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What Makes All Vaccines So Dangerous?
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2026/01/09/zeta-potential-vaccine-injuries-blood-sludging.aspx
Analysis by A Midwestern Doctor January 09, 2026

Story at-a-glance
- Vaccines often cause various side effects, making it hard to identify common causes — many of which overlap with other mysterious and “incurable” ailments
- Neurologist Andrew Moulden discovered that vaccines frequently trigger microstrokes, which can lead to a myriad of acute and chronic diseases
- Forgotten research from the 1960s shows that blood cell clumping is a root cause of many diseases — a belief also shared by Chinese Medicine
- Colloidal chemistry and zeta potential science reveal that positive charges around blood cells cause clumping. Agents with concentrated positive charges, such as aluminum and the COVID spike protein, are especially problematic
- Improving the physiologic zeta potential benefits a wide range of acute and chronic illnesses. A strong case can also be made that many conventional and holistic therapies work in part by enhancing zeta potential
Many medical problems stem from the diagnostic approach of physicians, especially with complex illnesses, which are often misdiagnosed and lead to ongoing patient struggles.
Complex conditions can present with varied symptoms across patients and resemble other illnesses (e.g., fibromyalgia vs. chronic fatigue syndrome). In turn, poorly trained physicians often default to psychiatric explanations, overlooking the actual causes.
As vaccine injuries have a wide range of symptoms, they have hence confused doctors for over 200 years (with many doctors in the past labeling them as “encephalitis”). Presently, I believe three main mechanisms underlie the myriad of chronic illnesses including vaccine injury:
• Immune dysfunction — Vaccines frequently cause chronic autoimmune disorders and varying degrees of immune suppression.
• Impaired circulation — Vaccines can impair fluid circulation by affecting the body’s zeta potential. This causes fluid clumping (i.e., micro blood clots and blood thickening) and obstructs blood flow in capillaries. Likewise, other factors can as well, and I believe one of the primary issues with COVID-19 and vaccine spike protein is that it carries a strong positive charge density, which triggers clumping in fluids throughout the body (hence why the vaccine became known as the “clot shot”).
• Cell danger response — When shocked, such as from a toxin or loss of blood flow, cells can enter a primitive state under threat, stopping normal mitochondrial function and creating inflammation. This temporary state can become chronic, underlying many severe conditions (particularly those which worsen rather than improve with treatment).
Treating this response has resolved conditions linked to vaccination, like autism, and, in complex illnesses, restoring health often requires first addressing the underlying cause of a patient’s illness and then resolving the cell danger response it triggers.
Note: While not the most potent tool for addressing each of these root cause illnesses, DMSO stands out for its broad therapeutic activity, which allows it to address all three.
This, I believe, accounts for why thousands of readers here have reported it was able to cure a myriad of seeming unrelated illnesses which did not respond to other therapies, but likewise why a fraction of people with those illnesses which typically responded to DMSO did not have a disease resolution from DMSO alone (as they required a stronger therapy to target the root cause of their illness).
While I always consider all three of these factors, I’ve long placed particular weight on circulatory obstructions, and I’ve long believed that patient outcomes would significantly improve if the medical system recognized and prioritized the zeta potential.
Andrew Moulden
Andrew Moulden was a Canadian neuroscientist and doctor specializing in neuropsychiatry. During his clinical training, he noticed that young children exhibited subtle neurological signs of stroke that his colleagues missed. Over time, he found these strokes often occurred soon after vaccination and could lead to severe neurological disorders like autism.
Note: Vaccine injury reports dating back to the early 1800s contain the same signs Moulden observed.
Moulden realized that the subtle stroke signs doctors look for in adults should also be assessed in children. Because these strokes in infants are often missed, many conditions are misdiagnosed or attributed to unknown causes. A major scientific challenge is making invisible issues visible. However, in neurology, disruptions in brain function, often due to impaired blood flow, can reveal stroke locations through careful physical examination.
Moulden found that cranial nerves in the brainstem, particularly in watershed areas with less redundant blood supply, were vulnerable to these strokes. Those strokes, caused by impaired blood flow, often due to increased blood thickness, were missed in infants, leading to conditions misdiagnosed or attributed to “unknown” causes. Key cranial nerves indicating vaccine-caused microstrokes (due to their blood supply) include:
• Cranial Nerve VI — Controls eye movement; damage causes inward eye resting or jerky side-to-side movement.1

Note: We’ve found CN VI is the nerve most frequently affected by COVID-19 injuries and I’ve lost count of how many people I know who developed subtle abnormalities in it after vaccinating.
• Cranial Nerve VII2 — Controls facial muscles; damage causes Bell’s Palsy,3 facial drooping, or asymmetry (e.g., this appeared to have happened to Justin Bieber during the COVID-19 vaccine campaign).

• Cranial Nerve IV — Levels eyes; damage causes head tilting to compensate for uneven eye height.4

Note: Often, you will see multiple cranial nerve issues on the same face (which suggests more parts of the brain lost their blood supply and hence that deeper neurological damage is also present). For example, cranial nerve deficits have long been observed after vaccine injuries and in autistic children.
Consider the case below of triplets who all received a hot pneumococcal vaccine,5,6 and in a few hours all had their cranial nerves stop functioning after which they rapidly became severely and permanently autistic — making it nearly irrefutable that this process caused their autism.
Once you know how to look for these symptoms (e.g., a loss of smooth eye motion), they are very easy to spot, and you will gradually become aware of how far-reaching the neurological damage resulting from vaccination can be (since any part of the brain can be affected). For example, these were two similar pictures readers sent in of their children who became severely disabled after vaccination.


Note: While cranial nerve issues are easiest to detect through observed motion, as the above pictures show, some of them can also be seen in static images. Remarkably, if you look at much older photos, facial asymmetries were much rarer. These pictures, for example, were collected by Forest Maready and mirror what I’ve seen (e.g., by looking at the walls of medical school class portraits and noticing how faces changed over the decades).7



Note: Decades of suppressed evidence link vaccines to sudden infant deaths. Moulden observed inward eye deviation before death and proposed vaccine-induced microstrokes affecting the CN VI nucleus disrupt the brain’s nearby respiratory center. Subsequent ICU studies show vulnerable infants can experience post-vaccination breathing cessation — survivable if monitored, fatal if unnoticed.”
Moulden’s work also suggested strokes were occurring in other watershed areas of the body, such as internal organs and speech centers. Evidence included:
• Autopsy studies show strokes in the internal organs of children with congenital rubella.
• Similar disease processes in teenagers and adults after HPV or anthrax vaccination (two particularly harmful vaccines).
• One of the most striking examples was the children of soldiers who received the anthrax vaccine and were born without limbs8 (thalidomide was also notorious for doing this by blocking the formation of new blood vessels9).

• Neurodegenerative processes in the elderly and psychiatric disorders being linked to detectable cranial nerve damage (something many of us also tragically witnessed after COVID vaccination).
Note: A major issue in conventional medicine is the failure to recognize that neurological damage can lead to psychiatric issues. Consequently, emotional changes in patients with nervous system injuries are often misattributed as the cause rather than a symptom of their illness.
Moulden thus began exploring which universal response was causing these microstrokes and how they could be treated. From this, he produced three videos describing the problem (which can be viewed here). Unfortunately, shortly before releasing a second series on the solutions for these injuries, he died under suspicious circumstances. However, we now have many clues as to what Moulden discovered.
Blood Sludging
In the medical world, a long-standing puzzle revolves around how small insults to the body can lead to widespread illness or even death. One key factor in this equation is blood sludging, a phenomenon observed for centuries where the blood clumps together and thickens under certain disease conditions. Melvin Knisely, Ph.D., in the mid-20th century made critical discoveries about this phenomenon.10
Knisely’s research, particularly with malaria-infected monkeys, revealed that certain severe illnesses could trigger significant blood sludging, starting in small vessels and eventually spreading to larger ones, which was typically fatal (unless prevented with the anticoagulant heparin).11 This thickening of blood can be likened to traffic jams, disrupting the body’s natural blood flow, and eventually leading to gridlock (death).
Additionally, he discovered that this systemic sludging could be seen externally through the eyes, providing a noninvasive way to assess this process throughout the body.

From this, Knisely discovered the greatest blood sludging was seen in critically ill hospital patients — something Pierre Kory, MD, also observed with point-of-care ultrasound, as once micro clots within the IVC became echogenic (visible), patients died shortly after.12 Likewise, multiple ultrasound researchers’ results showed blood sludging within patients.13,14
After learning of this, we attempted to replicate Knisely’s microscope and have been able to see the same sludging he observed 80 years ago in his patients. This video, for example, was taken from the eyes of a COVID-19 vaccine-injured patient:
Video Link
Likewise, this concept exists in other medical systems. Chinese Medicine, for example, ever since the (zeta potential-obstructing) smallpox vaccine was released, has come to view blood stasis as a primary cause of illness, and much of their blood stasis framework directly overlaps with the blood sludging model.
Note: Blood sludging was frequently observed in burns (which I believe explains why zeta potential restoring therapies and DMSO are so helpful for burns).

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Zeta Potential
When particles are placed in water, one of three things can happen:
• They don’t mix (e.g., oil floats to the top, sand sinks to the bottom).
• They dissolve (e.g., salt).
• They form a colloidal suspension (e.g., milk) in which each particle is repelled from the other and evenly distributed.
In the case of colloidal suspensions, their stability is determined by what causes their particles to come together (gravity separating things by weight, the inherent molecular attraction between objects), and what pushes them apart.15

The first method (zeta potential alteration) refers to the difference in charge between the water ions (which coat the colloidal particles) and the surrounding water.

Because electrical repulsion due to zeta potential is easier to adjust externally, it is typically the factor focused on when trying to improve colloidal dispersion (e.g., to eliminate blood sludging).
One of the most effective agents for collapsing zeta potential is aluminum (which explains why it’s frequently used to separate organic matter from water in sewage plants or to clot bleeding wounds). Moulden thus concluded that aluminum’s widespread use in vaccines likely accounted for many of their side effects. Similarly, consider the effect the COVID-19 vaccine’s spike protein has on the blood.16

The key thing to understand about zeta potential is that when its repulsion no longer suffices to overcome the attractive forces in a colloidal system, it will clump together, initially in small clumps (termed agglomerations), and then as the zeta potential worsens, form larger clumps.
Note: The normal zeta potential of a red blood cell is around -15.7 millivolts.17 Additionally, as red blood cells age, they lose their negatively charged sialic acid, which worsens their zeta potential.18

Thomas Riddick, a pioneer in this field, discovered that the body maintains blood zeta potential near the agglomeration threshold so it can clot in case of bleeding.19 With further study, Riddick found the degree of blood sludging or loss of physiologic zeta potential significantly varied from person to person (due to modern life disrupting it), and Knisely’s grading scale for blood flow in the eyes could be used to accurately predict who was at risk of an arrhythmia, a stroke, or a fatal heart attack.20
Most importantly, Riddick discovered that once the colloidal dispersion of the blood was fixed, heart arrhythmias normalized, and circulatory problems greatly improved.
Note: Many readers have shared with me that restoring their zeta potential improved their atrial fibrillation.
Riddick gradually discovered blood sludging was widespread in America and eventually concluded our food and water supply were contaminated with positive ions that were destructive to zeta potential. He attributed this to:
• Potassium is being replaced by sodium in processed foods
• Aluminum is being used in municipal water systems
• Aluminum kitchenware
• Aluminum is being added to many foods (e.g., most salt has aluminum added to keep it from caking)
• Many medications (e.g., antacids) are full of aluminum and other problematic metals
• Many foods are stored in metal cans (acidic foods leach these metals)
Note: The first head of the FDA fought to stop aluminum from entering general use but was muscled out by industry.21
Riddick also performed experiments that showed consuming water stored in metallic aluminum significantly impaired microcirculation. Sadly, we are now witnessing an increasing trend of storing water in aluminum cans (but fortunately, a few zeta-potential restoring bottled water brands still exist — which a few readers have shared dramatically improved their health, illustrating how sensitive some individuals can be to minor improvements in zeta potential).
Lastly, in addition to these, I believe EMFs, certain chronic infections, and humanity’s lack of electrical grounding to the Earth are significantly impairing humanity’s zeta potential.22 Likewise, I believe Riddick’s model (like many preliminary ones) was incomplete as he never accounted for the effect mass vaccination was having on zeta potential.
Note: I believe Knisely’s observations of profound blood sludging in the eyes of severely ill hospital patients account for why IV saline (which improves zeta potential) so frequently benefits people who are sick enough to require hospitalization. Likewise, Knisely also observed that certain agents, such as hydroxychloroquine, reversed blood sludging.
This led him to suspect a significant degree of the anti-malarial benefit of hydroxychloroquine actually arose from it reducing blood sludging; I also suspect this property may account for hydroxychloroquine’s value in treating autoimmune conditions and COVID-19 (both conditions linked to poor zeta potential).
Vaccines, Microbes, and Zeta Potential
Riddick also concluded that bacterial metabolism of proteins lowers their zeta potential by decarboxylating them.
Many sewage treatment systems (e.g., septic tanks) work under this principle, as over time, decarboxylation (which removes negative charges) destroys the colloidal stability of the organic matter suspended in wastewater, causing it to sludge at the bottom where it can later be removed and disposed of (in many cases unfortunately ending up in our soil as a “fertilizer” — which creates a host of subsequent issues).
Riddick next assessed how zeta potential changed in humans during acute infections. Much like Knisely had observed in the eyes of his acutely ill patients, Riddick consistently observed a decrease in physiologic zeta potential there during an infectious condition.
These observations were important because they provided a means to explain why the elderly (who cannot tolerate a further drop in their zeta potential without passing into the agglomeration threshold) are so much more vulnerable to infections like influenza (rather than simply feeling crummy from an unpleasant but manageable increase in fluid stagnation).
Sadly, it also likely explains their greater susceptibility to vaccine injuries (e.g., I’ve admitted a few patients to the hospital who suffered a classic zeta-potential collapse from a pneumococcal vaccine and readers here have shared a few similar examples).
Lastly, many microbes carry positive charges, which allow them to adhere to the negatively charged surfaces of the body. These hence cause them to disrupt zeta potential once they’ve sufficiently reproduced in the body.
This is a major problem in Lyme disease and chronic mold toxicity, which in part explains why therapies for those diseases often fail unless something (e.g., treating zeta potential) is also done to address the fluid stagnation they create (particularly within the lymphatics, which is required to drain the released toxins so herxheimer reactions do not occur). Fortunately, there are many ways to address this.
Ozone, for instance, oxidizes those charges, and I believe this accounts for the dramatic improvements sometimes observed after one receives an oxidative therapy.
Similarly, a 2022 paper that showed the spike protein directly impaired blood cell zeta potential also found that ivermectin dispersed blood cells, in which the spike protein had clumped together (which may explain the instantaneous normalization of vital signs sometimes seen after ivermectin is given to severely ill hospital patients).23
Protein Misfolding
Since folded proteins are essentially colloidal suspensions, ions that disrupt zeta potential can also cause protein misfolding and denaturing (something that also happens to egg whites when they are heated in a pan). I believe this is a key reason why the plaques found in Alzheimer’s disease (which are misfolded proteins) are found to contain aluminum.24
Likewise, the COVID spike protein (produced by the vaccines) has been linked to protein misfolding diseases such as Creutzfeldt-Jakob Disease, amyloidosis, and unusual fibrous (amyloid) clots embalmers have found within the vaccinated, which appear to result from misfolded clotting proteins the body can’t break down.25
Note: I have now received reports of those conditions (including CJD) responding to DMSO.
Lastly, it is critical to recognize that this zeta potential applies to many fluids besides blood, and I believe its ability to alter lymphatic and cerebrospinal fluid circulation plays a major role in why:
• Zeta potential regimens can eliminate toxins such as neurodegenerative protein deposits and improve cognition.
• Chinese medicine attributes blood stasis to autoimmunity, as congested lymph fluid creates inflammation.
Likewise, other critical properties for health (e.g., sufficient water within the body existing in a negatively-charged liquid crystalline state) also go hand-in-hand with the existing physiologic zeta potential.
Conclusion
Healthy fluid circulation is essential for health, and the zeta potential concept begins to explain why so many different conditions can lead to similar symptomatology. In the case of vaccines, this model explains why:
• Vaccines consistently cause harm.
• There is so much variability in vaccine injuries.
• Vaccine damage is cumulative, as existing impairment of the microcirculation (and other fluid circulations) will progressively worsen with each successive vaccine.
• Many infectious diseases can sometimes cause similar (but not as severe) injuries as vaccines.
Likewise, it’s critical to recognize that less severe impairments of zeta potential can also have significant physiologic consequences, and that a strong argument exists many of the consequences of aging (e.g., cognitive impairment and increased frailty) ultimately result from increasing disruption to the physiologic zeta potential as aging kidneys lose the ability to selectively excrete problematic ions (which is why longevity doctors had so much success averting cognitive decline with simple zeta potential regimens).
The zeta potential concept profoundly changed my medical practice, and I now believe that many effective holistic therapies work in part because they can restore physiologic zeta potential.
Once you know to look for it, it is truly eye opening how many different illnesses result from fluid stagnation within the body and how much hospital care could be improved by monitoring for zeta potential shifts.
Author’s Note: This is an abridged version of a longer article that discusses the topics mentioned here in more detail. That article, along with additional links and references, can be read here. Additionally, a companion article on how to restore the physiologic zeta potential can be read here. Finally, a companion article discussing how DMSO can be used to treat a wide range of neurological disorders, including brain injuries, paralysis and dementia can be read here.
A Note from Dr. Mercola About the Author
A Midwestern Doctor (AMD) is a board-certified physician from the Midwest and a longtime reader of Mercola.com. I appreciate AMD’s exceptional insight on a wide range of topics and am grateful to share it. I also respect AMD’s desire to remain anonymous since AMD is still on the front lines treating patients. To find more of AMD’s work, be sure to check out The Forgotten Side of Medicine on Substack.
- 1 Wikipedia, Abducens nerve, Accessed December 2025
- 2 Wikipedia, Facial nerve, Accessed December 2025
- 3 Wikipedia, Bell’s palsy, Accessed December 2025
- 4 Wikipedia, Trochlear nerve, Accessed December 2025
- 5 A Midwestern Doctor, July 12, 2024
- 6 @cmccaff542, x.com, October 13, 2025
- 7 Forrest Maready, January 18, 2017
- 8 Children’s Health Defense, November 9, 2020
- 9 Wikipedia, Thalidomide, Accessed December 2025
- 10 Wikipedia, Melvin Henry Knisely, Accessed December 2025
- 11 Angiology. 1964 Sep:15:411-6
- 12 Wikipedia, Inferior vena cava, Accessed December 2025
- 13 Science, 24 Dec 1982,Vol. 218, Issue 4579, pp. 1321-1323
- 14 Am Heart J. 1992 Oct;124(4):961-5
- 15 Wikipedia, Van der Waals force, Accessed December 2025
- 16 IJVTPR, Vol. 2 No. 2 (2022): COVID Aftermath
- 17 Exp Parasitol. 2012 Mar 21;131(2):245-251
- 18 Biologia 68, 762-765 (2013)
- 19, 21 American Water Works Association, 53(8), 1007-1030
- 20 A Midwestern Doctor, May 16, 2023
- 22 Earthing.com, Accessed December 2025
- 23 Int J Mol Sci. 2022 Dec 7;23(24):15480
- 24 J Alzheimers Dis. 2011;23(4):567-98
- 25 Biosci Rep. 2021 Aug 27;41(8):BSR20210611
Meal Fat Content Influences Muscle Building After Exercise
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/12/30/meal-fat-content-muscle-building.aspx
Analysis by Dr. Joseph Mercola December 30, 2025>

Story at-a-glance
- Low-fat protein after exercise delivers amino acids into your bloodstream faster, giving your muscles a stronger signal to repair and grow
- High-fat meals slow digestion and weaken your muscle-building response, even when the total amount of protein is the same
- A stronger and faster leucine surge from lean protein helps activate muscle repair more effectively, improving your recovery window
- Higher daily protein intake — around 0.8 grams per pound of ideal body weight — supports better muscle gain, fat loss, bone strength, and metabolic stability
- Simplifying your post-workout meal and choosing low-LA, low-fat protein sources help you recover more quickly and get better results from every training session
Muscle building depends on how quickly your body receives and uses amino acids after exercise, and that timing determines whether your workout translates into real progress or unnecessary soreness. Many people train hard but slow their own results with meal choices that interfere with this process. What you eat after training shapes the strength of your recovery signal, and the newest research underscores how sensitive this window is.
The structure of a meal — not just the amount of protein in it — influences the speed and effectiveness of muscle repair. Your body is constantly interpreting the nutrients you give it, and certain combinations accelerate the rebuilding phase while others hold it back. If you’ve ever wondered why similar workouts lead to completely different results from one person to another, this is one of the reasons.
Another piece that deserves attention is the level of daily protein intake needed to support consistent gains, especially if you train regularly. Many people mistake how much protein their body requires to maintain muscle and build more of it. The right intake supports stronger recovery, better composition changes, and a more resilient system overall.
Low-Fat Meals Trigger a Stronger Muscle-Building Signal
A recent study published in The American Journal of Clinical Nutrition investigated how different pork-based meals influence muscle protein synthesis after resistance training.1 While I don’t recommend pork due to its high level of linoleic acid (LA), the study reveals how different fat levels in your meals influence muscle growth.
The researchers compared three options — high-fat pork, low-fat pork, and a carbohydrate drink — to determine whether the fat content affects the body’s ability to repair and build muscle after exercise. This design allowed them to isolate fat as the key variable while keeping protein intake equal between the two pork meals.
• Healthy young adults completed exercise sessions before testing the meals — The study involved physically active adults who performed structured resistance exercise before consuming their assigned meal.2 Participants then underwent repeated blood draws and muscle biopsies, giving researchers highly accurate data on real-time muscle repair responses.
• Low-fat pork produced the strongest improvement in muscle-building activity — The low-fat pork meal triggered a sharper rise in myofibrillar protein synthesis, which is the process your body uses to repair and build muscle tissue after you train.
In contrast, the high-fat pork meal muted this muscle-building response so much that it looked similar to the carbohydrate drink. That means the fat in the meal affects your body’s ability to use the protein you just ate, even if the amount of protein is identical.3
• The most meaningful improvement was the faster leucine surge — Researchers reported that the low-fat meal produced a more rapid and higher peak in essential amino acids, especially leucine, compared to the high-fat meal.
Leucine acts like an ignition switch for muscle repair, and when it reaches your bloodstream quickly, your muscles begin rebuilding faster. With the high-fat meal, this leucine rise was delayed and smaller, which weakened the muscle-building signal. Faster amino acid absorption gives you an edge in rebuilding stronger muscle fibers.
• Time-based data showed slow digestion was the limiting factor — The high-fat pork slowed gastric emptying, meaning the food left the stomach more slowly. Slow emptying delays amino acid delivery into your bloodstream. By the time amino acids finally rose after the high-fat meal, the window for peak post-exercise sensitivity had already narrowed. If you train hard and expect optimal recovery, that timing mismatch works against you rather than for you.
• Additional signaling pathways confirmed the difference in response intensity — Measurements of pathways involved in muscle repair showed greater activation after the low-fat meal compared to the high-fat one. Although the mechanics varied across specific signaling proteins, the overall pattern matched the amino acid data: lean protein delivered a cleaner, stronger anabolic signal, while high-fat protein diluted that effect.
Higher Daily Protein Intake Strengthens Muscle, Bone, and Metabolic Health
A narrative review published in Nutrients investigated how eating protein well above the standard dietary recommendations affects trained adults who exercise regularly.4 The researchers evaluated how higher protein intake shapes lean mass, fat loss, metabolic markers, and bone health.
This review aimed to clarify whether consuming more protein than the minimum requirement delivers measurable physical benefits or simply exceeds what your body needs. Unlike narrow intervention trials, this work drew on controlled feeding studies, long-term training programs, and dietary assessments to determine how sustained high-protein intake affects whole-body physiology.
• Healthy, physically active adults showed distinct improvements with higher protein intake — The populations studied were composed largely of healthy adults who performed structured resistance or endurance training and had no chronic diseases affecting metabolism or muscle function. These individuals already consumed moderate protein before participating.
Across studies, those who increased daily protein intake experienced improvements in lean mass, reductions in fat mass, and measurable gains in bone-supportive markers. This indicates that higher protein intake supports multiple tissues, not just muscle.
The Recommended Dietary Allowance (RDA) is set at 0.8 grams of protein per kilogram of body weight, but many of the beneficial outcomes appeared at intakes two to three times higher. Most adults actually need about 0.8 grams of protein per pound of ideal body weight (or about 1.76 grams per kilogram).
• The greatest improvements involved increases in lean mass and decreases in body fat — The review found that elevated protein intake produced consistent increases in lean mass, meaning participants added more muscle tissue when they trained with higher protein intake. The improvements were not small; the researchers described significant increases in “fat-free body mass” across a range of training programs.
Fat mass reductions were also stronger in those consuming more protein, suggesting that protein supports a more favorable energy balance by increasing satiety and thermogenesis. Satiety refers to feeling full sooner and staying full longer, while thermogenesis refers to your body’s ability to generate heat by burning calories during digestion.
• Additional benefits appeared in strength performance and overall recovery — Higher protein intake supported better training quality by improving recovery markers and lowering soreness between workouts. Participants who consumed protein before sleep added strength and lean mass at a faster rate in several studies, as the amino acids delivered overnight supported continuous tissue repair.
Although the review did not quantify exact timelines, multiple trials demonstrated that protein consumed before bed enhanced the effect of evening training sessions. This gives you an actionable strategy: using pre-sleep protein to “extend” your anabolic window.
• Higher protein intake boosts muscle protein synthesis throughout the day, not just after workouts — This continuous elevation supports stronger remodeling of muscle tissue. Protein also enhances nitrogen balance, which reflects how effectively your body retains amino acids for tissue repair.
Nitrogen balance improves when you consume enough protein to exceed the amount your body breaks down. Enhanced nitrogen balance is associated with better recovery, stronger training adaptations, and increased functional capacity.
• Metabolic improvements reflected protein’s thermic and hormonal effects — Higher protein intake elevates diet-induced thermogenesis, meaning your body expends more energy digesting protein than digesting fat or carbohydrates. This effect supports fat loss by increasing total daily energy expenditure.
Protein-rich meals also stabilize blood sugar responses, supporting better metabolic health and preventing energy crashes that interfere with training. The review highlighted these effects as part of a broader metabolic advantage that high-protein diets offer active individuals.
Higher protein intakes also supported stronger bones when calcium intake was adequate. Protein stimulates bone-building pathways and supports the growth of muscle tissue, which applies healthy mechanical stress to bone. This dual effect promotes skeletal strength, offering you greater long-term resilience as you age or increase your training intensity.

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Simple Ways to Strengthen Your Muscle-Building Response
Your body responds quickly when you give it the right inputs at the right time, and the research shows that what you eat after training influences how strongly you recover and how much strength you gain. If your workouts feel harder than they should or your progress has slowed, your post-exercise habits are often the limiting factor.
These steps address the real root cause: delayed amino acid delivery from high-fat meals and inadequate daily protein intake. If you train consistently, these changes give you a noticeable advantage.
1. Choose lean, low-LA protein within an hour after training — If you want faster recovery, choose protein sources that are both low in fat and naturally lower in LA. I do not recommend pork or chicken, as both tend to accumulate high levels of LA. High-fat meals slow digestion and delay amino acid delivery, weakening the muscle-building signal triggered by your workout.
Lean, low-LA options such as grass fed beef, bison, or a high-quality whey isolate give your muscles rapid access to the amino acids they need while reducing the oxidative stress associated with excessive LA intake.
2. Get enough high-quality protein — and balance it with collagen-rich sources — If you deal with tightness, stiffness, or slow recovery, increasing your protein intake gives your body the raw materials it needs for both muscle repair and connective tissue support. Most adults do best with about 0.8 grams of protein per pound of ideal body weight (about 1.76 grams per kilogram).
Red meat provides excellent complete protein, but muscle meat alone lacks key amino acids required for tendon, ligament, cartilage, and fascia health.
To fill this gap, make sure roughly one-third of your protein comes from collagen-rich sources such as bone broth, pure gelatin powder without additives, oxtail, shanks, or grass fed ground beef that includes connective tissue. These foods supply glycine, proline, and hydroxyproline — amino acids that strengthen joints, rebuild tissues, ease inflammation, and support deeper sleep.
3. Spread your protein evenly across your day — If most of your daily protein ends up at dinner, shifting toward even distribution helps your body stay in repair mode for longer. Your muscles respond more effectively when amino acids arrive in regular intervals rather than in one large meal. By having balanced portions at breakfast, lunch, your post-exercise meal, and dinner, you support steadier energy, stronger recovery, and higher training output.
4. Use protein before sleep if your goal is faster progress — with one important caveat — If you’re training intensely or feeling sore longer than you’d like, a small early-evening protein serving strengthens overnight repair. I normally advise avoiding food for at least three hours before bed, because late eating disrupts metabolic rhythms and interferes with natural nighttime repair. That remains the preferred rule.
If you want the added recovery benefit, finish this serving two to three hours before bed so digestion is complete before you lie down. Grass fed raw yogurt or pure gelatin powder stirred into warm herbal tea supplies a steady drip of amino acids through the night. This helps you wake up stronger, less sore, and more ready for training — without disrupting your circadian rhythm.
5. Keep your post-workout meal simple so your body absorbs amino acids without competition — If you load your plate with large, complex meals after training, your digestive system has to process too many nutrients at once, which distracts from the goal of driving amino acids into your bloodstream quickly. Your body works far more efficiently when the post-exercise meal is streamlined and easy to digest.
By limiting extras — heavy starches, added fats, or multiple side dishes — you give your system a clear pathway to absorb protein rapidly. That simplicity helps you activate muscle repair sooner, especially if your digestion tends to be sluggish after exercise. These shifts give you far more control over your training outcomes, allowing every workout to translate into stronger muscles, healthier connective tissue, better sleep, and steady long-term progress.
FAQs About Meal Fat Content and Muscle Building
Q: Why does the fat content of my post-workout meal matter for muscle building?
A: Fat slows digestion, which delays the rise of amino acids in your bloodstream. The featured research showed that even when protein amounts were identical, low-fat meals produced a stronger and faster muscle-building response than high-fat meals. When digestion slows, you miss the window of peak post-exercise sensitivity, weakening the anabolic signal your workout created.
Q: What type of protein is best to eat after training?
A: Lean, low-LA protein sources provide the fastest amino acid delivery. Grass fed beef, bison, or a high-quality whey isolate support rapid uptake. Pork and chicken are not ideal due to their high LA content, which introduces oxidative stress and reduces recovery efficiency.
Q: How much protein do I actually need each day?
A: Most adults need about 0.8 grams of protein per pound of ideal body weight (1.76 grams per kilogram) — far higher than the outdated RDA. Higher protein intake supports better muscle repair, stronger bones, greater fat loss, and more stable metabolic function, especially if you train regularly.
Q: Should I eat protein before bed?
A: A small, early-evening protein serving meaningfully improves overnight recovery. The key is timing: finish the serving two to three hours before bed to protect circadian rhythm. Options like grass fed raw yogurt or pure gelatin in warm herbal tea provide a slow, steady amino acid supply that supports nighttime tissue repair.
Q: How do I design a post-workout meal that truly supports recovery?
A: Keep it simple and easy to digest. Prioritize lean protein, avoid added fats, and limit heavy sides. Your digestive system can then focus on rapidly absorbing amino acids rather than processing a complex meal. This simplicity strengthens the muscle-building response and helps you recover faster between training sessions.
The Importance of Exercise and Biological Youth for Longevity
Reproduced from original article: https://articles.mercola.com/sites/articles/archive/2025/12/09/exercise-biological-youth-longevity.aspx
Analysis by Dr. Joseph Mercola December 09, 2025
Story at-a-glance
- Maintaining “biological youth” is crucial for longevity. Exercise, particularly moderate activity and 150 to 180 minutes of weekly resistance training, is the most powerful intervention for slowing biological aging
- Optimal protein intake is about 0.8 grams per pound of ideal body weight. Protein quality matters, with collagen and glycine being especially important but often overlooked nutrients
- Moderate carbohydrate intake (40% to 55% of calories) is associated with lowest mortality risk. Long-term low-carb diets may impair metabolic flexibility and mitochondrial function
- Up to 99% of the U.S. population may have some degree of insulin resistance. The HOMA-IR test is a simple way to assess metabolic health
- Regular sun exposure is critical for health and longevity. Other key factors include adequate sleep, stress management, minimizing environmental toxins, and maintaining gut health
I spoke with Siim Land, author of the book “The Longevity Leap,” discussing key factors for optimizing health and lifespan. Maintaining “biological youth” is the single most important factor for longevity, but the question is how to achieve this as you get older.
Land’s book is 500 pages, with 8,000 references, so it’s a good resource to take a deep dive into the strategies that will help keep you biologically young. He’s a leader in the longevity field and walks the walk — he implements the programs he talks about and is a stellar example of taking good care of your biology. Chronologically, Land, who lives in Estonia, is 29, but he claims the biological ages of his organs are much lower — 17 years overall, with a 9-year-old liver.
These estimates are based on relatively new epigenetic and biological age tests, which are intriguing, but we don’t yet know if the results translate to longer lifespans. I personally do not put much trust in them and believe they are flawed. Land explains:1
“What does it mean if you have a liver of a 9-year-old? Does it mean that you’re going to live exponentially longer than someone else? We don’t have that data yet … I wouldn’t put a lot of emphasis on the tests themselves, much rather I would look at the traditional biomarkers, like glucose, inflammation … and those other things.”
Historically, many mistakes have been made in longevity research, particularly the focus on extreme calorie, carbohydrate and protein restriction:2
“The practical outcome would be that you’re eating very small amounts of food and you are becoming very frail and skinny. But in the actual world, we’re starting to see right now that frailty is a huge risk factor for early death and mortality. And malnutrition itself also increases the risk of a lot of different diseases, all-cause mortality and neurodegeneration and heart disease events.
Right now, I think the field has started to appreciate a lot more of these tangible, practical, functional outcomes, like muscle strength and body composition … other biomarkers that move more from the theoretical side of biological aging.”
Optimal Protein and Carbohydrate Intake for Longevity
Land and I agree that most adults need about 0.8 grams of protein per pound of ideal body weight (the weight you would ideally be, not necessarily the weight you are now), or for Europeans, approximately 1.76 grams of protein per kilogram, for appropriate muscle maintenance and growth.
“If you eat too much, then that could be problematic from the perspective of kidney health and homocysteine levels. If you’re eating too little, then that’s the risk of the sarcopenia and frailty,” Land notes. Regarding carbohydrates, we’re also in agreement that low-carb diets are not typically optimal for longevity.
Land cites research showing that moderate carbohydrate intake is associated with the lowest mortality risk. “With carbohydrates as well, it’s very commonly thought that eating too many carbs is going to be bad for your health. At least in observational studies, it’s the opposite — 40% to 55% of calories as carbohydrates is linked to the lowest risk, usually,” he says.3
Land argues that while low-carb diets can be beneficial in the short term for certain individuals, long-term carbohydrate restriction may impair metabolic flexibility:4
“In the short-term, someone might have pre-diabetes or insulin resistance, then in the short-term, it makes sense for them to maybe control the carbohydrate intake slightly to regain some of that insulin sensitivity. But chronic ketosis, chronic low-carb does impair long-term insulin sensitivity as well.”
Indeed, adequate carbohydrate intake is crucial for optimal mitochondrial function and overall health. It’s the optimal fuel for your mitochondria, but most people don’t consume enough healthy carbohydrates. If you’re metabolically healthy, most adults need 200 to 250 grams of carbohydrates daily as a minimum, while active individuals need closer to 400 grams. Chronically restricting carbohydrates can lead to increased stress hormone production and muscle breakdown.
Many people experience initial health improvements on low-carb diets, but these benefits are typically not sustainable long-term. The short-term benefits occur because you’re no longer feeding harmful bacteria in your gut, which decreases the production of endotoxins that can damage your overall health. In the long term, however, if you don’t consume enough healthy carbohydrates, your mitochondrial health will suffer.
While low-carb diets temporarily alleviate symptoms by starving harmful bacteria, they don’t resolve the underlying mitochondrial and gut health issues. A more sustainable approach involves addressing the root causes: improving mitochondrial function, reducing exposure to environmental toxins, including seed oils, endocrine-disrupting chemicals in plastics and electromagnetic fields (EMFs), and supporting a healthy gut microbiome balance.
The Most Powerful Intervention to Maintain Biological Youth
When asked how to maintain biological youth, Land states that exercise is likely the most powerful intervention:5
“Probably the single most powerful thing for biological aging is moderate exercise. Just maintaining physical activity, it just targets all the hallmarks of aging in a positive way. It improves all the organ function and it also improves the risk of all these chronic diseases as well. It targets everything that you need to do when it comes to slowing down biological aging.”
As highlighted in Dr. James O’Keefe’s landmark study,6 too much vigorous exercise can be detrimental, so finding the right balance is key. Land suggests that for vigorous exercise like resistance training, the sweet spot appears to be around 140 to 200 minutes per week.
Land has adjusted his own routine based on this data. “I’m doing about 180, maybe 150 to 180 minutes, of resistance training, and I’m training three times a week … cycling between upper body, lower body or push-pull leg split,” he says.7
I’ve also reduced my resistance training to three days per week based on potential risks of excessive training, but most people need to exercise more, not less. Moderate-intensity exercise like walking is an ideal form of physical activity, as it’s very hard to overdo it.

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The Importance of Protein Quality and Collagen
It’s not only protein quantity that’s important but also its quality and amino acid balance. Glycine and collagen, which are often overlooked, are among the most important. Land explains:8
“Glycine is conditionally essential, not essential, but that’s because your body makes 3 grams of glycine per day. But those 3 grams would be used for things, like creatine synthesis. But then you have 12 grams of glycine for collagen turnover, like optimal collagen turnover.”
Most people are deficient, as they’re likely only consuming 0 to 1 gram of collagen protein daily. About one-third of total body protein is collagen, so it’s crucial to consume adequate collagen, from foods like bone broth or grass fed ground beef, which contains connective tissue, or glycine to support connective tissue health.
The Prevalence of Insulin Resistance and Metabolic Dysfunction
The homeostasis model assessment of insulin resistance (HOMA-IR) is a test discovered in 1985, which is the gold standard for measuring insulin resistance. If you use HOMA-IR data, up to 99% of the U.S. population may have some degree of insulin resistance. Using this test is a simple way to assess your metabolic health.
You can figure out your HOMA-IR using two simple tests — your fasting blood glucose, which you can do at home, and then a fasting insulin level, which is an inexpensive test. Multiply those two numbers, and if you’re in the U.S., you divide by 405, and if you’re in Europe you have different units than the U.S. and need to divide by 22. If the result is below one, you’re not insulin resistant. The lucky less than 1% of the population does not have insulin resistance.
Land agrees this is a useful marker, while also emphasizing the importance of looking at multiple biomarkers to assess metabolic health.
The Importance of Sunlight and Vitamin D
We also discussed the critical importance of sunlight exposure and maintaining optimal vitamin D levels. Land, who lives in Estonia at a high latitude, maintains his vitamin D levels through a combination of sun exposure when possible, diet and supplementation when needed.
Sun is one of the most important factors for longevity, probably comparable to exercise. I think it’s almost biologically impossible to be healthy if you don’t have enough sun exposure. One way to help compensate, if you live in an area where year-round sunlight exposure isn’t practical, is using topical lanolin.
If you put lanolin on your skin before going in the sun, it will enhance vitamin D production from sunlight and helps reduce skin drying, cracks, wrinkles and fissures, so it’s especially useful if you’re concerned about photoaging.
However, if your diet is rich in vegetable oils, you should exercise extra caution with sun exposure. These oils contain high levels of linoleic acid (LA), an omega-6 fatty acid that easily oxidizes when exposed to ultraviolet (UV) light. When sunlight interacts with skin laden with these oils, it triggers their breakdown, resulting in inflammation and DNA damage.
Therefore, it’s advisable to limit sun exposure to earlier in the A.M. or later in the P.M. if you’ve been consuming these oils, ideally abstaining until you’ve eliminated seed oils for four to six months.
Practical Recommendations for Longevity
By focusing on foundational aspects of health — from mitochondrial function and gut health to exercise and nutrient balance — you may be able to significantly improve your long-term health outcomes. Several key strategies to optimize your health and longevity covered in the interview include:
• Exercise regularly, including moderate-intensity activity like walking and about 150 to 180 minutes of resistance training per week
• Consume adequate carbohydrates (200 to 400 g daily for most adults) from whole food sources to support metabolic health
• Prioritize protein quality, aiming for about 0.8 g per pound of lean body mass, with roughly one-third coming from collagen sources
• Get regular sun exposure and maintain optimal vitamin D levels
• Focus on gut health through diet, lifestyle and possibly targeted interventions
• Minimize exposure to environmental toxins, including seed oils, endocrine disruptors and EMFs
• Use simple tests like HOMA-IR to assess metabolic health regularly
• Prioritize sleep, stress management and overall lifestyle balance
You can find more details in Land’s book, “The Longevity Leap,” which provides a comprehensive overview of these topics and more, backed by extensive scientific references. As he describes:9
“I covered a lot of specific chronic diseases. I have a full chapter on kidney disease, metabolic syndrome, heart disease, three chapters on heart disease, actually, neurodegeneration and inflammation. I’m going into a lot of deep dives with a lot of these conditions.”
As research in longevity science continues to evolve, it’s clear that a proactive, comprehensive approach to health is crucial. Rather than seeking a single magic bullet, the path to longevity appears to lie in the consistent application of evidence-based health practices, regular self-monitoring and a willingness to adapt as new information emerges.
- 1, 2, 3, 4, 5, 7, 8, 9 Youtube, Dr. Mercola Interviews Siim Land
- 6 Missouri Medicine March-April 2023; 120(2): 155–162
Obesity Drives Alzheimer’s Through Fat Vesicles and Leptin
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/12/02/obesity-drives-alzheimers.aspx
Analysis by Dr. Joseph Mercola December 02, 2025
Story at-a-glance
- Obesity increases Alzheimer’s risk by altering how fat-derived vesicles communicate with the brain, causing amyloid proteins to misfold and form toxic plaques that damage neurons and impair cognition
- Specific lipids from obese individuals, including sphingolipids and ceramides, create oxidative stress in brain cells, reduce mitochondrial energy production, and accelerate the formation of sticky amyloid aggregates
- Excessive fat consumption promotes Alzheimer’s development, though balanced, controlled intake at lower concentrations helps inhibit amyloid aggregation and reduce disease risk
- Leptin resistance from obesity prevents this protective hormone from reaching the brain, disabling the cleanup process that normally breaks down amyloid proteins while worsening inflammation and cognitive decline
- Cellular health restoration requires eliminating four key factors — excess linoleic acid from vegetable oils, endocrine-disrupting chemicals, electromagnetic fields, and endotoxins in the gut
Despite advances in health care, the obesity epidemic in America continues to worsen. According to the latest data from the Centers for Disease Control and Prevention (CDC), 40.3% of adults are already obese,1 and nearly 7 out of 10 U.S. adults meet the criteria for obesity under a new, more comprehensive definition published in JAMA Network Open.2
The new standard — previously proposed by an international panel of experts in The Lancet Diabetes & Endocrinology3 — goes beyond body mass index (BMI) to include waist and hip measurements that reveal hidden fat conventional BMI misses.
The implications of these figures are serious, as excess body fat increases the risk of other health complications, such as diabetes and stroke.4
Now, new research shows that obesity is also a risk factor in the development of Alzheimer’s disease.5 Based on the findings, excess body fat alters how amyloid proteins fold, causing them to clump and eventually cause cognitive issues.6
Obesity Drives Brain Plaque Formation Through the Vesicles
In a study published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, researchers investigated how fat tissue communicates with the brain through microscopic particles known as vesicles. These are tiny cellular packages inside or outside the cell, and they carry fats, proteins, and genetic material.
The study’s focus was on whether these vesicles, released from human fat cells, influence the buildup of amyloid plaques — sticky clusters of protein thought to play a role in the development of Alzheimer’s disease.7
The researchers analyzed vesicles from adults with varying body fat levels and looked at how the fat-derived particles affected the behavior of amyloid proteins. Amyloid proteins are normally harmless, but when they begin to clump together, they form plaques that interfere with neuron communication.
• Obesity is a risk factor for Alzheimer’s disease — The team found that vesicles taken from people with more body fat changed the way amyloid molecules are assembled. These altered vesicles made amyloid clump faster and form denser, more toxic structures that are harder for the brain to clear away.
What makes this finding important is that it shows how your body fat obstructs cellular communication. The study revealed that when fat cells are overloaded, they send distorted signals through your vesicles. These signals carry lipids that change how brain proteins behave. In this case, those changes accelerate Alzheimer’s disease.
• The specific lipids inside the vesicles were not random — Obese individuals had vesicles rich in certain sphingolipids and ceramides — types of fats that directly influence inflammation and cell death. These compounds act like biological irritants, creating oxidative stress in neurons. Over time, that environment makes it easier for amyloid to stick together.
• The researchers also explored how these vesicles affect brain cells in a controlled lab setting — When human neural cells were exposed to vesicles from obese individuals, they observed increased cellular stress and decreased mitochondrial activity.
As you know, mitochondria are the cell’s energy factories. When they slow down, neurons lose energy, and their ability to process and clear waste — like amyloid — drops sharply. This loss of cellular energy is the same foundational issue that drives many chronic diseases, from diabetes to neurodegeneration.
• The study uncovered that these vesicles alter how amyloid folds at the molecular level — Normal amyloid proteins are flexible, but once these lipid-filled vesicles interact with them, the proteins take on a rigid structure — an abnormal configuration known to trigger plaque formation. This misfolding is what makes amyloid sticky, causing it to glue together into toxic aggregates that choke neurons.
Essentially, the lipid content of your fat vesicles rewires the shape of a brain protein that determines whether your neurons stay healthy or die.
• Too much fat of any kind is harmful — Another notable observation made by the researchers is how both saturated fat and unsaturated fat, at high levels, drive Alzheimer’s disease. In other words, even if you think you’re getting healthy fat from your diet, too much of it will eventually cause a reaction similar to consuming unhealthy fat:8
“[T]he convergent finding is that both saturated and unsaturated fatty acids can promote Aβ fibrillization at relatively high concentrations approaching lipotoxic conditions.”
• Striking a balance in fat consumption is important — In relation to the point above, controlling your fat intake can lower the risk of Alzheimer’s disease. According to the researchers:9
“Crucially some lipids exhibit concentration-dependent biphasic effects — promoting aggregation at higher levels yet inhibiting it at lower doses — highlighting the need for nuanced control of lipid microenvironments when considering therapeutic interventions or interpreting disease mechanisms.”
Another Study Examines the Obesity Angle of Alzheimer’s Disease
In a paper published in the International Journal of Molecular Sciences, researchers analyzed how obesity-driven changes in leptin directly increase the risk of dementia and Alzheimer’s disease. For context, leptin is a hormone produced by your body’s fat tissue that signals when you have eaten enough. From there, they focused on a concept called leptin resistance, which “perpetuates diseases such as dementia.”10
• What happens to your body when it begins to resist leptin — The researchers noted that leptin is strongly linked to impaired memory, slower learning, and higher risk for brain degeneration. Normally, leptin travels through the bloodstream to the brain, where it interacts with neurons in areas responsible for memory and learning, such as the hippocampus.
In healthy individuals, leptin supports the formation of new connections between brain cells and protects neurons from stress. But in people with obesity, the brain ignores leptin. The result is a double whammy — hunger control worsens, leading to more weight gain, while the brain loses one of its key protective hormones.
• Leptin influences how brain cells handle amyloid-beta — In normal conditions, leptin helps reduce amyloid levels by activating a cleanup process that breaks the protein down. However, once leptin resistance sets in, that cleanup machinery stalls. Amyloid proteins then start clumping faster, disrupting neural communication and fueling inflammation throughout the brain.
• Your weight plays a role in the secretion of leptin — The researchers showed that leptin production is affected by fat mass, and once your body becomes resistant to it, your risk of Alzheimer’s disease increases:11
“It has been shown that leptin is secreted by adipocytes and circulates in plasma in proportion to fat mass, and changes in body weight are associated with the possibility of developing AD [Alzheimer’s disease]. Therefore, it is not surprising that different investigations try to relate dysfunctional levels in leptin signalling with AD.
Thus, in some studies, low plasma leptin levels in old age have been found to be associated with an increased risk of cognitive decline and AD development.”
• Inflammation drives leptin resistance — As found in another study, obesity creates low-grade inflammation throughout the body.12 With this in mind, the featured study noted that this chronic state prevents leptin from crossing the blood-brain barrier (BBB) and into the central nervous system (CNS):13
“Low-grade inflammation due to obesity drives human C-reactive protein (CRP) production by hepatocytes in vitro and in vivo in humans. It has been found that peripheral human CRP can reduce the amount of human leptin that enters the CNS, preventing its transport across the BBB and into the median eminence. Furthermore, once inside the CNS, it reduces the physiological function of human leptin.”

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Tackle Obesity to Protect Your Brain Health
When it comes to managing obesity, the usual advice is to “eat less and move more.” However, this glosses over many important things that need to be addressed to help you lose weight effectively. The real issue runs deeper than restricting calories — it’s a cellular energy dysfunction. At its core, your mitochondria aren’t working efficiently, and that’s what drives stubborn fat, constant hunger, and low energy.
Fortunately, there’s hope to turn things around. You can rebuild your cellular health by targeting what’s interfering with it. As I discuss in my book “Your Guide to Cellular Health,” there are four major factors involved. I call them the Four E’s:
•Excess linoleic acid (LA) from vegetable oils
•Estrogen overload and endocrine-disrupting chemicals (EDCs)
•Electromagnetic fields (EMFs)
•Endotoxins from an unhealthy gut
Together, these elements act like toxins that suffocate your mitochondria and throw your metabolism into chaos. When you clear them out, your body’s natural energy systems start working again. Here’s how to do it, step-by-step.
1. Minimize vegetable oil intake — Seed oils are hiding everywhere, such as in restaurant meals, processed snacks, “healthy” dressings, and baked goods. These oils are loaded with LA, a toxin that damages your mitochondria when eaten excessively. Once your mitochondria are saturated with LA, your body can’t burn fuel efficiently, and fat begins to oxidize and impact cellular function. To start reversing the damage of LA:
•Eliminate industrial vegetable oils such as canola, soybean, sunflower, safflower, corn, and grapeseed from your pantry.
•Next, replace them with metabolically friendly fats like grass-fed butter, tallow, and ghee.
•Avoid conventionally grown chicken and pork, which are often high in LA due to their ultraprocessed feed.
•Cook your own food using healthy fats since most restaurants use vegetable oils.
•Check ingredient labels carefully — vegetable oils lurk in items like almond butter, hummus, and gluten-free chips.
Reducing LA intake is one of the fastest ways to improve mitochondrial efficiency and shift your metabolism from storing fat to burning it. I recommend keeping your overall consumption below 5 grams a day, but if you can keep it below 2 grams, that’s even better.
2. Cut back exposure on endocrine disruptors — Excess estrogen affects everyone. Too much of it interferes with thyroid function and suppresses mitochondrial activity. EDCs, which are synthetic chemicals that mimic estrogen, make the problem worse. They’re found in plastics, receipts, cosmetics, tap water, and even certain medications. You can reduce your exposure from EDCs by making a few key swaps:
•Use glass and/or stainless-steel containers instead of plastic. In addition, never heat your food in plastic.
•Choose natural personal care products without chemical fragrances or parabens.
•Limit exposure to synthetic estrogens found in birth control pills and hormone replacement therapies.
•Support hormonal balance by maintaining adequate progesterone levels — progesterone counteracts excess estrogen and promotes healthy metabolism.
3. Shield your cells from EMF damage — Electromagnetic fields emitted by cellphones, 5G towers, Wi-Fi routers, and Bluetooth devices interfere with how your cells handle calcium. Essentially, too much intracellular calcium triggers oxidative stress. You can protect yourself from EMFs with these lifestyle changes:
•Keep your phone in airplane mode when not in use, especially during your sleep.
•Turn off Wi-Fi at night and move electronics out of your bedroom.
•Choose wired internet connections whenever possible.
•Avoid Bluetooth earbuds that constantly bathe your brain in invisible radiation.
•Spend time grounding outdoors. This means walking barefoot on soil or sand to help discharge excess electrical stress naturally.
4. Repair your gut to reduce endotoxins — Gut health is an important pillar of optimal wellness, as it influences every aspect of your metabolism. When harmful bacteria overgrow, they release endotoxins — compounds that damage mitochondria and trigger inflammation throughout your body. This gut-driven toxicity slows metabolism and disrupts energy balance. To fix your gut, follow these recommendations:
•If you have gut problems, temporarily avoid high-fiber foods since fiber feeds bad bacteria in a damaged gut.
•Focus on simple, gentle carbohydrates like ripe fruit and white rice until symptoms calm down. Aim for 200 to 250 grams of healthy carbohydrates a day.
•Once your digestion stabilizes, gradually reintroduce cooked vegetables, roots, and starches. These feed beneficial bacteria that produce short-chain fatty acids like butyrate, which strengthen the gut lining and restore healthy immune balance.
Frequently Asked Questions (FAQs) About Obesity’s Influence on Alzheimer’s Disease
Q: How does obesity increase the risk of Alzheimer’s disease?
A: Obesity alters how the body communicates at the cellular level. Fat cells release vesicles, which are microscopic carriers of fats and proteins, that distort how brain proteins fold. These changes cause amyloid proteins to clump faster and form plaques in the brain, disrupting neuron communication and contributing to Alzheimer’s disease development.
Q: What role do vesicles and lipids play in Alzheimer’s disease?
A: Vesicles from obese individuals are high in harmful fats such as sphingolipids and ceramides, which promote inflammation and oxidative stress in the brain. These conditions make amyloid proteins more likely to stick together and form toxic plaques, accelerating neurodegeneration.
Q: How does leptin resistance connect obesity to dementia?
A: Leptin is a hormone that regulates hunger and supports brain health. In obesity, the brain becomes resistant to leptin, reducing its protective effects. This leads to impaired memory, slower learning, and an increased buildup of amyloid proteins, all of which heighten the risk for Alzheimer’s disease.
Q: What lifestyle factors can worsen or improve brain health related to obesity?
A: Excessive fat intake — whether from healthy or unhealthy sources — can promote harmful amyloid buildup. Balancing fat consumption and reducing obesity-related inflammation are key. Moreover, addressing cellular energy dysfunction through healthier mitochondrial function can protect both metabolic and brain health.
Q: What practical steps can help prevent obesity-related brain damage?
A: Addressing the four E’s will help manage obesity and restore optimal cellular health:
•Excess linoleic acid — Reduce intake to less than 5 grams per day.
•Endocrine disruptors (EDCs) — Products such as plastics hamper thyroid function.
•Electromagnetic field (EMF) exposure — Radiation emitted from these devices affects intracellular calcium, resulting in oxidative stress.
•Endotoxins — Harmful bacteria release these toxic byproducts, affecting mitochondrial function. Repair gut function to minimize production.
- 1 NCHS Data Brief No. 508, September 2024
- 2 JAMA Network Open October 15, 2025; 8;(10):e2537619
- 3 The Lancet Diabetes & Endocrinology January 14, 2025
- 4 NIH, Health Risks of Overweight and Obesity
- 5 Houston Methodist, October 2, 2025
- 6 NeuroscienceNews, October 2, 2025
- 7, 8, 9 Alzheimers Dement. 2025 Oct;21(10):e7060370603
- 10, 11, 13 Int J Mol Sci. 2022 May 6;23(9):5202
- 12 Cureus. 2022 Feb 28;14(2):e22711
Egg Yolk Compound Shows Promise in Osteoporosis Management
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/10/22/egg-yolk-compounds-osteoporosis.aspx
Analysis by Dr. Joseph Mercola October 22, 2025

Story at-a-glance
- Egg yolk proteins influence bone health by reducing bone breakdown and encouraging new bone growth, offering natural support against osteoporosis
- Research shows that certain egg yolk compounds shut down harmful “switches” in bone-destroying cells, helping prevent fractures and bone fragility
- The smallest protein fragments in eggs were found to be the most powerful, easily entering cells to trigger bone-building activity
- One egg yolk compound not only protected bones but also repaired fractures and improved strength in models of age-related bone loss and brittle-bone disease
- Choosing pasture-raised, low-linoleic acid eggs and combining them with collagen-rich foods and key nutrients like vitamin D, magnesium, and vitamin K2 helps build stronger bones and maintain independence as you age
Bone loss is silent until it isn’t. You wake up shorter, your back aches after simple chores, or a small misstep leads to a crack you didn’t see coming. Osteoporosis means bones lose strength and structure, which raises the odds of hip, spine, and wrist fractures and chips away at independence. Left unchecked, it reshapes daily life in ways that touch how you move, sleep, and even breathe.
Standard care leans on drugs that slow breakdown. That approach helps some people, yet it often leaves you stuck between trade-offs and side effects you didn’t sign up for. You want a path that supports everyday strength without significant risks or complexity. Your bones are living tissue that respond to the signals you send through food, sunlight, movement, and habits.
Your plan needs to restore balance — reducing excess breakdown while encouraging steady rebuilding. Food isn’t just fuel here. It’s information. Certain nutrients and proteins tell bone-building cells to get to work, and the right daily choices stack those messages in your favor.
Your job is straightforward: support your body’s natural repair systems and remove roadblocks that keep bones fragile. Eggs, long regarded as a dietary staple, are emerging as an unexpected ally in this fight. In the next section, you’ll see how this specific food source sends clear “build” signals to your skeleton and why that matters for real-world resilience.
Egg Yolk Proteins Help Guard Your Bones from Breaking Down
In a study published in Food Science of Animal Products, researchers tested whether proteins from egg yolks — broken down into smaller pieces called peptides — could affect osteoclasts, which are the cells that wear away bone. The big question was whether these natural compounds could slow or stop the bone loss that leads to osteoporosis.1
• Egg compound leads to less bone breakdown — The researchers discovered that certain water-soluble peptides in egg yolk cut down the number of bone-destroying cells. When they looked at the smallest peptides, the effect was even stronger. These tiny protein fragments not only reduced the number of cells that erode bone but also caused older ones to die off. In plain terms, that means less bone being eaten away and a better chance of keeping your skeleton strong.
• Egg compounds shut off harmful “switches” — Inside bone-destroying cells are pathways, like on/off switches, that tell them when to start breaking down bone. The smallest egg yolk peptides shut these switches off, stopping the damage at the root. If those switches stay on, bones get weaker and fractures become more likely.
• Multiple signals were stopped at once — These peptides didn’t just block one message — they cut off several signals that normally keep bone-eating cells alive and aggressive. That makes them more powerful than many drugs, which usually only work on one pathway at a time.
• The domino effect was interrupted — Normally, once those destructive messages start, they spread like falling dominoes until bone-eating enzymes get activated. With egg yolk peptides in play, that cascade was blocked before it could do damage. The end result: stronger, more resilient bones.
• Egg yolk isn’t just a food — It contains natural compounds that fight one of the biggest drivers of bone loss. Adding eggs to your diet gives your body another tool to help protect bone density and lower your risk of fractures, without relying only on risky medications.
Egg Yolk Proteins Build Stronger Bones from the Inside Out
A study published in the Journal of Functional Foods similarly looked at how natural proteins from egg yolks affect the cells in your body that create new bone.2 While earlier research showed that egg yolk proteins slow down bone breakdown, this one highlighted their role in helping bones grow stronger.
• Results showed stronger bone growth — The researchers found that egg yolk proteins helped bone-forming cells grow faster and deposit more calcium and minerals. The bones became denser and tougher, which lowers your risk of fractures.
• Small protein pieces worked best — The strongest effects came from the tiniest pieces of egg yolk protein. Because they’re so small, they easily get inside cells and kick-start the changes needed to build stronger bone tissue.
• Bone-building signals were switched on — The egg yolk proteins acted like a switch inside bone cells, telling them to grow, mature, and lay down more minerals. That signal made the cells work harder at reinforcing the skeleton, creating an ongoing cycle of bone building.
• A more balanced bone cycle — What makes this important is how it fits with the earlier findings. Some egg yolk compounds slowed bone breakdown, while these proteins boosted bone growth. Working together, they give your body both defense and rebuilding power, leaving your bones stronger than before.
Eggs contain special proteins that help your bones both resist damage and rebuild themselves. Adding eggs to your diet gives you a natural way to support bone strength, keep your mobility, and protect your independence as you age.

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Egg Yolk Protein D2 Sparks Real Bone Repair
In a study published in Regenerative Therapy, researchers identified a protein fragment from egg yolk, known as D2, that works after being swallowed and digested.3 Scientists tested it in animals with broken bones, age-related bone loss similar to menopause, and a genetic brittle-bone condition. In each case, D2 made bones stronger and tougher — exactly what you want if you need bones that hold up in daily life.
• Broken bones healed faster and stronger — Animals given the egg yolk protein daily after a fracture grew a thicker healing bridge over the break during the first month. These repairs also had denser bone in key areas, and strength tests showed they withstood more force within two weeks compared to untreated fractures. That translates into repairs that hold up better in daily movement.
• Age-related bone loss improved — In animals mimicking postmenopausal bone loss, the egg yolk protein restored some of the bone that had been lost and made the spine stronger after just a few weeks of use. Fractures in these animals also healed more steadily when the egg yolk protein was given, meaning faster recovery and fewer setbacks.
• Fragile bone disease improved — In animals bred to mimic brittle-bone disease, treatment with the egg yolk protein boosted bone volume and restored strength that had been lost. Even bone-forming cells in the lab began producing more of the key structural proteins after only a short exposure to the compound, pointing to a direct effect at the level of bone repair.
• The egg yolk protein survived digestion and spread through the body — Tests confirmed that the egg yolk protein remained active after being swallowed and entered the bloodstream, reaching organs where it could be used. That makes it practical for use outside of a lab or hospital setting.
Animals given the egg yolk protein for two weeks showed no weight changes or unusual behavior. Routine blood tests revealed no toxicity, and some measures even improved, such as lower triglycerides. This supports its role as a safe option for ongoing use.
• Bone-building cells multiplied — In both mouse and human cells, the egg yolk protein encouraged bone-forming cells to grow and mature while depositing more minerals. Even at very tiny amounts, the effect was strong, showing how powerful this protein fragment is at guiding cells to build bone.
Unlike treatments that only reduce bone breakdown, the egg yolk protein actively built new bone and improved its quality. The result was thicker healing tissue, tougher repaired fractures, and stronger bones overall — evidence of regeneration, not just protection.
How to Strengthen Your Bones Naturally with Food-Based Solutions
If your bones are thinning or you’re worried about osteoporosis, the real problem isn’t just low calcium — it’s the imbalance between bone breakdown and bone building. What the research on egg yolk proteins shows is that food has the power to help correct that imbalance at the cellular level. Your goal isn’t only to stop bone loss but also to encourage new bone growth so your skeleton stays strong. Here’s how to put this knowledge into action in your daily life.
1. Choose the right kind of eggs — Not all eggs are created equal. Factory-farmed eggs from corn- and soy-fed hens are loaded with linoleic acid (LA), a polyunsaturated fat that stirs up inflammation and damages your mitochondria — the tiny power plants inside your cells.
If you eat more than four of these eggs daily, you’re likely blowing past the recommended limit of 5 grams of LA. Switch to pasture-raised eggs, or better yet, eggs from hens that forage on grass and bugs. Some farms even use custom feed that produces eggs with far lower LA levels. These are the eggs that give you bone-strengthening compounds without the hidden damage.
2. Get collagen into your diet — About one-third of your bone structure is made of collagen, so you need a steady supply. Aim for protein to make up about 15% of your daily calories, with one-third of that coming from collagen.
The simplest way is to drink homemade bone broth from organic, grass fed bones. You can also slow-cook or pressure-cook cuts of meat rich in gelatin, or add high-quality collagen or gelatin supplements. Giving your body collagen means giving your bones the building blocks they rely on to stay tough and flexible.
3. Cover your nutrient bases — Calcium is important, but it only works well when paired with vitamin D, magnesium, and vitamin K2. Together, this combination makes sure calcium ends up in your bones and teeth — not stuck in your arteries, where it drives heart disease.
Egg yolks are especially valuable here because they are one of nature’s richest sources of vitamin K2 in the form of MK-4, the most bioactive and fast-acting subtype found in foods. This form of K2 is rare in the modern diet, yet it plays a central role in shuttling calcium into bones and away from soft tissues. Including pasture-raised egg yolks in your diet means you aren’t just getting bone-supporting proteins, you’re also giving your body one of the planet’s most potent natural sources of MK-4.
Get calcium from real foods like raw grass fed dairy, pasture-raised egg yolks, and even powdered eggshells. Add fermented foods, get daily sunlight exposure and consider a high-quality magnesium supplement — since it’s difficult to get enough from food alone — to keep your vitamin and mineral intake balanced so your bones use calcium efficiently.
4. Use movement and recovery as bone signals — Your bones respond to pressure. Walking, lifting weights, or even active gardening tells your body to “make this skeleton stronger.” But don’t forget rest — your body needs downtime to put nutrients like collagen, calcium, and egg-derived proteins to work. The cycle of stress and recovery is what drives bones to rebuild, just like it does with muscles.
5. Cut back on foods that weaken bones — Highly processed foods, sugary drinks, and packaged snacks all drive inflammation that speeds up bone loss. Every time you swap soda for water or trade fast food for whole food, you shift the balance in favor of bone building.
If you struggle with making big changes, start small. Add one more pasture-raised egg meal each week or cook up a pot of bone broth. Over time, these small changes add up, making your bones stronger and your daily life more stable.
FAQs About Egg Yolk Compounds for Osteoporosis
Q: How do eggs help protect against osteoporosis?
A: Egg yolks contain special proteins that influence bone cells directly. Some of these proteins slow down the cells that break down bone, while others stimulate the cells that build new bone. Together, they help restore balance in your skeleton, reducing bone loss and encouraging steady rebuilding.
Q: What kind of eggs should I eat for bone health?
A: Not all eggs are equal. Factory-farmed eggs from corn- and soy-fed hens are high in LA, a fat that damages your mitochondria and weakens your health. To get the bone benefits without the downsides, choose pasture-raised eggs or eggs from hens that forage naturally. These have far lower LA levels and more beneficial nutrients.
Q: Besides eggs, what other foods support stronger bones?
A: Your bones are one-third collagen and nearly all of your body’s calcium is stored in them. That means you need collagen-rich foods like bone broth, gelatin, and slow-cooked cuts of meat, along with calcium from raw grass fed dairy, egg yolks, and powdered eggshells. Pair these with vitamin D from sunlight exposure, magnesium, and vitamin K2 to make sure calcium gets delivered to your bones instead of your arteries.
Q: Can egg yolk compounds actually repair broken bones?
A: Yes, animal studies showed that a protein fragment from egg yolk not only improved bone strength but also sped up fracture healing. In models of postmenopausal bone loss and brittle-bone disease, this compound restored bone volume and durability. The research suggests egg yolk compounds don’t just protect bone — they actively rebuild it.
Q: What lifestyle habits make the biggest difference for bone health?
A: Bones respond to both movement and rest. Weight-bearing exercise like walking or resistance training tells your body to strengthen bones, while rest allows nutrients like collagen and calcium to do their repair work. Cutting out processed foods and sugary drinks reduces inflammation, and making small, steady changes — like swapping soda for water or adding an extra pasture-raised egg meal — keeps your bones stronger over time.
How Microplastics Accumulate in Your Brain and Other Organs
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/02/07/microplastic-in-the-brain.aspx
Analysis by Dr. Joseph Mercola February 07, 2025
STORY AT-A-GLANCE
- Research reveals microplastics are increasingly present in human organs, with brain tissue containing seven to 30 times more microplastic concentration than liver or kidney samples taken from 2016 and 2024 studies
- Microplastics originate from degrading plastic items and manufactured products, infiltrating oceans, soil and air, making them nearly impossible to avoid in our environment
- Nanoplastics (under 100 nanometers) cross the blood-brain barrier within two hours, contributing to inflammation and neurodegenerative diseases like Alzheimer’s through beta-amyloid peptide acceleration
- Laboratory studies indicate microplastics affect multiple body systems, causing digestive inflammation, respiratory issues, endocrine disruption and reproductive disorders, though human research remains challenging
- Practical ways to reduce exposure include filtering tap water, avoiding plastic packaging, using natural fiber clothing and choosing glass or metal containers over plastic ones
Most people enjoy eating seafood regularly or taking a relaxing, warm bath. While these seem harmless, research shows that they now come with an unseen invader — microplastics. These tiny plastic particles, often smaller than a grain of sand, are increasingly pervasive in our environment. In fact, they’re now in your brain and other organs.
Plastic Is Everywhere, and It’s Also in Your Brain
In a preprint study published in Research Square, researchers sought to find out the amount of micro- and nanoplastics (MNPs) currently embedded in the human body. For their experiment, they collected a total of 51 post-mortem tissue samples of liver, kidney and brain from 2016 and 2024. From there, the samples were subjected to a chemical test that created solid materials namely, polymer-based solids that can be detected by special equipment.1
The researchers discovered that the brain contains the highest concentration of MNPs — around seven to 30 times more — compared to liver or kidney samples. Moreover, the MNPs found in the brain typically range in the nanometer scale with shard-like properties. According to their findings:2
“A non-parametric analysis of variance (Kruskal-Wallis) confirmed that MNP concentrations in brains were significantly greater than all other tissues (P<0.0001).
Furthermore, from 2016 to 2024, there was a significant increase in MNP concentrations in both livers and brains. The predominant polymer found in all tissues was polyethylene, which independently displayed similarly increasing trends from 2016 to 2024 in the liver and brain.
The proportion of polyethylene in the brain (74%) appeared significantly greater relative to other polymers in comparison to the liver and kidney (44% to 57%), although kidney samples from 2024 also had increased relative PE (71%) …
The concentrations in liver and kidney were not as high (relative to brains) as we would have suspected, as these are ‘front line’ organs for xenobiotic uptake and clearance. That said, the lipophilic nature of plastics may make them easily handled by the liver, which has a major role in uptake and repackaging of dietary triglycerides and cholesterol.”
However, the researchers didn’t dive into the health effects of MNPs on human health, noting that this topic is better suited for a new study.3
Where Do Microplastics Come From?
Microplastics originate from various sources. Some are created when larger plastic items like bottles, bags and food packaging break down due to sunlight exposure, weathering and physical abrasion. Think of a plastic bottle left under the sun — it becomes brittle and eventually fragments into smaller and smaller pieces. These fragments are microplastics.
In other cases, microplastics are manufactured intentionally, such as microbeads used in certain cosmetics and personal care products (although many countries have now banned their use).
These tiny plastic particles have infiltrated nearly every corner of the environment. They’re found in our oceans, rivers and lakes, polluting the water and harming marine life. They’re also present in the soil, affecting plant growth and entering our food supply. Even the air you breathe contains microplastics, which lodge into your lungs when inhaled.4 This widespread contamination makes it nearly impossible to avoid exposure entirely.
When it comes to food, microplastics enter your system through various pathways. Marine animals, both predator and prey, ingest microplastics in the ocean, and these particles then accumulate in their tissues. This means that when you consume seafood, you’re also ingesting these microplastics.5
Similarly, microplastics in the soil are absorbed by plants, contaminating the growth and nutrition of fruits, vegetables and other crops.6 Plastic packaging used for food and beverages also shed microplastics, further contributing to your exposure.
Beyond food and water, you’ll encounter microplastics in many other everyday products, many of which you most likely own. For example, synthetic clothing, like polyester and nylon, sheds tiny plastic fibers during washing. These microfibers are a significant source of microplastic pollution in our waterways. While microbeads have been banned in many countries, some industrial processes still contribute to microplastic pollution.
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Microplastics and the Brain
Again, one of the most concerning aspects of microplastic pollution is their ability to reach the brain. The brain is protected by the blood-brain barrier, which normally prevents many harmful substances from entering the delicate brain tissue. However, nanoplastics (less than 100 nanometers), are able to cross this barrier7 in just two hours after they enter the body.
The concern is that these microscopic particles pile up in the brain over time, a process known as bioaccumulation. While research regarding the health impacts of MNPs is not definite yet, researchers theorizes that they provoke the immune system, thereby causing inflammation.8 Chronic inflammation in the brain has been linked to various neurological problems.
While research is still ongoing, there is concern that long-term exposure to MNPs and their subsequent accumulation in the brain contribute to the development of neurodegenerative diseases like Alzheimer’s.
As noted in an animal study published in the Journal of Hazardous Materials, once nanoplastics cross the blood-brain barrier, they contribute to neurotoxicity by accelerating the spread of beta-amyloid peptides, which is the main pathogenic protein of this condition.9
Unsolved Mystery — Researching the Impact of Microplastics
Studying the health effects of microplastics in humans is a complex challenge. It’s difficult to assess the impact of microplastics on human health because of ethical concerns.
This has caused scientists to resort to in vivo, in vitro and animal test models to monitor and study the impact of microplastics.10 But from this research, we’re now able to infer the likely consequences of microplastics on human health. Here’s what a 2023 study published in Yonsei Medical Journal have compiled:11
- Digestive system — Microplastics cause physical irritation to the gastrointestinal tract, leading to inflammation and digestive symptoms. This results in an imbalance in your gut microbiota, causing abdominal pain, bloating and changes in bowel habits.
- Respiratory system — The inhalation of microplastics causes oxidative stress in the airways, leading to coughing, sneezing and shortness of breath. Fatigue and dizziness will also occur due to low blood oxygen concentration.
- Endocrine health — Microplastics interfere with hormone health, disrupting your endocrine function. This leads to metabolic disorders, developmental problems and even lower fertility rates. Much of the reason for this is because microplastics typically have bisphenol A, a chemical that greatly affects endocrine health and the reproductive system.
Addressing the issue of microplastic pollution and its potential health impact requires collaborative efforts between scientists, governments and industries. Scientists need to conduct more research to understand the health effects, governments need to implement policies to reduce plastic pollution, and industries need to develop more sustainable alternatives to plastic.
“Considering the ubiquitous nature and long persistence of microplastics, it is necessary to make efforts to mitigate their exposure given their effects on entire generations and multiple generations.
In the future, in-depth research on the pollution status and hazards of marine microplastics, as well as the correlation between exposure to microplastics and diseases in humans, should be conducted; and based on these findings, human health should be protected by preventing and managing microplastics,” the researchers concluded.12
Take Control of Your Health in a Plastic World
While research is still ongoing, it’s clear that having foreign, microscopic objects embedded in your organs is not good for your health, or anyone’s health for that matter. Therefore, it’s important to take proactive steps to minimize your exposure while scientists continue to investigate the long-term effects.
Addressing the problem of microplastic pollution requires a collective effort. By combining individual actions with broader policy changes and industry innovation, we’ll move towards a future with less plastic contamination and a healthier environment for everyone. But in the meantime, implementing practical strategies at a personal level will help reduce microplastic exposure. Here are my top recommendations:
| Filter your tap water and avoid water bottled in plastic — If you need to buy bottled water, opt for glass bottles. Also make sure the filter you use to purify your tap water can filter out microplastics. |
| Boil hard tap water — If you have hard tap water, consider boiling it before using it for cooking or drinking, as hard water traps more microplastics. Recent research shows boiling hard tap water for five minutes removes up to 90% of the microplastics in the water. |
| Avoid plastic packaging — Opt for products packaged in glass, metal, or paper instead of plastic. This can significantly reduce the amount of plastic waste that breaks down into microplastics. At home, use wax paper, parchment paper or paper bags to store foods rather than plastic wrap. |
| Use reusable containers — Replace single-use plastic bottles, cups, and containers with reusable alternatives made from safer materials like stainless steel or glass. |
| Never microwave plastics — Heat can cause plastics to leach chemicals into food. Use glass or ceramic containers for microwaving. |
| Avoid plastic cutting boards — Use a wooden or glass cutting board instead. |
| Opt for natural fibers — Whenever possible, choose clothing and other textile products made from natural fibers like cotton, wool and linen, as synthetic fabrics such as polyester shed microfibers and leach xenoestrogens. |
| Wash synthetic clothes less frequently — When washing synthetic textiles, use a microfiber filter in your washing machine to trap synthetic fibers and prevent them from entering the water system. |
| Opt for food grade cosmetics and personal care products — Some cosmetics, toothpastes, and personal care products contain microbeads or other plastic particles. Look for products free of these materials. Ideally, opt for all-natural, food grade products. |
| Choose your children’s toys carefully — Replace plastic toys with those made from safe, nontoxic and sustainable materials. |
| Opt for natural cleaning products — Chemical cleaning products like soaps, cleansers and surface cleaners, usually contain microplastics and phthalates that affect your endocrine system. Replace them with natural alternatives like white vinegar, baking soda and essential oils. |
- 1, 2, 3 Res Sq [Preprint]. 2024 May 6:rs.3.rs-4345687, Results and Discussion
- 4 Journal of Hazardous Materials Volume 416, 15 August 2021, 126124, Abstract
- 5 NOAA, Ingestion
- 6 Journal of Hazardous Materials Advances Volume 17, February 2025, 100528, Effects of Microplastics on Agricultural Soils
- 7 Nanomaterials (Basel). 2023 Apr 19;13(8):1404, Abstract
- 8 Journal of Translational Medicine Volume 22, Article number: 959 (2024), Abstract
- 9 Journal of Hazardous Materials Volume 465, 5 March 2024, 133518, Abstract
- 10 Science of The Total Environment Volume 946, 10 October 2024, 174215, Toxicity to the Digestive System
- 11, 12 Yonsei Med J. 2023 Apr 20;64(5):301–308
Unlocking the Power of Methylene Blue
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/01/08/power-of-methylene-blue.aspx
Analysis by Dr. Joseph Mercola January 08, 2025
STORY AT-A-GLANCE
- Methylene blue enhances cellular energy production by integrating into the electron transport chain, cycling between oxidized and reduced forms to improve mitochondrial efficiency and resolve metabolic issues
- Clinical trials show methylene blue’s role in treating neurological conditions, including slowing progression of Alzheimer’s at doses of 16 mg daily
- Studies indicate methylene blue’s effectiveness in treating septic shock, reducing mortality rates, shortening hospital stays and improving blood pressure without significant adverse effects
- Research reveals methylene blue’s anticancer properties, particularly in chemoresistant ovarian tumors, by selectively targeting cancer cell mitochondria while sparing healthy cells from damage
- Safe dosage ranges from 5 mg to 50 mg daily, but requires medical supervision due to potential interactions with SSRIs and risks for those with kidney issues or G6PD deficiency
Few substances have captured my attention as profoundly as methylene blue. Earlier this year, I engaged in an in-depth discussion with Georgi Dinkov, a respected expert in metabolic health, who shed light on the multifaceted benefits of this remarkable compound.1
Methylene blue, a quinone-like molecule, is not just another supplement; it’s a powerful agent that can play an important role in cellular metabolism. By accepting and donating electrons, methylene blue enhances mitochondrial function, addressing issues like reductive stress that are often overlooked in conventional medicine.
This conversation with Dinkov highlights methylene blue’s role in reaching optimal health and treating a myriad of conditions, ranging from mental health disorders to acute medical emergencies.
Methylene Blue and the Electron Transport Chain
Methylene blue has the ability to integrate seamlessly into the electron transport chain (ETC), which plays a role in cellular energy generation. Unlike traditional antioxidants that either donate or accept electrons and subsequently require excretion, methylene blue possesses the unique capability to cycle between its oxidized and reduced forms indefinitely.
This continuous electron transfer process ensures sustained improvement in mitochondrial efficiency, which is key for energy production and overall cellular health. Dinkov emphasized that methylene blue acts as an emergency oxidant, stepping in to accept electrons even when essential co-actors like NAD+ are deficient.
This makes methylene blue capable of resolving metabolic issues associated with electron buildup and reductive stress. By maintaining the flow of electrons within the ETC, methylene blue prevents the stagnation that leads to cellular dysfunction and various health problems.
Methylene Blue for Enhanced Brain Health
The therapeutic potential of methylene blue is vast and varied, extending across a spectrum of neurological and psychological conditions. Dinkov shared insights into several studies where methylene blue, even at relatively low doses of 15 to 50 milligrams (mg), demonstrated significant benefits in treating treatment-resistant depression and psychosis.2
These findings are groundbreaking, suggesting that methylene blue enhances cognitive function and stabilizes mood by improving mitochondrial performance and reducing oxidative stress in the brain. Methylene blue enhances the benefits of niacinamide (vitamin B3) on brain health and metabolism.3 Furthermore, in terms of neurodegenerative diseases, methylene blue has shown remarkable promise.
A modified version of methylene blue, developed by a UK-based company, has been patented for Alzheimer’s treatment. Clinical trials have reported an astounding 80% reversal of Alzheimer’s symptoms in participants, according to Dinkov, highlighting methylene blue’s ability to not only halt but also reverse cognitive decline.4
These applications underscore the compound’s role in enhancing brain health by ensuring efficient energy production and mitigating the damaging effects of oxidative stress. A stabilized form of methylene blue known as hydromethylthionine (LMTM) also shows promise in treating mild to moderate Alzheimer’s disease.5
Unlike traditional methylene blue, LMTM is a stabilized dihydromesylate salt, which offers improved pharmacokinetic properties, including better brain uptake and longer half-life in humans. The study involved 1,162 patients across two Phase III trials and revealed a concentration-dependent activity of LMTM on cognitive decline and brain atrophy.
Notably, the optimal therapeutic dose was identified around 16 mg a day, which maximizes cognitive benefits without the diminishing returns observed at higher doses of 150 to 250 mg per day. This plateau effect underscores that beyond a certain concentration, no additional benefits are observed, aligning with the study’s findings that higher doses do not confer extra advantages.
Moreover, LMTM demonstrated significant benefits both alone and as an add-on to existing Alzheimer’s treatments. Patients receiving LMTM showed reduced cognitive decline and slower brain atrophy compared to those with lower plasma levels. This suggests that even at lower, more manageable doses, LMTM effectively slows the progression of Alzheimer’s by enhancing mitochondrial function.

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Methylene Blue’s Life-Saving Benefits in Septic Shock
Expanding methylene blue’s therapeutic applications, a systematic review and meta-analysis published in Critical Care Explorations evaluated the efficacy and safety of methylene blue in patients with septic shock,6 a condition with high mortality rates.
The analysis included six randomized controlled trials encompassing 302 patients and sought to determine whether methylene blue administration could improve outcomes compared to placebo or usual care.
The findings suggest that methylene blue may significantly reduce short-term mortality, shorten the duration of vasopressor use by approximately 31 hours and decrease hospital length of stay by about two days.
Additionally, methylene blue was associated with an increase in mean arterial pressure at six hours post-administration. Importantly, the study did not find an increase in adverse events.
Methylene blue functions by inhibiting endothelial and inducible nitric oxide synthase, thereby counteracting the profound vasodilation characteristic of septic shock. By restoring vascular tone, methylene blue helps maintain adequate organ perfusion and oxygenation, which are necessary for patient survival.
Methylene Blue for Cancer Treatment — Targeting Ovarian Tumors
Research is also exploring methylene blue as a treatment for ovarian cancer, particularly in cases resistant to conventional chemotherapies. A study published in Cancers (Basel) used a carboplatin-resistant ovarian cancer tumor model in mice to assess the impact of methylene blue on tumor growth.7
The findings revealed a significant in vivo reduction in tumor proliferation among mice treated with methylene blue compared to those receiving carboplatin alone or no treatment. Specifically, methylene blue demonstrated superior tumor suppression, highlighting its effectiveness against chemoresistant ovarian tumors.
Further in vitro analyses provided insights into the mechanisms underlying methylene blue’s anticancer effects. The study examined the impact of methylene blue on mitochondrial energetics in both cancerous and normal cell lines. Methylene blue altered the oxygen consumption rate and mitochondrial membrane potential in the ovarian cancer cells, suggesting enhanced mitochondrial respiration and induction of apoptosis.
In contrast, normal cells exhibited a markedly different response, with less pronounced changes in mitochondrial function, indicating a selective targeting of cancer cell mitochondria by methylene blue.
The combination of methylene blue with a mixture of lipoic acid and hydroxycitrate and carboplatin was investigated to evaluate synergistic effects. While the combination therapy showed a modest enhancement in tumor response compared to methylene blue alone, the difference was not statistically significant. Importantly, the metabolic therapies did not induce toxicity or weight loss in the treated mice, underscoring the favorable safety profile of methylene blue-based treatments.
By targeting the altered mitochondrial function and inducing apoptosis in chemoresistant cancer cells, methylene blue offers a novel approach that could improve treatment outcomes for patients facing limited options. The differential response between cancerous and normal cells also suggests that methylene blue selectively targets tumor metabolism, minimizing harm to healthy tissues.
Methylene Blue in Emergency Situations, Including Heart Attack
Beyond its chronic health benefits, methylene blue proves invaluable in acute medical emergencies. Dinkov elaborated on its effectiveness in treating conditions such as cyanide and carbon monoxide poisoning. In these scenarios, methylene blue acts swiftly to restore cellular respiration by accepting electrons and facilitating the utilization of oxygen, thereby reversing the toxic effects of these poisons.
I also recommend having methylene blue readily available at home in case of a heart attack. While sudden death is the most common symptom of heart disease, surviving individuals face the serious threat of reperfusion injury, where cellular dysfunction and death may worsen following the restoration of blood flow.
Methylene blue administration significantly mitigates tissue damage; however, proper dosage is important to avoid overdose. Administer methylene blue within minutes of the cardiac event to meet the critical time threshold.
In cases of stroke or heart attack, even a single dose below 50 mg may be life-saving. This rapid benefit makes methylene blue an essential tool in emergency medicine, offering a quick and efficient means to counteract metabolic crises.
I strongly advocate for the inclusion of methylene blue in emergency kits, as its ability to stabilize metabolic function swiftly provides an additional layer of protection against sudden, life-threatening metabolic disturbances. The potential of methylene blue to act as a universal antidote in various poisoning scenarios underscores its significance in both medical and emergency settings.
Methylene Blue and Antiaging Benefits
The antiaging properties of methylene blue is another exciting frontier that Dinkov passionately discussed.8 Studies have indicated that methylene blue reverses aging in human cells by maintaining optimal mitochondrial function and reducing oxidative damage, which are key factors in the aging process. Daily doses ranging from 5 mg to 50 mg help achieve the necessary concentration for these benefits without causing discoloration in urine or tissues.
Moreover, when combined with red light therapy, methylene blue’s effects are significantly amplified. This synergy promotes cellular rejuvenation and longevity by enhancing mitochondrial efficiency and reducing oxidative stress, thereby combating the visible signs of aging and supporting overall cellular health.
Dinkov mentioned an innovative approach where methylene blue is used in a dilution similar to mouthwash as an oral rinse, offering antiseptic benefits without the harsh side effects of conventional mouthwashes.9 This application not only leverages methylene blue’s metabolic benefits but also integrates it into daily routines for enhanced health and longevity.
Beyond the primary benefits discussed, methylene blue exhibits several other promising properties that could significantly enhance various aspects of health and medicine. Dinkov mentioned that methylene blue acts as a powerful aromatase inhibitor at sub-micromolar concentrations, which could have implications in managing hormone-related conditions.10
Additionally, methylene blue’s ability to enhance the flow of electrons within the electron transport chain makes it a versatile supplement for addressing a wide range of metabolic disturbances. Dinkov also introduced the concept of the “Methylene Blue Test of Health,” where the dosage at which an individual’s urine begins to turn blue serves as an indicator of their metabolic health.11
A lower dosage threshold for this coloration suggests better metabolic function, while higher thresholds may indicate underlying health issues such as cancer or diabetes, which are characterized by extreme reduction states in cells.
This innovative approach provides a simple yet effective method for individuals to monitor their metabolic health and take proactive measures to address any issues. As research continues to unfold, the full spectrum of methylene blue’s benefits will likely expand, positioning it as a cornerstone in both preventative and therapeutic health strategies.
Safety and Dosage Considerations
While the benefits of methylene blue are substantial, Dinkov highlighted the importance of appropriate dosing to avoid severe adverse effects that may occur with high doses, particularly serotonin syndrome — a fatal condition caused by excessive serotonin levels in the brain.
Methylene blue is a potent monoamine oxidase type A (MAO-A) inhibitor, which may dangerously elevate serotonin levels when combined with selective serotonin reuptake inhibitors (SSRIs) or other serotonergic drugs. I would advise strong caution for anyone ever to take an SSRI drug, as I don’t believe anyone benefits from them.
Further, at doses exceeding 30 mg to 50 mg, methylene blue may cause temporary blue discoloration of urine and, occasionally, the tongue. Although harmless, this effect is startling if unexpected. High doses may also interfere with pulse oximeter readings, leading to inaccurate assessments of blood oxygen levels.
Individuals with severe renal insufficiency should use methylene blue with caution and under close medical supervision, as impaired kidney function affects drug clearance. Additionally, methylene blue is contraindicated for patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency due to the risk of hemolytic anemia.
Common side effects associated with methylene blue include mild and transient gastrointestinal discomfort, such as nausea and diarrhea. Allergic reactions, ranging from skin rashes to life-threatening anaphylaxis, are also possible. Neurological effects like headaches and confusion may occur.
Cardiovascular effects, though less common, may include increased blood pressure and palpitations. Furthermore, methylene blue interacts with various medications, particularly antidepressants and antimalarials, altering their efficacy or causing adverse reactions.
To mitigate these risks, Dinkov recommends lower daily doses of methylene blue, typically between 5 mg to 15 mg, especially for long-term use. These dosages are sufficient to harness its metabolic benefits without significantly increasing the risk of serotonin syndrome. Additionally, Dinkov pointed out that while higher doses (up to 50 mg) have shown efficacy in certain therapeutic applications, they must be approached with caution and under professional supervision.
If you’re considering methylene blue supplementation, consult with a knowledgeable health care professional to tailor the dosage to your specific needs and avoid harmful interactions with other medications.
My Recommendations for Methylene Blue Use
There are three types of methylene blue typically sold — industrial-grade, chemical-grade (laboratory-grade) and pharmaceutical-grade. The only one you should use is the pharmaceutical-grade variety in solid, capsule or tablet form. Avoid using any solutions of methylene blue as dissolving it in water leads to a significant decrease in its effectiveness after 48 to 72 hours.
Methylene blue is a popular choice in aquarium maintenance due to its antifungal, antiparasitic and oxygen-transporting capabilities. It’s commonly used to alleviate fish stress, combat fungal infections and eliminate external parasites like Ich (white spot disease). However, aquarium-grade methylene blue often contains harmful contaminants, including heavy metals, which pose serious health risks to your aquatic pets.
To ensure the safety and well-being of your pets, I strongly advise against using methylene blue products designed for aquariums in any pet-related applications. Instead, choose pharmaceutical-grade methylene blue, which undergoes rigorous testing to confirm it is free from harmful impurities.
Personally, I have eliminated my regular intake of methylene blue, finding that daily walks by the ocean are an excellent way to manage reductive stress naturally. However, in scenarios where I might not have access to the ocean, I would consider taking 5 mg of methylene blue daily, adjusting to 3 mg if I were 75 pounds lighter in weight, and doing so six days a week.
It’s essential to emphasize that the appropriate and legal way to use methylene blue is through a prescription from a qualified physician. If you’re contemplating the use of methylene blue for your health, I strongly encourage you to consult with your doctor to determine if it’s suitable for your specific needs and circumstances.
Proteins Linked to Alzheimer’s Disease Now Observable in Real Time
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/12/31/proteins-linked-to-alzheimers-disease.aspx
Analysis by Dr. Joseph Mercola December 31, 2024
STORY AT-A-GLANCE
- Nearly 7 million Americans currently have Alzheimer’s disease. Projections show this number will increase to 13 million by 2050, according to the Alzheimer’s Association
- A study used liquid-based atomic force microscopy to visualize beta-amyloid protein development in real-time, identifying “superspreader” fibrils that accelerate disease progression across brain tissue
- Three major toxins that damage mitochondrial function are excessive linoleic acid (LA) intake, endocrine-disrupting chemicals from microplastics and electromagnetic field (EMF) exposure from electronic devices
- Certain pathogenic bacteria strains like Collinsella, Lachnospira, and Veillonella increase Alzheimer’s risk, while probiotic strains like Eubacterium nodatum produce protective benefits through short-chain fatty acids
- Prevention strategies include optimizing vitamin D levels, maintaining low fasting insulin, avoiding gluten and casein, exercising regularly and challenging your mind with new skills
According to the Alzheimer’s Association, nearly 7 million Americans are currently diagnosed with Alzheimer’s disease, the most common type of dementia. Furthermore, the situation is expected to worsen — by 2050, around 13 million Americans are projected to be diagnosed with this neurodegenerative disease.1
Alzheimer’s disease remains challenging for modern medicine to diagnose and treat. However, a recent study2 has made a breakthrough in understanding how the disease progresses, creating a foundation for future clinicians and researchers to build upon to create better treatment plans.
A Breakthrough in Observing Alzheimer’s Disease Progression
In a study3 published in Science Advances, researchers were able to visualize the development of amyloid-beta proteins to see how Alzheimer’s disease spreads. Beta-amyloid proteins have been observed using a variety of methods, several of which were reviewed in the study:
“Methodological advances have been able to resolve the ultrastructure of Aβ and tau protein aggregates formed along the primary nucleation pathway using cryo-electron microscopy (cryo-EM) and solid-state nuclear magnetic resonance spectroscopy.
Likewise, the aggregation kinetics and toxicity of these proteins have been investigated using ultrasensitive fluorescence-based assays, nanopore devices, and circular dichroism.
Details on the morphology, on-surface assembly, and chemical structure of Aβ and tau protein aggregates have also been made accessible using standard atomic force microscopy (AFM), video-rate AFM, and infrared spectroscopy.”
For context, beta-amyloid proteins aggregate in the brain, and they’re suspected of playing a key role in the development of Alzheimer’s. Hence, they’re what researchers usually focus on to find therapeutic solutions.4 Previous staining methods used for observational analysis distort the protein structures.
To find new ways to analyze the mechanisms of Alzheimer’s disease, the team used liquid-based atomic force microscopy (AFM). As explained by the authors:5
“Building on the observations from previous secondary nucleation studies, we postulated that it should be feasible with a high-resolution AFM to record elementary information such as oligomer size, shape, and adsorption site on individual fibrils with sub-10-nm diameter. Operating the AFM in an aqueous solution medium would allow the diffusion of oligomers on the fibril surface.”
Tracking the Progression of Alzheimer’s Disease in Real Time
Once the team settled on the methodology, they moved onto testing. To start, they agitated beta-amyloid samples for 30 minutes at room temperature. Then, they set up different experiments to observe the growth and progression protein aggregates from 30 seconds to 250 hours:6
“Nanoscale imaging supported by atomic-scale molecular simulations tracked the adsorption and proliferation of oligomeric assemblies at nonperiodically spaced catalytic sites on the fibril surface. Upon confirming that fibril edges are preferential binding sites for oligomers during embryonic stages, the secondary fibrillar size changes were quantified during the growth stages.”
From their observations of protein fibril development in real time, they were able to classify some of them as “superspreaders” based on their surface anatomy. Specifically, these superspreaders “feature highly active edges and surfaces where new protein molecules accumulate, eventually forming longer fibrils that may spread across brain tissue.”
As they spread, more protein aggregation occurs, effectively progressing the hallmarks of Alzheimer’s disease. Ultimately, the research team hopes that this breakthrough in fibril analysis will be able to help improve the diagnosis and monitoring of neurodegenerative diseases. “This work brings us another step closer to better understanding how these proteins spread in brain tissue of Alzheimer’s disease,” says Peter Nirmalraj, one of the authors of the study.7
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Mitochondrial Dysfunction Is at the Heart of Alzheimer’s Disease
As researchers continue to come up with new tools to help diagnose and treat Alzheimer’s better, following a healthy lifestyle is important to reduce your risk. Prevention is by far your best option. I believe addressing mitochondrial dysfunction is key to protecting cognitive function, which is achieved by improving your cellular health.
The first thing to address is your diet. A study published in Neurology noted that eating an inflammatory diet raises your risk of dementia.8 In addition, I believe that there are three major toxins damaging your mitochondrial function by affecting intracellular calcium, which subsequently impacts cellular health.
Essentially, when calcium within your cells increase, your body produces superoxide and nitric oxide. These two combine to form peroxynitrite, a potent reactive oxygen species that contributes to poor health. Three pervasive toxins that raise intracellular calcium levels and drive peroxynitrite formation include:
1. Excessive linoleic acid (LA) consumption — LA is an omega-6 polyunsaturated fat (PUFA) found most abundantly in seed and vegetable oils and processed foods. I believe it is one of the most pernicious toxins of the Western diet, driving inflammation and chronic diseases among the populace.
Overconsumption negatively impacts your metabolic rate and gut microbiome, which are key factors for optimal health. To protect your health, I recommend keeping your LA intake below 5 grams a day.
Note that it’s virtually impossible to avoid LA, as most foods inherently have them, and your body does need some of it. The key is to avoid excess.
2. Endocrine-disrupting chemicals (EDCs) — Microplastics are so prevalent in our environment that humans ingest approximately a credit card’s worth of plastic every week.9 These microplastics contain endocrine-disrupting chemicals (EDCs), particularly phthalates and bisphenol A (BPA).
When these substances enter the body, they activate and overstimulate estrogen receptors. This increased estrogen activity raises intracellular calcium levels, which in turn leads to peroxynitrite formation.
To reduce your exposure, the first line of defense is minimizing your dependence on plastic products, such as bottled water and single-use food containers. Bringing a glass container and reusable tumbler for your water when going outside will significantly cut down your plastic usage. For additional strategies, read my article “How Microplastics Affect Your Reproductive Health.”
3. Electromagnetic field (EMF) exposure — The devices you use every day emit EMFs that activate voltage-gated calcium channel (VGCC) receptors within your cells. This triggers calcium influx, catalyzing peroxynitrite production.10
Major sources of EMFs include your cellphone, Bluetooth devices, wireless computer accessories and smart appliances that connect to your home’s Wi-Fi. For practical strategies on protecting yourself from EMFs, read my article “Study: Phone Radiation Kills Cheek Cells.”
Keep Your Gut Flora Healthy to Protect Cognitive Function
Your gut microbiome is one of the most crucial aspects for achieving optimal health. Research11 has shown that it plays a role in various functions, such as modulating the immune system, glucose metabolism and reducing insulin resistance. In addition to these findings, a study12 published in Scientific Reports showed that certain bacterial strains in the gut increased the risk of Alzheimer’s disease.
In the study, the researchers singled out strains such as Collinsella, Lachnospira and Veillonella as contributors to the risk of Alzheimer’s disease. According to the study authors:13
“In our analyses, Collinsella from the phylum Actinobacteria was identified as a risk factor for AD (Alzheimer’s disease) in both the discovery and replication samples … Importantly, an increased abundance of this genus has also been observed in AD transgenic mice and AD patients. Our findings provide evidence at the human genome-wide level of a connection between Collinsella and AD that supports previous observational studies …
In addition, we identified two Firmicutes genera as risk factors for AD (Lachnospira and Veillonella), with Veillonella being validated in the replication sample. Recently, it was reported that AD patients have an abundance of Veillonella in their oral microbiome. In the gut, it has been shown that an overabundance of species like V.parvula promotes intestinal inflammation …
The dual association of oral and gut abundance of Veillonella with disease points to this genus as a target for therapeutics and a potential bridge between conditions like gut inflammation and periodontitis with AD.”
The researchers also identified strains that provide protective benefits against Alzheimer’s disease, such as Eubacterium nodatum and Eisenbergiella. These produce short-chain fatty acids (SCFAs), particularly butyrate, from dietary carbohydrates.14
Butyrate nourishes your colonic epithelial cells, reinforcing the intestinal barrier. SCFAs also stimulate mucin production, creating a protective shield against harmful bacteria. Akkermansia also produces SCFAs, and research has shown that Alzheimer’s patients tend to have very low levels of this important keystone species.15
Carbohydrates Help Support Your Gut Health
Nurturing oxygen-intolerant beneficial bacteria, including Akkermansia, will strengthen your intestinal lining to create an environment that promotes overall wellness. On the other hand, low levels of oxygen-intolerant bacteria will lead to increased intestinal permeability, also known as leaky gut.
This causes openings in the intestinal barrier, allowing toxins, undigested food particles and harmful microbes to enter your bloodstream, resulting in systemic inflammation and chronic health issues.
To create an environment that allows your gut microbiome to thrive, increasing your intake of carbohydrates is a priority. Ashley Armstong provides some good recommendations for gut-friendly carbs, which include:
- Well-cooked white rice
- Sourdough bread
- Root vegetables like potatoes and sweet potatoes
- Fresh, ripe fruits
- Masa harina, or traditionally made tortillas
Also remember to include fermented foods. I’m a big believer of making your own fermented vegetables at home because they’re both simple and cost-effective to prepare. I don’t recommend buying commercially prepared fermented vegetables, as they often contain artificial sweeteners and additives, negating the benefits of fermented foods in the first place.
Additional Strategies to Prevent Alzheimer’s Disease
Aside from optimizing your gut health and mitochondrial function, there’s a plethora of helpful Alzheimer’s prevention strategies, several of which are outlined below:
| Avoid gluten and casein (primarily wheat and pasteurized dairy, but not dairy fat, such as butter) — As noted in a 2022 study,16 your blood-brain barrier is negatively affected by gluten. When bacteria enter your blood stream, the risk of Alzheimer’s disease increases. Other cognitive disorders are linked to a weakened blood-brain barrier as well, such as Parkinson’s disease, anxiety and depression. |
| Make sure you’re getting enough animal-based omega-3 fats — Omega-3 fats, namely EPA and DHA, help by preventing cell damage caused by Alzheimer’s disease, thereby slowing down its progression and lowering your risk of developing the disorder. That said, omega-3s are PUFAs, so don’t overdo it. |
| Optimize your vitamin D level with safe sun exposure — Strong links between low levels of vitamin D in Alzheimer’s patients and poor outcomes on cognitive tests have been revealed. In a 2023 study,17 increasing vitamin D reduced dementia risk by 40%.
The best way to get vitamin D is through sensible sun exposure, aiming for a blood level between 60 ng/mL and 80 ng/mL. However, you need to purge seed oils from your body before going into the sun at solar noon. The LA in your skin oxidizes when exposed to sunlight, causing inflammation and skin damage. To protect your skin, avoid sun exposure during solar noon for four to six months as you work on removing LA from your body. Stick to sunlight during early morning and late afternoon in the meantime. For additional skin defense, your can take astaxanthin, a low-dose aspirin or molecular hydrogen. Niacinamide cream will also lower your risk of skin damage. |
| Keep your fasting insulin levels below 3 — Insulin resistance is linked to accelerated brain aging, as well as neurodegeneration.18 |
| Eat a nutritious diet, rich in folate — Vegetables, without question, are your best form of folate. Avoid supplements like folic acid, which is the inferior synthetic version of folate. Research shows that folate is a protective factor against Alzheimer’s disease.19 |
| Avoid and eliminate mercury and aluminum from your body — Dental amalgam fillings, which are 50% mercury by weight, are one of the major sources of heavy metal toxicity. Make sure you use a biological dentist to have your amalgams removed. Sources of aluminum include antiperspirants, nonstick cookware and vaccine adjuvants. |
| Make sure your iron isn’t elevated and donate blood if it is — A study20 published in Aging Medicine shows that excess iron increases your risk of Alzheimer’s disease by initiating the Fenton reaction, leading to increased oxidative stress. |
| Exercise regularly — Exercise triggers beneficial changes that support cognitive function. Particularly, it’s been shown to improve blood flow to the brain, leading to an increase in biomarkers related to improved neuronal plasticity and better cell survival.21 |
| Eat blueberries and other antioxidant-rich foods — Wild blueberries, which have high anthocyanin and antioxidant content, are known to guard against neurological diseases. |
| Challenge your mind daily — Mental stimulation, such as learning to play a musical instrument, is associated with a decreased risk of Alzheimer’s.22 |
| Avoid anticholinergics and statin drugs — Drugs that block acetylcholine, a nervous system neurotransmitter, have been shown to increase your risk of dementia. These drugs include certain nighttime pain relievers, antihistamines, sleep aids, certain antidepressants, medications to control incontinence and certain narcotic pain relievers.
Statin drugs are particularly problematic because they suppress the synthesis of cholesterol, deplete your brain of CoQ10 and neurotransmitter precursors, and prevent adequate delivery of essential fatty acids and fat-soluble antioxidants to your brain by inhibiting the production of the indispensable carrier biomolecule known as low-density lipoprotein. |
- 1 Alzheimer’s Association, “Facts and Figures”
- 2 Science Advances, Vol 10, Issue 43, October 25, 2024
- 3 Science Advances, Vol 10, Issue 43, October 25, 2024, Introduction
- 4 News-Medical.net, October 28, 2024
- 5, 6 Science Advances, Vol 10, Issue 43, October 25, 2024, Abstract
- 7 Wiley Analytical Science, October 29, 2024
- 8 Neurology. 2021 Dec 14;97(24):e2381–e2391, Abstract
- 9 World Wildlife Fund, Assessing Plastic Ingestion from Nature to People
- 10 Open Journal of Veterinary Medicine, 11, 57-86, Abstract
- 11 Gut Microbes. 2024 Jan 4;16(1):229786, Diet with Probiotics and Their Impact on Gut Health
- 12, 13, 14 Scientific Reports volume 13, Article number: 5258 (2023), Discussion
- 15 Critical Reviews in Microbiology, 2023, 49(2), 151-176
- 16 Am J Lifestyle Med. 2022 Jan 11;16(1):32–35, Abstract
- 17 Alzheimers Dement (Amst). 2023 Mar 1;15(1):e12404, Highlights
- 18 Int J Mol Sci. 2021 Sep 15;22(18):9987, Abstract
- 19 Front Neurosci. 2021 Apr 14;15:661198, Abstract
- 20 Aging Med (Milton). 2024 Oct 22;7(5):649–667, Iron Overload/Accumulation and Increase Risk of AD
- 21 Front Aging Neurosci. 2023 Aug 4;15:1243869, Conclusion
- 22 Aging Ment Health. 2021 Apr;25(4):593-601, Abstract
The Role of Vitamin D Deficiency in Mental Illness
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/12/23/vitamin-d-deficiency-mental-illness.aspx
Analysis by Dr. Joseph Mercola December 23, 2024
STORY AT-A-GLANCE
- Vitamin D receptors exist throughout your brain, affecting mental health by regulating neurotransmitters and reducing inflammation. Deficiency is linked to depression, anxiety and psychosis
- Mental health patients show higher rates of vitamin D deficiency, caused by reduced sun exposure, obesity and other factors
- Studies show vitamin D supplementation improves depression symptoms, particularly in elderly and adolescent patients. Optimal blood levels range from 60 to 80 ng/mL
- Safe sun exposure remains the best source of vitamin D, but those consuming seed oils should wait four to six months after elimination before increasing sun exposure; if regular sun exposure isn’t feasible, vitamin D supplementation may be necessary
- Protective strategies for safe sun exposure include taking astaxanthin (12 mg daily), using niacinamide cream, pre-exposure baby aspirin and molecular hydrogen supplementation
Vitamin D receptors are not just limited to your skeletal system for bone health — they’re also present in various brain regions like your hippocampus, substantia nigra and cerebellum.
This hints at vitamin D’s key role in neurological development and the functioning of your nervous system. When your body lacks sufficient vitamin D, it disrupts neurotransmitter release, affects neurotrophic factors and impairs neuroprotection.1
These disruptions are linked to mood and behavioral changes, contributing to psychiatric conditions such as depression, anxiety and even psychosis. Moreover, vitamin D helps modulate inflammation, which is often elevated in mental health disorders. This is why optimizing your vitamin D levels is important for both physical health and maintaining your mental well-being.
Vitamin D Deficiency and Its Prevalence in Mental Health Conditions
Vitamin D deficiency is common, affecting over half of the global population regardless of age or ethnicity.2 For individuals battling psychiatric disorders, the rates of deficiency are even higher. Studies indicate that psychiatric patients often have lower vitamin D levels compared to the general population.
Factors contributing to this deficiency include reduced sunlight exposure due to time spent indoors, poor dietary intake and obesity, which sequesters vitamin D in fat tissues. Additionally, certain psychiatric medications lead to weight gain, further complicating vitamin D status.3
This widespread deficiency is concerning because low levels of vitamin D have been linked to a higher incidence of various mental health issues, including depression, schizophrenia and anxiety disorders4 — each affected in unique ways.
In depression, low vitamin D levels are associated with increased symptoms and a higher risk of developing the disorder. Vitamin D may protect the hippocampus during stress-related dysregulation and support the release of dopamine, a neurotransmitter involved in mood regulation.5
Schizophrenia, a chronic mental health disorder characterized by distorted thinking and perceptions, is another area of interest concerning vitamin D’s benefits. Research reveals a high prevalence of vitamin D deficiency among individuals with schizophrenia, particularly those experiencing acute episodes.6
Some studies have also found a strong association between low vitamin D levels and the severity of schizophrenia symptoms, suggesting that vitamin D could play a role in cognitive function and neuroprotection.7 In psychotic spectrum diseases like schizophrenia, deficiency is often linked to poorer outcomes and increased symptom severity, due to reduced neuroprotection and impaired neurotransmission.
The Impact of Vitamin D on Specific Mental Health Conditions
Neurodevelopmental disorders, including autism and attention-deficit hyperactivity disorder (ADHD), also show significant correlations with vitamin D levels, where supplementation has been found to improve behavioral and cognitive symptoms.8
Some research also indicates that individuals with bipolar disorder often exhibit lower levels of vitamin D compared to those without the condition. For instance, higher levels of vitamin D binding protein have been observed in bipolar patients, suggesting a link between vitamin D metabolism and mood regulation.9
Additionally, vitamin D plays a role in sleep-wake disorders, where deficiency disrupts circadian rhythms and leads to poor sleep quality.10 Optimizing vitamin D levels is therefore a promising therapeutic strategy for many mental health conditions. Studies have shown that vitamin D supplementation leads to improvements in depressive symptoms, particularly in individuals with existing deficiencies.
For instance, elderly patients with depression, adolescents and those recovering from acute illnesses have all benefited from increased vitamin D intake. In the context of schizophrenia, adding vitamin D to standard antipsychotic treatments has been linked to better cognitive outcomes and reduced symptom severity.11
Neuroinflammation, the inflammation of the nervous tissue, plays a role in many neurological and mental disorders, including traumatic brain injury, Alzheimer’s disease and vascular dementia. Vitamin D has emerged as a promising agent in combating neuroinflammation due to its anti-inflammatory and immunomodulatory properties.12
Animal studies, such as those conducted on rats with traumatic brain injury, have also demonstrated that vitamin D supplementation shifts microglial cells toward an anti-inflammatory state, reducing brain edema and protecting the blood-brain barrier.

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Vitamin D Helps Relieve Depression and Anxiety
A meta-analysis published in the Journal of Affective Disorders explored the effectiveness of vitamin D supplementation in managing primary depression.13 The study reviewed 18 randomized controlled trials to assess whether vitamin D alleviates depressive symptoms in adults. The findings revealed a significant overall reduction in depression scores among those who received vitamin D supplements compared to those who received a placebo.
Notably, the benefits were more pronounced in individuals with baseline vitamin D levels exceeding 20 ng/mL, where the reduction in depressive symptoms was substantial. This suggests that higher levels of vitamin D may be necessary to achieve meaningful improvements in depression.
A study published in The American Journal of Geriatric Psychiatry also revealed a compelling association between vitamin D deficiency and increased depressive symptoms in older adults.14 The study analyzed data from 299 participants, with over 60% classified as either vitamin D deficient or insufficient.
These individuals exhibited higher scores on the Geriatric Depression Scale, particularly in the dysphoria and meaninglessness subdomains. This negative correlation suggests that lower vitamin D levels are directly linked to heightened feelings of sadness, hopelessness and a lack of purpose — core elements of depression. Notably, the study found that higher vitamin D sufficiency levels, nearing 95.5 ng/mL, were associated with minimal to no depressive symptoms.
These results underscore the crucial role that adequate vitamin D plays in maintaining mental health, highlighting the potential of VD supplementation as a strategic intervention to alleviate depressive symptoms in older populations. Anxiety disorders, much like depression, significantly impact your daily life and overall well-being.
Separate research highlights that low vitamin D levels are not only associated with increased symptoms of depression but also with heightened anxiety.15 Vitamin D’s antioxidant and anti-inflammatory properties play a role in mitigating the oxidative stress and inflammation that are key players in the pathophysiology of anxiety disorders.
Brain regions such as the prefrontal cortex and hippocampus, which are involved in regulating mood and anxiety, contain vitamin D receptors and the enzyme necessary for activating vitamin D. This suggests that adequate vitamin D levels are essential for maintaining the health and functionality of these brain areas. Supplementing with vitamin D has also been found to help reduce anxiety symptoms.16
Maximizing the Benefits of Sunlight for Vitamin D Production
While vitamin D supplements are widely available, sunlight remains the gold standard for vitamin D synthesis in your body. Beyond just vitamin D production, sun exposure offers additional health advantages. In fact, elevated vitamin D levels often indicate healthy sun exposure, which may explain many of the health benefits traditionally attributed to vitamin D alone, including reduced mental health benefits, cancer risk and enhanced longevity.
One important factor that’s often overlooked in sun exposure discussions, however, is the impact of dietary oils, particularly seed oils. If you regularly consume seed oils, you’ll need to exercise extra caution with sun exposure. These oils contain high amounts of linoleic acid (LA), which becomes problematic when exposed to ultraviolet radiation. The interaction between sunlight and LA-rich skin triggers inflammation and DNA damage.
For this reason, it’s advisable to limit sun exposure to earlier in the morning or later in the afternoon if you’ve been consuming these oils regularly. A safe approach is to wait four to six months after eliminating these oils from your diet before increasing sun exposure. Several personal characteristics also influence how your body tolerates and responds to sunlight:
• Skin pigmentation — Melanin serves as a natural sunscreen. People with darker skin need longer sun exposure to produce the same amount of vitamin D as those with lighter skin.
• Body composition — Fat tissue stores fat-soluble compounds, including oxidized seed oils. Those with higher body fat percentages may need to be more cautious, as stored oils extend the risk period even after dietary changes.
Guidelines for Safe Sun Exposure
The simplest way to gauge appropriate sun exposure is the “sunburn test.” Monitor your skin for any signs of redness. If you don’t notice even slight pinkness, you’re likely within a safe exposure range. Always avoid sunburn, as it indicates damage. As you reduce LA stores in your body, your susceptibility to sunburn and skin cancer decreases significantly.
These recommendations account for both optimal vitamin D production and protection against oxidative stress while your body eliminates stored LA so during the transition period:
• Until you’ve been seed oil-free for six months, avoid direct sun 2 to 3 hours before and after solar noon. While complete tissue clearance of seed oils takes about two years, the six-month mark typically allows enough detoxification for beneficial sun exposure during peak hours.
• Remember that during Daylight Saving Time (summer months), solar noon occurs at 1 PM, not 12 PM. This means peak sunlight hours are roughly 10 AM to 4 PM during these months.
• As your body eliminates stored seed oils over the initial six months, gradually increase sun exposure closer to solar noon. Start with early morning or late afternoon sun, slowly working toward midday exposure as your tissues become cleaner and more resilient to UV light.
If sun exposure is necessary before your body has cleared seed oils, consider these protective measures:
1. Astaxanthin supplementation — Take 12 milligrams daily to enhance skin resistance to sun damage.
2. Topical niacinamide — Apply vitamin B3 cream before sun exposure to protect against UV-induced DNA damage.
3. Pre-exposure aspirin — Taking a baby aspirin 30 to 60 minutes before sun exposure may reduce skin cancer risk by preventing LA conversion to harmful oxidized linoleic acid metabolites (OXLAMs).
4. Molecular hydrogen — This compound helps neutralize free radicals and reduces oxidative stress while maintaining beneficial reactive oxygen species.
Vitamin D Supplementation Tips
If regular sun exposure isn’t feasible, vitamin D supplementation may be necessary. However, the current definition of vitamin D deficiency (less than 20 ng/mL) has been shown to be inadequate for good health and disease prevention. While sufficiency begins around 40 ng/mL (100 nmol/L in European measurements), the target range for optimal health is 60 to 80 ng/mL (150 to 200 nmol/L). To optimize your vitamin D levels:
- Test your levels twice a year
- Adjust sun exposure or supplementation based on the results
- Retest after three to four months to confirm you’ve reached target levels
- Continue monitoring to maintain optimal levels
Remember that everyone’s relationship with the sun is unique. Listen to your body’s signals and adjust your exposure accordingly. The goal is to harness the benefits of sunlight while avoiding sunburn. Further, keep in mind that the interplay between vitamin D and mental health is intricate and multifaceted. While supplementation shows promise, it’s not a one-size-fits-all solution.
Vitamin D deficiency could be both a consequence of mental illness — due to factors like reduced sunlight exposure and poor diet — and a contributing factor to the severity and resistance to treatment of these conditions. Therefore, addressing vitamin D levels should be part of a holistic approach to mental health care, alongside dietary improvements, physical activity and other psychosocial interventions.
However, ensuring adequate vitamin D levels through safe sun exposure and supplementation when necessary is a valuable component in supporting your mental well-being. By taking proactive steps to manage your vitamin D status, you contribute positively to your overall mental health and resilience against psychiatric disorders.
- 1, 2, 3, 4, 5, 8, 10, 11 Medicina (Kaunas). 2023 Nov 21;59(12):2056
- 6, 7, 9, 12 Diseases. 2024 Jun 20;12(6):131
- 13 J Affect Disord. 2024 Jan 1:344:653-661. doi: 10.1016/j.jad.2023.10.021. Epub 2023 Oct 16
- 14 The American Journal of Geriatric Psychiatry July 2024, Volume 32, Issue 7, P808-820
- 15, 16 Curr Nutr Rep. 2022 Sep 13;11(4):675–681
How to Assess the Protein Needs of Older Adults
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/12/04/protein-needs-older-adults.aspx
Analysis by Dr. Joseph Mercola December 04, 2024
STORY AT-A-GLANCE
- Protein needs become crucial for older adults, but many Americans over 50 don’t meet recommended intakes. Both insufficient and excessive protein consumption leads to health issues
- Proteins, composed of amino acids, are essential for bodily functions. Your body requires 20 amino acids, including nine essential ones that must be obtained through diet
- Studies show 31% to 50% of older adults don’t meet protein recommendations. This deficiency correlates with lower intake of essential nutrients and decreased physical functioning
- Your ability to perform daily activities is closely tied to your protein intake. If you’re not meeting your protein needs, you’re more likely to experience limitations in activities of daily living such as standing for longer periods, walking upstairs, preparing meals and walking for a quarter mile
- Protein should make up about 15% of your daily calories. More specifically, most adults need about 0.8 grams of protein per pound of ideal body weight. Quality, timing and distribution of protein consumption throughout the day are important factors in maintaining muscle health and overall vitality
As you enter your golden years, your protein needs become increasingly important for maintaining health and functionality. A recent analysis of data from the National Health and Nutrition Examination Survey (NHANES) reveals, however, that many Americans over 50 are not meeting their recommended daily protein intake.1 This deficiency puts you at risk of a host of health issues, particularly as you age.
The study examined protein intakes, associated dietary patterns and physical functioning in adults aged 51 and older, shedding light on the importance of adequate protein consumption for healthy aging.
However, it’s important to optimize protein intake, as consuming either too much or too little is problematic. If you eat too much protein, it may harm your kidney health and homocysteine levels. But if you eat too little, there’s a risk of sarcopenia, an age-related condition characterized by the loss of muscle mass and function, and frailty.2
The Vital Role of Proteins in Your Body
You might not think about it often, but proteins are working tirelessly in your body every moment of the day. These remarkable molecules are essential for building and repairing your tissues, including your muscles and organs. They’re also important for the proper functioning of your enzymes, hormones and immune system components. But what exactly are proteins made of?
They’re composed of smaller units called amino acids, some of which your body can’t produce on its own. These “essential” amino acids must come from your diet, which is why it’s important to consume protein-rich foods like meat, eggs and dairy products. By ensuring a varied diet with these protein sources, you’re providing your body with the building blocks it needs to function optimally.
When you eat protein, your body doesn’t simply absorb it whole. Instead, it breaks down the protein into its individual amino acids. As explained by the educational platform Osmosis from Elsevier,3 these amino acids are then reformed into new proteins in your body.
These newly formed proteins perform a vast array of functions, from fighting infections to helping your cells divide. At its most basic, a protein is like a string of beads, with each bead representing an amino acid. These strings then twist and fold into complex shapes, giving each protein its unique structure and function.
Most amino acids have a central carbon atom bonded to an amino group, a carboxylic acid group, a hydrogen atom and a unique sidechain. This structure is why they’re called amino acids.
The 20 Amino Acids Your Body Needs
While nature has produced hundreds of amino acids, your body only uses about 20 of them to create virtually every type of protein it needs. Those 20 proteins include:
| Alanine | Arginine | Asparagine | Aspartic acid |
| Cysteine | Glutamic acid | Glutamine | Glycine |
| Histidine | Isoleucine | Leucine | Lysine |
| Methionine | Phenylalanine | Prolene | Serine |
| Threonine | Tryptophan | Tyrosine | Valine |
Each of these amino acids plays a role in your body’s functions. For example, leucine is important for muscle growth and repair. Not all amino acids are created equal when it comes to your dietary needs, however. Of the 20 amino acids your body uses, some are considered nonessential because your body produces them on its own. These include alanine, asparagine, aspartic acid, glutamic acid and serine.
However, don’t let the term “nonessential” fool you — these amino acids are still crucial for your health. They’re simply called nonessential because you don’t need to get them directly from your diet. On the other hand, there are nine essential amino acids that your body can’t produce — histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan and valine.
You must obtain these from the foods you eat, which is why a varied, protein-rich diet is so important.
There’s a third category of amino acids that falls between essential and nonessential: conditionally essential amino acids. These include arginine, cysteine, glutamine, glycine, proline and tyrosine. Under normal circumstances, your body produces these amino acids. However, during times of illness, stress or intense physical activity, your body’s ability to produce these amino acids may not be sufficient to meet your increased needs.
In these situations, it becomes necessary to consume these amino acids through your diet. This is why your protein needs change depending on your age, health status and activity level.

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The Surprising Truth About Protein Intake in Older Adults
You might assume that most Americans easily meet or exceed their protein requirements, but the data tell a different story. A substantial proportion of older adults — between 31% and 50% — did not even meet the highly conservative recommended protein intake of 0.8 grams per kilogram of body weight per day.4
The problem becomes more pronounced with age, as the likelihood of meeting protein recommendations decreases in older age groups. This trend is particularly worrying because it coincides with the age range when sarcopenia becomes more prevalent. When you don’t meet your protein needs, it’s not just your muscles that suffer.
The study found that adults not meeting the protein recommendation were more likely to have lower intakes of several essential nutrients.5 These include fiber, various B vitamins, choline, vitamins C, A, D, E and K, as well as important minerals like zinc, calcium, phosphorus, magnesium and selenium. Many of these are considered nutrients of public health concern due to their widespread under-consumption. This nutrient shortfall has far-reaching effects on your health.
For instance, zinc insufficiency impairs your immune function and slows wound healing — issues that become increasingly problematic as you age. The combination of low protein and micronutrient deficiencies may increase your risk of common age-related issues such as falls, pressure sores, osteoporosis, muscle weakness and even premature mortality.
The Link Between Protein and Physical Functioning
Your ability to perform daily activities is also closely tied to your protein intake. The study found a positive association between achieving the recommended protein intake and self-reported physical functioning.
If you’re not meeting your protein needs, you’re more likely to experience limitations in activities of daily living such as stooping, crouching, kneeling, standing or sitting for longer periods, walking upstairs, preparing meals and walking for a quarter mile.6
These findings align with other research showing that higher protein diets improve physical functioning, particularly in activities like walking, climbing stairs and lifting heavy items.7 While the current study doesn’t prove causation, it suggests that ensuring adequate protein intake could play a role in maintaining your independence and quality of life as you age.
The Benefits of Increased Protein Intake for Older Adults
Epidemiological and experimental evidence supports the notion that in some cases older adults may benefit from protein intake higher than the current recommended dietary allowance (RDA).
A seminal study from the Health, Aging, and Body Composition Study revealed that older community-dwellers consuming around 1.2 grams of protein per kilogram of body weight daily lost 40% less lean muscle tissue in their arms and legs over a three-year follow-up compared to those ingesting 0.8 grams per kilogram.8
Similar findings were observed in two independent cohorts from the Women’s Health Initiative and the Framingham Offspring study, where protein intake of approximately 1.2 grams per kilogram of body weight was associated with better grip strength preservation.9 Several systematic reviews and meta-analyses have shown that protein intakes higher than the RDA are linked to improved physical function and reduced risk of sarcopenia in older adults.10
These findings have led several expert groups to issue updated nutritional recommendations for maintaining and improving lean body mass and function in old age, suggesting daily protein intakes of at least 1 to 1.2 grams per kilogram of body weight for healthy older individuals.11
Finding Your Protein Sweet Spot
So, how do you determine the right amount of protein for your body? The study suggests that both too little and too much protein can be detrimental to muscle health. While low protein intake (less than 0.8 grams per kilogram of body weight per day) was associated with a lower risk of low muscle mass, it didn’t provide significant protection against sarcopenia overall. The optimal range in this study was between 0.8 and 1.3 grams of protein per kilogram of body weight per day.
As a rule, protein should make up about 15% of your daily calories. Approximately one-third of this protein, or about 5%, should be collagen. More specifically, most adults need about 0.8 grams of protein per pound of ideal body weight (the weight you would ideally be, not necessarily the weight you are now), or for Europeans, approximately 1.76 grams of protein per kilogram.
So, while the conventional recommendation is 0.8 grams per KILO of TOTAL bodyweight, my recommendation is 0.8 grams per POUND of IDEAL bodyweight — including for seniors. This ends up being significantly higher than the conventional recommendation.
To determine your ideal bodyweight, you need to figure out your lean body mass. Take your current weight and subtract your body fat percentage. For example, if you weigh 160 pounds and have 20% body fat, your lean body mass is 128 pounds (160 x 0.8). Multiply that by 0.8, and you’ve got your daily protein target: 102.4 grams.
This might seem like a lot, but spread it out over your meals, and it’s totally doable. Aim for about 33 grams per meal if you’re eating three times a day. In another example, if your ideal weight is 135 pounds, your protein requirement would be 108 grams. Divided into two meals, that would be 54 grams per meal. For reference, there’s approximately 7 grams of protein in each ounce of steak, so a 5-ounce steak would give you 35 grams of high-quality protein.
For children, the average amount per meal is around 5 to 10 grams, while young adults typically can get away with 20 grams per meal. For most normal-weight adults, 30 grams per meal is the minimum you need to stimulate muscle protein synthesis. To find your personal protein sweet spot, consider factors such as your age, activity level and overall health status.
Quality and Timing Matter: Optimizing Protein Intake
When it comes to protein intake, quality and timing are just as important as quantity. Protein quality is sometimes expressed using the digestible indispensable amino acid score (DIAAS), which measures the systemic bioavailability of indispensable amino acids from specific foods, mixed meals or supplements.
Most animal food sources provide excellent quality protein (DIAAS ≥100), while whey falls into the high-quality category (DIAAS = 75–99). Leucine content is a key factor in protein quality, as it stimulates muscle protein synthesis through the activation of specific signaling pathways. To maximize muscle health, some experts recommend ingesting 25 to 30 grams of high-quality protein with at least 2.5 grams of leucine at each meal.12
Your eating pattern also matters, with current recommendations encouraging older individuals to distribute protein intake evenly across meals rather than concentrating it in a single sitting. Additionally, consuming protein-rich meals in close proximity to exercise routines, particularly resistance training, enhances muscle anabolic responses and supports overall muscle health.13
While optimizing your protein intake is important, it’s just one piece of the puzzle when it comes to maintaining muscle health and vitality as you age. Other factors are also associated with muscle strength and sarcopenia, including physical activity, overall diet quality and gut microbiome diversity. A holistic approach to healthy aging is best for preserving muscle mass and function.