall quality of life.”
“Under-recognized” is medical speak for “we’ve been ignoring this massive problem for decades.”
So imagine yourself lying in that hospital bed, grateful to be alive, while doctors explain your discharge instructions. Nobody mentions that there’s a two-thirds chance you won’t be able to think straight for months – maybe years. Nobody suggests cognitive testing. Nobody connects you with brain specialists who might be able to help.
You get sent home to discover your mental decline on your own, wondering if you’re going crazy.
How to protect yourself before crisis strikes
The harsh truth is that once your heart goes into cardiogenic shock, the brain damage is probably already happening. Your best defense is to ensure your heart never reaches that point.
Here’s how to keep your heart so strong it never fails catastrophically:
Ditch the foods that are literally poisoning your cardiovascular system. Processed junk, sugar-loaded garbage, and those toxic seed oils they put in everything are creating chronic inflammation that’s slowly destroying your heart and blood vessels.
Feed your heart the nutrients it actually needs to stay strong. CoQ10, magnesium, omega-3s, and hawthorn berry are beneficial for your cardiovascular system.
Stop treating symptoms and start fixing root causes. High blood pressure, insulin resistance, and chronic stress are all warning signs that your heart is headed for trouble. Most doctors just want to throw pills at these problems instead of actually solving them.
Get real testing that can catch problems before they kill you. Standard heart tests often miss early problems that advanced testing can identify years in advance. For example, talk to a holistic doctor about C-reactive protein (CRP) and fibrinogen, two tests that measure levels of inflammation in the body.
Improve your body’s detoxification systems. Environmental toxins, heavy metals, and chronic infections are all attacking your cardiovascular system. Your liver, kidneys, and lymphatic system need support to protect your heart from this toxic assault.
Your heart and brain are connected, whether doctors admit it or not
What happens to your heart directly affects your brain. When your cardiovascular system breaks down, your brain pays the price. The medical system might want to treat these as separate issues, but your body knows better.
Thousands of people are walking around right now thinking they’re “heart attack survivors” when they’re actually brain damage victims who don’t even know what happened to them.
If you are ready to give your heart the protection it needs, consider Jonathan Landsman’s Cardiovascular Docu-Class, featuring 22 leading heart health experts who understand the real connection between heart and brain health. These aren’t the same doctors who ignore cognitive damage – these are experts who know how to prevent heart disease before it destroys your life and your mind. Get lifetime access to strategies that could save both your heart and your ability to think clearly.
Sources for this article include:
The Hidden Key to Boundless Energy
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/04/06/the-hidden-key-to-boundless-energy.aspx
Analysis by Dr. Joseph Mercola April 06, 2025
STORY AT-A-GLANCE
- Modern environmental factors including seed oils, endocrine disruptors, estrogens and EMFs allow harmful gut bacteria to proliferate, producing endotoxins that severely compromise mitochondrial function and reduce cellular energy production
- While ketogenic diets provide short-term benefits, long-term carbohydrate restriction impairs mitochondrial function and creates reductive stress in cells, necessitating a more balanced approach
- Excessive consumption of omega-6-rich seed oils severely damages mitochondrial function and makes skin more susceptible to sun damage, making these processed oils one of the biggest threats to health
- A healthy gut environment requires proper cellular energy to maintain low oxygen levels, allowing beneficial bacteria to thrive and produce protective short-chain fatty acids that strengthen your intestinal barrier
- Restoring health requires systematically reducing exposure to environmental toxins while gradually reintroducing healthy carbohydrates to support mitochondrial function and maintain proper gut bacteria balance
In my interview with Sean Kim of Growth Minds, we discussed the decades I’ve spent searching for the best ways to help you reclaim your health.1 When you consider how different modern lifestyles are from our ancestors’ days, it reveals many clues about why you might feel tired, run-down or prone to illness. Those ancestors had their own health challenges, but they weren’t swimming in artificial chemicals, electromagnetic fields and processed seed oils that drive chronic diseases.
You face these threats every day, and your body is likely struggling as a result. I’ve devoted my life to understanding how food, environment and daily habits affect you at the cellular level. That journey led me to study how your mitochondria produce the energy you need. Mitochondria are known as your cells’ power stations.
They depend on proper fuel, stable hormone levels and minimal toxic exposures to keep you thriving. If those factors are off balance, you’ll feel it. The question is: how do you get them back on track?
While a ketogenic diet or intermittent fasting help you lose weight initially, they’re a short-term fix with long-term consequences. As I explained to Kim, there’s a deeper story about how your body responds to various fuels, especially when you’ve been under stress or exposed to toxic influences.
You have to look at your gut, your hormone systems and your environment to fully understand what’s going on and restore optimal health. When I first explored diets high in fat and extremely low in carbohydrates, I saw benefits for some people in specific circumstances. Over time, however, I discovered that your system needs more than a strict low-carb diet provides.
Rethinking What It Means to Eat Well
In my interview with Kim, I made it clear that I used to be a leading advocate of ketogenic diets. I even wrote a No. 1 bestselling book on the topic. Many people have used a ketogenic diet with good outcomes for weight loss and insulin control, and I believed that kind of diet could support you in turning your health around. The results people experienced weren’t imaginary. Many of them had real successes.
Over time, however, more detailed research into mitochondrial function made me change my stance. It’s not enough to measure your short-term results. You have to look at what happens over many years. If you keep forcing your body into a state of ultra-low carbohydrate intake, you risk backing up electron flow in your mitochondria. That jammed-up electron flow weakens your cells’ ability to produce steady energy, a phenomenon otherwise known as reductive stress.
It also encourages shifts in your gut bacteria that harm you more than help you. You need healthy gut bacteria to make short-chain fatty acids, which keep your colon lining strong and keep harmful pathogens in check. A balanced intake of healthy carbohydrates is key once you’ve corrected the root concerns. Your brain needs glucose, and while you can survive on fewer carbs for a while, it’s easy to slip into a stressful metabolic state if you don’t consume enough healthy carbs.
How Your Environment Shapes Your Health
Everyday toxins also affect you at the cellular level. Throughout our talk, I explained to Kim that I’ve identified four main stressors that diminish your mitochondrial energy production. These factors silently harm your gut health, disrupt your hormones and trigger damaging oxidative stress.
First, you have the overconsumption of omega-6 seed oils, which are rich in linoleic acid. These highly processed cooking oils are the single biggest nutritional danger you face. You’ll find them in countless packaged foods, snack items and restaurant meals. The main reason why excess LA causes disease is that it prevents your mitochondria from working well. It also makes sun exposure more damaging due to the accumulation of these fats in your skin cells.
Second, you have excess endocrine-disrupting chemicals (EDCs) in your environment. These come from plastics, personal care products and even certain pesticides and mimic hormones, like estrogen, in your body. Many of these endocrine-disrupting chemicals reduce fertility and create hormonal imbalances. Xenoestrogens found in everyday items like plastic are one example of EDCs with widespread reach.
It’s also important to minimize exposure to synthetic estrogens, such as those found in hormone replacement therapy and oral contraceptives. Estrogen increases intracellular calcium levels and decreases mitochondrial function. In fact, estrogen dominance is nearly as dangerous as excessive LA intake when it comes to destroying your mitochondrial function.
The third significant threat to cellular health comes from pervasive exposure to electromagnetic fields (EMFs) due to the proliferation of wireless technologies. EMFs increase calcium ion concentrations within cells, resulting in the production of harmful free radicals.
Together, widespread exposure to LA in seed oils, EDCs in plastics and EMFs impair your cells’ ability to generate energy efficiently. This energy deficit makes it challenging to sustain the oxygen-free gut environment necessary for beneficial bacteria to flourish.
As your gut barrier weakens, it allows harmful substances to breach your intestinal wall and enter your bloodstream. This intrusion triggers a systemic inflammatory response, with wide-ranging effects on your health. Of particular concern is the proliferation of oxygen-tolerant bacteria, which are not ideally suited for the gut environment.
These microorganisms produce a potent form of endotoxin — the fourth major threat to your cellular health — known as lipopolysaccharide (LPS). When LPS enters your bloodstream through a compromised gut barrier, it leads to a severe condition known as endotoxemia, which often progresses to septic shock — a state of systemic inflammation that’s sometimes fatal.
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Restoring Gut Health as Your Foundation
A healthy gut is pivotal to your well-being. In my interview with Kim, I explained that if your healthy gut bacteria can’t thrive, your body faces one hurdle after another. An oxygen-free environment is necessary for beneficial bacteria that create short-chain fatty acids such as butyrate, propionate and acetate to thrive. These compounds help keep your colon lining strong by nourishing the cells that line your gut wall.
Your body needs cellular energy to keep oxygen levels low in your colon, however. So, if your mitochondria aren’t functioning properly and your cellular energy is low, you’re likely to have excess oxygen in your colon that boosts harmful bacteria.
The end result is an upsurge in toxic byproducts, including more potent forms of endotoxin. That’s why simply cutting carbohydrates might seem to help in the short term: if you starve harmful bacteria of their favorite fuels, they don’t multiply so fast.
Yet you pay for it later by ultimately decreasing the cellular energy you need for robust digestion and a healthy metabolism. A diet that includes high-quality fiber from vegetables and other sources of healthy carbohydrates is key, but if you have a compromised gut, it’s important to start with easier-to-digest options, like white rice or slowly sipping dextrose water daily for a week or two.
You want to steer clear of a low-carb diet, especially long term. If you keep your body in a constant energy deficit, you’re only compounding your mitochondrial problems. You’re also setting yourself up for increased stress hormone release, which breaks down your lean muscle tissue to make emergency glucose.
By cutting out mitochondrial poisons and nourishing your gut with healthy carbohydrates, you give your body the chance to restore that protective mucus layer, keep oxygen levels low in your colon and restore mitochondrial health for increased cellular energy.
When you remove the factors that destroy your cellular energy, you can then enjoy moderate to higher carbohydrate intake without wrecking your metabolic function. This might mean 200 to 350 grams of quality carbohydrates in a day, but the exact amount varies by your personal needs, activity level and genetics. The key is to focus on real, whole-food sources instead of ultraprocessed carbs that contain seed oils and refined sugar.
Let me emphasize once more that you should clear out the elements causing harm before you increase your carbohydrate intake. That means cutting back on omega-6-rich seed oils, limiting endocrine-disrupting chemicals, reducing EMF exposure and repairing your gut so it’s able to handle more fiber.
Practical Steps to Tame the Toxins
During my discussion with Kim, we touched on ways to reduce exposure to chemicals and stressors, so you enhance your health from the inside out. If you want to limit microplastics and hormone-disrupting substances, start by cutting down on plastic packaging.
Swap plastic containers for glass whenever possible, and avoid heating foods in plastic. Be mindful of personal care items with synthetic fragrances or complex chemical blends. Even so-called “organic” products often contain compounds that destabilize your hormones, so read labels carefully.
You also want to be wary of your Wi-Fi router and the constant signals from your phone. If you keep your phone by your bed at night, you’re exposing your body to nonstop EMFs. Turning off your wireless devices or switching to airplane mode gives your cells a break, but a better option is to turn off your Wi-Fi at night — or even shut off the power to your bedroom.
Also, try wired internet at home and see whether you notice improvements in your sleep or focus. As you move beyond eating well, also look into ways to speed up the removal of toxins. Sweating is one of the best methods. Traditional exercise does the job as you increase circulation, but an infrared sauna takes it further if you have access to one.
Grounding, or walking barefoot on natural surfaces like sand or soil, also helps reduce extra electrical charges in your body. You still want to watch out for walking barefoot on unnaturally hard floors every day, which promotes the development of joint or foot issues. Even so, a dose of nature is calming, and you might find that grounding on natural surfaces like grass or the ocean is a soothing method to connect with your environment.
During the interview, I also noted that sunlight is both beneficial and at times harmful, depending on your overall health. You absolutely need adequate sun exposure to help your body produce vitamin D and provide other benefits. However, if you’re carrying an excessive amount omega-6 seed oils in your skin cells, they’re prone to oxidation when exposed to sunlight, increasing the risk of skin damage.
Too many of these oxidizable fats in your tissues magnifies any negative effects from UV rays. To maximize the benefits of sun exposure and minimize the risks, eliminate seed oils from your diet. I recommend avoiding sun during peak hours (from 10 a.m. to 4 p.m. in most U.S. regions) until you’ve been seed-oil-free for at least six months.
The Promise of Future Health Innovations
As I told Kim, I believe technology itself becomes a friend if it’s harnessed in the right way. Yes, you should reduce EMF exposure from your phone and your Wi-Fi. Still, advanced computer systems, including artificial intelligence, help you monitor your health in real time.
In the near future, you might use AI-driven software that tracks your daily habits, recognizes patterns in your hormone levels and reminds you to make adjustments to your diet or supplement routine. It’s like having a health coach who’s always there, offering personalized feedback based on data from wearable devices or blood tests.
Progress in the field of mitochondrial research is also advancing at a rapid pace. We’ve come a long way in understanding how molecules like coenzyme Q10 help push electrons through your mitochondrial chain. Further investigations could pinpoint more specific strategies to optimize that electron flow, so you generate energy without building up damaging free radicals.
I’m particularly excited about new insights into gut therapies that restore the colon’s oxygen-free environment, such as an approach that combines targeted probiotics with supportive nutrients to revive the cells lining your gut.
Doing so would let beneficial microbes flourish and block harmful bacteria from expanding. This holds the promise of turning gut health into a more precise science, where you measure shifts in your microbiome composition and match specific interventions for faster results.
As these new approaches gain traction, I’m working to gather data and share it with you. I’m driven by a mission to show you that your body already has the blueprint for abundant energy and balanced hormones. The problem is interference. Environmental pollutants, seed oils and stressors have created roadblocks. If you reduce them systematically, you’ll give yourself a fresh start.
Charting Your Path to Lasting Vitality
In my interview with Kim, I emphasized that your mitochondria lie at the heart of your health story. They decide whether you have the energy to thrive or whether you struggle with chronic fatigue and cellular stress. By addressing the four main stressors — seed oils, endocrine-disrupting chemicals, endotoxins and EMFs — you free up your mitochondria to run at full power. You stop feeding the processes that tear down your gut and your energy.
You also open the door for a truly balanced diet, one that includes not just healthy fats and proteins, but also the right kind of carbohydrates. You deserve to feel vibrant, and your cells are programmed to help you get there.
Clear away plastic toxins, turn off your Wi-Fi at night, choose glass bottles and avoid consuming seed oils. As your gut health improves, introduce better fiber sources that feed your beneficial gut microbes and support mucin production, which protects you from leaky gut.
If you take these steps, you’ll likely see a positive ripple effect. Your thyroid might perk up, your hormones rebalance and your gut wall becomes sturdier. In time, you might even be able to tolerate moderate sun exposure without burning as easily, since your cell membranes are no longer packed with unhealthy fats.
No matter where you are in your health journey, let this knowledge empower you — you can fix the hidden obstacles that drain your energy and derail your gut, and feel confident in a plan that nourishes you from your cells outward, letting you enjoy a fuller life.
This is what I hope you’ll take away from my conversation with Kim: you have more control over your well-being than you realize. When you align your habits with what your body needs, you unleash the boundless energy that’s been waiting inside you all along.
Probiotics Offer New Hope for Alzheimer’s and Other Neurodegenerative Diseases
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/03/20/probiotics-alzheimers-neurodegenerative-diseases.aspx
Analysis by Dr. Joseph Mercola March 20, 2025
STORY AT-A-GLANCE
- Probiotics may influence brain function through the gut-brain axis, offering benefits for neurodegenerative diseases like Alzheimer’s and Parkinson’s by improving gut health and reducing inflammation
- Studies suggest a link between gut health and cognitive function, indicating that an improved gut microbiome enhances mental health and may reduce inflammation associated with neurodegeneration
- Research indicates that probiotics could play a role in managing Alzheimer’s and Parkinson’s, offering a noninvasive treatment option that helps slow or reverse cognitive decline
- Biologically, the action of probiotics involves several interconnected pathways. By restoring a healthy balance of gut bacteria, probiotics reduce the production of harmful substances like lipopolysaccharides (LPS) that trigger inflammation in the brain
- Further studies are needed to confirm the long-term benefits of probiotics in neurodegenerative disease management, emphasizing the importance of continued research in this area
Neurodegenerative diseases (NDs) are disorders characterized by the progressive loss of structure or function of neurons, leading to their eventual death. This decline disrupts essential brain functions, resulting in symptoms that significantly impair daily living and overall quality of life.
Common neurodegenerative diseases include Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS).1 Individuals affected by these conditions often experience memory loss, impaired movement, and difficulties with speech and coordination. As the diseases advance, patients may face severe cognitive and physical challenges, necessitating extensive care and support.
Neurodegenerative diseases now affect millions worldwide, with Alzheimer’s alone responsible for approximately 60% to 70% of dementia cases.2 On the other hand, the prevalence of Parkinson’s disease is expected to double by 2040, underscoring a growing public health concern.3 Additionally, ALS affects about 2 per 100,000 people in Europe and the U.S., with no known cure currently available.4
Risk Factors Associated with Neurodegenerative Diseases
Understanding the underlying causes of NDs is complex, as they often involve a combination of factors. For example, genetic mutations can predispose individuals to conditions like Alzheimer’s and Parkinson’s. According to a review published in the NPJ Parkinson’s Disease journal, genetic factors are linked to 56% to 79% of the risk for developing Alzheimer’s disease.5
• Environmental toxins — Exposure to heavy metals and pesticides, may contribute to neuronal damage. According to the aforementioned study:
“Several studies have suggested that lead (Pb), arsenic (As), and methyl mercury (MeHg) are also neurotoxins and can disrupt brain function, cause cognitive dysfunction, and increase the risk of AD and PD by disrupting mRNA splicing, the ubiquitin-proteasome system, the electron transport chain, and oxidative stress.”6
• Lifestyle factors — Poor diet, lack of exercise and chronic stress exacerbate NDs by affecting overall brain health and function. The progression from these underlying causes to full-blown NDs involves a cascade of biological events. Neurons, the brain’s communication cells, begin to lose their structure and function due to factors like oxidative stress and inflammation.
This deterioration disrupts the brain’s ability to process information, leading to symptoms such as memory loss and impaired motor skills. Over time, the cumulative effect of these disruptions results in the characteristic decline associated with NDs.
• Diagnosing NDs can be challenging — Often, symptoms overlap with other conditions, making it difficult to pinpoint the exact disease. For instance, memory loss could be attributed to normal aging, stress, or other medical issues, leading to potential misdiagnosis. Additionally, the lack of definitive biomarkers for many NDs means that diagnosis often relies on clinical assessments and patient history, which can be subjective and vary between practitioners.
• Limitations in diagnostic tools complicate the process — Imaging techniques like MRI and CT scans show brain changes, but these are not always specific to NDs. Blood tests and genetic screenings may offer clues but are not conclusive.
As a result, patients may undergo a lengthy diagnostic journey, experiencing uncertainty and anxiety while seeking answers. This underscores the need for more precise and reliable diagnostic methods to improve early detection and treatment outcomes.
Beyond the immediate symptoms, neurodegenerative diseases lead to profound emotional and financial burden for patients and their families. The progressive nature of these disorders often results in loss of independence, increased healthcare costs and emotional stress. Addressing these multifaceted challenges is crucial in improving patient outcomes and enhancing the quality of life for those affected.
Breakthrough Research Shows Probiotics’ Role in Alzheimer’s Disease Management
A recent study published in the journal Nutrients7 investigated the impact of probiotics on individuals diagnosed with Alzheimer’s disease. The research, conducted by Taiwanese researchers, aimed to determine whether introducing specific beneficial bacteria could influence cognitive function and reduce disease markers.
• Investigating the effects of probiotics — The study involved 60 elderly participants who were diagnosed with Alzheimer’s disease. They were assigned to either a probiotic treatment group or a placebo group over a 12-week period.
The probiotic group consumed a milk product containing strains such as Lactobacillus acidophilus, Lactobacillus casei, Bifidobacterium bifidum, and Lactobacillus fermentum. The primary goal was to assess any changes in cognitive function and Alzheimer’s disease markers as a result of the probiotic intervention.
• Probiotics improve cognitive function — Significant improvements were seen in the group that received probiotics compared to the placebo group. The probiotic group showed a notable increase in their Mini-Mental State Examination (MMSE) scores, indicating enhanced cognitive function. In contrast, those who took the placebo experienced a decline in their MMSE scores over the same period.
• Probiotics’ positive effects against inflammation — The probiotic group demonstrated a reduction in inflammation markers, which are often elevated in Alzheimer’s patients. “Considering these findings, specific probiotics demonstrate robust and effective antioxidant capabilities,” the study authors report.8
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Probiotics Reduce Inflammation and Oxidative Stress
The mechanism behind these improvements is believed to involve the gut-brain axis, a communication network between the gastrointestinal tract and the brain.
• Probiotics balance your gut health — Probiotics help maintain a healthy balance of gut microbiota, which in turn influence brain function. By promoting a diverse and balanced microbiome, probiotics may reduce systemic inflammation and oxidative stress, both of which are implicated in the progression of Alzheimer’s disease. For more information on how gut health affects your mental health, read “Gut Health’s Impact on Mental Well-Being.”
• Benefits of SCFAs — Short-chain fatty acids (SCFAs) are metabolites produced by beneficial bacteria in the gut. SCFAs have been shown to support brain health by providing energy to neurons and reducing inflammation. The increased abundance of Lactobacillus species in the probiotic group likely contributed to higher SCFA levels, fostering an environment conducive to cognitive stability and improvement.
• Benefits are observed in a short amount of time — Cognitive improvements were observed after just 12 weeks of probiotic supplementation, suggesting that the benefits of probiotics can manifest relatively quickly. This rapid response underscores the potential of probiotics as a viable intervention for slowing or even reversing aspects of cognitive decline in Alzheimer’s patients.
Comparing the effects of probiotics to other variables in the study, probiotics consistently outperformed the placebo in all measured outcomes. While both groups participated in the same environment and received similar care apart from the probiotic intervention, only the probiotic group showed meaningful improvements in physiological markers related to brain health. This stark contrast emphasizes the specific role that probiotics play in enhancing brain health.
Probiotics’ Mechanisms of Action Against Neurodegenerative Disorders
Biologically, the action of probiotics involves several interconnected pathways. By restoring a healthy balance of gut bacteria, probiotics reduce the production of harmful substances like lipopolysaccharides (LPS) that trigger inflammation in the brain.9
• Enhancing the integrity of the gut barrier — They prevent the leakage of proinflammatory agents into the bloodstream, which could otherwise reach the brain and exacerbate neuroinflammation.10
• Affecting neurotransmitter production — Probiotics influence the production of neurotransmitters such as dopamine and gamma-aminobutyric acid (GABA).11 These chemicals are crucial for mood regulation and cognitive function. By increasing the levels of these neurotransmitters, probiotics contribute to improved mental health and cognitive resilience against the degenerative processes of Alzheimer’s disease.
Four Ways to Support Your Brain Through Gut Health
Your gut microbiome acts as a second brain, directly influencing your cognitive function and neurological health, and how you nourish it plays a significant role in your risk for neurodegenerative conditions. For example, a study published in Scientific Reports showed that certain bacterial strains in the gut, such as Collinsella, Lachnospira, and Veillonella, increased the risk of Alzheimer’s disease.12
However, they also identified strains that provide protective benefits against Alzheimer’s disease, such as Eubacterium nodatum and Eisenbergiella. These produce short-chain fatty acids (SCFAs), particularly butyrate, from dietary carbohydrates.
Butyrate nourishes your colonic epithelial cells, reinforcing the intestinal barrier. SCFAs also stimulate mucin production, creating a protective shield against harmful bacteria. Akkermansia muciniphila also produces SCFAs, and research has shown that Alzheimer’s patients tend to have very low levels of this important keystone species.13 Here are four proven strategies geared toward optimizing the Akkermansia in your gut to enhance your brain health:
1. Increase Akkermansia through targeted diet and supplementation — Prioritize foods and supplements that promote the growth of Akkermansia. Include well-cooked, prebiotic-rich vegetables and fiber sources that nourish this crucial bacterium.
Consider high-quality supplements specifically designed to enhance Akkermansia levels, supporting gut barrier integrity and reducing brain inflammation. Avoid processed foods and high-fat diets that can hinder Akkermansia growth.
2. Enhance beneficial short-chain fatty acids — Focus on increasing butyrate-producing bacteria alongside Akkermansia to protect against amyloid buildup in the brain. Incorporate fermented foods and resistant starches that feed these beneficial microbes.
Tailor your carbohydrate intake to support your unique microbiome, aiming for at least 250 grams of targeted carbs daily, and adjust based on your activity level to optimize Akkermansia and short-chain fatty acid production.
3. Support your gut-brain connection — Optimize your gut barrier integrity to prevent inflammatory compounds from reaching your brain. This includes removing inflammatory processed foods and supporting the growth of protective bacteria like Akkermansia, which strengthens your intestinal lining.
Maintain a balanced diet with sufficient carbohydrates tailored to your microbiome, and use pharmaceutical-grade supplements as needed to sustain Akkermansia levels.
4. Address systemic inflammation by promoting Akkermansia diversity — Lower inflammation throughout your body by enhancing microbiome diversity, with a specific emphasis on increasing Akkermansia.
Eliminate vegetable oils and other proinflammatory fats that damage gut bacteria, and incorporate foods that reduce inflammatory markers while supporting Akkermansia growth. Regularly monitor biomarkers such as C-reactive protein levels to track your progress in reducing systemic inflammation and maintaining a healthy gut microbiome.
Additional Strategies to Prevent Alzheimer’s Disease
Aside from optimizing your gut health and Akkermansia levels, there’s a plethora of helpful Alzheimer’s prevention strategies, several of which are outlined below:
• Avoid gluten and casein (primarily wheat and pasteurized dairy, but not dairy fat, such as butter) — As noted in a 2022 study,14 your blood-brain barrier is negatively affected by gluten. When bacteria enter your bloodstream, the risk of Alzheimer’s disease increases. Other cognitive disorders are linked to a weakened blood-brain barrier as well, such as Parkinson’s disease, anxiety and depression.
• Make sure you’re getting enough animal-based omega-3 fats — Omega-3 fats, namely 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. That said, omega-3s are PUFAs, so don’t overdo it.
• 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 a 2023 study,15 increasing vitamin D reduced dementia risk by 40%.
The best way to get vitamin D is through sensible sun exposure, aiming for a blood level between 60 and 80 ng/mL. However, you need to purge vegetable oils from your body before going into the sun at solar noon. The LA in your skin oxidizes when exposed to sunlight, causing inflammation and skin damage.
To protect your skin, avoid sun exposure during solar noon for four to six months as you work on removing LA from your body. Stick to sunlight during early morning and late afternoon in the meantime. For additional skin defense, you can take astaxanthin, a low-dose aspirin or molecular hydrogen. Niacinamide cream will also lower your risk of skin damage.
• Keep your fasting insulin levels below 3 — Insulin resistance is linked to accelerated brain aging, as well as neurodegeneration.16
• Eat a nutritious diet, rich in folate — Vegetables, without question, are your best form of folate. Avoid supplements like folic acid, which is the inferior synthetic version of folate. Research shows that folate is a protective factor against Alzheimer’s disease.17
• 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, nonstick cookware and vaccine adjuvants.
• Make sure your iron isn’t elevated and donate blood if it is — A study18 published in Aging Medicine shows that excess iron increases your risk of Alzheimer’s disease by initiating the Fenton reaction, leading to increased oxidative stress.
• Exercise regularly — Exercise triggers beneficial changes that support cognitive function. Particularly, it’s been shown to improve blood flow to the brain, leading to an increase in biomarkers related to improved neuronal plasticity and better cell survival.19
• 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, such as learning to play a musical instrument, is associated with a decreased risk of Alzheimer’s.20
• 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.
Frequently Asked Questions (FAQs) About Probiotics and Neurodegenerative Diseases
Q: How do probiotics impact neurodegenerative diseases like Alzheimer’s?
A: Probiotics influence brain function through the gut-brain axis by restoring gut microbiome balance, reducing inflammation, and improving cognitive function. Studies suggest that beneficial bacteria can slow or even reverse aspects of cognitive decline in conditions like Alzheimer’s and Parkinson’s.
Q: What research supports the benefits of probiotics for Alzheimer’s patients?
A: A study published in Nutrients found that Alzheimer’s patients who took probiotics for 12 weeks showed improved cognitive function and reduced inflammation compared to a placebo group. These improvements were measured using the Mini-Mental State Examination (MMSE) and inflammatory markers.
Q: What mechanisms make probiotics beneficial for brain health?
A: Probiotics help reduce inflammation by lowering harmful substances like lipopolysaccharides (LPS), enhancing gut barrier integrity, and influencing neurotransmitter production (e.g., dopamine and GABA). They also promote the production of short-chain fatty acids (SCFAs), which support brain health.
Q: Can improving gut health help prevent neurodegenerative diseases?
A: Yes. A diverse gut microbiome, particularly the presence of beneficial bacteria like Akkermansia muciniphila, plays a crucial role in reducing inflammation and protecting against neurodegeneration. Consuming prebiotic-rich foods, fermented foods, and maintaining a fiber-rich diet can support gut health.
Q: What other lifestyle changes can support brain health and reduce Alzheimer’s risk?
A: In addition to probiotics, strategies like avoiding processed foods, eliminating heavy metal exposure (e.g., mercury and aluminum), maintaining optimal vitamin D and omega-3 levels, exercising regularly, and engaging in mental stimulation activities can help prevent cognitive decline and support brain health.
- 1 Int J Mol Sci. 2020 Dec 14;21(24):9500
- 2, 7, 8 Nutrients. 2023 Dec 20;16(1):16
- 3 Clinical Medicine, Volume 20, Issue 4, July 2020, Pages 393-398
- 4 Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 20(3–4), 264–274
- 5, 6 NPJ Parkinsons Dis. 2021 Aug 11;7:70
- 9 Front Immunol. 2021 Feb 26;12:578386
- 10 Front Immunol. 2023 Apr 24;14:1143548
- 11 Front Microbiol. 2023 Aug 17;14:1216674
- 12 Scientific Reports, Volume 13, Article number: 5258 (2023)
- 13 Critical Reviews in Microbiology, 49(2), 151–176
- 14 Am J Lifestyle Med. 2022 Jan 11;16(1):32–35, Abstract
- 15 Alzheimers Dement (Amst). 2023 Mar 1;15(1):e12404, Highlights
- 16 Int J Mol Sci. 2021 Sep 15;22(18):9987, Abstract
- 17 Front Neurosci. 2021 Apr 14;15:661198, Abstract
- 18 Aging Med (Milton). 2024 Oct 22;7(5):649–667, Iron Overload/Accumulation and Increase Risk of AD
- 19 Front Aging Neurosci. 2023 Aug 4;15:1243869
- 20 Aging Ment Health. 2021 Apr;25(4):593-601
How Microplastics Accumulate in Your Brain and Other Organs
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/02/07/microplastic-in-the-brain.aspx
Analysis by Dr. Joseph Mercola February 07, 2025
STORY AT-A-GLANCE
- Research reveals microplastics are increasingly present in human organs, with brain tissue containing seven to 30 times more microplastic concentration than liver or kidney samples taken from 2016 and 2024 studies
- Microplastics originate from degrading plastic items and manufactured products, infiltrating oceans, soil and air, making them nearly impossible to avoid in our environment
- Nanoplastics (under 100 nanometers) cross the blood-brain barrier within two hours, contributing to inflammation and neurodegenerative diseases like Alzheimer’s through beta-amyloid peptide acceleration
- Laboratory studies indicate microplastics affect multiple body systems, causing digestive inflammation, respiratory issues, endocrine disruption and reproductive disorders, though human research remains challenging
- Practical ways to reduce exposure include filtering tap water, avoiding plastic packaging, using natural fiber clothing and choosing glass or metal containers over plastic ones
Most people enjoy eating seafood regularly or taking a relaxing, warm bath. While these seem harmless, research shows that they now come with an unseen invader — microplastics. These tiny plastic particles, often smaller than a grain of sand, are increasingly pervasive in our environment. In fact, they’re now in your brain and other organs.
Plastic Is Everywhere, and It’s Also in Your Brain
In a preprint study published in Research Square, researchers sought to find out the amount of micro- and nanoplastics (MNPs) currently embedded in the human body. For their experiment, they collected a total of 51 post-mortem tissue samples of liver, kidney and brain from 2016 and 2024. From there, the samples were subjected to a chemical test that created solid materials namely, polymer-based solids that can be detected by special equipment.1
The researchers discovered that the brain contains the highest concentration of MNPs — around seven to 30 times more — compared to liver or kidney samples. Moreover, the MNPs found in the brain typically range in the nanometer scale with shard-like properties. According to their findings:2
“A non-parametric analysis of variance (Kruskal-Wallis) confirmed that MNP concentrations in brains were significantly greater than all other tissues (P<0.0001).
Furthermore, from 2016 to 2024, there was a significant increase in MNP concentrations in both livers and brains. The predominant polymer found in all tissues was polyethylene, which independently displayed similarly increasing trends from 2016 to 2024 in the liver and brain.
The proportion of polyethylene in the brain (74%) appeared significantly greater relative to other polymers in comparison to the liver and kidney (44% to 57%), although kidney samples from 2024 also had increased relative PE (71%) …
The concentrations in liver and kidney were not as high (relative to brains) as we would have suspected, as these are ‘front line’ organs for xenobiotic uptake and clearance. That said, the lipophilic nature of plastics may make them easily handled by the liver, which has a major role in uptake and repackaging of dietary triglycerides and cholesterol.”
However, the researchers didn’t dive into the health effects of MNPs on human health, noting that this topic is better suited for a new study.3
Where Do Microplastics Come From?
Microplastics originate from various sources. Some are created when larger plastic items like bottles, bags and food packaging break down due to sunlight exposure, weathering and physical abrasion. Think of a plastic bottle left under the sun — it becomes brittle and eventually fragments into smaller and smaller pieces. These fragments are microplastics.
In other cases, microplastics are manufactured intentionally, such as microbeads used in certain cosmetics and personal care products (although many countries have now banned their use).
These tiny plastic particles have infiltrated nearly every corner of the environment. They’re found in our oceans, rivers and lakes, polluting the water and harming marine life. They’re also present in the soil, affecting plant growth and entering our food supply. Even the air you breathe contains microplastics, which lodge into your lungs when inhaled.4 This widespread contamination makes it nearly impossible to avoid exposure entirely.
When it comes to food, microplastics enter your system through various pathways. Marine animals, both predator and prey, ingest microplastics in the ocean, and these particles then accumulate in their tissues. This means that when you consume seafood, you’re also ingesting these microplastics.5
Similarly, microplastics in the soil are absorbed by plants, contaminating the growth and nutrition of fruits, vegetables and other crops.6 Plastic packaging used for food and beverages also shed microplastics, further contributing to your exposure.
Beyond food and water, you’ll encounter microplastics in many other everyday products, many of which you most likely own. For example, synthetic clothing, like polyester and nylon, sheds tiny plastic fibers during washing. These microfibers are a significant source of microplastic pollution in our waterways. While microbeads have been banned in many countries, some industrial processes still contribute to microplastic pollution.
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Microplastics and the Brain
Again, one of the most concerning aspects of microplastic pollution is their ability to reach the brain. The brain is protected by the blood-brain barrier, which normally prevents many harmful substances from entering the delicate brain tissue. However, nanoplastics (less than 100 nanometers), are able to cross this barrier7 in just two hours after they enter the body.
The concern is that these microscopic particles pile up in the brain over time, a process known as bioaccumulation. While research regarding the health impacts of MNPs is not definite yet, researchers theorizes that they provoke the immune system, thereby causing inflammation.8 Chronic inflammation in the brain has been linked to various neurological problems.
While research is still ongoing, there is concern that long-term exposure to MNPs and their subsequent accumulation in the brain contribute to the development of neurodegenerative diseases like Alzheimer’s.
As noted in an animal study published in the Journal of Hazardous Materials, once nanoplastics cross the blood-brain barrier, they contribute to neurotoxicity by accelerating the spread of beta-amyloid peptides, which is the main pathogenic protein of this condition.9
Unsolved Mystery — Researching the Impact of Microplastics
Studying the health effects of microplastics in humans is a complex challenge. It’s difficult to assess the impact of microplastics on human health because of ethical concerns.
This has caused scientists to resort to in vivo, in vitro and animal test models to monitor and study the impact of microplastics.10 But from this research, we’re now able to infer the likely consequences of microplastics on human health. Here’s what a 2023 study published in Yonsei Medical Journal have compiled:11
- Digestive system — Microplastics cause physical irritation to the gastrointestinal tract, leading to inflammation and digestive symptoms. This results in an imbalance in your gut microbiota, causing abdominal pain, bloating and changes in bowel habits.
- Respiratory system — The inhalation of microplastics causes oxidative stress in the airways, leading to coughing, sneezing and shortness of breath. Fatigue and dizziness will also occur due to low blood oxygen concentration.
- Endocrine health — Microplastics interfere with hormone health, disrupting your endocrine function. This leads to metabolic disorders, developmental problems and even lower fertility rates. Much of the reason for this is because microplastics typically have bisphenol A, a chemical that greatly affects endocrine health and the reproductive system.
Addressing the issue of microplastic pollution and its potential health impact requires collaborative efforts between scientists, governments and industries. Scientists need to conduct more research to understand the health effects, governments need to implement policies to reduce plastic pollution, and industries need to develop more sustainable alternatives to plastic.
“Considering the ubiquitous nature and long persistence of microplastics, it is necessary to make efforts to mitigate their exposure given their effects on entire generations and multiple generations.
In the future, in-depth research on the pollution status and hazards of marine microplastics, as well as the correlation between exposure to microplastics and diseases in humans, should be conducted; and based on these findings, human health should be protected by preventing and managing microplastics,” the researchers concluded.12
Take Control of Your Health in a Plastic World
While research is still ongoing, it’s clear that having foreign, microscopic objects embedded in your organs is not good for your health, or anyone’s health for that matter. Therefore, it’s important to take proactive steps to minimize your exposure while scientists continue to investigate the long-term effects.
Addressing the problem of microplastic pollution requires a collective effort. By combining individual actions with broader policy changes and industry innovation, we’ll move towards a future with less plastic contamination and a healthier environment for everyone. But in the meantime, implementing practical strategies at a personal level will help reduce microplastic exposure. Here are my top recommendations:
| Filter your tap water and avoid water bottled in plastic — If you need to buy bottled water, opt for glass bottles. Also make sure the filter you use to purify your tap water can filter out microplastics. |
| Boil hard tap water — If you have hard tap water, consider boiling it before using it for cooking or drinking, as hard water traps more microplastics. Recent research shows boiling hard tap water for five minutes removes up to 90% of the microplastics in the water. |
| Avoid plastic packaging — Opt for products packaged in glass, metal, or paper instead of plastic. This can significantly reduce the amount of plastic waste that breaks down into microplastics. At home, use wax paper, parchment paper or paper bags to store foods rather than plastic wrap. |
| Use reusable containers — Replace single-use plastic bottles, cups, and containers with reusable alternatives made from safer materials like stainless steel or glass. |
| Never microwave plastics — Heat can cause plastics to leach chemicals into food. Use glass or ceramic containers for microwaving. |
| Avoid plastic cutting boards — Use a wooden or glass cutting board instead. |
| Opt for natural fibers — Whenever possible, choose clothing and other textile products made from natural fibers like cotton, wool and linen, as synthetic fabrics such as polyester shed microfibers and leach xenoestrogens. |
| Wash synthetic clothes less frequently — When washing synthetic textiles, use a microfiber filter in your washing machine to trap synthetic fibers and prevent them from entering the water system. |
| Opt for food grade cosmetics and personal care products — Some cosmetics, toothpastes, and personal care products contain microbeads or other plastic particles. Look for products free of these materials. Ideally, opt for all-natural, food grade products. |
| Choose your children’s toys carefully — Replace plastic toys with those made from safe, nontoxic and sustainable materials. |
| Opt for natural cleaning products — Chemical cleaning products like soaps, cleansers and surface cleaners, usually contain microplastics and phthalates that affect your endocrine system. Replace them with natural alternatives like white vinegar, baking soda and essential oils. |
- 1, 2, 3 Res Sq [Preprint]. 2024 May 6:rs.3.rs-4345687, Results and Discussion
- 4 Journal of Hazardous Materials Volume 416, 15 August 2021, 126124, Abstract
- 5 NOAA, Ingestion
- 6 Journal of Hazardous Materials Advances Volume 17, February 2025, 100528, Effects of Microplastics on Agricultural Soils
- 7 Nanomaterials (Basel). 2023 Apr 19;13(8):1404, Abstract
- 8 Journal of Translational Medicine Volume 22, Article number: 959 (2024), Abstract
- 9 Journal of Hazardous Materials Volume 465, 5 March 2024, 133518, Abstract
- 10 Science of The Total Environment Volume 946, 10 October 2024, 174215, Toxicity to the Digestive System
- 11, 12 Yonsei Med J. 2023 Apr 20;64(5):301–308
Unlocking the Power of Methylene Blue
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/01/08/power-of-methylene-blue.aspx
Analysis by Dr. Joseph Mercola January 08, 2025
STORY AT-A-GLANCE
- Methylene blue enhances cellular energy production by integrating into the electron transport chain, cycling between oxidized and reduced forms to improve mitochondrial efficiency and resolve metabolic issues
- Clinical trials show methylene blue’s role in treating neurological conditions, including slowing progression of Alzheimer’s at doses of 16 mg daily
- Studies indicate methylene blue’s effectiveness in treating septic shock, reducing mortality rates, shortening hospital stays and improving blood pressure without significant adverse effects
- Research reveals methylene blue’s anticancer properties, particularly in chemoresistant ovarian tumors, by selectively targeting cancer cell mitochondria while sparing healthy cells from damage
- Safe dosage ranges from 5 mg to 50 mg daily, but requires medical supervision due to potential interactions with SSRIs and risks for those with kidney issues or G6PD deficiency
Few substances have captured my attention as profoundly as methylene blue. Earlier this year, I engaged in an in-depth discussion with Georgi Dinkov, a respected expert in metabolic health, who shed light on the multifaceted benefits of this remarkable compound.1
Methylene blue, a quinone-like molecule, is not just another supplement; it’s a powerful agent that can play an important role in cellular metabolism. By accepting and donating electrons, methylene blue enhances mitochondrial function, addressing issues like reductive stress that are often overlooked in conventional medicine.
This conversation with Dinkov highlights methylene blue’s role in reaching optimal health and treating a myriad of conditions, ranging from mental health disorders to acute medical emergencies.
Methylene Blue and the Electron Transport Chain
Methylene blue has the ability to integrate seamlessly into the electron transport chain (ETC), which plays a role in cellular energy generation. Unlike traditional antioxidants that either donate or accept electrons and subsequently require excretion, methylene blue possesses the unique capability to cycle between its oxidized and reduced forms indefinitely.
This continuous electron transfer process ensures sustained improvement in mitochondrial efficiency, which is key for energy production and overall cellular health. Dinkov emphasized that methylene blue acts as an emergency oxidant, stepping in to accept electrons even when essential co-actors like NAD+ are deficient.
This makes methylene blue capable of resolving metabolic issues associated with electron buildup and reductive stress. By maintaining the flow of electrons within the ETC, methylene blue prevents the stagnation that leads to cellular dysfunction and various health problems.
Methylene Blue for Enhanced Brain Health
The therapeutic potential of methylene blue is vast and varied, extending across a spectrum of neurological and psychological conditions. Dinkov shared insights into several studies where methylene blue, even at relatively low doses of 15 to 50 milligrams (mg), demonstrated significant benefits in treating treatment-resistant depression and psychosis.2
These findings are groundbreaking, suggesting that methylene blue enhances cognitive function and stabilizes mood by improving mitochondrial performance and reducing oxidative stress in the brain. Methylene blue enhances the benefits of niacinamide (vitamin B3) on brain health and metabolism.3 Furthermore, in terms of neurodegenerative diseases, methylene blue has shown remarkable promise.
A modified version of methylene blue, developed by a UK-based company, has been patented for Alzheimer’s treatment. Clinical trials have reported an astounding 80% reversal of Alzheimer’s symptoms in participants, according to Dinkov, highlighting methylene blue’s ability to not only halt but also reverse cognitive decline.4
These applications underscore the compound’s role in enhancing brain health by ensuring efficient energy production and mitigating the damaging effects of oxidative stress. A stabilized form of methylene blue known as hydromethylthionine (LMTM) also shows promise in treating mild to moderate Alzheimer’s disease.5
Unlike traditional methylene blue, LMTM is a stabilized dihydromesylate salt, which offers improved pharmacokinetic properties, including better brain uptake and longer half-life in humans. The study involved 1,162 patients across two Phase III trials and revealed a concentration-dependent activity of LMTM on cognitive decline and brain atrophy.
Notably, the optimal therapeutic dose was identified around 16 mg a day, which maximizes cognitive benefits without the diminishing returns observed at higher doses of 150 to 250 mg per day. This plateau effect underscores that beyond a certain concentration, no additional benefits are observed, aligning with the study’s findings that higher doses do not confer extra advantages.
Moreover, LMTM demonstrated significant benefits both alone and as an add-on to existing Alzheimer’s treatments. Patients receiving LMTM showed reduced cognitive decline and slower brain atrophy compared to those with lower plasma levels. This suggests that even at lower, more manageable doses, LMTM effectively slows the progression of Alzheimer’s by enhancing mitochondrial function.
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Methylene Blue’s Life-Saving Benefits in Septic Shock
Expanding methylene blue’s therapeutic applications, a systematic review and meta-analysis published in Critical Care Explorations evaluated the efficacy and safety of methylene blue in patients with septic shock,6 a condition with high mortality rates.
The analysis included six randomized controlled trials encompassing 302 patients and sought to determine whether methylene blue administration could improve outcomes compared to placebo or usual care.
The findings suggest that methylene blue may significantly reduce short-term mortality, shorten the duration of vasopressor use by approximately 31 hours and decrease hospital length of stay by about two days.
Additionally, methylene blue was associated with an increase in mean arterial pressure at six hours post-administration. Importantly, the study did not find an increase in adverse events.
Methylene blue functions by inhibiting endothelial and inducible nitric oxide synthase, thereby counteracting the profound vasodilation characteristic of septic shock. By restoring vascular tone, methylene blue helps maintain adequate organ perfusion and oxygenation, which are necessary for patient survival.
Methylene Blue for Cancer Treatment — Targeting Ovarian Tumors
Research is also exploring methylene blue as a treatment for ovarian cancer, particularly in cases resistant to conventional chemotherapies. A study published in Cancers (Basel) used a carboplatin-resistant ovarian cancer tumor model in mice to assess the impact of methylene blue on tumor growth.7
The findings revealed a significant in vivo reduction in tumor proliferation among mice treated with methylene blue compared to those receiving carboplatin alone or no treatment. Specifically, methylene blue demonstrated superior tumor suppression, highlighting its effectiveness against chemoresistant ovarian tumors.
Further in vitro analyses provided insights into the mechanisms underlying methylene blue’s anticancer effects. The study examined the impact of methylene blue on mitochondrial energetics in both cancerous and normal cell lines. Methylene blue altered the oxygen consumption rate and mitochondrial membrane potential in the ovarian cancer cells, suggesting enhanced mitochondrial respiration and induction of apoptosis.
In contrast, normal cells exhibited a markedly different response, with less pronounced changes in mitochondrial function, indicating a selective targeting of cancer cell mitochondria by methylene blue.
The combination of methylene blue with a mixture of lipoic acid and hydroxycitrate and carboplatin was investigated to evaluate synergistic effects. While the combination therapy showed a modest enhancement in tumor response compared to methylene blue alone, the difference was not statistically significant. Importantly, the metabolic therapies did not induce toxicity or weight loss in the treated mice, underscoring the favorable safety profile of methylene blue-based treatments.
By targeting the altered mitochondrial function and inducing apoptosis in chemoresistant cancer cells, methylene blue offers a novel approach that could improve treatment outcomes for patients facing limited options. The differential response between cancerous and normal cells also suggests that methylene blue selectively targets tumor metabolism, minimizing harm to healthy tissues.
Methylene Blue in Emergency Situations, Including Heart Attack
Beyond its chronic health benefits, methylene blue proves invaluable in acute medical emergencies. Dinkov elaborated on its effectiveness in treating conditions such as cyanide and carbon monoxide poisoning. In these scenarios, methylene blue acts swiftly to restore cellular respiration by accepting electrons and facilitating the utilization of oxygen, thereby reversing the toxic effects of these poisons.
I also recommend having methylene blue readily available at home in case of a heart attack. While sudden death is the most common symptom of heart disease, surviving individuals face the serious threat of reperfusion injury, where cellular dysfunction and death may worsen following the restoration of blood flow.
Methylene blue administration significantly mitigates tissue damage; however, proper dosage is important to avoid overdose. Administer methylene blue within minutes of the cardiac event to meet the critical time threshold.
In cases of stroke or heart attack, even a single dose below 50 mg may be life-saving. This rapid benefit makes methylene blue an essential tool in emergency medicine, offering a quick and efficient means to counteract metabolic crises.
I strongly advocate for the inclusion of methylene blue in emergency kits, as its ability to stabilize metabolic function swiftly provides an additional layer of protection against sudden, life-threatening metabolic disturbances. The potential of methylene blue to act as a universal antidote in various poisoning scenarios underscores its significance in both medical and emergency settings.
Methylene Blue and Antiaging Benefits
The antiaging properties of methylene blue is another exciting frontier that Dinkov passionately discussed.8 Studies have indicated that methylene blue reverses aging in human cells by maintaining optimal mitochondrial function and reducing oxidative damage, which are key factors in the aging process. Daily doses ranging from 5 mg to 50 mg help achieve the necessary concentration for these benefits without causing discoloration in urine or tissues.
Moreover, when combined with red light therapy, methylene blue’s effects are significantly amplified. This synergy promotes cellular rejuvenation and longevity by enhancing mitochondrial efficiency and reducing oxidative stress, thereby combating the visible signs of aging and supporting overall cellular health.
Dinkov mentioned an innovative approach where methylene blue is used in a dilution similar to mouthwash as an oral rinse, offering antiseptic benefits without the harsh side effects of conventional mouthwashes.9 This application not only leverages methylene blue’s metabolic benefits but also integrates it into daily routines for enhanced health and longevity.
Beyond the primary benefits discussed, methylene blue exhibits several other promising properties that could significantly enhance various aspects of health and medicine. Dinkov mentioned that methylene blue acts as a powerful aromatase inhibitor at sub-micromolar concentrations, which could have implications in managing hormone-related conditions.10
Additionally, methylene blue’s ability to enhance the flow of electrons within the electron transport chain makes it a versatile supplement for addressing a wide range of metabolic disturbances. Dinkov also introduced the concept of the “Methylene Blue Test of Health,” where the dosage at which an individual’s urine begins to turn blue serves as an indicator of their metabolic health.11
A lower dosage threshold for this coloration suggests better metabolic function, while higher thresholds may indicate underlying health issues such as cancer or diabetes, which are characterized by extreme reduction states in cells.
This innovative approach provides a simple yet effective method for individuals to monitor their metabolic health and take proactive measures to address any issues. As research continues to unfold, the full spectrum of methylene blue’s benefits will likely expand, positioning it as a cornerstone in both preventative and therapeutic health strategies.
Safety and Dosage Considerations
While the benefits of methylene blue are substantial, Dinkov highlighted the importance of appropriate dosing to avoid severe adverse effects that may occur with high doses, particularly serotonin syndrome — a fatal condition caused by excessive serotonin levels in the brain.
Methylene blue is a potent monoamine oxidase type A (MAO-A) inhibitor, which may dangerously elevate serotonin levels when combined with selective serotonin reuptake inhibitors (SSRIs) or other serotonergic drugs. I would advise strong caution for anyone ever to take an SSRI drug, as I don’t believe anyone benefits from them.
Further, at doses exceeding 30 mg to 50 mg, methylene blue may cause temporary blue discoloration of urine and, occasionally, the tongue. Although harmless, this effect is startling if unexpected. High doses may also interfere with pulse oximeter readings, leading to inaccurate assessments of blood oxygen levels.
Individuals with severe renal insufficiency should use methylene blue with caution and under close medical supervision, as impaired kidney function affects drug clearance. Additionally, methylene blue is contraindicated for patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency due to the risk of hemolytic anemia.
Common side effects associated with methylene blue include mild and transient gastrointestinal discomfort, such as nausea and diarrhea. Allergic reactions, ranging from skin rashes to life-threatening anaphylaxis, are also possible. Neurological effects like headaches and confusion may occur.
Cardiovascular effects, though less common, may include increased blood pressure and palpitations. Furthermore, methylene blue interacts with various medications, particularly antidepressants and antimalarials, altering their efficacy or causing adverse reactions.
To mitigate these risks, Dinkov recommends lower daily doses of methylene blue, typically between 5 mg to 15 mg, especially for long-term use. These dosages are sufficient to harness its metabolic benefits without significantly increasing the risk of serotonin syndrome. Additionally, Dinkov pointed out that while higher doses (up to 50 mg) have shown efficacy in certain therapeutic applications, they must be approached with caution and under professional supervision.
If you’re considering methylene blue supplementation, consult with a knowledgeable health care professional to tailor the dosage to your specific needs and avoid harmful interactions with other medications.
My Recommendations for Methylene Blue Use
There are three types of methylene blue typically sold — industrial-grade, chemical-grade (laboratory-grade) and pharmaceutical-grade. The only one you should use is the pharmaceutical-grade variety in solid, capsule or tablet form. Avoid using any solutions of methylene blue as dissolving it in water leads to a significant decrease in its effectiveness after 48 to 72 hours.
Methylene blue is a popular choice in aquarium maintenance due to its antifungal, antiparasitic and oxygen-transporting capabilities. It’s commonly used to alleviate fish stress, combat fungal infections and eliminate external parasites like Ich (white spot disease). However, aquarium-grade methylene blue often contains harmful contaminants, including heavy metals, which pose serious health risks to your aquatic pets.
To ensure the safety and well-being of your pets, I strongly advise against using methylene blue products designed for aquariums in any pet-related applications. Instead, choose pharmaceutical-grade methylene blue, which undergoes rigorous testing to confirm it is free from harmful impurities.
Personally, I have eliminated my regular intake of methylene blue, finding that daily walks by the ocean are an excellent way to manage reductive stress naturally. However, in scenarios where I might not have access to the ocean, I would consider taking 5 mg of methylene blue daily, adjusting to 3 mg if I were 75 pounds lighter in weight, and doing so six days a week.
It’s essential to emphasize that the appropriate and legal way to use methylene blue is through a prescription from a qualified physician. If you’re contemplating the use of methylene blue for your health, I strongly encourage you to consult with your doctor to determine if it’s suitable for your specific needs and circumstances.
Understanding the Root Causes of Dyslipidemia in Atherosclerotic Cardiovascular Disease
Reproduced from original OMNS article (OrthoMolecular News Service):
http://orthomolecular.org/
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Orthomolecular Medicine News Service, January 10, 2025
Richard Z. Cheng, M.D., Ph.D., Thomas E. Levy, M.D., J.D.
Highlights
A paradigm shift from the cholesterol-centric focus on symptom management to addressing the root causes of ASCVD has demonstrated potential for prevention and reversal, as shown by our recently reported 10 ASCVD reversal cases (1).
Abstract
Dyslipidemia has long been the primary target for atherosclerotic cardiovascular disease (ASCVD) treatment. However, we have recently presented compelling evidence demonstrating that dyslipidemia is an intermediary mechanistic step, not a root cause of ASCVD, and that the American Heart Association’s decades-long cholesterol-centric dogma is both unreasonable and potentially unethical, bordering on criminal negligence (2).
In our international consultation services, we have shifted from this outdated paradigm to an orthomolecular medicine-based integrative approach, focusing on restoring biochemical balance (between nutrients and toxins) and physiological harmony (among various hormones). Using this approach, we recently reported a series of 10 successful ASCVD reversal cases (1).
This paper explores the multifactorial root causes contributing to dyslipidemia, including dietary factors, nutritional deficiencies, infections, physical inactivity, and hormonal imbalances. Special attention is given to the roles of high-carbohydrate diets, ultra-processed foods, seed oils (containing high amounts of omega-6 PUFA), and high-fructose consumption. The effects of micronutrient deficiencies, such as those of vitamins B, C, D, E, and magnesium, are examined in the context of lipid metabolism. Additionally, the paper highlights the impact of chronic infections, sedentary lifestyles, and hormonal dysregulation on lipid abnormalities.
Understanding these key root causes provides a foundation for more effective prevention and treatment strategies (3). In future papers, we plan to explore these topics in greater detail, advocating for a paradigm shift from cholesterol-centric management to addressing the underlying causes of dyslipidemia and ASCVD.
Introduction
Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of morbidity and mortality worldwide. For decades, cholesterol and dyslipidemia have been central to ASCVD management strategies. However, our prior critiques of the cholesterol-centric paradigm have underscored that dyslipidemia is not the root cause but rather an intermediary mechanism of ASCV (2). Here we explore the multifactorial root causes underlying dyslipidemia, and advocate for prevention and treatment strategies that address these root causes. We focus here on categorizing the primary root causes contributing to ASCVD through dyslipidemia. More comprehensive discussions on these root causes will be presented where appropriate in subsequent papers in this series.
1. Dietary factors and dyslipidemia
- High-carbohydrate diets have been strongly associated with dyslipidemia, particularly characterized by increased triglycerides and decreased HDL cholesterol levels (4–6). This effect is especially pronounced with high glycemic index carbohydrates (5). The mechanism may involve reduced clearance of LDL particles and increased production of their precursors (7). Carbohydrate-induced hypertriglyceridemia occurs when dietary carbohydrate exceeds 55% of energy intake, despite reduced dietary fat (8). This paradoxical effect may be due to enhanced intestinal de novo lipogenesis and mobilization of stored lipids (9). However, the impact of carbohydrates on lipid metabolism is complex, with some studies suggesting that low-carbohydrate diets may have beneficial effects on atherogenic dyslipidemia (10).
- Low-carbohydrate ketogenic diets (KDs) have shown promising effects in improving metabolic disorders, particularly dyslipidemia. KDs can lead to significant reductions in triglycerides, total cholesterol, and LDL cholesterol, while increasing HDL cholesterol (11,12). These diets have been found to improve insulin sensitivity, reverse atherogenic dyslipidemia, and reduce inflammatory biomarkers associated with cardiovascular disease (13,14). KDs have also demonstrated benefits in managing obesity, metabolic syndrome, and type 2 diabetes (15,16). Studies have shown that KDs can decrease fasting serum insulin concentrations, improve LDL particle size, and reduce postprandial lipemia (11,12). While the optimal carbohydrate proportion and diet duration require further investigation, KDs appear to be a safe and effective approach for treating metabolic disorders (17,18).
- Ultra-processed foods and dyslipidemia. High consumption of ultra-processed foods (UPF) has been shown to be associated with an increased risk of dyslipidemia and other cardiometabolic disorders. Multiple prospective cohort studies have found that individuals with higher UPF intake have significantly greater odds of developing hypertriglyceridemia, low HDL cholesterol, and hypercholesterolemia (19,20). This association has been observed in both adults and adolescents (21,22). Systematic reviews and meta-analyses confirm these findings, reporting consistent positive associations between UPF consumption and increased risk of dyslipidemia, as well as diabetes, hypertension, and obesity (23,24). Longitudinal studies in children have also shown that higher UPF intake is associated with elevated total cholesterol and triglyceride levels (25). Proposed mechanisms include altered food matrix, toxicity from additives, and processing-induced contaminants affecting lipid metabolism, gut microbiota, and inflammatory pathways (26).
- Seed oils (rich in omega-6 PUFA) and dyslipidemia. Research suggests that high intake of omega-6 polyunsaturated fatty acids (PUFAs) from seed oils may contribute to inflammation, oxidative stress, and atherosclerosis (27). Despite recommendations for omega-6 PUFA consumption, some studies indicate potential long-term side effects, including hyperinsulinemia and increased cancer risk (28). Flaxseed and its oil, rich in omega-3 fatty acids, have demonstrated positive impacts on cardiovascular risk factors and dyslipidemia (29,30). Adjusting the omega-6 to omega-3 PUFA ratio may be crucial in managing chronic diseases (30). During cooking, both omega-3 and omega-6 high PUFA seed oils are readily oxidized, become rancid, and may produce harmful trans-fats (72).
- High fructose (found in HFCS and fruits). Research suggests that high fructose consumption, particularly from high-fructose corn syrup (HFCS), may contribute to dyslipidemia and other metabolic disorders. Studies have shown that fructose intake can increase postprandial triglycerides, LDL cholesterol, and apolipoprotein B levels (32,33). Fructose consumption has also been linked to visceral adiposity, insulin resistance, and hepatic de novo lipogenesis (fatty liver disease) (34,35). The metabolic effects of fructose differ from glucose due to its rapid hepatic conversion and extraction (36). While some studies found no significant metabolic differences between HFCS and sucrose (37), others suggest that HFCS consumption at 25% of energy requirements can increase cardiovascular disease risk factors comparably to fructose (32). Recent research emphasizes the synergistic effects of glucose and fructose on lipid metabolism, supporting public health efforts to reduce sugar intake (38,39).
2. Nutritional deficiency and dyslipidemia
Many vitamins and micronutrients play critical roles in lipid and energy metabolism, and deficiencies—whether isolated or combined—can lead to metabolic disturbances. Below are some key examples:
- B vitamins. Niacin and vitamin B6 have shown significant potential in managing dyslipidemia and associated cardiovascular risks. Niacin supplementation can lower triglycerides, LDL, and VLDL levels while increasing HDL (40). B vitamin supplementation improves lipid metabolism and reduces inflammation in patients with stable coronary artery disease (41). Animal studies have demonstrated antihyperlipidemic and hepatoprotective effects of vitamin B6 (42). Deficiencies in vitamins B6 and B12 are frequently reported in hyperlipidemic patient (43). Higher dietary niacin intake is associated with a reduced risk of dyslipidemia (44).
- Vitamin C and dyslipidemia. Research demonstrates that vitamin C supplementation can improve lipid profiles by lowering total cholesterol, LDL cholesterol, and triglycerides, particularly in individuals with hypercholesterolemia or diabetes (45–47). Some studies also report increases in HDL cholesterol (48,49). Beneficial effects of vitamin C have been observed across diverse groups, including diabetics, hemodialysis patients, and oil workers exposed to petroleum fumes (50,51). A meta-analysis of 13 randomized controlled trials confirmed that vitamin C supplementation significantly reduces LDL cholesterol and triglycerides in hypercholesterolemic individuals (46). The effects of vitamin C vary depending on dosage, duration, and individual health status (47). Dr. Linus Pauling’s pioneering work on vitamin C and cardiovascular disease laid the foundation for understanding its role in vascular health, indirectly linking it to lipid metabolism. We plan to dedicate a paper to further explore Pauling’s insights and their relevance to dyslipidemia and ASCVD. One of us (TEL) discusses vitamin C’s role in improving lipid profiles, combating oxidative stress, and supporting vascular health in the books Primal Panacea (52) and Stop America’s Number One Killer (53).
- Vitamin D and dyslipidemia. Vitamin D deficiency is significantly associated with dyslipidemia. Studies reveal that individuals with lower serum 25-hydroxyvitamin D levels are more likely to exhibit abnormal lipid profiles, including elevated total cholesterol, LDL, and triglycerides, and decreased HDL (54–57). This relationship persists even after adjusting for confounding factors. Vitamin D deficiency is linked to alterations in metabolomic profiles, particularly sphingolipid pathway (58). Interactions with other micronutrients, such as vitamin A, zinc, and magnesium, may influence vitamin D’s impact on lipid metabolism (59). Our recent comprehensive review of vitamin D demonstrates that maintaining optimal serum levels above 40 ng/mL reduces the risk of cardiovascular disease incidence and mortality (60) (accepted for publication by Nutrients).
- Vitamin E and dyslipidemia. Vitamin E has shown anti-atherosclerotic properties (61). Research on vitamin E and dyslipidemia shows mixed results. Some studies suggest that vitamin E supplementation can improve lipid profiles in dyslipidemic patients, reducing total cholesterol, LDL-C, and triglycerides (62,63). Higher serum vitamin E levels have been associated with a more favorable lipid profile (64). Vitamin E supplementation has been shown to suppress elevated plasma lipid peroxides and increase serum antioxidant activity (65). The impact of antioxidative vitamins on lipid profiles varies based on dosage, duration, and individual health status (47).
- Magnesium and dyslipidemia. Hypomagnesemia has been linked to metabolic abnormalities and dyslipidemia (66–70). Studies report negative correlations between serum magnesium and triglycerides, LDL, and total cholesterol, while positive correlations are observed with HDL cholesterol (70,71).
3. Infections and dyslipidemia
- Infections promote dyslipidemia. Dyslipidemia is a common complication in HIV-infected patients and those with COVID-19, associated with increased severity and mortality (72). It is characterized by elevated total cholesterol, LDL, and triglycerides, with decreased HDL (73,74). The pathogenesis involves inflammation, oxidative stress, and lipid peroxidation (75). These lipid abnormalities may increase cardiovascular risk in HIV patients (76,77). Research suggests a significant association between oral infections, particularly periodontitis, and systemic metabolic disturbances. Periodontitis has been linked to increased risk of cardiovascular diseases and dyslipidemia (78,79). Studies have found higher levels of total cholesterol, LDL cholesterol, and triglycerides, along with lower HDL cholesterol, in individuals with periodontitis (80,81). Chronic oral infection with Porphyromonas gingivalis, a key periodontal pathogen, has been shown to accelerate atheroma formation by altering lipid profiles in animal models (82). The relationship between periodontitis and hyperlipidemia appears bidirectional, with elevated triglycerides potentially modulating inflammatory responses to periodontal pathogens (83). The underlying mechanisms involve systemic inflammation, metabolic endotoxemia, and genetic factors that influence both oral infections and cardiometabolic diseases (84). These findings highlight the complex interplay between oral health and systemic metabolism.
- Infection control improves dyslipidemia. Periodontal treatment has been shown to improve lipid control (85). Eradication of Helicobacter pylori infection may decrease the risk of dyslipidemia (86).
4. Physical inactivity and dyslipidemia/high cholesterol
Research consistently shows an inverse relationship between physical activity (PA) and dyslipidemia. Higher PA levels are associated with increased HDL-C and decreased triglycerides in both men and women (87,88). Sedentary behavior increases the risk of dyslipidemia, while moderate-to-vigorous PA (MVPA) may reduce this risk (89,90). The prevalence of dyslipidemia is high in some populations, with limited awareness and treatment (91). Individuals meeting PA guidelines have lower odds of dyslipidemia, even with poor diet quality (91). However, adults with hypercholesterolemia are less likely to meet PA recommendations compared to those without (92). PA patterns, including timing and intensity, may influence lipid profiles differently (90). Overall, habitual PA is associated with more favorable lipid profiles and reduced cardiovascular disease risk (93,94).
5. Hormonal imbalance and dyslipidemia/high cholesterol
- Thyroid dysfunction, particularly hypothyroidism, is strongly associated with dyslipidemia and increased cardiovascular risk (95,96). Both overt and subclinical hypothyroidism can lead to elevated total cholesterol, LDL cholesterol, and apolipoprotein B levels, while potentially affecting HDL cholesterol and triglycerides (97,98). These lipid abnormalities are primarily due to reduced LDL receptor activity and altered regulation of cholesterol biosynthesis (99). Thyroid hormone replacement therapy has been shown to improve lipid profiles in overt hypothyroidism, but its benefits in subclinical hypothyroidism remain debated (99,100). Recent studies have also highlighted the role of thyroid hormones in regulating HDL function and cholesterol efflux (98). Given the prevalence of thyroid dysfunction and its impact on lipid metabolism, screening for thyroid disorders is recommended in patients with dyslipidemia (101).
- Cortisol imbalance significantly contributes to dyslipidemia, high cholesterol, and increased cardiovascular risk. Excess cortisol, such as in Cushing’s syndrome, is associated with elevated triglycerides, total cholesterol, and LDL cholesterol levels (102). Similarly, stress-induced cortisol elevation disrupts lipid metabolism, promoting atherogenesis and increasing the risk of atherosclerosis (103). Conversely, patients with metabolic syndrome and low cortisol levels exhibit less pronounced lipid disturbances (104). Elevated basal cortisol levels and reduced circadian variability have been linked to unfavorable lipid profiles, particularly in individuals with depressive and anxiety disorders (105). Additionally, the cortisol-to-DHEA ratio has been positively correlated with atherogenic lipid profiles in HIV patients with lipodystrophy (106). Glucocorticoid therapy, a common cause of cortisol excess, can lead to dyslipidemia and hypertension, further heightening cardiovascular disease risk (107). Excess cortisol is also strongly associated with obesity, hypertension, and metabolic syndrome (108,109). Furthermore, studies have found that elevated long-term cortisol levels, as measured in scalp hair, are linked to a history of cardiovascular disease (110). In obesity, higher cortisol concentrations are directly correlated with an increased risk of cardiovascular comorbidities (111). These findings highlight the multifaceted role of cortisol in dyslipidemia and emphasize the need to manage cortisol levels to mitigate cardiovascular risks effectively.
- Estrogen imbalance significantly impacts lipid metabolism and cholesterol levels. During menopause, estrogen deficiency leads to increased total cholesterol, LDL cholesterol, and triglycerides, while decreasing HDL cholesterol (112). High maternal estradiol levels can induce dyslipidemia in newborns by upregulating HMGCR expression in fetal hepatocytes (113). Estrogen administration in premenopausal women increases VLDL and HDL constituents, enhancing VLDL apoB and HDL apoA-I production (114). In postmenopausal women, estrogen therapy lowers LDL cholesterol levels (115). Estrogen treatment in cholesterol-fed rabbits attenuates atherosclerosis development by modulating lipoprotein metabolism (116,117). Endogenous sex hormones play a role in regulating lipid metabolism in postmenopausal women, with SHBG associated with a more favorable lipid profile (118). Estrogen administration in postmenopausal women decreases LDL cholesterol and hepatic triglyceride lipase activity while increasing HDL cholesterol (119).
- Progesterone imbalance can significantly impact lipid metabolism and cholesterol levels. Progesterone administration in rats led to increased hepatic triglycerides and cholesterol esters, while decreasing plasma cholesterol levels (120). In cultured cells, progesterone inhibited cholesterol biosynthesis (121). Dyslipidemia affected ovarian steroidogenesis in mice through oxidative stress, inflammation, and insulin resistance (122). In premenopausal women, ovarian lipid metabolism influenced circulating lipids (123). Estrogen plus progesterone replacement therapy in postmenopausal women lowered lipoprotein[a] levels and improved overall lipid profiles (124). High-dose medroxyprogesterone decreased total, LDL, and HDL cholesterol in postmenopausal women (125). In children, progesterone/estradiol ratios were associated with LDL-cholesterol levels (126). Female runners with menstrual irregularities showed altered steroid hormone and lipid profiles compared to eumenorrheic counterparts (127).
- Testosterone imbalance can significantly impact lipid metabolism and cholesterol levels. Research suggests a complex relationship between testosterone and lipid profiles. Low testosterone levels are associated with adverse lipid profiles, including higher total cholesterol and triglycerides, and lower high-density lipoprotein (HDL) cholesterol (128,129). Conversely, higher testosterone levels correlate with increased HDL cholesterol in men, particularly those with cardiovascular disease (130,131). Testosterone deficiency may contribute to hypercholesterolemia through altered expression of hepatic PCSK9 and LDL receptors (132). The effect of testosterone on lipids varies with age, gender, race/ethnicity, and menopausal status (133). Exogenous testosterone administration in hypogonadal men may improve lipid profiles by decreasing LDL and total cholesterol, although it may also decrease HDL cholesterol (134). While testosterone’s influence on lipids is evident, its overall impact on cardiovascular disease risk remains unclear and requires further investigation (134,135).
Conclusion
Dyslipidemia, long regarded as a primary target in ASCVD management, is increasingly understood as an outcome of complex, multifactorial root causes. These root causes include dietary factors, such as high-carbohydrate diets, ultra-processed foods, seed oils, and high-fructose consumption, which significantly influence lipid metabolism. Nutritional deficiencies, including vitamins B, C, D, and E, and magnesium, further exacerbate dyslipidemia, while chronic infections and physical inactivity compound cardiovascular risk. Hormonal imbalances, including dysfunctions in thyroid hormones, estrogen, progesterone, testosterone, and cortisol, also play a pivotal role in lipid abnormalities.
Addressing these underlying factors presents an opportunity to move beyond the traditional cholesterol-centric paradigm. Strategies such as dietary modifications, increased physical activity, infection control, and optimization of nutritional and hormonal balance can significantly improve lipid profiles, reduce cardiovascular risk, and even reverse ASCVD in some cases, as we have demonstrated in our recent report (1).
By focusing on the root causes of dyslipidemia, healthcare providers can offer more personalized and effective interventions, shifting the emphasis from symptom management to true disease prevention and reversal. This approach has the potential to improve not only ASCVD outcomes but also overall cardiovascular health and longevity. Future studies should prioritize the integration of these multifaceted strategies into clinical practice, emphasizing the importance of addressing the root causes of dyslipidemia for sustainable cardiovascular health.
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Proteins Linked to Alzheimer’s Disease Now Observable in Real Time
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/12/31/proteins-linked-to-alzheimers-disease.aspx
Analysis by Dr. Joseph Mercola December 31, 2024
STORY AT-A-GLANCE
- Nearly 7 million Americans currently have Alzheimer’s disease. Projections show this number will increase to 13 million by 2050, according to the Alzheimer’s Association
- A study used liquid-based atomic force microscopy to visualize beta-amyloid protein development in real-time, identifying “superspreader” fibrils that accelerate disease progression across brain tissue
- Three major toxins that damage mitochondrial function are excessive linoleic acid (LA) intake, endocrine-disrupting chemicals from microplastics and electromagnetic field (EMF) exposure from electronic devices
- Certain pathogenic bacteria strains like Collinsella, Lachnospira, and Veillonella increase Alzheimer’s risk, while probiotic strains like Eubacterium nodatum produce protective benefits through short-chain fatty acids
- Prevention strategies include optimizing vitamin D levels, maintaining low fasting insulin, avoiding gluten and casein, exercising regularly and challenging your mind with new skills
According to the Alzheimer’s Association, nearly 7 million Americans are currently diagnosed with Alzheimer’s disease, the most common type of dementia. Furthermore, the situation is expected to worsen — by 2050, around 13 million Americans are projected to be diagnosed with this neurodegenerative disease.1
Alzheimer’s disease remains challenging for modern medicine to diagnose and treat. However, a recent study2 has made a breakthrough in understanding how the disease progresses, creating a foundation for future clinicians and researchers to build upon to create better treatment plans.
A Breakthrough in Observing Alzheimer’s Disease Progression
In a study3 published in Science Advances, researchers were able to visualize the development of amyloid-beta proteins to see how Alzheimer’s disease spreads. Beta-amyloid proteins have been observed using a variety of methods, several of which were reviewed in the study:
“Methodological advances have been able to resolve the ultrastructure of Aβ and tau protein aggregates formed along the primary nucleation pathway using cryo-electron microscopy (cryo-EM) and solid-state nuclear magnetic resonance spectroscopy.
Likewise, the aggregation kinetics and toxicity of these proteins have been investigated using ultrasensitive fluorescence-based assays, nanopore devices, and circular dichroism.
Details on the morphology, on-surface assembly, and chemical structure of Aβ and tau protein aggregates have also been made accessible using standard atomic force microscopy (AFM), video-rate AFM, and infrared spectroscopy.”
For context, beta-amyloid proteins aggregate in the brain, and they’re suspected of playing a key role in the development of Alzheimer’s. Hence, they’re what researchers usually focus on to find therapeutic solutions.4 Previous staining methods used for observational analysis distort the protein structures.
To find new ways to analyze the mechanisms of Alzheimer’s disease, the team used liquid-based atomic force microscopy (AFM). As explained by the authors:5
“Building on the observations from previous secondary nucleation studies, we postulated that it should be feasible with a high-resolution AFM to record elementary information such as oligomer size, shape, and adsorption site on individual fibrils with sub-10-nm diameter. Operating the AFM in an aqueous solution medium would allow the diffusion of oligomers on the fibril surface.”
Tracking the Progression of Alzheimer’s Disease in Real Time
Once the team settled on the methodology, they moved onto testing. To start, they agitated beta-amyloid samples for 30 minutes at room temperature. Then, they set up different experiments to observe the growth and progression protein aggregates from 30 seconds to 250 hours:6
“Nanoscale imaging supported by atomic-scale molecular simulations tracked the adsorption and proliferation of oligomeric assemblies at nonperiodically spaced catalytic sites on the fibril surface. Upon confirming that fibril edges are preferential binding sites for oligomers during embryonic stages, the secondary fibrillar size changes were quantified during the growth stages.”
From their observations of protein fibril development in real time, they were able to classify some of them as “superspreaders” based on their surface anatomy. Specifically, these superspreaders “feature highly active edges and surfaces where new protein molecules accumulate, eventually forming longer fibrils that may spread across brain tissue.”
As they spread, more protein aggregation occurs, effectively progressing the hallmarks of Alzheimer’s disease. Ultimately, the research team hopes that this breakthrough in fibril analysis will be able to help improve the diagnosis and monitoring of neurodegenerative diseases. “This work brings us another step closer to better understanding how these proteins spread in brain tissue of Alzheimer’s disease,” says Peter Nirmalraj, one of the authors of the study.7
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Mitochondrial Dysfunction Is at the Heart of Alzheimer’s Disease
As researchers continue to come up with new tools to help diagnose and treat Alzheimer’s better, following a healthy lifestyle is important to reduce your risk. Prevention is by far your best option. I believe addressing mitochondrial dysfunction is key to protecting cognitive function, which is achieved by improving your cellular health.
The first thing to address is your diet. A study published in Neurology noted that eating an inflammatory diet raises your risk of dementia.8 In addition, I believe that there are three major toxins damaging your mitochondrial function by affecting intracellular calcium, which subsequently impacts cellular health.
Essentially, when calcium within your cells increase, your body produces superoxide and nitric oxide. These two combine to form peroxynitrite, a potent reactive oxygen species that contributes to poor health. Three pervasive toxins that raise intracellular calcium levels and drive peroxynitrite formation include:
1. Excessive linoleic acid (LA) consumption — LA is an omega-6 polyunsaturated fat (PUFA) found most abundantly in seed and vegetable oils and processed foods. I believe it is one of the most pernicious toxins of the Western diet, driving inflammation and chronic diseases among the populace.
Overconsumption negatively impacts your metabolic rate and gut microbiome, which are key factors for optimal health. To protect your health, I recommend keeping your LA intake below 5 grams a day.
Note that it’s virtually impossible to avoid LA, as most foods inherently have them, and your body does need some of it. The key is to avoid excess.
2. Endocrine-disrupting chemicals (EDCs) — Microplastics are so prevalent in our environment that humans ingest approximately a credit card’s worth of plastic every week.9 These microplastics contain endocrine-disrupting chemicals (EDCs), particularly phthalates and bisphenol A (BPA).
When these substances enter the body, they activate and overstimulate estrogen receptors. This increased estrogen activity raises intracellular calcium levels, which in turn leads to peroxynitrite formation.
To reduce your exposure, the first line of defense is minimizing your dependence on plastic products, such as bottled water and single-use food containers. Bringing a glass container and reusable tumbler for your water when going outside will significantly cut down your plastic usage. For additional strategies, read my article “How Microplastics Affect Your Reproductive Health.”
3. Electromagnetic field (EMF) exposure — The devices you use every day emit EMFs that activate voltage-gated calcium channel (VGCC) receptors within your cells. This triggers calcium influx, catalyzing peroxynitrite production.10
Major sources of EMFs include your cellphone, Bluetooth devices, wireless computer accessories and smart appliances that connect to your home’s Wi-Fi. For practical strategies on protecting yourself from EMFs, read my article “Study: Phone Radiation Kills Cheek Cells.”
Keep Your Gut Flora Healthy to Protect Cognitive Function
Your gut microbiome is one of the most crucial aspects for achieving optimal health. Research11 has shown that it plays a role in various functions, such as modulating the immune system, glucose metabolism and reducing insulin resistance. In addition to these findings, a study12 published in Scientific Reports showed that certain bacterial strains in the gut increased the risk of Alzheimer’s disease.
In the study, the researchers singled out strains such as Collinsella, Lachnospira and Veillonella as contributors to the risk of Alzheimer’s disease. According to the study authors:13
“In our analyses, Collinsella from the phylum Actinobacteria was identified as a risk factor for AD (Alzheimer’s disease) in both the discovery and replication samples … Importantly, an increased abundance of this genus has also been observed in AD transgenic mice and AD patients. Our findings provide evidence at the human genome-wide level of a connection between Collinsella and AD that supports previous observational studies …
In addition, we identified two Firmicutes genera as risk factors for AD (Lachnospira and Veillonella), with Veillonella being validated in the replication sample. Recently, it was reported that AD patients have an abundance of Veillonella in their oral microbiome. In the gut, it has been shown that an overabundance of species like V.parvula promotes intestinal inflammation …
The dual association of oral and gut abundance of Veillonella with disease points to this genus as a target for therapeutics and a potential bridge between conditions like gut inflammation and periodontitis with AD.”
The researchers also identified strains that provide protective benefits against Alzheimer’s disease, such as Eubacterium nodatum and Eisenbergiella. These produce short-chain fatty acids (SCFAs), particularly butyrate, from dietary carbohydrates.14
Butyrate nourishes your colonic epithelial cells, reinforcing the intestinal barrier. SCFAs also stimulate mucin production, creating a protective shield against harmful bacteria. Akkermansia also produces SCFAs, and research has shown that Alzheimer’s patients tend to have very low levels of this important keystone species.15
Carbohydrates Help Support Your Gut Health
Nurturing oxygen-intolerant beneficial bacteria, including Akkermansia, will strengthen your intestinal lining to create an environment that promotes overall wellness. On the other hand, low levels of oxygen-intolerant bacteria will lead to increased intestinal permeability, also known as leaky gut.
This causes openings in the intestinal barrier, allowing toxins, undigested food particles and harmful microbes to enter your bloodstream, resulting in systemic inflammation and chronic health issues.
To create an environment that allows your gut microbiome to thrive, increasing your intake of carbohydrates is a priority. Ashley Armstong provides some good recommendations for gut-friendly carbs, which include:
- Well-cooked white rice
- Sourdough bread
- Root vegetables like potatoes and sweet potatoes
- Fresh, ripe fruits
- Masa harina, or traditionally made tortillas
Also remember to include fermented foods. I’m a big believer of making your own fermented vegetables at home because they’re both simple and cost-effective to prepare. I don’t recommend buying commercially prepared fermented vegetables, as they often contain artificial sweeteners and additives, negating the benefits of fermented foods in the first place.
Additional Strategies to Prevent Alzheimer’s Disease
Aside from optimizing your gut health and mitochondrial function, there’s a plethora of helpful Alzheimer’s prevention strategies, several of which are outlined below:
| Avoid gluten and casein (primarily wheat and pasteurized dairy, but not dairy fat, such as butter) — As noted in a 2022 study,16 your blood-brain barrier is negatively affected by gluten. When bacteria enter your blood stream, the risk of Alzheimer’s disease increases. Other cognitive disorders are linked to a weakened blood-brain barrier as well, such as Parkinson’s disease, anxiety and depression. |
| Make sure you’re getting enough animal-based omega-3 fats — Omega-3 fats, namely 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. That said, omega-3s are PUFAs, so don’t overdo it. |
| 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 a 2023 study,17 increasing vitamin D reduced dementia risk by 40%.
The best way to get vitamin D is through sensible sun exposure, aiming for a blood level between 60 ng/mL and 80 ng/mL. However, you need to purge seed oils from your body before going into the sun at solar noon. The LA in your skin oxidizes when exposed to sunlight, causing inflammation and skin damage. To protect your skin, avoid sun exposure during solar noon for four to six months as you work on removing LA from your body. Stick to sunlight during early morning and late afternoon in the meantime. For additional skin defense, your can take astaxanthin, a low-dose aspirin or molecular hydrogen. Niacinamide cream will also lower your risk of skin damage. |
| Keep your fasting insulin levels below 3 — Insulin resistance is linked to accelerated brain aging, as well as neurodegeneration.18 |
| Eat a nutritious diet, rich in folate — Vegetables, without question, are your best form of folate. Avoid supplements like folic acid, which is the inferior synthetic version of folate. Research shows that folate is a protective factor against Alzheimer’s disease.19 |
| 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, nonstick cookware and vaccine adjuvants. |
| Make sure your iron isn’t elevated and donate blood if it is — A study20 published in Aging Medicine shows that excess iron increases your risk of Alzheimer’s disease by initiating the Fenton reaction, leading to increased oxidative stress. |
| Exercise regularly — Exercise triggers beneficial changes that support cognitive function. Particularly, it’s been shown to improve blood flow to the brain, leading to an increase in biomarkers related to improved neuronal plasticity and better cell survival.21 |
| 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, such as learning to play a musical instrument, is associated with a decreased risk of Alzheimer’s.22 |
| 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. |
- 1 Alzheimer’s Association, “Facts and Figures”
- 2 Science Advances, Vol 10, Issue 43, October 25, 2024
- 3 Science Advances, Vol 10, Issue 43, October 25, 2024, Introduction
- 4 News-Medical.net, October 28, 2024
- 5, 6 Science Advances, Vol 10, Issue 43, October 25, 2024, Abstract
- 7 Wiley Analytical Science, October 29, 2024
- 8 Neurology. 2021 Dec 14;97(24):e2381–e2391, Abstract
- 9 World Wildlife Fund, Assessing Plastic Ingestion from Nature to People
- 10 Open Journal of Veterinary Medicine, 11, 57-86, Abstract
- 11 Gut Microbes. 2024 Jan 4;16(1):229786, Diet with Probiotics and Their Impact on Gut Health
- 12, 13, 14 Scientific Reports volume 13, Article number: 5258 (2023), Discussion
- 15 Critical Reviews in Microbiology, 2023, 49(2), 151-176
- 16 Am J Lifestyle Med. 2022 Jan 11;16(1):32–35, Abstract
- 17 Alzheimers Dement (Amst). 2023 Mar 1;15(1):e12404, Highlights
- 18 Int J Mol Sci. 2021 Sep 15;22(18):9987, Abstract
- 19 Front Neurosci. 2021 Apr 14;15:661198, Abstract
- 20 Aging Med (Milton). 2024 Oct 22;7(5):649–667, Iron Overload/Accumulation and Increase Risk of AD
- 21 Front Aging Neurosci. 2023 Aug 4;15:1243869, Conclusion
- 22 Aging Ment Health. 2021 Apr;25(4):593-601, Abstract
The Role of Vitamin D Deficiency in Mental Illness
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/12/23/vitamin-d-deficiency-mental-illness.aspx
Analysis by Dr. Joseph Mercola December 23, 2024
STORY AT-A-GLANCE
- Vitamin D receptors exist throughout your brain, affecting mental health by regulating neurotransmitters and reducing inflammation. Deficiency is linked to depression, anxiety and psychosis
- Mental health patients show higher rates of vitamin D deficiency, caused by reduced sun exposure, obesity and other factors
- Studies show vitamin D supplementation improves depression symptoms, particularly in elderly and adolescent patients. Optimal blood levels range from 60 to 80 ng/mL
- Safe sun exposure remains the best source of vitamin D, but those consuming seed oils should wait four to six months after elimination before increasing sun exposure; if regular sun exposure isn’t feasible, vitamin D supplementation may be necessary
- Protective strategies for safe sun exposure include taking astaxanthin (12 mg daily), using niacinamide cream, pre-exposure baby aspirin and molecular hydrogen supplementation
Vitamin D receptors are not just limited to your skeletal system for bone health — they’re also present in various brain regions like your hippocampus, substantia nigra and cerebellum.
This hints at vitamin D’s key role in neurological development and the functioning of your nervous system. When your body lacks sufficient vitamin D, it disrupts neurotransmitter release, affects neurotrophic factors and impairs neuroprotection.1
These disruptions are linked to mood and behavioral changes, contributing to psychiatric conditions such as depression, anxiety and even psychosis. Moreover, vitamin D helps modulate inflammation, which is often elevated in mental health disorders. This is why optimizing your vitamin D levels is important for both physical health and maintaining your mental well-being.
Vitamin D Deficiency and Its Prevalence in Mental Health Conditions
Vitamin D deficiency is common, affecting over half of the global population regardless of age or ethnicity.2 For individuals battling psychiatric disorders, the rates of deficiency are even higher. Studies indicate that psychiatric patients often have lower vitamin D levels compared to the general population.
Factors contributing to this deficiency include reduced sunlight exposure due to time spent indoors, poor dietary intake and obesity, which sequesters vitamin D in fat tissues. Additionally, certain psychiatric medications lead to weight gain, further complicating vitamin D status.3
This widespread deficiency is concerning because low levels of vitamin D have been linked to a higher incidence of various mental health issues, including depression, schizophrenia and anxiety disorders4 — each affected in unique ways.
In depression, low vitamin D levels are associated with increased symptoms and a higher risk of developing the disorder. Vitamin D may protect the hippocampus during stress-related dysregulation and support the release of dopamine, a neurotransmitter involved in mood regulation.5
Schizophrenia, a chronic mental health disorder characterized by distorted thinking and perceptions, is another area of interest concerning vitamin D’s benefits. Research reveals a high prevalence of vitamin D deficiency among individuals with schizophrenia, particularly those experiencing acute episodes.6
Some studies have also found a strong association between low vitamin D levels and the severity of schizophrenia symptoms, suggesting that vitamin D could play a role in cognitive function and neuroprotection.7 In psychotic spectrum diseases like schizophrenia, deficiency is often linked to poorer outcomes and increased symptom severity, due to reduced neuroprotection and impaired neurotransmission.
The Impact of Vitamin D on Specific Mental Health Conditions
Neurodevelopmental disorders, including autism and attention-deficit hyperactivity disorder (ADHD), also show significant correlations with vitamin D levels, where supplementation has been found to improve behavioral and cognitive symptoms.8
Some research also indicates that individuals with bipolar disorder often exhibit lower levels of vitamin D compared to those without the condition. For instance, higher levels of vitamin D binding protein have been observed in bipolar patients, suggesting a link between vitamin D metabolism and mood regulation.9
Additionally, vitamin D plays a role in sleep-wake disorders, where deficiency disrupts circadian rhythms and leads to poor sleep quality.10 Optimizing vitamin D levels is therefore a promising therapeutic strategy for many mental health conditions. Studies have shown that vitamin D supplementation leads to improvements in depressive symptoms, particularly in individuals with existing deficiencies.
For instance, elderly patients with depression, adolescents and those recovering from acute illnesses have all benefited from increased vitamin D intake. In the context of schizophrenia, adding vitamin D to standard antipsychotic treatments has been linked to better cognitive outcomes and reduced symptom severity.11
Neuroinflammation, the inflammation of the nervous tissue, plays a role in many neurological and mental disorders, including traumatic brain injury, Alzheimer’s disease and vascular dementia. Vitamin D has emerged as a promising agent in combating neuroinflammation due to its anti-inflammatory and immunomodulatory properties.12
Animal studies, such as those conducted on rats with traumatic brain injury, have also demonstrated that vitamin D supplementation shifts microglial cells toward an anti-inflammatory state, reducing brain edema and protecting the blood-brain barrier.
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Vitamin D Helps Relieve Depression and Anxiety
A meta-analysis published in the Journal of Affective Disorders explored the effectiveness of vitamin D supplementation in managing primary depression.13 The study reviewed 18 randomized controlled trials to assess whether vitamin D alleviates depressive symptoms in adults. The findings revealed a significant overall reduction in depression scores among those who received vitamin D supplements compared to those who received a placebo.
Notably, the benefits were more pronounced in individuals with baseline vitamin D levels exceeding 20 ng/mL, where the reduction in depressive symptoms was substantial. This suggests that higher levels of vitamin D may be necessary to achieve meaningful improvements in depression.
A study published in The American Journal of Geriatric Psychiatry also revealed a compelling association between vitamin D deficiency and increased depressive symptoms in older adults.14 The study analyzed data from 299 participants, with over 60% classified as either vitamin D deficient or insufficient.
These individuals exhibited higher scores on the Geriatric Depression Scale, particularly in the dysphoria and meaninglessness subdomains. This negative correlation suggests that lower vitamin D levels are directly linked to heightened feelings of sadness, hopelessness and a lack of purpose — core elements of depression. Notably, the study found that higher vitamin D sufficiency levels, nearing 95.5 ng/mL, were associated with minimal to no depressive symptoms.
These results underscore the crucial role that adequate vitamin D plays in maintaining mental health, highlighting the potential of VD supplementation as a strategic intervention to alleviate depressive symptoms in older populations. Anxiety disorders, much like depression, significantly impact your daily life and overall well-being.
Separate research highlights that low vitamin D levels are not only associated with increased symptoms of depression but also with heightened anxiety.15 Vitamin D’s antioxidant and anti-inflammatory properties play a role in mitigating the oxidative stress and inflammation that are key players in the pathophysiology of anxiety disorders.
Brain regions such as the prefrontal cortex and hippocampus, which are involved in regulating mood and anxiety, contain vitamin D receptors and the enzyme necessary for activating vitamin D. This suggests that adequate vitamin D levels are essential for maintaining the health and functionality of these brain areas. Supplementing with vitamin D has also been found to help reduce anxiety symptoms.16
Maximizing the Benefits of Sunlight for Vitamin D Production
While vitamin D supplements are widely available, sunlight remains the gold standard for vitamin D synthesis in your body. Beyond just vitamin D production, sun exposure offers additional health advantages. In fact, elevated vitamin D levels often indicate healthy sun exposure, which may explain many of the health benefits traditionally attributed to vitamin D alone, including reduced mental health benefits, cancer risk and enhanced longevity.
One important factor that’s often overlooked in sun exposure discussions, however, is the impact of dietary oils, particularly seed oils. If you regularly consume seed oils, you’ll need to exercise extra caution with sun exposure. These oils contain high amounts of linoleic acid (LA), which becomes problematic when exposed to ultraviolet radiation. The interaction between sunlight and LA-rich skin triggers inflammation and DNA damage.
For this reason, it’s advisable to limit sun exposure to earlier in the morning or later in the afternoon if you’ve been consuming these oils regularly. A safe approach is to wait four to six months after eliminating these oils from your diet before increasing sun exposure. Several personal characteristics also influence how your body tolerates and responds to sunlight:
• Skin pigmentation — Melanin serves as a natural sunscreen. People with darker skin need longer sun exposure to produce the same amount of vitamin D as those with lighter skin.
• Body composition — Fat tissue stores fat-soluble compounds, including oxidized seed oils. Those with higher body fat percentages may need to be more cautious, as stored oils extend the risk period even after dietary changes.
Guidelines for Safe Sun Exposure
The simplest way to gauge appropriate sun exposure is the “sunburn test.” Monitor your skin for any signs of redness. If you don’t notice even slight pinkness, you’re likely within a safe exposure range. Always avoid sunburn, as it indicates damage. As you reduce LA stores in your body, your susceptibility to sunburn and skin cancer decreases significantly.
These recommendations account for both optimal vitamin D production and protection against oxidative stress while your body eliminates stored LA so during the transition period:
• Until you’ve been seed oil-free for six months, avoid direct sun 2 to 3 hours before and after solar noon. While complete tissue clearance of seed oils takes about two years, the six-month mark typically allows enough detoxification for beneficial sun exposure during peak hours.
• Remember that during Daylight Saving Time (summer months), solar noon occurs at 1 PM, not 12 PM. This means peak sunlight hours are roughly 10 AM to 4 PM during these months.
• As your body eliminates stored seed oils over the initial six months, gradually increase sun exposure closer to solar noon. Start with early morning or late afternoon sun, slowly working toward midday exposure as your tissues become cleaner and more resilient to UV light.
If sun exposure is necessary before your body has cleared seed oils, consider these protective measures:
1. Astaxanthin supplementation — Take 12 milligrams daily to enhance skin resistance to sun damage.
2. Topical niacinamide — Apply vitamin B3 cream before sun exposure to protect against UV-induced DNA damage.
3. Pre-exposure aspirin — Taking a baby aspirin 30 to 60 minutes before sun exposure may reduce skin cancer risk by preventing LA conversion to harmful oxidized linoleic acid metabolites (OXLAMs).
4. Molecular hydrogen — This compound helps neutralize free radicals and reduces oxidative stress while maintaining beneficial reactive oxygen species.
Vitamin D Supplementation Tips
If regular sun exposure isn’t feasible, vitamin D supplementation may be necessary. However, the current definition of vitamin D deficiency (less than 20 ng/mL) has been shown to be inadequate for good health and disease prevention. While sufficiency begins around 40 ng/mL (100 nmol/L in European measurements), the target range for optimal health is 60 to 80 ng/mL (150 to 200 nmol/L). To optimize your vitamin D levels:
- Test your levels twice a year
- Adjust sun exposure or supplementation based on the results
- Retest after three to four months to confirm you’ve reached target levels
- Continue monitoring to maintain optimal levels
Remember that everyone’s relationship with the sun is unique. Listen to your body’s signals and adjust your exposure accordingly. The goal is to harness the benefits of sunlight while avoiding sunburn. Further, keep in mind that the interplay between vitamin D and mental health is intricate and multifaceted. While supplementation shows promise, it’s not a one-size-fits-all solution.
Vitamin D deficiency could be both a consequence of mental illness — due to factors like reduced sunlight exposure and poor diet — and a contributing factor to the severity and resistance to treatment of these conditions. Therefore, addressing vitamin D levels should be part of a holistic approach to mental health care, alongside dietary improvements, physical activity and other psychosocial interventions.
However, ensuring adequate vitamin D levels through safe sun exposure and supplementation when necessary is a valuable component in supporting your mental well-being. By taking proactive steps to manage your vitamin D status, you contribute positively to your overall mental health and resilience against psychiatric disorders.
- 1, 2, 3, 4, 5, 8, 10, 11 Medicina (Kaunas). 2023 Nov 21;59(12):2056
- 6, 7, 9, 12 Diseases. 2024 Jun 20;12(6):131
- 13 J Affect Disord. 2024 Jan 1:344:653-661. doi: 10.1016/j.jad.2023.10.021. Epub 2023 Oct 16
- 14 The American Journal of Geriatric Psychiatry July 2024, Volume 32, Issue 7, P808-820
- 15, 16 Curr Nutr Rep. 2022 Sep 13;11(4):675–681
Low Magnesium Linked to Increased DNA Damage in Healthy Adults
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/12/02/low-magnesium-dna-damage.aspx
Analysis by Dr. Joseph Mercola December 02, 2024
STORY AT-A-GLANCE
- Low magnesium levels, especially when combined with high homocysteine, significantly increase DNA damage in healthy adults, accelerating cellular aging and increasing the risk of chronic degenerative diseases
- Magnesium plays a crucial role in DNA replication, repair and stability. It acts as a cofactor for enzymes involved in these processes and helps maintain the double helix structure
- Magnesium is essential for brain health, regulating NMDA receptors, modulating immune responses and acting as an antioxidant. It also supports synaptic plasticity, learning and memory functions
- Adequate magnesium levels are vital for blood sugar control, insulin sensitivity and cellular energy production. Magnesium deficiency leads to insulin resistance and metabolic disorders like Type 2 diabetes
- To optimize magnesium levels, consider supplements like magnesium threonate, consume magnesium-rich foods and try alternative methods such as Epsom salt baths or topical application for better absorption
There’s a critical link between magnesium levels and the integrity of your DNA, according to research published in the European Journal of Nutrition.1 The study, conducted on healthy middle-aged Australians, revealed that low magnesium levels, especially when combined with high homocysteine, significantly increase DNA damage.
This finding underscores the vital role magnesium plays in maintaining your genetic health and staving off age-related diseases. As the fourth most abundant mineral in your body, magnesium is involved in over 600 enzymatic reactions, including those crucial for DNA replication and repair.
Ensuring adequate magnesium intake could be a key factor in protecting your genetic material and promoting healthy aging. In fact, by examining various biomarkers of DNA damage, researchers have shed light on how magnesium deficiency might accelerate cellular aging and increase your risk of developing chronic degenerative diseases.
The Hidden Dangers of Magnesium Deficiency
While magnesium’s importance for bone health and nerve function is well-known, its role in safeguarding your DNA is less recognized. The study found that participants with lower magnesium levels exhibited higher frequencies of micronuclei (MN) and nucleoplasmic bridges (NPBs) in their cells.2 These are telltale signs of DNA damage and chromosomal instability.
Essentially, when your body lacks sufficient magnesium, it struggles to efficiently replicate and repair DNA, leaving your genetic material vulnerable to damage. This vulnerability manifests as increased oxidative stress and a higher likelihood of DNA strand breaks. Over time, these effects accumulate, leading to premature aging of your tissues and organs.
The research suggests that chronic magnesium deficiency might create a state of persistent oxidative stress in your body, similar to the effects seen with deficiencies in other crucial micronutrients like zinc.3
The Homocysteine Connection: A Double-Edged Sword
The study didn’t just focus on magnesium; it also examined the interplay between magnesium levels and homocysteine, an amino acid linked to various health issues when present in high concentrations. Researchers discovered a significant negative correlation between magnesium and homocysteine levels. In other words, as magnesium levels decreased, homocysteine levels tended to increase.4
This relationship is noteworthy because elevated homocysteine is associated with an increased risk of neurodegenerative diseases, cardiovascular problems and pregnancy complications. Participants with both low magnesium and high homocysteine levels showed the highest frequency of DNA damage markers.
This synergistic effect suggests that the combination of magnesium deficiency and elevated homocysteine could be particularly detrimental to your genetic health, accelerating the aging process and increasing your susceptibility to age-related diseases.5
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Unraveling the Mechanisms of Magnesium’s Protective Effects
To understand why magnesium is so crucial for your DNA’s integrity, it’s important to look at its role in various cellular processes. Magnesium acts as a cofactor for enzymes involved in DNA replication and repair, such as DNA polymerase and DNA ligases. When magnesium levels are low, these enzymes can’t function optimally, leading to errors in DNA replication and inefficient repair of damaged DNA.6
Additionally, magnesium plays a role in maintaining the stability of DNA and RNA structures. It helps neutralize the negative charges on DNA phosphate groups, contributing to the overall stability of the double helix structure.
The study also hints at magnesium’s involvement in epigenetic regulation and protein modification processes that are crucial for maintaining genomic integrity.7 By ensuring adequate magnesium levels, you’re providing your cells with the tools they need to protect and maintain your genetic material effectively.
Magnesium’s Role in Protecting Your Brain’s Delicate Balance
Your brain’s health depends on a delicate balance of various processes, and magnesium plays a key role in maintaining this equilibrium. Recent research reveals how magnesium acts as a gatekeeper for N-methyl-D-aspartate (NMDA) receptors, which are vital for learning and memory.8 By regulating these receptors, magnesium helps prevent excessive glutamate activity, which leads to inflammation and neuronal damage.
Additionally, magnesium has been found to influence the production of substance P, a neuropeptide involved in pain perception and inflammatory responses. Low magnesium levels increase substance P, exacerbating neuroinflammation.9 Furthermore, magnesium’s interplay with calcium in your neurons is critical. By limiting calcium influx, magnesium helps prevent a cascade of events that could otherwise result in intensified inflammation and neuronal injury.
This balancing act extends to magnesium’s role in modulating immune responses, particularly through its interaction with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), a key player in inflammatory processes. By inhibiting NF-κB activation, magnesium helps dampen the expression of proinflammatory genes, reducing overall brain inflammation.10
The Hidden Power of Magnesium as an Antioxidant
While not typically classified as an antioxidant, emerging research suggests that magnesium plays a role in your body’s defense against oxidative stress.11 This is particularly important for your brain health, as oxidative stress is a significant contributor to cognitive decline and neurodegenerative diseases.
Studies have shown that magnesium deficiency is associated with increased markers of oxidative stress, including modified lipids, proteins and DNA. Importantly, magnesium appears to support your body’s antioxidant defense mechanisms. One key way it does this is by stabilizing superoxide dismutase (SOD), a critical enzyme that converts harmful superoxide radicals into less reactive molecules.12
This stabilization of SOD provides a unique link between magnesium and your antioxidant defense system. Magnesium’s involvement in various cellular processes, including mitochondrial function and fatty acid metabolism, further contributes to its role in managing oxidative stress.
By supporting these fundamental processes, magnesium helps maintain cellular health and resilience against oxidative damage. This antioxidant-like activity of magnesium adds another layer to its neuroprotective properties, helping to slow the progression of age-related cognitive decline and neurodegenerative disorders.13
Magnesium’s Impact on Your Brain’s Plasticity and Memory
Recent discoveries have also unveiled magnesium’s role in synaptic plasticity, your brain’s ability to form and reorganize connections between neurons.14 This process is fundamental to learning, memory and cognitive flexibility.
Research has shown that presynaptic intracellular magnesium is instrumental in mediating the transition between two crucial synaptic configurations: one involved in encoding new information and learning, and another responsible for storing and recalling memories.15 This insight highlights magnesium’s importance not just in maintaining neural health but in actively shaping your cognitive processes.
Studies on animal models of Alzheimer’s disease have demonstrated that magnesium supplementation enhances cognitive function and synaptic plasticity. Moreover, in a rat model of Alzheimer’s, magnesium sulfate supplementation improved cognitive function, synaptic plasticity and even the morphology of dendritic spines — the tiny protrusions on neurons that receive input from other neurons.16
These findings suggest that maintaining optimal magnesium levels could be crucial for preserving cognitive function as you age.17
Magnesium for Blood Sugar Control and Cellular Energy Production
Your body’s intricate blood sugar control system also relies on magnesium. This essential nutrient is involved in the function of your pancreatic beta cells, which produce insulin to regulate blood glucose levels.18 When you eat, these cells respond by releasing insulin to help your body store glucose as glycogen, primarily in your liver and muscle cells.
Magnesium is vital for this process, acting as a cofactor for enzymes involved in glucose metabolism and insulin signaling. If your magnesium levels are low, your beta cells may struggle to produce and release insulin effectively, leading to blood sugar imbalances. Furthermore, magnesium deficiency impairs the activity of glucokinase, an enzyme that acts as a glucose sensor in beta cells and controls the rate of glucose entry into these cells.19
Without adequate magnesium, your body’s ability to sense and respond to changes in blood glucose levels may be compromised, setting the stage for metabolic disorders like Type 2 diabetes. Low magnesium levels also contribute to insulin resistance by altering the activity of the insulin receptor and its downstream signaling pathways. Conversely, insulin resistance leads to increased urinary magnesium loss, further depleting your body’s magnesium stores.20
This creates a self-perpetuating cycle that’s difficult to break. Studies have shown that individuals with Type 2 diabetes often have lower intracellular magnesium concentrations compared to those without diabetes.21
Beyond its effects on insulin and glucose metabolism, magnesium is essential for your cells’ energy production processes. It acts as a cofactor for numerous enzymes involved in glycolysis and the Krebs cycle, two key pathways in cellular energy generation. In the absence of sufficient magnesium, these enzymes may not function optimally, leading to reduced energy production and metabolic inefficiencies.22
It’s important to remember that magnesium’s benefits are far-reaching. Adequate magnesium intake helps maintain healthy blood pressure, support proper muscle and nerve function and promote strong bones.
There are also positive correlations between magnesium levels and other important nutrients like folate and vitamin B12, suggesting that magnesium status is an indicator of overall nutritional health.23 By prioritizing your magnesium intake, you’re not just protecting your DNA, brain or blood sugar; you’re supporting your body’s overall function and resilience.
How to Optimize Your Magnesium Levels
More than half of Americans don’t get enough magnesium daily,24 and this deficiency is even more widespread in certain groups. Various health conditions and lifestyle choices increase magnesium loss from your body. For example, if you have diabetes or drink alcohol regularly, you’re at higher risk of magnesium deficiency.
Your magnesium levels are also affected by lack of sleep and stress. Even short periods of stress might lower your magnesium. When it comes to supplements, I prefer magnesium threonate because it’s particularly good at entering cells, including those in your brain and mitochondria.
However, if you’re new to magnesium supplements, it’s best to start slowly with magnesium citrate to find the right dose for you. This method, called “bowel tolerance,” helps you determine how much magnesium your body needs. Like vitamin C, excessive oral magnesium results in loose stools, indicating that you’ve surpassed your optimal intake. This natural safeguard makes magnesium toxicity highly unlikely.
Start with 200 milligrams (mg) of magnesium citrate per day and gradually increase until you notice your stools becoming slightly loose. This indicates you’ve found your ideal dose. From there, try other types of magnesium if you want.
Take magnesium threonate with or without food. If you’re also taking calcium supplements, it’s good to take them together. Fitness enthusiasts might benefit from a pre-workout regimen that includes calcium and magnesium in a 1:2 ratio. While a 1:1 ratio of magnesium to calcium is often recommended, most diets are already high in calcium. So, you might need two to three times more magnesium than calcium in your supplements to balance things out.
Remember, blood tests aren’t always reliable for checking your magnesium levels, especially in muscles and bones. Instead, tracking what you eat is a more practical way to make sure you’re getting enough magnesium. Foods that are high in magnesium include:
| Raw milk and homemade yogurt | Broccoli |
| White rice | Bok choy |
| Potato | Turnip greens |
| Dried seaweed or agar | Brussels sprouts |
Aside from food and oral supplements, alternative methods to increase your magnesium levels include:
• Epsom salt baths — Soaking in magnesium sulfate-rich water enables transdermal (skin) absorption, circumventing your digestive system.
• Topical application — Create a concentrated Epsom salt solution using the following steps:
◦Heat 6 ounces of water and dissolve 7 tablespoons of Epsom salt
◦Once cooled, transfer to a dropper bottle
◦Apply directly to your skin
◦For enhanced absorption, follow with fresh aloe vera gel
As we continue to uncover the intricate ways in which nutrients interact with our genes and cellular processes, the importance of maintaining optimal magnesium levels becomes increasingly clear. To ensure healthy aging and disease prevention, prioritize getting an adequate intake of magnesium.
- 1, 2, 3, 4, 5, 6, 7, 23 European Journal of Nutrition June 12, 2024
- 8, 9, 10, 11, 12, 13, 14, 15, 16, 17 Front. Endocrinol., 25 September 2024 Sec. Cellular Endocrinology, Volume 15 – 2024
- 18, 19, 20, 21, 22 Front. Nutr., 25 September 2024 Sec. Nutritional Epidemiology, Volume 11 – 2024
- 24 Oregon State University, “Micronutrient Inadequacies in the US Population: An Overview” Micronutrient Deficiencies and Inadequacies
Reigniting Hope: Managing Systemic Lupus Erythematosus with Integrative Orthomolecular Medicine
Reproduced from original article:
https://orthomolecular.acemlna.com/p_v.php?l=1&c=333&m=337&s=a8c8fe7bea3fdaa4efae896c7612b3de
Orthomolecular Medicine News Service, November 16, 2024
Richard Z. Cheng, M.D., Ph.D.
OMNS (Nov 16, 2024) A recent story from Shanghai highlights the difficult journey of SLE patients. A woman named Shabai, after two decades battling this autoimmune disease and suffering kidney failure requiring dialysis, sought relief through assisted death in Switzerland. In her final social media post on October 24, 2024, she expressed gratitude for a ‘wonderful life,’ offering a heartfelt farewell with her father. Shabai’s story has ignited public empathy, underscoring the profound impact of SLE on physical and emotional well-being.
Having been asked to write about SLE, I aim to explore how integrative orthomolecular medicine can offer effective management strategies for this complex condition. Through a holistic approach that addresses root causes, nutrient support, and lifestyle factors, integrative orthomolecular medicine opens new avenues for reducing symptoms and enhancing quality of life. Patients with SLE should not give up hope; there are promising strategies that can empower them to live healthier, fuller lives despite their diagnosis.
Introduction: Systemic Lupus Erythematosus (SLE) is a complex autoimmune disease characterized by the production of autoantibodies and immune complex formation, affecting multiple organ systems.
While the exact etiology remains unclear, an integrative orthomolecular approach can provide insights into the root causes and intermediary mechanisms involved in SLE development and progression.
Root Causes Contributing to SLE:
- Unhealthy Diet: High consumption of carbohydrates, omega-6 polyunsaturated fatty acids (PUFAs), and ultra-processed foods may contribute to inflammation and immune dysregulation in SLE (1).
- A high-carbohydrate diet is associated with increased SLE risk (2). Specifically, women in the highest quintile of carbohydrate consumption had a nearly twofold increased risk compared to those in the lowest quintile (2). This suggests that diets high in carbohydrates may contribute to the development of SLE in this population.
- Overconsumption of omega-6 seed oil: Research suggests that an imbalanced omega-6 to omega-3 ratio, a global trend, may contribute to autoimmune diseases like systemic lupus erythematosus (SLE) (3). Omega-3 fatty acids have anti-inflammatory properties and may benefit autoimmune conditions (4-6). Research on mice demonstrated that omega-3-rich diets could reduce autoantibody production and kidney damage in SLE models (7). The complex relationship between dietary fats and autoimmunity is further highlighted by findings that both excessive omega-6 intake and reduced omega-3 consumption may exacerbate autoimmune diseases (8).
- Ultra-processed foods: Recent studies suggest a link between ultra-processed food (UPF) intake and increased risk of systemic lupus erythematosus (SLE), particularly in women. Higher UPF consumption was associated with a >50% increased SLE risk and doubled risk for anti-dsDNA+ SLE (9).
- Dietary toxins in plant-based foods: Lectins, found in many plant-based foods, have been identified as potential contributors to autoimmune diseases, including systemic lupus erythematosus (SLE). These carbohydrate-binding proteins can resist digestion, enter the bloodstream, and trigger immune responses (10,11). Lectins may disrupt intestinal barrier integrity, leading to various autoimmunities (11). While some researchers caution against labeling plant compounds as “anti-nutrients” (12), others emphasize the potential risks of lectins, oxalates, and other plant-based toxins (13,14). Natural plant metabolites have been explored as potential remedies for SLE due to their immunomodulatory properties (15). Environmental factors, including toxic chemicals, are believed to contribute significantly to autoimmune diseases (16). Oxidative stress, arising from both endogenous and exogenous sources, has been identified as a unifying theme in the pathogenesis of SLE and other autoimmune conditions (17).
- Environmental Toxins: Exposure to chemicals, pesticides, and heavy metals may trigger autoimmune responses. Occupational exposure to crystalline silica has been studied as a possible trigger for SLE (18).
- Environmental toxins and chemicals have been implicated in the development and exacerbation of systemic lupus erythematosus (SLE) and other autoimmune conditions. Various studies have linked exposure to silica, solvents, pesticides, heavy metals, and endocrine disruptors like bisphenol A (BPA) and bisphenol F (BPF) to increased SLE risk (19-21). These toxins can trigger autoimmunity through multiple mechanisms, including epigenetic alterations, immune dysregulation, antioxidant depletion, and barrier degradation in genetically susceptible individuals (22). Cigarette smoking, oral contraceptives, and postmenopausal hormone therapy have also been associated with SLE incidence, while alcohol consumption may decrease risk (23). Environmental exposures can lead to chronic inflammation, tissue damage, and the release of self-antigens, potentially contributing to the development of autoimmunity (24). Further research is needed to fully elucidate the complex interactions between environmental factors and genetic susceptibility in SLE pathogenesis (25).
- Heavy metals exposure has been linked to autoimmune diseases, including SLE (20,26). Metals such as mercury, cadmium, and lead can disrupt immune responses, potentially exacerbating immune tolerance issues and chronic inflammation (27-29). These metals can affect both innate and adaptive immunity, leading to chronic inflammation and disrupted immune tolerance (30,31). This exposure triggers immune dysregulation through pathways like oxidative stress, genetic predisposition, and epigenetic alterations (26,31,32).
- Infections: Infections play a crucial role in the etiopathogenesis and exacerbation of systemic lupus erythematosus (SLE) (33,34). Various pathogens, particularly viruses like Epstein-Barr virus, can trigger autoimmunity through molecular mimicry and immune dysregulation (35,36). SLE patients are more susceptible to infections due to genetic factors and immunosuppressive treatments (37). Bacterial infections, including periodontal disease, may contribute to SLE pathogenesis by exposing nuclear autoantigens and stimulating Toll-like receptors (TLRs) 2 and 4 (38,39). Periodontal disease is associated with increased inflammatory markers and may be a risk factor for cardiovascular disease in SLE patients (40). Preventive measures, such as screening for chronic infections before immunosuppressive therapy, are crucial in managing SLE patients (35,37).
- Nutrient Deficiencies: Insufficient intake of vitamins and micronutrients, especially B vitamins, vitamins C, D3, and K2, as well as magnesium and selenium, may contribute to immune dysfunction in SLE (1). Vitamin D deficiency, in particular, has been linked to increased SLE activity (1). Vitamin D deficiency is prevalent in systemic lupus erythematosus (SLE) patients and associated with increased disease activity (41). Low vitamin D levels correlate with higher autoantibody production, B cell hyperactivity, and interferon-α activity in SLE patients (42). Vitamin D plays a crucial role in immune regulation and may contribute to autoimmune disease pathogenesis (43). Supplementation with vitamin D has shown potential in reducing inflammatory markers and disease activity in SLE patients (44). Factors such as photosensitivity, photoprotection, and postmenopausal status are associated with vitamin D deficiency in SLE patients (41,45). Hydroxychloroquine use may help prevent vitamin D deficiency (45). While the relationship between vitamin D and SLE is complex, addressing vitamin D deficiency may have benefits beyond bone health for SLE patients (46,47).
- Mental Health and Stress: Emotional or physical stress can trigger SLE flares (18). Chronic stress may contribute to immune system dysregulation.
- Genetics: SLE has a strong genetic component, with multiple genetic variants associated with increased susceptibility (18).
- Hormonal Imbalance: SLE often manifests or worsens during periods of hormonal fluctuations, such as puberty, pregnancy, or menopause (18). Hormonal imbalances play a significant role in the pathogenesis of autoimmune diseases, particularly systemic lupus erythematosus (SLE). The higher prevalence of SLE in women, especially during reproductive years, suggests a strong influence of sex hormones (48,49). Studies have shown that SLE patients exhibit abnormal hormone levels, including elevated estrogen and prolactin, and decreased androgens (50,51). These hormonal alterations affect both innate and adaptive immune responses, contributing to disease development and progression (52). Estrogen, in particular, can exert pro-inflammatory effects through genomic and non-genomic pathways, influencing B cell maturation and selection (53,54). Additionally, environmental factors such as estrogenic endocrine disruptors may trigger or alter autoimmune disease onset (53). The complex interplay between sex hormones, cytokines, and the immune system highlights the importance of hormonal balance in SLE pathogenesis (55). Notably, dehydroepiandrosterone (DHEA) has shown promise as a potential treatment for SLE. Multiple studies have demonstrated that DHEA supplementation (200 mg/day) can reduce disease activity, decrease corticosteroid requirements, and improve health-related quality of life in SLE patients (56-59). DHEA has also been found to have a protective effect against corticosteroid-induced osteopenia (58).
- Ultraviolet Radiation: Sunlight, particularly UVB rays, is a well-established trigger for SLE flares (18).
- Lifestyle Factors: Smoking is both a potential flare trigger and a risk factor for SLE, increasing the risk of skin and kidney problems (18).
Intermediary Mechanisms in SLE
- Leaky Gut: Increased intestinal permeability, or “leaky gut,” is a common underlying cause of autoimmunity (60). In SLE, this can lead to undigested food particles entering the bloodstream, triggering immune responses and potentially causing molecular mimicry.
- Elevated Oxidative Stress: SLE patients exhibit high levels of oxidative stress, which can damage cellular components and contribute to inflammation (61). This may be exacerbated by nutrient deficiencies and environmental toxins.
- Impaired Mitochondrial Function: Mitochondrial dysfunction has been implicated in various autoimmune diseases and may play a role in SLE pathogenesis (62).
- Insulin Resistance in SLE: Insulin resistance (IR) is more prevalent in systemic lupus erythematosus (SLE) patients compared to healthy controls, increasing the risk of cardiovascular disease and type 2 diabetes mellitus (63). SLE patients exhibit higher C-peptide levels and elevated HOMA2-IR-C-peptide index, independent of traditional cardiovascular risk factors (64). IR in SLE is associated with disease activity, inflammation markers, and damage over time (64,65). Oxidative stress, indicated by increased malondialdehyde levels, correlates with IR in SLE patients (66). Type B insulin resistance syndrome, characterized by autoantibodies to insulin receptors, can occur in SLE patients and may respond to immunosuppressive treatment (67,68). Cyclophosphamide and mycophenolate mofetil have been successfully used to treat SLE-associated type B insulin resistance (69). Understanding these mechanisms can lead to better treatment strategies for SLE patients with IR.
- Immune System Dysregulation: SLE is characterized by an imbalance of T-helper cell subsets (Th1/Th2/Th17) and regulatory T-cells (Tregs), contributing to tissue damage and increased proinflammatory responses (1).
- Autoantibody Production: The hallmark of SLE is the production of autoantibodies, particularly antinuclear antibodies (ANA), which target the body’s own tissues (18).
- Complement Activation: Intravascular activation and conversion of complement contribute to increased capillary permeability and tissue damage in SLE (61).
- Cytokine Imbalance: SLE patients exhibit elevated levels of proinflammatory cytokines, including IFN-γ, TNF, IL-4, IL-6, IL-10, IL-12, IL-17, and IL-18, while IL-2 levels are typically lower compared to healthy controls (1).
Integrative Intervention:
- Healthy diet: A 2022 study found that low carbohydrate intake, improved self-reported symptoms in SLE patients (70). While not specific to SLE, a 2023 case report on a very low calorie ketogenic diet (VLCKD) for rheumatic disorders found: “VLCKD allowed the patient to achieve weight goal, better management of joint pain, headache episodes and normalization of inflammatory indices (71). A review on diet and SLE management stated: “Currently, a diet rich in vitamin- and mineral-rich foods and MUFA/PUFA with moderate energy consumption is recommended to control the inflammatory findings of the disease and the complications and co-morbidities resulting from SLE therapy” (1).
- Nutritional supplements: Supplementation of vitamins, micronutrients, antioxidants and mitochondrial nutrients, often at high doses, has shown various effectiveness on autoimmune diseases, including SLE.
- High dose vitamin B1 (thiamine): High-dose thiamine has shown benefits for autoimmune diseases like rheumatoid arthritis, lupus, and Hashimoto’s thyroiditis. These findings suggest potential broader applications for autoimmune skin conditions (72-79).
- High dose vitamin B2 (riboflavin): High-dose vitamin B2 (riboflavin) has shown potential benefits in managing autoimmune diseases, primarily due to its role in reducing oxidative stress, supporting mitochondrial function, and modulating immune responses (80-82).
- High dose vitamin B3 (niacin/nicotinamide): Vitamin B3 (niacin/nicotinamide) shows promise in treating various autoimmune and inflammatory conditions. High doses of nicotinamide can reduce regulatory T cells and alter immune tolerance (83). In dermatology, it has been used to treat autoimmune skin diseases in dogs (84) and shows potential for treating acne, rosacea, and photoaging in humans (85,86). Nicotinamide has also been investigated for preventing type 1 diabetes (87) and as a cytoprotectant in immune system disorders (88). Recent studies demonstrate its ability to suppress T cell activation and pro-inflammatory cytokine production in juvenile idiopathic arthritis (89). Additionally, niacin has shown potential in enhancing remyelination in aging central nervous systems by rejuvenating macrophage/microglia function (90). These findings suggest that vitamin B3 may have therapeutic applications across various autoimmune and inflammatory conditions.
- High dose vitamin B5 (pantothenic acid): Recent research suggests a potential role for vitamin B5 and vitamin D in autoimmune diseases, including systemic lupus erythematosus (SLE). Vitamin B5 has been shown to inhibit Th17 cell differentiation and related autoimmune diseases by impeding PKM2 nuclear translocation (91). It may also have paradoxical effects on inflammatory and anti-inflammatory cytokines (29). Vitamin B5 deficiency can have significant health consequences (92).
- High dose vitamin B6 (pyridoxine): Research suggests that vitamin B6 supplementation may have beneficial effects for autoimmune conditions like systemic lupus erythematosus (SLE). Higher intake of vitamin B6 was associated with a reduced risk of active disease in SLE patients (93). High-dose vitamin B6 demonstrated strong anti-inflammatory properties in monocytes by downregulating key inflammatory mediators (94). It also prevented excessive inflammation by reducing sphingosine-1-phosphate accumulation (95). In critically ill patients, vitamin B6 supplementation increased immune responses (96). Vitamin B6 deficiency is associated with inflammation, and supplementation may improve immune function (97). However, very high doses of vitamin B6 can cause peripheral neuropathy, so appropriate dosing is crucial (98).
- High dose vitamin B7 (biotin): Recent research suggests potential benefits of vitamin B7 supplementation for autoimmune disorders. High-dose biotin (vitamin B7) has shown promise in treating progressive multiple sclerosis by promoting remyelination and enhancing energy production (99), although studies of biotin on SLE are limited.
- High dose vitamin C (ascorbic acid): Recent studies suggest that vitamin C supplementation may have beneficial effects in treating autoimmune diseases like Systemic Lupus Erythematosus (SLE) and rheumatoid arthritis by regulating cytokines, modulating immune responses, and reducing oxidative stress (100). High-dose vitamin C treatment has been shown to increase glucocorticoid activity and potentially control autoimmune diseases (101). In SLE patients, combined vitamin C and E supplementation decreased lipid peroxidation but did not affect endothelial function (102). Vitamin C intake was inversely associated with SLE disease activity in a 4-year prospective study (103).
- High dose vitamin D: Recent research suggests a potential role for vitamin D in autoimmune diseases, including systemic lupus erythematosus (SLE). Vitamin D deficiency has been associated with autoimmune disorders, including SLE (104). Up to 69% of SLE patients were found to be vitamin D deficient in one study, compared to only 22% of healthy controls without antinuclear antibodies (ANA) (42). While a randomized trial found no significant effect of high-dose vitamin D on SLE disease activity, it did demonstrate a corticosteroid-sparing effect (105). Some SLE patients develop anti-vitamin D antibodies, which are associated with anti-dsDNA antibodies (106). The concept of acquired vitamin D resistance may explain the need for high-dose vitamin D therapy in autoimmune diseases (107,108). Vitamin D supplementation is increasingly recommended for SLE patients (109).
- The recent trials of CAM treatments for SLE indicate that supplements such as vitamin D, omega 3 fatty acids, N-acetyl cysteine and turmeric show some promise for reducing SLE disease activity (80).
- PBMT (Photobiomodulation therapy): PBMT shows promise in treating autoimmune diseases like multiple sclerosis (MS) and systemic lupus erythematosus (SLE). Studies demonstrate that PBMT, particularly using wavelengths of 670nm and 830nm, can modulate immune responses by increasing anti-inflammatory cytokines like IL-10 and decreasing pro-inflammatory cytokines such as IFN-γ (110,111). PBMT also reduces nitric oxide production, potentially alleviating nitrosative stress in MS patients (111). In experimental autoimmune encephalomyelitis, a mouse model of MS, 670nm light treatment reduced disease severity and modulated cytokine production (112). For SLE, both extracorporeal photochemotherapy and ultraviolet-A1 irradiation therapy have shown clinical improvements (113). Additionally, photodynamic therapy with 5-aminolevulinic acid successfully treated skin ulcers in an SLE patient (114). These findings suggest that various forms of light therapy could be valuable in managing autoimmune diseases.
- Methyelene Blue: Recent research suggests that methylene blue and metabolic modulators may have therapeutic potential for systemic lupus erythematosus (SLE) and other autoimmune diseases. Methylene blue has shown promise in reducing symptoms of experimental autoimmune encephalomyelitis by modulating immune responses and activating the AMPK/SIRT1 pathway (115). Metabolic disturbances, including oxidative stress and altered lipid profiles, have been observed in SLE patients (53). Normalizing T cell metabolism through inhibition of glycolysis and mitochondrial metabolism has demonstrated efficacy in treating lupus in animal models and human cells (116). Other potential therapeutic approaches include methimazole, which prevents experimental SLE in mice (117), and histone deacetylase inhibitors, which may reverse epigenetic dysregulation in SLE (118). DNA methylation patterns have also emerged as important biomarkers and potential therapeutic targets in SLE (119).
- Stem cell therapy for SLE: Stem cell therapy, particularly using mesenchymal stem cells (MSCs), has shown promise in treating systemic lupus erythematosus (SLE) (120), a chronic autoimmune disease affecting multiple organs. MSCs demonstrate immunomodulatory effects, inhibiting inflammatory factors and pathways while promoting regulatory T cells (121-123). Clinical trials have indicated that MSC therapy is generally safe and can improve disease activity, reduce autoantibodies, and ameliorate organ dysfunction in SLE patients (123,124). However, challenges remain, including potential complications and variable efficacy (123,124). Further research is needed to optimize stem cell therapy for SLE, including investigating MSC modification methods to enhance their immunosuppressive effects (121,125).
Summary of Key Benefits:
- Healthy Diets Low in Carbohydrates, Omega-6 PUFAs, Plant-Based Toxins, and Ultra-Processed Foods: A diet focused on low carbohydrates, reduced omega-6 polyunsaturated fatty acids (PUFAs), minimal plant-based toxins (like lectins and oxalates), and limited ultra-processed foods can help lower inflammation, support metabolic health, and improve immune regulation. This dietary approach may alleviate symptoms, reduce flare-ups, and promote overall well-being for individuals with SLE and other autoimmune conditions by addressing key dietary triggers of inflammation and immune dysregulation.
- Vitamin B1: Potential for reducing autoimmune symptoms.
- Vitamin B2: Supports oxidative stress reduction and immune modulation.
- Vitamin B3: Shows promise for treating inflammatory conditions.
- Vitamin B5: May inhibit inflammatory pathways.
- Vitamin B6: Anti-inflammatory effects with improved immune function.
- Vitamin B7: Promotes energy and remyelination in certain cases.
- Vitamin C: Reduces oxidative stress and supports immune modulation.
- Vitamin D: Associated with reduced disease activity and immune regulation benefits.
- PBMT (Photobiomodulation Therapy): Modulates immune response by increasing anti-inflammatory cytokines (like IL-10) and reducing pro-inflammatory cytokines. PBMT also supports cellular energy production and reduces oxidative stress, making it beneficial for managing inflammation and symptoms in SLE and other autoimmune conditions.
- Methylene Blue: Enhances mitochondrial function, reduces oxidative stress, and modulates immune responses. Methylene blue’s impact on the AMPK/SIRT1 pathway may support energy production and reduce inflammation, which could benefit autoimmune diseases, including SLE.
- Hormonal Balance: Hormonal balance helps regulate immune responses, reduces autoimmune disease activity, decreases corticosteroid needs, and improves quality of life, especially in conditions like SLE.
- Detox of Heavy Metals: Reduces the toxic load that may exacerbate autoimmune conditions. By eliminating metals like mercury, cadmium, and lead, patients can improve immune tolerance, decrease chronic inflammation, and support overall immune system health.
Conclusion: Addressing root causes and intermediary mechanisms in SLE through integrative methods offers promise for improved outcomes. By combining nutritional, environmental, and lifestyle modifications with targeted interventions for immune regulation and oxidative stress, SLE patients may experience relief and enhanced quality of life. Integrative orthomolecular medicine presents a holistic, patient-centered approach to nurturing resilience and optimism in the face of chronic autoimmune challenges.
Through this integrative orthomolecular approach, we have observed significant improvements in our patients’ quality of life (126,127). In many cases, these methods have even contributed to reversing symptoms of various autoimmune diseases. This experience reinforces the potential of integrative medicine to provide renewed hope and health to those facing the challenges of autoimmune conditions.
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