Nutrition

now browsing by category

“Let food be thy medicine, and medicine be thy food” ~ Hippocrates.
Doctors should be taught this in medical school, as well as “First, do no harm”.

 

Why Arthritis Gets Worse in the Winter Months


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/12/30/why-arthritis-worsens-in-winter.aspx


Analysis by Dr. Joseph Mercola     
December 30, 2025

why arthritis worsens in winter

Story at-a-glance

  • Cold weather worsens arthritis symptoms by thickening joint fluid, slowing blood flow, and tightening muscles, which amplifies pain and stiffness
  • Drops in barometric pressure cause tendons and muscles to expand, adding extra pressure to already inflamed joints and increasing discomfort
  • Reduced sunlight during winter lowers vitamin D levels, weakening bones and increasing inflammation, while inactivity further restricts circulation
  • Eliminating seed oils, boosting vitamin K2, optimizing vitamin D, and sipping warm bone broth help reduce inflammation, strengthen cartilage, and restore flexibility
  • Daily movement, heat therapy, and sunlight exposure keep joints lubricated, improve circulation, and help you stay active and pain-free all winter long

Arthritis is one of the most common causes of chronic pain worldwide, and for millions of people, the suffering intensifies when temperatures drop. Cold air doesn’t cause arthritis, but it changes how your body feels it. When the temperature falls, the thick fluid that keeps your joints gliding smoothly turns sluggish. That’s when your knees ache, your fingers feel tight, and simple tasks like standing or opening a jar remind you that your joints aren’t happy.

When the air gets colder, your circulation slows and your muscles tighten. You might notice that your hands feel clumsy, your knees ache a little sooner, or your morning routine takes longer than it used to. These small shifts reflect how your body adapts to the season — conserving heat but at the cost of flexibility and comfort. Add shorter days, less sunlight, and reduced activity, and your joints start to feel the strain.

The impact of winter on arthritis goes beyond temperature. It’s a story of how lifestyle, environment, and biology collide. Understanding that connection gives you a powerful advantage — because once you know why the pain worsens, you can do something about it.

Cold Weather Thickens Joint Fluid and Strains Your Joints

In a Cedars-Sinai article, Dr. Mariko Ishimori explains that your joints “operate best in temperate weather,” and when temperatures fall, the synovial fluid inside them thickens.1 This fluid acts like motor oil for your body — keeping your joints smooth and cushioned.

When it becomes thick, your movements feel stiff, and even simple actions like walking or gripping an object trigger discomfort. The colder air doesn’t damage joints directly, but it alters their performance, making existing inflammation more noticeable.

Barometric pressure drops create internal pressure on swollen joints — Changes in barometric pressure — the force exerted by the atmosphere — cause tendons and muscles to expand, putting added strain on joints that already have limited space. “A drop in barometric pressure can cause muscles and tendons to expand, which can put more stress on an already crowded joint,” Ishimori explains.

This physical expansion presses against sensitive joint capsules, making the surrounding tissues feel tight and sore. Many people living with arthritis even notice that their joints start aching before a storm hits, because they sense these atmospheric shifts sooner than the weather forecast does.

Reduced circulation in the cold slows recovery and heightens pain — Low temperatures constrict blood vessels, decreasing the flow of oxygen and nutrients to your joints. Poor circulation means slower healing and greater stiffness, especially in your knees, hips, and hands.

Staying warm — layering clothing and soaking in hot baths — is important to counteract this restricted blood flow. Warming your body helps relax muscles, improve joint lubrication, and reduce stiffness. Even moderate heat therapy supports better mobility throughout the day.

Movement remains the best natural remedy for winter stiffness — Exercise, according to Dr. Ishimori, is “the single best thing you can do to stave off arthritis pain.” Regular movement strengthens the muscles supporting your joints, releases endorphins that act as natural painkillers, and improves flexibility.

Start small with gentle stretches or short walks and gradually increase activity levels. Stretching before outdoor activity helps prevent injury and warms up tight tissues. For example, rolling your wrists and ankles or bending your knees helps prepare your body to handle temperature changes more comfortably.

Nutrition and vitamin D play a major role in pain management — Eating anti-inflammatory foods and maintaining vitamin D levels help significantly reduce winter pain. Vitamin D deficiency, common even in sunny climates, contributes to bone loss and greater joint discomfort. Optimizing your vitamin D levels supports bone strength and helps control inflammation.

Eating nutrient-rich foods such as leafy greens, and fermented products also helps maintain your body’s natural defenses against winter joint stress.

Maintaining a healthy weight protects your joints from further damage — Every pound of excess body weight wears down cartilage faster, increasing pain and stiffness in weight-bearing joints. Staying active through low-impact exercises such as swimming or walking, while adopting a nutrient-dense diet, helps relieve this pressure naturally.

Small, consistent actions — such as cutting processed foods and seed oils — help balance metabolism while easing physical strain. Even modest weight loss significantly reduces pain, showing how lifestyle changes directly affect joint resilience.

Cold Weather Habits and Immune Changes Drive Winter Joint Pain

A report from Proliance Orthopedic Associates focuses on how colder weather triggers multiple biological and behavioral changes that worsen arthritis. This includes lifestyle factors — reduced movement, dietary changes, and immune activity — that amplify inflammation. People often move less, eat more inflammatory foods, and spend less time in the sun during the winter months. Together, these behaviors make joints ache, muscles tighten, and pain feel more pronounced.

Decreased physical activity leads to weaker muscles and stiffer joints — Shorter days and low temperatures discourage people from maintaining daily movement routines, which directly affects joint function. When muscles lose strength, they provide less support and shock absorption for joints, creating more friction and pain.

Reduced circulation from inactivity slows oxygen delivery and waste removal, compounding inflammation. It’s important to stay active through indoor-friendly workouts — swimming, yoga, treadmill walking, or tai chi — that maintain mobility and help your joints stay lubricated, even when you don’t feel like going outside.

Immune system shifts during winter fuel inflammation — Cold weather doesn’t just chill your skin — it activates your immune system in subtle but significant ways. In autoimmune conditions like rheumatoid arthritis, this immune reactivity intensifies inflammatory cascades that damage joint tissue.

This overactivity increases stiffness and swelling, especially when combined with stress or poor diet. Keeping your immune system balanced through regular movement, nutrient-dense food, and consistent sleep routines helps blunt these winter flare-ups.

Heat therapies restore comfort and circulation naturally — Tools like paraffin baths, warm compresses, saunas, and hot tubs help relax stiff tissues and restore flexibility. Heat increases blood flow to inflamed joints, flushing out inflammatory compounds while supplying oxygen and nutrients. Regular heat exposure encourages a feedback loop of comfort and confidence — when your joints feel looser, you’re more likely to move, and that movement maintains long-term function.

Self-care and proactive management reduce flare-ups year-round — Joint pain is often manageable through daily choices, even without medical intervention. Staying hydrated, dressing warmly, and keeping your environment comfortable all help reduce stiffness.

Save This Article for Later – Get the PDF Now

Download PDF

How to Stop Winter from Making Your Arthritis Worse

Cold weather makes joint pain feel sharper and stiffness last longer, but that doesn’t mean you’re powerless against it. Winter affects your body in predictable ways — it slows circulation, thickens joint fluid, tightens muscles, and lowers vitamin D. On top of that, most people move less, eat differently, and spend more time indoors surrounded by dry heat and artificial light.

All of these factors increase inflammation and strain your joints. The good news is that by addressing the real cause of winter flare-ups — cellular inflammation and sluggish metabolism — you can stay flexible, comfortable, and active through the cold months. Here’s where to start:

1. Warm up from the inside out to protect your joints — When your body temperature drops, the synovial fluid in your joints thickens, making every movement feel stiff. Staying warm isn’t just about comfort — it directly affects how easily your joints move. Dress in layers, use a heating pad before bed, and take warm baths or short sauna sessions to improve circulation.

If you work at a desk, keep a small hot water bottle nearby for added warmth. Think of it as “priming the oil” in your joints before you start your day. Once your muscles are warm, even a short walk or light stretch session feels smoother and less painful.

2. Remove inflammatory seed oils and switch to healthier fats — Vegetable oils like soybean, corn, safflower, and sunflower oil are high in linoleic acid (LA) that feeds inflammation that worsens in cold weather. They increase oxidative stress and damage mitochondria — the tiny engines that produce energy in your cells.

During winter, when your circulation slows, your body has an even harder time clearing those inflammatory byproducts. Replace those oils with nourishing fats like grass fed butter, ghee, and tallow. These fats strengthen cellular membranes, reduce oxidative damage, and keep you warm by supporting efficient energy production.

3. Get your vitamin D and K2 balance right to prevent winter joint stiffness — Less sunlight in winter means less vitamin D, which leads to weaker bones and stiffer joints. Vitamin D works best alongside vitamin K2 — which directs calcium into bones and out of soft tissues like cartilage — and magnesium.

I recommend getting daily sunlight whenever possible, even for 15 minutes, to optimize your vitamin D levels. Test your vitamin D levels every six months, and aim for a range between 60 and 80 ng/mL (150 to 200 nmol/L). If your levels are lower, adjust your daily sunlight or supplement with vitamin D3 accordingly.

4. Sip warm bone broth throughout the day for joint nourishment and circulation — Cold weather reduces blood flow to your extremities, starving your joints of nutrients. Bone broth helps reverse that. Made from grass fed bones and cartilage-rich cuts like oxtail, it contains collagen, glycine, glucosamine, and chondroitin — compounds that rebuild cartilage and reduce pain.

Sip it warm throughout the day instead of cold drinks. The warmth promotes circulation while the nutrients repair the tissues that cushion your joints. If your mornings feel achy, start your day with a mug of broth instead of coffee.

5. Move daily — but adapt your routine for winter — Staying active keeps inflammation under control, but cold weather changes how your body responds to exercise. If long outdoor walks feel too harsh, switch to indoor activities like yoga, stretching, or short resistance sessions, such as blood flow restriction (BFR) training.

Movement keeps your lymphatic system — your body’s built-in waste-removal system — active and prevents swelling around your joints. Try this rhythm: stretch indoors, step outside for sunlight exposure, then return to a warm environment. The temperature contrast boosts blood flow, improves flexibility, and helps your joints “remember” how to move freely, even in winter.

If you feel every cold snap in your knees or fingers, these steps aren’t just about comfort — they’re about taking back control. When you warm your body, nourish your joints, and protect your mitochondria, winter stops being something you endure and becomes something you move through with confidence.

FAQs About Why Arthritis Feels Worse in the Winter

Q: Why does arthritis feel worse during the winter months?

A: Cold weather thickens the lubricating fluid inside your joints and slows circulation, making your movements feel stiff and painful. Drops in barometric pressure also cause muscles and tendons to expand, which puts more pressure on inflamed joints. Combined with reduced sunlight, lower vitamin D levels, and less physical activity, this creates a perfect storm for pain and inflammation.

Q: What can I do to reduce arthritis pain when it’s cold outside?

A: Start by keeping your body warm from the inside out. Dress in layers, use heating pads or warm baths, and move your body daily to keep joints lubricated. Gentle indoor exercises like yoga or stretching are ideal. Staying hydrated and maintaining a steady room temperature also make a noticeable difference.

Q: How does diet affect joint pain in winter?

A: Certain fats make inflammation worse, especially LA in seed oils like soybean, corn, sunflower, and safflower oil. Replacing them with nourishing fats like grass fed butter, ghee, or tallow reduces oxidative stress and supports joint health. Adding more anti-inflammatory foods — such as leafy greens, fermented vegetables and grass fed animal products — helps your body control inflammation and maintain flexibility.

Q: Why are vitamin D and K2 so important for joint health in winter?

A: Less sunlight means less vitamin D, which weakens bones and raises inflammation levels. Vitamin D works together with vitamin K2 to move calcium into bones instead of soft tissues like cartilage. Keeping both in balance strengthens your joints and helps prevent stiffness. Aim for daily sun exposure when possible, or consider supplementing to maintain optimal levels.

Q: What are simple habits that keep arthritis under control all winter?

A: Warm your body daily, eat nutrient-rich foods, move regularly, and avoid sitting for long periods. Sip bone broth to nourish your joints, stretch before outdoor activity, and use heat therapies to improve flexibility. Small, consistent changes — such as cutting out seed oils, keeping your vitamin D levels up, and staying warm — help you stay active and pain-free all season long.

– Sources and References

Black Pepper — The King of Spices and Its Surprising Superpowers


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/09/03/black-pepper-digestion-flavor-absorption.aspx


Analysis by Dr. Joseph Mercola     
September 03, 2025

black pepper digestion flavor absorption

Story at-a-glance

  • Piperine, the active compound in black pepper, stimulates the trigeminal nerve system, creating a unique tingling or warming sensation beyond taste and smell
  • Adding freshly ground black pepper at the table activates multiple senses and increases meal satisfaction by giving you more control over flavor
  • Whole peppercorns preserve their flavor and aroma far longer than pre-ground pepper, making fresh grinding the most effective way to unlock its health and sensory benefits
  • Black, white, and green peppercorns offer distinct flavor profiles and can be rotated to keep meals interesting and support a broader range of sensory stimulation
  • Research shows that when you season food yourself, your brain perceives the meal as more enjoyable and rewarding — supporting healthier eating habits over time

Most people don’t think twice about the black pepper shaker on the table, but that ordinary spice holds a far more powerful role than it gets credit for. Used across continents for thousands of years, black pepper earned its place not just as a flavor enhancer, but as a compound deeply tied to how you experience food, digest it, and benefit from it. What makes black pepper so effective is how it works with your body, not just your taste buds.

It sharpens flavor, supports better digestion, and helps your system absorb more from the food you’re already eating. But what really sets it apart is how your brain responds when you’re the one adding it — giving you more control, more satisfaction, and a better shot at enjoying healthy meals long-term. Let’s look at what modern research has uncovered about why this spice deserves a lot more attention — and how using it strategically could change the way you eat.

Your Brain Likes It When You Add the Pepper Yourself

Research published in the International Journal of Gastronomy and Food Science analyzed why black pepper has earned the nickname “the king of spices” and what makes it so enduringly popular.1 The researchers reviewed the cultural history, global trade patterns, culinary functions, and biochemical actions of black pepper, with a special focus on how piperine — the active compound in pepper — affects flavor perception and consumer experience.

Black pepper plays a unique psychological role in dining — One of the most interesting takeaways is how people enjoy food more when they add the pepper themselves. The authors suggest this boosts engagement, satisfaction, and personalization, a phenomenon similar to what psychologists call the “IKEA effect.”

This is the idea that you value something more when you play a role in creating or customizing it. In the case of black pepper, adding it yourself gives you a sense of control and ownership over your food.

Letting people season their food creates a better eating experience — Researchers found that personal seasoning habits — adding black pepper at the table rather than during cooking — tend to result in greater enjoyment and stronger flavor recognition.

The act of adding pepper is more than just functional; it becomes part of the meal’s ritual and enhances the multisensory eating experience. This simple choice taps into your personal taste preferences, which vary from person to person depending on genetics, gut health, and even your mood.

Pepper’s sharp bite triggers a unique sensory system — Black pepper doesn’t just stimulate your taste buds. It activates what scientists call the trigeminal nerve system, a set of nerve endings responsible for detecting heat, cold, and chemical irritation.

This system is separate from taste and smell, yet it plays a huge role in how you experience flavor. Piperine is a “chemesthetic” agent, meaning it gives you a burning or tingling sensation through chemical stimulation rather than heat or spice in the traditional sense.

Piperine heightens flavor without additives — Unlike common flavor enhancers like MSG, piperine doesn’t carry the stigma or negative health associations. It sharpens flavor perception, helping you detect and enjoy other ingredients more fully.2 This makes black pepper an effective tool for people trying to enjoy bold flavors without synthetic ingredients.

Piperine’s impact is strongest when added fresh — The research emphasizes that ground pepper loses its aromatic compounds quickly — sometimes in a matter of weeks — while whole peppercorns retain their pungency for years.

That’s why freshly ground pepper delivers a much stronger sensory impact than pre-ground varieties. The timing and method of pepper use also matter: adding it after cooking or at the table preserves more of its aroma and flavor-enhancing power.

Pepper’s Benefits Come from a Complex Mix of Compounds

Piperine is just one of many bioactive ingredients in black pepper. The essential oil of the pepper fruit also contains limonene, β-caryophyllene, α-pinene, and sabinene — each contributing to the aroma, flavor, and possibly even biological effects of pepper. These compounds interact with your nose, mouth, and nervous system in ways that amplify the dining experience far beyond simple taste.

Your body processes piperine slowly, extending its effects — Piperine has a long-lasting effect in your mouth and throat, where it creates a lingering warming or burning sensation. The study describes how piperine is often felt most strongly in the front of the tongue and sometimes the throat, depending on how it’s consumed. This adds to its complexity and helps explain why pepper is often described as “hot,” even though it isn’t a thermal sensation like chili.

Black pepper’s sensory profile is deeply layered — Beyond its pungency, black pepper delivers what the researchers call “top notes” and “base notes.” These include citrus-like brightness from limonene and earthy, woody undertones from compounds like β-caryophyllene. The result is a spice that doesn’t just taste “spicy” but offers a full sensory spectrum that changes with preparation and form — whole, crushed, or ground.

Pepper taps into sensory personalization, a powerful motivator — This personalization effect makes meals more enjoyable and even helps you eat healthier foods more consistently. When flavor feels satisfying, you’re more likely to stick with your nutrition goals, especially when reducing processed additives or junk food. That’s why chefs who remove table seasoning are missing an opportunity to enhance the guest experience.

This simple spice has been underestimated in modern food science — Although pepper is nearly universal in kitchens and dining rooms, most people overlook its sensory and psychological power. This study reframes pepper not just as a condiment, but as a functional, sensory-enhancing ingredient that plays a bigger role in eating satisfaction and flavor perception than previously recognized.

Save This Article for Later – Get the PDF Now

Download PDF

How to Use Black Pepper to Boost Flavor, Digestion, and Nutrient Absorption

If you’re trying to improve how your food tastes without relying on artificial flavor enhancers, black pepper is one of the simplest and most effective tools you’ve got. But there’s more to this spice than just its burn.

Used correctly, black pepper supports digestion and amplifies nutrient absorption. The key is using it at the right time and in the right way, so your body and taste buds both get the most out of it. Here’s how to start using black pepper intentionally to enhance both the flavor and function of your meals:

1. Use whole peppercorns and grind them fresh at the table — Pre-ground pepper loses its flavor and aromatic oils quickly. When you grind whole peppercorns fresh, you’re getting the full spectrum of volatile compounds, like limonene and β-caryophyllene, that deliver both flavor and function. Add it after cooking or just before eating to preserve the sensory punch.

2. Add it yourself, don’t let the kitchen decide for you — Seasoning your food at the table isn’t just about taste — it engages your brain and enhances enjoyment. When you control the amount and placement of pepper, it activates your sensory system more fully. That makes meals more satisfying and helps you stick to healthier food choices without feeling deprived.

3. Pair black pepper with nutrient-dense foods to boost absorption — Piperine, the main compound in black pepper, makes it easier for your body to absorb nutrients like selenium, beta-carotene, and even curcumin from turmeric.3 Use it when eating colorful veggies, grass fed meat, or pastured eggs to enhance the bioavailability of what you’re already eating.

4. Use black pepper to make simple meals more satisfying — Even the most basic foods, like eggs, rice, or steamed vegetables, taste richer and more complex when you add freshly ground black pepper. It stimulates multiple senses at once, which tells your brain the meal is more enjoyable and rewarding. If you’re trying to eat healthier without giving up flavor, this small shift helps you feel more satisfied with less effort or added ingredients.

5. Rotate pepper types to keep your taste buds engaged — Black, green, and white peppercorns all offer different flavor profiles — black for heat and aroma, white for a milder, earthy note, and green for herbal freshness. If you get bored with your food easily, rotating these varieties makes healthy meals feel exciting again. Bonus: variety stimulates different sensory pathways, which keeps your brain more engaged at mealtime.

FAQs About Black Pepper

Q: What makes black pepper different from other spices?

A: Black pepper stimulates multiple sensory systems — taste, smell, and chemesthesis — through its active compound, piperine. This gives it a unique ability to enhance flavor and digestion while also supporting antioxidant and antimicrobial activity.

Q: How does black pepper improve digestion and nutrient absorption?

A: Piperine boosts digestive enzymes and increases stomach acid, which helps your body break down food more effectively. It also improves the absorption of key nutrients like curcumin, selenium, and beta-carotene.

Q: Why is freshly ground pepper better than pre-ground?

A: Pre-ground pepper quickly loses its essential oils and aromatic compounds. Whole peppercorns retain their potency for years, making freshly ground pepper a more flavorful and effective option for enhancing both taste and health benefits.

Q: What’s the benefit of adding pepper at the table instead of during cooking?

A: When you season your food yourself, it creates a more satisfying and personalized eating experience. This simple act of control boosts enjoyment and makes you more likely to stick with healthier meals.

Q: Do different types of peppercorns offer different benefits?

A: Yes. Black pepper has the strongest flavor and highest piperine content, while white pepper offers a milder, earthy profile, and green pepper delivers a fresh, herbal taste. Rotating these keeps your meals interesting and stimulates different sensory pathways.

Adenomyosis Is a Hidden, Estrogen-Driven Cause of Severe Period Pain


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/08/23/adenomyosis-symptoms-causes-natural-treatment.aspx


Analysis by Dr. Joseph Mercola     
August 23, 2025

adenomyosis symptoms causes natural treatment

Story at-a-glance

  • Adenomyosis is often mistaken for bad period pain or endometriosis, but it involves tissue growing into the uterine muscle, causing swelling, heavy bleeding, and knife-like cramps
  • Many women suffer for years without a diagnosis because doctors misinterpret symptoms or rely on outdated assumptions that the condition only affects older women
  • Research shows adenomyosis leads to serious complications like infertility, miscarriage, preeclampsia, and dangerously low hemoglobin levels requiring emergency transfusions
  • Estrogen overload is the main driver of adenomyosis, and it’s made worse by birth control, plastics, vegetable oils, and hormone-disrupting chemicals found in everyday products
  • You can start reversing estrogen dominance naturally by cutting synthetic hormones, avoiding xenoestrogens, restoring metabolism with the right carbs, and using natural progesterone

If your period pain feels unbearable — like a deep, throbbing ache or stabbing cramps that knock the wind out of you — it’s not something to brush off. Pain that severe isn’t normal. For millions of women, it’s the body’s warning signal for something deeper that’s often misunderstood or completely missed.

You’ve likely been told that heavy bleeding, pelvic pressure, and fatigue are just part of being a woman. But what if those symptoms point to a disease that’s quietly hijacking your uterus and flooding your body with inflammation? That’s the reality for countless women who are dismissed, misdiagnosed, or left in the dark for years, sometimes decades. This condition, known as adenomyosis, doesn’t always show up clearly on a scan.

It’s not taught well in medical school. And it’s rarely mentioned in mainstream conversations about women’s health. But it’s there, silently reshaping lives, month after month. I want to walk you through what the research now shows — why it happens, who’s at risk, and what your options actually are. The science is evolving fast, and the data is clear: you don’t have to live like this. Let’s take a look at the overlooked patterns and newest discoveries about this underdiagnosed disease.

Most Women Are Told Their Pain Is Normal — It Isn’t

From the women suffering through debilitating cramps to the doctors mislabeling it as “just a bad period,” an article in The Hearty Soul pulls back the curtain on how widespread yet invisible adenomyosis is.1 It presents differently from endometriosis and takes a devastating toll on a woman’s social life, mental well-being, and ability to function day to day.

Symptoms often mimic other conditions, which causes many women to go undiagnosed — Unlike endometriosis, adenomyosis causes the uterine wall itself to thicken and expand, sometimes doubling or tripling in size. Women describe the pain as knife-like cramping that strikes during menstruation, along with painful sex, bloating, pelvic pressure, and severe bleeding that disrupts quality of life.

There’s a cultural normalization of these symptoms, but just because menstrual pain is common doesn’t mean it’s normal.

Doctors often dismiss or misinterpret these symptoms, further delaying diagnosis — Gynecologist Dr. Shamitha Kathurusinghe, who points out that many doctors are themselves misinformed: “There’s a lot of misinformation because there’s a lot of misunderstanding that comes from messaging that doctors are getting.” That means women aren’t just being ignored — they’re being actively misled into thinking their symptoms don’t warrant investigation.

The lack of awareness creates a cycle of isolation and suffering — Many women miss work, cancel plans, and lose relationships because of the unpredictability and severity of their symptoms. Yet they often remain silent out of embarrassment or fear of being labeled “dramatic.”

Adenomyosis doesn’t always come with symptoms, making it harder to catch early — The condition is often silent for years, only showing up after other reproductive complications arise. But when it does cause symptoms, it mimics endometriosis or fibroids, which complicates diagnosis and treatment decisions.

Younger Women Are Now at Risk — and Doctors Aren’t Catching It

A review published in the Journal of Clinical Medicine revealed just how often adenomyosis is missed or misunderstood in clinical settings.2 The paper compiled data from dozens of high-quality studies to explore how adenomyosis affects everything from fertility to miscarriage risk. The review focused on women of reproductive age and made clear that current diagnostic and treatment approaches are still not consistent, even among specialists.

Adenomyosis is now being found in much younger women than previously thought — The conventional view has been that this condition primarily affects women in their 40s or 50s, especially those who’ve already had children.

But the paper highlighted that focal forms of adenomyosis — where lesions are isolated rather than spread throughout the uterine muscle — are now increasingly being diagnosed in women in their 30s and even younger. These women often present with fertility problems or abnormal bleeding, but their symptoms are dismissed or misattributed to something else.

There’s a strong link between adenomyosis and pregnancy complications — Women with adenomyosis have a much higher risk of miscarriage, preterm birth, preeclampsia (dangerously high blood pressure during pregnancy), and delivering babies that are smaller than normal for their gestational age.

These risks are especially pronounced when the adenomyosis is diffuse, meaning it spreads across a wider area of the uterus rather than being confined to one spot. This type of tissue growth interferes with the placenta’s ability to attach and develop normally.

Even though diagnostic tools exist, global guidelines are still not aligned — so your doctor’s advice may depend on where you live — While some countries are adopting advanced classification systems based on imaging criteria, others still lack a formal system to define or grade adenomyosis severity. That means two women with the exact same symptoms often get completely different diagnoses and treatments depending on which clinic or country they visit.

The biological explanation lies in how the tissue invades the uterine muscle and disrupts its structure — Researchers believe that tissue from the uterine lining becomes embedded in the muscle wall either through mechanical injury — such as from surgery — or through a faulty junction between the endometrium and the myometrium — the inner and outer layers of the uterus.

Once this tissue is inside the muscle, it thickens and swells with each menstrual cycle, causing inflammation, scarring, and impaired uterine function.

Several theories explain how adenomyosis starts, but most point to a breakdown in your uterine architecture — One theory, called tissue injury and repair, suggests that repeated damage to the uterine lining causes abnormal healing responses, leading to invasion of the muscle by uterine lining cells.

Another theory proposes that stem cells in the uterus misfire and turn into the wrong kind of tissue, embedding themselves where they don’t belong. In either case, the result is the same: a uterus that’s constantly inflamed, structurally compromised, and metabolically inefficient.

Save This Article for Later – Get the PDF Now

Download PDF

Adenomyosis Isn’t Just Painful — It Leads to Emergency Room Visits

An overview from Johns Hopkins Medicine highlights how adenomyosis becomes medically dangerous, not just inconvenient or uncomfortable.3 While the condition is often brushed off as a heavy period, the article makes clear that some women bleed so much they end up severely anemic, requiring blood transfusions just to restore basic function.

Gynecologic oncologist Dr. Mildred Chernofsky explains that adenomyosis involves tissue that grows into the muscular wall of the uterus and bleeds every month like normal uterine lining. But because it’s trapped in the muscle, it causes inflammation, swelling, and massive blood loss.

The most severe cases involve hemoglobin levels dropping to life-threatening lows — According to Chernofsky, “I may see patients that bleed until they have a hemoglobin level of 7 grams per deciliter and are extremely anemic.” Normal hemoglobin levels for women range from 12 to 16 g/dL. When blood levels drop this low, women often experience fatigue, dizziness, fainting, shortness of breath, and lightheadedness.

Most women don’t even realize their uterus has enlarged until the symptoms are advanced — The uterus becomes spongy, heavy, and balloon-like. This bloating feels like constant pressure in your lower abdomen or a sense of fullness that doesn’t go away. Yet during physical exams, doctors often don’t recognize the warning signs unless they specifically palpate the uterus and check for size, shape, and density irregularities.

Diagnosing adenomyosis still depends heavily on imaging, and MRI remains the most accurate tool — While an ultrasound is usually the first step, it’s not always sensitive  enough to pick up on deeper tissue invasion. “MRI provides incredibly high-resolution images and shows us the thickness of the endometrial-myometrial junction,” says Chernofsky. That junction — the boundary where the uterine lining meets the muscle — is usually where the disease starts.

Adenomyosis often gets confused with two other conditions: endometriosis and fibroids, but the treatments are different — While all three cause pelvic pain and heavy bleeding, they originate in different tissues and require different approaches. Endometriosis involves tissue outside the uterus. Fibroids are benign tumors. Adenomyosis, on the other hand, is diffuse tissue growth inside the uterine wall, and can’t simply be “cut out” the way fibroids sometimes are.

Surgery is often used as a last resort — Unlike fibroids, adenomyosis tissue spreads throughout the uterus and often has fingerlike projections that invade the muscle. That makes it difficult to remove piece by piece. This means that for women with severe, unrelenting symptoms, removing the uterus becomes conventional medicine’s go-to permanent solution.

How to Stop Feeding the Root Cause of Adenomyosis

If you’ve been dealing with symptoms like heavy bleeding, intense cramping, or a constantly bloated abdomen — and you suspect or know you have adenomyosis — then it’s time to focus on the root of the issue: excess estrogen. Estrogen dominance fuels this disease.4 That includes both the estrogen your body produces and the synthetic or food-based estrogens you’re exposed to without realizing it.

You’re not powerless here. You can start taking control today. The goal is to block what’s driving this disease while rebuilding your energy and restoring balance. If you’re looking to avoid hormonal treatments like birth control pills or you’re looking for alternatives to surgery, these five steps will help you move forward.

1. Cut off the estrogen at the source — If you’re on birth control or hormone replacement therapy, and you’re dealing with adenomyosis symptoms, those drugs are likely making things worse. Synthetic estrogens increase tissue growth inside your uterus.5

You’ll also want to stay far away from plastics, conventional cleaning products, and chemical-laden beauty products — these all contain xenoestrogens, which mimic estrogen in your body. Switch to glass containers, and use natural or homemade personal care and cleaning options.

2. Use natural progesterone to block the damage — Natural progesterone is your anti-estrogen. It doesn’t just relieve symptoms — it actually blocks the effects of both estrogen and cortisol. That’s a powerful combination. But don’t rush into it. If your diet is still holding you back from making energy at the cellular level, progesterone won’t have its full effect. First, rebuild your metabolic foundation.

Once your diet supports mitochondrial energy production, introducing a natural progesterone, as described below, makes a noticeable difference.

3. Fix your metabolism with the right carbs — not fewer — If you’ve been doing keto or low-carb, stop. Shift toward 250 grams of carbs per day, and more if you’re very active. This is what your cells need to make adenosine triphosphate (ATP), the fuel that powers everything from brain function to hormone balance.

Start with white rice and whole fruit. Add well-cooked root vegetables next. Hold off on raw greens, whole grains and beans until your gut is healthy, meaning your bowel habits, bloating, and overall comfort are under control.

4. Filter your toxins, especially vegetable oils — Linoleic acid (LA), the dominant fat in vegetable oils, mimics estrogen, contributing to estrogen dominance. As a result, LA disrupts hormonal balance along with mitochondrial function. Cut out all forms of vegetable oils, including from processed foods, restaurant meals, and even nuts and seeds. Replace them with tallow, grass fed butter, or ghee.

5. Know your prolactin level — Many people believe they’re low in estrogen due to bloodwork, when they actually have high levels in their organs. This is because serum estrogen levels are not representative of estrogen that’s stored in tissues. Estrogen is often low in plasma but high in tissues. Prolactin levels serve as a reliable indicator of estrogen activity, as estrogen directly stimulates your pituitary gland to produce prolactin.

When prolactin levels are elevated, it signals increased estrogen receptor activation, whether from your body’s own estrogen production or environmental exposures to endocrine-disrupting chemicals in microplastics and other pollutants. This relationship is particularly significant when combined with low thyroid function, making prolactin an important marker for identifying hormonal imbalance.

FAQs About Adenomyosis

Q: What is adenomyosis and how is it different from other conditions like endometriosis or fibroids?

A: Adenomyosis is a condition where the tissue that normally lines your uterus grows into the muscular wall of the uterus itself. This causes the uterus to swell and leads to intense cramps, heavy bleeding, and chronic pelvic pain. Unlike endometriosis (where tissue grows outside the uterus) or fibroids (benign tumors), adenomyosis spreads through the uterine muscle and can’t be removed surgically in the same way.

Q: Why do so many women go undiagnosed with adenomyosis?

A: Doctors often misinterpret adenomyosis symptoms or attribute them to other conditions. Symptoms like painful periods, bloating, and fatigue are frequently dismissed as “normal,” especially in younger women. Additionally, imaging tools like ultrasound don’t always catch the disease. MRI is more accurate but less commonly used, so many women are left undiagnosed or misdiagnosed for years.

Q: What are the long-term risks of untreated adenomyosis?

A: Left untreated, adenomyosis often leads to severe anemia from chronic blood loss, requiring emergency care or blood transfusions. It also increases the risk of pregnancy complications, including miscarriage, preeclampsia, and preterm birth. Over time, the ongoing inflammation and uterine damage leads to reduced fertility and significant declines in quality of life.

Q: What is the root cause of adenomyosis and how do I address it?

A: The underlying driver of adenomyosis is excess estrogen, including both natural estrogen and environmental estrogens from plastics, chemicals, and synthetic hormones. To lower your estrogen load, cut out vegetable oils and processed foods, reduce chemical exposures and birth control pills, use natural progesterone and support your metabolism through strategic dietary shifts and mitochondrial repair.

Q: What steps can I take today to start feeling better?

A: Start by eliminating hormone disruptors like synthetic birth control and chemical-laden products. Shift to a higher-carb, whole-food diet to rebuild your mitochondrial function. Add natural progesterone and monitor prolactin levels to get a more accurate picture of your true estrogen burden and hormonal balance.

Simply Removing Vaccine Mandates Without Optimal Nutritional Immunity May Do More Harm to the MAHA Movement

Reproduced from original OMNS article (OrthoMolecular News Service):
http://orthomolecular.org/


Subscribe to the free Orthomolecular Newsletter: http://orthomolecular.org/subscribe.html
Go to the OMNS Archive: http://orthomolecular.org/resources/omns/index.shtml

Orthomolecular Medicine News Service, September 22, 2025

By Richard Z. Cheng, M.D., Ph.D., Editor-in-Chief

Florida’s recent elimination of school vaccine mandates has polarized the nation. For some, this is a long-awaited victory for personal freedom. For others, it is a reckless gamble that will unleash epidemics of preventable diseases.

From the perspective of Orthomolecular Medicine (OM), canceling mandates is the right step forward for freedom and medical choice. But freedom without foundation is fragility. To truly succeed, removing mandates must be paired with building strong nutritional immunity. Otherwise, we risk not only health setbacks but also undermining the credibility and momentum of the MAHA movement (Make America Healthy Again).


MAHA’s Promise – and Its Responsibility

MAHA represents a historic opportunity: to reclaim health from the pharmaceutical establishment and restore it to the people. Rejecting coercive mandates affirms that health decisions belong to individuals and families, not bureaucracies.

But if the movement is perceived only as “anti-vaccine,”it risks public backlash. Outbreaks of measles, pertussis, or other diseases in poorly nourished, immune-fragile populations would hand the media and medical establishment their favorite headline: “MAHA endangers lives.“This would discredit reform and stall momentum for decades.


Nutritional Immunity: The Stronger Shield

Orthomolecular medicine has long emphasized the true foundation of health: biochemical sufficiency.

  • Vitamin D – essential for immune regulation; deficiency is widespread in the U.S.
  • Vitamin C – the master antioxidant; critical in infection defense at gram-level intakes.
  • Zinc and selenium – trace minerals vital for antiviral immunity.
  • Magnesium and omega-3 fats – essential for inflammation control and immune balance.
  • Nutrition – a low-carb, nutrient-dense diet stabilizes metabolism and strengthens host defenses.
  • Avoidance of ultraprocessed foods – refined carbs, industrial seed oils, and additives weaken immunity, fuel chronic inflammation, and accelerate metabolic fragility.

Without this “nutritional immunity,”America is like an army without armor – vulnerable, regardless of vaccine policy.


Freedom + Nutritional Immunity = Resilience

Canceling vaccine mandates is a necessary step to restore freedom. But true freedom is not only the absence of coercion – it is the presence of resilience.

  • Children and elderly are safest when both vaccine coercion is ended and nutritional immunity is built.
  • Poorer communities benefit most from nutrient sufficiency programs that reduce disease risk.
  • The establishment loses power when MAHA is framed as visionary and science-based, not reckless.

The Orthomolecular Path Forward

For MAHA to succeed, it must champion freedom plus resilience:

  1. End coercion – Cancel mandates and protect medical freedom as a fundamental right.
  2. Launch a national nutritional immunity program – Ensure access to vitamin D, vitamin C, zinc, and nutrient education in schools, workplaces, and nursing homes.
  3. Measure what matters – Track population vitamin D levels, nutrient sufficiency, and reductions in chronic disease, not just vaccine uptake.
  4. Maintain safeguards – Voluntary vaccines remain accessible, while communities are strengthened through nutrition and lifestyle health.

Conclusion

The real choice is not mandates versus no mandates. The real choice is fragility versus resilience.

Canceling mandates is a victory for freedom – but to secure health and credibility, MAHA must also lead a revolution in nutritional immunity. With optimal nutrition, metabolic health, and true prevention, MAHA can become a transformative force in American healthcare.

Make America Healthy Again must mean more than rejecting coercion. It must mean building strength from within. To truly succeed, MAHA must also mean: Make America Nutritious Again.


About the Author

Richard Z. Cheng, M.D., Ph.D.Editor-in-Chief, Orthomolecular Medicine News Service

Dr. Cheng is a U.S.-based, NIH-trained, board-certified physician specializing in integrative cancer therapy, orthomolecular medicine, functional & anti-aging medicine. He maintains active practices in both the United States and China.

A Fellow of the American Academy of Anti-Aging Medicine and a Hall of Fame inductee of the International Society for Orthomolecular Medicine, Dr. Cheng is a leading advocate for nutrition-based, root-cause health strategies. He also serves as an expert reviewer for the South Carolina Board of Medical Examiners, and co-founded both the China Low Carb Medicine Alliance and the Society of International Metabolic Oncology.

Dr. Cheng offers online Integrative Orthomolecular Medicine consultation services.
📰 Follow his latest insights on Substack: https://substack.com/@rzchengmd


Orthomolecular Medicine

Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org

Find a Doctor

To locate an orthomolecular physician near you: http://orthomolecular.org/resources/omns/v06n09.shtml

The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.

Editorial Review Board:

Jennifer L. Aliano, M.S., L.Ac., C.C.N. (USA)
Albert G. B. Amoa, MB.Ch.B, Ph.D. (Ghana)
Seth Ayettey, M.B., Ch.B., Ph.D. (Ghana)
Ilyès Baghli, M.D. (Algeria)
Greg Beattie, Author (Australia)
Barry Breger, M.D. (Canada)
Ian Brighthope, MBBS, FACNEM (Australia)
Gilbert Henri Crussol, D.M.D. (Spain)
Carolyn Dean, M.D., N.D. (USA)
Ian Dettman, Ph.D. (Australia)
Susan R. Downs, M.D., M.P.H. (USA)
Ron Ehrlich, B.D.S. (Australia)
Hugo Galindo, M.D. (Colombia)
Gary S. Goldman, Ph.D. (USA)
William B. Grant, Ph.D. (USA)
Claus Hancke, MD, FACAM (Denmark)
Patrick Holford, BSc (United Kingdom)
Ron Hunninghake, M.D. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Dwight Kalita, Ph.D. (USA)
Felix I. D. Konotey-Ahulu, M.D., FRCP (Ghana)
Peter H. Lauda, M.D. (Austria)
Fabrice Leu, N.D., (Switzerland)
Alan Lien, Ph.D. (Taiwan)
Homer Lim, M.D. (Philippines)
Stuart Lindsey, Pharm.D. (USA)
Pedro Gonzalez Lombana, M.D., Ph.D. (Colombia)
Diana MacKay (Gifford-Jones), M.P.P. (Canada)
Victor A. Marcial-Vega, M.D. (Puerto Rico)
Juan Manuel Martinez, M.D. (Colombia)
Mignonne Mary, M.D. (USA)
Dr.Aarti Midha M.D., ABAARM (India)
Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)
Karin Munsterhjelm-Ahumada, M.D. (Finland)
Sarah Myhill, MB, BS (United Kingdom)
Tahar Naili, M.D. (Algeria)
Zhiwei Ning, M.D., Ph.D. (China)
Zhiyong Peng, M.D. (China)
Pawel Pludowski, M.D. (Poland)
Isabella Akyinbah Quakyi, Ph.D. (Ghana)
Selvam Rengasamy, MBBS, FRCOG (Malaysia)
Jeffrey A. Ruterbusch, D.O. (USA)
Gert E. Schuitemaker, Ph.D. (Netherlands)
Thomas N. Seyfried, Ph.D. (USA)
Han Ping Shi, M.D., Ph.D. (China)
T.E. Gabriel Stewart, M.B.B.CH. (Ireland)
Jagan Nathan Vamanan, M.D. (India)
Dr. Sunil Wimalawansa, M.D., Ph.D. (Sri Lanka)

Andrew W. Saul, Ph.D. (USA), Founding & Former Editor
Richard Cheng, M.D., Ph.D. (USA), Editor-In-Chief
Associate Editor: Robert G. Smith, Ph.D. (USA)
Editor, Japanese Edition: Atsuo Yanagisawa, M.D., Ph.D. (Japan)
Editor, Chinese Edition: Richard Cheng, M.D., Ph.D. (USA)
Editor, Norwegian Edition: Dag Viljen Poleszynski, Ph.D. (Norway)
Editor, Arabic Edition: Moustafa Kamel, R.Ph, P.G.C.M (Egypt)
Editor, Korean Edition: Hyoungjoo Shin, M.D. (South Korea)
Editor, Spanish Edition: Sonia Rita Rial, PhD (Argentina)
Editor, German Edition: Bernhard Welker, M.D. (Germany)
Associate Editor, Arabic Edition: Ayman Kamel, DVM, MBA (Egypt)
Associate Editor, German Edition: Gerhard Dachtler, M.Eng. (Germany)
Assistant Editor: Michael Passwater (USA)
Contributing Editor: Thomas E. Levy, M.D., J.D. (USA)
Contributing Editor: Damien Downing, M.B.B.S., M.R.S.B. (United Kingdom)
Contributing Editor: W. Todd Penberthy, Ph.D. (USA)
Contributing Editor: Michael J. Gonzalez, N.M.D., Ph.D. (Puerto Rico)
Technology Editor: Michael S. Stewart, B.Sc.C.S. (USA)
Associate Technology Editor: Robert C. Kennedy, M.S. (USA)
Legal Consultant: Jason M. Saul, JD (USA)

Comments and media contact: editor@orthomolecular.org OMNS welcomes but is unable to respond to individual reader emails. Reader comments become the property of OMNS and may or may not be used for publication.

This article may be reprinted free of charge provided 1) that there is clear attribution to the Orthomolecular Medicine News Service, and 2) that both the OMNS free subscription link http://orthomolecular.org/subscribe.html and also the OMNS archive link http://orthomolecular.org/resources/omns/index.shtml are included.

Riordan Clinic | Orthomolecular.org
3100 N Hillside Ave
Wichita, Kansas 67219
United States

Vitamin B6 Lawsuits in Australia: Science, Safety, and the Truth Behind the Headlines

Reproduced from original OMNS article (OrthoMolecular News Service):
http://orthomolecular.org/


Subscribe to the free Orthomolecular Newsletter: http://orthomolecular.org/subscribe.html
Go to the OMNS Archive: http://orthomolecular.org/resources/omns/index.shtml

Orthomolecular Medicine News Service, August 27, 2025

by Richard Z. Cheng, M.D., Ph.D
Editor-in-Chief, Orthomolecular Medicine News Service

Editor’s Note – OMNS receives many thoughtful reader questions, but our current platform doesn’t support public Q&A. To foster more dialogue, I’ll share selected letters and replies on my Substack (👉 https://substack.com/@rzchengmd). OMNS will continue publishing articles from our editors and authors; this Substack Q&A is simply a complementary channel. I hope OMNS will add interactive features in the future so all editors can join the conversation. – Richard Z. Cheng, M.D., Ph.D., Editor-in-Chief

Summary – Recent headlines from Australia report lawsuits alleging nerve damage from vitamin B6 supplements. Understandably, this has sparked public concern: If vitamin B6 (pyridoxine) is essential for life, how can it also be accused of causing serious harm? And could these cases be used to further restrict public access to this vital nutrient?

What’s missing in these situations is not the value of supplementation itself – nutrient therapy remains a critical tool for health – but the way it is applied. In integrative orthomolecular medicine (IOM), no nutrient should be ever used as a stand-alone intervention. B6, like any vitamin or mineral, is prescribed in the context of the whole person: paired with essential cofactors, integrated with dietary and lifestyle measures, adjusted for individual biochemistry, and monitored for both safety and effectiveness. When supplementation is isolated from this broader IOM framework, its benefits can be reduced, and the risk of side effects increases – a gap that conventional guidelines and unsupervised use too often overlook.


1. What Is Vitamin B6 and Why Do We Need It?

Vitamin B6 is crucial for:

  • 🧠 Neurotransmitter synthesis – serotonin, dopamine, GABA (1,2)
  • 🍽 Amino acid metabolism – energy and brain chemistry (1)
  • 🛡 Immune function – supporting antibody production (3)
  • 🧬 Gene regulation – via one-carbon metabolism (4)
  • ❤️ Homocysteine control – with B12 and folate (5)

Deficiency can lead to depression, irritability, fatigue, poor immunity, cracked lips, and-in severe cases-anemia or seizures (1).


2. Why Is B6 Linked to Toxicity in the News?

Peripheral neuropathy (nerve damage) from B6 supplementation has been documented- but typically in cases of:

  • High-dose pyridoxine HCl >200-500 mg/day for many months or years (6,7)
  • Missing key nutrient cofactors (magnesium, B2, B12, folate)
  • Underlying metabolism issues that impair conversion of pyridoxine to its active form P5P (8,9)

Key points:

  • Most cases are reversible after stopping supplementation (6)
  • Active P5P form appears to have a lower risk profile (8)
  • The U.S. NIH Upper Limit is set at 100 mg/day (1), yet many clinical protocols use 50-200 mg/day safely under supervision (10,11)

3. Vitamin B6 Toxicity: Mechanisms

To better understand the controversy, it is important to review the biological mechanisms by which excessive B6 can rarely cause harm:

  • Dose and Duration – Most cases involve long-term intake of pyridoxine hydrochloride at >200-500 mg/day for months or years (6,7).
  • Impaired Conversion to P5P – Pyridoxine must be converted in the liver to its active form, pyridoxal-5′-phosphate (P5P). When conversion is impaired (due to genetic variants, liver detox stress, or toxins), unmetabolized pyridoxine may accumulate and act as a functional antagonist, blocking active B6 pathways (8,9).
  • Cofactor Deficiencies as Amplifiers – Low magnesium, riboflavin (B2), B12, or folate can impair pyridoxine utilization, amplifying the risk of neuropathy (8,12).
  • Reversibility – In most reported cases, symptoms improve or resolve after discontinuation of high-dose supplementation. Persistent neuropathy is rare and usually linked to extremely high or hidden intakes (6,8).

👉 These mechanisms reinforce the orthomolecular principle: nutrients like B6 should never be used in isolation, but rather in synergy with cofactors, tailored to individual biochemistry, and monitored for both safety and benefit.


4. Other Factors That May Increase B6 Sensitivity

Even moderate doses can cause problems if certain conditions are present:

  • Poor diet – high in carbs, ultra-processed foods, and low in protein (1,3).
  • Chronic toxin exposure – Environmental toxins (e.g., heavy metals, pesticides, solvents) and certain medications (e.g., isoniazid, hydralazine) (13).
  • Deficiency of other B-vitamins – Low B2 (riboflavin) or B12 (8,9).
  • Low magnesium or zinc (8,12).
  • Liver detox impairment (9).
  • Genetic variants.

Integrative orthomolecular practice always considers these co-factors-addressing them can both reduce toxicity risk and maximize therapeutic benefit from B6.


5. The Australian Lawsuits – What We Know

Media reports suggest long-term use of B6 before neuropathy symptoms.

However:

  • Doses, forms, and co-nutrient context are not disclosed
  • Literature shows dose and form are critical to safety (6,7)
  • In orthomolecular practice, unsupervised high-dose pyridoxine without cofactors is poor practice

6. Australia’s Regulatory Climate

The Therapeutic Goods Administration (TGA) already has some of the world’s strictest supplement rules.

  • Since 2022, warning labels are required on products with >10 mg/day B6, claiming neuropathy can occur even below 50 mg/day (14).
  • In 2025, the TGA proposed making products with 50-200 mg/day “pharmacist-only” (14,15).

This approach ignores decades of safe clinical use and individualized dosing principles. The risk is that lawsuits may push regulators toward even tighter restrictions, reducing access to safe, effective nutrient therapy.


7. Real-World Cases: Lessons from Australia

Prof. Ian Brighthope, my colleague on the OMNS editorial board, recently highlighted a striking case of vitamin B6 toxicity in Australia. Dr. Mary Buchanan, a general practitioner, developed progressive muscle weakness and peripheral neuropathy after unknowingly consuming excess B6 from over-the-counter magnesium tablets.

“I couldn’t walk – 100 metres was a struggle,”she recounted. Even a year after stopping, her recovery has been slow and incomplete.

➡️ Read Prof. Bright hope’s article here

This case illustrates two key issues Prof. Brighthope has emphasized:

  1. Hidden intake sources – B6 is found not only in supplements but also in energy drinks, cereals, and weight-loss shakes, leading to cumulative exposure well beyond safe levels.
  2. Regulatory response – Australia’s Therapeutic Goods Administration (TGA) has mandated warning labels for products with >10 mg/day of B6, after recognizing that neuropathy has been reported even at lower intakes when multiple products are combined.

8. Integrative Orthomolecular Medicine’s Perspective

In IOM, B6 is:

  • Personalized – Based on genetics, diet, symptoms (10).
  • Synergistic – Always paired with magnesium, B2, B12, folate, zinc (8,10).
  • Lifestyle-integrated – Supported by low-carb, nutrient-dense diet, toxin reduction, exercise, hormone balance.
  • Clinically monitored – Doses above 50-100 mg/day used only with follow-up for symptoms or labs (1,10).

9. Hormones and B6 Need.

Thyroid, adrenal, and sex hormones can change how your body uses B6:

  • Thyroid hormones – B6 intake can influence thyroid function; supplementation may lower high TSH in hypothyroidism (16).
  • Adrenal hormones – Corticosteroids may increase B6 needs (17-19).
  • Sex hormones – Estrogens may compete with B6; adequate B6 supports progesterone and testosterone synthesis (20).

10. Facts vs. Myths

Facts

  • Toxicity is rare and dose-dependent (6,8)
  • Active P5P form is better tolerated (8)
  • Most cases reverse after stopping (6)

🚫 Myths

  • “Any dose above the RDA is dangerous”- false
  • “All B6 forms are equally risky”- false
  • “B6 toxicity is always permanent”- false

11. Safe Supplementation Guidelines

Use Case Form Dose Notes
General support P5P or pyridoxine 10-50 mg/day Long-term safe (1)
Therapeutic (e.g., PMS, CTS) P5P preferred 100-200 mg/day Monitor if >3 months (10,11)
Neuropathy present Switch to P5P or stop < 50 mg/day Symptoms often reversible (6,8)

Always pair B6 with magnesium, B2, B12, folate, and zinc for optimal effect (8,10)


12. Bottom Line

Vitamin B6 is an essential nutrient and, when used wisely, a safe and powerful health tool. The Australian lawsuits highlight a need for better education on form, dose, and synergy – not fear-driven restrictions that may deny people access to safe, effective therapy.


About the Author

Richard Z. Cheng, M.D., Ph.D.Editor-in-Chief, Orthomolecular Medicine News Service

Dr. Cheng is a U.S.-based, NIH-trained, board-certified physician specializing in integrative cancer therapy, orthomolecular medicine, functional & anti-aging medicine. He maintains active practices in both the United States and China.

A Fellow of the American Academy of Anti-Aging Medicine and a Hall of Fame inductee of the International Society for Orthomolecular Medicine, Dr. Cheng is a leading advocate for nutrition-based, root-cause health strategies. He also serves as an expert reviewer for the South Carolina Board of Medical Examiners, and co-founded both the China Low Carb Medicine Alliance and the Society of International Metabolic Oncology.

Dr. Cheng offers online Integrative Orthomolecular Medicine consultation services.

📰 Follow his latest insights on Substack: https://substack.com/@rzchengmd


References

1. Office of Dietary Supplements – Vitamin B6 [Internet]. [cited 2025 Aug 9]. Available from: https://ods.od.nih.gov/factsheets/VitaminB6-HealthProfessional/

2. Kennedy DO. B Vitamins and the Brain: Mechanisms, Dose and Efficacy–A Review. Nutrients. 2016 Jan 27;8(2):68.

3. Wintergerst ES, Maggini S, Hornig DH. Contribution of selected vitamins and trace elements to immune function. Ann Nutr Metab. 2007;51(4):301-23.

4. Finkelstein JD. Methionine metabolism in mammals. J Nutr Biochem. 1990 May;1(5):228-37.

5. Malinow MR, Bostom AG, Krauss RM. Homocyst(e)ine, diet, and cardiovascular diseases: a statement for healthcare professionals from the Nutrition Committee, American Heart Association. Circulation. 1999 Jan 5;99(1):178-82.

6. Dalton K, Dalton MJ. Characteristics of pyridoxine overdose neuropathy syndrome. Acta Neurol Scand. 1987 July;76(1):8-11.

7. Albin RL, Albers JW, Greenberg HS, Townsend JB, Lynn RB, Burke JM, et al. Acute sensory neuropathy-neuronopathy from pyridoxine overdose. Neurology. 1987 Nov;37(11):1729-32.

8. Schellack N, Yotsombut K, Sabet A, Nafach J, Hiew FL, Kulkantrakorn K. Expert Consensus on Vitamin B6 Therapeutic Use for Patients: Guidance on Safe Dosage, Duration and Clinical Management. Drug Healthc Patient Saf. 2025 Apr 7;17:97-108.

9. Hadtstein F, Vrolijk M. Vitamin B-6-Induced Neuropathy: Exploring the Mechanisms of Pyridoxine Toxicity. Adv Nutr. 2021 Oct 1;12(5):1911-29.

10. Brush MG, Bennett T, Hansen K. Pyridoxine in the treatment of premenstrual syndrome: a retrospective survey in 630 patients. Br J Clin Pract. 1988 Nov;42(11):448-52.

11. Ellis JM, Folkers K. Clinical aspects of treatment of carpal tunnel syndrome with vitamin B6. Ann N Y Acad Sci. 1990;585:302-20.

12. Gröber U, Schmidt J, Kisters K. Magnesium in Prevention and Therapy. Nutrients. 2015 Sept 23;7(9):8199-226.

13. Parry GJ, Bredesen DE. Sensory neuropathy with low-dose pyridoxine. Neurology. 1985 Oct;35(10):1466-8.

14. Administration (TGA) TG. Peripheral neuropathy with supplementary vitamin B6 (pyridoxine) | Therapeutic Goods Administration (TGA) [Internet]. Therapeutic Goods Administration (TGA); 2022 [cited 2025 Aug 9]. Available from: https://www.tga.gov.au/news/safety-updates/peripheral-neuropathy-supplementary-vitamin-b6-pyridoxine

15. NewsGP [Internet]. [cited 2025 Aug 9]. newsGP – Sweeping vitamin B6 restrictions proposed. Available from: https://www1.racgp.org.au/newsgp/clinical/sweeping-vitamin-b6-restrictions-proposed

16. Li L, Wang J, Chen J. Relationship between vitamin B6 intake and thyroid function in US adults: NHANES 2007-2012 results. PLoS One. 2025;20(4):e0321688.

17. Chang HY, Tzen JTC, Lin SJ, Wu YT, Chiang EPI. Long-term prednisolone treatments increase bioactive vitamin B6 synthesis in vivo. J Pharmacol Exp Ther. 2011 Apr;337(1):102-9.

18. Mahuren JD, Dubeski PL, Cook NJ, Schaefer AL, Coburn SP. Adrenocorticotropic hormone increases hydrolysis of B-6 vitamers in swine adrenal glands. J Nutr. 1999 Oct;129(10):1905-8.

19. Allgood VE, Powell-Oliver FE, Cidlowski JA. The influence of vitamin B6 on the structure and function of the glucocorticoid receptor. Ann N Y Acad Sci. 1990;585:452-65.

20. Rose DP. The interactions between vitamin B6 and hormones. Vitam Horm. 1978;36:53-99.


Orthomolecular Medicine

Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org

Find a Doctor

To locate an orthomolecular physician near you: http://orthomolecular.org/resources/omns/v06n09.shtml

The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.

Editorial Review Board:

Jennifer L. Aliano, M.S., L.Ac., C.C.N. (USA)
Albert G. B. Amoa, MB.Ch.B, Ph.D. (Ghana)
Seth Ayettey, M.B., Ch.B., Ph.D. (Ghana)
Ilyès Baghli, M.D. (Algeria)
Greg Beattie, Author (Australia)
Barry Breger, M.D. (Canada)
Ian Brighthope, MBBS, FACNEM (Australia)
Gilbert Henri Crussol, D.M.D. (Spain)
Carolyn Dean, M.D., N.D. (USA)
Ian Dettman, Ph.D. (Australia)
Susan R. Downs, M.D., M.P.H. (USA)
Ron Ehrlich, B.D.S. (Australia)
Hugo Galindo, M.D. (Colombia)
Gary S. Goldman, Ph.D. (USA)
William B. Grant, Ph.D. (USA)
Claus Hancke, MD, FACAM (Denmark)
Patrick Holford, BSc (United Kingdom)
Ron Hunninghake, M.D. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Dwight Kalita, Ph.D. (USA)
Felix I. D. Konotey-Ahulu, M.D., FRCP (Ghana)
Peter H. Lauda, M.D. (Austria)
Fabrice Leu, N.D., (Switzerland)
Alan Lien, Ph.D. (Taiwan)
Homer Lim, M.D. (Philippines)
Stuart Lindsey, Pharm.D. (USA)
Pedro Gonzalez Lombana, M.D., Ph.D. (Colombia)
Diana MacKay (Gifford-Jones), M.P.P. (Canada)
Victor A. Marcial-Vega, M.D. (Puerto Rico)
Juan Manuel Martinez, M.D. (Colombia)
Mignonne Mary, M.D. (USA)
Dr.Aarti Midha M.D., ABAARM (India)
Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)
Karin Munsterhjelm-Ahumada, M.D. (Finland)
Sarah Myhill, MB, BS (United Kingdom)
Tahar Naili, M.D. (Algeria)
Zhiwei Ning, M.D., Ph.D. (China)
Zhiyong Peng, M.D. (China)
Pawel Pludowski, M.D. (Poland)
Isabella Akyinbah Quakyi, Ph.D. (Ghana)
Selvam Rengasamy, MBBS, FRCOG (Malaysia)
Jeffrey A. Ruterbusch, D.O. (USA)
Gert E. Schuitemaker, Ph.D. (Netherlands)
Thomas N. Seyfried, Ph.D. (USA)
Han Ping Shi, M.D., Ph.D. (China)
T.E. Gabriel Stewart, M.B.B.CH. (Ireland)
Jagan Nathan Vamanan, M.D. (India)
Dr. Sunil Wimalawansa, M.D., Ph.D. (Sri Lanka)

Andrew W. Saul, Ph.D. (USA), Founding Editor
Richard Cheng, M.D., Ph.D. (USA), Editor-In-Chief
Associate Editor: Robert G. Smith, Ph.D. (USA)
Editor, Japanese Edition: Atsuo Yanagisawa, M.D., Ph.D. (Japan)
Editor, Chinese Edition: Richard Cheng, M.D., Ph.D. (USA)
Editor, Norwegian Edition: Dag Viljen Poleszynski, Ph.D. (Norway)
Editor, Arabic Edition: Moustafa Kamel, R.Ph, P.G.C.M (Egypt)
Editor, Korean Edition: Hyoungjoo Shin, M.D. (South Korea)
Editor, Spanish Edition: Sonia Rita Rial, PhD (Argentina)
Editor, German Edition: Bernhard Welker, M.D. (Germany)
Associate Editor, Arabic Edition: Ayman Kamel, DVM, MBA (Egypt)
Associate Editor, German Edition: Gerhard Dachtler, M.Eng. (Germany)
Assistant Editor: Michael Passwater (USA)
Contributing Editor: Thomas E. Levy, M.D., J.D. (USA)
Contributing Editor: Damien Downing, M.B.B.S., M.R.S.B. (United Kingdom)
Contributing Editor: W. Todd Penberthy, Ph.D. (USA)
Contributing Editor: Michael J. Gonzalez, N.M.D., Ph.D. (Puerto Rico)
Technology Editor: Michael S. Stewart, B.Sc.C.S. (USA)
Associate Technology Editor: Robert C. Kennedy, M.S. (USA)
Legal Consultant: Jason M. Saul, JD (USA)

Comments and media contact: editor@orthomolecular.org OMNS welcomes but is unable to respond to individual reader emails. Reader comments become the property of OMNS and may or may not be used for publication.

Click here to see a web copy of this news release: http://orthomolecular.activehosted.com/p_v.php?c=466&m=404&s=a8c8fe7bea3fdaa4efae896c7612b3de&d=0&v=2&l

This article may be reprinted free of charge provided 1) that there is clear attribution to the Orthomolecular Medicine News Service, and 2) that both the OMNS free subscription link http://orthomolecular.org/subscribe.html and also the OMNS archive link http://orthomolecular.org/resources/omns/index.shtml are included.

Riordan Clinic | Orthomolecular.org
3100 N Hillside Ave
Wichita, Kansas 67219
United States

 

Titanium Dioxide in Processed Foods Disrupts Gut Hormones and Blood Sugar


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/08/20/titanium-dioxide-food-additive-health-risks.aspx


Analysis by Dr. Joseph Mercola     
August 20, 2025

Story at-a-glance

  • Titanium dioxide is a common food additive used to whiten and brighten processed foods, but studies show it disrupts gut hormone signaling, impairs blood sugar control, and contributes to metabolic dysfunction
  • Even without causing visible gut damage, titanium dioxide shuts down the production of hormones that are key to appetite regulation, insulin response, and digestive timing
  • Research shows titanium dioxide particles interfere with how stem cells in your gut mature, preventing them from becoming hormone-producing cells and leading to a silent breakdown in metabolic communication
  • Titanium dioxide also damages intestinal structures responsible for nutrient absorption and weakens your gut barrier, which triggers inflammation, nutrient deficiencies, and leaky gut
  • Despite growing international bans, titanium dioxide is still legal in the U.S. and appears in foods marketed to children, supplements, and toothpaste, often without clear labeling

You eat it without knowing. Titanium dioxide is added to thousands of processed foods to make them look brighter, smoother, and more appealing. It’s what gives sandwich cookies their crisp white filling and powdered donuts their snowy coating. You’ll find it in breath mints, gum, coffee creamers, and even children’s chewable vitamins. It serves no nutritional purpose — and yet it’s everywhere.

The problem isn’t just that it’s unnecessary. The smallest form of this additive — titanium dioxide nanoparticles — is now being linked to serious metabolic disruption. We’re talking about measurable shifts in blood sugar control, gut hormone activity, and even the way your intestines absorb nutrients.1 And this isn’t rare contamination or occasional exposure.

If you eat processed food regularly, you’re likely swallowing trillions of these particles every day. What makes it more dangerous is how quietly it works. Unlike toxic chemicals that inflame or destroy tissue outright, titanium dioxide interferes with how your gut functions at the cellular level, long before you feel anything is wrong. The latest findings are forcing a deeper look at what these particles do once they enter your body — and why their impact goes far beyond what most food safety regulations account for.

Titanium Dioxide Hijacks Your Gut’s Hormone Signals

A study published in Food and Chemical Toxicology tested how titanium dioxide — the whitening additive found in many processed foods — affects your body at the cellular level.2 Researchers used both intestinal cells grown in the lab and live mice to find out if these tiny particles mess with how your gut talks to your brain and pancreas. Their goal? To see how titanium dioxide affects hunger cues, digestion, and blood sugar regulation.

Mice given food containing titanium dioxide had trouble controlling their blood sugar — The mice were fed chow mixed with 1% food-grade titanium dioxide, which matches how much people, especially children, get from their diets. Over time, their blood sugar went up, and their ability to handle glucose after eating got worse. In simple terms, their metabolism started looking like the early stages of diabetes.

Even though their gut tissue looked normal, the hormone system inside was disrupted — The intestines weren’t visibly damaged. But inside, key hormone-producing cells weren’t working properly. These cells normally release hormones like glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and cholecystokinin (CCK), which help control appetite, signal fullness, manage insulin, and regulate how fast your stomach empties. Titanium dioxide interfered with these cells’ development and function.

The gut hormones that regulate appetite and insulin were nearly shut off — Hormones that are supposed to be released after meals dropped significantly in the exposed mice. Without these hormones, the body doesn’t know when to stop eating, how much insulin to release, or how to properly manage blood sugar. The problem isn’t just what you eat — it’s how your body responds to it.

The disruption came from how gut stem cells matured, not from visible damage or inflammation — Stem cells in the gut are supposed to develop into different cell types, including those that make hormones. But titanium dioxide exposure changed that process. Instead of maturing into functional hormone-producing cells, the stem cells were redirected, leading to a breakdown in gut signaling. There was no tissue destruction, just a silent failure in communication.

This breakdown in signaling makes it harder to feel full or maintain stable energy — When GLP-1 and PYY levels drop, your brain doesn’t register fullness, and your pancreas doesn’t get the right message to release insulin. Your digestion speeds up or slows down unpredictably. That means more hunger, energy crashes, and blood sugar swings, all of which raise your risk for chronic disease.

Titanium Dioxide Is Widespread in Processed Foods Despite Risks

A report from U.S. Right to Know highlighted findings from the Food and Chemical Toxicology study and emphasized how everyday food exposure adds up, especially for children.3 According to the article, many common snack foods, from sandwich cookies to colorful candies, contain titanium dioxide in nanoparticle form.

Children are more vulnerable to harm — This is because of their lower body weight and, often, higher consumption of processed foods. U.S. Right to Know pointed out that food-grade titanium dioxide is banned in the European Union due to safety concerns, but remains widely used in the U.S. without any warning label.

Hormone disruption occurred without obvious physical damage — Unlike toxins that inflame or destroy tissue, titanium dioxide nanoparticles work in a more insidious way. The news piece explained that the damage occurs at the molecular level — blocking your body’s ability to sense food and regulate insulin.

Titanium dioxide has been linked to cancer, gut inflammation, and brain health concerns — Research in animal and cell studies has connected titanium dioxide exposure to DNA damage, which raises cancer risk, intestinal inflammation, metabolic disorders tied to obesity, and even brain diseases like Alzheimer’s.

The International Agency for Research on Cancer classifies it as “possibly carcinogenic to humans,” and in 2021 the European Food Safety Authority declared it unsafe for food use.4

Despite bans overseas, titanium dioxide is still allowed in U.S. food, with limited oversight — France banned titanium dioxide in 2020, followed by the European Union in 2022. But in the U.S., it’s still legal and often hides on labels under vague terms like “artificial color.”

The U.S. Food and Drug Administration (FDA) considers it “generally recognized as safe” as long as it makes up less than 1% of the food’s weight — but doesn’t require labeling of particle size or full disclosure. New York lawmakers are now pushing legislation to ban it and require transparency in food chemicals.

Save This Article for Later – Get the PDF Now

Download PDF

Titanium Dioxide Nanoparticles Shrink Nutrient Absorption and Damage Gut Structure

Published in NanoImpact, a related study investigated how chronic exposure to titanium dioxide nanoparticles impacts human intestinal cells using a lab-grown cell model that mimics the small intestine.5 Unlike previous studies that focused on immune or hormonal effects, this one focused specifically on the digestive lining — how nutrients are absorbed and what happens to the gut’s protective barrier after repeated exposure.

Researchers found serious disruptions to nutrient uptake and gut cell structure — The study showed that exposure to titanium dioxide nanoparticles reduced the absorption of key nutrients, including iron, zinc, and essential fatty acids.

It also caused the loss of microvilli, the microscopic fingerlike projections that line your intestine and help your body absorb food efficiently. These structural changes appeared after just a few days of exposure, with more damage accumulating over time.

The gut’s “filter system” started to break down, making it more vulnerable to toxins and bacteria — One of the most important findings was the disruption of tight junction proteins — cellular “gatekeepers” that keep harmful substances from leaking through your gut wall.

When these are weakened, your gut barrier becomes permeable, allowing partially digested food particles, toxins, and bacteria to escape into your bloodstream. This condition, often referred to as “leaky gut,” has been linked to systemic inflammation, autoimmune problems, and chronic disease.

Key nutrient transporters were downregulated, reducing how much your gut could absorb from food — The study found a significant decrease in the expression of key nutrient transporters. That means even if you’re eating a nutrient-rich diet, your gut isn’t able to pull those nutrients into your bloodstream effectively. It’s not a deficiency of food — it’s a breakdown in the machinery that makes food useful.

The changes occurred without inflammation, making them harder to detect, but just as damaging — There was no cell death, bleeding, or overt toxicity. Instead, the titanium dioxide triggered subtle dysfunctions like changes in cell behavior, suppressed nutrient uptake, and weakened structural integrity. This kind of silent disruption is especially dangerous because it’s easy to overlook until larger problems emerge.

Oxidative stress was a major driver of the structural damage — Titanium dioxide nanoparticles increased the production of reactive oxygen species (ROS), unstable molecules that damage DNA, proteins, and cell membranes. The study confirmed that oxidative stress was one of the main biological mechanisms driving the breakdown of microvilli and weakening of tight junctions.

When left unchecked, this stress leads to long-term degradation of gut function and makes recovery more difficult. The researchers emphasized that repeated exposure to titanium dioxide, especially from daily processed food consumption, amplifies the negative effects. The more often your gut lining is exposed to these particles, the more structural damage accumulates, and the more likely nutrient malabsorption becomes.

How to Avoid Titanium Dioxide in Your Food

If your goal is to protect your gut, balance your blood sugar, and avoid harmful hormone disruption, your first step is removing the source of the problem. Titanium dioxide is legal but not safe — and avoiding it takes strategy, not guesswork. Most food labels won’t warn you clearly, and many processed items marketed to children are among the worst offenders. Here’s how to avoid it in your food:

1. Cut out processed snacks, gums, and candies — Titanium dioxide is most common in white or brightly colored sweets like mints, marshmallows, powdered donuts, frosting, and chewing gum. It’s also used in some dairy substitutes and protein bars. If you’re regularly eating foods with shiny, smooth coatings or pure-white fillings, it’s time to check the label — or better yet, avoid those products altogether.

2. Look for short ingredient lists with real foods only — The more processed an item is, the more likely it is to contain titanium dioxide. Aim for whole-food ingredients you recognize. If the label mentions “artificial color,” “color added,” “colored with titanium dioxide,” or “E171” (its label in some international products), steer clear. But beware — not all products have to list it, especially if it’s part of a blend. When in doubt, skip it.

3. Avoid ultraprocessed items, especially those marketed to children — Foods aimed at children, like colorful cereals, gummies, and snack packs, are some of the biggest sources of titanium dioxide. If you’re a parent, I strongly recommend avoiding these items. Even small amounts eaten daily could trigger long-term metabolic effects based on the research.

4. Choose supplements carefully — Many chewable vitamins, probiotics, and over-the-counter pills use titanium dioxide to make tablets look smooth and white. Always check supplement labels, especially if the pill is bright white or has a glossy coating. Opt for capsules, powders, or brands that clearly state “titanium dioxide free.”

5. Buy from brands and stores that ban titanium dioxide — Some natural food brands and grocery chains have banned titanium dioxide from their products altogether. Look for stores with published “no artificial additives” policies, and stick to brands that commit to clean ingredients. It’s one of the easiest ways to shop smarter without needing to decode every label.

FAQs About Titanium Dioxide

Q: What is titanium dioxide and why is it added to food?

A: Titanium dioxide is a whitening agent used in thousands of processed foods to enhance color and visual appeal. It’s commonly found in white or brightly colored candies, frostings, powdered donuts, breath mints, coffee creamers, and even supplements. It has no nutritional benefit and is used purely for appearance.

Q: How does titanium dioxide affect my gut and metabolism?

A: Research shows that titanium dioxide nanoparticles interfere with hormone-producing cells in your gut.6 These hormones control appetite, blood sugar, and digestion. Disrupting them causes blood sugar spikes, poor insulin signaling, increased hunger, and higher risk for conditions like insulin resistance and metabolic syndrome.

Q: Does titanium dioxide damage my gut without causing symptoms?

A: Yes. Titanium dioxide doesn’t visibly inflame or destroy gut tissue. Instead, it silently alters how gut stem cells mature and how nutrients are absorbed. It reduces microvilli, which absorb food, weakens your gut barrier — leading to leaky gut — and triggers oxidative stress that erodes intestinal function over time.7

Q: Is titanium dioxide banned in other countries?

A: Yes. France banned it in 2020, and the European Union followed in 2022. The European Food Safety Authority declared it unsafe in 2021. In contrast, the U.S. FDA still allows its use and classifies it as “generally recognized as safe,” with no requirement to list particle size or include it on all labels.8

Q: How do I avoid titanium dioxide in my diet?

A: Start by cutting out highly processed foods, especially those with shiny coatings or white fillings. Read ingredient lists and avoid products that mention “titanium dioxide,” “artificial color,” or “E171.” Check supplements, personal care items, and toothpaste as well. Opt for brands and retailers that prohibit titanium dioxide use entirely.

How to Avoid and Treat Digital Eye Strain


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2025/03/27/digital-eye-strain.aspx


Analysis by Dr. Joseph Mercola     
March 27, 2025

digital eye strain

STORY AT-A-GLANCE

  • Digital eye strain affects 55% to 81% of screen users, causing blurred vision, tired eyes, headaches and neck pain due to extended exposure to digital devices
  • Environmental factors like improper lighting, workspace setup and screen positioning contribute to eye strain and worsen symptoms
  • Taking regular breaks and limiting screen time help reduce eye strain by resting eye muscles and normalizing blink rates
  • Nutrition plays a key role in eye health, with anthocyanins from berries and carotenoids (lutein and zeaxanthin) from egg yolks acting as natural blue light filters
  • Digital strain extends beyond eyes to overall health, causing sleep disturbances, musculoskeletal issues and even skin conditions like “screen dermatitis”

Our modern world has become undeniably tethered to digital devices. Indeed, the last decade has seen a massive surge in digital device usage across all age groups. This constant connectivity has brought with it a significant health concern: digital eye strain.

Digital eye strain, also known as computer vision syndrome (CVS), is a cluster of ocular, musculoskeletal and even behavioral problems triggered by extended exposure to digital screens, including blurred vision, tired eyes, headaches and neck pain.

As we rely more and more on screens, understanding digital eye strain and how to mitigate its effects becomes increasingly important. The good news is that research is providing valuable insights into both the causes and solutions for this widespread issue.

Many Factors Contribute to Digital Eye Strain

A review published in the journal Medicina explored the environmental, visual and physical factors that contribute to digital eye strain.1 The aim of this review was to consolidate the latest scientific findings to better equip eye care professionals and individuals with effective strategies to manage this widespread condition.

The review of numerous studies highlighted that asthenopia, a condition commonly known as eye strain or eye fatigue, is remarkably prevalent among people who regularly use visual display terminals like computer screens. In fact, studies show that anywhere from 55% to as high as 81% of screen users experience asthenopia.

Interestingly, while some research is still unclear on whether age directly impacts asthenopia during computer use, there’s evidence suggesting that starting screen use at a young age makes asthenopia more likely.

Furthermore, people over 30 are more prone to developing dry eyes specifically related to digital screen use. It’s also worth noting that women appear to report asthenopia more frequently than men, suggesting sex may play a role in the experience of these symptoms.

Beyond general eye strain, the Medicina review emphasized that using screens for extended periods disrupts various aspects of vision and eye function. For instance, prolonged close-up work on devices like cellphones has been linked to a condition called acute acquired comitant esotropia (AACE), particularly in younger individuals. This condition, where the eyes turn inward, leads to double vision and, if persistent, results in amblyopia, also known as lazy eye.

The type of device and how you use it also significantly influences the degree of eye strain. The review points out that prolonged smartphone and computer use is associated with higher levels of myopia, or nearsightedness, compared to using tablets or watching TV. Intriguingly, studies examining the link between screen use and intraocular pressure (IOP), the pressure inside your eye, have also yielded important findings.

One study discovered a small but notable increase in IOP linked to smartphone use, and this pressure change became more pronounced in low-light conditions. This is particularly relevant for individuals with conditions like normal tension glaucoma, where using smartphones in dim settings could elevate IOP further.

Environmental factors at your workspace also have a considerable impact on eye comfort while using screens, according to the review. Overhead lighting that shines onto the screen reduces text contrast, leading to increased eye fatigue and discomfort. Conversely, adjustable task lighting has been shown to provide relief for both visual and muscle strain, while also improving posture.

Work and Lifestyle Habits Affect Digital Eye Strain

Work habits, particularly the duration of screen use, play a key role in digital eye strain. The Medicina review highlights that extended hours spent on screens correlate directly with more pronounced visual symptoms. To counteract this, structuring computer work with frequent breaks is essential.

Schedules incorporating short breaks, such as micro-breaks every 15 minutes or five-minute breaks every 30 minutes, not only boost work efficiency but also help reduce eye and muscle discomfort.

Furthermore, excessive screen time, especially smartphone use, significantly affects sleep quality, leading to shorter sleep duration and reduced sleep efficiency. Studies have confirmed that this disruption of sleep patterns is just one of many physical and psychological side effects associated with too much screen time. It’s also been found that spending more than four hours a day on screens significantly increases the risk of developing dry eye syndrome, especially in older adults.

Additionally, lifestyle choices such as smoking introduce further risk, as smoking is a known risk factor for various eye conditions, including dry eye and cataracts, further complicating digital eye strain. Device-related factors, such as screen angle and display quality, also matter. Improper viewing angles, particularly screens positioned too high, are identified as a major risk factor for digital eye strain.

Poor screen resolution and screen glare exacerbate eye strain severity, with small screens and font sizes increasing eye strain due to focus issues. Furthermore, 3D stereoscopic displays and virtual reality headsets introduce additional strain on accommodation, convergence and tear dynamics, causing symptoms like motion sickness and fatigue, especially in women using VR headsets.

Save This Article for Later – Get the PDF Now

Download PDF

Digital Screen Use Affects Your Eyes and Overall Health

The health of your eye’s surface is just one area impacted by digital screen use. The Medicina review discusses how prolonged screen use impairs spontaneous blinking, leading to increased tear film evaporation and ocular discomfort. Reduced blinking frequency and duration contribute to dry eye disease.

To combat this, the review suggests preventive measures such as taking eye rest breaks, practicing blinking exercises and modifying environmental factors like humidity. Blinking exercises, like closing your eyes for short durations and squeezing eyelids, help reduce dry eye disease symptoms and improve tear film quality. Using desktop humidifiers also enhance tear film stability and eye comfort.2

Digital eye strain extends beyond just your eyes, however. People who spend up to 12 hours daily on digital screens can experience headaches, sleep disturbances and musculoskeletal issues, including neck, shoulder and back pain. Improper posture, screen position and non-ergonomic furniture contribute to these musculoskeletal problems.

Smartphone use, in particular, often leads to abnormal neck bending, increasing muscle fatigue and pain. Furthermore, prolonged screen use also affects wrists, arms and hands, leading to carpal tunnel syndrome due to pressure on wrist tendons. Some individuals also develop “screen dermatitis,” a skin condition characterized by redness and irritation.

Nutrition Is a Key Component in Easing Digital Eye Strain

Can what you eat actually help your eyes cope with all that screen time? That’s the question explored in a compelling review published in the journal Nutrients.3 This research dives into the role of nutrition, specifically certain micronutrients found in supplements and foods, to lessen the symptoms of digital eye strain.

Oxidative damage and ongoing inflammation are major culprits in why digital eye strain develops. According to the Nutrients review, eating the right nutrients is a way to ease those bothersome eye symptoms. For instance, anthocyanins are the pigments that give berries and colorful vegetables their vibrant hues, and they’re celebrated for their antioxidant, anti-inflammatory and immune-boosting abilities.

Studies included in the review indicate that anthocyanins improve eye muscle function, which is key for focusing and reducing eye strain. Specifically, bilberry extract, rich in anthocyanins, has been shown to enhance the responsiveness of eye muscles after short periods of screen use, suggesting these nutrients could help eyes recover from the strain of digital devices.

Furthermore, anthocyanins also alleviate those subjective feelings of tired eyes and blurred vision that are common complaints among heavy screen users.

Another set of powerful nutrients discussed in the review are carotenoids, especially lutein and zeaxanthin. These are macular carotenoids, meaning they are highly concentrated in the macula, the central part of your retina responsible for sharp, central vision. Lutein and zeaxanthin act as a natural defense against blue light, the high-energy light emitted from digital screens, by filtering it out and neutralizing harmful free radicals produced by blue light exposure.

The review points out that maintaining good levels of these carotenoids is linked to better visual performance, reducing glare sensitivity, improving contrast and lessening overall visual fatigue — all symptoms associated with digital eye strain. These carotenoids aren’t just beneficial for vision; research suggests they also play a role in reducing psychological stress and improving sleep quality, which are often disrupted by excessive screen time.

Practical Tips to Prevent and Relieve Digital Eye Strain

Dealing with digital eye strain in our screen-filled lives can feel like an unavoidable part of the day, but it doesn’t have to be that way. The good news is, there are straightforward steps to ease the strain and make your eyes more comfortable. By making a few simple adjustments to your habits and environment, you lessen the impact of digital devices on your vision and overall well-being. Let’s get into some practical ways to start protecting your eyes today.

1. Embrace regular eye breaks — If you’re spending hours in front of a screen, taking regular visual breaks is paramount. While the 20/20/20 rule — look 20 feet away for 20 seconds every 20 minutes — is a common recommendation, recent studies suggest that even this isn’t sufficient for everyone and longer breaks are necessary.4,5

Try to take a five-minute break for every hour of screen time. During these breaks, make sure you’re not just switching to another screen. Instead, get up, walk around, stretch and let your eyes completely relax from focusing up close. This is important for giving those tired eye muscles a rest and letting your blink rate return to normal, which helps keep your eyes properly moisturized.6

2. Avoid blue light exposure before bed — It’s really important to manage your exposure to blue light from screens, especially in the hours leading up to bedtime. Screen use before bed interferes with sleep, and lack of good sleep worsens eye strain.

To help with this, try to avoid screens after sunset. Also, in the evenings, dimming the lights in your home and using warmer light sources instead of bright, cool lights makes a difference. If you absolutely must use screens at night, consider using blue light filters on your devices or wearing blue light-blocking glasses.

3. Limit your overall screen time — One of the most direct ways to reduce digital eye strain is simply to cut down on screen time. Think about how much time you actually need to spend looking at screens for work and leisure. Are there areas where you can reduce usage?

Consider setting specific times for checking emails or social media, rather than constantly being connected. Perhaps swap some screen-based leisure activities for hobbies that don’t involve screens, like reading a physical book, going for a walk or spending time with friends and family face-to-face.

4. Optimize nutrition for eye health — Anthocyanins, the colorful pigments in berries, help reduce eye fatigue and improve muscle function. Lutein and zeaxanthin, carotenoids found in leafy green vegetables and egg yolks, act like internal blue light filters and antioxidants.

Your eyes are also highly susceptible to and damaged by polyunsaturated fats (PUFAs) such as linoleic acid (LA), so avoid consuming seed oils (also known as vegetable oils) and stay clear of processed foods, fast food meals and most restaurant food, which typically contain them.

5. Spend more time outdoors — Getting outside more often is beneficial for your eyes. When you’re outdoors, you’re naturally looking at things in the distance, which gives your eye muscles a break from the constant close-up focus required by screens.

Sunlight is also different from artificial indoor lighting and screen light, and this has a positive effect on eye health. Plus, spending time outdoors is great for overall well-being, reducing stress and improving mood, which indirectly helps with physical symptoms like eye strain. Make an effort to incorporate regular outdoor time into your day, even if it’s just a walk during lunch breaks.

Frequently Asked Questions About Digital Eye Strain

Q: What exactly is digital eye strain, and how do I know if I have it?

A: Digital eye strain, also known as computer vision syndrome, is what happens when your eyes get tired and strained from too much screen time. You might notice symptoms like blurry vision, dry or irritated eyes, headaches, and even neck and shoulder pain. If you’re spending a lot of time on digital devices and experiencing these discomforts, it’s likely digital eye strain. It’s a common issue in our tech-heavy world.

Q: Why do screens cause my eyes to feel so tired and blurry?

A: Screens cause eye strain for a couple of main reasons. First, you blink much less when you’re focused on a screen, which dries out your eyes — blinking is like your eye’s natural windshield wiper.7 Second, the muscles in your eyes get tired from constantly focusing on a fixed, close-up point for extended periods. These factors combined lead to that blurry, fatigued feeling you get after prolonged screen use.

Q: Are children more susceptible to digital eye strain than adults, and are their symptoms different?

A: Children are in the high-risk group for digital eye strain, and it’s something to really keep an eye on. Children often spend even more time on screens than adults, and their eyes are still developing, which makes them more vulnerable.

Some studies suggest screen use in children could be linked to nearsightedness.8 Unlike adults who often self-manage, children might not always express their discomfort clearly, or understand why they’re feeling it, making proactive management important.

Q: Besides just eye breaks, are there changes I can make to my workspace setup to ease eye strain?

A: How set up your workspace makes a difference in reducing eye strain. Your screen position should be about arm’s length away and slightly below eye level. Adjustable task lighting is also great because, unlike overhead lights that cause glare, it lets you direct light where you need it without shining directly on your screen. Small ergonomic tweaks add up to a more comfortable screen-using experience.

Q: Can my diet play a role in managing digital eye strain?

A: Yes, what you eat supports your eye health in the face of digital eye strain. Specific nutrients like anthocyanins and carotenoids as especially beneficial. Anthocyanins help reduce eye fatigue and carotenoids improve visual performance and protect against blue light. Your eyes are highly susceptible to and damaged by polyunsaturated fats (PUFAs) such as linoleic acid (LA) in seed oils, so eliminate the processed foods that contain them.

Understanding the Root Causes of Dyslipidemia in Atherosclerotic Cardiovascular Disease

Reproduced from original OMNS article (OrthoMolecular News Service):
http://orthomolecular.org/


Subscribe to the free Orthomolecular Newsletter: http://orthomolecular.org/subscribe.html
Go to the OMNS Archive: http://orthomolecular.org/resources/omns/index.shtml
Orthomolecular Medicine News Service, January 10, 2025

Richard Z. Cheng, M.D., Ph.D., Thomas E. Levy, M.D., J.D.

Highlights

A paradigm shift from the cholesterol-centric focus on symptom management to addressing the root causes of ASCVD has demonstrated potential for prevention and reversal, as shown by our recently reported 10 ASCVD reversal cases (1).

Abstract

Dyslipidemia has long been the primary target for atherosclerotic cardiovascular disease (ASCVD) treatment. However, we have recently presented compelling evidence demonstrating that dyslipidemia is an intermediary mechanistic step, not a root cause of ASCVD, and that the American Heart Association’s decades-long cholesterol-centric dogma is both unreasonable and potentially unethical, bordering on criminal negligence (2).

In our international consultation services, we have shifted from this outdated paradigm to an orthomolecular medicine-based integrative approach, focusing on restoring biochemical balance (between nutrients and toxins) and physiological harmony (among various hormones). Using this approach, we recently reported a series of 10 successful ASCVD reversal cases (1).

This paper explores the multifactorial root causes contributing to dyslipidemia, including dietary factors, nutritional deficiencies, infections, physical inactivity, and hormonal imbalances. Special attention is given to the roles of high-carbohydrate diets, ultra-processed foods, seed oils (containing high amounts of omega-6 PUFA), and high-fructose consumption. The effects of micronutrient deficiencies, such as those of vitamins B, C, D, E, and magnesium, are examined in the context of lipid metabolism. Additionally, the paper highlights the impact of chronic infections, sedentary lifestyles, and hormonal dysregulation on lipid abnormalities.

Understanding these key root causes provides a foundation for more effective prevention and treatment strategies (3). In future papers, we plan to explore these topics in greater detail, advocating for a paradigm shift from cholesterol-centric management to addressing the underlying causes of dyslipidemia and ASCVD.

Introduction

Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of morbidity and mortality worldwide. For decades, cholesterol and dyslipidemia have been central to ASCVD management strategies. However, our prior critiques of the cholesterol-centric paradigm have underscored that dyslipidemia is not the root cause but rather an intermediary mechanism of ASCV (2). Here we explore the multifactorial root causes underlying dyslipidemia, and advocate for prevention and treatment strategies that address these root causes. We focus here on categorizing the primary root causes contributing to ASCVD through dyslipidemia. More comprehensive discussions on these root causes will be presented where appropriate in subsequent papers in this series.

1. Dietary factors and dyslipidemia

  • High-carbohydrate diets have been strongly associated with dyslipidemia, particularly characterized by increased triglycerides and decreased HDL cholesterol levels (4–6). This effect is especially pronounced with high glycemic index carbohydrates (5). The mechanism may involve reduced clearance of LDL particles and increased production of their precursors (7). Carbohydrate-induced hypertriglyceridemia occurs when dietary carbohydrate exceeds 55% of energy intake, despite reduced dietary fat (8). This paradoxical effect may be due to enhanced intestinal de novo lipogenesis and mobilization of stored lipids (9). However, the impact of carbohydrates on lipid metabolism is complex, with some studies suggesting that low-carbohydrate diets may have beneficial effects on atherogenic dyslipidemia (10).
  • Low-carbohydrate ketogenic diets (KDs) have shown promising effects in improving metabolic disorders, particularly dyslipidemia. KDs can lead to significant reductions in triglycerides, total cholesterol, and LDL cholesterol, while increasing HDL cholesterol (11,12). These diets have been found to improve insulin sensitivity, reverse atherogenic dyslipidemia, and reduce inflammatory biomarkers associated with cardiovascular disease (13,14). KDs have also demonstrated benefits in managing obesity, metabolic syndrome, and type 2 diabetes (15,16). Studies have shown that KDs can decrease fasting serum insulin concentrations, improve LDL particle size, and reduce postprandial lipemia (11,12). While the optimal carbohydrate proportion and diet duration require further investigation, KDs appear to be a safe and effective approach for treating metabolic disorders (17,18).
  • Ultra-processed foods and dyslipidemia. High consumption of ultra-processed foods (UPF) has been shown to be associated with an increased risk of dyslipidemia and other cardiometabolic disorders. Multiple prospective cohort studies have found that individuals with higher UPF intake have significantly greater odds of developing hypertriglyceridemia, low HDL cholesterol, and hypercholesterolemia (19,20). This association has been observed in both adults and adolescents (21,22). Systematic reviews and meta-analyses confirm these findings, reporting consistent positive associations between UPF consumption and increased risk of dyslipidemia, as well as diabetes, hypertension, and obesity (23,24). Longitudinal studies in children have also shown that higher UPF intake is associated with elevated total cholesterol and triglyceride levels (25). Proposed mechanisms include altered food matrix, toxicity from additives, and processing-induced contaminants affecting lipid metabolism, gut microbiota, and inflammatory pathways (26).
  • Seed oils (rich in omega-6 PUFA) and dyslipidemia. Research suggests that high intake of omega-6 polyunsaturated fatty acids (PUFAs) from seed oils may contribute to inflammation, oxidative stress, and atherosclerosis (27). Despite recommendations for omega-6 PUFA consumption, some studies indicate potential long-term side effects, including hyperinsulinemia and increased cancer risk (28). Flaxseed and its oil, rich in omega-3 fatty acids, have demonstrated positive impacts on cardiovascular risk factors and dyslipidemia (29,30). Adjusting the omega-6 to omega-3 PUFA ratio may be crucial in managing chronic diseases (30). During cooking, both omega-3 and omega-6 high PUFA seed oils are readily oxidized, become rancid, and may produce harmful trans-fats (72).
  • High fructose (found in HFCS and fruits). Research suggests that high fructose consumption, particularly from high-fructose corn syrup (HFCS), may contribute to dyslipidemia and other metabolic disorders. Studies have shown that fructose intake can increase postprandial triglycerides, LDL cholesterol, and apolipoprotein B levels (32,33). Fructose consumption has also been linked to visceral adiposity, insulin resistance, and hepatic de novo lipogenesis (fatty liver disease) (34,35). The metabolic effects of fructose differ from glucose due to its rapid hepatic conversion and extraction (36). While some studies found no significant metabolic differences between HFCS and sucrose (37), others suggest that HFCS consumption at 25% of energy requirements can increase cardiovascular disease risk factors comparably to fructose (32). Recent research emphasizes the synergistic effects of glucose and fructose on lipid metabolism, supporting public health efforts to reduce sugar intake (38,39).

2. Nutritional deficiency and dyslipidemia

Many vitamins and micronutrients play critical roles in lipid and energy metabolism, and deficiencies—whether isolated or combined—can lead to metabolic disturbances. Below are some key examples:

  • B vitamins. Niacin and vitamin B6 have shown significant potential in managing dyslipidemia and associated cardiovascular risks. Niacin supplementation can lower triglycerides, LDL, and VLDL levels while increasing HDL (40). B vitamin supplementation improves lipid metabolism and reduces inflammation in patients with stable coronary artery disease (41). Animal studies have demonstrated antihyperlipidemic and hepatoprotective effects of vitamin B6 (42). Deficiencies in vitamins B6 and B12 are frequently reported in hyperlipidemic patient (43). Higher dietary niacin intake is associated with a reduced risk of dyslipidemia (44).
  • Vitamin C and dyslipidemia. Research demonstrates that vitamin C supplementation can improve lipid profiles by lowering total cholesterol, LDL cholesterol, and triglycerides, particularly in individuals with hypercholesterolemia or diabetes (45–47). Some studies also report increases in HDL cholesterol (48,49). Beneficial effects of vitamin C have been observed across diverse groups, including diabetics, hemodialysis patients, and oil workers exposed to petroleum fumes (50,51). A meta-analysis of 13 randomized controlled trials confirmed that vitamin C supplementation significantly reduces LDL cholesterol and triglycerides in hypercholesterolemic individuals (46). The effects of vitamin C vary depending on dosage, duration, and individual health status (47). Dr. Linus Pauling’s pioneering work on vitamin C and cardiovascular disease laid the foundation for understanding its role in vascular health, indirectly linking it to lipid metabolism. We plan to dedicate a paper to further explore Pauling’s insights and their relevance to dyslipidemia and ASCVD. One of us (TEL) discusses vitamin C’s role in improving lipid profiles, combating oxidative stress, and supporting vascular health in the books Primal Panacea (52) and Stop America’s Number One Killer (53).
  • Vitamin D and dyslipidemia. Vitamin D deficiency is significantly associated with dyslipidemia. Studies reveal that individuals with lower serum 25-hydroxyvitamin D levels are more likely to exhibit abnormal lipid profiles, including elevated total cholesterol, LDL, and triglycerides, and decreased HDL (54–57). This relationship persists even after adjusting for confounding factors. Vitamin D deficiency is linked to alterations in metabolomic profiles, particularly sphingolipid pathway (58). Interactions with other micronutrients, such as vitamin A, zinc, and magnesium, may influence vitamin D’s impact on lipid metabolism (59). Our recent comprehensive review of vitamin D demonstrates that maintaining optimal serum levels above 40 ng/mL reduces the risk of cardiovascular disease incidence and mortality (60) (accepted for publication by Nutrients).
  • Vitamin E and dyslipidemia. Vitamin E has shown anti-atherosclerotic properties (61). Research on vitamin E and dyslipidemia shows mixed results. Some studies suggest that vitamin E supplementation can improve lipid profiles in dyslipidemic patients, reducing total cholesterol, LDL-C, and triglycerides (62,63). Higher serum vitamin E levels have been associated with a more favorable lipid profile (64). Vitamin E supplementation has been shown to suppress elevated plasma lipid peroxides and increase serum antioxidant activity (65). The impact of antioxidative vitamins on lipid profiles varies based on dosage, duration, and individual health status (47).
  • Magnesium and dyslipidemia. Hypomagnesemia has been linked to metabolic abnormalities and dyslipidemia (66–70). Studies report negative correlations between serum magnesium and triglycerides, LDL, and total cholesterol, while positive correlations are observed with HDL cholesterol (70,71).

3. Infections and dyslipidemia

  • Infections promote dyslipidemia. Dyslipidemia is a common complication in HIV-infected patients and those with COVID-19, associated with increased severity and mortality (72). It is characterized by elevated total cholesterol, LDL, and triglycerides, with decreased HDL (73,74). The pathogenesis involves inflammation, oxidative stress, and lipid peroxidation (75). These lipid abnormalities may increase cardiovascular risk in HIV patients (76,77). Research suggests a significant association between oral infections, particularly periodontitis, and systemic metabolic disturbances. Periodontitis has been linked to increased risk of cardiovascular diseases and dyslipidemia (78,79). Studies have found higher levels of total cholesterol, LDL cholesterol, and triglycerides, along with lower HDL cholesterol, in individuals with periodontitis (80,81). Chronic oral infection with Porphyromonas gingivalis, a key periodontal pathogen, has been shown to accelerate atheroma formation by altering lipid profiles in animal models (82). The relationship between periodontitis and hyperlipidemia appears bidirectional, with elevated triglycerides potentially modulating inflammatory responses to periodontal pathogens (83). The underlying mechanisms involve systemic inflammation, metabolic endotoxemia, and genetic factors that influence both oral infections and cardiometabolic diseases (84). These findings highlight the complex interplay between oral health and systemic metabolism.
  • Infection control improves dyslipidemia. Periodontal treatment has been shown to improve lipid control (85). Eradication of Helicobacter pylori infection may decrease the risk of dyslipidemia (86).

4. Physical inactivity and dyslipidemia/high cholesterol

Research consistently shows an inverse relationship between physical activity (PA) and dyslipidemia. Higher PA levels are associated with increased HDL-C and decreased triglycerides in both men and women (87,88). Sedentary behavior increases the risk of dyslipidemia, while moderate-to-vigorous PA (MVPA) may reduce this risk (89,90). The prevalence of dyslipidemia is high in some populations, with limited awareness and treatment (91). Individuals meeting PA guidelines have lower odds of dyslipidemia, even with poor diet quality (91). However, adults with hypercholesterolemia are less likely to meet PA recommendations compared to those without (92). PA patterns, including timing and intensity, may influence lipid profiles differently (90). Overall, habitual PA is associated with more favorable lipid profiles and reduced cardiovascular disease risk (93,94).

5. Hormonal imbalance and dyslipidemia/high cholesterol

  • Thyroid dysfunction, particularly hypothyroidism, is strongly associated with dyslipidemia and increased cardiovascular risk (95,96). Both overt and subclinical hypothyroidism can lead to elevated total cholesterol, LDL cholesterol, and apolipoprotein B levels, while potentially affecting HDL cholesterol and triglycerides (97,98). These lipid abnormalities are primarily due to reduced LDL receptor activity and altered regulation of cholesterol biosynthesis (99). Thyroid hormone replacement therapy has been shown to improve lipid profiles in overt hypothyroidism, but its benefits in subclinical hypothyroidism remain debated (99,100). Recent studies have also highlighted the role of thyroid hormones in regulating HDL function and cholesterol efflux (98). Given the prevalence of thyroid dysfunction and its impact on lipid metabolism, screening for thyroid disorders is recommended in patients with dyslipidemia (101).
  • Cortisol imbalance significantly contributes to dyslipidemia, high cholesterol, and increased cardiovascular risk. Excess cortisol, such as in Cushing’s syndrome, is associated with elevated triglycerides, total cholesterol, and LDL cholesterol levels (102). Similarly, stress-induced cortisol elevation disrupts lipid metabolism, promoting atherogenesis and increasing the risk of atherosclerosis (103). Conversely, patients with metabolic syndrome and low cortisol levels exhibit less pronounced lipid disturbances (104). Elevated basal cortisol levels and reduced circadian variability have been linked to unfavorable lipid profiles, particularly in individuals with depressive and anxiety disorders (105). Additionally, the cortisol-to-DHEA ratio has been positively correlated with atherogenic lipid profiles in HIV patients with lipodystrophy (106). Glucocorticoid therapy, a common cause of cortisol excess, can lead to dyslipidemia and hypertension, further heightening cardiovascular disease risk (107). Excess cortisol is also strongly associated with obesity, hypertension, and metabolic syndrome (108,109). Furthermore, studies have found that elevated long-term cortisol levels, as measured in scalp hair, are linked to a history of cardiovascular disease (110). In obesity, higher cortisol concentrations are directly correlated with an increased risk of cardiovascular comorbidities (111). These findings highlight the multifaceted role of cortisol in dyslipidemia and emphasize the need to manage cortisol levels to mitigate cardiovascular risks effectively.
  • Estrogen imbalance significantly impacts lipid metabolism and cholesterol levels. During menopause, estrogen deficiency leads to increased total cholesterol, LDL cholesterol, and triglycerides, while decreasing HDL cholesterol (112). High maternal estradiol levels can induce dyslipidemia in newborns by upregulating HMGCR expression in fetal hepatocytes (113). Estrogen administration in premenopausal women increases VLDL and HDL constituents, enhancing VLDL apoB and HDL apoA-I production (114). In postmenopausal women, estrogen therapy lowers LDL cholesterol levels (115). Estrogen treatment in cholesterol-fed rabbits attenuates atherosclerosis development by modulating lipoprotein metabolism (116,117). Endogenous sex hormones play a role in regulating lipid metabolism in postmenopausal women, with SHBG associated with a more favorable lipid profile (118). Estrogen administration in postmenopausal women decreases LDL cholesterol and hepatic triglyceride lipase activity while increasing HDL cholesterol (119).
  • Progesterone imbalance can significantly impact lipid metabolism and cholesterol levels. Progesterone administration in rats led to increased hepatic triglycerides and cholesterol esters, while decreasing plasma cholesterol levels (120). In cultured cells, progesterone inhibited cholesterol biosynthesis (121). Dyslipidemia affected ovarian steroidogenesis in mice through oxidative stress, inflammation, and insulin resistance (122). In premenopausal women, ovarian lipid metabolism influenced circulating lipids (123). Estrogen plus progesterone replacement therapy in postmenopausal women lowered lipoprotein[a] levels and improved overall lipid profiles (124). High-dose medroxyprogesterone decreased total, LDL, and HDL cholesterol in postmenopausal women (125). In children, progesterone/estradiol ratios were associated with LDL-cholesterol levels (126). Female runners with menstrual irregularities showed altered steroid hormone and lipid profiles compared to eumenorrheic counterparts (127).
  • Testosterone imbalance can significantly impact lipid metabolism and cholesterol levels. Research suggests a complex relationship between testosterone and lipid profiles. Low testosterone levels are associated with adverse lipid profiles, including higher total cholesterol and triglycerides, and lower high-density lipoprotein (HDL) cholesterol (128,129). Conversely, higher testosterone levels correlate with increased HDL cholesterol in men, particularly those with cardiovascular disease (130,131). Testosterone deficiency may contribute to hypercholesterolemia through altered expression of hepatic PCSK9 and LDL receptors (132). The effect of testosterone on lipids varies with age, gender, race/ethnicity, and menopausal status (133). Exogenous testosterone administration in hypogonadal men may improve lipid profiles by decreasing LDL and total cholesterol, although it may also decrease HDL cholesterol (134). While testosterone’s influence on lipids is evident, its overall impact on cardiovascular disease risk remains unclear and requires further investigation (134,135).

Conclusion

Dyslipidemia, long regarded as a primary target in ASCVD management, is increasingly understood as an outcome of complex, multifactorial root causes. These root causes include dietary factors, such as high-carbohydrate diets, ultra-processed foods, seed oils, and high-fructose consumption, which significantly influence lipid metabolism. Nutritional deficiencies, including vitamins B, C, D, and E, and magnesium, further exacerbate dyslipidemia, while chronic infections and physical inactivity compound cardiovascular risk. Hormonal imbalances, including dysfunctions in thyroid hormones, estrogen, progesterone, testosterone, and cortisol, also play a pivotal role in lipid abnormalities.

Addressing these underlying factors presents an opportunity to move beyond the traditional cholesterol-centric paradigm. Strategies such as dietary modifications, increased physical activity, infection control, and optimization of nutritional and hormonal balance can significantly improve lipid profiles, reduce cardiovascular risk, and even reverse ASCVD in some cases, as we have demonstrated in our recent report (1).

By focusing on the root causes of dyslipidemia, healthcare providers can offer more personalized and effective interventions, shifting the emphasis from symptom management to true disease prevention and reversal. This approach has the potential to improve not only ASCVD outcomes but also overall cardiovascular health and longevity. Future studies should prioritize the integration of these multifaceted strategies into clinical practice, emphasizing the importance of addressing the root causes of dyslipidemia for sustainable cardiovascular health.

References:

1. Cheng RZ, Duan L, Levy TE. A Holistic Approach to ASCVD: Summary of a Novel Framework and Report of 10 Case Studies. Orthomol Med News Serv [Internet]. 2024 Nov 27;20(20). Available from: https://orthomolecular.org/resources/omns/v20n20.shtml

2. Cheng RZ, Levy TE. The Mismanagement of ASCVD: A Call for Root Cause Solutions Beyond Cholesterol. Orthomol Med News Serv [Internet]. 2025 Jan 2 [cited 2025 Jan 5]; Available from: https://orthomolecular.activehosted.com/index.php?action=social&chash=0bb4aec1710521c12ee76289d9440817.345

3. Cheng RZ. Integrative Orthomolecular Medicine Protocol for ASCVD [Internet]. 2024. Available from: https://www.drwlc.com/blog/2024/08/01/integrative-orthomolecular-medicine-protocol-for-ascvd/

4. Polacow VO, Lancha Junior AH. [High-carbohydrate diets: effects on lipid metabolism, body adiposity and its association with physical activity and cardiovascular disease risk]. Arq Bras Endocrinol Metabol. 2007 Apr;51(3):389–400.

5. Shin WK, Shin S, Lee Jo koo. Carbohydrate Intake and Hyperlipidemia among Population with High‐Carbohydrate Diets: The Health Examinees Gem Study – Shin – 2021 – Molecular Nutrition & Food Research – Wiley Online Library. Mol Nutr Food Res [Internet]. [cited 2024 Dec 29]; Available from: https://onlinelibrary.wiley.com/doi/10.1002/mnfr.202000379

6. Jackson RL, Yates MT, McNerney CA, Kashyap ML. Diet and HDL Metabolism: High Carbohydrate vs. High Fat Diets. In: Malmendier CL, Alaupovic P, editors. Lipoproteins and Atherosclerosis [Internet]. Boston, MA: Springer US; 1987 [cited 2024 Nov 5]. p. 165–72. Available from: https://doi.org/10.1007/978-1-4684-1268-0_24

7. Houttu V, Grefhorst A, Cohn DM, Levels JHM, Roeters van Lennep J, Stroes ESG, et al. Severe Dyslipidemia Mimicking Familial Hypercholesterolemia Induced by High-Fat, Low-Carbohydrate Diets: A Critical Review. Nutrients. 2023 Feb 15;15(4):962.

8. Parks EJ. Effect of dietary carbohydrate on triglyceride metabolism in humans. J Nutr. 2001 Oct;131(10):2772S-2774S.

9. Stahel P, Xiao C, Lewis GF. Control of intestinal lipoprotein secretion by dietary carbohydrates. Curr Opin Lipidol. 2018 Feb;29(1):24–9.

10. Musunuru K. Atherogenic dyslipidemia: cardiovascular risk and dietary intervention. Lipids. 2010 Oct;45(10):907–14.

11. Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gómez AL, Scheett TP, et al. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr. 2002 Jul;132(7):1879–85.

12. Hickey JT, Hickey L, Yancy WS, Hepburn J, Westman EC. Clinical use of a carbohydrate-restricted diet to treat the dyslipidemia of the metabolic syndrome. Metab Syndr Relat Disord. 2003 Sep;1(3):227–32.

13. O’Neill BJ. Effect of low-carbohydrate diets on cardiometabolic risk, insulin resistance, and metabolic syndrome. Curr Opin Endocrinol Diabetes Obes. 2020 Oct;27(5):301–7.

14. Zhang W, Guo X, Chen L, Chen T, Yu J, Wu C, et al. Ketogenic Diets and Cardio-Metabolic Diseases. Front Endocrinol. 2021;12:753039.

15. Moreno-Sepúlveda J, Capponi M. [The impact on metabolic and reproductive diseases of low-carbohydrate and ketogenic diets]. Rev Med Chil. 2020 Nov;148(11):1630–9.

16. Sakr HF, Sirasanagandla SR, Das S, Bima AI, Elsamanoudy AZ. Low-Carbohydrate Ketogenic Diet for Improvement of Glycemic Control: Mechanism of Action of Ketosis and Beneficial Effects. Curr Diabetes Rev. 2023;19(2):e110522204580.

17. Charlot A, Zoll J. Beneficial Effects of the Ketogenic Diet in Metabolic Syndrome: A Systematic Review. Diabetology. 2022 Apr 24;3(2):292–309.

18. Kayode TO, Rotimi ED, Afolayan AO, Kayode AAA. Ketogenic diet: A nutritional remedy for some metabolic disorders. J Educ Health Sport. 2020 Aug 10;10(8):180–8.

19. Donat-Vargas C, Sandoval-Insausti H, Rey-García J, Moreno-Franco B, Åkesson A, Banegas JR, et al. High Consumption of Ultra-Processed Food is Associated with Incident Dyslipidemia: A Prospective Study of Older Adults. J Nutr. 2021 Aug 7;151(8):2390–8.

20. Scaranni P de O da S, de Oliveira Cardoso L, Griep RH, Lotufo PA, Barreto SM, da Fonseca M de JM. Consumption of ultra-processed foods and incidence of dyslipidemias: the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Br J Nutr. 2022 Apr 22;1–22.

21. Lima LR, Nascimento LM, Gomes KRO, Martins M do C de CE, Rodrigues MTP, Frota K de MG. [Association between ultra-processed food consumption and lipid parameters among adolescents]. Cienc Saude Coletiva. 2020 Oct;25(10):4055–64.

22. Beserra JB, Soares NI da S, Marreiros CS, Carvalho CMRG de, Martins M do C de CE, Freitas B de JES de A, et al. [Do children and adolescents who consume ultra-processed foods have a worse lipid profile? A systematic review]. Cienc Saude Coletiva. 2020 Dec;25(12):4979–89.

23. Vitale M, Costabile G, Testa R, D’Abbronzo G, Nettore IC, Macchia PE, et al. Ultra-Processed Foods and Human Health: A Systematic Review and Meta-Analysis of Prospective Cohort Studies. Adv Nutr Bethesda Md. 2024 Jan;15(1):100121.

24. Mambrini SP, Menichetti F, Ravella S, Pellizzari M, De Amicis R, Foppiani A, et al. Ultra-Processed Food Consumption and Incidence of Obesity and Cardiometabolic Risk Factors in Adults: A Systematic Review of Prospective Studies. Nutrients. 2023 May 31;15(11):2583.

25. Leffa PS, Hoffman DJ, Rauber F, Sangalli CN, Valmórbida JL, Vitolo MR. Longitudinal associations between ultra-processed foods and blood lipids in childhood. Br J Nutr. 2020 Aug 14;124(3):341–8.

26. Juul F, Vaidean G, Lin Y, Deierlein AL, Parekh N. Ultra-Processed Foods and Incident Cardiovascular Disease in the Framingham Offspring Study. J Am Coll Cardiol. 2021 Mar 30;77(12):1520–31.

27. DiNicolantonio JJ, O’Keefe J. The Importance of Maintaining a Low Omega-6/Omega-3 Ratio for Reducing the Risk of Autoimmune Diseases, Asthma, and Allergies. Mo Med. 2021;118(5):453–9.

28. Yam D, Eliraz A, Berry EM. Diet and disease–the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet. Isr J Med Sci. 1996 Nov;32(11):1134–43.

29. Vashishtha V, Barhwal K, Kumar A, Hota SK, Chaurasia OP, Kumar B. Effect of seabuckthorn seed oil in reducing cardiovascular risk factors: A longitudinal controlled trial on hypertensive subjects. Clin Nutr Edinb Scotl. 2017 Oct;36(5):1231–8.

30. Fawzy M, Nagi HM, Mourad R. BENEFICIAL EFFECT OF FLAXSEED AND FLAXSEED OIL BY ADJUSTING OMEGA6:OMEGA3 RATIO ON LIPID METABOLISM IN HIGH CHOLESTEROL DIET FED RATS. J Spec Educ Res. 2020 Apr 1;2020(58):117–42.

31. Obi J, Sakamoto T, Furihata K, Sato S, Honda M. Vegetables containing sulfur compounds promote trans-isomerization of unsaturated fatty acids in triacylglycerols during the cooking process. Food Res Int. 2025 Jan 1;200:115425.

32. Stanhope KL, Bremer AA, Medici V, Nakajima K, Ito Y, Nakano T, et al. Consumption of fructose and high fructose corn syrup increase postprandial triglycerides, LDL-cholesterol, and apolipoprotein-B in young men and women. J Clin Endocrinol Metab. 2011 Oct;96(10):E1596-1605.

33. Stanhope KL, Medici V, Bremer AA, Lee V, Lam HD, Nunez MV, et al. A dose-response study of consuming high-fructose corn syrup-sweetened beverages on lipid/lipoprotein risk factors for cardiovascular disease in young adults. Am J Clin Nutr. 2015 Jun;101(6):1144–54.

34. Stanhope KL, Havel PJ. Fructose consumption: potential mechanisms for its effects to increase visceral adiposity and induce dyslipidemia and insulin resistance. Curr Opin Lipidol. 2008 Feb;19(1):16–24.

35. Tappy L, Lê KA. Metabolic effects of fructose and the worldwide increase in obesity. Physiol Rev. 2010 Jan;90(1):23–46.

36. Schaefer EJ, Gleason JA, Dansinger ML. Dietary fructose and glucose differentially affect lipid and glucose homeostasis. J Nutr. 2009 Jun;139(6):1257S-1262S.

37. Angelopoulos TJ, Lowndes J, Zukley L, Melanson KJ, Nguyen V, Huffman A, et al. The effect of high-fructose corn syrup consumption on triglycerides and uric acid. J Nutr. 2009 Jun;139(6):1242S-1245S.

38. Gugliucci A. Sugar and Dyslipidemia: A Double-Hit, Perfect Storm. J Clin Med. 2023 Aug 31;12(17):5660.

39. Stanhope KL. Role of fructose-containing sugars in the epidemics of obesity and metabolic syndrome. Annu Rev Med. 2012;63:329–43.

40. Dayi T, Hoca M. Niasin Dislipidemi Riskini Azaltmada Potansiyel Bir Ajan Mıdır? İstanbul Gelişim Üniversitesi Sağlık Bilim Derg. 2022 Aug 29;(17):626–35.

41. Liu M, Wang Z, Liu S, Liu Y, Ma Y, Liu Y, et al. Effect of B vitamins supplementation on cardio-metabolic factors in patients with stable coronary artery disease: A randomized double-blind trial. Asia Pac J Clin Nutr. 2020;29(2):245–52.

42. Zhang Q, Zhang DL, Zhou XL, Li Q, He N, Zhang J, et al. Antihyperlipidemic and Hepatoprotective Properties of Vitamin B6 Supplementation in Rats with High-Fat Diet-Induced Hyperlipidemia. Endocr Metab Immune Disord Drug Targets. 2021;21(12):2260–72.

43. Al-Qusous MN, Al Madanat WKJ, Mohamed Hussein R. Association of Vitamins D, B6, and B12 Deficiencies with Hyperlipidemia Among Jordanian Adults. Rep Biochem Mol Biol. 2023 Oct;12(3):415–24.

44. Altschul R, Hoffer A, Stephen JD. Influence of nicotinic acid on serum cholesterol in man. Arch Biochem Biophys. 1955 Feb;54(2):558–9.

45. Chaudhari HV, Dakhale GN, Chaudhari S, Kolhe S, Hiware S, Mahatme M. The beneficial effec of vitamin C suppllemtation on serum lipids in type 2 diabetic patients: a randomized double blind study. Int J Diabetes Metab. 2012;20(2):53–8.

46. McRae MP. Vitamin C supplementation lowers serum low-density lipoprotein cholesterol and triglycerides: a meta-analysis of 13 randomized controlled trials. J Chiropr Med. 2008 Jun;7(2):48–58.

47. Mohseni S, Tabatabaei-Malazy O, Shadman Z, Khashayar P, Mohajeri-Tehrani M, Larijani B. Targeting dyslipidemia with antioxidative vitamins C, D, and E; a systematic review of meta-analysis studies. J Diabetes Metab Disord. 2021 Oct 21;20(2):2037–47.

48. Ness AR, Khaw KT, Bingham S, Day NE. Vitamin C status and serum lipids. Eur J Clin Nutr. 1996 Nov;50(11):724–9.

49. Cerná O, Ramacsay L, Ginter E. Plasma lipids, lipoproteins and atherogenic index in men and women administered vitamin C. Cor Vasa. 1992;34(3):246–54.

50. El Mashad GM, ElSayed HM, Nosair NA. Effect of vitamin C supplementation on lipid profile, serum uric acid, and ascorbic acid in children on hemodialysis. Saudi J Kidney Dis Transplant Off Publ Saudi Cent Organ Transplant Saudi Arab. 2016;27(6):1148–54.

51. George-Opuda IM, Etuk EJ, Elechi-Amadi KN, Okolonkwo BN, Adegoke OA, Ohaka TP, et al. Vitamin C Supplementation Lowered Atherogenic Lipid Parameters among Oil and Gas Workers Occupationally Exposed to Petroleum Fumes in Port Harcourt, Rivers State, Nigeria. J Adv Med Pharm Sci. 2024 Feb 19;26(3):45–52.

52. Levy TE, Gordon G. Primal Panacea. 2012 Second Printing edition. Henderson, NV: Medfox Publishing; 2011. 352 p.

53. Levy TE. Stop America’s #1 Killer: MD JD Levy, MD Julian Whitaker: 9780977952007: Amazon.com: Gateway [Internet]. [cited 2019 Jul 6]. Available from: https://www.amazon.com/Stop-Americas-Killer-MD-Levy/dp/0977952002/ref=sr_1_1?crid=2GE3D8VO3QMJL&keywords=stop+america+s+%231+killer&qid=1562416934&s=gateway&sprefix=stop+america%2Caps%2C428&sr=8-1

54. Sharba ZF, Shareef RH, Abd BA, Hameed EN. Association between Dyslipidemia and Vitamin D Deficiency: a Cross-Sectional Study. Folia Med (Plovdiv). 2021 Dec 31;63(6):965–9.

55. Chaudhuri JR, Mridula KR, Anamika A, Boddu DB, Misra PK, Lingaiah A, et al. Deficiency of 25-Hydroxyvitamin D and Dyslipidemia in Indian Subjects. J Lipids. 2013;2013:1–7.

56. Jiang X, Peng M, Chen S, Wu S, Zhang W. Vitamin D deficiency is associated with dyslipidemia: a cross-sectional study in 3788 subjects. Curr Med Res Opin. 2019 Jun 3;35(6):1059–63.

57. Doddamani DS, Shetty DP. The Association between Vitamin D Deficiency and Dyslipidemia. In 2020 [cited 2025 Jan 5]. Available from: https://www.semanticscholar.org/paper/The-Association-between-Vitamin-D-Deficiency-and-Doddamani-Shetty/50aa5e70d0f7a9edc9d72c5c7a8b0af5fca58866

58. Mousa H, Elrayess MA, Diboun I, Jackson SK, Zughaier SM. Metabolomics Profiling of Vitamin D Status in Relation to Dyslipidemia. Metabolites. 2022 Aug 22;12(8):771.

59. Khosravi-Boroujeni H, Ahmed F, Sarrafzadegan N. Is the Association between Vitamin D and Metabolic Syndrome Independent of Other Micronutrients? Int J Vitam Nutr Res Int Z Vitam- Ernahrungsforschung J Int Vitaminol Nutr. 2015 Dec;85(5–6):245–60.

60. Grant WB, Wimalawansa SJ, Pludowski P, Cheng RZ. Vitamin D: Evidence-Based Health Benefits and Recommendations for Population Guidelines. Nutrients [Internet]. Available from: www.mdpi.com/journal/nutrients

61. Saggini A, Anogeianaki A, Angelucci D, Cianchetti E, D’Alessandro M, Maccauro G, et al. Cholesterol and vitamins: revisited study. J Biol Regul Homeost Agents. 2011;25(4):505–15.

62. Vasanthi B, Kalaimathi B. Therapeutic Effect of Vitamin E in Patients with Dyslipidaemia. In 2012 [cited 2025 Jan 5]. Available from: https://www.semanticscholar.org/paper/Therapeutic-Effect-of-Vitamin-E-in-Patients-with-Vasanthi-Kalaimathi/2856f54306f952ff20d346526b46f31e4b462e23

63. Manimegalai R, Geetha A, Rajalakshmi K. Effect of vitamin-E on high fat diet induced hyperlipidemia in rats. Indian J Exp Biol. 1993 Aug;31(8):704–7.

64. Barzegar-Amini M, Ghazizadeh H, Seyedi SMR, Sadeghnia HR, Mohammadi A, Hassanzade-Daloee M, et al. Serum vitamin E as a significant prognostic factor in patients with dyslipidemia disorders. Diabetes Metab Syndr. 2019;13(1):666–71.

65. Szczeklik A, Gryglewski RJ, Domagala B, Dworski R, Basista M. Dietary supplementation with vitamin E in hyperlipoproteinemias: effects on plasma lipid peroxides, antioxidant activity, prostacyclin generation and platelet aggregability. Thromb Haemost. 1985 Aug 30;54(2):425–30.

66. Guerrero-Romero F, Rodríguez-Morán M. Magnesium and dyslipidemia [Internet]. 1st Edition. CRC Press; 2019 [cited 2025 Jan 5]. Available from: https://www.taylorfrancis.com/chapters/edit/10.1201/9780429029141-5/magnesium-dyslipidemia-fernando-guerrero-romero-martha-rodr%C3%ADguez-mor%C3%A1n

67. Levy T. Magnesium: Reversing Disease: Levy MD, Jd: 9780998312408: Amazon.com: Books [Internet]. 2019 [cited 2022 Feb 12]. Available from: https://www.amazon.com/Magnesium-Reversing-MD-Jd-Levy/dp/0998312401/ref=pd_lpo_2?pd_rd_i=0998312401&psc=1

68. Dean C. The Magnesium Miracle (Second Edition): Dean M.D. N.D., Carolyn: 9780399594441: Amazon.com: Books [Internet]. 2017 [cited 2022 Feb 12]. Available from: https://www.amazon.com/Magnesium-Miracle-Second-Carolyn-Dean/dp/0399594442

69. Mishra S, Padmanaban P, Deepti G, G.Sarkar, Sumathi S, Toora BD. Serum Magnesium and Dyslipidemia in Type-2 Diabetes Mellitus. Biomed Res-Tokyo [Internet]. 2012 [cited 2025 Jan 5]; Available from: https://www.semanticscholar.org/paper/Serum-Magnesium-and-Dyslipidemia-in-Type-2-Diabetes-Mishra-Padmanaban/8d23a2bd9017cb57bb6ddda98789ba81c176b53c

70. Sajjan N, Shamsuddin M. A study of serum magnesium and dyslipidemia in type 2 diabetes mellitus patients. Int J Clin Biochem Res. 2016;3(1):36.

71. Deepti R, Nalini G, Anbazhagan. RELATIONSHIP BETWEEN HYPOMAGNESEMIA AND DYSLIPIDEMIA IN TYPE 2 DIABETES MELLITUS. Asian J Pharm Res Health Care [Internet]. 2014 Jul 1 [cited 2025 Jan 5]; Available from: https://www.semanticscholar.org/paper/RELATIONSHIP-BETWEEN-HYPOMAGNESEMIA-AND-IN-TYPE-2-Deepti-Nalini/5fd9c00eacce8aa45f93c3e5ea0961969ec3223b

72. Hariyanto TI, Kurniawan A. Dyslipidemia is associated with severe coronavirus disease 2019 (COVID-19) infection. Diabetes Metab Syndr. 2020;14(5):1463–5.

73. Lo J. Dyslipidemia and lipid management in HIV-infected patients. Curr Opin Endocrinol Diabetes Obes [Internet]. 2011 Apr [cited 2024 Dec 29];18(2). Available from: https://journals.lww.com/co-endocrinology/abstract/2011/04000/dyslipidemia_and_lipid_management_in_hiv_infected.9.aspx

74. Green ML. Evaluation and management of dyslipidemia in patients with HIV infection. J Gen Intern Med. 2002 Oct 1;17(10):797–810.

75.Feingold KR, Grunfeld C. The Effect of Inflammation and Infection on Lipids and Lipoproteins. In: Feingold KR, Anawalt B, Blackman MR, Boyce A, Chrousos G, Corpas E, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000 [cited 2024 Dec 29]. Available from: http://www.ncbi.nlm.nih.gov/books/NBK326741/

76. Kulasekaram R, Peters BS, Wierzbicki AS. Dyslipidaemia and cardiovascular risk in HIV infection. Curr Med Res Opin. 2005 Nov;21(11):1717–25.

77. Kotler DP. HIV and Antiretroviral Therapy: Lipid Abnormalities and Associated Cardiovascular Risk in HIV-Infected Patients. JAIDS J Acquir Immune Defic Syndr. Sept. 1, 20008;49:S79–85.

78. Mattila KJ, Pussinen PJ, Paju S. Dental infections and cardiovascular diseases: a review. J Periodontol. 2005 Nov;76(11 Suppl):2085–8.

79. Ma W, Zou Z, Yang L, Lin D, Guo J, Shan Z, et al. Exploring the bi-directional relationship between periodontitis and dyslipidemia: a comprehensive systematic review and meta-analysis. BMC Oral Health. 2024 Apr 29;24(1):508.

80. Moeintaghavi A, Haerian-Ardakani A, Talebi-Ardakani M, Tabatabaie I. Hyperlipidemia in patients with periodontitis. J Contemp Dent Pract. 2005 Aug 15;6(3):78–85.

81. Nibali L, D’Aiuto F, Griffiths G, Patel K, Suvan J, Tonetti MS. Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case-control study. J Clin Periodontol. 2007 Nov;34(11):931–7.

82. Maekawa T, Takahashi N, Tabeta K, Aoki Y, Miyashita H, Miyauchi S, et al. Chronic Oral Infection with Porphyromonas gingivalis Accelerates Atheroma Formation by Shifting the Lipid Profile. Cardona PJ, editor. PLoS ONE. 2011 May 19;6(5):e20240.

83. Cutler CW, Shinedling EA, Nunn M, Jotwani R, Kim BO, Nares S, et al. Association between periodontitis and hyperlipidemia: cause or effect? J Periodontol. 1999 Dec;70(12):1429–34.

84. Janket SJ, Javaheri H, Ackerson LK, Ayilavarapu S, Meurman JH. Oral Infections, Metabolic Inflammation, Genetics, and Cardiometabolic Diseases. J Dent Res. 2015 Sep;94(9 Suppl):119S-27S.

85. Fentoğlu O, Sözen T, Oz SG, Kale B, Sönmez Y, Tonguç MO, et al. Short-term effects of periodontal therapy as an adjunct to anti-lipemic treatment. Oral Dis. 2010 Oct;16(7):648–54.

86. Park Y, Kim TJ, Lee H, Yoo H, Sohn I, Min YW, et al. Eradication of Helicobacter pylori infection decreases risk for dyslipidemia: A cohort study. Helicobacter. 2021 Apr;26(2):e12783.

87. Dancy C, Lohsoonthorn V, Williams MA. Risk of dyslipidemia in relation to level of physical activity among Thai professional and office workers. Southeast Asian J Trop Med Public Health. 2008 Sep;39(5):932–41.

88. Meireles De Pontes L. Standard of physical activity and influence of sedentarism in the occurrence of dyslipidemias in adults. Fit Perform J. 2008 Jul 1;7(4):245–50.

89. Zhou J, Zhou Q, Wang DP, Zhang T, Wang HJ, Song Y, et al. [Associations of sedentary behavior and physical activity with dyslipidemia]. Beijing Da Xue Xue Bao. 2017 Jun 18;49(3):418–23.

90. Wang X, Wang Y, Xu Z, Guo X, Mao H, Liu T, et al. Trajectories of 24-Hour Physical Activity Distribution and Relationship with Dyslipidemia. Nutrients. 2023 Jan 9;15(2):328.

91. Mutalifu M, Zhao Q, Wang Y, Hamulati X, Wang YS, Deng L, et al. Joint association of physical activity and diet quality with dyslipidemia: a cross-sectional study in Western China. Lipids Health Dis. 2024 Feb 10;23(1):46.

92. Churilla JR, Johnson TM, Zippel EA. Association of physical activity volume and hypercholesterolemia in US adults. QJM Mon J Assoc Physicians. 2013 Apr;106(4):333–40.

93. Gordon DJ, Witztum JL, Hunninghake D, Gates S, Glueck CJ. Habitual physical activity and high-density lipoprotein cholesterol in men with primary hypercholesterolemia. The Lipid Research Clinics Coronary Primary Prevention Trial. Circulation. 1983 Mar;67(3):512–20.

94. Delavar M, Lye M, Hassan S, Khor G, Hanachi P. Physical activity, nutrition, and dyslipidemia in middle-aged women. Iran J Public Health. 2011 Dec;40(4):89–98.

95. Brenta G, Fretes O. Dyslipidemias and hypothyroidism. Pediatr Endocrinol Rev PER. 2014 Jun;11(4):390–9.

96. Neves C, Alves M, Medina JL, Delgado JL. Thyroid diseases, dyslipidemia and cardiovascular pathology. Rev Port Cardiol Orgao Of Soc Port Cardiol Port J Cardiol Off J Port Soc Cardiol. 2008 Oct;27(10):1211–36.

97. Peppa M, Betsi G, Dimitriadis G. Lipid abnormalities and cardiometabolic risk in patients with overt and subclinical thyroid disease. J Lipids. 2011;2011:575840.

98. Jung KY, Ahn HY, Han SK, Park YJ, Cho BY, Moon MK. Association between thyroid function and lipid profiles, apolipoproteins, and high-density lipoprotein function. J Clin Lipidol. 2017;11(6):1347–53.

99. Duntas LH, Brenta G. A Renewed Focus on the Association Between Thyroid Hormones and Lipid Metabolism. Front Endocrinol. 2018;9:511.

100. Liberopoulos EN, Elisaf MS. Dyslipidemia in patients with thyroid disorders. Horm Athens Greece. 2002;1(4):218–23.

101.Asranna A, Taneja RS, Kulshreshta B. Dyslipidemia in subclinical hypothyroidism and the effect of thyroxine on lipid profile. Indian J Endocrinol Metab. 2012 Dec;16(Suppl 2):S347-349.

102. Arnaldi G, Scandali VM, Trementino L, Cardinaletti M, Appolloni G, Boscaro M. Pathophysiology of dyslipidemia in Cushing’s syndrome. Neuroendocrinology. 2010;92 Suppl 1:86–90.

103. Marcondes FK, Das Neves VJ, Costa R, Sanches A, Sousa T, Sampaio Moura MJC, et al. Dyslipidemia Induced by Stress. In: Kelishadi R, editor. InTech; 2012 [cited 2025 Jan 5]. Available from: http://www.intechopen.com/books/dyslipidemia-from-prevention-to-treatment/dyslipidemia-induced-by-stress

104. Nadolnik L, Polubok V, Gonchar K. Blood Cortisol Level in Patients with Metabolic Syndrome and Its Correlation with Parameters of Lipid and Carbohydrate Metabolisms. Int J Biochem Res Rev. 2020 Dec 31;149–58.

105. Veen G, Giltay EJ, DeRijk RH, van Vliet IM, van Pelt J, Zitman FG. Salivary cortisol, serum lipids, and adiposity in patients with depressive and anxiety disorders. Metabolism. 2009 Jun;58(6):821–7.

106. Christeff N, Melchior JC, de Truchis P, Perronne C, Nunez EA, Gougeon ML. Lipodystrophy defined by a clinical score in HIV-infected men on highly active antiretroviral therapy: correlation between dyslipidaemia and steroid hormone alterations. AIDS Lond Engl. 1999 Nov 12;13(16):2251–60.

107. Sholter DE, Armstrong PW. Adverse effects of corticosteroids on the cardiovascular system. Can J Cardiol. 2000 Apr;16(4):505–11.

108. Anagnostis P, Athyros VG, Tziomalos K, Karagiannis A, Mikhailidis DP. Clinical review: The pathogenetic role of cortisol in the metabolic syndrome: a hypothesis. J Clin Endocrinol Metab. 2009 Aug;94(8):2692–701.

109. van der Valk ES, Savas M, van Rossum EFC. Stress and Obesity: Are There More Susceptible Individuals? Curr Obes Rep. 2018 Jun;7(2):193–203.

110. Manenschijn L, Schaap L, van Schoor NM, van der Pas S, Peeters GMEE, Lips P, et al. High long-term cortisol levels, measured in scalp hair, are associated with a history of cardiovascular disease. J Clin Endocrinol Metab. 2013 May;98(5):2078–83.

111. Vicennati V, Pasqui F, Cavazza C, Pagotto U, Pasquali R. Stress-related development of obesity and cortisol in women. Obes Silver Spring Md. 2009 Sep;17(9):1678–83.

112. Torosyan N, Visrodia P, Torbati T, Minissian MB, Shufelt CL. Dyslipidemia in midlife women: Approach and considerations during the menopausal transition. Maturitas. 2022 Dec;166:14–20.

113. Meng Y, Lv PP, Ding GL, Yu TT, Liu Y, Shen Y, et al. High Maternal Serum Estradiol Levels Induce Dyslipidemia in Human Newborns via a Hepatic HMGCR Estrogen Response Element. Sci Rep. 2015 May 11;5:10086.

114. Schaefer EJ, Foster DM, Zech LA, Lindgren FT, Brewer HB, Levy RI. The effects of estrogen administration on plasma lipoprotein metabolism in premenopausal females. J Clin Endocrinol Metab. 1983 Aug;57(2):262–7.

115. Wahl P, Walden C, Knopp R, Hoover J, Wallace R, Heiss G, et al. Effect of estrogen/progestin potency on lipid/lipoprotein cholesterol. N Engl J Med. 1983 Apr 14;308(15):862–7.

116. Henriksson P, Stamberger M, Eriksson M, Rudling M, Diczfalusy U, Berglund L, et al. Oestrogen-induced changes in lipoprotein metabolism: role in prevention of atherosclerosis in the cholesterol-fed rabbit. Eur J Clin Invest. 1989 Aug;19(4):395–403.

117. Kushwaha RS, Hazzard WR. Exogenous estrogens attenuate dietary hypercholesterolemia and atherosclerosis in the rabbit. Metabolism. 1981 Apr;30(4):359–66.

118. Mudali S, Dobs AS, Ding J, Cauley JA, Szklo M, Golden SH, et al. Endogenous postmenopausal hormones and serum lipids: the atherosclerosis risk in communities study. J Clin Endocrinol Metab. 2005 Feb;90(2):1202–9.

119. Applebaum-Bowden D, McLean P, Steinmetz A, Fontana D, Matthys C, Warnick GR, et al. Lipoprotein, apolipoprotein, and lipolytic enzyme changes following estrogen administration in postmenopausal women. J Lipid Res. 1989 Dec;30(12):1895–906.

120. Gandarias JM, Abad C, Lacort M, Ochoa B. [Effect of progesterone on rat plasma and liver lipid levels (author’s transl)]. Rev Esp Fisiol. 1979 Dec;35(4):470–3.

121. Metherall JE, Waugh K, Li H. Progesterone inhibits cholesterol biosynthesis in cultured cells. Accumulation of cholesterol precursors. J Biol Chem. 1996 Feb 2;271(5):2627–33.

122. Abreu JM, Santos GB, Carvalho MDGDS, Mencarelli JM, Cândido BRM, Prado BBDP, et al. Dyslipidemia’s influence on the secretion ovarian’s steroids in female mice. Res Soc Dev. 2021 Oct 12;10(13):e298101321369.

123. Jensen JT, Addis IB, Hennebold JD, Bogan RL. Ovarian Lipid Metabolism Modulates Circulating Lipids in Premenopausal Women. J Clin Endocrinol Metab. 2017 Sep 1;102(9):3138–45.

124. Soma MR, Osnago-Gadda I, Paoletti R, Fumagalli R, Morrisett JD, Meschia M, et al. The lowering of lipoprotein[a] induced by estrogen plus progesterone replacement therapy in postmenopausal women. Arch Intern Med. 1993 Jun 28;153(12):1462–8.

125. Grönroos M, Lehtonen A. Effect of high dose progestin on serum lipids. Atherosclerosis. 1983 Apr;47(1):101–5.

126. Srinivasan SR, Sundaram GS, Williamson GD, Webber LS, Berenson GS. Serum lipoproteins and endogenous sex hormones in early life: observations in children with different lipoprotein profiles. Metabolism. 1985 Sep;34(9):861–7.

127. Thompson DL, Snead DB, Seip RL, Weltman JY, Rogol AD, Weltman A. Serum lipid levels and steroidal hormones in women runners with irregular menses. Can J Appl Physiol Rev Can Physiol Appl. 1997 Feb;22(1):66–77.

128. Haring R, Baumeister SE, Völzke H, Dörr M, Felix SB, Kroemer HK, et al. Prospective association of low total testosterone concentrations with an adverse lipid profile and increased incident dyslipidemia. Eur J Cardiovasc Prev Rehabil Off J Eur Soc Cardiol Work Groups Epidemiol Prev Card Rehabil Exerc Physiol. 2011 Feb;18(1):86–96.

129. Zhang N, Zhang H, Zhang X, Zhang B, Wang F, Wang C, et al. The relationship between endogenous testosterone and lipid profile in middle-aged and elderly Chinese men. Eur J Endocrinol. 2014 Apr;170(4):487–94.

130. Page ST, Mohr BA, Link CL, O’Donnell AB, Bremner WJ, McKinlay JB. Higher testosterone levels are associated with increased high-density lipoprotein cholesterol in men with cardiovascular disease: results from the Massachusetts Male Aging Study. Asian J Androl. 2008 Mar;10(2):193–200.

131. Nordøy A, Aakvaag A, Thelle D. Sex hormones and high density lipoproteins in healthy males. Atherosclerosis. 1979 Dec;34(4):431–6.

132. Cai Z, Xi H, Pan Y, Jiang X, Chen L, Cai Y, et al. Effect of testosterone deficiency on cholesterol metabolism in pigs fed a high-fat and high-cholesterol diet. Lipids Health Dis. 2015 Mar 7;14:18.

133. Self A, Zhang J, Corti M, Esani M. Correlation between Sex Hormones and Dyslipidemia. Am Soc Clin Lab Sci. 2019 Oct 14;ascls.119.002071.

134. Monroe AK, Dobs AS. The effect of androgens on lipids. Curr Opin Endocrinol Diabetes Obes. 2013 Apr;20(2):132–9.

135. Gutai J, LaPorte R, Kuller L, Dai W, Falvo-Gerard L, Caggiula A. Plasma testosterone, high density lipoprotein cholesterol and other lipoprotein fractions. Am J Cardiol. 1981 Nov;48(5):897–902.

 


Orthomolecular Medicine

Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org

Find a Doctor

To locate an orthomolecular physician near you: http://orthomolecular.org/resources/omns/v06n09.shtml

The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.

Editorial Review Board:

Albert G. B. Amoa, MB.Ch.B, Ph.D. (Ghana)
Seth Ayettey, M.B., Ch.B., Ph.D. (Ghana)
Ilyès Baghli, M.D. (Algeria)
Barry Breger, M.D. (Canada)
Ian Brighthope, MBBS, FACNEM (Australia)
Gilbert Henri Crussol, D.M.D. (Spain)
Carolyn Dean, M.D., N.D. (USA)
Ian Dettman, Ph.D. (Australia)
Susan R. Downs, M.D., M.P.H. (USA)
Ron Ehrlich, B.D.S. (Australia)
Hugo Galindo, M.D. (Colombia)
Gary S. Goldman, Ph.D. (USA)
William B. Grant, Ph.D. (USA)
Claus Hancke, MD, FACAM (Denmark)
Patrick Holford, BSc (United Kingdom)
Ron Hunninghake, M.D. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Dwight Kalita, Ph.D. (USA)
Felix I. D. Konotey-Ahulu, M.D., FRCP (Ghana)
Peter H. Lauda, M.D. (Austria)
Fabrice Leu, N.D., (Switzerland)
Alan Lien, Ph.D. (Taiwan)
Homer Lim, M.D. (Philippines)
Stuart Lindsey, Pharm.D. (USA)
Pedro Gonzalez Lombana, M.D., Ph.D. (Colombia)
Victor A. Marcial-Vega, M.D. (Puerto Rico)
Juan Manuel Martinez, M.D. (Colombia)
Mignonne Mary, M.D. (USA)
Dr.Aarti Midha M.D., ABAARM (India)
Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)
Karin Munsterhjelm-Ahumada, M.D. (Finland)
Sarah Myhill, MB, BS (United Kingdom)
Tahar Naili, M.D. (Algeria)
Zhiyong Peng, M.D. (China)
Isabella Akyinbah Quakyi, Ph.D. (Ghana)
Selvam Rengasamy, MBBS, FRCOG (Malaysia)
Jeffrey A. Ruterbusch, D.O. (USA)
Gert E. Schuitemaker, Ph.D. (Netherlands)
Thomas N. Seyfried, Ph.D. (USA)
Han Ping Shi, M.D., Ph.D. (China)
T.E. Gabriel Stewart, M.B.B.CH. (Ireland)
Jagan Nathan Vamanan, M.D. (India)

Andrew W. Saul, Ph.D. (USA), Founding Editor
Richard Cheng, M.D., Ph.D. (USA), Editor-In-Chief
Associate Editor: Robert G. Smith, Ph.D. (USA)
Editor, Japanese Edition: Atsuo Yanagisawa, M.D., Ph.D. (Japan)
Editor, Chinese Edition: Richard Cheng, M.D., Ph.D. (USA)
Editor, Norwegian Edition: Dag Viljen Poleszynski, Ph.D. (Norway)
Editor, Arabic Edition: Moustafa Kamel, R.Ph, P.G.C.M (Egypt)
Editor, Korean Edition: Hyoungjoo Shin, M.D. (South Korea)
Editor, Spanish Edition: Sonia Rita Rial, PhD (Argentina)
Editor, German Edition: Bernhard Welker, M.D. (Germany)
Associate Editor, German Edition: Gerhard Dachtler, M.Eng. (Germany)
Assistant Editor: Michael Passwater (USA)
Contributing Editor: Thomas E. Levy, M.D., J.D. (USA)
Contributing Editor: Damien Downing, M.B.B.S., M.R.S.B. (United Kingdom)
Contributing Editor: W. Todd Penberthy, Ph.D. (USA)
Contributing Editor: Ken Walker, M.D. (Canada)
Contributing Editor: Michael J. Gonzalez, N.M.D., Ph.D. (Puerto Rico)
Technology Editor: Michael S. Stewart, B.Sc.C.S. (USA)
Associate Technology Editor: Robert C. Kennedy, M.S. (USA)
Legal Consultant: Jason M. Saul, JD (USA)

Comments and media contact: editor@orthomolecular.org OMNS welcomes but is unable to respond to individual reader emails. Reader comments become the property of OMNS and may or may not be used for publication.

Click here to see a web copy of this news release: https://orthomolecular.acemlna.com/p_v.php?l=1&c=351&m=346&s=a8c8fe7bea3fdaa4efae896c7612b3de

This news release was sent to brenton.satman@gmail.com. If you no longer wish to receive news releases, please reply to this message with “Unsubscribe” in the subject line or simply click on the following link: unsubscribe . To update your profile settings click here .

This article may be reprinted free of charge provided 1) that there is clear attribution to the Orthomolecular Medicine News Service, and 2) that both the OMNS free subscription link http://orthomolecular.org/subscribe.html and also the OMNS archive link http://orthomolecular.org/resources/omns/index.shtml are included.

Riordan Clinic | Orthomolecular.org
3100 N Hillside Ave
Wichita, Kansas 67219
United States

The Miracles of High-Dose Orthomolecular Nutrition: A Tribute to Dr. Bruce Ames

Reproduced from original OMNS article (OrthoMolecular News Service):
http://orthomolecular.org/


Subscribe to the free Orthomolecular Newsletter: http://orthomolecular.org/subscribe.html
Go to the OMNS Archive: http://orthomolecular.org/resources/omns/index.shtml
Orthomolecular Medicine News Service, December 27, 2024

Richard Z. Cheng, M.D., Ph.D.

Dr. Bruce Ames, a trailblazer in biochemistry and a passionate advocate for nutrition and health, passed away recently at the age of 95. A distinguished member of the National Academy of Sciences and the recipient of numerous awards, including the National Medal of Science, he was inducted into the Orthomolecular Medicine Hall of Fame. Known for his groundbreaking scientific work and his commitment to improving public health, Dr. Ames leaves behind a remarkable legacy that has profoundly influenced how we think about nutrition and wellness.

Over his long and productive career, Dr. Ames revolutionized our understanding of the relationship between nutrition, disease, and longevity. His contributions to the field of orthomolecular nutrition—the science of optimizing health through high doses of vitamins and minerals—have inspired countless researchers, doctors, and health advocates around the world. His vibrant 95-year life stands as a testament to the principles he championed, much like his peers Linus Pauling, Abram Hoffer, and Roger Williams, all of whom lived beyond 90 years and were pioneers of this transformative approach to health.

v20n25-BruceAmes.png


Dr. Bruce Ames: A Life Dedicated to Health and Nutrition

Dr. Ames is perhaps best known for the Ames Test, a simple yet revolutionary tool for detecting harmful, DNA-damaging chemicals. But it was his later work in nutrition that cemented his reputation as a visionary. He introduced the Triage Theory, which proposed that when essential nutrients are in short supply, the body prioritizes immediate survival over long-term health. This theory has profound implications for understanding chronic diseases, aging, and how even small deficiencies in vitamins or minerals can have lasting effects on our health.

Dr. Ames believed that optimizing nutrition wasn’t just about avoiding deficiencies; it was about thriving. He advocated for using high doses of key nutrients to repair cells, support energy production, strengthen the immune system, and even reduce the risk of diseases like heart disease, diabetes, and cancer. His message was simple but powerful: nutrition is the foundation of health and longevity.


The Synergistic Roles of 40+ Vitamins and Micronutrients

Dr. Ames often highlighted the intricate interplay of over 40 essential vitamins and minerals, emphasizing their synergistic roles in maintaining optimal health. He demonstrated how these nutrients work together to support countless biochemical processes essential for vitality and disease prevention.

1. Interconnected Biochemical Pathways

Dr. Ames explained that micronutrients do not work in isolation. For example:

  • Magnesium activates enzymes necessary for DNA repair and energy metabolism.
  • B Vitamins (e.g., B6, B12, and folate) are essential for methylation processes that regulate gene expression and prevent DNA damage.
  • Vitamin C and Vitamin E act together to neutralize free radicals, protecting cells from oxidative stress.

2. Addressing Subclinical Deficiencies

He stressed that even mild deficiencies in any single nutrient can disrupt these pathways, compounding health issues over time. For instance:

  • A deficiency in selenium or zinc can weaken the antioxidant network, leaving cells vulnerable to damage despite adequate levels of other nutrients.

3. Comprehensive Supplementation

Dr. Ames championed comprehensive supplementation to ensure that all micronutrients are present in sufficient amounts. This approach aligns with his Triage Theory, which warns of the long-term consequences of nutrient scarcity:

  • Chronic deficiencies lead to DNA damage, mitochondrial dysfunction, and accelerated aging.
  • Comprehensive supplementation helps address these deficiencies, promoting both short-term health and long-term vitality.

“The Triage Theory provides a mechanistic rationale for such damage: shortage of a nutrient triggers a built-in rationing mechanism that allocates the scarce nutrient to proteins needed for immediate survival (survival proteins), at the expense of those needed for long-term survival (longevity proteins)” – Bruce Ames

4. Micronutrient Synergy and Healthspan

By ensuring an optimal balance of all 40+ essential vitamins and minerals, Dr. Ames showed that we could enhance energy production, reduce inflammation, and improve resilience against chronic diseases.


What Is Orthomolecular Nutrition?

Orthomolecular nutrition focuses on providing the body with optimal levels of essential nutrients to achieve the best possible health. While traditional dietary recommendations aim to prevent acute deficiency diseases like scurvy or rickets, orthomolecular nutrition goes a step further by addressing the nutrient levels needed for long-term health and vitality.

Here are some of the ways high-dose nutrients can transform health:

1. Supporting Cellular Health

Nutrients like vitamin C and vitamin E act as antioxidants, protecting cells from damage caused by stress and aging. For example:

  • Vitamin C boosts the immune system, fights infections, and supports skin health.
  • Vitamin E protects against heart disease by preventing damage to blood vessels.

“Folic acid deficiency does the same thing as radiation.” – Bruce Ames

2. Boosting Energy Production

Key nutrients such as B vitamins, magnesium, and coenzyme Q10 support mitochondria, the powerhouses of our cells. By improving mitochondrial function, these nutrients enhance energy levels and reduce fatigue.

3. Strengthening the Immune System

High-dose vitamin D helps regulate the immune system, while zinc supports the production of infection-fighting cells. Together, they fortify the body’s defenses against illness.

“Vitamin D activates serotonin production in the brain.” – Bruce Ames

4. Preventing Chronic Disease

Dr. Ames’ Triage Theory highlights how even minor nutrient shortages can lead to DNA damage, accelerated aging, and chronic diseases like cancer, diabetes, and cardiovascular conditions. High-dose supplementation helps prevent these issues before they arise.


Why Conventional Guidelines Aren’t Enough

The standard dietary guidelines, like the Recommended Dietary Allowance (RDA), focus on preventing immediate nutrient deficiencies. However, these levels often fall short of what’s needed to support long-term health. Dr. Ames argued that most people suffer from subclinical deficiencies—nutrient levels that may not cause obvious symptoms but still contribute to chronic diseases over time.

For example:

  • Vitamin D levels recommended by the RDA are sufficient to prevent rickets but inadequate for reducing inflammation and improving bone strength.
  • Niacin (Vitamin B3) in high doses can improve cholesterol levels and support heart health, far beyond the RDA’s minimal requirements.

Orthomolecular nutrition bridges this gap by focusing on nutrient levels that promote optimal health rather than just preventing disease.


Real-World Benefits of High-Dose Nutrition

1. Managing Chronic Conditions

Orthomolecular approaches have shown success in managing and even reversing chronic diseases:

  • Heart Disease: High doses of niacin improve cholesterol levels and reduce plaque buildup.
  • Diabetes: Nutrients like alpha-lipoic acid and chromium enhance insulin sensitivity and regulate blood sugar levels.
  • Cognitive Decline: Omega-3 fatty acids and antioxidants protect the brain from aging and neurodegenerative diseases.

2. Cancer Prevention and Support

Nutrients like selenium and vitamin C have been shown to reduce cancer risk. High-dose vitamin C, in particular, has a unique ability to target cancer cells while sparing healthy ones, offering a complementary approach to conventional treatments.

3. Enhancing Longevity

Orthomolecular nutrition addresses the root causes of aging by repairing DNA damage, improving energy production, and reducing inflammation, helping people live longer, healthier lives.


Honoring Dr. Ames’ Vision

“An optimum intake of micronutrients and metabolites, which varies with age and genetic constitution, would tune up metabolism and give a marked increase in health, particularly for the poor and elderly, at little cost.” – Bruce Ames

Dr. Ames dedicated his life to understanding how nutrition impacts our health at the deepest levels. His work in orthomolecular medicine has inspired a global movement to prioritize nutrition as the foundation of health and longevity. As we reflect on his contributions, we are reminded of the transformative power of optimal nutrition. Dr. Ames once emphasized that our diet profoundly shapes our health—a fundamental truth that underpins his life’s work. By embracing his vision of high-dose orthomolecular nutrition, we can continue his mission to create a healthier, more vibrant world for generations to come. With orthomolecular nutrition, we can not only Make America Healthy Again, but also Make the World Healthy Again.


Orthomolecular Medicine

Orthomolecular medicine uses safe, effective nutritional therapy to fight illness. For more information: http://www.orthomolecular.org

Find a Doctor

To locate an orthomolecular physician near you: http://orthomolecular.org/resources/omns/v06n09.shtml

The peer-reviewed Orthomolecular Medicine News Service is a non-profit and non-commercial informational resource.

Editorial Review Board:

Albert G. B. Amoa, MB.Ch.B, Ph.D. (Ghana)
Seth Ayettey, M.B., Ch.B., Ph.D. (Ghana)
Ilyès Baghli, M.D. (Algeria)
Barry Breger, M.D. (Canada)
Ian Brighthope, MBBS, FACNEM (Australia)
Gilbert Henri Crussol, D.M.D. (Spain)
Carolyn Dean, M.D., N.D. (USA)
Ian Dettman, Ph.D. (Australia)
Susan R. Downs, M.D., M.P.H. (USA)
Ron Ehrlich, B.D.S. (Australia)
Hugo Galindo, M.D. (Colombia)
Gary S. Goldman, Ph.D. (USA)
William B. Grant, Ph.D. (USA)
Claus Hancke, MD, FACAM (Denmark)
Patrick Holford, BSc (United Kingdom)
Ron Hunninghake, M.D. (USA)
Bo H. Jonsson, M.D., Ph.D. (Sweden)
Dwight Kalita, Ph.D. (USA)
Felix I. D. Konotey-Ahulu, M.D., FRCP (Ghana)
Peter H. Lauda, M.D. (Austria)
Fabrice Leu, N.D., (Switzerland)
Alan Lien, Ph.D. (Taiwan)
Homer Lim, M.D. (Philippines)
Stuart Lindsey, Pharm.D. (USA)
Pedro Gonzalez Lombana, M.D., Ph.D. (Colombia)
Victor A. Marcial-Vega, M.D. (Puerto Rico)
Juan Manuel Martinez, M.D. (Colombia)
Mignonne Mary, M.D. (USA)
Dr.Aarti Midha M.D., ABAARM (India)
Jorge R. Miranda-Massari, Pharm.D. (Puerto Rico)
Karin Munsterhjelm-Ahumada, M.D. (Finland)
Sarah Myhill, MB, BS (United Kingdom)
Tahar Naili, M.D. (Algeria)
Zhiyong Peng, M.D. (China)
Isabella Akyinbah Quakyi, Ph.D. (Ghana)
Selvam Rengasamy, MBBS, FRCOG (Malaysia)
Jeffrey A. Ruterbusch, D.O. (USA)
Gert E. Schuitemaker, Ph.D. (Netherlands)
Thomas N. Seyfried, Ph.D. (USA)
Han Ping Shi, M.D., Ph.D. (China)
T.E. Gabriel Stewart, M.B.B.CH. (Ireland)
Jagan Nathan Vamanan, M.D. (India)

Andrew W. Saul, Ph.D. (USA), Founding Editor
Richard Cheng, M.D., Ph.D. (USA), Editor-In-Chief
Associate Editor: Robert G. Smith, Ph.D. (USA)
Editor, Japanese Edition: Atsuo Yanagisawa, M.D., Ph.D. (Japan)
Editor, Chinese Edition: Richard Cheng, M.D., Ph.D. (USA)
Editor, Norwegian Edition: Dag Viljen Poleszynski, Ph.D. (Norway)
Editor, Arabic Edition: Moustafa Kamel, R.Ph, P.G.C.M (Egypt)
Editor, Korean Edition: Hyoungjoo Shin, M.D. (South Korea)
Editor, Spanish Edition: Sonia Rita Rial, PhD (Argentina)
Editor, German Edition: Bernhard Welker, M.D. (Germany)
Associate Editor, German Edition: Gerhard Dachtler, M.Eng. (Germany)
Assistant Editor: Michael Passwater (USA)
Contributing Editor: Thomas E. Levy, M.D., J.D. (USA)
Contributing Editor: Damien Downing, M.B.B.S., M.R.S.B. (United Kingdom)
Contributing Editor: W. Todd Penberthy, Ph.D. (USA)
Contributing Editor: Ken Walker, M.D. (Canada)
Contributing Editor: Michael J. Gonzalez, N.M.D., Ph.D. (Puerto Rico)
Technology Editor: Michael S. Stewart, B.Sc.C.S. (USA)
Associate Technology Editor: Robert C. Kennedy, M.S. (USA)
Legal Consultant: Jason M. Saul, JD (USA)

 

Riordan Clinic | Orthomolecular.org
3100 N Hillside Ave
Wichita, Kansas 67219
United States

From Farm to Health — A Vision for Regenerative Agriculture and Metabolic Wellness


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/11/24/regenerative-agriculture-metabolic-wellness.aspx


Analysis by Dr. Joseph Mercola     
November 24, 2024

STORY AT-A-GLANCE

  • Ashley Armstrong, co-founder of Angel Acres Egg Co., shifted from fitness coaching to health advocacy after discovering the connection between dietary choices and autoimmune issues
  • Adequate carbohydrate intake — approximately 250 grams daily — is necessary for metabolic health, while low-carb diets increase cortisol and disrupt thyroid function
  • Body temperature measurements three times daily provide a better indicator of metabolic health than conventional blood work, with 98.6 degrees F midday indicating normal function
  • Polyunsaturated fatty acids (PUFAs) and phytoestrogens in modern diets interfere with thyroid function and estrogen detoxification, leading to metabolic disruptions
  • Armstrong promotes regenerative farming practices, producing low-PUFA eggs and freeze-dried egg yolks while advocating for sustainable agriculture over conventional farming methods

I recently interviewed Ashley Armstrong, co-founder of Angel Acres Egg Co. and a leading advocate for regenerative agriculture. Ashley’s unique perspective bridges the gap between optimal health practices and sustainable farming, offering invaluable insights into how our food systems and dietary choices profoundly impact well-being.

Ashley began her health journey alongside her sister, Sarah, under the moniker “Strong Sisters.” Initially focused on weightlifting and resistance training, they documented their progress and reveled in the empowerment that came with physical strength. “It was so empowering … It’s you versus you,” Ashley shared.1

However, their path took a significant turn when both encountered health issues linked to their dietary choices, particularly the prevalence of polyunsaturated fatty acids (PUFAs) and processed ingredients. Sarah was diagnosed with a form of lupus at 21, prompting them to seek alternatives to conventional medicine.

“We went down rabbit holes of keto, fasting, carnivore, all of that … we felt relief initially … and then those decisions caught up to us. After about two years, we stumbled upon the work of Dr. Ray Pete, and the rest is history,” Ashley explained,2 emphasizing their shift toward understanding thyroid and metabolic health as interconnected facets of systemic well-being.

The Role of Carbohydrates in Metabolic Health

The importance of carbohydrates in maintaining metabolic rate and thyroid function is often overlooked. Ashley said, “Carbohydrates are vital. They’re optimal. They’re required. They’re necessary.” Part of their importance is linked to their effects on body temperature. She explained:3

“It’s up to you as an individual to find what carbs work well for you, focus on those for a period of time. Work on implementing more slowly, increasing those that work well for you, because that, over time, is going to raise your metabolic rate. As you raise your metabolic rate, your body temperature rises.

And that is the whole goal. We want to be hot. We don’t just want to look good. We want to be hot inside of us, because all the functions in our body, they run off of enzymes. And enzyme reaction rates depend on temperature.”

She criticized the dogmatic low-carb approaches prevalent in certain health communities, advocating instead for a personalized strategy to carbohydrate intake. By categorizing carbs into a traffic light system — green, yellow and red — my newest book, “Your Guide to Cellular Health: Unlocking the Science of Longevity and Joy,” provides a practical framework for you to identify and incorporate beneficial carbohydrates into your diet.

It’s important to meet a certain carbohydrate threshold, approximately 250 grams a day, to support metabolic functions. If you don’t reach that threshold, you’re going to run into health troubles. Low-carbohydrate diets, for instance, increase cortisol. Short-term elevation of cortisol is protective and necessary for survival.

However, chronic elevation leads to detrimental health effects, including muscle wasting, bone density loss and impaired cognitive function. Further, consuming enough healthy carbohydrates not only supports metabolic rate but also ensures the proper conversion of inactive thyroid hormone (T4) into its active form (T3), a process necessary for cellular energy production.

Measuring Health Beyond Conventional Blood Work

Ashley recommends the use of body temperature as a metric for assessing your metabolic health. Unlike conventional blood tests, which provide only a snapshot and are influenced by various external factors, body temperature measurements offer a continuous, real-time indicator of metabolic rate. “If your body temperature is rising, that’s a clear sign your cellular utilization of T3 is happening,” Ashley explained.4

She advocates for taking body temperature three times a day — upon waking, 30 to 45 minutes after breakfast and midday. This approach is effective because T3 levels are generally higher in the morning and decline as the day progresses. This routine allows you to monitor your metabolic trends and make informed dietary adjustments.

Ashley highlighted, “This is an easy tool … because blood work still doesn’t tell you whether your mitochondria are actually using that thyroid hormone T3.”5

Ideally, use a basal body temperature thermometer to measure your temperature, as they measure to 100th of a degree. A consistently low body temperature indicates a sluggish metabolism, while a morning body temperature of approximately 98 degrees F signifies healthy thyroid function. By midday, a temperature around 98.6 degrees F typically indicates a normal metabolic response.

Ashley also highlighted the limitations of conventional thyroid panels, which often focus solely on thyroid-stimulating hormone (TSH) levels. She stressed the importance of comprehensive thyroid testing, including free T3, reverse T3 and T4, to gain a true understanding of thyroid health and metabolic function.

Save This Article for Later – Get the PDF Now

Download PDF

The Dual Threat of PUFAs and Phytoestrogens

We also covered the detrimental effects of PUFAs, like linoleic acid (LA), and phytoestrogens on metabolic health. Ashley noted, “PUFAs damage our ability to detoxify estrogen,” explaining how these substances interfere with your body’s ability to convert T4 to T3, thereby lowering metabolic rates.6 This disruption not only hampers energy production but also fosters an environment conducive to autoimmune conditions and other health issues.

LA is found in seed oils, processed foods and even some seemingly healthy options like chicken, nuts and seeds. While it’s believed to be an essential fatty acid that your body needs, the modern Western diet typically provides far more than necessary. Optimizing your mitochondrial function is necessary for improving your cellular energy, but LA is a mitochondrial poison and also damages your gut health.

She also addressed the pervasive nature of phytoestrogens in the modern diet, particularly through soy and flax products. “Phytoestrogens have been shown to activate estrogen receptors in the same way we’re eating that through fake dairy products, soy milk, soy cheese,” Ashley warned. The accumulation of these estrogen-like compounds exacerbates metabolic disruptions, leading to estrogen dominance and further impeding thyroid function.

Exposure to endocrine-disrupting chemicals (EDCs) like phthalates and bisphenol A (BPA), often from microplastics, also overstimulates your estrogen receptors. Estrogen increases intracellular calcium levels, leading to peroxynitrite formation, a potent reactive oxygen species that contributes to poor health.

As bioenergetic researcher Georgi Dinkov explained in our previous interview, estrogen is carcinogenic and antimetabolic, radically reducing the ability of your mitochondria to create cellular energy. Many people believe that they are low in estrogen due to bloodwork, when they actually have high levels in their organs. This is because serum estrogen levels are not representative of estrogen that’s stored in tissues. Estrogen may be low in plasma, but high in tissues.

A better option for gauging estrogen levels in fat and tissues is a prolactin blood test. Estrogen promotes the production of prolactin, which is a hormone produced by the pituitary gland. Once you’ve dialed in your diet by reducing LA and consuming healthy carbs, an effective strategy that helps counteract estrogen excess is natural progesterone.

Transforming Agriculture — Regenerative Practices for Superior Nutrition

Ashley’s expertise as a chicken farmer is deeply intertwined with her health advocacy. She spearheads a movement toward regenerative agriculture, focusing on feeding chickens a diet low in PUFAs and free from harmful additives. “Our row crop farm partners are producing our grains that our chickens are eating regeneratively,” she explained, underscoring the importance of soil health and sustainable farming practices in producing nutrient-dense animal products.7

This commitment to regenerative practices enhances the nutritional profile of the eggs and ensures that the chickens are healthier and more robust. “We’re working with Mother Nature, with our row crop partners,” Ashley affirmed, highlighting the synergy between sustainable farming and optimal human health.8

One of the most exciting developments discussed was the introduction of freeze-dried egg yolks. This innovative product addresses the perishability and logistical challenges of traditional egg consumption while preserving the rich nutrient profile of the yolks. When you freeze-dry food, specifically egg yolks, you essentially remove all the moisture, reducing perishability and extending the shelf life.

These freeze-dried yolks are not only nutrient-dense but also versatile, allowing you to incorporate them into various dishes, like smoothies, without worrying about spoilage. Freeze-dried egg yolks offer a convenient, long-lasting source of essential nutrients like choline and vitamin K2. Ashley emphasized their role in supporting neurotransmitter function and overall metabolic health.

Choline is part of an important neurotransmitter called acetylcholine, which is part of the parasympathetic nervous system. Unfortunately, conventional health and agricultural systems prioritize profitability over health and sustainability. The dominance of Big Pharma and Big Agriculture has led to widespread use of harmful PUFAs, phytoestrogens and other additives that compromise both human and environmental health.

Ashley explained the economic challenges faced by small-scale farmers within these systems. “Farmers have to get off the farm jobs to support their farm,” she lamented, pointing out the unsustainable nature of current agricultural practices.9 Our collaborative efforts aim to create alternative markets and support structures that make regenerative farming viable and profitable, thereby ensuring the production of healthier food products.

She also touched upon the systemic issues perpetuated by federal subsidies, which have historically favored certain crops, leading to the overproduction of soy and corn — primary sources of PUFAs and phytoestrogens.

“The Farm Bill has subsidized the production of certain crops, and we’ve overproduced so much that now the costs are so low for feed producers,” Ashley explained.10 By shifting consumer demand toward regenerative and sustainable farming practices, we will gradually diminish the influence of these subsidies and promote a healthier, more resilient agricultural system.

Practical Steps to Enhance Metabolic Health

For those looking to improve their metabolic health, Ashley provided actionable advice rooted in her expertise. She emphasized the importance of:

  1. Ensuring a sufficient intake of healthy carbohydrates to support metabolic functions and thyroid health.
  2. Using body temperature measurements as a real-time indicator of metabolic rate and thyroid function.
  3. Avoiding foods high in PUFAs like LA and phytoestrogens to prevent metabolic disruptions and support thyroid hormone utilization.
  4. Incorporating nutrient-dense foods, including saturated fats and egg yolks to provide essential vitamins and minerals without harmful additives.
  5. Supporting regenerative agriculture by choosing products from regenerative farms to ensure the intake of healthier, sustainably produced food.

Ashley’s work serves as a reminder of the power of informed, sustainable practices. By prioritizing whole foods, minimizing harmful additives and supporting ethical farming methods, it’s possible to create a healthier, more resilient society.

Building a Sustainable, Healthy Future

As consumers become more aware of the profound connections between their dietary choices and overall health, the demand for regenerative products will naturally increase. This, in turn, will incentivize more farmers to adopt sustainable practices, creating a positive feedback loop that benefits both individuals and the planet.

Ashley concluded, “Health shouldn’t be hard. You shouldn’t be overwhelmed, and you are not forever broken if you give the body the tools it needs, remove the metabolic breaks and use simple body temperature measurements.”11 Her holistic approach underscores the interconnectedness of diet, agriculture and systemic health, offering a roadmap for individuals to achieve optimal well-being.

Ashley and I also discussed the forthcoming launch of the revolutionary Mercola Health Coach app and Mercola Health Labs. These initiatives will change how individuals access and interpret their health data, making comprehensive lab testing more accessible and affordable.

The Mercola Health Coach app will provide personalized monitoring and recommendations that support your best possible health. Food Buddy, an integral part of the Mercola Health Coach, is designed to help you effectively navigate daily food choices to reach optimal wellness.

Mercola Health Labs will offer a range of lab tests at a fraction of the current costs, with plans to provide some tests for free along with supplement purchases. This initiative is designed to empower you to take control of your health without the financial and logistical barriers associated with conventional lab testing. If you’d like to join the waitlist for the Mercola Health Coach app, click here.

As we continue to develop tools like the Mercola Health Coach app and expand regenerative farming partnerships, the vision of a healthier, more sustainable future becomes increasingly attainable.

We are pioneering a movement that not only transforms individual health but also redefines our relationship with the food we consume and the environment we inhabit. By empowering individuals with knowledge and supporting farmers with sustainable practices, we are laying the foundation for a thriving future.