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Vitamin D Deficiency and Fatty Liver — A Growing Health Concern with Actionable Solutions
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/10/09/vitamin-d-deficiency-and-fatty-liver.aspx
Analysis by Dr. Joseph Mercola October 09, 2026
Story at-a-glance
- Vitamin D deficiency is strongly linked to fatty liver disease, a growing metabolic disorder that often develops silently until serious damage occurs
- Research in aging mice suggests that vitamin D influences liver fat metabolism at the genetic level, helping restore fat-burning genes while dialing down fat-storage ones. These findings point to a potential role in supporting liver health as you age
- In a study of aged mice, a vitamin D3-enriched diet significantly reduced liver fat accumulation, and in cultured liver cells, vitamin D helped restore normal mitochondrial structure — effects seen only in the older, vitamin D-insufficient animals
- A 2021 research review highlights vitamins E, B12, and folate, which are involved in fat metabolism, antioxidant defense, and inflammatory balance in the liver
- Practical solutions include eliminating vegetable oils, which are high in linoleic acid, strategic sun exposure, testing your vitamin D levels (aiming for 60 to 80 ng/mL) and combining vitamin D3 with magnesium and K2 when supplementing
One of the fastest-rising metabolic disorders today affects your liver, quietly and without warning. Fatty liver disease is becoming increasingly common worldwide, yet most people have no idea their liver is in trouble until serious damage sets in.
This isn’t just a condition that strikes the unhealthy or overweight. A growing body of research is uncovering hidden drivers behind fatty liver, including something that rarely gets enough attention: nutrient depletion. And topping that list is vitamin D.
Vitamin D is often framed as a bone-health vitamin, but that’s just a fraction of the story. Your liver relies on it to manage fat metabolism, regulate inflammation and maintain energy production inside your cells. As your vitamin D levels drop, which happens with age and indoor living, your liver’s ability to function properly may begin to falter.
Additional research shows another layer: In animal and cell studies, vitamin D appears to act on liver metabolism at the genetic level, not just support it. If those findings hold up in people, they could have meaningful implications for how liver health is supported during aging and metabolic stress.
Vitamin D Flips a Key Mitochondrial Switch Linked to Liver Fat in Aging Mice
A 2024 animal and cell study published in Experimental & Molecular Medicine investigated how vitamin D3 supplementation can affect age-related fatty liver disease in mice.1 Researchers focused on the role of a mitochondrial protein called Mic60, which helps keep your liver cells’ energy systems working. The goal was to understand how aging disrupts this process and whether vitamin D could help restore it.
• Older animals with low vitamin D had more fat in the liver — The study looked at 22-month-old mice — elderly by mouse standards — compared with young adult mice. Older mice fed a standard diet had lower vitamin D levels and much higher fat accumulation in their livers, while those fed a vitamin D3-enriched diet (20,000 IU per kilogram of feed, compared with 1,000 IU/kg in the standard diet) for 18 weeks saw marked improvement. In addition, liver fat accumulation and the abnormal increase in liver weight were both significantly reduced.
• Fat-burning genes dropped with age, but vitamin D restored them — In older animals, genes that break down fat, such as PPARα and CPT-1, were significantly suppressed. These are also the same ones your liver uses to burn fat for energy. In the aged mice, vitamin D supplementation reversed this pattern, restoring these genes, and lowering genes that drive fat uptake and storage. This dual action appeared to shift the aged mouse liver away from fat storage and back toward fat-burning.
• Blood fatty acid levels tracked with vitamin D status — Circulating free fatty acid levels were inversely related to vitamin D levels, with lower free fatty acids in the mice that had higher vitamin D, suggesting less incoming fat reaching the liver. This points to a better balance between fat uptake and fat breakdown, a stability that is often disrupted in older adults with metabolic issues.
• Vitamin D helped restore mitochondrial structure — Levels of Mic60, a protein that helps organize the mitochondria’s inner folds (cristae), were reduced in the livers of older mice. When Mic60 is depleted, mitochondria lose their normal structure and liver cells, beginning the fat-accumulation process. Vitamin D restored Mic60 levels in the aged mice, and in cultured liver cells, electron microscope imaging showed vitamin D helped mitochondria recover their normal structure after Mic60 was depleted. The researchers also found that the vitamin D receptor binds directly to the gene that makes Mic60, switching it on.
• Aging cells hoard fat, but vitamin D countered it — To see how cellular aging affects this protein, researchers treated human liver-derived cells (HepG2) with the drug doxorubicin to push them into an aged, senescent state. Mic60 levels dropped, and the cells began storing fat and showing signs of cellular aging. Vitamin D prevented the fat buildup and restored Mic60 levels, although the study did not report that it reversed the markers of cellular aging themselves.*
It’s worth keeping in mind that these findings come from mice and cultured cells. The authors themselves note that further studies are needed to determine whether the loss of Mic60 plays the same role in age-related fatty liver disease in humans.2
*These findings are from laboratory or animal research and may not directly apply to human health.
How Vitamins Interact with Liver Metabolism at a Molecular Level
In a 2021 review article published in Liver Research, scientists summarized research on how key vitamins relate to the progression of fatty liver disease.3 They explored how deficiencies in vitamins D, E, B9 and B12, among others, may disrupt liver metabolism. The authors noted that impaired vitamin metabolism is believed to play a critical role in disease progression, with inadequate levels potentially contributing to a cascade of inflammation, insulin resistance, and oxidative stress.
• Connections exist between vitamin levels and the severity of liver damage — The studies reviewed found that lower blood levels of vitamin D were associated with more severe fat accumulation and inflammatory liver damage, while low vitamin B12 was associated with elevated liver enzymes. However, the authors noted B12’s protective role remains controversial. Insufficient vitamin E intake was linked to a higher grade of fat buildup in the liver.
• Different vitamins impact your liver in very different ways — Vitamin E is described as a powerful antioxidant that may help cool down inflammation, limit fat uptake into liver cells, and protect cells from dying. The authors also caution that high-dose vitamin E has been linked to increased mortality in one study, and that its safety and effectiveness need further evaluation.
Meanwhile, vitamin D is involved in regulating immune responses and insulin sensitivity, while folate supports one-carbon (methylation) metabolism, and B12 acts as a cofactor in mitochondrial fat handling — processes that help your liver metabolize nutrients and fats. The review suggests each of these vitamins may play a distinct role in fatty liver disease, with deficiencies linked to worse outcomes.
• Vitamin D deficiency was linked to insulin resistance and poor liver function — The researchers noted that vitamin D deficiency appears in 55% of people with fatty liver disease, and that low levels of this nutrient may contribute to insulin resistance, one of the main drivers behind fat buildup in your liver.
Experimental models suggest that vitamin D may support how the pancreas secretes insulin and how cells throughout the body respond to it. The authors propose that when vitamin D runs low, insulin resistance may worsen, which in turn favors fat storage in the liver over fat burning.
• Vitamin D also modulated the immune system’s activity in the liver — Your liver is deeply involved in your immune function. The review describes how vitamin D helps regulate immune cells in the liver, especially through a family of toll-like receptors that are often activated by toxins and bacterial fragments in the blood. In animal studies, vitamin D deficiency increased activation of these receptors, which in turn. triggered inflammatory signaling that contributed to fat buildup and inflammation in the liver.
• Vitamin deficiencies may worsen metabolic stress on the liver — Without enough of these nutrients, your liver may struggle to balance fat metabolism, manage oxidative stress, and keep inflammation in check. These disruptions are compounded by modern diets and environmental stressors, which is why a nutrient-dense whole food diet matters for liver health. The authors are clear, however, that vitamin supplementation trials have produced inconsistent results so far, and that more clinical trials are needed to confirm whether these nutrients can change the course of fatty liver disease.
How to Support Your Liver Health and Raise Your Vitamin D Levels
Understanding how vitamin D interacts with your liver at the cellular level gives you a reason to act early and support your liver health before problems progress.
If you’ve been diagnosed with fatty liver disease, or you suspect your liver is under stress from poor metabolic health, work with your health care provider — and know that addressing the underlying drivers, such as inflammation, oxidative stress, and the metabolic imbalances that keep your liver stuck in survival mode, is key.
Most people focus only on reducing fat in their liver, but they overlook a factor research increasingly links to fatty liver disease: vitamin depletion. Because your liver stores and regulates key vitamins, deficiencies can make it harder for your liver to recover. Emerging research, much of it in animal and cell models, suggests vitamin D may play a role in calming inflammation, supporting insulin sensitivity and limiting fat buildup in liver cells. To give your liver the support it needs, here’s where to start:
1. Start by fixing the root: Cut out vegetable oils — If you’re still using canola, soybean, sunflower or generic “vegetable oil,” you’re flooding your cells with linoleic acid (LA), a polyunsaturated fat that oxidizes easily, builds up in your skin and increases your risk of skin damage if you get sun exposure during peak hours (10 a.m. to 4 p.m.).
Cut these oils from your diet for four to six months before getting high-intensity midday sun exposure. Replace them with healthier fats like tallow, grass fed butter, and ghee. As LA levels in your tissues gradually drop, your skin becomes less prone to sunburn, and your liver has one less metabolic stressor to contend with.
2. Use sunlight strategically to rebuild your vitamin D stores — Your skin was designed to make vitamin D from the sun. To raise your vitamin D levels naturally, spend time in direct sunlight with bare skin exposed daily, ideally outside peak hours if you’re still transitioning off vegetable oils. Again, once you’ve been off them for four to six months, solar noon becomes the optimal time. Use the “sunburn test” — cover up just before your skin starts to turn pink.
This lets you harness the sun’s benefits without burning, while supporting the healthy vitamin D levels your liver and immune system rely on.
3. Test your vitamin D levels and personalize your approach — Get your vitamin D levels tested at least twice a year and aim for a level between 60 and 80 ng/mL (150 to 200 nmol/L). This isn’t just about bone health — it’s about supporting healthy insulin sensitivity, inflammatory balance, and immune function. Testing gives you a starting point and helps you track real progress. That said, talk to your health care provider about whether this testing is appropriate for you.
4. Supplement smart: If you supplement, pair vitamin D3 with magnesium and K2 — If you’re indoors often or live far from the equator, supplementation is often needed to maintain healthy levels, and vitamin D3 appears to work best when combined with magnesium and vitamin K2.
In fact, an analysis of GrassrootsHealth participant data found that people taking neither magnesium nor vitamin K2 needed 244% more supplemental vitamin D for half of them to reach 40 ng/mL, compared with those taking both.4 These nutrients appear to work as a team, with vitamin K2 helping direct calcium to your bones and away from your arteries.
5. Use food to replenish liver-supportive vitamins — Real nourishment starts with real food. Eat liver-supportive nutrients daily, like pasture-raised eggs and grass fed beef liver. Think of your meals as nutrient delivery systems, not just fuel, but repair tools your liver depends on. Everyday food choices are one of the most powerful tools you have to support your liver: give it what it’s missing, and remove what’s hurting it.
FAQs About Vitamin D and Fatty Liver Disease
Q: What’s the real connection between vitamin D and fatty liver disease?
A: Vitamin D appears to play a key role in keeping your liver metabolically active. Research in mice and liver cells found that the vitamin D receptor directly switches on the gene for Mic60, a protein that helps your mitochondria keep their structure and burn fat. In that research, low vitamin D in aged mice went hand in hand with a shift toward fat storage — a silent shift that may contribute to the development of fatty liver disease, even in people who eat reasonably well or don’t drink alcohol.
Q: What does the research show about vitamin D supplementation and liver fat?
A: The evidence comes mainly from animal and cell research. In a study of aged mice, a vitamin D3-enriched diet significantly reduced liver fat accumulation and restored levels of Mic60, and in cultured liver cells vitamin D prevented the fat buildup triggered by cellular aging. The effects were seen only in the older animals, which had insufficient vitamin D levels to begin with — young mice showed no such benefit. Whether the same holds true in people, particularly older adults who don’t get enough sun or have low vitamin D levels, still needs to be confirmed in human studies.
Q: What other vitamins are important for liver health?
A: In addition to vitamin D, a review from Liver Research highlights vitamins E, B12, folate (B9), C, and A as potential contributors to liver health.5 Vitamin E may help calm inflammation. B12 and folate are involved in fat metabolism and gene expression. Vitamin C supports antioxidant defenses and may help limit oxidative stress in liver cells, though the review notes its link to fatty liver disease remains debated. Each vitamin appears to play a unique role in keeping your liver resilient against metabolic stress.
Q: What does the vitamin D receptor do in the liver?
A: The vitamin D receptor (VDR) is how vitamin D exerts many of its effects. According to the Liver Research review, VDR is found at high levels in the liver’s immune cells and in hepatic stellate cells — the cells mainly responsible for liver scarring — where it has been reported to counter TGF-β signaling, the main pro-scarring pathway in the liver.6 In the Experimental & Molecular Medicine study, silencing VDR in liver cells also lowered levels of the mitochondrial protein Mic60, while vitamin D treatment brought them back up.7 Together, these findings suggest vitamin D may help support healing and immune balance in the liver at the genetic level.
Q: How do I raise my vitamin D levels and support my liver naturally?
A: Start by cutting out vegetable oils like canola, soybean, and sunflower oil. These flood your system with LA, which may add to the metabolic burden on your liver. Spend time in the sun each day, exposing your skin until just before it starts to turn pink (not burn).
Test your vitamin D levels regularly and aim for 60 to 80 ng/mL. If you need to supplement, pair D3 with magnesium and K2. And eat real food rich in liver-supportive nutrients like pastured eggs and whole fruits.
This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.
Could This Overlooked Vitamin Be the Key to Healthier Bones?
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/08/31/vitamin-k-healthier-bones.aspx
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/08/31/vitamin-k-healthier-bones.aspx
Analysis by Dr. Joseph Mercola August 31, 2026
Story at-a-glance
- Vitamin K does far more than support blood clotting; research in mice found it helps regulate the constant cycle of removing old bone and building new bone — a process that influences long-term bone strength
- Researchers identified a vitamin K-dependent protein called GAS6 that acts as a messenger between bone-building cells and bone-removing cells, helping coordinate the remodeling process that keeps your skeleton healthy
- Bone-building cells use vitamin K at remarkably high levels; researchers found that the enzymes responsible for vitamin K activity were 10 to 40 times more abundant in bone-building cells than in bone-removing cells, a sign that bone-building cells are among the body’s heaviest users of vitamin K, on par with the liver
- Foods rich in vitamin K2, including egg yolks, liver, Gouda, Brie, and fermented foods such as natto, help direct calcium into your bones and teeth instead of allowing it to accumulate in soft tissues
- Protecting your bones involves more than getting enough calcium; adequate protein, healthy vitamin D levels, regular weight-bearing exercise, avoiding soft drinks, and reducing seed oils all support the cellular energy and nutrient balance required for healthy bone remodeling
Your skeleton is never finished. Every day it tears down old bone and lays down new bone in its place, a constant remodeling process that quietly determines whether your frame stays strong or slowly weakens with age. When people set out to protect that process, they reach almost reflexively for calcium and vitamin D, and stop there.
Yet, another nutrient has been linked to bone health for decades while rarely earning the same attention: vitamin K, found in leafy green vegetables, egg yolks, certain animal foods, and fermented foods. That oversight matters, because bone loss rarely announces itself.
Osteoporosis, a disease marked by weak, fragile bones that break more easily, often develops silently for years before the first warning signs appear, whether a loss of height, a stooped posture, or a fracture from a minor fall. Left unaddressed, it raises the risk of disability, chronic pain, and lost independence. For years, the link between vitamin K and bone strength was just that, a link researchers could see but not explain.
Recent research has finally moved beyond that association, tracing how this overlooked vitamin reaches into bone tissue and helps regulate the cells that break old bone down, part of the constant renewal that keeps a skeleton sound. What that work uncovered reframes vitamin K as far more than a clotting nutrient — and points to a hidden communication system that may help determine how strong your bones remain over time.
Vitamin K Helps Direct the Cells That Shape Your Skeleton
For a study published in Bone Research, researchers sought to determine exactly how vitamin K influences bone health at the cellular level.1 For years, scientists observed that people with lower vitamin K intake often had lower bone mineral density and higher fracture risk, but the biological explanation remained unclear.
A second clue comes from people with atrial fibrillation. A meta-analysis of observational studies found that those taking warfarin, a drug that blocks vitamin K, had higher rates of hip and spine fractures than those on anticoagulants that leave vitamin K alone. Together these clues made the missing piece clear: No one had shown what vitamin K actually does inside bone.
Instead of looking only at bone density measurements, the researchers examined the communication network between the cells that build bone and the cells that remove old bone. Their goal was to identify the specific vitamin K-dependent proteins involved in this process and determine how they affect skeletal strength.
• Vitamin K plays an active role in bone renewal — By disrupting a vitamin K-dependent pathway in mice, researchers uncovered one of the ways vitamin K helps regulate bone remodeling. The experiment showed that vitamin K influences the activity of osteoclasts, the cells responsible for removing old bone so it can be replaced with new tissue.*
On its own, this finding complicates the simple picture — when researchers shut down this vitamin K pathway in the bone-building cells, the mice ended up with more bone, not less, because they produced fewer bone-removing cells.
• A newly identified protein turned out to be the missing link — One of the study’s most important discoveries was a protein called growth arrest specific 6, or GAS6. Bone-building cells released this vitamin K-dependent protein, which acted like a messenger between the cells that build bone and the cells that break old bone down. When more GAS6 was present, bone-removing cells grew larger and became more active. When GAS6 levels dropped, fewer of these cells developed.
At first glance, a nutrient that ramps up bone removal sounds like bad news for your skeleton. But removal isn’t damage; it’s how bone clears microscopic wear and keeps fresh tissue cycling in. What matters isn’t whether bone is removed, but whether removal stays matched to replacement. This is where vitamin K-dependent signaling appears to earn its keep: helping keep that balance in tune rather than letting either side run unchecked.
• Vitamin K helped bone-removing cells fuse into larger cells — Bone-removing cells don’t start out fully formed. Several smaller immature cells need to combine to create a larger cell capable of breaking down old bone tissue. The researchers found that GAS6 helped drive this joining process. In laboratory experiments, adding GAS6 increased both the number and size of bone-removing cells, while blocking GAS6 reduced their formation.
Notably, GAS6 did this by driving the fusion step specifically — the physical merging of smaller cells — rather than switching on the genes that make a bone-removing cell in the first place. Vitamin K’s influence here is about coordinating how these cells come together, not acting on a single cell in isolation.
• The study also revealed where vitamin K exerts much of its influence inside bone tissue — Researchers found that the enzymes responsible for vitamin K’s activity were expressed at levels roughly 10 to 40 times higher in osteoblasts than in bone-resorbing cells. Their abundance in osteoblasts was comparable to levels found in the liver, where vitamin K plays a central role in activating clotting factors.
This tells you that bone-building cells are major users of vitamin K. Rather than acting as a passive nutrient that simply supports mineralization, vitamin K functions inside highly active cellular pathways that help coordinate skeletal maintenance throughout life.
• Bone remodeling occurs every day, whether you notice it or not — The cells involved constantly remove older bone and replace it with new tissue. According to the researchers, vitamin K-dependent signaling helps regulate this process by controlling the maturation of osteoclasts through GAS6.
When researchers increased this signaling in mice, bone removal rose and density fell; when they blocked it, fewer bone-removing cells formed. The direction of the effect tracks the strength of the signal.
This reinforces the importance of obtaining vitamin K from nutrient-dense foods such as leafy green vegetables for vitamin K1 and certain animal foods and fermented foods for vitamin K2. Strong bones are not built by calcium alone. They depend on an entire communication system inside bone tissue, and this study identified one of the key messengers that keeps that system running efficiently.
Two caveats keep this in perspective. The bone measurements were done in male mice, and human bone cells weren’t tested — so the study maps a mechanism rather than proving an effect in people. And human trials of vitamin K supplements for bone density have produced mixed results, which is part of why pinning down how the vitamin works has mattered so much.
*These findings are from laboratory or animal research and may not directly apply to human health.
Support the Nutrients That Keep Bone Remodeling Balanced
Strong bones depend on much more than calcium. The featured study suggests that vitamin K helps regulate the cellular communication system involved in how much bone gets removed and replaced over time. If you focus only on minerals while ignoring the nutrients that direct bone remodeling, you miss an important part of the equation. Focus first on supplying the raw materials your skeleton uses every day to maintain its strength.
1. Prioritize vitamin K2-rich foods every day — What this study makes clear is how deeply vitamin K is woven into bone biology; these signaling proteins can’t function without it at all. That’s a reason to make sure your diet reliably supplies vitamin K, chiefly K2 from animal and fermented foods, rather than to treat any single pathway as a lever to push harder.
Focus on grass fed and pasture-raised animal foods such as egg yolks, liver, and tallow, along with fermented foods that naturally contain vitamin K2. Unlike vitamin K1, which is abundant in leafy greens, vitamin K2 plays a key role in directing calcium into your bones and teeth instead of allowing it to accumulate in soft tissues.
Certain cheeses are also excellent sources of vitamin K2. Gouda and Brie are among the richest dietary sources, particularly when made with traditional animal rennet. If you already enjoy cheese, choosing these varieties (preferably grass fed) offers a simple way to increase your vitamin K2 intake while supporting bone health. Fermented foods deserve special attention as well.
Natto, a traditional fermented soybean food, contains the highest known concentration of MK-7, a highly bioavailable form of vitamin K2 that remains active in your body longer than many other forms. Even small amounts provide a substantial boost in K2 intake.
Because vitamin K2 is fat-soluble, absorption improves when you consume it with healthy fats such as grass fed butter or ghee. I also recommend viewing vitamin K2 as part of a larger nutrient team that includes vitamin D and magnesium.
These nutrients work together to support proper calcium placement, bone remodeling, and cellular energy production. If your diet consistently falls short of vitamin K2-rich foods, an MK-7 supplement is another option worth discussing with your health care provider.
The exception is if you take a vitamin K antagonist such as warfarin. These drugs work specifically by blocking vitamin K, so adding an MK-7 supplement can interfere with how the medication controls clotting. If you are on one of these drugs, do not add vitamin K2 without talking to the prescriber who manages it.
2. Build your diet around nutrient-dense protein — Bone is not just a mineral structure. A large portion of your skeleton consists of protein. I recommend consuming about 0.6 to 0.8 grams of protein per pound (1.32 to 1.76 grams per kilogram) of your ideal body weight, with one-third coming from collagen-rich sources like slow-cooked meats or bone broth.
If you’re an older adult concerned about age-related bone loss, this step becomes even more important because both muscle and bone depend on adequate protein for maintenance and repair.
3. Support healthy vitamin D levels through sensible sun exposure — Vitamin D remains one of the most important nutrients for skeletal health because it helps regulate calcium metabolism and supports bone remodeling. Regular sunlight exposure also promotes cellular energy production and supports overall metabolic health.
Aim for a vitamin D blood level between 60 and 80 ng/mL (150 to 200 nmol/L). If you consume seed oils and other major sources of linoleic acid (LA), avoid intense midday sun for at least six months, since LA is a polyunsaturated fat that oxidizes easily, builds up in your skin, and increases your risk of skin damage.
Note: Talk to your health care provider about whether this testing is appropriate for you.
4. Remove foods and drinks that work against bone health — Ultraprocessed foods do more than crowd out nutritious foods. Many contain seed oils that are loaded with LA, a polyunsaturated fat that accumulates in your tissues and interferes with mitochondrial function over time. Your mitochondria are the tiny energy-producing structures inside your cells, including the cells responsible for building and maintaining bone.
When mitochondrial energy production declines, bone-forming cells become less efficient, inflammation rises, and the balance between bone formation and bone breakdown shifts in the wrong direction. I recommend eliminating seed oils, packaged snack foods, fried foods, margarine, and other highly processed products that contribute little nutritional value.
Replace them with whole foods such as fruit, root vegetables, pasture-raised animal foods, grass fed butter, ghee, and properly prepared vegetables. Every meal becomes an opportunity to strengthen the nutritional foundation that supports healthy bone remodeling.
One major but often overlooked problem is soft drinks. Many sodas contain phosphoric acid, which disrupts the balance between calcium and phosphorus in your body. When that balance shifts in the wrong direction, your body may draw on its calcium reserves, including those in your bones, to compensate. Over time, this places additional strain on your skeletal reserves. Every soda you skip helps protect the minerals your bones depend on.
Iron balance matters as well. While it is an important mineral, excessive levels contribute to inflammation and may impair the cells responsible for building new bone. If you’re an adult who regularly consumes iron-fortified foods or large amounts of red meat, keeping an eye on your iron status is another important step toward supporting long-term bone strength.
5. Make strength-building movement part of your weekly routine — Bones respond to physical demand. Walking, resistance training, carrying groceries, climbing stairs, and other weight-bearing activities send a signal that stronger bones are required.
If traditional weight training feels intimidating, start with bodyweight exercises and gradually increase the challenge. Blood flow restriction training, also known as BFR or KAATSU training, is another option that stimulates muscle and bone adaptations with lighter loads. Treat it like a long-term challenge. Every workout gives your skeleton another reason to stay strong.
FAQs About Vitamin K for Healthy Bones
Q: What does vitamin K do for my bones?
A: Vitamin K helps regulate the process of bone remodeling, the continuous cycle in which old bone is removed and new bone is built. In the featured Bone Research study, vitamin K-dependent proteins helped coordinate communication between bone-building cells and bone-removing cells — a process researchers believe supports healthy bone structure over time, though this has not yet been confirmed in people.2
Q: Is vitamin K1 the same as vitamin K2?
A: Both forms belong to the vitamin K family, but they’re found in different foods and play somewhat different roles. Vitamin K1 is abundant in leafy green vegetables, while vitamin K2 is found in foods such as egg yolks, liver, certain cheeses, and fermented foods. Vitamin K2 is especially important for directing calcium into your bones and teeth rather than allowing it to accumulate in soft tissues.
Q: What foods contain the most vitamin K2?
A: Some of the richest sources include natto, Gouda cheese, Brie cheese, egg yolks, liver, and other grass fed or pasture-raised animal foods. Natto contains exceptionally high amounts of MK-7, a form of vitamin K2 that remains active in the body for an extended period.
Q: Why are soft drinks and processed foods harmful to bone health?
A: Many soft drinks contain phosphoric acid, which can disrupt the balance between calcium and phosphorus and may increase the amount of calcium drawn from your bones. Ultraprocessed foods often contain seed oils rich in LA, which interferes with mitochondrial energy production. Because bone-building cells require large amounts of energy, impaired mitochondrial function makes it harder for your body to maintain strong bones.
Q: What else supports strong bones besides vitamin K?
A: Bone health depends on multiple factors working together. Adequate protein intake, collagen-rich foods, healthy vitamin D levels, regular weight-bearing exercise, and avoiding seed oils and other ultraprocessed foods all help support the cells responsible for maintaining bone strength. Strong bones result from a coordinated system, not a single nutrient acting alone.
This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.
This Silent Health Crisis Is Now Affecting Nearly 800 Million People
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/08/25/chronic-kidney-disease-worldwide.aspx
Analysis by Dr. Joseph Mercola August 25, 2026
Story at-a-glance
- Chronic kidney disease now affects an estimated 788 million adults worldwide, roughly one in seven adults, making it one of the largest and fastest-growing chronic health challenges on the planet
- Most people with kidney disease are in the early stages and often have no obvious symptoms, allowing damage to progress silently for years before it’s discovered
- Kidney disease extends far beyond the kidneys themselves; impaired kidney function contributes to more than one in 10 cardiovascular deaths worldwide by increasing strain on the heart and blood vessels
- High fasting blood sugar, high blood pressure, and excess body weight were identified as leading contributors to kidney disease-related disability and premature death, highlighting the importance of metabolic health
- Taking action early by improving blood sugar control, supporting healthy blood pressure, eating potassium-rich whole foods, staying physically active, and monitoring kidney function offers the best opportunity to preserve kidney health long term
Chronic kidney disease is a gradual loss of your kidneys’ ability to filter waste, balance fluids, and regulate the minerals your body depends on. What makes it so dangerous is how quietly it begins. Early on, you may notice nothing at all, or you may shrug off vague signs like fatigue, swelling in your legs or feet, or subtle changes in urination. By the time the damage makes itself obvious, much of it has often already been done.
That silence is exactly what makes a recent global analysis so unsettling. Drawing on health data spanning more than three decades and hundreds of countries and territories, researchers set out to measure how far this condition has actually spread, and what they uncovered suggests it has become one of the most widespread chronic threats to human health, with consequences that reach well past the kidneys and into the heart itself.1
The detail that deserves your attention most, though, isn’t the sheer size of the problem. It’s that the majority of people whose kidneys are already in trouble have no idea, because the early stages do their damage without raising an alarm. That gap, between how common this condition has become and how rarely it gets caught in time, is the real story. And it starts with what this landmark analysis revealed about the true scope of the crisis.
Kidney Disease Quietly Became One of the World’s Biggest Health Threats
Published in The Lancet, this global analysis examined chronic kidney disease trends across 204 countries and territories between 1990 and 2023. Researchers drew on published studies, household surveys, treatment registries, and national health records to determine how many adults were affected, how many died from the condition, and which risk factors contributed most heavily to the burden of disease.2
Their findings revealed that chronic kidney disease is no longer a niche medical problem; it’s become one of the largest health challenges facing adults worldwide.
• The number of affected adults more than doubled in three decades — According to the analysis, 788 million adults were living with chronic kidney disease in 2023, compared to 378 million in 1990. Researchers reported that the global prevalence reached 14.2% of adults, meaning roughly one in seven adults now has some level of kidney damage or impaired kidney function.3
For you, that reframes the question — kidney disease is no longer a problem confined to a high-risk few, which means the odds it’s relevant to you personally are higher than you might assume.
• Most people are stuck in the silent stages — The overwhelming majority of cases occurred in stages 1 through 3. These are the earlier phases of kidney disease, when the kidneys still perform much of their job but damage has already begun. Researchers estimated that stage 1 through stage 3 disease accounted for a combined prevalence of 13.9% of adults worldwide.
This matters because early kidney disease rarely causes obvious symptoms. You can feel completely normal while damage progresses in the background. That creates a challenge, but it also creates an opportunity. If you identify the problem early, you have a much larger window to address the factors that drive further decline.
• Kidney disease reaches far beyond the kidneys themselves — The analysis found that chronic kidney disease ranked as the ninth leading cause of death globally in 2023, accounting for approximately 1.48 million deaths. Researchers also calculated that impaired kidney function contributed to 11.5% of cardiovascular deaths worldwide.
Unhealthy kidneys place extra stress on your entire circulatory system. Your kidneys help regulate fluid levels, blood pressure, and numerous chemical signals throughout the body. As kidney function declines, the strain extends to the heart and blood vessels, increasing the likelihood of serious cardiovascular problems.
• Blood sugar emerged as the biggest contributor to kidney-related health loss — When researchers compared risk factors, high fasting blood glucose accounted for the largest share of kidney-related disability-adjusted life years — a measure that combines years lost to illness and to premature death — at 31.9%. High systolic blood pressure (24.5%) and excess body weight (23.5%) followed closely behind, while dietary factors accounted for 17.6%.
Because these figures come from an observational analysis, they show how strongly each factor is associated with kidney-related health loss — not that any one directly causes it. Even so, improving blood sugar control, maintaining healthy blood pressure, and managing excess weight may help address the factors contributing the greatest share of kidney-related health loss worldwide.
• Age dramatically increased the burden, but the trend affected all adults — Researchers observed that both the prevalence and severity of chronic kidney disease rose steadily with age. More advanced stages became increasingly common among older adults, while the contribution of high blood pressure to kidney-related disease burden also increased with advancing age.
Yet the findings were not limited to seniors. The study focused on adults beginning at age 20, highlighting that kidney damage often develops decades before severe symptoms appear. If you think of kidney health as a long-term challenge rather than an old-age problem, you gain a major advantage. Every positive step you take today gives your kidneys a better chance of functioning well years from now.
Support Your Kidney Health and Lower Your Risk
The findings from this global analysis point to a simple reality: Chronic kidney disease rarely begins in the kidneys alone. The biggest contributors were high blood sugar, high blood pressure, and excess body weight. That means the most effective strategy is to address the metabolic and lifestyle factors that place stress on your kidneys year after year.
High blood pressure deserves special attention because it doesn’t just accompany kidney disease — it also contributes to it. Over time, elevated pressure damages the tiny blood vessels inside your kidneys, reducing their ability to filter waste efficiently, while declining kidney function often pushes blood pressure even higher. The earlier you address the factors that strain both your blood vessels and your kidneys, the greater your opportunity to preserve kidney function for decades.
The following strategies are for prevention and early-stage risk reduction; anyone with diagnosed kidney disease should treat potassium, protein, and fluid targets as clinician-directed, because the right numbers flip once function is significantly impaired.
1. Make blood sugar control your first priority — High fasting blood sugar was the largest contributor to kidney disease burden worldwide. When blood sugar remains elevated, excess glucose damages the small blood vessels that allow your kidneys to filter waste effectively. Focus on improving metabolic health with whole foods, adequate protein, and healthy carbohydrates that match your activity level.
For most adults, that means approximately 250 grams of carbohydrates daily, with higher amounts if you’re physically active. Prioritize ripe fruit, root vegetables, and other nutrient-dense carbohydrate sources while eliminating ultraprocessed foods, including seed oils and sugary beverages.
Because protein is essential for maintaining muscle and metabolic health, aim for roughly 0.8 grams of protein per pound (or 1.76 grams per kilogram) of ideal body weight, with approximately one-third coming from collagen-rich sources like slow-cooked meats or bone broth.
2. Improve your blood pressure by improving your metabolism — High blood pressure ranked among the leading contributors to chronic kidney disease worldwide. Yet blood pressure often reflects deeper metabolic problems rather than an isolated condition. Excess weight, poor blood sugar control, chronic stress, and nutrient imbalances all place additional strain on your blood vessels and kidneys.
If you’re carrying excess weight, improving body composition often reduces pressure on both systems simultaneously. Daily movement, strength training, adequate sleep, and stress reduction support healthy blood pressure while helping protect your kidneys from further wear and tear. Even a daily walking routine creates meaningful improvements over time.
3. Restore a healthy sodium-to-potassium balance — Many people focus exclusively on reducing salt, but healthy blood pressure depends heavily on maintaining the proper balance between sodium and potassium. The larger problem is that most dietary sodium comes from ultraprocessed foods that contain very little potassium while delivering excess sugar, phosphate additives, seed oils, and other compounds that increase your kidneys’ workload.
Instead of aggressively restricting salt, focus on removing ultraprocessed foods and replacing them with whole-food potassium sources such as ripe fruit, root vegetables, and well-cooked greens. This strategy supports fluid balance, healthy blood pressure, and kidney function at the same time. It also reduces exposure to additives that place additional stress on kidney tissue.
One important exception: If you already have diagnosed kidney disease, especially stage 3b or beyond, don’t increase dietary potassium without checking with your doctor and knowing your latest labs. Once kidney function is significantly reduced, the kidneys can’t clear potassium efficiently, and too much can become dangerous. The advice to raise potassium applies to prevention and early-stage risk reduction, not to established, more advanced disease.
4. Optimize vitamin D through sensible sun exposure and daily movement — Vitamin D helps regulate the hormonal system that controls blood pressure and fluid balance. When vitamin D levels remain low, that system may become overstimulated, which research has linked to increased tension in your blood vessels and added strain on your kidneys.
Regular sun exposure helps to support vitamin D production, cellular energy generation, and healthy circulation. Aim for a vitamin D level between 60 and 80 ng/mL (150 to 200 nmol/L). If you still consume significant amounts of seed oils and other sources of linoleic acid (LA), avoid intense sun exposure until you have reduced those foods for at least six months.
This is because LA is a polyunsaturated fat that oxidizes easily, builds up in your skin, and increases your risk of skin damage. Pair sunlight with regular movement. An hour of walking, cycling, swimming, or similar activity each day improves circulation, supports healthy blood sugar levels, and reduces pressure on your kidneys’ filtering units. If you’re just getting started, even 10-minute sessions create momentum.
5. Stay hydrated, reduce unnecessary kidney stress, and screen early — For healthy kidneys, hydration helps dilute and remove waste while lowering kidney-stone risk, and thirst is usually a reliable guide. If you’ve been diagnosed with kidney disease, fluid needs can change — sometimes downward — so follow your doctor’s guidance rather than thirst alone.
Pale yellow urine also generally reflects adequate hydration. If you have a history of kidney stones, pay attention to foods high in oxalates, including spinach, sweet potatoes, and figs.
Pairing oxalate-containing foods with calcium-rich foods helps bind oxalates in your digestive tract so fewer reach your kidneys. At the same time, reduce phosphorus from processed foods, colas, and fast-food meats, since excess phosphorus disrupts mineral balance and places additional strain on kidney tissue.
If you have high blood pressure, diabetes, obesity, a family history of kidney disease, or other metabolic risk factors, make kidney screening part of your routine. Ask specifically for two tests: an eGFR (estimated glomerular filtration rate), which estimates how much blood your kidneys filter each minute, and a urine albumin-to-creatinine ratio (uACR), which catches protein leaking through damaged filters — often the earliest warning sign, before eGFR has budged.
Because early-stage kidney disease often produces no symptoms, these simple tests help identify problems long before significant damage occurs.
If you are considering kidney-function or vitamin D testing, talk to your health care provider about whether they’re appropriate for you.
FAQs About Chronic Kidney Disease
Q: What is chronic kidney disease and why is it called a silent health crisis?
A: Chronic kidney disease is a gradual loss of kidney function that often develops without obvious symptoms. Many people remain unaware they have it because early-stage kidney disease rarely causes noticeable problems. By the time symptoms become clear, significant damage has often already occurred.
Q: How common is chronic kidney disease?
A: According to the global analysis published in The Lancet, an estimated 788 million adults were living with chronic kidney disease in 2023. The condition now affects roughly one in seven adults worldwide and has more than doubled in prevalence since 1990.
Q: What are the biggest factors driving chronic kidney disease?
A: The leading contributors identified in the research were high fasting blood sugar, high blood pressure, and excess body weight. These metabolic factors damage the blood vessels that supply the kidneys and increase the strain placed on the kidneys over time.
Q: How does kidney disease affect the rest of the body?
A: Kidney disease affects far more than waste filtration. The kidneys help regulate blood pressure, fluid balance, and numerous chemical signals throughout your body. As kidney function declines, the risk of cardiovascular disease rises substantially. Researchers estimated that impaired kidney function contributes to 11.5% of cardiovascular deaths worldwide.
Q: What are the most important steps to protect kidney health?
A: Focus on addressing the root causes of kidney damage before permanent decline occurs. Maintain healthy blood sugar levels, improve blood pressure through better metabolic health, restore a healthy sodium-to-potassium balance with whole foods, optimize vitamin D through sensible sun exposure and regular movement, stay hydrated, and monitor kidney function early if you have risk factors such as diabetes, obesity, high blood pressure, or a family history of kidney disease.
This article is for informational purposes only and does not constitute medical advice. Consult a qualified health care provider before making changes to your health regimen.
Why Phosphate-Loaded Sodas Hammer Your Metabolism Harder Than Sugar
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/08/24/phosphate-loaded-sodas-metabolism-damage.aspx
Analysis by Dr. Joseph Mercola August 24, 2026
Story at-a-glance
- A single can of cola floods your system with nearly 100% absorbable inorganic phosphate, triggering hormonal shifts that disrupt vitamin D, calcium balance, and kidney function
- Phosphate in soda raises levels of FGF23, a hormone that accelerates vascular calcification, weakens bones, and increases your long-term risk of heart attack or stroke, even if your labs are normal
- Unlike natural sources, phosphate additives in soda are rapidly absorbed and bypass digestive safeguards, placing a silent burden on your kidneys and arteries with every sip
- When combined with high-fructose corn syrup (HFCS), soda creates a metabolic double hit — HFCS promotes liver fat, raises uric acid, and drives insulin resistance, while phosphate sabotages hormonal and mineral balance
- Replacing soda with sparkling citrus water, magnesium glycinate, and vitamin K2 helps support your bones, protect your heart, and reverse the silent damage phosphate leaves behind
A single can of cola delivers more than just refined sugar — it delivers a metabolic ambush that your body absorbs within minutes. While most people know to worry about the high-fructose corn syrup (HFCS) lurking in soft drinks, few realize that the real damage comes from the phosphate hidden in plain sight.
Phosphoric acid is added to cola for flavor and shelf life, but what it delivers is a rapid spike in inorganic phosphate, a form your body absorbs almost entirely. Your bloodstream reacts fast. Within just 30 to 60 minutes, phosphate levels surge — and with them, a hormone called fibroblast growth factor 23 (FGF23). That one surge sets off a hormonal chain reaction that disrupts calcium absorption, suppresses vitamin D, stresses your kidneys, and begins laying the groundwork for hardening of your arteries.
Unlike the sugar in soda, phosphate acts more like a stealth hormone disruptor. It hijacks your endocrine system with every sip. And it doesn’t matter how healthy you think you are. Even young adults with no chronic conditions have shown elevated FGF23 levels within hours of a single phosphate load.
What’s worse, this phosphate exposure is virtually unregulated by your body. While natural food sources contain phosphate bound in protein or phytate, which slows absorption, sodas deliver inorganic phosphates that enter your system quickly. This largely bypasses your digestive safeguards and leaves your organs to clean up the mess.
It’s a burden your kidneys never signed up for and one your arteries pay for over time. That’s why the real danger in soda isn’t just about sugar — it’s about what happens when fructose and phosphate collide in the same can. Let’s take a closer look at the two ingredients side by side.
What’s Really in a Can of Cola?
When you crack open a can of soda, you’re not just sipping something sweet. You’re taking in a concentrated mix of biologically active compounds that hit your metabolism hard. Each 12-ounce serving of cola contains ingredients that work against your health in different ways — and some are far more damaging than they appear.
• High-fructose corn syrup (HFCS-55, ~39 grams of total sugar) — HFCS-55 is made of roughly 55% fructose and 45% glucose. While glucose raises blood sugar and stimulates insulin, it’s the fructose component that does the deeper damage. Your liver takes the hit first.
Fructose gets funneled directly into your liver’s fat-making process, increasing your liver’s fat load and elevating triglycerides. At the same time, it spikes uric acid, which increases oxidative stress, raises blood pressure, and damages mitochondria. Over time, this combination drives insulin resistance — the foundational defect in obesity, diabetes, and cardiovascular disease.
• Phosphoric acid (~50 to 60 milligrams (mg) of elemental phosphorus) — This is where things turn hormonal. Unlike phosphate found in whole foods, the phosphate in cola is inorganic and nearly 100% bioavailable. That means your body absorbs almost all of it, quickly. Within minutes, it forces your kidneys and bones to compensate.
You’ll see a spike in FGF23 — a hormone that lowers vitamin D, impairs calcium metabolism, and forces your kidneys to waste phosphate in an effort to protect your bloodstream. Repeated exposure increases vascular stiffness and elevates cardiovascular risk, even in people without existing kidney problems.
• Caffeine, caramel color, and artificial flavors — Don’t dismiss the trace components. Caffeine itself increases calcium loss in your urine, compounding the calcium-phosphate imbalance created by phosphoric acid.
Caramel color, especially the ammonia-sulfite processed kind, adds another layer of risk by introducing advanced glycation end products (AGEs). These compounds contribute to inflammation, oxidative stress, and tissue aging. Artificial flavors may seem harmless, but their unknown interactions with your gut and liver remain poorly studied.
Each of these ingredients hits a different pathway — metabolic, endocrine, vascular — but the real problem is how they interact. Fructose depletes adenosine triphosphate (ATP) and raises uric acid. Phosphate hijacks your hormone signaling. Add caffeine and AGEs, and you’ve got a cocktail that does far more than add inches to your waistline.
How Inorganic Phosphate Hijacks Your Hormones and Stresses Your Kidneys
When you eat whole foods, like meat, eggs, or legumes, the phosphate they contain is naturally bound to proteins or plant compounds like phytate. Your body takes its time breaking those down, and you only absorb about 40% to 60% of the phosphate in a typical meal. That’s a manageable load.
But the phosphate in soda doesn’t play by those rules. Phosphoric acid is a form of inorganic phosphate that’s not bound to anything. It bypasses digestion and enters your bloodstream at nearly 100% absorption. Within 30 to 60 minutes, your blood phosphate level spikes. And your body scrambles to respond.
• FGF23 is the hormone that flips your metabolism into damage control — This sudden phosphate flood triggers a spike in FGF23.1 This hormone is produced by your bones to get rid of excess phosphate, but FGF23 suppresses the enzyme 1α-hydroxylase, which your kidneys need to convert vitamin D into its active form, calcitriol. Without calcitriol, your body struggles to absorb calcium, shutting down bone turnover and starving your cells of calcium even when your diet is sufficient.
• Your body tries to rebalance, and your skeleton pays the price — As calcium levels drop, your parathyroid glands kick in. They release parathyroid hormone (PTH), which pulls calcium out of your bones to bring blood levels back up. But this leaching process weakens bone structure over time. If you’re regularly drinking cola, your bones are constantly being tapped to fix a problem that started in your soda can.
• A silent source of wear and tear on your kidneys — With every phosphate spike, your kidneys start dumping phosphate into your urine to keep blood levels in check. This ongoing flush seems protective, but it comes at a cost: micro-damage, oxidative stress, and accelerated wear on delicate filtering structures. Over time, even small, repeated injuries add up, especially if you’re already dealing with other metabolic stressors like insulin resistance or high uric acid.
How Phosphate Hardens Your Arteries and Raises Your Risk of a Heart Attack
You don’t need kidney disease for phosphate to wreck your heart. Even if your lab tests look normal, chronically high phosphate levels, like the ones triggered by regular soda consumption, quietly damage your blood vessels and heart over time. The damage starts in your bloodstream, but it doesn’t stay there.
• Your arteries aren’t supposed to turn into bone, but that’s what happens — Under normal conditions, smooth muscle cells in your arterial walls stay flexible and elastic. But when exposed to persistently elevated phosphate, those same cells begin expressing genes typically seen in bone-forming cells. This process turns pliable arteries into rigid, calcium-laced pipes. Once this transformation begins, it’s extremely difficult to reverse.
• Your hormonal defense system collapses — High phosphate doesn’t just activate bone-building pathways in your arteries. It also disrupts the protective feedback loop between FGF23 and a protein called α-Klotho.2
These two normally work together to regulate phosphate and calcium balance. But when phosphate keeps flooding your system, this balance breaks. Klotho levels drop, oxidative stress goes up, and arterial walls stiffen.3 That stiffening drives up blood pressure and reduces blood flow, setting the stage for a heart attack or stroke.
• Phosphate raises your risk of dying from heart disease — A 2024 meta-analysis showed that people in the highest phosphate quartile had a 44% greater risk of cardiovascular death compared to those with lower phosphate levels, even if their kidney function was perfectly normal.4 This isn’t about end-stage disease or rare cases. It’s about everyday exposures, like the phosphate in your soda, quietly eroding your cardiovascular resilience year after year.
The Collateral Damage You Don’t See — Kidney Strain, Bone Loss, and Faster Aging
The impact of high-phosphate sodas goes far beyond your arteries. What starts as a seemingly harmless beverage choice quickly spreads into a web of silent damage that hits multiple systems in your body. If you’re drinking cola regularly, you’re stacking the odds against your kidneys, bones, and even your longevity.
• Phosphate overload speeds up kidney decline, even before symptoms show up — If you already have mild kidney dysfunction, high-phosphate intake pushes that damage into overdrive. Diets rich in inorganic phosphate, like what’s found in sodas and ultraprocessed foods, accelerate the progression of chronic kidney disease.5
Your kidneys are forced to work overtime to dump excess phosphate from your bloodstream, which increases oxidative stress and causes scarring in the nephrons — the tiny filters inside your kidneys that clean your blood. Over time, this leads to progressive loss of kidney function, even in people who aren’t diabetic or hypertensive. And because kidney damage is largely symptomless until advanced stages, you may not even know it’s happening.
• Soda pulls calcium out of your skeleton and leaves it brittle — Women who drink cola four or more times per week have significantly lower BMD in the hip, one of the most fracture-prone areas of the skeleton.6 The combination of high phosphate and low calcium absorption makes bones porous and weak, raising the risk of osteoporosis and fractures.
• Excess phosphate accelerates the biological clock — Phosphate affects you down to the cellular level. High phosphate levels activate mTOR, a key regulator of growth and metabolism.7
While mTOR has beneficial roles in controlled settings, chronic overactivation leads to DNA damage,8 increased cellular replication errors, and premature senescence — a state where cells stop dividing and enter a permanent state of aging. This isn’t just about disease — it’s about quality of life. Phosphate-laden sodas rob you of resilience, making it harder for your body to recover, repair, and maintain the energy you need to thrive.
Fructose in Soda Still Damages Your Metabolism
Fructose in soda isn’t off the hook. You’ll find about 22 grams of it in every can of HFCS-sweetened soda, and that’s more than enough to create metabolic chaos in the wrong context. But unlike phosphate, which hits hard no matter what, you do have some leverage when it comes to fructose’s effects.
• Fructose goes straight to your liver and turns into fat — Unlike glucose, which is used by nearly every cell in your body, fructose has a narrow processing window — it’s metabolized almost entirely in your liver.
When your liver is already loaded with energy (especially in sedentary or overfed states), it begins converting that fructose into fat. This results in fat droplets building up inside your liver cells and elevates triglycerides in your bloodstream. Over time, this fat buildup contributes to insulin resistance, fatty liver disease, and rising cardiovascular risk.
• Fructose metabolism generates uric acid as a byproduct — High uric acid levels drive inflammation. They impair nitric oxide availability in your blood vessels, reducing their ability to relax and regulate pressure. Elevated uric acid also promotes oxidative stress through the generation of reactive oxygen species (ROS), further damaging the endothelium — the delicate lining of your arteries. This sets the stage for high blood pressure, kidney strain, and accelerated aging.
•Fructose feeds the wrong microbes and fuels leaky gut — Too much fructose also disrupts your gut. It feeds opportunistic bacteria in your small intestine, creating dysbiosis — a microbial imbalance that weakens your gut barrier. When that happens, endotoxins seep into your bloodstream. These toxic fragments drive systemic inflammation, contributing to joint pain, brain fog, and autoimmune flare-ups.
• Fructose isn’t harmful in small, buffered doses — The damage from fructose largely depends on how and when you consume it. When eaten with fiber-rich whole foods like fruit, fructose does far less harm. The fiber slows absorption, and the nutrients in whole fruit counterbalance the inflammatory effects. But in soda, you’re drinking a fast-acting dose with zero buffering — just straight metabolic stress.
How to Protect Yourself from the Hidden Damage in Soda
If you’ve been drinking soda regularly, even just a few cans per week, your body is already dealing with the consequences. That phosphate-fructose combo doesn’t just affect your blood sugar or waistline. It hijacks your hormones, leaches calcium from your bones, stiffens your arteries, and stresses your kidneys.
But the good news is, you’re not stuck. You can take control starting today by removing the source and supporting your body’s natural defenses. Whether you’re an athlete using energy drinks, a parent reaching for a cola, or just looking to break a soda habit, these steps will help you protect your metabolism and cellular health.
1. Swap soda for sparkling water with fresh citrus — If you’re drinking cola — even the diet kind — you’re getting a dose of inorganic phosphate that hits your bloodstream fast. Switch to sparkling mineral water and squeeze in some lemon or lime. You’ll get flavor, hydration, and a small amount of citrate, which helps support kidney function without adding phosphate or HFCS.
2. Ditch phosphate-loaded energy drinks and reach for coconut water with sea salt — If you’re an athlete or just someone who relies on energy drinks or sports colas, those are hammering your kidneys and arteries every time you sip. Coconut water mixed with a pinch of sea salt offers natural electrolytes without the phosphate hit, helping your cells rehydrate and recover without metabolic fallout.
3. Use maple-salt rice bars instead of commercial gels — If you’re using sports gels or preworkout drinks with cola flavoring or phosphoric acid, it’s time to upgrade. Cook some white rice, mix in a little maple syrup and sea salt, press it into a pan, and let it chill. You’ll get slow-burning carbs, no added phosphate, and a better energy profile that doesn’t disrupt your insulin response.
4. Shield your system with magnesium glycinate — If you drink soda now and then — maybe socially or during travel — take 200 to 400 mg of magnesium glycinate with it. This helps bind phosphate, restore calcium balance, and reduce the risk of vascular and kidney damage. It’s a simple tool to soften the metabolic blow.
5. Use vitamin K2 (MK-7) daily to guard your arteries — Vitamin K2 activates matrix-Gla protein, which prevents calcium from getting deposited in soft tissues like your arteries. I recommend 100 to 200 micrograms per day. If you’ve ever had a history of soda drinking, this is a long-term investment in your vascular health. If you’ve already been exposed for years, don’t panic. Your body has the capacity to recover, but only if you remove the drivers and give it the nutrients it needs to repair.
FAQs About Phosphate-Loaded Sodas
Q: What makes soda harmful beyond the sugar content?
A: While HFCS in soda is damaging to liver and metabolic health, the phosphate — especially in the form of phosphoric acid — delivers a faster and more disruptive blow. Inorganic phosphate is absorbed almost instantly, spiking the hormone FGF23, which suppresses vitamin D, disrupts calcium metabolism, and stresses your kidneys and arteries.
Q: How does phosphate affect my bones and heart?
A: Inorganic phosphate triggers hormonal shifts that leach calcium from your bones, weaken your skeleton, and harden your arteries. The rise in FGF23 and drop in active vitamin D impair calcium handling, while high phosphate levels drive smooth muscle cells in your arteries to behave like bone cells, increasing cardiovascular risk even in healthy individuals.
Q: What are the long-term risks of drinking cola regularly?
A: Regular soda consumption increases your risk for chronic kidney disease, osteoporosis, vascular calcification, and premature aging. Studies show that even people without kidney disease experience microdamage to their filtering systems and a significant increase in cardiovascular mortality risk when phosphate levels remain elevated.
Q: Is HFCS still a problem in soda?
A: Yes. HFCS in soda drives fat production in your liver, raises uric acid, and fuels gut dysbiosis. However, the effects of fructose are context-dependent — fructose in fruit behaves differently than HFCS in soda due to the presence of fiber and protective nutrients. In soda, fructose is unbuffered, rapidly absorbed, and synergistically harmful alongside phosphate.
Q: What can I do to protect myself if I’ve been drinking soda?
A: Eliminate soda and similar phosphate-loaded drinks. Replace them with sparkling water and natural electrolyte options like coconut water with sea salt. Use magnesium glycinate (200 to 400 mg) to buffer phosphate exposure and consider taking vitamin K2 (100 to 200 mcg daily) to help prevent calcium from depositing in your arteries. These steps support bone, kidney, and cardiovascular recovery.
- 1 Pflugers Arch. 2024 Nov 27;477(3):495-508
- 2 Scientific Reports November 13, 2024
- 3 Nutrients 2024, 16(11), 1599
- 4 Bone 2016 Nov 12;100:87-93
- 5 Clinical Journal of the American Society of Nephrology March 20, 2025
- 6 The American Journal of Clinical Nutrition October 2006, Volume 84, Issue 4, Pages 936-942
- 7 J Am Soc Nephrol. 2016 Feb 12;27(9):2810-2824
- 8 Nutrients 2025, 17(9), 1587
Normal Vitamin B12 Levels May Still Be Too Low for Brain Health
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/07/28/normal-vitamin-b12-levels-brain-health.aspx
Analysis by Dr. Joseph Mercola July 28, 2026
Story at-a-glance
- Research suggests “normal” vitamin B12 levels are insufficient for optimal brain health, especially in older adults, despite being above the standard medical threshold
- Vitamin B12 helps your nerves work well by protecting them with a special coating, allowing brain messages to travel quickly and clearly
- A study of healthy older adults showed that lower B12 levels, even within the “normal” range, were linked to slower thinking and brain signals
- Signs of low B12 include brain fog, memory issues, tingling in hands and feet, and mood swings; these symptoms often develop gradually
- Rich sources of B12 include grass fed meat, eggs, and dairy; supplementation is often necessary for vegans, older adults or those taking certain medications like metformin
You might think that if your doctor says your vitamin B12 levels are “normal,” your brain is safe and sound. But what if even “normal” levels could be hiding sneaky problems with your thinking or memory? This research is shaking things up, showing that what’s “normal” might not be enough.1
Vitamin B12 is a nutrient your body needs to keep your blood pumping and your brain sharp. You get it from foods like grass fed meat, eggs, and dairy, and it’s like a power-up for your nerves and cells. As you age, your brain leans on B12 to stay fast and clear.
However, a 2025 study with healthy older adults found that even if your B12 isn’t super low, it could still affect how well your brain works.2 Let’s dig into what this study uncovered, how B12 keeps your brain buzzing and simple steps to protect your mind as you get older.
Why Vitamin B12 Is Your Brain’s Best Friend
Vitamin B12 is a big deal for your brain health. It’s like a key that unlocks energy in your body. It helps your cells build DNA — think of DNA as your body’s instruction book — and it wraps your nerves in a protective layer, kind of like insulation on electrical wires. This keeps your brain signals moving fast and smooth. But what happens if you don’t have enough B12? It’s like those wires getting frayed — signals slow down, and you might feel it in your hands, legs, or even your memory.
• What does vitamin B12 do for your brain? You need B12 to keep your nerves healthy and your brain sharp. It builds that protective coating, called myelin, around your nerves. This coating makes sure signals zip from one part of your brain to another without a hitch. Without enough B12, that coating wears thin, and your brain doesn’t work as well as it should.
• What happens when your B12 is low? If your B12 dips, your nerves and brain feel the pinch. You might notice tingling in your hands or feet, feel weaker than usual, or struggle to remember things. It’s like a phone with a bad signal — messages don’t get through clearly. Low B12 even messes with your mood, leaving you feeling down or jittery. The tricky part? These changes sneak up on you slowly.
• Is “normal” B12 really enough? Doctors usually say your B12 is “normal” if it’s above 148 pmol/L — a number they measure in your blood. This cutoff is based on what’s average for most people, not necessarily what keeps your brain at its best. It’s like saying your car’s OK as long as it starts — but is it running smoothly? For older adults, this study, published in Annals of Neurology, hints that “normal” doesn’t cut it for top-notch brain health.3
• Should you rethink “normal”? Here’s the big question: What if “normal” B12 levels aren’t enough as you age? Even if your levels aren’t dangerously low, they might not fully shield your brain from slowing down or wearing out. Think of it like having just enough gas to limp to the next station — you’ll get there, but it’s not the smoothest ride.
What Scientists Discovered About B12 and Your Brain
Scientists studied 231 healthy older adults, averaging 71 years old, to see how B12 affects the brain. These weren’t people with obvious B12 troubles — their average level was 414.8 pmol/L, well above the “low” mark. But the researchers used some tricks to peek at their brain health. They tested how fast signals travel from the eyes to the brain, how quick these adults were at thinking tasks and used MRI scans to check inside their heads.
• What did they find? Lower B12 levels — even if still “normal” — were linked to:
◦Slower brain signals, like a lagging internet connection.
◦Slower thinking, especially as you get older.
◦More white spots on brain scans, showing possible damage or aging. Those spots are like scuff marks on your brain’s wiring, showing wear and tear.
• What’s the deal with active vs. inactive B12? B12 has two faces. The “active” form is like a worker fixing your nerves, keeping your brain sharp. The “inactive” form is like that worker taking a nap — it’s there but not helping. The study showed that too much inactive B12 might actually signal trouble, even if your total B12 looks fine.
How to Keep Your Brain Happy with Vitamin B12
So, what does this mean for you? If you’ve had a blood test, you might see a B12 number like 300 or 400 pmol/L. That’s above the “low” line, but this study suggests it’s not enough to keep your brain in peak shape as you age. You might feel a bit foggy, take longer to recall names, or notice your thoughts aren’t as quick. These could be signs your brain needs more B12.
• What signs should you watch for? Your brain might nudge you if your B12’s lagging. Look out for:
◦Feeling foggy or slow, like your thoughts are stuck in mud.
◦Struggling to remember names or little details.
◦Tingling in your hands or feet.
◦Mood swings, like feeling blue or edgy.
These clues are often quiet, so pay attention, as they could mean your brain needs a B12 boost. Not sure where you stand? Talk to your doctor — they can check your levels.
• How do you read your B12 number? Your B12 level shows up as a number like 300 pmol/L on a blood test. Above 148 is “normal,” but this study hints that for brain health, you need more, especially as you age.
How Can You Boost Your B12?
Here are simple tips to optimize your B12:
1. Eat B12-rich foods like grass fed meat, eggs, and dairy.
2. Consider supplements — If you’re vegan or your body doesn’t absorb B12 well, a supplement could be your best bet. Oral or intramuscular vitamin B12 supplements help restore adequate levels, depending on the severity of the deficiency.4
Oral supplementation is generally effective for mild to moderate deficiency, with dosages ranging from 1,000 to 2,000 micrograms daily. Intramuscular injections, typically administered monthly, are more suitable for patients with severe deficiency or those with malabsorption issues.
3. Check your levels — Ask your doctor for a test, especially if you’re over 50 or feel off. Routine blood tests every six to 12 months allow for early intervention to maintain B12 levels.
4. Check your medications — Certain medications, like metformin, are linked to vitamin B12 deficiency. Patients on long-term metformin therapy should discuss supplementation options with their health care providers to determine the best approach based on individual needs and risk factors.
Wrapping It Up
You’ve seen how vitamin B12 is a superstar for your brain. Even “normal” levels aren’t enough to keep your mind sharp as you age. This study of older adults showed that lower B12 — even if it’s not super low — slows your thinking and leaves wear marks on your brain. Plus, too much “inactive” B12 spells trouble.
Your brain deserves better than the bare minimum. By eating B12-rich foods or taking a supplement, you help keep it humming. So, check your B12 — grab some eggs or grass fed meat, think about a supplement if needed, and talk to your doctor if you’re wondering where your levels stand. Your brain’s your control center; give it the boost it craves.
FAQs — Your B12 Questions Answered
Q: What are the best foods for B12?
A: Grass fed meat, eggs, and dairy. If you’re vegan, consider supplementation.
Q: How do I know if my B12 is too low?
A: You might feel tired, foggy, or tingly in your hands or feet. A blood test is the sure way to find out. Pay attention to subtle symptoms, as they can indicate an early stage of deficiency.
Q: Can I get too much B12?
A: It’s usually safe — your body flushes out extra. But super high levels hint at other issues, so ask your doctor.
Q: Should I take a B12 supplement?
A: If you eat B12-rich foods, you might not need one. But if you’re vegan, older, or taking medications like metformin, a supplement helps keep your brain happy. Consult with a health care professional to determine the appropriate dosage and form of B12 supplementation for your individual needs.
Q: How does B12 help my brain?
A: It protects your nerves and speeds up brain signals. Low B12 slows you down and muddles your memory. Optimal B12 levels are important for helping your brain stay sharp.
The Role of Sun Exposure in Optimizing Your Cellular Health
Reproduced from original article:
“https://articles.mercola.com/sites/articles/archive/2026/07/25/sun-exposure-cellular-health.aspx
Analysis by Dr. Joseph Mercola July 25, 2026
Story at-a-glance
- Just like plants, you need sunlight to thrive, as there’s a biological mechanism in your body that transforms sunlight into cellular energy
- When the sun’s rays touch your skin, your body captures the red and near-infrared light and converts them into electrons. Your body then uses these electrons to feed the electron transport chain and create ATP in your mitochondria
- Reductive stress is a biological mechanism that could be hampering your ability to create sufficient cellular energy. If going out in the sun makes you feel worse, you may need to first resolve reductive stress in your body
- Grounding to the earth and using methylene blue can help get rid of the excessive electrons that have accumulated in your mitochondria. However, it is crucial to address the root causes of reductive stress
- Beyond vitamin D production, sunlight exposure helps optimize melatonin production and anchors the circadian rhythm for better sleep, making it a crucial but underrated factor in overall health maintenance
The role of sun exposure for your well-being is a topic that’s close to my heart, and for more than two decades it’s one of the top recommendations that I stand firm on. One of the benefits, of course, is that it allows you to optimize your vitamin D levels — however, the benefits far surpass that, as it actually awakens the essence of your biology.
In this podcast, I go into the details on why getting optimal sun exposure is one of the cornerstones of health, particularly the role it plays in optimizing your cellular energy. I encourage you to listen to it in its entirety as it will help you understand this groundbreaking information that will help you reach optimal health.
Just Like Plants, You Cannot Thrive Without Sunlight
There’s no question that the sun powers every form of life on the planet. Plants, for example, cannot survive without sunlight, as they need it for photosynthesis. When the sun’s rays shine on a plant, the electrons in the chloroplasts, a sac-like organelle that contains chlorophyll molecules, convert the solar energy to structural energy in the form of glucose. This then fuels the biological processes in the plant.
You, on the other hand, mostly rely on the foods you eat as an energy source. Take note that I said “mostly,” because did you know that you also have the capacity to use sunlight to produce cellular energy?
In low light, a plant can survive for a time. However, it will not thrive — its leaves will not become green and lush, it will not produce beautiful flowers, and its growth will be stunted. The same can happen to humans. You cannot reach your full health potential unless you’re getting regular sun exposure.
There is one caveat to this, however. If you’ve been eating a diet high in vegetable oils or seed oils, you need to approach sun exposure with caution, as these oils increase your risk of sunburn. That’s why I recommend avoiding high-intensity sun exposure unless you’ve been off these oils for at least four to six months. I’ll explain why further below.
Sunlight Is the Unrecognized Nutrient You Cannot Live Without
Just like plants, you need sunlight to thrive, as there’s a biological mechanism in your body that transforms sunlight into cellular energy. I’m actually in the process of doing some experiments and have set up a mitochondrial research lab to study this theory more closely.
But basically, here’s how it works — your body, when exposed to the sun, collects electrons from solar energy that are used for mitochondrial energy production. This is why failing to get enough sun exposure can have severe consequences for your health.
Your body primarily gets its energy from the foods you eat. When you digest food in your intestine, it is ultimately metabolized to tiny molecules called acetyl-Coenzyme A.
As acetyl-Coenzyme A enters the mitochondria and goes through the Krebs cycle, it is converted into electrons, which are then carried by NADH and FADH2 into the electron transport chain (ETC). This final stage of cellular respiration is where the electrons are transformed by your body into adenosine triphosphate (ATP) — the fuel on which your body runs. To help you understand, here’s an illustration of how cellular energy is created.
Your Cellular Health Also Relies on Sun Exposure
In the case of sun exposure, when the sun’s rays touch your skin, your body captures the red and near-infrared light and converts them into electrons. Your body then uses these electrons to feed the ETC and create ATP in your mitochondria.
A single electron transport chain can produce 100 ATPs per second. Considering that every single mitochondrion contains 100,000 electron chains, that means you’re producing 10 million ATP molecules per second.
And when you multiply that by 40 quadrillion — that’s the number of mitochondria you have in your body — that means you’re producing 400 million quadrillion ATPs per second.
If you’re optimally healthy, then typically you’re producing enough ATP per day to fuel all the cellular functions of your entire body. But if you’re not creating enough ATPs, then you won’t have enough cellular energy for all processes. The result? Some “nonessential” processes are then downregulated to conserve energy. The available fuel goes to essential life-preserving processes and little else.
Not only will you feel miserable and experience fatigue as a result of this, but it will also put you at high risk of basically every chronic degenerative disease known to man today, including cancer, diabetes, and heart disease. That’s why I call this my unified theory of cellular health.
This is why you need sunlight. Although it follows a different yet equally complex series of steps as when you use energy from food, it ultimately leads to the same result — the transfer of electrons into the ETC of your mitochondria, which boosts your cellular health.
To help you better understand the difference between how your body creates cellular energy from your food versus from the sun and the complex steps involved, I created the 2-D illustration below.
Most People Hide from the Sun
Getting enough sun exposure is one of the most beneficial yet underrated strategies to help achieve optimal health. Apart from exposing you to beneficial red and near-infrared light that contributes to cellular energy production and other health benefits, it also helps optimize your vitamin D levels and melatonin production, which helps anchor your circadian rhythm to help you better sleep at night.
Unfortunately, a significant portion of the population isn’t getting enough sun exposure. According to a survey published in Medium,1 58.8% of Americans say they spend one hour or less outdoors daily, while one-third are only getting 30 minutes of outdoor time, or less. Women and young adults in particular spend more time indoors.
The Keys to Safer Sun Exposure
There’s no doubt that spending time outdoors in bright sunlight is one of the fundamental strategies to regain and maintain your health, so whenever you have an opportunity to go outdoors, do it. It is really important for you to get your one hour of sun exposure around solar noon (12 noon, or 1 p.m. during Daylight Saving Time) to reap the maximum solar benefits.
Wear as little clothing as possible to expose large areas of your skin. Consider doing outdoor activities as well, such as walking or engaging in a regular exercise routine. However, as mentioned earlier, it’s important to avoid high-intensity sun exposure until you’ve been off seed oils for about six months, as these oils significantly raise your risk of sunburn.
These oils are rich in linoleic acid (LA), an omega-6 fat that is highly prone to oxidation when exposed to ultraviolet (UV) radiation. When sunlight interacts with skin containing these oils, it causes the oils to break down, leading to inflammation and DNA damage.
So, while you’re reducing vegetable oils in your diet, temporarily avoid peak sunlight hours, which are typically an hour before and after solar noon. In most of the U.S. during summer, this means staying out of direct sun from 11 a.m. to 3 p.m. during Daylight Saving Time, or 10 a.m. to 2 p.m. in Standard Time.
Over time, as your body detoxes the accumulated seed oils, you can gradually increase your time in the sun. Eventually, you will be able to enjoy an hour or more of peak sunlight hours.
The Importance of Addressing Reductive Stress
I’ve been practicing medicine for four decades now, and back when I still used to see patients, I’ve encountered those who say that when they go out in the sun, they end up feeling worse, as if their body is warning them to stop doing what they’re doing and get out of the sun.
The fact is that your body will never lie to you. If it’s telling you to get out of the sun, then there could be something else you need to pay attention to. So, if you experience this paradox, then it boils down to resolving reductive stress — this biological mechanism could be hampering your ability to create sufficient cellular energy.
Reductive stress, to put it simply, means you have too many electrons backed up in your electron transport chain in your mitochondria. In my interview with molecular biologist Brad Marshall, he explains:
“The calories in food are just electrons between the carbon and the hydrocarbon bonds … Those electrons between the carbon and the hydrogen, that’s where the energy is. And so, we have these systems where the electrons flow through the cell, and we use that electron flow to create ATP, and the ATP moves our body.
The electrons move on electron carriers, which are things like NAD. NAD, when it has electrons, is NADH, and when it loses the electrons, it’s NAD+. You want a balance of NAD+ and NADH. Then the electron flow works.
What happens is, we get too many electrons in the system. We get too many NADH and not enough NAD+. And that can happen because we’re allowing too much fuel into the system. That’s usually why it happens. To use an analogy, cars used to have carburetors. A carburetor takes in fuel and air and mixes the fuel and the air together.”
When there’s a surplus of electrons in your body, it can clog up the series of complexes that are occurring in your electron transport chain. Think of it like pouring a liquid from a big bottle into a small funnel — if there’s too much and you pour too quickly, it will overflow and spill, becoming unusable.
Reductive stress can cause damage, as the surplus of electrons prevent the ETC from transferring them down to Complex IV and they prematurely combine with oxygen to create reactive oxygen species.
Reductive stress also slows down your metabolism and energy production. It’s like your body’s systems are overwhelmed with energy they can’t properly use, which leads to decreased efficiency and damage over time. Molecular biology can be complicated, so I encourage you to watch my interview with Marshall to get a better understanding of this topic.
Grounding Can Help Address Reductive Stress
Addressing reductive stress means getting rid of the excess electrons that have accumulated in your mitochondria as a result of your inability to create sufficient cellular energy. Fortunately, there are two methods you can use that I highly recommend. One is being connected to the earth.
Have you ever tried walking on a carpet in a low-humidity environment, such as during a cold winter morning, then touching a metal doorknob? You’ll get an electric shock. But contrary to common belief, it’s not the electrons coming from the doorknob into your hand; rather, it’s the other way around.
The reductive stress that you built out is grounded to that doorknob because the humidity is low and not acting as an insulation. So, when your finger connects to the metal, you discharge the electrons as a spark. This can be surprising, but it’s a good thing, as you’re releasing your surplus of electrons and not slowing down your mitochondrial energy production.
Another way for you to release your surplus of electrons is by grounding — this is basically being electrically reconnected to the earth’s surface. You can do this by walking barefoot, lying on the ground, or being submerged in water.
However, if you live in North America, as I do, then grounding may not do you much good, as you’re being exposed to “dirty electricity” brought about by distortions of high voltage transients in the electricity supplied to homes and buildings. Modern electronic devices are the main reason why these distortions occur. So, if you do grounding, you may discharge your surplus of electrons but you’re also gaining unhealthy frequencies from the earth.
There are a couple of exceptions, though — if you live in a really remote area and if you ground to the ocean. In mountain areas where there’s no power and the nearest substation is miles away, the ground is most likely healthy and you can connect to the earth there.
As for the ocean, it is such a massive sink that it will accept those electrons. Aside from having salt, which is a good conductor, it gives you a continuous and stable connection to the earth’s natural electrical state, allowing an efficient transfer of surplus electrons in your ETC back to the earth.
Using Methylene Blue
I don’t particularly recommend resorting to drugs, but I believe methylene blue, said to be the oldest drug in existence today, can be a great alternative to grounding in helping you create enough cellular energy. Developed in 1876 by German chemist Heinrich Caro,2 it is the first synthesized drug and has a rich history as both a dye and drug — in the textile industry, it is used as a dye for blue jeans.
When scientists discovered its medical properties, it became the first synthetic compound to be used as a drug, and was used to treat malaria, methemoglobinemia (a condition where hemoglobin cannot release oxygen effectively to body tissues), and as an antidote to cyanide poisoning.
This medicine has powerful metabolic effects, and in reductive stress, it can provide benefits by acting as a powerful electron acceptor that temporarily removes the bottleneck created by faulty metabolism so it can function again and continue producing cellular energy. If there’s a block anywhere in the electron transport chain, methylene blue simply transfers the electrons straight to oxygen, bypassing the obstruction.
The only concern about methylene blue is you need a prescription to purchase it. For human use, the safest option is pharmaceutical grade methylene blue, for which you need a prescription.
Never use industrial grade methylene blue (which is often used for cleaning fish tanks), as it is frequently contaminated with heavy metals. Instead, have your physician write you a prescription to a compounding pharmacy. One of the better ones I have found is Town & Country compounding pharmacy.
These compounded pills can easily be made into 50-milligram capsules, but since you only need 5 mg once a day, one 50 mg pill can be enough for 10 doses. Take a 50-milligram pill (be careful when opening it, as the dye can stain your hands and countertop) and put it into 50 cubic centimeters (cc) of water, or just under 2 ounces.
Measure out 5 cc, which would be about a tablespoon, and then save the rest. If you are using it to optimize the benefits of sun exposure, it is best to take it approximately 30 minutes before going out into the sun.
Get to the Root Cause of Reductive Stress
All of that said, when it comes to optimizing your cellular health, I advise going to the root cause instead of just relying on methylene blue and grounding. Although helpful, you cannot achieve your body’s full potential if you do not address your excessive LA intake, optimize your gut microbiome, lower your estrogen burden, and get rid of EMFs.
These four key culprits wreak havoc on your mitochondrial function, so addressing them is a crucial step to successfully bring back your cellular health. Once you’ve taken control of these four factors, your body will start to recover, repair, and regenerate, and you’ll regain the ability to increase your mitochondrial function and the ability to increase cellular energy.
I urge you to listen to this podcast until the end. You may need to listen to it several times to fully grasp these complex processes, as they can be quite complicated — it took me almost 50 years to fully comprehend these concepts, but I guarantee that once you implement them, you will be far closer to taking control of your health.
The cause of fatigue that most doctors fail to discover
Reproduced from original article:
https://www.naturalhealth365.com/researchers-uncover-a-hidden-vitamin-deficiency-behind-fatigue-that-most-doctors-never-test-for.html
Edit Lang, staff writer June 1, 2026
(NaturalHealth365) Millions of people wake up exhausted every day and hear the same advice: sleep more, reduce stress and exercise more. Now, a new study published in the peer-reviewed journal Nutrients points to something far more specific and overlooked. Researchers in Japan found that shortfalls in two common vitamins quietly drive fatigue and low motivation in otherwise healthy adults.
Moreover, the blood marker that reveals the problem almost never shows up on a standard checkup.
Researchers at Osaka Metropolitan University measured blood levels of homocysteine, folate, and vitamin B12 in roughly 600 healthy Japanese adults. Homocysteine is a compound in the blood that rises when B12 and folate levels drop too low.
Participants then completed validated fatigue and motivation tests. Men with higher homocysteine levels reported significantly more physical fatigue. Women with elevated homocysteine showed reduced motivation. Furthermore, researchers called the connection potentially the first report of this kind in healthy adults.
Why a little-known blood marker may explain the fatigue your doctor keeps dismissing
Homocysteine has long been connected to serious health problems. Higher levels link to heart disease, mental decline, and a greater chance of bone fractures. But until now, no study had formally tied homocysteine to everyday fatigue and motivation in otherwise healthy people.
Consequently, this finding adds a new dimension to a biomarker most people have never heard of and that most doctors rarely check outside of heart risk testing.
Vitamin B12 and folate help the body produce healthy red blood cells, support DNA synthesis, and keep the nervous system functioning properly. When either nutrient falls short, homocysteine builds up in the blood. That build-up drives oxidative stress and disrupts a key cellular process tied to energy production and brain chemical balance.
In other words, fatigue and low motivation are not vague complaints. They are the felt result of cellular systems running short on fuel.
What normal lab results are hiding from millions of exhausted people
Western medicine flags B12 deficiency only at severe levels. A result below 200 pg/mL often prompts no action at all. Yet research consistently shows that a functional shortfall can produce real symptoms long before a formal diagnosis appears.
Cellular processes slow down even when numbers fall technically within the normal range. Similarly, the same gap applies to folate, which doctors check even less often.
Most people who feel chronically tired hear that their labs look fine. What those results typically miss is homocysteine. That single marker reveals whether B12 and folate are actually doing their jobs at the cellular level.
A normal B12 reading alone is not enough to keep homocysteine in check. Therefore, testing homocysteine directly closes a gap that standard panels leave wide open.
Steps that can shift energy and motivation starting now
Request a homocysteine test at your next appointment and treat the number as a direct energy marker. Healthy homocysteine levels are below 7-8 micromoles per liter. Most labs only flag results above 15 as a problem.
However, research suggests that even levels between 9 and 12 raise cardiovascular and brain health risk in meaningful ways. Knowing the number gives a far more useful picture of B12 and folate status than a standard serum B12 test alone.
Choose active forms of B12 and folate rather than the cheapest option on the shelf. Methylcobalamin is the brain-ready form of B12 and absorbs better than cyanocobalamin, the man-made form found in most budget supplements. Methylfolate is the usable form of folate, and people with MTHFR gene variants need methylfolate the most.
Those variants prevent the body from converting folic acid into folate it can use, and a large share of the population carries them without knowing. As a result, choosing active forms skips the conversion step entirely.
Support the full range of nutrients involved in energy production, not B vitamins alone. Iron, magnesium, vitamin D, and CoQ10 all play key roles in cellular energy and often run low alongside B12 and folate. Additionally, a diet built around pasture-raised eggs, wild-caught fish, organic leafy greens, and organ meats naturally supplies B12, folate, and the supporting nutrients that help the body absorb and use them.
Avoiding alcohol, which depletes folate, and acid-blocking drugs, which impair B12 absorption, also helps preserve the gains from food and supplementation.
The energy question Western medicine keeps answering with the wrong test
Fatigue ranks among the most common complaints in primary care and is one of the most brushed aside. Doctors tell patients to manage stress, sleep better, and move more. Meanwhile, homocysteine rarely gets tested.
Functional B12 and folate targets rarely come up in conversation. And almost no one asks whether the body has the raw materials needed to produce energy at the cellular level.
Sources for this article include:
The Ancient Bacterium That Eats Roundup
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Reproduced from original article:
https://sayerji.substack.com/p/how-bacillus-subtilis-is-quietly
A ubiquitous microorganism found in healthy soil and traditional foods the world over may be the missing link in restoring planetary and human health from the ground up.
One ancient and extremely powerful bacterium — in our soil, our fermented foods, and our own gut — is dismantling glyphosate, protecting our cardiovascular system, modulating our immunity, and reminding us that “germs” have always been the medicine
There is a quiet, almost poetic symmetry in the way Nature responds to human folly.
We have saturated our soils with a synthetic molecule designed to dismantle the shikimate pathway — the very pathway that bacteria in our guts depend on to make the amino acids that become our neurotransmitters, our connective tissue, our immune signals. We were told this molecule was safe for us because humans don’t possess the shikimate pathway. What we were not told, for decades, is that we are not only human. The 99% of our holobiont selves that is microbial in origin does possess the shikimate pathway. Glyphosate, by mechanism, is an antibiotic against the very organisms that make us who we are.
And yet, hidden within the same biosphere we have so casually poisoned, there exists a single, humble bacterium that can take this molecule apart — bond by bond — while at the same time producing some of the most therapeutically powerful biomolecules known to medicine. It lives in the soil beneath our feet. It lives in the fermented foods of every traditional cuisine that survived industrialization. It lives in the rhizospheres of our food crops. And — as researchers have come to recognize only in the past two decades — it lives in our own gastrointestinal tracts, where it has been working as a quiet commensal partner for as long as our species has existed.
Its name is Bacillus subtilis.
This is the story of how one ancestral microbe braids together nearly every thread of the microbiome revolution: the extensibility of our biology through microbial partners, the continuity between soil and gut that makes us inseparable from the living Earth, the restorative intelligence of microbial life that can heal damage our own genome cannot even register, and the ancestral dietary inheritance through which our forebears continuously renewed this relationship long before any of us had the language to name it.
Before we go further into the science, a single image to anchor what we mean when we say “we.” Da Vinci’s Vitruvian Man — the Renaissance icon of human perfection as a self-contained, geometrically complete being — has been reimagined in contemporary microbiome science as the Holobiont: a body inseparable from the trillions of microbes, fungi, viruses, and food-derived signaling molecules with which it lives in constant biochemical conversation.
The Damage Glyphosate Does to the Holobiont
To understand why the B. subtilis story matters, we must first sit with the scale of what glyphosate has done.
Glyphosate is the active ingredient in Roundup and is the most widely applied herbicide in agricultural history. It is sprayed onto Roundup-Ready GM crops, used as a pre-harvest desiccant on conventional wheat and oats, and applied to fields, lawns, parks, and roadsides on every inhabited continent. Its industrial defenders have repeated, for nearly half a century, that glyphosate is safe for mammals because mammals do not possess the shikimate pathway — the metabolic route through which plants, fungi, and bacteria synthesize the aromatic amino acids phenylalanine, tyrosine, and tryptophan.
The argument is technically true and biologically dishonest. We do not possess the shikimate pathway. Our microbiome does. The bacteria of our gut — including the Lactobacillus and Bifidobacterium species that ferment our foods, modulate our immunity, produce our B-vitamins, and govern the gut-brain axis — depend on the shikimate pathway.¹ ² So do many fungi in our mycobiome. So do many soil organisms that build the living substrate beneath every meal we have ever eaten.
What the published research has now made unambiguously clear — across in vitro studies, animal models, and metabolomic analyses — is that glyphosate exposure selectively suppresses many of the beneficial members of the gut community while leaving certain pathogens relatively unscathed. Lactobacillus and Bifidobacterium have been shown to be more susceptible to glyphosate than Clostridium perfringens and certain Salmonella strains.³ The shikimate pathway has been documented as transcriptionally active across a meaningful fraction of human gut microbes,⁴ and metabolomic studies in rats have confirmed accumulation of shikimate-pathway intermediates — the biochemical fingerprint of glyphosate inhibition — inside living animals exposed to environmentally relevant doses.⁵ Samsel and Seneff first articulated the broader implications of this mechanism for chronic human disease in their 2013 Entropy review on glyphosate’s suppression of cytochrome P450 enzymes and microbial amino acid biosynthesis.¹
This is the meaning of glyphosate’s harm: it is not a “human toxin” in the narrow toxicological sense. It is a holobiont toxin. It targets the inner ecology that constitutes 99% of our genetic identity. Because the body it was poisoning was never recognized as a body by the regulatory science that approved it, the damage was allowed to accumulate, generation upon generation, until it now shows up in the epidemic curves of celiac disease, IBD, autism, depression, autoimmunity, and the metabolic disorders that increasingly define the modern human condition.
When we ask what glyphosate “does” to a person, the honest answer is: it does not act on the person at all. It acts on the microbial communities through which the person exists.
Bacillus subtilis: The Bacterium We Forgot We Knew
And yet, in the very soil that conventional agriculture has carpet-bombed, an older lineage of bacteria carries on its ancient work. Among them is Bacillus subtilis.
B. subtilis is one of the most studied organisms in all of biology. It is the textbook gram-positive bacterium, the model organism for sporulation, the workhorse of fermentation laboratories around the world. For most of the twentieth century, microbiologists classified it as a soil bacterium — a tidy designation that allowed us to think of it as separate from us, “out there” in the dirt. That classification has been quietly overturned.
In 2009, researchers at Royal Holloway University in London, working with strains isolated directly from ileum biopsies and fecal samples of healthy humans, demonstrated that B. subtilis had adapted to life inside the human gastrointestinal tract.⁶ The bacterium could sporulate anaerobically, secrete antimicrobials against pathogens, and form protective biofilms along the gut wall. Their conclusion was unambiguous: B. subtilis and other spore-formers should be considered “gut commensals rather than solely soil microorganisms.”⁶ Subsequent reviews have confirmed and extended this view, noting that B. subtilis spores survive cooking temperatures, the acidity of the stomach, and the bile of the small intestine — and that they germinate, grow, and contribute metabolically once they reach the gut.⁷
This is itself a small microbiome revolution. B. subtilis is not “out there” — it is, and has always been, part of us. Our ancestors, foraging unwashed roots and tubers, eating naturally fermented foods, drinking unfiltered spring water, breathing air thick with soil dust during planting and harvest, were continuously inoculated with this organism. It travelled with us, in us, alongside us, across continents and millennia. The boundary between the soil’s microbiome and ours, between the field and the gut, was never the hard line modern hygiene imagined it to be. It was, as the herbalist Paul Schulick named it, a life bridge — and B. subtilis is one of the species that walks it.
How Our Ancestors Met This Bacterium Every Day
Long before “probiotic” became a marketing word, B. subtilis was already a daily dietary inheritance for human beings across the planet. It lived in the foods our ancestors knew were sacred — foods so often associated with longevity and vitality that traditional cultures built entire ritual practices around their preparation.
The most celebrated dietary source is natto, the traditional Japanese fermented soybean dish in which Bacillus subtilisvar. natto converts cooked soybeans into one of the most nutrient-dense, bioactive foods in the human dietary record.⁸ Eaten daily for centuries in regions of Japan associated with exceptional cardiovascular health and bone density,⁹ natto is a living culture — every spoonful contains billions of active B. subtilis organisms along with the cascade of bioactive molecules they produce.
But natto is only the most famous example. B. subtilis and its close relatives are involved in fermentation of:
- Kinema, thua nao, and pe-poke — the soybean ferments of Nepal, Thailand, and Myanmar, dietary parallels to natto with their own indigenous Bacillus strains
- Dawadawa, iru, and ogiri — West African condiments fermented from locust bean, soybean, or melon seed, central to the cuisines of Nigeria, Ghana, Senegal, and surrounding regions
- Cheonggukjang — the rapidly-fermented Korean soybean paste, traditionally aged on rice straw rich in wild Bacillus
- Doenjang and chunjang — slower Korean fermented bean pastes carrying Bacillus alongside the more famous Aspergillus and Lactobacillus communities
- Raw, unwashed root vegetables — carrots, beets, parsnips, and tubers pulled from healthy living soil carry B. subtilis spores on their surface, which is one reason traditional cuisines historically did not over-sterilize their produce, and why ‘eating dirt’ (albeit healthy sources in very small quantities) may be an essential part of health.
- Wild and properly-tended honey — honey collected from hives surrounded by biodiverse pasture and forest harbors Bacillus species among its broader microbial signature [learn more about the microbial wonders of raw honey here]
- Aged hay, grass-finished animal products, and raw milk from animals on pasture — B. subtilis was historically named hay bacillus because it was first cultivated from hay; pastured-animal foods naturally carry this organism
What this means, in plain biological terms, is that B. subtilis exposure was continuous for our ancestors. Not a once-a-week event. A daily, almost hourly inoculation through food, water, air, and soil contact. The modern lifestyle — sterile kitchens, washed produce, pasteurized everything, sealed packaged foods, dirt-free hands — has functionally eliminated this exposure for most people living in industrialized societies. We have, in effect, severed one of the oldest continuous microbial relationships in the human evolutionary record.
What This Bacterium Actually Does for Us
The reason B. subtilis mattered so deeply to our ancestors is not romantic. It is biochemical. This single organism is one of the most prolific producers of therapeutically active molecules in the entire microbial world. The peer-reviewed literature on its secondary metabolites now spans thousands of papers. A short list of what B. subtilis makes, while alive in our food or in our gut, includes:
Nattokinase. Produced during the fermentation of soy, nattokinase is a serine protease with potent fibrinolytic activity — it dissolves fibrin, the protein scaffold that holds blood clots together.¹⁰ It is one of the most extensively studied natural cardiovascular compounds in the literature, with documented effects on blood viscosity, atherosclerotic plaque, blood pressure, and circulatory function.¹⁰ ¹¹ Daily natto consumption has been associated, in Japanese population studies, with lower cardiovascular mortality and reduced stroke risk.⁹
Vitamin K2 as menaquinone-7 (MK-7). B. subtilis var. natto is, by a wide margin, the richest known biological source of MK-7 — the long-chain form of vitamin K2 with the longest half-life in human serum.⁸ ¹² MK-7 activates osteocalcin (which directs calcium into bone) and matrix Gla protein (which keeps calcium out of arterial walls). The clinical implications are significant: MK-7 supplementation has been associated with reduced arterial calcification, improved bone density in postmenopausal women, and lower cardiovascular mortality.¹² A 100-gram serving of natto contains roughly 1 milligram of MK-7, an amount essentially impossible to obtain from any other food.¹²
Surfactin. A cyclic lipopeptide and one of the most powerful biosurfactants known. Recent research has documented surfactin’s ability to enhance secretory IgA production, increase intestinal villus height, upregulate tight-junction proteins (claudin-1, occludin, ZO-1) that maintain gut barrier integrity, and reduce intestinal inflammation in models of induced colitis.¹³ Surfactin also has documented antiviral activity, including against enveloped viruses, and has been shown to inhibit the VEGF pathway involved in tumor angiogenesis — making it an emerging candidate in oncology research.¹⁴
Subtilisin and related proteases. Powerful protein-digesting enzymes that contribute to the breakdown of dietary proteins (including the difficult-to-digest gluten proteins of wheat) and to the catabolism of damaged proteins in tissues. B. subtilis proteases are part of the reason traditional fermented soy foods are more digestible than unfermented soy.
Bacteriocins and antimicrobial peptides. A broad arsenal of compounds — subtilin, mycosubtilin, fengycin, iturin, plipastatin — with documented activity against pathogenic bacteria (including methicillin-resistant Staphylococcus aureus), pathogenic fungi (including Candida albicans), and certain viruses.¹⁴ These compounds are part of how B. subtilis in our gut helps maintain the microbial balance that resists opportunistic infections.
Folate, riboflavin, biotin, and other B-vitamins. Like many beneficial gut commensals, B. subtilis contributes directly to the synthesis of essential cofactors our own cells cannot produce.⁷
Immune-modulating spore-coat proteins. Even before germination, B. subtilis spores interact with gut-associated lymphoid tissue (GALT), training the immune system, biasing it toward tolerance rather than reactivity, and contributing to the gut-immune axis that determines so much of our overall health.⁷
This is the supra-human principle in plain biochemistry. We could not, with our human genome alone, make these molecules. We borrow them — daily, ancestrally, through diet and exposure — from a microbial partner whose chemical capabilities vastly exceed our own.
The Clinical Picture: What Happens When We Restore the Relationship
The literature on B. subtilis as a probiotic supplement has matured considerably in recent years, and the clinical signal is consistent. A recent open-label pilot trial conducted by the Center for Applied Health Sciences using Bacillus subtilisAB22™ at 1 billion CFU per day for six weeks documented, in healthy adult volunteers, statistically significant improvements in:¹⁵
- Bloating (baseline scores nearly halving, from 4.0 to 2.0)
- Flatulence (4.3 to 2.6)
- Abdominal discomfort (trending improvement)
- Enthusiasm and well-being (significant increases)
- Fatigue, anxiety, and nervousness (significant decreases)
- TNF-α — a central pro-inflammatory cytokine implicated in systemic inflammation, fatigue, mood disturbance, and chronic disease — showed a statistically significant decrease in serum levels¹⁵
The TNF-α reduction is, biologically, the most important data point. It provides a measurable mechanistic anchor for the mood, energy, and gut comfort improvements: when systemic inflammation decreases, the entire neuroendocrine-immune axis recalibrates. The gut-brain axis is no longer a metaphor; it is a measurable cascade of cytokines, neuroactive metabolites, and vagal signaling that B. subtilis demonstrably modulates.¹³ ¹⁵
This is the AB22™ form of Bacillus subtilis that I selected for CardioNK™, my own cardiovascular-regenerative formulation.¹⁶ CardioNK was built around what I call the Regenerative Natto Complex: a single ancient ferment delivering nattokinase (2 billion colony-forming units (CFU) and 10,800 fibrinolytic units per dose, anchored to the dose range used in the clinical literature), AB22® Bacillus subtilis itself, and MK-7 — all three of which originate from the same organism, working in the same biological synergy our ancestors received every time they ate a bowl of natto. Layered on top are EA-613™ hyper-soluble ellagic acid and pterostilbene for additional polyphenolic vascular and metabolic support.¹⁶ The design philosophy was simple: instead of fragmenting the natto ferment into isolated, decontextualized molecules, deliver them the way Nature delivered them — together, in their evolved synergy, with the parent organism still present.
Bs-15 Discovery: A Microbial Answer to a Synthetic Problem
And now we return to the soil — and to the deepest expression of B. subtilis‘s capacity to heal what industrial chemistry has broken.
In 2015, a research team from the Shandong Institute of Pomology, working with Rutgers University and the Chinese Academy of Agricultural Sciences, published a study in Genetics and Molecular Research with the unassuming title ”Glyphosate biodegradation and potential soil bioremediation by Bacillus subtilis strain Bs-15.”¹⁷
The Bs-15 strain had been isolated from the rhizosphere — the thin, living layer of soil clinging to plant roots — of a pepper plant. Earlier work had shown that this strain promoted plant growth and suppressed disease. What Yu and colleagues set out to test was whether Bs-15 could do something even more remarkable: take a synthetic, organophosphorus molecule that resists chemical, hydrolytic, and photolytic breakdown — and dismantle it.
The results were striking.
Bs-15 not only survived glyphosate exposure; it thrived in it. The bacterium tolerated glyphosate concentrations up to 40,000 mg/L — a concentration vastly higher than anything an ecosystem would ever encounter.¹⁷ It could use glyphosate as both a carbon and a phosphorus source, meaning the molecule that the industry treats as a permanent contaminant was, for Bs-15, a meal. Under optimized conditions, Bs-15 degraded approximately 65% of glyphosate in liquid culture within 60 hours. In non-sterile soil, where Bs-15 worked in concert with the native microbial community, degradation reached 71.57% within four days.¹⁷
Even more telling was what happened to the overall microbial ecosystem when Bs-15 was introduced. Using BIOLOG ECO microplate analysis — a standard ecological method for measuring functional diversity in microbial communities — the researchers found that glyphosate-contaminated soils inoculated with Bs-15 showed significantly greater functional diversity across five separate indices (Shannon, Shannon uniformity, Simpson, McIntosh, and McIntosh uniformity) than uninoculated controls.¹⁷ The bacterium was not only degrading the herbicide; it was restoring the biological complexity the herbicide had collapsed.
In other words: Bs-15 was healing the soil.
Subsequent research has extended this story. Engineered glyphosate oxidase enzymes derived from Bacillus species have demonstrated catalytic efficiency toward glyphosate increased by more than a thousand-fold, with selectivity for glyphosate over related molecules.¹⁸ A 2023 study published in Environmental Microbiology further documented that B. subtilis naturally adapts to glyphosate exposure not primarily through mutation but through reducing uptake of the herbicide — a remarkably elegant survival strategy that preserves the integrity of its own shikimate pathway.¹⁹ The bacterium, in other words, recognizes glyphosate as a threat and protects itself.
The Threads, Braided
This is where the deeper pattern emerges, and where the microbiome lens earns its keep.
First — extensibility. The human genome cannot break down glyphosate. Our liver enzymes do not metabolize it cleanly; what little processing occurs is largely passive, and the bulk of the molecule is excreted in a form structurally similar to what entered. Likewise, our genome cannot produce nattokinase, MK-7, surfactin, or the antimicrobial peptides that protect us from opportunistic pathogens. None of this is part of “our” 1% of the holobiont. Yet B. subtilis — an organism that lives both in soil and in our own intestines, and that we have eaten ancestrally for millennia — can do all of it. This is the supra-human principle in action. We extend our biological capability through our microbial partners. What we cannot metabolize, they metabolize for us. What we cannot synthesize, they synthesize for us. What we cannot defend ourselves against, they defend us against. The holobiont is the unit of physiology — not the human body in isolation.
Second — continuity. The same species that lives in pepper-plant rhizospheres also lives in fermented soybeans, in raw honey, in hay, in pasture-finished dairy, and in the human gut. It travels between soil and body, between field and digestive tract, through every traditional food culture our species ever developed. There is no clean separation. When industrial agriculture poisons the soil microbiome, it is poisoning a continuous biological tissue that includes our own. When we sterilize, pasteurize, and chemically wash our food into lifelessness, we are severing the same continuity. Conversely, when we eat natto, when we honor fermented traditions, when we restore the soil’s microbiome through wild-soil inoculation and regenerative farming — we are restoring an organ of our own extended physiology.
Third — restorative intelligence. The Bs-15 study is not a story of a single bacterium overpowering a single toxin. It is a story of a community coming back to life. The most important finding in the paper is not the degradation percentage — it is the functional diversity indices. Bs-15’s presence allowed dozens of other microbial species, suppressed by glyphosate, to recover. The bacterium acted as a keystone, a starting point from which a whole ecology re-assembled itself. This is the signature of biological intelligence at the ecosystem scale: not the linear “kill the bad thing” logic of biocide chemistry, but the recursive, generative logic of life restoring life through relationship.
Fourth — ancestral inheritance. Every culture that survived industrialization with their cardiovascular, skeletal, and digestive health intact had B. subtilis in their daily food. Not as a supplement. As a tradition. The Japanese have natto. The Koreans have cheonggukjang. The Nepalese have kinema. The West Africans have dawadawa. The Europeans had hay-fermented dairy, traditionally aged cheeses, root cellars where vegetables remained in contact with their soil microbiome. This was not nutritional coincidence. It was, across the entire human species, the dietary expression of a multi-million-year coevolutionary partnership.
What This Means
The implications, set in the context of two decades of microbiome research, are quietly enormous.
It means that the most widely applied herbicide on Earth — a molecule that regulatory science declared “safe” because it didn’t directly poison the eukaryotic human cell — is, by mechanism, an antibiotic against the holobiont. The harm has always been there. We simply lacked the conceptual framework to see it.
It means that our gut, our soil, and our food are not separate domains but continuous biological tissue, and that what we do to one of them we do to all of them. The “life bridge” between the inside and outside of the body has never been metaphor. It is a measurable, molecularly mediated continuity carried by organisms like B. subtilis.
It means that the cardiovascular, immune, mood, and gut benefits documented in the clinical literature on natto, nattokinase, and MK-7 are not isolated nutraceutical effects. They are the recovery of a relationship — the restoration of biological information our ancestors received every day, and that most modern humans have lost.
And it means — perhaps most importantly — that Nature has not abandoned us. Even after decades of poisoning, the bacteria that can heal the damage are still there. Still in the soil. Still in the rhizospheres of plants. Still in the fermented foods of every traditional cuisine that has survived. Still in our own guts, waiting for us to stop eradicating them. They are waiting. They are willing. They are, by their very metabolism, for life.
The work of restoration, then, is not heroic and it is not technological. It is humble and ecological. Stop the spraying. Restore the soil. Eat the ferments — natto, dawadawa, kinema, real raw honey, real raw foods from real living soil. Take the spore-form probiotics, particularly clinically validated strains like AB22™, when ferment access is limited. Honor the diversity. Recognize, finally, that the body we are trying to heal does not end at our skin and that the medicine has always been in relationship — with the microbes, with the soil, with each other, and with the living Earth from which we have never truly been separate.
Bacillus subtilis knew this all along.
It was waiting for us to catch up.
References
- Samsel, A., & Seneff, S. (2013). Glyphosate’s suppression of cytochrome P450 enzymes and amino acid biosynthesis by the gut microbiome: Pathways to modern diseases. Entropy, 15(4), 1416–1463.
- Mesnage, R., & Antoniou, M. N. (2020). Computational modelling shows that indigenous gut microorganisms metabolise the herbicide glyphosate. bioRxiv. https://doi.org/10.1101/870105
- Shehata, A. A., Schrödl, W., Aldin, A. A., Hafez, H. M., & Krüger, M. (2013). The effect of glyphosate on potential pathogens and beneficial members of poultry microbiota in vitro. Current Microbiology, 66(4), 350–358.
- Puigbò, P., Leino, L. I., Rainio, M. J., Saikkonen, K., Saloniemi, I., & Helander, M. (2022). Does glyphosate affect the human microbiota? Life, 12(5), 707. (Computational analysis of shikimate pathway prevalence in gut microbiome.)
- Mesnage, R., Teixeira, M., Mandrioli, D., Falcioni, L., Ducarmon, Q. R., Zwittink, R. D., Mazzacuva, F., Caldwell, A., Halket, J., Amiel, C., Panoff, J. M., Belpoggi, F., & Antoniou, M. N. (2021). Use of shotgun metagenomics and metabolomics to evaluate the impact of glyphosate or Roundup MON 52276 on the gut microbiota and serum metabolome of Sprague-Dawley rats. Environmental Health Perspectives, 129(1), 017005.
- Hong, H. A., Khaneja, R., Tam, N. M. K., Cazzato, A., Tan, S., Urdaci, M., Brisson, A., Gasbarrini, A., Barnes, I., & Cutting, S. M. (2009). Bacillus subtilis isolated from the human gastrointestinal tract. Research in Microbiology, 160(2), 134–143.
- Lefevre, M., Racedo, S. M., Ripert, G., Housez, B., Cazaubiel, M., Maudet, C., Jüsten, P., Marteau, P., & Urdaci, M. C. (2024). Spore-based probiotic Bacillus subtilis: Current applications in humans and future perspectives. Fermentation, 10(2), 78. https://doi.org/10.3390/fermentation10020078
- Sumi, H., Hamada, H., Tsushima, H., Mihara, H., & Muraki, H. (1987). A novel fibrinolytic enzyme (nattokinase) in the vegetable cheese natto; a typical and popular soybean food in the Japanese diet. Experientia, 43(10), 1110–1111.
- Nagata, C., Wada, K., Tamura, T., Konishi, K., Goto, Y., Koda, S., Kawachi, T., Tsuji, M., & Nakamura, K. (2017). Dietary soy and natto intake and cardiovascular disease mortality in Japanese adults: The Takayama study. American Journal of Clinical Nutrition, 105(2), 426–431.
- Chen, H., McGowan, E. M., Ren, N., Lal, S., Nassif, N., Shad-Kaneez, F., Qu, X., & Lin, Y. (2018). Nattokinase: A promising alternative in prevention and treatment of cardiovascular diseases. Biomarker Insights, 13, 1177271918785130.
- Kurosawa, Y., Nirengi, S., Homma, T., Esaki, K., Ohta, M., Clark, J. F., & Hamaoka, T. (2015). A single-dose of oral nattokinase potentiates thrombolysis and anti-coagulation profiles. Scientific Reports, 5, 11601.
- Sato, T., Inaba, N., & Yamashita, T. (2020). MK-7 and its effects on bone quality and strength. Nutrients, 12(4), 965; and Schurgers, L. J., Teunissen, K. J. F., Hamulyák, K., Knapen, M. H. J., Vik, H., & Vermeer, C. (2007). Vitamin K-containing dietary supplements: Comparison of synthetic vitamin K1 and natto-derived menaquinone-7. Blood, 109(8), 3279–3283.
- Wu, Y., Liu, Y., Zhou, L., Ye, W., Liu, Y., Sun, J., Wang, X., & Wang, W. (2024). Surfactin from Bacillus subtilisenhances immune response and contributes to the maintenance of intestinal microbial homeostasis. Microbiology Spectrum, 12(12), e00918-24.
- Caulier, S., Nannan, C., Gillis, A., Licciardi, F., Bragard, C., & Mahillon, J. (2019). Overview of the antimicrobial compounds produced by members of the Bacillus subtilis group. Frontiers in Microbiology, 10, 302; and Wu, Y. S., Ngai, S. C., Goh, B. H., Chan, K. G., Lee, L. H., & Chuah, L. H. (2017). Anticancer activities of surfactin and potential application of nanotechnology assisted surfactin delivery. Frontiers in Pharmacology, 8, 761.
- Center for Applied Health Sciences (CAHS). (2024). The Efficacy and Tolerability of Bacillus subtilis AB22™: A Pilot Clinical Study on Gut Health, Mood, and Immunomodulation. Open-label proof-of-concept pilot trial, 1×10⁹ CFU daily, 42 days, n=10 healthy adult volunteers. Primary endpoints: adverse events, VAS gastrointestinal/mood/stress measures, serum cytokine panel including TNF-α. Amplified Ingredients, LLC.
- Regenerate Company. CardioNK™ Product Documentation: Regenerative Natto Complex (nattokinase 10,800 FU, AB22® Bacillus subtilis, vitamin K2 MK-7), EA-613™ hyper-soluble ellagic acid, and pterostilbene. https://regeneratecompany.com/products/cardionk
- Yu, X. M., Yu, T., Yin, G. H., Dong, Q. L., An, M., Wang, H. R., & Ai, C. X. (2015). Glyphosate biodegradation and potential soil bioremediation by Bacillus subtilis strain Bs-15. Genetics and Molecular Research, 14(4), 14717–14730. https://doi.org/10.4238/2015.November.18.37
- Qin, Y., Wu, G., Guo, Y., Ke, D., Yin, J., Wang, D., Fan, X., Liu, Z., Ruan, L., & Hu, Y. (2020). Engineered glyphosate oxidase coupled to spore-based chemiluminescence system for glyphosate detection. Analytica Chimica Acta, 1133, 39–47; and Delprat, N., Martins, L. O., Blum, L. J., Aymard, C. M. G., Leca-Bouvier, B., Octobre, G., & Doumèche, B. (2023). User-friendly one-step disposable signal-on bioassay for glyphosate detection in water samples. Biosensors & Bioelectronics, 241, 115689.
- Schwedt, I., Schöne, K., Eckert, M., Pizzinato, M., Winkler, L., Knotkova, B., Richts, B., Hau, J. L., Steuber, J., Mireles, R., Noda-Garcia, L., Fritz, G., Mittelstädt, C., Hertel, R., & Commichau, F. M. (2023). The low mutational flexibility of the EPSP synthase in Bacillus subtilis is due to a higher demand for shikimate pathway intermediates. Environmental Microbiology, 25(12), 3604–3622.
Vitamin A and Thyroid Hormone Are Crucial for Good Eyesight
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/04/22/vitamin-a-thyroid-hormone-good-eyesight.aspx
Analysis by Dr. Joseph Mercola April 22, 2026
Story at-a-glance
- Vitamin A and thyroid hormone work together during eye development to build the tiny region of your retina responsible for your sharpest vision
- The center of your retina contains a dense cluster of specialized cone cells that allow you to read fine print, recognize faces, and see detail clearly, even though this area makes up only a small portion of the eye
- Researchers found that early blue-detecting cone cells transform into red and green cones as the eye develops, a process driven by vitamin A metabolism and thyroid hormone signaling
- Nutrients from your diet — including vitamins A, C, and E along with carotenoids like lutein and zeaxanthin — help protect retinal tissue from oxidative damage that contributes to vision decline
- Supporting eye health through nutrient-dense foods, stable metabolism, regular movement and healthy sleep habits strengthens the biological systems that protect your eyesight as you age
The tiny patch of retina that lets you read these words, recognize a loved one’s face across a room, or thread a needle is smaller than the head of a pin — yet it generates roughly half of everything you see. New research from Johns Hopkins University reveals that vitamin A and thyroid hormone work together to build this remarkable structure.
The study, published in the Proceedings of the National Academy of Sciences, used lab-grown retinal tissue to overturn a long-held assumption about how the eye organizes its light-sensing cells and opens a new path toward understanding why central vision is so vulnerable to disease.1 Separately, eye specialists at Johns Hopkins Medicine emphasize that the nutrients you consume directly shape the long-term health and resilience of your eyes.
Vitamins, carotenoids and protective minerals all defend retinal tissue from the oxidative damage that drives age-related vision loss. Together, these insights reinforce a straightforward idea: your food choices influence not only how well your eyes age but how they were built in the first place.
Scientists Discover How Vitamin A and Thyroid Hormone Help Create Sharp Vision
For the PNAS study, researchers used lab-grown pieces of retinal tissue called organoids to observe how the eye develops over time.2 These tiny lab-grown models let the team observe, in real time, how light-sensing cells sort themselves into position at the center of the retina. Their focus was the foveola — the spot that lets you read fine print, recognize faces, and see detail. Even though this area makes up only about 2% of your retina, it produces about 50% of what you see.
• Sharp vision forms when certain eye cells change into more precise ones — Early in development, the center of the retina contains a mix of cone cells, including some that detect blue light. As the eye matures, that area ends up filled almost entirely with red- and green-detecting cones, which provide the sharpest vision. The researchers discovered that these blue cones don’t move away as scientists once believed.
Instead, many of them gradually change into red and green cones. This overturns an assumption that shaped eye research for nearly three decades — that blue cones physically migrated out of the foveola rather than transforming in place.3 The results show that the retina actively reshapes itself during development to produce clearer vision.
• Vitamin A helps control which types of light-sensing cells form — One important step in this process involves a substance made from vitamin A called retinoic acid. In the developing retina, a special enzyme breaks down retinoic acid in the center of the eye.
Think of it like a sculptor removing material to reveal a shape — the retina clears away retinoic acid in precisely the right spot so that red and green cones, rather than blue ones, fill the center of your vision. This step matters because retinoic acid encourages the formation of blue cones. When the retina reduces this chemical, fewer blue cones appear and more red and green cones develop instead.
The study showed that when researchers increased retinoic acid levels in their lab-grown retinal tissue, blue cones increased while red and green cones decreased. In simple terms, too much of this vitamin A compound pushes the retina toward the wrong cell types for clear central vision.
• Thyroid hormone finishes the job by converting the remaining cells — The second signal in this process involves thyroid hormone activity inside the retina. The scientists identified strong activity of an enzyme that increases thyroid hormone signaling in the center of the eye.
This signal encourages the remaining blue cones to switch into red and green cones. The researchers reported that sustained thyroid hormone activity helped generate the cone cells responsible for high-resolution vision. Thyroid hormone helps turn less useful cone cells into the ones needed for sharp eyesight.
• Your retina behaves like brain tissue — Your retina is actually part of your central nervous system, along with your brain and spinal cord. Tissues in this system require large amounts of cellular energy to function properly.
In fact, the retina is one of the most metabolically active tissues in your body, consuming oxygen at a rate comparable to your brain. Because thyroid hormones regulate metabolism and energy production, strong thyroid function supports the demanding energy needs of retinal cells.
Bioenergetic researcher Georgi Dinkov points out that this classification helps explain why thyroid activity has such a direct influence on vision quality — the retina simply can’t maintain normal function without robust energy production.4 Physiologist Ray Peat similarly recommended vitamin A and thyroid support for people with poor eyesight, especially older adults, because both sustain the metabolic processes that keep retinal cells healthy.
How Vitamin A and Thyroid Hormone Shape the Center of Your Vision
Together, these signals build the part of your eye responsible for clear sight. The developing retina uses a two-step system to shape the foveola. Vitamin A metabolism limits the formation of blue cones in the center of your retina.
Thyroid hormone then converts the remaining cells into red and green cones. The result is a dense cluster of highly specialized photoreceptors that produce extremely sharp vision. Without this coordinated process, the center of the retina would contain the wrong mix of cells and visual clarity would decline.
• This also explains why the center of vision is vulnerable to disease — Researchers emphasize that the foveola is often the first region damaged in macular degeneration. This condition gradually destroys central vision, making it difficult to read, drive, or recognize faces. Because the foveola relies on a very precise arrangement of cone cells, even small disruptions lead to noticeable vision loss. Understanding how these cells form gives scientists new insight into how vision problems develop.
• This discovery could lead to treatments that restore vision — The researchers view this work as an early step toward repairing damaged retinal tissue. Study leader Robert L. Johnston Jr. described the discovery as “a key step toward understanding the inner workings of the center of the retina.”5 By recreating the same biological signals in laboratory models, researchers hope to produce healthy photoreceptor cells that could replace damaged ones.
• The long-term goal is to rebuild the eye’s most important vision cells — Scientists involved in the project envision producing carefully designed populations of photoreceptors that could be transplanted into the eye. These cells would integrate with the existing retina and restore lost visual function.
Although this work is still in early stages, identifying how vitamin A signaling and thyroid hormone shape cone cells gives researchers a blueprint for developing future therapies aimed at restoring eyesight.
Nutrition Supplies the Protective Compounds That Defend Your Eyesight
The same retinal cells that vitamin A and thyroid hormone helped build during development still depend on a steady nutrient supply throughout your life. Once those cells are in place, your daily food choices determine how well they hold up.
Guidance from Johns Hopkins Medicine highlights how daily food choices shape the health of your retina and other delicate eye structures.6 Ophthalmologist Dr. Mona Kaleem, from the Wilmer Eye Institute at Johns Hopkins Medicine, explains that many people focus on diet only for weight control or heart health, yet the same nutrients influence visual performance across your lifespan.
The nutrients required for healthy vision come directly from the foods you eat. Vitamins, carotenoids, flavonoids and minerals all work together to protect eye structures and support visual function. Building meals around nutrient-dense foods increases the supply of these protective compounds.
Certain nutrients help preserve vision quality and defend the eyes from age-related decline. Diet provides compounds that protect eye tissue from damage and deterioration caused by oxidative stress — the gradual cellular wear created by normal metabolism and environmental exposure. These protective compounds help maintain the structures that allow you to read, drive and recognize faces as you age.
• Antioxidants act as a protective shield for the delicate cells inside your eyes — Antioxidants play a major role in protecting the eye from damage caused by unstable molecules called oxidizing agents. These unstable molecules damage cells over time and contribute to aging in many organs, including the eye.
By neutralizing these harmful molecules, antioxidants slow the processes that lead to cellular damage and tissue breakdown. This protective effect supports the health of the retina, lens and other structures required for clear vision. Maintaining a steady supply of antioxidant nutrients through diet therefore supports the long-term durability of your eyesight.
• Several vitamins work together to maintain healthy eye tissue — Three antioxidant vitamins play especially important roles in eye health: vitamins A, C, and E. Each one protects eye structures through different biological actions. Vitamin C accumulates in the aqueous humor — the clear fluid located in front of the eye lens — where it serves as a protective antioxidant and helps prevent age-related cataracts.
Cataracts occur when the normally clear lens of the eye becomes cloudy, leading to blurred vision, glare sensitivity and difficulty seeing at night. By helping neutralize oxidative damage in eye tissues, vitamin C supports the clarity of the structures that focus light.
• Plant pigments help filter damaging light and support retinal health — Another important group of compounds includes carotenoids. These natural pigments give many fruits and vegetables their vibrant colors. Two carotenoids stand out for eye health: lutein and zeaxanthin. These compounds accumulate directly in the light-sensitive tissue at the back of the eye.
Their presence inside retinal tissue supports visual function and protects cells exposed to constant light. Foods such as leafy greens, berries and certain fruits supply these compounds. By regularly eating foods rich in these pigments, you reinforce the protective systems that help your retina handle daily exposure to light and oxidative stress.
• Certain plant compounds strengthen the nerve pathways that carry visual signals — Flavonoids are another group of plant compounds linked to eye health. Flavonoids appear in many foods including berries, citrus fruits, tea, and dark chocolate. These compounds influence the function of retinal ganglion cells — specialized nerve cells that carry visual information from your eye to your brain.
When these cells work efficiently, signals from your retina travel more effectively through the optic nerve and reach your brain’s visual processing centers. This biological connection highlights how plant compounds contribute not only to eye structure but also to the communication pathways required for vision.
• Mineral nutrients also protect your eyes from degenerative diseases — In addition to vitamins and plant compounds, selenium is an important mineral involved in eye protection. Selenium functions as a preventive antioxidant and plays a role in defending the eye against degenerative conditions.
Selenium deficiency has been associated with thyroid eye disease, a condition that affects the tissues around the eyes and can cause swelling, discomfort, and visual disturbances. Adequate selenium intake therefore supports both antioxidant defenses and normal thyroid-related eye function.
How to Support the Nutrients and Signals That Protect Your Eyesight
Your eyesight depends on the health of your retina and the light-sensing cells that allow you to read, recognize faces, and see fine detail. When your retina lacks the nutrients and metabolic signals required for healthy photoreceptors, vision declines over time. Focus first on restoring the biological foundations that support retinal cells — nutrient status, cellular energy production and metabolic health.
When you strengthen those foundations, the structures responsible for sharp vision remain resilient as you age. The following steps address the root causes that influence retinal health and the development of the photoreceptor cells discussed earlier. Adopted consistently, these habits reinforce the same biological systems that built your retina’s sharpest vision cells in the first place.
1. Build your diet around foods that supply vitamin A and retinal nutrients — Vitamin A supports the pigments inside photoreceptor cells that allow your eyes to detect light. Prioritize whole food sources because they provide the nutrient in its natural form alongside supporting compounds. Focus on foods such as pastured egg yolks, grass fed liver, dairy products, and dark leafy greens, along with vegetables like carrots and spinach.
These foods also provide important carotenoids such as lutein and zeaxanthin, which concentrate in the retina and help protect the light-sensitive tissue at the back of your eye. If you already eat these foods regularly, you’re providing your retina with the raw materials needed to support healthy photoreceptors and maintain strong night vision.
2. Eat a variety of colorful plant foods that protect retinal tissue — Antioxidant nutrients defend eye cells from oxidative stress that damages delicate retinal structures over time. Use color as a simple guide — the more variety on your plate, the broader the range of protective compounds reaching your retina.
Aim to include several brightly colored fruits and vegetables each day — berries, citrus and peppers are excellent examples. These foods supply carotenoids, flavonoids and vitamin C that support retinal function and the nerve cells that carry visual signals from your eyes to your brain.
3. Protect mitochondrial energy production in your retinal cells — Your retina demands enormous amounts of cellular energy to convert light into visual signals. Protecting mitochondrial function is key because energy production drives every process inside your photoreceptor cells.
Replace seed oils — including soybean, canola, corn and sunflower — with heat-stable fats like grass fed butter, ghee or tallow. These seed oils are high in linoleic acid (LA), a polyunsaturated fat that, in excess, damages the mitochondria your retinal cells depend on for energy.
4. Protect your eyes and sleep by managing nighttime light exposure Artificial light from phones, computers and indoor lighting exposes your eyes to large amounts of blue wavelengths late at night. This light signals your brain to stay awake and suppresses melatonin production in the brain, which disrupts sleep cycles.
Limit screen exposure in the evening and reduce bright artificial lighting after sunset whenever possible. If you spend long hours on digital devices, blue-blocking glasses in the evening help support healthy circadian rhythms and better sleep, which also supports overall metabolic health.
While limiting artificial blue light at night protects your circadian rhythm, getting natural sunlight exposure during the day is equally important — sunlight stimulates dopamine production in your retina, which helps protect against myopia, and supports healthy vitamin D levels that benefit overall metabolic function.
5. Strengthen blood flow to your retina through regular movement — Your retina depends on a network of extremely small blood vessels that deliver oxygen and nutrients. High blood pressure damages those vessels and restricts circulation to the eye. Daily movement is important because exercise lowers blood pressure and improves circulation. Regular physical activity also helps balance insulin and leptin levels, both of which influence metabolic health and retinal function.
6. Support thyroid function and metabolic balance to protect your retina — Your retina belongs to your central nervous system and requires significant cellular energy. Thyroid hormone regulates the metabolic rate that produces that energy, which explains why thyroid activity influences vision. If thyroid function slows, retinal cells struggle to maintain the energy required for clear sight.
Support thyroid function by maintaining strong metabolic health. This starts with eating adequate carbohydrates and balanced protein so your body produces enough cellular energy. Most adults function best with roughly 250 grams of carbohydrates daily and about 0.8 grams of protein per pound of lean body mass (or about 1.76 grams per kilogram), with about one-third of that protein coming from collagen-rich sources like bone broth.
Selenium also plays a direct role here — as noted earlier, this mineral supports both antioxidant defenses in the eye and healthy thyroid function. Good sources include pasture-raised eggs, grass fed beef, organ meats and wild-caught seafood like sardines. When your metabolism runs efficiently, the retinal cells responsible for sharp vision receive the energy they need to function properly.
Optimizing thyroid health requires a holistic approach that includes dietary adjustments, lifestyle changes and careful consideration before relying on hormone therapies. For a deeper look at how to support your thyroid naturally, see my past interview with Dr. Alan Christianson, a leading expert in thyroid disorders, in “Unraveling the Mysteries of Thyroid Health.”
FAQs About Vitamin A and Thyroid Hormone for Eyesight
Q: Why are vitamin A and thyroid hormone important for eyesight?
A: Vitamin A and thyroid hormone work together to shape the part of your eye responsible for sharp central vision. During development, vitamin A signaling helps control which types of light-sensing cells form in the retina, while thyroid hormone converts remaining cells into the red and green cones that produce the highest visual resolution. This coordinated process builds the foveola — the small region that allows you to read fine print, recognize faces, and see detail clearly.
Q: What’s the foveola and why does it matter for vision?
A: The foveola is a tiny area in the center of your retina that produces the sharpest vision. Even though it makes up only about 2% of the retina, it accounts for roughly half of your visual perception. This region contains a dense cluster of specialized cone cells that detect color and fine detail, making it essential for tasks like reading, driving, and recognizing faces.
Q: How does nutrition influence the long-term health of your eyes?
A: Nutrients from your diet help protect the delicate tissues inside your eyes from damage caused by oxidative stress and aging. Vitamins A, C, and E support different protective systems in the eye, while plant pigments such as lutein and zeaxanthin accumulate in the retina and help shield it from light-related stress. Minerals like selenium also support antioxidant defenses and healthy thyroid-related eye function.
Q: Which foods support healthy retinal cells and vision?
A: Foods rich in vitamin A and protective carotenoids help supply the raw materials needed for healthy photoreceptors. Examples include pastured egg yolks, grass fed liver, dairy products, leafy greens, carrots, and spinach. Colorful fruits and vegetables such as berries, citrus, and peppers provide additional antioxidants and plant compounds that support retinal tissue and the nerve pathways involved in vision.
Q: What lifestyle habits help protect eyesight as you age?
A: Several everyday habits support long-term eye health. Eating nutrient-dense whole foods, avoiding seed oils, maintaining stable blood sugar levels and getting regular physical activity all help protect the retina. Managing nighttime light exposure to support healthy sleep cycles and maintaining strong thyroid and metabolic health also help ensure retinal cells receive the energy and nutrients they need to function properly.
Vitamin E’s Therapeutic Benefits in Bone and Joint Disorders
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/03/05/vitamin-e-bone-joint-health.aspx
Analysis by Dr. Joseph Mercola March 05, 2026
Story at-a-glance
- Vitamin E is gaining attention in orthopedics because it influences inflammation, oxidative stress, and immune signaling, all of which shape how your bones and joints maintain strength over time
- Osteoporosis develops when bone breakdown outpaces rebuilding, and studies show vitamin E helps suppress this activity, reduce inflammatory cytokines, and support antioxidant defenses involved in bone preservation
- Research also links vitamin E to improved outcomes in osteoarthritis, fracture healing, implant longevity, arthrofibrosis, and osteomyelitis, suggesting broader musculoskeletal relevance beyond bone density alone
- Many people fall short on vitamin E because the most common sources come packaged with high linoleic acid, which raises your antioxidant demand beyond what diet alone typically supplies
- Choosing the right vitamin E supplement matters, since natural full-spectrum forms provide greater biological activity than synthetic versions, especially for bone and joint support
Your bones and joints influence how comfortably you move, how well you recover from physical stress, and how resilient your body remains over time. Many orthopedic conditions develop gradually, shaped by more than calcium intake or bone density alone. Inside your tissues, inflammation, oxidative stress, and immune imbalance can slowly disrupt the processes that maintain bone strength and joint integrity.
That is where vitamin E has begun to draw more attention. Best known as an antioxidant, it is now being examined more closely for its role in supporting bone and joint tissue, with researchers exploring how it may help preserve the structural strength your musculoskeletal system relies on across many different stages of life.1
Vitamin E Helps Slow the Bone Breakdown That Drives Osteoporosis
Osteoporosis is the most common orthopedic condition affecting older adults, and it develops when bones gradually lose both mass and internal strength. This decline increases the risk of fragility fractures, especially in the hip, spine, and wrist. Among women over 65, about one in four is affected, and lifetime fracture risk in osteoporosis may reach as high as 40%, making it one of the most widespread and serious age-related skeletal conditions.2
• Your bones are not static structures — They are constantly being renewed through a process called bone remodeling. Old or damaged bones are broken down and replaced with new bone to preserve strength and structure over time.
This cycle depends on two main types of cells: osteoclasts, which remove old bone, and osteoblasts, which build new bone in its place. Osteoporosis develops when the breakdown side of this cycle becomes too active, leaving the bone thinner and more fragile.
• Vitamin E interferes with the molecular “on switch” that drives osteoclast formation — A review published in IntechOpen describes a central molecular signaling system that acts like a biological “on switch” for osteoclast formation. When this signaling becomes overactive, the body produces more osteoclasts, and bone loss accelerates.
Vitamin E has been highlighted as a nutrient that interferes with this process by reducing the signals that drive osteoclast development and increasing natural regulators that help keep bone breakdown in check.
• Inflammation also plays an important role in osteoporosis — Inflammatory cytokines act as chemical messengers that can stimulate osteoclast activity. The IntechOpen review reports that vitamin E inhibits cytokines such as TNF-α, IL-1, IL-6, and IL-27, all of which are linked to bone resorption.
• Oxidative stress accelerates osteoclast activity — Vitamin E decreases malondialdehyde, a marker of lipid damage caused by oxidative stress, while increasing antioxidant enzymes such as superoxide dismutase and glutathione peroxidase. These shifts matter because oxidative stress can promote osteoclast activity, and the antioxidant role of vitamin E is tied directly to suppressing bone-resorbing processes.
• Not all forms of vitamin E appear equally active in bone tissue — Vitamin E exists in different forms, including tocopherols and tocotrienols, and these do not always behave the same way in the body. In laboratory models where bone-building cells and bone-resorbing cells interact, tocotrienols reduced the signals that normally tell the body to form more osteoclasts.
Researchers also found that α-tocotrienols lowered c-Fos, an important molecular switch that helps immature cells develop into fully active osteoclasts, while alpha-tocopherol, the form used in most standard supplements, did not show the same effect.3
• Population data links higher vitamin E intake with lower osteoporosis risk — An analysis of data from the U.S. National Health and Nutrition Examination Survey (NHANES) involving 5,800 U.S. adults aged 50 and older found that higher dietary vitamin E intake was associated with lower osteoporosis risk.
Each additional 1 milligram per day corresponded to a 4% reduction in risk, and those in the highest intake group showed substantially reduced odds compared with the lowest intake group. Vitamin E intake also showed a stronger association with lower osteoporosis risk among participants with a history of hormone use, suggesting that hormonal context may shape skeletal outcomes in older adults.4
The rising risk of osteoporosis highlights the importance of maintaining adequate vitamin E levels as a beneficial strategy to support bone health. Learn more in “Hip Fractures from Osteoporosis Predicted to Double by 2050.”
Vitamin E in Other Orthopedic Conditions
Vitamin E’s relevance in orthopedics extends beyond osteoporosis, because many bone and joint problems involve the same internal stressors that wear down tissue over time. A narrative synthesis published in The Indian Journal of Orthopaedics highlights several orthopedic settings where vitamin E appears to influence tissue stability and healing:5,6
• Osteoarthritis — This involves the gradual degeneration of cartilage, the smooth tissue that cushions your joints. Vitamin E’s antioxidant and anti-inflammatory effects may help mitigate cartilage degeneration triggered by mechanical stress or free radical injury. Low vitamin E levels in blood or synovial fluid have also been correlated with more significant osteoarthritis progression.
One study cited in the review involved patients with late-stage knee osteoarthritis, where 400 IU of alpha-tocopherol daily for two months led to reduced pain, stiffness, and functional limitation. These improvements were accompanied by differences in oxidative stress markers in both blood and synovial fluid (the lubricating fluid inside your joints).
• Fracture healing — Bone healing occurs in stages, including callus formation, where temporary scaffolding stabilizes the fracture while new bone is built. A systematic review of animal studies reported that alpha-tocopherol demonstrated a significant positive influence on bone formation during late callus remodeling.
The review also summarizes findings from an osteoporotic fracture model where alpha-tocopherol improved the stage of fracture healing compared with untreated osteoporotic controls. This improvement was accompanied by significantly higher activity of antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase during the early phase of repair.
• Joint replacement and implant longevity — In joint replacement surgery, implant materials slowly experience wear over time. Tiny debris particles can trigger inflammation and bone erosion around the prosthesis, contributing to loosening.
Meta-analyses cited in the review found that when vitamin E is incorporated into highly crosslinked polyethylene liners, a common implant material, it helps improve resistance to oxidative degradation and reduce wear-related bone loss around the implant.
• Post-surgical scar tissue — After orthopedic surgery, some patients develop excessive scar tissue inside the joint, which can restrict movement. This complication is called arthrofibrosis. Vitamin E’s local antioxidant and anti-inflammatory properties were reported to mitigate arthrofibrosis while improving final range of motion and weight-bearing symmetry.
• Osteomyelitis — Osteomyelitis is a serious bone infection, often caused by Staphylococcus aureus bacteria, that can destroy tissue and impair healing. The review highlights an animal study where titanium implants coated with a vitamin E phosphate layer showed lower bacterial levels, higher bone mineral density, and less bone tissue death, compared with uncoated implants.
• Tendon and ligament injuries — Some research suggests vitamin E may reduce swelling and tissue damage after musculoskeletal injury through its effects on inflammatory cytokines. The review notes preliminary suggestions that vitamin E could support healing after anterior cruciate ligament (ACL) tears or sprains by reducing excess scar buildup and protecting collagen fibers.
Across these orthopedic applications, the review presents vitamin E as a promising adjunct, with its consistent effects on inflammation, oxidative stress, and tissue healing.
The Role of Estrogen and Vitamin E in Postmenopausal Bone Health
Estrogen is often presented as a key protector of bone density, especially for women entering menopause. You’ve likely heard that once estrogen production declines, bone loss speeds up — and that’s true to a degree. After menopause, women typically lose bone mass at a faster rate, and this is commonly attributed to lower circulating estrogen levels.
What’s less widely recognized is how estrogen behaves in tissues compared to the bloodstream, and why vitamin E’s antiestrogenic activity may be especially relevant in this context.7,8,9
• Estrogen is not simply low across the board after menopause — Even when blood levels decline, estrogen can remain elevated in fat and other tissues, creating a hormonal environment that still favors estrogenic activity.
The use of hormone replacement therapy (HRT) intensifies this further by increasing estradiol and estrone concentrations within adipose tissue, while also reducing androgens like testosterone. The result is not a clean reversal of deficiency, but rather an increase in estrogen signaling where it already tends to accumulate.
• This is significant for bone health because estrogen affects more than bone density — In excess, estrogen contributes to higher intracellular calcium levels, increased oxidative stress, and suppressed mitochondrial function, which undermine bone regeneration and cellular energy metabolism.
It also fuels inflammatory processes that, over time, damage tissue and disrupt the balance of bone turnover. In this hormonal terrain, bone loss can continue or worsen despite estrogen being present in high amounts at the tissue level.
• Vitamin E helps rebalance the hormonal environment — It acts as a natural estrogen antagonist, blocking receptor activation, limiting estrogen’s stimulatory effects, and inhibiting aromatase, the enzyme that converts androgens into estrogens. These actions help blunt the excess estrogenic activity that accumulates in tissues, particularly in fat.
By doing so, vitamin E helps restore a more stable foundation for bone remodeling, not by increasing estrogen, but by limiting its dominance where it becomes counterproductive.
This perspective challenges the assumption that more estrogen is always better for bones. It also opens a path for targeted nutrient support that doesn’t carry the risks of pharmacological hormone manipulation. For women navigating midlife bone loss, and for anyone experiencing hormone-related disruptions in skeletal health, restoring hormonal balance through vitamin E may offer a safer and more sustainable foundation for long-term skeletal resilience.
Why Many People Don’t Get Enough Vitamin E from Their Diet Alone
Vitamin E exists in many foods, but that doesn’t mean you’re getting enough of it. One reason is that many common vitamin E sources, such as nuts, seeds, and vegetable oils, also come packaged with high amounts of linoleic acid (LA), an unstable omega-6 fat that increases oxidative stress. Instead of correcting a deficiency, these foods increase your demand for antioxidants like vitamin E, so you end up needing more just to keep up with the damage it generates.
• Some plant-based sources contain trade-offs that affect absorption — Beans and other legumes provide small amounts of vitamin E, but they also contain antinutrients such as lectins. In sensitive individuals, these compounds irritate the gut lining and interfere with nutrient absorption, making dietary vitamin E harder to utilize even when intake looks adequate.
• There are better options that provide vitamin E without the drawbacks — These include fresh fruits and vegetables such as pumpkin, asparagus, red bell peppers, tomatoes, kiwi, and mango. Pasture-raised, grass fed meats like beef and bison also contribute meaningful vitamin E, especially when you’re aiming to keep your LA intake low. These foods deliver vitamin E in a form your body absorbs more efficiently, especially when eaten alongside healthy fats.
• Modern diet is dominated by processed foods and industrial seed oils — For every gram of LA you eat, your vitamin E requirement goes up. This means someone eating 20 to 30 grams of LA per day, which is typical on a Western diet, would need far more vitamin E than what food alone can reasonably supply. This is why supplementing is a practical tool to counteract the effects of LA.
• Vitamin E supplementation becomes less necessary as LA burden declines — If you keep your LA intake below 5 grams per day for about three years, you may no longer need vitamin E supplements regularly, or you may only need them occasionally. If you do have a meal high in LA, taking a vitamin E capsule afterward helps protect your body from the effects of that specific meal.
Once your LA levels are lower, you’ll only need around 2 milligrams (mg) of vitamin E for every gram of LA you consume. With a recommended daily LA intake of 5 grams or less, that works out to about 10 mg of vitamin E per day, which is a relatively small amount. For best absorption, it’s ideal to take vitamin E with a healthy fat source, like coconut oil.
How to Choose the Right Vitamin E Supplement
Not all vitamin E supplements are created equal. Many products on the market use synthetic vitamin E, which is less biologically active than the natural form. Synthetic versions are often listed as alpha-tocopherol acetate, and the “acetate” label is a common sign that the product is not the same form of vitamin E found in food.
• Another issue is that many synthetic supplements are racemic — This means they contain a mix of mirror-image forms called isomers, like left and right hands. Your body strongly prefers one “handed” form of vitamin E. Only the “D” isomer provides health benefits, while the “L” isomer does not. In synthetic products, half of the vitamin E comes from this ineffective form, which significantly reduces the supplement’s overall potency.
• That is why label details matter — A high-quality supplement will list d-alpha-tocopherol, which indicates the natural D form. A label that says dl-alpha-tocopherol signals a synthetic mixture.
• Full-spectrum vitamin E provides broader benefits — For the best results, look for a supplement that provides the full range of vitamin E forms, including tocotrienols such as the beta, gamma, and delta types, in the natural D configuration. These different forms of vitamin E work synergistically to provide a wider range of health benefits.
• Choose a clean, food-based supplement without industrial additives — I recommend looking for a food-based supplement that contains all eight forms of vitamin E and avoids soy, soybean oil, and genetically engineered (GE) ingredients. Many lower-quality supplements use GE derivatives from corn, soy, or cottonseed, so choosing a clean, naturally sourced product helps ensure you are getting the highest-quality form available.
Frequently Asked Questions (FAQs) About Vitamin E and Bone Health
Q: What does vitamin E have to do with bone health?
A: Vitamin E influences the biological systems that control how your bones are maintained over time. Research shows it affects the activity of osteoclasts, the cells responsible for breaking down old bone, and helps regulate inflammatory and oxidative processes that accelerate skeletal weakening as you age.
Q: How might vitamin E help with osteoporosis?
A: Vitamin E has been shown to interfere with signals that drive excessive bone breakdown, including pathways involved in osteoclast formation. It also reduces inflammatory cytokines linked to bone resorption and supports antioxidant defenses that help protect bone tissue from oxidative damage, which plays a major role in osteoporosis progression.
Q: Why don’t I get enough vitamin E from food alone?
A: Many foods rich in vitamin E, such as nuts, seeds, and vegetable oils, are also high in linoleic acid (LA), which increases oxidative stress and raises your body’s demand for vitamin E. On a modern diet dominated by processed foods and seed oils, your requirement often exceeds what food alone can realistically supply.
Q: Are vitamin E supplements good for me?
A: Supplementing with vitamin E can be helpful, especially if you have a high LA burden or are trying to support bone and joint health during aging. Vitamin E is fat-soluble and provides antioxidant protection in tissues where oxidative stress contributes to degeneration, although the benefits depend heavily on using the right form.
Q: What should I look for in a high-quality vitamin E supplement?
A: Look for a natural form labeled d-alpha-tocopherol, not synthetic dl-alpha-tocopherol or acetate-based products. The best supplements include the full spectrum of vitamin E compounds, especially tocotrienols, and avoid soy, seed oils, and genetically engineered additives for cleaner, more effective support.
- 1, 5 JOIO 59, 1364–1380 (2025)
- 2, 3 IntechOpen, November 6, 2023
- 4 Front Endocrinol (Lausanne). 2024 Oct 21:15:1410581
- 6 Indian Journal of Orthopaedics 59(9) June 2025
- 7 J Clin Endocrinol Metab. 2024 Jul 10;110(2):511–522
- 8 Biomedicine & Pharmacotherapy June 2018, Volume 102, Pages 403-411 (Archived)
- 9 To Extract Knowledge from Matter February 9, 2025