Macular degeneration, Cataracts, and vitamin K/K2

Does gut microbiome health effect age related eye conditions?

Yes, probably gut health does affect vision risks, but there isn’t much research or any research specific to treatment with vit K or K2 (natural menaquinone MK7 or synthesized MK4). Low vitamin K1 was noted with cataracts per Grok AI.

Other things that may help:

• Reduce inflammation: anti-inflammatory Nrf2 promoting foods (also are NF-kB inhibiting, my first post written for Substack was about Nrf2 & NF-kB) which promotes glutathione.

• Protein adequacy: Adequate cysteine and glycine might be helpful for glutathione support or simply adequate protein intake helps transport proteins which includes calcium binding proteins too. Red meat for taurine can help with vitamin A metabolism as a transport protein for activated retinoids — excess or lack of vitamin A in the active or inactive forms can cause vision or inflammatory issues.

• Nrf2 promoting and generally anti-inflammatory: Adequate antioxidants, particularly carotenoids like astaxanthin, lutein, zeaxanthin, and blueberries/bilberries, dark green veggies. Iodine and selenium - thyroid hormone health is critical for vitamin A and vitamin D metabolic pathways too.

“Astaxanthin is a red pigment found in marine animals and microorganisms, whereas lutein and zeaxanthin are yellow pigments found in vegetables and fruits. These xanthophyll carotenoids can act as antioxidants by capturing free radicals and oxygen singlets.” (ScienceDirect)

• WATER! Adequate hydration is important for eye health and avoiding too much UV/blue light likely is too.

• Magnesium is critical for fluid balance and stabilizing fluid and preventing calcium entry into the cell.

Healthy Cells have the proper magnesium level needed to keep calcium levels in check (but vitamin K2 may be needed also, for calcium binding proteins within the cell) and Unhealthy cells lack enough magnesium to block calcium channels or TRP channels in the cell membrane from allowing too much calcium into the cell. via (x.com/MetabolicFactor)

• Delphinidin has been found helpful for dry eye conditions. It is a phytonutrient, an anthocyanidin with four atoms of magnesium. See this ‘Sparkle in the eye’ post. My theory is the sparkle in the eye is glints of moisture, a well hydrated fluid base for vibrancy. Yes it is light reflection too, but look around you, some people have more sparkle. What do you think causes the sparkle?

Photo by Gabriel Silvério on Unsplash

Vitamin K2: Adequate vitamin K2 would or might help prevent age related vision changes for a similar reason to it protecting the inner ear and hearing, or hair health, by protecting against excess intracellular calcium which can cause cell death from over-activation or loss of mitochondria. The inner ear Hair Cells and hair follicle cells on our scalp are very dependent on mitochondrial function and the vitamin K2 protects them from calcium imbalance.

More details, x.com AI, with some additions by me and prior post links.

Me: What are some underlying risk factors associated with macular degeneration or cataracts? Or some comorbid conditions? Is premature balding or hair loss associated with age related vision degeneration?

Grok3: Underlying Risk Factors and Comorbid Conditions for Macular Degeneration and Cataracts

(Query link)

Age-Related Macular Degeneration (AMD):

• Risk Factors:

  • Age: Primary risk factor, especially over 50.

  • Genetics: Family history and specific gene variants (e.g., CFH, ARMS2).

  • Smoking: Significantly increases risk.

  • UV Light Exposure: Prolonged exposure may contribute.

  • Diet: Low intake of antioxidants (vitamins C, E, zinc, lutein, zeaxanthin) and omega-3 fatty acids.

  • Obesity: Higher BMI linked to increased risk.

  • Hypertension: Poorly controlled blood pressure.

  • Cardiovascular Disease: Linked to vascular changes in the retina.

• Comorbid Conditions:

  • Cardiovascular diseases (e.g., atherosclerosis, heart disease).

  • Hypertension and diabetes (affect retinal blood vessels).

  • Obesity-related conditions (e.g., metabolic syndrome).

  • Chronic inflammatory conditions (e.g., arthritis).

Cataracts:

• Risk Factors:

  • Age: Most common after 60.

  • UV Radiation: Cumulative exposure to sunlight.

  • Smoking and Alcohol: Heavy use increases risk.

  • Diabetes: Accelerates cataract formation due to high blood sugar.

  • Steroid Use: Long-term corticosteroid use.

  • Eye Trauma or Surgery: Physical damage or prior procedures.

  • Genetics: Family history of early cataracts.

• Comorbid Conditions:

  • Diabetes (most significant, due to lens protein glycation).

  • Hypertension and cardiovascular disease.

  • Obesity and metabolic syndrome.

  • Chronic kidney disease (linked to metabolic imbalances).

  • Autoimmune diseases (e.g., rheumatoid arthritis, linked to steroid use).

Premature Balding/Hair Loss and Age-Related Vision Degeneration: There is no direct, well-established link between premature balding (e.g., androgenetic alopecia) and age-related vision degeneration (AMD or cataracts). However, some indirect associations may exist:

• Hormonal Factors: Androgenetic alopecia is driven by dihydrotestosterone (DHT). Elevated DHT or hormonal imbalances may be linked to systemic inflammation or cardiovascular issues, which are risk factors for AMD and cataracts.

• Cardiovascular Connection: Premature balding has been associated with increased cardiovascular risk (e.g., coronary artery disease) in some studies. Since cardiovascular disease is a risk factor for AMD, there could be an indirect overlap.

• Oxidative Stress and Inflammation: Both hair loss and vision degeneration involve oxidative stress and inflammation. Conditions like metabolic syndrome, which elevate systemic inflammation, could theoretically contribute to both.

• Limited Evidence: No large-scale studies directly connect premature balding to AMD or cataracts. Any association is speculative and likely mediated through shared risk factors like cardiovascular health or aging processes.

Summary: AMD and cataracts share risk factors like aging, smoking, UV exposure, and cardiovascular/metabolic conditions. Comorbidities often include diabetes, hypertension, and obesity. Premature balding is not directly linked to vision degeneration but may share indirect pathways through cardiovascular risk or inflammation. Maintaining a healthy lifestyle (e.g., diet rich in antioxidants, UV protection, no smoking) can reduce risks for both eye conditions.

If you want me to search for recent studies or posts on X about balding and vision degeneration, let me know!

Disclaimer: Grok is not a doctor; please consult one. Don't share information that can identify you.

Vitamin K2 and Mitochondria

Me: Mitochondrial dysfunction seems to be a related risk to early hair loss or hearing changes but that seemed less linked to vision changes when I was doing a deep dive on ototoxicity. Apparently Hair cells of the inner ear and hair follicles on the head have particularly large mitochondria associated with them. / both of those conditions were also comorbid/related to later dementia risk. Vision risk seemed slightly less associated. calcium binding proteins that use vitamin K2 as a cofactor seemed involved in the inner ear risks - poor gut microbiome making too little vitamin K2 I think as the world wide diet average is really not rich in vitamin K2 itself - suggesting to me that humans depended on healthy gut microbes to make it for our calcium binding protein needs as we need quite a lot more of it for that then we need vitamin K for blood clotting roles. maybe even a gram per day of vitamin K2 compared to 150 mcg of K1 for coagulation cofactors. / any comment or anything about K2 and macular degeneration?

• *See my Ototoxicity series for more about this topic.

• **Note that the powder K2 product I had found was a mistake - a bad product. Dr. Mercola or Life Extension have vitamin K2 products that don’t have the negative of an excess filler, calcium phosphate that is used in the bulk powder product I had mentioned early in the series. I now encourage a focus on restoring the gut microbiome with zinc, resistant starch and a Mega SporeBiotic (Microbiome Labs) type of probiotic that contains Bacillis subtilis or other butyrate producing species. Bifidobacterium would help but chimeric spike tends to knock that out. Gut health is critical in many aspects of aging or chronic degenerative disease.

• Readers can order the Mega SporeBiotic or other professional brand supplements at 20-25% off through Fullscript, a wholesale professional dispensary, by signing up under my account. (Sign up here.)

• You would also be able to order from protocols I have shared on that site (search my archives here for ‘protocol’: Leptin Resistance, PCOS, Lymphedema (Salicylate excess), Cardiometabolic Protocol), or order directly from their catalog except, supplements by the company Ortho Molecular Products will need to have a plan/recommendation from me to allow purchase and the system notifies me if you want to order one. Look for a plan from me after you place the request - give me a day or two to get the email. Orders over $50 get free shipping and the company is fast. *Affiliate links, thank you for purchasing if you do, as I make a small amount of money from your purchases.

Document link & Reference List for the Ototoxicity & vit K2 series

Grok3: Your deep dive into mitochondrial dysfunction, hair loss, hearing changes, and their potential links to vitamin K2 and calcium-binding proteins is fascinating and touches on some cutting-edge areas of research. Let’s unpack this and address your specific question about vitamin K2 and macular degeneration (AMD), while also commenting on the broader context you’ve raised.

Mitochondrial Dysfunction and Shared Pathways

You’re correct that mitochondrial dysfunction is implicated in both hair loss (e.g., androgenetic alopecia) and hearing changes (e.g., age-related hearing loss or ototoxicity). Hair follicles and inner ear hair cells (cochlear hair cells) are highly metabolically active, relying on robust mitochondrial function to meet their energy demands. Mitochondria in these cells are critical for ATP production and managing oxidative stress. Dysfunction—whether due to aging, toxins, or genetic predisposition—can lead to cell death or impaired function, contributing to hair loss or hearing loss.

• Hair Loss: Mitochondrial dysfunction in hair follicle stem cells may impair their regenerative capacity, exacerbated by oxidative stress or hormonal factors like DHT. Studies suggest that mitochondrial DNA mutations or reduced mitochondrial efficiency correlate with premature balding.

• Hearing Loss: Inner ear hair cells are particularly vulnerable to mitochondrial damage due to their high energy needs and exposure to oxidative stress (e.g., from noise or ototoxic drugs). Mitochondrial mutations (e.g., MT-RNR1) are linked to sensorineural hearing loss.

• Dementia Link: Mitochondrial dysfunction is a known contributor to neurodegenerative diseases, including dementia. Oxidative stress, impaired energy metabolism, and inflammation from dysfunctional mitochondria can damage neurons over time. Both hair loss and hearing loss have been associated with increased dementia risk, potentially as markers of systemic aging or vascular/metabolic stress.

Vision changes (e.g., AMD, cataracts) also involve mitochondrial dysfunction, but the link appears less direct than for hair or hearing. Retinal pigment epithelial (RPE) cells in AMD rely on mitochondria for energy and to combat oxidative stress from light exposure. However, the retina’s unique environment (e.g., high oxygen consumption, intense light exposure) means other factors like lipofuscin accumulation or drusen formation may overshadow mitochondrial contributions in AMD progression.

Vitamin K2, Calcium-Binding Proteins, and Inner Ear Risks

Your hypothesis about vitamin K2, calcium-binding proteins, and gut microbiome is insightful. Vitamin K2 (menaquinones) is critical for activating calcium-binding proteins, such as matrix Gla protein (MGP) and osteocalcin, which regulate calcium deposition in tissues. Unlike vitamin K1 (phylloquinone, abundant in leafy greens and primarily for coagulation), K2 is less prevalent in diets and heavily dependent on gut microbial synthesis (e.g., from bacteria like Lactobacillus or Bifidobacterium) or fermented foods (e.g., natto, cheese).

• Inner Ear and Calcium: Calcium homeostasis is crucial in the inner ear, where calcium-binding proteins (e.g., calbindin, calretinin) regulate signaling in hair cells. Dysregulated calcium, potentially from insufficient K2-activated proteins, could exacerbate mitochondrial stress or ototoxicity. For example, ototoxic drugs like aminoglycosides disrupt calcium signaling, and poor K2 status might worsen this by impairing protective proteins.

• K2 Requirements: You’re right that K2 needs for calcium regulation likely exceed K1 needs for coagulation. While K1 requirements are ~90–120 mcg/day for clotting, K2 doses for optimal calcium metabolism (e.g., preventing vascular calcification or bone loss) may be higher—studies suggest 100–1000 mcg/day of K2 (MK-7 or MK-4) for therapeutic effects. The gram-per-day estimate you mentioned seems high, as most studies use microgram doses, but it underscores the reliance on gut microbes when dietary K2 is scarce.

• Gut Microbiome: Modern diets (low in fermented foods) and antibiotic use can impair gut microbial K2 production, potentially leading to subclinical deficiencies. This could affect tissues like the inner ear, where calcium regulation is critical.

Vitamin K2 and Macular Degeneration

There’s limited direct research linking vitamin K2 to AMD, but let’s explore the plausible connections based on available evidence and your hypothesis:

1. Calcium Regulation and Drusen Formation:

   • In AMD, drusen (yellow deposits under the retina) contain calcium and lipids, suggesting dysregulated calcium metabolism. Vitamin K2 activates MGP, which inhibits ectopic calcification in soft tissues (e.g., blood vessels). Theoretically, K2 deficiency could contribute to calcium deposition in drusen, worsening AMD. However, no studies have directly confirmed K2’s role in drusen formation.

   • A 2017 study on vascular calcification suggested K2 supplementation (180–360 mcg/day MK-7) reduced arterial stiffness, which could indirectly benefit retinal vasculature, a factor in wet AMD. Poor retinal blood flow is a risk for AMD progression, so K2’s vascular benefits might be relevant.

2. Mitochondrial Support:

   • K2 has antioxidant properties and may support mitochondrial function by reducing oxidative stress. Since mitochondrial dysfunction in RPE cells contributes to AMD, K2 could theoretically protect retinal cells. However, this is speculative, as most K2 research focuses on bone and cardiovascular health.

   • A 2020 review on vitamin K suggested its role in reducing inflammation (via NF-κB pathways), which could mitigate chronic inflammation in AMD. Inflammation drives AMD progression, so K2 might offer indirect benefits.

3. Gut Microbiome and Systemic Health:

   • A dysfunctional gut microbiome, producing less K2, could exacerbate systemic inflammation or metabolic issues (e.g., diabetes, obesity), which are AMD risk factors. Improving gut health (e.g., via probiotics or fermented foods) might increase K2 availability and support overall health, potentially reducing AMD risk indirectly.

   • No studies have quantified K2 levels in AMD patients or linked microbiome-derived K2 to retinal health.

4. Current Evidence:

   • A 2021 study on vitamin K status and eye health found that low K1 (not K2) was associated with increased cataract risk, but AMD was not significantly linked. K2’s role in AMD remains underexplored.

   • Anecdotal reports on platforms like X mention K2 supplementation for general eye health, but these lack scientific rigor. For example, a 2024 X post claimed K2 “helped with vision clarity,” but no clinical data supported this.

   • Most K2 research focuses on osteoporosis, cardiovascular disease, and diabetes, with doses of 100–360 mcg/day MK-7 showing benefits. These conditions are AMD comorbidities, so K2 might have secondary benefits for retinal health.

Comments on Your Hypothesis

Your idea that humans evolved to rely on gut microbes for K2, given low dietary intake, is plausible. Evolutionary diets likely included fermented or animal-based foods (e.g., organ meats) providing K2, supplemented by microbial synthesis. Modern diets, high in processed foods and low in fermented products, may create a K2 deficit, especially if gut dysbiosis is present. This could impair calcium-binding proteins across tissues, including the inner ear and potentially the retina.

The weaker link between mitochondrial dysfunction and vision (compared to hair/hearing) makes sense, as AMD involves complex factors like lipofuscin, complement system activation, and VEGF-driven angiogenesis, which may dilute mitochondrial contributions. However, K2’s role in systemic health (vascular, inflammatory, metabolic) suggests it could still be relevant for AMD prevention, even if not a primary factor.

Recommendations and Gaps

• K2 and AMD: No direct evidence links K2 supplementation to AMD prevention or treatment. However, given its safety (doses up to 360 mcg/day MK-7 are well-tolerated) and benefits for comorbidities (e.g., cardiovascular health, diabetes), it might be a reasonable adjunct for at-risk individuals. Consult a doctor before supplementing, especially if on anticoagulants, as K2 can interact with drugs like warfarin.

• Diet and Gut Health: Increase K2 intake via fermented foods (natto, sauerkraut, certain cheeses) and support gut health with prebiotics/probiotics to enhance microbial K2 production. This could benefit systemic health, including eyes.

• Research Gaps: Clinical trials on K2 and AMD are needed, particularly measuring K2 status in AMD patients and testing supplementation effects on drusen or retinal function. Studies on K2’s role in retinal mitochondrial health are also lacking.

• Other Nutrients for AMD: Focus on established AMD-protective nutrients: lutein, zeaxanthin (10–20 mg/day), omega-3s (DHA/EPA), and antioxidants (vitamins C/E, zinc). The AREDS2 formula is evidence-based for slowing AMD progression.

Final Thoughts

Your hypothesis about K2, calcium-binding proteins, and mitochondrial dysfunction is a compelling framework for understanding systemic aging risks. While K2’s role in AMD is not well-studied, its benefits for vascular health, inflammation, and potentially mitochondrial function make it a plausible candidate for supporting retinal health indirectly. The stronger links between K2 and inner ear/hair follicle health highlight tissue-specific differences in mitochondrial and calcium dynamics. Until more research emerges, optimizing K2 through diet and gut health is a low-risk strategy that aligns with overall health goals.

If you’d like, I can search X or recent literature for more on K2 and AMD or dive deeper into mitochondrial dysfunction in these conditions. Let me know!

Disclaimer: Grok is not a doctor; please consult one. Don't share information that can identify you.

High dose vitamin K2 supplements aren’t available but Bacillus subtilis is in the probiotic product called Mega SporeBiotic by Microbiome Labs.

Me: The very high ~ 1 gram per day amount was my own extrapolation from successful animal based studies using K2 supplementation over time to reduce calcification of aging risks.... it worked very well, but seriously, those animals were being given ~ 1 gram per day human dose equivalent and YES there are no comparable human studies at that dosage and no supplementation at that level available and Natto is the richest human K2 food but a serving only gives ~ a few mg at the most. What it would be giving though is live culture probiotic of the K2 producing species Bacillus subtilis.

Grok3: Your extrapolation from animal studies to a ~1 gram per day human-equivalent dose of vitamin K2 is a bold and intriguing hypothesis, and it’s great that you’re critically analyzing the data while acknowledging the lack of human studies at such high doses. Let’s dive into your points about high-dose K2, animal studies, natto, and the potential role of Bacillus subtilis as a probiotic for K2 production, while tying this back to macular degeneration (AMD) and systemic aging risks like calcification.

High-Dose K2 in Animal Studies

You’re correct that some animal studies use very high doses of vitamin K2 (often MK-4 or MK-7) to achieve significant reductions in age-related calcification, particularly in models of vascular or soft-tissue calcification. These studies often aim to mimic accelerated aging or disease states (e.g., atherosclerosis, kidney disease) and report impressive outcomes, such as reduced arterial stiffness or calcium deposits.

• Animal Dosing Context:

  • Animal studies often use doses scaled to body weight, but direct extrapolation to humans is tricky due to differences in metabolism, absorption, and physiology. For example, a rat given 100 mg/kg of K2 (MK-4) might receive a human-equivalent dose (HED) that sounds massive—potentially approaching your ~1 g/day estimate—when adjusted for body surface area or metabolic rate. A common conversion factor (e.g., rat-to-human) divides animal dose by ~6–12, depending on the model.

  • Example: A 100 mg/kg dose in a 0.2 kg rat = 20 mg/day for the rat. For a 70 kg human, the HED might be ~200–500 mg/day, not far from your 1 g estimate. Some studies push even higher doses to maximize effects.

  • Outcomes: High-dose K2 in animals often activates matrix Gla protein (MGP) and other calcium-regulating proteins, preventing ectopic calcification in arteries, kidneys, or other tissues. This aligns with your focus on calcification as a systemic aging risk.

• Why It Works:

  • K2’s role in carboxylating MGP and osteocalcin ensures calcium is directed to bones and teeth, not soft tissues. High doses may saturate these pathways, providing robust protection against calcification, especially in models with extreme calcium dysregulation.

  • Anti-inflammatory and antioxidant effects of K2 (e.g., via NF-κB suppression) may also contribute, as chronic inflammation drives aging-related damage.

• Human Relevance:

  • No human studies have tested K2 at ~1 g/day, likely due to safety, cost, and regulatory concerns. Typical human trials use 100–360 mcg/day (0.1–0.36 mg) of MK-7 or 1–10 mg/day of MK-4, showing benefits for bone health, vascular elasticity, and diabetes markers.

  • At high doses, K2 is considered safe (no known toxicity ceiling), but megadoses could theoretically interact with anticoagulants (e.g., warfarin) or affect gut microbiota. Long-term effects of gram-level doses are unknown.

Natto, K2 Content, and Bacillus subtilis

You’re spot-on about natto being the richest dietary source of K2 (specifically MK-7) and its role as a delivery vehicle for Bacillus subtilis, the K2-producing probiotic. Let’s break this down:

• K2 in Natto:

  • A typical 50–100 g serving of natto provides 800–1000 mcg (0.8–1 mg) of MK-7, far more than other foods like cheese (10–50 mcg/100 g) or organ meats (~5–10 mcg/100 g). Your estimate of “a few mg” is reasonable for larger or highly fermented servings, but 1–2 mg is likely the upper end.

  • Even at 1–2 mg/day, natto falls far short of your 1 g/day extrapolation. To reach gram-level K2 via diet alone is impractical, reinforcing your point about reliance on microbial synthesis or supplementation.

• Bacillus subtilis as a Probiotic:

  • Bacillus subtilis in natto is a spore-forming bacterium that produces MK-7 during fermentation. When consumed, it can survive the stomach’s acidic environment and colonize the gut temporarily, potentially boosting endogenous K2 production.

  • Unlike typical gut microbes (e.g., Lactobacillus), B. subtilis is not a permanent resident but can contribute to K2 synthesis while present. Studies show natto consumption increases serum MK-7 levels, partly due to direct K2 intake and partly due to microbial activity.

  • This aligns with your earlier point about humans historically relying on gut microbes for K2, especially when dietary sources were scarce. Natto’s live cultures could enhance this natural system, unlike supplements, which provide K2 without probiotic benefits.

• Implications for Systemic Health:

  • By increasing K2 availability, B. subtilis could reduce calcification risks (e.g., in arteries or kidneys), which are linked to aging and AMD comorbidities like cardiovascular disease. A healthier gut microbiome might also lower systemic inflammation, benefiting retinal health indirectly.

  • No studies have directly tested B. subtilis supplementation for AMD or vision outcomes, but its role in K2 production makes it a plausible candidate for supporting calcium metabolism and mitochondrial health.

K2, Calcification, and Macular Degeneration

Your focus on calcification as a unifying risk factor is particularly relevant for AMD, as drusen (calcium- and lipid-rich deposits in the retina) are a hallmark of the disease. Let’s connect the dots:

• Calcification in AMD:

  • Drusen contain hydroxyapatite (a calcium phosphate mineral), similar to vascular calcifications. Dysregulated calcium metabolism in retinal pigment epithelial (RPE) cells may contribute to drusen formation, paralleling ectopic calcification elsewhere.

  • MGP, activated by K2, inhibits calcification in soft tissues. If K2 deficiency impairs MGP function, it could theoretically exacerbate drusen formation or retinal calcification, worsening AMD. No studies have measured MGP activity in AMD retinas, but the analogy to vascular calcification is compelling.

• High-Dose K2 and AMD:

  • Your 1 g/day extrapolation suggests a therapeutic threshold for overcoming systemic calcification risks. In AMD, such doses might maximize MGP activation, potentially slowing drusen progression or protecting retinal vasculature. However, this is speculative, as even human studies at 360 mcg/day MK-7 show benefits for vascular health without targeting eyes specifically.

  • Animal models of AMD (e.g., mice with ApoE or complement factor H mutations) could test high-dose K2 to see if it reduces drusen or retinal inflammation, but no such studies exist yet.

• Mitochondrial and Inflammatory Links:

  • High-dose K2 might support RPE mitochondrial function by reducing oxidative stress, as seen in some in vitro studies. This could protect against AMD’s early stages, where mitochondrial damage in RPE cells is a driver.

  • Inflammation (e.g., via complement activation) fuels AMD. K2’s anti-inflammatory effects, if scalable at high doses, could mitigate this, but current doses (100–360 mcg) already show modest anti-inflammatory benefits.

• Current Evidence:

  • As noted previously, no direct studies link K2 to AMD prevention or treatment. A 2021 study found low K1 (not K2) associated with cataracts but not AMD. Indirectly, K2’s benefits for cardiovascular health (e.g., reduced arterial stiffness in trials) could support retinal blood flow, a factor in wet AMD.

  • X posts occasionally mention K2 for “eye health,” but these are anecdotal and lack specificity to AMD.

Practical Considerations

• Achieving High K2 Levels:

  • Your 1 g/day target is unattainable via diet (natto’s 1–2 mg/serving is the ceiling) or current supplements (highest doses are ~1–10 mg MK-4 or 360 mcg MK-7). Developing a B. subtilis-based probiotic optimized for K2 production could bridge this gap, but no such product exists commercially.

  • Fermented foods like natto remain the best strategy for combining K2 and probiotics. Regular consumption (e.g., 50 g/day) could provide ~1 mg K2 plus microbial benefits, supporting your gut-K2 hypothesis.

• Safety of High Doses:

  • K2 has no known upper limit for toxicity, but gram-level doses are untested in humans. Potential risks include interactions with medications (e.g., warfarin) or unforeseen effects on gut microbiota or calcium metabolism. Animal studies suggest safety, but human trials are needed.

• AMD Prevention:

  • While awaiting K2-AMD research, focus on proven strategies: AREDS2 supplements (lutein, zeaxanthin, zinc, vitamins C/E), UV protection, smoking cessation, and a diet rich in omega-3s and antioxidants.

  • Adding natto or K2 supplements (100–360 mcg/day MK-7) is low-risk and may benefit AMD comorbidities (e.g., cardiovascular health, diabetes), even if direct retinal effects are unproven.

Comments on Your Hypothesis

Your extrapolation from animal studies is a creative leap, highlighting the potential for high-dose K2 to address systemic calcification and aging risks. The B. subtilis angle is particularly exciting, as it bridges dietary K2, gut health, and endogenous production—a natural system disrupted by modern diets. While 1 g/day is far beyond current human protocols, it underscores the need for research into optimal K2 dosing for non-skeletal outcomes like AMD or dementia.

The weaker link between K2 and AMD (vs. hair/hearing) likely reflects the retina’s complex pathology (drusen, complement, VEGF), where calcification is one of many drivers. Still, your focus on calcium-binding proteins and microbial K2 production aligns with emerging views on aging as a systemic, mitochondria- and inflammation-driven process.

Next Steps

• Research Gaps: Trials testing K2 (even at 1–10 mg/day) in AMD models or patients could clarify its role in drusen formation or retinal health. Studies on B. subtilis probiotics for K2 production are also needed, especially for calcification-related diseases.

• Practical Action:

  • Incorporate natto regularly (e.g., 50 g/day) for K2 and B. subtilis. If natto’s taste is a barrier, MK-7 supplements (100–360 mcg/day) are an alternative.

  • Support gut health with prebiotics (e.g., inulin, resistant starch) to enhance microbial K2 synthesis. *and/or add the Mega SporeBiotic product by Microbiome Labs. (Microbiome Labs)

  • Monitor cardiovascular and metabolic health, as these influence AMD risk and may benefit from K2.

• Consult a Doctor: Before experimenting with high-dose K2 (even if theoretically achievable), discuss with a healthcare provider, especially if you’re on medications or have health conditions.

If you’d like me to search for recent X posts, new studies on K2/AMD, or details on B. subtilis probiotics, let me know! I can also dig into specific animal studies you’re referencing to refine the dose extrapolation. [*That was done already, in the ototoxicity series]

Disclaimer: Grok is not a doctor; please consult one. Don't share information that can identify you.

There is value in doing your own research. A comment shared that early vision degeneration was reversed successfully with blueberry type changes and…. the doctor who had done the initial diagnosis then refused to believe there had been any problems… How could someone reverse this issue? ….. Not with that doctor’s help.

• See my page Resistant Starch/Butyrate and How Much Butyrate? on jenniferdepew.com for more information about a gut healthy diet. Also page Membranes/Inflammation and Membranes (about glyphosate in part).

• My Colitis Protocol post. …. and don’t forget the pomegranate!

• Pomegranate products would help vision health and overall microbiome and other inflammatory risks.

Disclaimer: I am not a doctor either, I am a Registered Dietitian and am sharing this information within the guidelines of Fair Use for educational purposes and it is not intended to provide individual health care guidance.