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Kidney Stones in Children Are Becoming More Prevalent — Here’s Why and How to Fight Them
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/05/16/kidney-stones-in-children.aspx
Analysis by Dr. Joseph Mercola May 16, 2024
STORY AT-A-GLANCE
- Cases of kidney stones among children are increasing, and although less common than in adults, it could become a lifelong battle
- Oxalates, which are found in many plant foods, are a contributing factor to the rising cases of kidney stones. When these compounds bind with calcium, they form calcium oxalate crystals, which are microscopic and razor-sharp, and can cause significant tissue damage
- By optimizing your metabolic flexibility, you can maintain a low-oxygen environment in your gut. This allows healthy obligate anaerobes, which can help metabolize and eliminate oxalates, to thrive
- Removing high-oxalate foods from your diet is the first step to minimize their harmful effects and help heal your gut. Some strategies that can aid in eliminating oxalates are also discussed here
Kidney stones are hard masses that form from the chemicals in the urine when there’s too much waste and too little liquid. They can be as small as a grain of sand, or as big as a pebble — in some cases, they can grow as large as a golf ball. As your body works to eliminate the stone, it can lead to irritation or blockage, causing intense pain and other symptoms.1
In adults, kidney stones are a common health complaint, with 8 out of 1,000 adults being diagnosed yearly.2 Alarmingly, cases among children are increasing as well.
Is Your Child at Risk of Developing Kidney Stones?
According to an article in ABC7,3 kidney stones have become more prevalent in children over the last 20 years. Although less common than in adults, it could still be a lifelong battle. The article tells the story of Alex Zellers, a 4-year-old with a rare genetic disease called cystinuria, which caused him to develop enlarged kidney stones that had to be surgically removed.4
“One stone in his kidney was the size of a golf ball. The other, in his bladder, was the size of a lacrosse ball. ‘It’s just like a giant dense egg. It’s just a big mass,’ described Kate, Alex’s mother.”
In the article, Dr. Greg Tasian, a pediatric urologist with Children’s Hospital of Philadelphia, explains how kidney stones form, saying “Your body doesn’t absorb certain amino acids and that cystine accumulates and crystallizes in the urine forming stones early in life.”
And although Alex’s condition is rare, Tasian claims that he is seeing an increase in young patients with kidney stones and says that several lifestyle factors are to blame, such as eating more ultraprocessed foods, excessive of use antibiotics and being chronically dehydrated, especially during hot weather.5
However, there could be another more significant contributing factor, and it’s found in the foods you eat — even those that are considered healthy.
Oxalates Are Linked to Kidney Stones, but What Are They?
Oxalates are natural compounds found in many plant foods, including beans, grains, seeds and nuts, fruits, berries and herbs.6 They’re also called dicarboxylic acid, meaning they are composed of two carbon dioxide (CO2) molecules.
However, having two carboxyl groups (COOH), causes them to lose protons under physiological conditions. This leaves them with a negative charge, which then allows them to bind to positively charged ions like calcium.
Chemically, oxalate is a salt; and as with other salts, it forms crystals that your body innately has a limited capacity to process. When oxalates bind with calcium, they form calcium oxalate crystals, which are microscopic and razor-sharp and can cause significant tissue damage. And because they are not soluble, they can accumulate.
This is what causes kidney stones to form. Calcium stones are the primary type, making up 80% of kidney stones.7 But contributing to the formation of kidney stones is just one of the ways oxalates wreak havoc on your health. These compounds can affect numerous body functions and cause a wide range of symptoms.
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A High-Oxalate Diet Can Lead to Joint Pain, Digestive Problems and Skin Irritation
Excessive oxalates can affect your absorption of essential nutrients and lead to mineral deficiencies. When they accumulate in your joints, they can cause crystals, similar to those in the kidneys, to form. This can trigger inflammation and joint pain, resembling symptoms of gout or arthritis.
In your urinary tract, oxalates can cause irritation, discomfort and an increased risk of urinary tract infections (UTIs). The razor-sharp crystals can also make urination painful, and contribute to irritable bladder syndrome, which is characterized by frequent, urgent and/or painful urination.
Meanwhile, bloating, gas, diarrhea and abdominal pain can arise when oxalates affect your intestinal tract, especially in people with sensitive digestive systems or who have irritable bowel syndrome (IBS).
There’s also research linking a high-oxalate diet with fibromyalgia symptoms, and while still not fully understood, the theory is that oxalate crystals may be causing inflammation in the muscles and connective tissues, causing widespread pain and fatigue.
Once your body tries to eliminate oxalates, they can be excreted through your skin, particularly if your kidneys can no longer process the excessive amounts of oxalates in your system. This can form crystalline deposits on your skin, causing irritation, rash and intense itching.
I struggled with this health problem 15 years ago, when I developed a rash that caused such intense itching it made me lose sleep. When scratched, the rash would turn into hard nodules that would last for months or years.
I tried numerous natural interventions, including icing the affected area and applying aloe gel, but could not find any long-lasting solution — it was only when I addressed the oxalates in my diet that I was able to find relief.
Oxalates Can Interfere With Your Cellular Functions
Another way that oxalates harm your health is by disrupting enzyme functions that are essential to cellular energy production. Oxalate ions can bind to the enzymes in the mitochondrial electron transport chain, which are essential for adenosine triphosphate (ATP) production.
Your mitochondria produce ATP, which is why they are called the “powerhouses” of your cells. ATP is the currency of your cellular energy and is the lifeblood of cellular processes. It powers everything, including processes like muscle contraction, nerve impulse propagation, synthesis of essential biomolecules and the maintenance of cellular homeostasis.
When oxalates disrupt ATP production, it can lead to decreased energy production and increased oxidative stress within cells. This then leads to a broader range of metabolic and physiological dysfunctions.
Avoid These High-Oxalate Foods
Everyone needs to be concerned about oxalates, not just those dealing with kidney stones or other chronic health issues, metabolic inflexibility or mineral imbalances. The first step is to identify high-oxalate foods and remove them from your diet, until your gut is healed.
I recently interviewed Sally Norton, who is an esteemed authority on oxalates. Her expertise is indeed invaluable for anyone seeking to understand this topic. In our discussion, she specified the foods that are particularly loaded with oxalates. You may be surprised, as some of these are on many people’s “healthy foods” list:
• Spinach — Their oxalate levels can be as high as 600 to 800 mg per 100 grams.
• Almonds — Almonds generally contain about 122 mg of oxalates per 100 grams. However, all nuts in general are particularly problematic, since they contain linoleic acid (LA). Even macadamia nuts can add to your toxic load, as they contain oleic acid, which could just be as bad as LA.
“These seeds from the trees are designed with all these multiple anti-nutrients to kick you in the gut. All the anti-nutrients are gut toxic. They’re all causing some degree of gut damage. Nuts are just designed to be indigestible. They’re designed to dismantle your ability to digest food. If you want a healthy gut, you don’t want nuts kicking your gut over and over again,” says Norton.
• Peanut butter — Peanut butter can have around 140 mg per 100 grams.
• Sweet potatoes — They contain about 30 mg of oxalates per 100 grams. (Although this is considered high compared to other vegetables, it’s actually much lower than spinach or nuts)
• Figs — They have approximately 40 mg per 100 grams.
In addition to spinach, high-oxalate leafy greens that are considered “superfoods” are Swiss chard and beet greens, so you may want to avoid them if you’re sensitive to oxalates or are struggling with kidney stones.
You may also want to avoid these collagen-rich protein sources until your gut is healed, as collagen breakdown can lead to oxalate production and aggravate your condition:
- Bone broth
- Gelatin
- Animal skins, tendon and ligaments
- Meat cuts with connective tissues such as oxtail, neck and shank
- Organ meats like heart and liver
Healing Your Gut Can Help Address Oxalate Toxicity
I mentioned above that healing your gut health is crucial to help curb the effects of oxalates, but before you do that, you need to address your metabolic inflexibility. This refers to your body’s diminished ability to switch between burning fuel sources, mainly carbohydrates and fats.
When you’re metabolically inflexible, it can affect your body’s ability to produce energy. This can have a profound impact on your gut health, particularly your large intestine, as it hinders your body’s ability to maintain a low-oxygen environment in this organ.
You need a low-oxygen environment in your large intestine because not only does it help keep pathogenic bacteria in check, but it also allows healthy obligate anaerobes to thrive. These are a primitive type of bacteria that cannot survive when exposed to oxygen.
So what do obligate anaerobes have to do with oxalate toxicity? It turns out that there are obligate anaerobes that can digest oxalate crystals, called Oxalobacter formongines.8 These beneficial bacteria thrive in a low-oxygen environment and have a unique ability to efficiently metabolize oxalates.
Using specific enzymes, Oxalobacter bacteria break down oxalate crystals into formate and carbon dioxide. The carbon dioxide then helps retain the low-oxygen environment in your intestine, allowing these primitive organisms to thrive and support your health. Through simple passive diffusion, the crystals are released and wind up in your intestine where the Oxalobacter continues to digest them until the oxalate toxicity issues disappear.
To put it simply, you need to optimize your metabolic flexibility so you can maintain a low-oxygen environment in your gut and allow Oxalobacter bacteria to radically reduce the level of oxalates in your tissues.
I believe this is the ultimate cure for most kidney stones. It’s far more efficient and effective than the conventional approach for this common health condition, as it goes straight to the root cause of the problem.
Step 1 in healing your gut would be to eliminate linoleic acid (LA) from your diet, as LA precipitates the formation of peroxynitrites that ravage mitochondrial function and impede energy production, forcing your body to rely on glycolysis in the cytoplasm of your cells rather than the electron transport chain (ETC) of your mitochondria.
This, in turn, results in the impairment of your gut by allowing oxygen leakage into your gut that kills beneficial bacteria and allows pathogenic bacteria to thrive.
There’s No Quick Way to Detox Oxalates
If you or your children struggle with kidney stones or have other signs of oxalate toxicity, I encourage you to watch my interview with Norton, as we discuss many strategies and food choices that can help minimize the harmful effects of oxalates or aid in their elimination.
Aside from limiting your intake of high-oxalate foods mentioned above, here are some key recommendations to remember:
| Increase your calcium intake — When you consume foods high in calcium or take calcium supplements, they can bind to oxalates in the intestines and prevent them from being absorbed. They will also help facilitate oxalate excretion through your stool. Foods rich in calcium include dairy products and leafy greens. |
| Stay hydrated — Drinking sufficient water will help flush out oxalates through your urine and keep kidney stones from forming. |
| Optimize your gut health — Promote a healthy gut microbiome by consuming probiotic-rich foods like yogurt, kefir and fermented vegetables. This will help support the growth of Oxalobacter and other beneficial bacteria. |
| Citrate consumption — Citrate, found in citrus fruits like lemons and oranges, can help by binding with calcium and oxalate, thereby reducing the formation of kidney stones. Avoid over-supplementation with ascorbic acid, however, as high doses can convert into oxalate. Ascorbic acid is the most common form of vitamin C used in dietary supplements. |
| Cook high-oxalate foods well — Cooking methods that involve boiling can help reduce oxalate content in foods as the oxalates will leach into the cooking water. |
| Topical calcium for oxalate-related skin irritations — Applying topical calcium can alleviate your symptoms by precipitating oxalates at the site. |
Remember that healing your body takes time — don’t expect results overnight. It’s a marathon, not a sprint. In some cases, it may take two years to two-and-a-half years after following a low-oxalate diet to see the effects, and they may not be pleasant.
For example, you may suddenly get sicker, as your kidneys are finally cleaned up and can excrete oxalate more efficiently. This means your body is tapping into deeper deposits. Possible side effects can include gastritis, migraines, anxiety attacks, gout and other types of toxic reactions.
Your uric acid may also increase, as it is replacing the oxalic acid. In this instance, this means you’re clearing oxalate. You may also notice tartar buildup on your teeth, gritty stools, gritty eyes, hemorrhoids and burning stools — all these are symptoms that your body is healing itself.
Cellular Energy — The Very Essence of Life
My personal struggle with the skin irritation triggered by oxalates 15 years ago is an eye-opener. It’s what I consider the pivotal turning point in my health journey, as it is the best illustration of just how crucial it is to have a healthy, well-functioning microbiome to your overall health.
Unfortunately, virtually none of us have a healthy gut microbiome. This is a result mainly because of large multinational corporations taking advantage of us and steering us toward unnatural products that end up harming our mitochondria and ultimately our ability to create cellular energy.
I believe that your ability to produce sufficient cellular energy is the single most important factor to fuel your body’s innate repair and regeneration processes so it can recover from diseases and any type of health obstacle.
With that said, I will be releasing a new book this summer that delves into the science of cellular energy. In this book, I’ll explain in detail the biochemical pathways that provide energy to your cells, as well as also how disrupting these pathways can put you or your loved ones at risk of progressively worsening health issues.
I’ll also share practical strategies to help support your mitochondrial health and enhance your cellular energy production through healthy food choices, lifestyle changes and proper supplementation. This book is a definite must-read, as it can help you rediscover the foundational strategies to heal your body and ward off diseases, so stay tuned.
Oxalates — The Hidden Dangers in ‘Healthy’ Foods
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/04/28/oxalates-in-food.aspx
Analysis by Dr. Joseph Mercola April 28, 2024
STORY AT-A-GLANCE
- Oxalates, or dicarboxylic acids, are natural compounds found in many foods like leafy greens and nuts. Despite their simple carbon dioxide-based structure, they can form harmful crystals in the body and disrupt biological processes
- Oxalates can bind to calcium to form insoluble crystals that may lead to kidney stones and other health issues
- Oxalates can also inhibit crucial enzymes in the mitochondrial electron transport chain, reducing energy production and increasing oxidative stress
- If you struggle with chronic health issues related to mineral imbalances or metabolic inflexibility, minimizing your oxalate intake is advisable
- Foods high in oxalates that should be avoided if sensitive include spinach, almonds, peanut butter and sweet potatoes
In today’s episode, I am thrilled to welcome back Sally Norton, an esteemed authority on oxalates, whose expertise is invaluable for anyone seeking to understand this topic.
Norton has dedicated years to meticulously analyzing data and compiling an authoritative guide on oxalates, “Toxic Superfoods: How Oxalate Overload Is Making You Sick — and How to Get Better.” In it, she reviews how and why foods we’ve been told are healthy can undermine your health.
Her academic background includes a bachelor’s degree in nutritional science from Cornell University and her master’s degree in public health from the University of North Carolina, Chapel Hill. In this interview, we explore the broader implications of oxalates on health, Norton’s personal journey with oxalate sensitivity, and her innovative solutions for common nutritional misunderstandings.
What Are Oxalates?
Oxalates are natural compounds found in many foods, including leafy greens, nuts, and seeds. Another term for oxalate is dicarboxylic acid, which is made up by two carbon dioxide (CO2) molecules. As I’ve discussed in previous articles, CO2 is essential for health and life itself, so how is it that two CO2 molecules together cause so much harm?
The key problem with oxalates is not their CO2 origin but rather their ability to form crystals that interfere with normal biological processes. Dicarboxylic acids, such as oxalate, are characterized by having two carboxyl groups (COOH), which can lose protons under physiological conditions, leaving them with a negative charge.
This negative charge allows them to bind positively charged ions like calcium. When oxalates bind with calcium, they form calcium oxalate crystals, which are not soluble and can accumulate, leading to the formation of kidney stones or other tissue deposits.
Moreover, the electromagnetic properties of these charged oxalate ions can interfere with cellular functions. For example, the negatively charged oxalate can disrupt enzyme functions that are crucial for cellular energy production.
The enzymes in the mitochondrial electron transport chain, which are vital for ATP (energy) production, can be inhibited by the binding of oxalate ions, resulting in decreased energy production and increased oxidative stress within cells. In this way, oxalates contribute to broader metabolic and physiological dysfunctions.
This paradoxical nature of oxalates — arising from a simple and essential molecule like CO2 but leading to complex health challenges — illustrates the nuanced interactions within human biochemistry. In essence, the “charging” of dicarboxylic acids like oxalate transforms them into reactive molecules that can disrupt normal cellular processes through electromagnetic interactions.
As a result, people with compromised kidney function aren’t the only ones who need to be concerned about oxalates. Just about anyone struggling with chronic health issues related to mineral imbalances and/or metabolic flexibility may be adversely impacted by them and would do well to minimize their intake.
Oxalate Rashes Are a Common Symptom of Oxalate Toxicity
Oxalate toxicity can cause several problems that are very common, such as oxalate rashes — intensely itchy rashes that have no apparent cause. I struggled with that for 15 years before I finally discovered the cause. While using my aloe vera plants helped me, the best solution is to avoid oxalate-rich foods, as they’re what’s causing it.
Topical calcium citrate can also help resolve those itchy rashes. The reason topical calcium citrate works so well is twofold. Calcium binds to and forms precipitates with oxalates. It also addresses the calcium and electrolyte interference caused by oxalates.
“This interference with electrolytes and calcium is a major toxic effect,” Norton says. “And as the immune system is trying to deal with those oxalates in the subdermis, you’re getting additional electrolyte disturbances.
I don’t really know the mechanism of why that calcium topically is so powerful, but it’s amazing [for] any skin injury, People who are doing hair removal or whatever, damaging their skin, putting calcium on top of it, it just heals like overnight …
Interestingly, you can see it in the primary hyperoxaluria literature where high oxalate levels turn fascia and other connective tissues into calcified sheets. You can see it in the X-rays in kids that end up dying of oxalate poisoning that, just because the body is high oxalate, it causes calcification in tissues …
Calcium encourages oxalate clearing depending on how much oxalate is already in the diet, but once you’re low in oxalate, adding more calcium can increase the mobilization of oxalate.”
Citrate, such as fresh-squeezed lemon juice, taken internally, will also help dissolve oxalates.
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Oxalate-Rich Foods to Avoid
In the interview, Norton specifies several foods that are particularly high in oxalate and need to be avoided if you’re sensitive. Top examples include:
• Spinach — Typically, spinach can have oxalate levels as high as 600-800 mg per 100 grams
• Almonds — Almonds generally contain about 122 mg of oxalates per 100 grams. Nuts in general tend to be problematic, not only for oxalates but also for linoleic acid. As noted by Norton:
“These seeds from the trees are designed with all these multiple anti-nutrients to kick you in the gut. All the anti-nutrients are gut toxic. They’re all causing some degree of gut damage. Nuts are just designed to be indigestible. They’re designed to dismantle your ability to digest food. If you want a healthy gut, you don’t want nuts kicking your gut over and over again.”
• Peanut butter — Peanut butter can have around 140 mg per 100 grams
• Sweet potatoes — They contain about 30 mg of oxalates per 100 grams, which is considered high compared to other vegetables but much lower than spinach or nuts
• Figs — Figs have approximately 40 mg per 100 grams
Surprisingly, collagen-rich protein sources, including gelatin, bone broth, animal skins, tendons and ligaments, meat cuts that include a lot of connective tissues such as oxtail, neck and shank, and organ meats like heart and liver, can also be aggravating if you’re sensitive to oxalates or struggle with recurring kidney stones. So, it is wise to avoid oxalates until your gut is healed and you can tolerate them.
Decreased Mitochondrial Energy Production Contributes to Oxalate Toxicity
Metabolic inflexibility refers to your body’s reduced ability to switch between fuel sources, particularly between carbohydrates and fats, efficiently. This inflexibility can impair your energy production capabilities. When energy production is compromised, especially at the cellular level in the gut lining, it impairs your body’s ability to maintain a low oxygen environment in the large intestine, which is required to keep pathogenic bacteria in check.
The large intestine is typically an anaerobic (low oxygen) environment where beneficial bacteria thrive. These bacteria are crucial for various functions, including maintaining the integrity of the gut barrier and modulating immune responses.
A healthy gut with a properly maintained anaerobic environment supports the growth of beneficial obligate anaerobes, such as the keystone species Akkermansia. When the oxygen gradient is disturbed due to insufficient energy production (as seen in metabolically inflexible individuals), it allows facultative anaerobes (bacteria that can utilize oxygen when available) to proliferate.
These bacteria often produce endotoxins, also known as lipopolysaccharides (LPS), which can cause inflammation if they translocate across the compromised gut barrier into the systemic circulation.
Oxalates indirectly contribute to this scenario by exacerbating mitochondrial dysfunction and reducing cellular energy production. This reduction in ATP production can impair the maintenance of the anaerobic conditions necessary in the large intestine, facilitating the overgrowth of facultative anaerobes and the subsequent production of endotoxins.
The Intricate Relationship Between Gut Bacteria and Oxalates
Another important bacterium is Oxalobacter formigenes, a beneficial bacterium in the gut that plays a crucial role in the metabolism and regulation of bodily oxalate levels. It digests oxalate crystals and basically signals the gut wall to excrete oxalate for its own nourishment.
In this way, Oxalobacter helps reduce the concentration of oxalate in your gut, which can consequently lower the risk of oxalate crystallization and the formation of kidney stones and other health problems. However, the relationship between oxalates and Oxalobacter also has a hazardous aspect.
While these bacteria can mitigate some of the risks associated with high oxalate levels, their presence and effectiveness can be compromised if the oxalate levels become too high or if the gut environment becomes inhospitable due to other dietary or metabolic imbalances.
Excessive oxalates can overwhelm the gut system, inhibit other beneficial gut flora, and contribute to a reduction in Oxalobacter populations, thus diminishing their protective role. But the reason oxalates are able to overwhelm your system goes right back to having low or impaired metabolism again.
Your body’s inability to produce cellular energy to maintain the oxygen gradient in your gut causes the Oxalobacter to disappear in the first place, which allows the oxalates to accumulate. It’s basically a self-perpetuating cycle in the wrong direction. As noted by Norton:
“It’s this vicious cycle because one of the major ways that oxalate itself is toxic is by breaking down cellular production of ATP. It blocks the last step of glycolysis. It blocks Complex II.
It causes all this oxidative stress and inflammation that messes up the mitochondria. It’s messing up the membranes of the mitochondria in the cell. So, this is one of its mechanisms of harm. And then you have these redundant ways in which the energy production is being destroyed.
And unfortunately, the body really tries hard to look like everything’s fine. So, this can go on under the hood for decades. Then suddenly in your late 30s or in your 40s, you suddenly feel old and broken.”
How to Minimize the Harmful Effects of Oxalates
We cover a lot of ground in this interview, so here’s a quick summary of the strategies and food choices discussed that can help minimize the harmful effects of oxalates or aid in their elimination:
| Limit high-oxalate foods — This is of course a no-brainer. Reducing your intake of foods known to be high in oxalates such as spinach, almonds, and peanut butter will decrease your overall oxalate load. |
| Increase your calcium intake — Consuming foods high in calcium or using calcium supplements can bind to oxalates in the gut, preventing their absorption and facilitating their excretion through the stool. Foods rich in calcium include dairy products, leafy greens, and fortified foods. |
| Hydrate adequately — Drinking sufficient water is crucial as it helps to flush out oxalates through the urine and prevents kidney stones from forming. |
| Balance your collagen intake — While collagen is extremely beneficial, it’s important to moderate its intake if you are sensitive to oxalates, given that collagen breakdown can lead to oxalate production. So, do consume sources of collagen like bone broth, but do so in moderation. |
| Optimize your gut health — Promoting a healthy gut microbiome by consuming probiotic-rich foods like yogurt, kefir and fermented vegetables can support the growth of beneficial bacteria, including those that can degrade oxalates like Oxalobacter. |
| Citrate consumption — Citrate, found in citrus fruits like lemons and oranges, can help by binding with calcium and oxalate, thereby reducing the formation of kidney stones. Avoid over-supplementation with ascorbic acid, however, as high doses can convert into oxalate. Ascorbic acid is the most common form of vitamin C used in dietary supplements. |
| Cook high-oxalate foods well — Cooking methods that involve boiling can help reduce oxalate content in foods as the oxalates will leach into the cooking water. |
| Topical calcium for oxalate-related skin irritations — If oxalates are causing skin irritations, applying topical calcium can alleviate symptoms by precipitating oxalates at the site. |
More Information
To learn more, pick up a copy of “Toxic Superfoods: How Oxalate Overload Is Making You Sick — and How to Get Better.” You can also find more information on her website, SallyKNorton.com, or follow her on YouTube, Facebook, Twitter/X and Instagram.
Can This Unique Raspberry Protect Your Heart?
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/02/01/endothelial-health.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.
Analysis by Dr. Joseph Mercola February 01, 2024
STORY AT-A-GLANCE
- Your endothelium is the collective group of cells that line your blood vessels, representing about 1% of your body mass and a surface area of 5,000 square meters
- The endothelium is directly involved in a number of diseases, including heart disease, diabetes and chronic kidney failure
- Black raspberry decreases markers of inflammation and improves endothelial function, reducing risk factors of cardiovascular disease
- Drinking green tea is associated with an increase in flow-mediated dilation (FMD) of the brachial artery, a measure of endothelium function
- Pomegranate, grape seed extract and garlic are other natural compounds that support endothelial health
Your endothelium is the collective group of cells that line your blood vessels. Representing about 1% of your body mass and a surface area of 5,000 square meters, the endothelium has been described as a “multifunctional endocrine organ strategically placed between the vessel wall and the circulating blood.”1
To put this into perspective, a single layer of endothelial cells lines the inner surface of your entire vascular system, separating your blood from the vessel wall. This “tissue-blood barrier” is semipermeable and plays a key role in regulating the transfer of molecules as well as vascular homeostasis.2
While endothelial dysfunction — an early sign of atherosclerosis3 — is a hallmark of many diseases, including cardiovascular disease, there are a host of natural options to protect your endothelium and keep it healthy.
The Role of Your Endothelium on Overall Health
While once regarded as a simple barrier, the endothelium is now regarded as a dynamic endocrine organ that has a major influence on human health. In the International Journal of Biological Sciences, it’s noted:4
“The endothelium was once thought of as the ‘cellophane wrapper’ of the vascular tree, with no other specific functions than affording selective permeability to water and electrolytes. However, enormous advances since the 1980’s have led to an understanding of the complex functions of this large endocrine organ. Vascular endothelial cells line the entire circulatory system, from the heart to the smallest capillaries.
These cells have very distinct and unique functions that are paramount to vascular biology. These functions include fluid filtration, such as in the glomeruli of the kidneys, blood vessel tone, hemostasis, neutrophil recruitment, and hormone trafficking.”
In addition to serving as a physical barrier, endothelial cells metabolize, synthesize and release vasoactive and other compounds that affect vascular tone, blood pressure, blood flow, coagulation, fibrinolysis, inflammation, immunological reactions and more.
“Any perturbation affecting the capacity and equilibrium of the endothelium as a physical barrier and to metabolize, synthesize and release these substances will cause endothelial dysfunction, which contributes to the development and progression of cardiovascular diseases,” according to a review in the World Journal of Cardiology.5 Further, the endothelium is directly involved in a number of diseases, including:6
| Peripheral vascular disease | Stroke | Heart disease |
| Diabetes | Insulin resistance | Chronic kidney failure |
| Tumor growth and metastasis | Venous thrombosis | Viral infectious diseases |
Black Raspberry and Other Natural Options for Endothelial Health
A healthy lifestyle, including diet and exercise, supports endothelial function,7 but so, too, do a variety of substances from nature.
| Black raspberry — Anthocyanins, the most abundant flavonoids in black raspberries, have anti-inflammatory and anti-angiogenic effects, meaning they help prevent angiogenesis, which may promote cancer. In human intestinal microvascular endothelial cells and human esophageal microvascular endothelial cells, black raspberry extract had both anti-angiogenic and anti-inflammatory effects.8
In a study on patients with metabolic syndrome, black raspberry also increased circulating endothelial progenitor cells (EPCs) and improved cardiovascular risks after 12 weeks.9 Separate research, also on people with metabolic syndrome, similarly revealed that black raspberry significantly decreased inflammatory cytokines, improving vascular endothelial function.10 Animal studies also suggest that black raspberry decreases markers of inflammation and improves endothelial function, reducing risk factors of cardiovascular disease.11 Flavonoids like those in black raspberries even alleviate the vascular endothelial barrier dysfunction that’s induced by advanced glycation end products.12 It’s believed that metabolism of flavonoids is involved in their beneficial role in cardiovascular health, as metabolism increases flavonoids’ vascular efficacy, “resulting in a diversity of structures of varying bioactivity in human endothelial cells.”13 |
| Green tea — Drinking green tea is associated with an increase in flow-mediated dilation (FMD) of the brachial artery, a measure of endothelium function. “The beneficial effect of green tea on endothelial function may be attributed to its high flavonoid content.
As has been shown, epigallocatechin gallate, a major catechin in tea, acutely improves endothelial function in humans with coronary artery disease,” researchers explained in the European Journal of Preventive Cardiology.14 Green tea also increases nitric oxide production by endothelial cells and may boost vascular function via anti-inflammatory pathways. According to the European Journal of Preventive Cardiology scientists:15
Green tea is also a rich source of quercetin. In one study of 30 men with coronary heart disease, consuming quercetin-rich polyphenol extract led to an increase in flow-mediated dilation of arteries, signaling improved endothelial health.16 It also inhibits platelet aggregation and has vasorelaxant properties that help lower blood pressure and prevent cardiac hypertrophy, in which the heart muscles thickens. |
| Black chokeberry — Black chokeberry (Aronia melanocarpa), known for its astringent berries, is another concentrated source of beneficial phenolic compounds, including proanthocyanidins, flavanols, anthocyanins, flavonoids and chlorogenic and caffeic acids.17
Black chokeberry extracts significantly induce endothelial cells nitric oxide (NO) production, even at relatively low concentrations. NO plays an important role in vascular function and endothelial cell dysfunction may impair NO production, increasing the risk of cardiovascular diseases. Writing in the Journal of Food Biochemistry, researchers explained:18
|
Grape seed extract — Grape seed extract contains antioxidant proanthocyanidins, a type of polyphenol that may also benefit endothelial function, thereby protecting heart health. Writing in the journal Nutrients, scientists from Tokyo Medical and Dental University noted:19
In the study of middle-aged adults with prehypertension, participants received either low-dose or high-dose grape seed proanthocyanidin extract or a placebo for 12 weeks. Grape seed extract improved vascular elasticity, while high-dose grape seed extract also decreased blood pressure.20 |
| Pomegranate — Due to its high polyphenol content, pomegranate acts against oxidative stress and is useful for endothelial dysfunction. Pomegranate contains antihypertensive, antiatherogenic, antihyperglycemic and anti-inflammatory compounds that protect heart health by improving endothelial function.
In describing its protective role in endothelial dysfunction, researchers with Federal University of Espirito Santo in Vitoria, Brazil, explained:21
Many of pomegranate’s — known as “the jewel of autumn” — beneficial polyphenols are stored in the peel, which is why pomegranate peel powder is one of my favorite supplements. Research shows pomegranate peel contains more than twice the amounts of antioxidants — specifically phenolics, flavonoids and proanthocyanidins — than the pulp, for instance, and has been shown to protect low-density lipoprotein against oxidation to a far greater degree than pulp.22,23 Other research found polyphenol-rich pomegranate peel extract improved endothelial dysfunction in mice by modulating gut microbiota.24 |
| Garlic — Garlic is a powerful antioxidant that may help fight reactive oxygen species (ROS) in your body. In one study, aged garlic extract reduced ROS, helping to prevent endothelial dysfunction.25 Garlic’s therapeutic properties may act synergistically to support heart health and protect against heart-related events like heart attack.
Aged garlic extract supplementation may increase microcirculation, helping to prevent the atherosclerotic process, while a garlic-herb preparation blocked atherosclerosis progression 1.5-fold in postmenopausal women, with the benefit lasting for 12 months.26 Further, according to a review published in the journal Antioxidants:
Among garlic’s protective effects is the ability to lower blood pressure levels. Aged black garlic (ABG), which contains more antioxidants than raw garlic,27 may be particularly beneficial. While it’s unknown exactly how garlic may lower blood pressure, scientists noted that ABG extract helps improve vasodilation and levels of endothelial nitric oxide synthase (eNOS), among other benefits.28 |
| Fibrinolytic enzymes — The connection between enzymes and the endothelium was highlighted during the COVID-19 pandemic. Studies suggested damage to the endothelium contributed to the development of blood clots, or thrombosis, in the blood vessels of severely ill COVID-19 patients.29
When physicians at the Yale School of Medicine began running clotting tests on their patients,30 levels of Von Willebrand factor (VWF), a clotting protein released by endothelial cells, were found to be significantly elevated, which suggested that damaged endothelial cells may be releasing large quantities of VWF, leading to clots.31 “Our findings show that endotheliopathy is present in COVID-19 and is likely to be associated with critical illness and death. Early identification of endotheliopathy and strategies to mitigate its progression might improve outcomes in COVID-19,” the researchers concluded.32 Under healthy conditions, blood cells can pass through the endothelium lining blood vessels, but when exposed to viral infections and other inflammatory agents, the endothelium becomes sticky and releases VWF. The end result is a cascade of clotting and inflammation, both characteristics of severe COVID-19. In the European Heart Journal it’s stated, “COVID-19, particularly in the later complicated stages, represents an endothelial disease.”33 This is where enzymes come in. One study reported three case studies of patients with severe COVID‐19 respiratory failure who were treated with tissue plasminogen activator (tPA), a serine protease enzyme found on endothelial cells that’s involved in fibrinolysis, or the breakdown of blood clots.34 All three patients benefitted from the treatment. Beyond COVID-19, another study involved 1,062 people with mild hyperlipidemia and/or mild atherosclerosis. They took the fibrinolytic enzyme nattokinase, which “effectively managed the progression of atherosclerosis and hyperlipidemia with a significant improvement in the lipid profile.”35 Significant reduction in carotid artery intima-media thickness, a measure of the extent of arterial thickening related to endothelial dysfunction, was noted, with improvement rates ranging from 66.5% to 95.4%. When using these enzymes for fibrinolytic therapy they need to be taken on an empty stomach, at least one hour before or two hours after meals. Lumbrokinase, which is about 300 times stronger than serrapeptase and nearly 30 times stronger than nattokinase,36 is my strong personal preference and recommendation if you are using a fibrinolytic enzyme. |
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Endothelial Health Depends on a Healthy Lifestyle
Protecting endothelial health is much like protecting heart health — it involves a comprehensive, healthy lifestyle. A sedentary lifestyle, smoking, excess alcohol37 and ultraprocessed foods can all negatively affect endothelial health, while exercise38 and fresh, whole foods, including citrus fruits and dark green vegetables, are protective.39
In addition to black raspberry and the other natural substances above, coenzyme Q10 (CoQ10), a fat-soluble antioxidant, also acts directly on your endothelium, dilating your blood vessels and lowering blood pressure.40,41 CoQ10 is associated with significant improvements in endothelial dysfunction.42 By the age of 65, your body typically produces only about half the amount of CoQ10 it did at 2543 so supplementation with CoQ10 or its reduced form ubiquinol is helpful in some cases.
- 1, 2 Pathophysiology June 2008, Volume 15, Issue 1, Pages 49-67
- 3 Open Cardiovasc Med J. 2010; 4: 302–312
- 4, 6 Int J Biol Sci. 2013; 9(10): 1057–1069
- 5 World J Cardiol. 2015 Nov 26; 7(11): 719–741
- 7 Metabolism December 2011, Volume 60, Issue 12, Pages 1736-1740
- 8 Microvascular Research January 2015, Volume 97, Pages 167-180
- 9 J Med Food. 2016 Apr;19(4):346-52. doi: 10.1089/jmf.2015.3563. Epub 2016 Feb 18
- 10 Phytother Res. 2014 October;28(10);1492-8
- 11 Journal of Food Biochemistry September 12, 2021
- 12 Nutrients. 2022 Mar; 14(5): 1026
- 13 The Journal of Nutrition February 3, 2016
- 14 European Journal of Cardiovascular Prevention and Rehabilitation, Volume 15, Issue 3, 1 June 2008, Pages 300–305
- 15 European Journal of Cardiovascular Prevention and Rehabilitation, Volume 15, Issue 3, 1 June 2008, Pages 300–305, Clinical implications
- 16 Pharmacogn Rev. 2016 Jul-Dec; 10(20): 84–89., Cardiovascular disease prevention
- 17, 18 J Food Biochem. 2016 Aug; 40(4): 404–410
- 19, 20 Nutrients. 2019 Dec; 11(12): 2844
- 21 Curr Pharm Des. 2020;26(30):3684-3699. doi: 10.2174/1381612826666200406152147
- 22 Food Chemistry May 2006; 96(2): 254-260
- 23 Foodnavigator.com July 19, 2008
- 24 Scientific Reports volume 9, Article number: 14150 (2019)
- 25 Antioxidants (Basel). 2020 Jul; 9(7): 619., 5.1 Garlic Properties
- 26 Antioxidants (Basel). 2020 Jul; 9(7): 619., 5.2.2. Cardiovascular Diseases
- 27 Food Chem. 2016 May 15:199:135-9. doi: 10.1016/j.foodchem.2015.11.128. Epub 2015 Nov 30
- 28 Nutrients, 2022; 14(3), Discussion
- 29, 30, 31 The Scientist November 3, 2020
- 32 The Lancet Haematology June 30, 2020
- 33 European Heart Journal, Volume 41, Issue 32, 21 August 2020, Pages 3038–3044, doi: 10.1093/eurheartj/ehaa623
- 34 Diapharma, Tissue Plasminogen Activator
- 35 Front. Cardiovasc. Med., 22 August 2022
- 36 Townsend Letter May 2018
- 37 European Journal of Physiology June 4, 2023
- 38 J Cardiovasc Transl Res. 2022; 15(3): 604–620
- 39 Cleveland Clinic, Endothelium
- 40 Molecular Aspects of Medicine. 1994;15(1):s257-s263
- 41 Circ Res. 1989;65(1):1-21
- 42 Atherosclerosis April 2012, Volume 221, Issue 2, Pages 311-316
- 43 Int J Mol Sci. 2020 Sep; 21(18): 6695., Intro
Can Taking CoQ10 Prevent Heart Disease?
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/01/15/coq10-heart-disease.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.
Analysis by Dr. Joseph Mercola January 15, 2024
STORY AT-A-GLANCE
- A number of studies support the use of CoQ10 for heart health; much of CoQ10’s cardioprotective effects involve its antioxidant effects and ability to produce ATP
- People who took CoQ10 were also less likely to experience a nonfatal or fatal heart attack over 12 months compared to those who did not
- Low levels of CoQ10 are associated with an increased risk of heart failure, with the severity of heart failure correlated with the severity of CoQ10 deficiency
- Supplementing with CoQ10 for eight to 12 weeks can significantly reduce CRP, tumor necrosis factor alpha (TNF-α) and IL-6, measures of widespread inflammation
- By the age of 65, your body typically produces only about half the amount it did at 25, so supplementation with CoQ10 or its reduced form ubiquinol is helpful in some cases
Coenzyme Q10 (CoQ10) is a fat-soluble antioxidant your body uses for energy production. While it’s found in nearly every cell in your body, the highest levels are in your heart, liver and kidneys.1 CoQ10 plays a role in the production of adenosine triphosphate (ATP),2 a compound involved in cells’ energy storage and the synthesis of nucleic acids.
CoQ10 must be present in the inner mitochondrial membrane in order for energy from carbohydrates and fats to be converted into ATP, which is the form of energy cells use.3 As a member of the ubiquinone family, humans can synthesize CoQ10 as well as consume it via their diet, in foods like grass fed beef, sardines and herring. It’s estimated that dietary CoQ10 accounts for about 25% of plasma CoQ10 levels.4
Genetic alterations in metabolism, poor diet, oxidative stress, chronic conditions, certain medications and aging can all interfere with CoQ10 production, however, leading to CoQ10 deficiency. If you don’t get enough of this important compound, your heart health could suffer, as CoQ10 is a key player in heart health. In fact, 75% of ischemic heart disease patients have low levels of CoQ10.5
CoQ10’s Role in Heart Health
Preventing heart disease requires a comprehensive approach involving healthy diet, daily movement and stress management. So, taking any supplement alone, including CoQ10, shouldn’t be considered a panacea to preventing heart disease. That said, heart health is CoQ10’s claim to fame.
Many conditions, including heart disease, appear to be rooted in mitochondrial dysfunction.6 Cardiac muscle cells have about 5,000 mitochondria per cell,7 where CoQ10 concentrates.
For further comparison, mitochondria make up about 35% of the volume of cardiac tissue and only 3% to 8% of the volume of skeletal muscle tissue.8 Brown University researchers conducted a study to determine which micronutrients are best for your heart.9 They unveiled an evidence-based map that quantifies the impact of micronutrients on cardiovascular outcomes.
Out of 27 micronutrients, three — omega-3 fats, folic acid and CoQ10 — came out on top. CoQ10 decreased all-cause mortality events, according to the Journal of the American College of Cardiology study.10 Much of CoQ10’s cardioprotective effects involve its antioxidant effects and ability to produce ATP.11 A number of studies support the use of CoQ10 for heart health, including the following conditions:
1. Heart attack — Taking CoQ10 daily within three days of a heart attack reduces the risk of a subsequent heart attack and chest pain, while lowering the likelihood of dying from heart disease.12 People who took CoQ10 were also less likely to experience a nonfatal or fatal heart attack over 12 months compared to those who did not.13
The number needed to treat, or NNT, which describes how many people have to take a particular drug to avoid one incidence of a medical issue, was 34 to prevent one nonfatal heart attack and 60 to prevent one fatal heart attack.
“Clinicians should consider adding coenzyme Q10 to the treatment regimen of high-risk patients of myocardial infarction,” the researchers wrote in Cureus. “… Using coenzyme Q10 as a supplement will improve the quality of life of such patients.”14
2. Heart failure — Supplementing with CoQ10 may improve heart failure, in which the heart cannot pump enough blood for your body. Low levels of CoQ10 are associated with an increased risk of heart failure, with the severity of heart failure correlated with the severity of CoQ10 deficiency.
“Emerging data suggest that the harmful effects of reactive oxygen species are increased in people with heart failure, and coenzyme Q10 may help to reduce these toxic effects because of its antioxidant activity,” according to a study published in the Cochrane Database of Systematic Reviews.15 Further, the Cureus study scientists also highlighted CoQ10’s potential for improving heart failure:16
“Coenzyme Q10 reduces admission in heart failure and reduces the episodes of pulmonary edema in heart failure … coenzyme Q10 improves 6 minute walk time in patients with heart failure … supplement of coenzyme Q10 reduces the risk of all cause-death, worsening of heart failure, and cardiovascular death.”
3. Atrial fibrillation (Afib) — Scavenging of reactive oxygen species (ROS) and a reduction in oxidative stress are an essential part of keeping the heart functioning normally,17 including helping to ward off Afib,18 an abnormal, often rapid, heart rhythm that occurs when the atria, your heart’s upper chambers, beat out of sync with the ventricles, the heart’s lower chambers. It’s a common symptom in those with heart failure or heart disease.
In one study, 102 patients with Afib were divided into two groups. One group was given a CoQ10 supplement while the other group was given a placebo. After 12 months of supplementation, 12 people in the placebo group had Afib episodes compared to only three people in the CoQ10 group.19 Levels of malondialdehyde, a known biomarker of oxidative stress, also went down significantly in the CoQ10 group.
4. Blood pressure — CoQ10 acts directly on your endothelium, dilating your blood vessels and lowering blood pressure.20,21 CoQ10 also decreases aldosterone, a hormone that makes you retain salt and water.22,23 When aldosterone goes down, excess salt and water are excreted through your kidneys, often causing your blood pressure to go down.
In a systematic review and meta-analysis of 17 trials, CoQ10 supplementation significantly decreased systolic blood pressure as well as diastolic blood pressure, though the diastolic was not statistically significant.24
5. Stroke — Systemic inflammation, oxidative stress and nerve cell damage play a role in stroke development. Research suggests supplementing with CoQ10 can reduce ischemic lesions and improve outcomes in patients who have been treated with a statin drug after having a stroke (statins reduce CoQ10 levels in your body).25
6. Lower inflammation — C-reactive protein (CRP) is a marker for inflammation, and when your CRP is elevated, it suggests you have a heightened risk for heart disease.26 CoQ10 supplementation was found to significantly reduce levels of circulating CRP, with researchers explaining:27
“This meta-analysis provides evidence for CoQ10 supplementation to reduce the level of inflammatory mediators in the general population and proposes that daily supplementation of 300-400 mg CoQ10 show superior inhibition of inflammatory factors.”
Two other markers for inflammation are gamma-glutamyl transferase (GGT),28 which is an early marker of heart failure, and N-terminal pro b-type natriuretic peptide (NT-proBNP).29
There’s an association between the levels of these two markers and ubiquinol, the reduced version of CoQ10 (aka ubiquinone). When ubiquinol is supplemented, both these markers go down and genes associated with them are downregulated.30,31
Supplementing with 60 milligrams (mg) to 500 mg of CoQ10 for eight to 12 weeks can also significantly reduce not only CRP but also tumor necrosis factor alpha (TNF-α) and IL-6;32,33 additional measures of widespread inflammation. Ubiquinol has also been found to improve vascular function in older adults, such that researchers suggested it “may hold promise for treating age-related vascular dysfunction.”34
Aging, Statins Are Two Drivers of CoQ10 Deficiency
Your production of CoQ10 peaks around the age of 25, then begins to decline. By the age of 65, your body typically produces only about half the amount it did at 25.35 In addition to aging, statin cholesterol-lowering drugs are also well known to deplete CoQ10.
Statins block HMG coenzyme A reductase in your liver, which is how they reduce cholesterol. But this is also the same enzyme that makes CoQ10, making depletion likely. Statin-induced CoQ10 deficiency may be responsible for the myopathic — or relating to muscle control — side effects often attributed to these drugs.
Interestingly, LDL cholesterol is the major carrier of CoQ10 in your circulation, so it’s also been suggested that the decrease in CoQ10 among statin users is related to the decrease in LDL.36
In addition to statins, beta-blockers for high blood pressure and tricyclic antidepressant medications may also lower levels of CoQ10, as can fibric acid derivatives for cholesterol, such as gemfibrozil (Lopid).37
Depending on your age and health status, supplementation may be necessary to keep your CoQ10 levels high enough for optimal health. Young people are able to use CoQ10 supplements quite well, but older people do better with ubiquinol, as it’s more readily absorbed.
If you take a statin drug, you need at least 100 mg to 200 mg of ubiquinol or CoQ10 per day, or more. Ideally, you’ll want to work with your physician to determine your ideal dose. However, generally the sicker you are, the more you need.
The suggested dose is usually 30 mg to 100 mg per day if you’re healthy, or 60 to 1,200 mg daily if you’re sick or have underlying health conditions.38 If you have an active lifestyle, exercise a lot or are under a lot of stress, you may want to increase your dose to 200 to 300 mg per day.
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CoQ10 May Boost Your Overall Health
It’s not only your heart health that benefits from CoQ10. The nutrient is also useful for age-related diseases, with some studies suggesting it can increase lifespan in animal models.39 Benefits have also been found for improving fertility in older women and reducing fertility decline in men.40 It may also stop the progression of nonalcoholic fatty liver disease (NAFLD)41 and help relieve migraine headaches.42
CoQ10 is also protective of the kidneys and may be useful in cases of acute kidney injury due to sepsis, drugs like nonsteroidal anti-inflammatories and other causes.43 In short, “CoQ10 is essential for the health of virtually all human tissues and organs,” as a review in the Journal of Pharmacy & BioAllied Sciences puts it,44 so if you’re older and don’t think you’re getting enough from diet alone, this is one supplement you may want to consider.
- 1 StudyFinds, Can Taking CoQ10 Prevent Heart Disease? December 5, 2023
- 2, 3, 4 Linus Pauling Institute, Coenzyme Q10
- 5, 11, 13, 14, 16 Cureus. 2021 Feb; 13(2): e13137
- 6 Integr Med (Encinitas). 2014;13(4):35-43
- 7 PeerJ. 2018;6:e4790
- 8 Am J Physiol Heart Circ Physiol. 2014;307(3):H346-52
- 9, 10 Journal of the American College of Cardiology December 13, 2022, Volume 80, Issue 24, Pages 2269-2285
- 12, 37 Mount Sinai, Coenzyme Q10
- 15 Cochrane Database Syst Rev. 2021; 2021(2): CD008684
- 17 Antioxidants (Basel). 2020;9(4)
- 18, 19 J Investig Med. 2015;63(5):735-9
- 20 Molecular Aspects of Medicine. 1994;15(1):s257-s263
- 21 Circ Res. 1989;65(1):1-21
- 22 Am J Physiol. 1965;208:1275-80
- 23 Molecular Aspects of Medicine. 1994;15(1):s265-s272
- 24 High Blood Press Cardiovasc Prev. 2018 Mar;25(1):41-50. doi: 10.1007/s40292-018-0247-2. Epub 2018 Jan 12
- 25 Nutr Neurosci. 2019;22(4):264-272
- 26 Clinics. 2016;71(4):235-42
- 27 Molecular Nutrition & Food Research April 28, 2023
- 28 Nutr Metab. 2016;13:37
- 29 Clin Res Cardiol. 2010;99(7):445-52
- 30 BMC Res Notes. 2014; 7: 427
- 31 Biofactors. 2015 Jan-Feb;41(1):35-43. doi: 10.1002/biof.1198
- 32 Pharmacol Res. 2017;119:128-136
- 33 Pharmacol Res. 2019;148:104290
- 34 Hypertension. 2018;71:1056–1063
- 35 Int J Mol Sci. 2020 Sep; 21(18): 6695
- 36 Int J Mol Sci. 2020 Sep; 21(18): 6695., 3. Clinical Consequences of CoQ10 Deficiency
- 38 Comprehensive Reviews in Food Science and Safety. 2020;19(2):574-594
- 39, 40 Nutrients. 2019 Sep; 11(9): 2221
- 41 Arch Med Res. 2014;45(7):589-95
- 42 Acta Neurol Scand. 2019 Mar;139(3):284-293. doi: 10.1111/ane.13051. Epub 2018 Dec 3
- 43 Cell Mol Biol Lett. 2022; 27: 57
- 44 J Pharm Bioallied Sci. 2011 Jul-Sep; 3(3): 466–467
Vitamin C, B1 and Hydrocortisone Dramatically Reduce Mortality From Sepsis
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/12/20/vitamin-c-b1-hydrocortisone-sepsis-mortality.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.
Analysis by Dr. Joseph Mercola December 20, 2023
STORY AT-A-GLANCE
- Sepsis is caused by an aggressive, out-of-control immune response to an infection in the bloodstream. Each year, an estimated 1 million Americans get sepsis and up to half of them die
- Giving patients IV vitamin C with hydrocortisone and thiamine (vitamin B1) for two days reduced mortality nearly five-fold, from 40% to 8.5%
- Lab testing shows that while neither vitamin C or hydrocortisone alone can prevent cell death following exposure to toxins produced by bacteria, when given in combination, the concoction does protect the cells
Editor’s Note: This article is a reprint. It was originally published April 5, 2017.
Sepsis1 is a progressive disease process caused by an aggressive, dysfunctional immune response to an infection in the bloodstream. It starts with symptoms of infection that can progress to septic shock.
Unless treated — and the earlier the better — sepsis can result in extremely low blood pressure that is unresponsive to fluid replacement, weakening of the heart, and multiple-organ failure. Sepsis is a common hospital-acquired infection,2,3 but common illnesses such as bronchitis, pneumonia, strep throat or kidney infection can also turn septic, as can localized infections caused by bacteria, fungi or viruses.
The condition becomes particularly problematic and deadly if the infection involves methicillin-resistant or vancomycin-resistant Staphylococcus aureus (MRSA or VRSA) bacteria. Each year, an estimated 1 million Americans get sepsis4 and up to half of them die.5,6 Treatment can be a challenge, and is becoming even more so as drug-resistant infections become more prevalent.
According to the Agency for Healthcare Research and Quality, sepsis is the most expensive condition being treated in U.S. hospitals, costing more than $20 billion in 20117 and $24 billion in 2014.8 The good news is a critical care physician just may have found a way to save tens of thousands of lives and billions of dollars each year using two readily available vitamins and a steroid.
Vitamin C and Thiamine — An Inexpensive Cure for Sepsis
Vitamin C is well-known for its ability to prevent and treat infectious diseases. Previous research has shown it effectively lowers pro-inflammatory cytokines and C-reactive protein.9,10 Influenza,11 encephalitis and measles12 have all been successfully treated with high-dose vitamin C.
Studies have even shown vitamin C is selectively cytotoxic to cancer cells by generating hydrogen peroxide when administered intravenously (IV) in high doses. It also has a number of heart and cardiovascular benefits.
The anti-infective power of vitamin C has now been demonstrated yet again by Dr. Paul Marik, a critical care doctor at Sentara Norfolk General Hospital in East Virginia. Last January, when faced with yet another deathly ill patient, Marik decided to try a combination of intravenous (IV) vitamin C with hydrocortisone as a last-ditch effort to save the woman’s life.13
He’d recently read a colleague’s paper on vitamin C, and he knew vitamin C acts like the steroid hydrocortisone, so on a hunch, he administered the two together. It worked. While everyone expected her to die, the woman made a remarkable overnight recovery. As reported by NBC4i News:14
“The staff couldn’t believe it, so they tried it again and again — with the same results. They added a third element, thiamine, to the IV treatment as well. Today, they have used the treatment on about 150 patients and they say the result is the same …
A researcher at Old Dominion University, John Catravas, Ph.D., … did an independent lab study that confirms the treatment’s effectiveness.”
Interestingly, Marik used a relatively small amount of vitamin C — only 1.5 grams IV. Most natural medicine physicians tend to use 25 grams or more when giving IV vitamin C, more than 20 times the dose used here. One can only wonder how much more effective a larger dose would be.
It’s All About the Right Combination of Ingredients
For the first two or three patients, only vitamin C and hydrocortisone were used. Marik then decided to add thiamine for a number of reasons. Importantly, it’s required for metabolism of some of the metabolites of vitamin C.
Research has also shown many patients with sepsis are vitamin deficient, and when thiamine is given, it reduces mortality. Septic shock patients who receive thiamine have also been shown to have a reduced risk of renal failure.
Marik’s retrospective before-after clinical study,15,16 published in the journal Chest, showed that giving patients IV vitamin C with hydrocortisone and thiamine (vitamin B1) for two days reduced mortality nearly five-fold, from 40% to 8.5%.
Of the 50 patients treated, only four died — and none of them actually died from sepsis. They died from their underlying disease.
Interestingly, further lab testing found that while neither vitamin C nor hydrocortisone alone are able to prevent cell death following exposure to toxins produced by bacteria, when given in combination, the concoction does protect the cells. Turns out Marik’s hunch had been a truly inspired one.
Other research has also shown thiamine reduces mortality from sepsis and helps protect against renal failure, which is why Marik decided to add it to his mixture.
The treatment has now become part of the hospital’s standard of care for sepsis, and will hopefully become standard of care for sepsis elsewhere as well. As noted by Marik, sepsis kills about 1,000 people each day in the U.S. — that’s like having three jumbo jets crash each day.
Sepsis kills more than breast cancer, colon cancer and AIDS combined, and here’s a treatment that is not only profoundly effective, but also has no side effects and is inexpensive, readily available and simple to administer. Patients and doctors really have nothing to lose by trying it.
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Potential Contraindication
While more research is needed to validate the findings, vitamin C and thiamine (vitamin B1) administration is so safe there’s really no need to avoid it. It certainly isn’t going to make the situation worse — unless you happen to be glucose-6-phosphate dehydrogenase (G6PD) deficient (a genetic disorder).17
G6PD is an enzyme your red blood cells need to maintain membrane integrity. High-dose IV vitamin C is a strong pro-oxidant, and giving a pro-oxidant to a G6PD-deficient individual can cause their red blood cells to rupture, which could have disastrous consequences.
Fortunately, G6PC deficiency is relatively uncommon, and can be tested for. People of Mediterranean and African descent are at greater risk of being G6PC deficient. Worldwide, G6PD deficiency is thought to affect 400 million individuals, and in the U.S., an estimated 1 in 10 African American males have it.18
Anecdotal Evidence Suggests Near-Infrared Light May Protect Against Kidney Failure
On a side note, your risk of kidney failure — which is a very common outcome of sepsis — may be reduced or prevented by shining a near-infrared light on the area. I know, that sounds too amazing to be true, but according to Michael Hamblin, Ph.D., a photodynamic therapy researcher, the anecdotal evidence for this is quite strong.
“Kidney failure is the third leading cause of death. These are old folks who are dying from kidney failure. You can’t really give them transplants because they’re elderly. You put a near-infrared LED array where their kidneys are and it seems to work like a dream. [But] it’s hardly been studied at all,” Hamblin said.
Again, the worst that could happen is nothing, as red and near-infrared light (630 to 830 nanometer range) is quite safe.
Other Health Benefits of Thiamine
Thiamine or vitamin B1,19 found in pork, dark leafy greens, wheat germ, green peas, lentils and nuts,20 is perhaps best known for its role in cellular production of energy and supporting normal neuronal activity. However, it also has a wide range of other health benefits.21 According to the Mayo Clinic, studies confirm thiamine can be helpful for a long list of diseases and disorders, including:22
- Metabolic and mitochondrial disorders23
- Blood clots and clogged arteries24
- Cerebellar ataxia (movement disorder caused by neurological damage)25
- Coma26
- Kidney dysfunction27
Research28 published in 2013 also found thiamine supplementation can improve cardiac function in those with heart failure. Overall, patients with heart failure tend to be deficient in thiamine, as well as other micronutrients. Thiamine deficiency has also been linked to delirium,29 thyroid fatigue and Hashimoto’s (a thyroid autoimmune disorder).30 These and other health effects may help explain why thiamine works so well (in conjunction with vitamin C and hydrocortisone) for sepsis.
For general health purposes, adult men and women need about 1.2 and 1.1 milligrams (mg) of thiamine respectively each day. Also be aware that thiamine conversion is dependent on having sufficient amounts of sulfur. Good sources of dietary sulfur include organic pastured eggs, legumes, garlic, onion, Brussel sprouts, asparagus, kale and wheat germ.
Moreover, all B vitamins, including thiamine, are produced within your gut31 provided you have a healthy gut microbiome. So, eating real food, ideally organic, along with fermented foods will provide your microbiome with important fiber and beneficial bacteria to help optimize your internal vitamin B production.
To Avoid Sepsis, Understand the Cause
With sepsis affecting more than a million Americans each year, how can you avoid becoming a statistic? First, be aware that ANY infection can lead to sepsis. While it’s typically associated with hospital-acquired infections, nearly half of all cases are in fact the result of an infection acquired outside a hospital setting.32
Part of what makes it so deadly is that people typically do not suspect it, and the longer you wait to treat it, the deadlier it gets. As noted in a special report on sepsis by Consumer Reports:33
“Whenever the body develops an infection, the immune system normally kicks in, producing chemicals to fight the infection. But sometimes — either because the triggering bacteria is unusually powerful or because the person’s immune system is already weakened by other health problems — those chemicals are set loose in the bloodstream and course through the body.
Instead of just fighting the local infection, those chemicals unleashed by the immune system cause widespread inflammation and damage tissues in the liver, kidneys, heart and other organs.
Within hours, blood clots can begin to form, and damage to blood vessels causes blood pressure to drop, which in turn slows the delivery of vital nutrients to those organs already under attack. In the final stages, the heart weakens and organs begin to fail.”
According to the Centers for Disease Control and Prevention, you’re at higher risk for sepsis if you have:
- Chronic disease — A vast majority — 7 out of 10 — of people who develop sepsis have some kind of chronic health condition. Those with diabetes, lung, kidney or liver disease tend to be particularly susceptible to infection, which raises the risk.
- Weakened immune system, AIDS or cancer.
- Recently spent time in a hospital, nursing home or other health care facility, as exposure to infection-causing bacteria is common in these places.
Common Sense Strategies to Reduce Your Risk of Sepsis
While health care workers have a responsibility to prevent infections that could potentially turn septic and to educate patients about warning signs of sepsis, you can lower your own risk by:
• Promptly treating urinary tract infections (UTIs) — UTIs are the second most common type of infection in the body, sending more than 8 million people to their health care providers every year in the U.S. alone,34 and one-quarter of sepsis cases are related to urinary tract infections.
Conventional treatment typically involves antibiotics, but research shows 90% of UTIs can be successfully treated with D-Mannose, a naturally occurring sugar that’s closely related to glucose.
• Properly clean skin wounds — About 1 in 10 sepsis cases are due to skin infections, so always take the time to properly clean and care for wounds and scrapes. Wash the wound with mild soap and water to clean out dirt and debris, then cover with a sterile bandage. Diabetics should follow good foot care to avoid dangerous foot infections.
• Avoid infections in hospitals — When visiting a health care facility, be sure to wash your own hands, and remind doctors and nurses to wash theirs (and/or change gloves) before touching you or any equipment being used on you.
If you have to undergo a colonoscopy or other testing using a flexible medical scope, remember to call and ask how they clean their scopes and what kind of cleaning solution they use. If the answer is glutaraldehyde (brand name Cidex), find another hospital or clinic — one that uses peracetic acid. This preliminary legwork will significantly decrease your risk of contracting an infection from a contaminated scope.
In the video below, Andrew Saul, Ph.D., co-author of the book, “Hospitals and Health: Your Orthomolecular Guide to a Shorter, Safer Hospital Stay,” discusses the dangers of hospital stays, the type of patient that tends to get killed the most, and how you can protect your health and life in the event you have to spend time in a hospital.
- 1 Mayo Clinic, Sepsis
- 2 JAMA Internal Medicine 2010;170(4):347-353
- 3 EurekAlert! February 22, 2010
- 4 National Center for Health Statistics Data Brief No. 62 June 2011
- 5 PharmacoEconomics. 2004;22(14):895-906
- 6 NIH. Sepsis. September 2023
- 7 Agency for Healthcare Research and Quality Healthcare Cost and Utilization Project Statistical Brief No. 160 August 2013
- 8 Canadian Medical Association Journal 2017;18:E2-3
- 9 Journal of Translational Medicine 2012; 10: 189
- 10 Riordan Clinic Press Release October 2012
- 11 Journal of Manipulative and Physiological Therapeutics 1999 Oct;22(8):530-3
- 12 Clinical Guide to the Use of Vitamin C by Fredrick R. Klenner, MD
- 13 NPR March 23, 2017
- 14 NBC4i.com March 23, 2017
- 15 Chest 2016. doi: 10.1016/j.chest.2016.11.036
- 16 Dr. Malcolm Kendrick, January 28, 2017
- 17, 18 NIH.gov Glucose-6-Phosphate Dehydrogenase Deficiency
- 19 Harvard T.H. School oof Public Health. Thiamin — Vitamin B1
- 20 Livestrong.com, Foods High in B Vitamins
- 21 Oregon State University, Thiamine
- 22 Mayo Clinic Proceedings. Thiamine. June 2019
- 23 Mol Genet Metab. 2017 Nov; 122(3): 1–9
- 24 Restorative Medicine Thiamine (Vitamin B1)
- 25 BMJ Case Rep. 2013; 2013: bcr2012007302
- 26 Merck Manual. Symptoms of Thiamine Deficiency
- 27 Nephrol Dial Transplant. 2011 Jul; 26(7): 2137–2144
- 28 Heart Failure July 2013, DOI: 10.1111/chf.12037
- 29 Innovations in Clinical Neuroscience 2013 Apr; 10(4): 26–32
- 30 Thyroidpharmacist.com February 3, 2015
- 31 Nutrition Reviews 1942; 1(1): 4-5
- 32, 33 Consumer Reports August 23, 2016
- 34 Urology Care Foundation Summer 2016
Popular Heartburn Meds Linked to Osteoporosis
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/12/19/ppi-osteoporosis.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.
Analysis by Dr. Joseph Mercola December 19, 2023
STORY AT-A-GLANCE
- An estimated 12.3 million Americans over 50 are affected by osteoporosis (“porous bone” or low bone density), and an additional 47 million younger Americans are in the early stages. Worldwide, the prevalence is 18.3%
- Rates of hip fractures vary from tenfold to a hundredfold between countries, showing that low bone density is not a consequence of aging per se, but is dependent on lifestyle factors, including the use of certain drugs such as proton pump inhibitors (PPIs), the most popular heartburn medications on the market
- PPIs are only recommended for short-term use, yet 60% of users report staying on the drug for more than one year; 31% are still on them after three years. More than 60% are also taking them to treat conditions for which these drugs are not indicated, such as indigestion
- Dozens of studies show rates of hip fractures are elevated among both long- and short-term users of PPIs, and at all dose levels
- More recent research suggests one of the primary ways by which PPIs damage bone may be by way of collagen, as these drugs have been shown to inhibit collagen production through several mechanisms of action
Americans spend a whopping $13 billion a year on over-the-counter (OTC) antacids (acid neutralizers) and OTC and prescription proton pump inhibitors (PPIs), which are the most popular heartburn medications on the market.1 It’s estimated that more than 15% of the population are on PPIs.2,3
Prescription PPIs like Nexium, Dexilant, Prilosec, Zegerid, Prevacid, Protonix, Aciphex and Vimovo inhibit acid production in your stomach and are routinely used to treat gastroesophageal reflux disease (GERD), a condition affecting about 20% of the U.S. population.4 OTC versions like Prilosec OTC, Zegerid OTC and Prevacid 24HR are also available.
Once prescribed, your doctor may keep you on a PPI drug for years, despite label warnings suggesting they be used only for short periods. One of the potential ramifications of long-term use of heartburn medication is osteoporosis. In the Nutrition Facts video above,5 Dr. Michael Greger reviews the evidence for this.
Your Osteoporosis Risk Is Highly Modifiable
As of 2020, an estimated 12.3 million Americans over 50 were affected by osteoporosis (“porous bone” or low bone density), and an additional 47 million younger Americans were in the early stages.6 Worldwide, the prevalence is 18.3%, according to data cited by Greger.
If your bones are getting compromised in your 40s or even 30s, your life expectancy, not to mention quality of life, will be seriously lowered. As noted by Greger, the good news is, osteoporosis is not an inevitable outcome even in advanced age, as lifestyle has been shown to play the greatest role in its development.
Rates of hip fractures vary from tenfold to a hundredfold between countries,7 showing that low bone density is not a consequence of aging per se, but is dependent on things like diet, exercise, alcohol use — and the use of certain drugs, including:8
- PPIs and H2 blockers
- Antidepressants, anti-anxiety and antipsychotic drugs
- Antiparkinsonian drugs
- Benzodiazepines and other sedatives
- Systemic corticosteroids
PPIs Linked to Bone Fractures
The link between PPIs and brittle bone is strong enough that the U.S. Food and Drug Administration issued a safety alert on it in 2010, warning that the use of these drugs increases the risk of wrist, hip and spine fractures. As noted in that safety announcement:9
“The new safety information is based on FDA’s review of several epidemiological studies that reported an increased risk of fractures of the hip, wrist, and spine with proton pump inhibitor use.
Some studies found that those at greatest risk for these fractures received high doses of proton pump inhibitors or used them for one year or more. The majority of the studies evaluated individuals 50 years of age or older and the increased risk of fracture primarily was observed in this age group.
While the greatest increased risk for fractures in these studies involved people who had been taking prescription proton pump inhibitors for at least one year or who had been taking high doses of the prescription medications (not available over-the-counter), as a precaution, the ‘Drug Facts’ label on the OTC proton pump inhibitors (indicated for 14 days of continuous use) also is being revised to include information about this risk.
Healthcare professionals and users of proton pump inhibitors should be aware of the possible increased risk of fractures of the hip, wrist, and spine with the use of proton pump inhibitors, and weigh the known benefits against the potential risks when deciding to use them.”
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FDA Safety Alert Is Out of Date
However, in March 2011, the FDA removed the warning for PPIs sold over the counter, claiming they had “concluded that fracture risk with short-term low dose PPI use is unlikely.” The caveat, of course, is that users of OTC PPIs must then strictly follow usage recommendations to avoid the risk of bone fractures.
OTC PPIs are not to be used for more than 14 days in a row, up to three times in a single year. Chances are, many users do not stick to these parameters, and since there’s no warning label, they might not think anything of it.
According to one survey, 60% of PPI users stayed on the drug for more than one year, and 31% were still on them after three years. More than 60% were also taking them to treat conditions for which these drugs are not indicated, such as indigestion.10 So, overuse is clearly a problem.
What’s more, as noted by Greger, as of 2023 there are dozens of studies showing rates of hip fractures are elevated among both long- and short-term users, and at all dose levels. So, the FDA’s safety alert is seriously outdated.
PPIs and the Risk of Bone Fractures
Studies showing a clear link between PPI usage and bone fractures include a prospective study11 published in 2009, which found that use of the PPI omeprazole was “a significant and independent predictor of vertebral fractures,” with a 3.50 relative risk compared to nonusers.
Relative risk ratio refers to the probability of an event occurring in the exposed group versus the probability of the same event occurring in a nonexposed group.12 So, in this case, PPI users were 3.5 times, or 350%, more likely to fracture their spines during the six-year follow-up compared to those who did not use the drug.
A meta-analysis13 published in 2016, which looked at 18 studies involving a total of 244,109 fracture cases, concluded PPI use was associated with a “modestly” increased risk of all fractures, including hip and spine fractures.
Here, pooled analysis showed PPI use raised the relative risk of hip fracture by 1.26 times, and this was true both for short-term (less than one year) and long-term (more than one year) use. The relative risk of spine fracture was also 1.58 times higher, and any-site fractures 1.33 times higher among PPI users.
How PPIs Cause Osteoporosis
As for how PPIs cause osteoporosis, studies suggest they can affect bone density by:
| Inducing hypochlorhydria (a state where production of hydrochloric acid production is absent or very low), which inhibits calcium absorption14 |
| Dysregulating bone resorption, which is essential for healthy bone15 |
| Secondary hyperparathyroidism caused by a negative calcium balance16 |
| PPI-induced hypergastrinemia resulting in parathyroid hypertrophy or hyperplasia17 |
| Gut microbiome alterations18 |
| Hypomagnesemia (low magnesium)19 |
Interestingly, more recent research suggests one of the primary ways by which PPIs damage bone may actually be by way of collagen, as these drugs have been shown to:20
- Inhibit Type 1 collagen found in bone by increasing the release of calcium and deoxypyridinoline (the latter of which provides structural stiffness to Type 1 collagen)
- Inhibit the gene expression of several collagen types
- Reduce total collagen levels by inhibiting expression of dimethylarginine dimethylaminohydrolase (DDAH)
- Impair vitamin B12 absorption, which can lead to elevated homocysteine. High homocysteine increases the risk of fractures by altering the quality of collagen21
As noted in a 2020 paper in the Frontiers in Endocrinology:22
“PPIs may actually target the ECM [extracellular matrix] in general and members of the collagen family in particular to influence bone pathophysiology including increasing the risk of osteoporosis and osteoporotic fractures …”
Other Risks Associated With PPIs
Dependency is also a real risk. Research cited by Greger found that just two months of PPI therapy in healthy volunteers induced “acid-related symptoms” when the drug was withdrawn.23 Besides bone fractures, other health risks associated with PPIs include:24
| Kidney disease25 |
| Intestinal infections, including Clostridioides difficile infection — In one study, those taking PPIs had a 1.7 to 3.7 times increased risk of developing C. difficile or Campylobacter infection compared to nonusers26 |
| Stomach cancer |
| Gastrointestinal polyps |
| Pneumonia |
| Heart disease27 and heart attacks, even if you have no prior history of cardiovascular disease28 |
| Erectile dysfunction |
| Premature death |
| Higher risk of knee replacement29 |
| Dementia30 and Alzheimer’s disease31,32 — In one study, PPIs were found to cause statistically and clinically significant impairments in the participants’ executive functions, visual memory and planning function after just one week of use33 |
Natural Remedies for Treating Occasional Reflux Problems
As explained in “Keys to Optimal Digestion” and “Why You Should Never Take Antacids for Digestive Reflux,” stomach acid serves several important functions, such as breaking down proteins, killing ingested pathogens, ensuring optimal nutrient absorption, and regulating the rest of the digestion process.
If you use acid-blockers, you’re compromising your entire digestive system. You may also be compromising your bone health and significantly raising your risk of osteoporosis and serious bone fractures that take a long time to heal.
So, if you suffer from occasional heartburn, indigestion and other minor reflux symptoms, forgo the PPIs and try one or more of the following nondrug alternatives instead:34,35,36,37,38
| Aloe juice — The juice of the aloe plant naturally helps reduce inflammation, which may ease symptoms of acid reflux. Drink about one-half cup of aloe juice before meals. To avoid its laxative effect, look for a brand in which the laxative component has been removed. |
| Apple cider vinegar (raw, unfiltered) — Take 1 tablespoon of raw unfiltered apple cider vinegar in a large glass of water before or directly after meals. |
| Astaxanthin — When compared to a placebo, this potent antioxidant was found to reduce symptoms of acid reflux, especially for individuals with pronounced H. pylori infection.39 The researchers concluded a daily dose of 40 mg of astaxanthin was effective for reflux reduction. |
| Baking soda — One-half to 1 teaspoon of baking soda (sodium bicarbonate) in an 8-ounce glass of water, or orange juice, will help neutralize your stomach acid and ease the burn of acid reflux. While I do not advise this as an ongoing remedy, it is effective on an “emergency” basis when you are in excruciating pain. |
| Ginger root — Ginger has a gastroprotective effect by suppressing H. pylori. It also accelerates gastric emptying which, when impaired, contributes to heartburn. Add two or three slices of fresh ginger root to 2 cups of hot water and let it steep for several minutes. Drink it about 20 minutes prior to your meal. |
| Sauerkraut — Consuming sauerkraut or cabbage juice will stimulate your body to produce stomach acid. |
| Glutamine — The amino acid glutamine has been shown to address gastrointestinal damage caused by H. pylori. Glutamine is found in many foods, including beef, chicken, dairy products, eggs, fish and selected fruits and vegetables. L-glutamine is widely available as a supplement. |
| Ripe papaya or a papain supplement — Papaya contains papain, an enzyme useful for breaking down both protein and carbohydrates. |
| Fresh pineapple or bromelain supplement — Bromelain is a proteolytic enzyme found in pineapple that helps digest proteins. |
| Pepsin supplement — Like bromelain, pepsin is a proteolytic enzyme involved in protein digestion.40 |
| Betaine HCI supplement — Betaine HCl is the hydrochloride salt of betaine, not to be confused with betaine or trimethylglycine (TMG). As noted in a 2020 review paper:41 “… the most common recommendation for the use of betaine HCl supplements is usually implemented using an empirical test for low stomach acid whereby increasing doses of betaine HCl are given during sequential meals until such time as an uncomfortable sensation is noticed by the patient.
Along with improvements in symptoms of dyspepsia (or laboratory analysis of improved protein digestion), the lack of side effects acts is an empirical confirmation that low gastric acid production was contributing to poor digestion and/or dyspeptic symptoms.” |
| Bitters — Bitters have a long history of use in herbal medicinal traditions to promote digestion and/or to relieve digestive complaints.42 |
| Slippery elm — Slippery elm coats and soothes your mouth, throat, stomach and intestines, and contains antioxidants that may help address inflammatory bowel conditions. Because it stimulates nerve endings in your gastrointestinal tract, it is useful for increasing mucus secretion, which has a protective effect against ulcers and excess acidity. |
| Vitamin D — Vitamin D is important for your gut health. Once your vitamin D levels are optimized, you will benefit from your body’s production of about 200 antimicrobial peptides that will help eradicate gut infections. |
| Zinc — Your stomach needs zinc to produce stomach acid, so make sure your body has the necessary raw ingredients. The recommended daily amount for adults is 8 to 11 mg. Zinc-rich foods include oysters, lobster, beef, cashew nuts, beans and raw yogurt. A zinc supplement can be used if you rarely eat these foods.43 |
Talk to Your Doctor About Getting Off PPIs
If you’re currently on a PPI, I strongly recommend working with your doctor to wean off it, as inhibiting stomach acid can raise your risk of other, far more serious health conditions, including:44
| Osteoporosis | Asthma |
| Depression | Gallbladder disease |
| Migraines | Macular degeneration |
| Autoimmune conditions, including but not limited to Celiac disease, Type 1 juvenile diabetes, Grave’s disease (hyperthyroid), lupus, multiple sclerosis (MS), rheumatoid arthritis and ulcerative colitis |
The best and safest way to do that is to work with your doctor to lower the dose you’re taking while simultaneously implementing the following lifestyle modifications:
- Avoid reflux triggers and/or any food that irritates your stomach
- Avoid processed foods and sugar
- Eat a Mediterranean diet, focused on fruits, healthy fats, lean meats, nuts and vegetables. Research published in the Journal of the American Medical Association Otolaryngology — Head & Neck Surgery found a Mediterranean diet was as effective as PPIs in treating acid reflux symptoms45
- Reseed your gut with beneficial bacteria from traditionally fermented foods or a high-quality probiotic supplement
- Thoroughly chew each bite of food
Once you get down to the lowest dose of the PPI, you can start substituting with an over-the-counter H2 blocker like Pepcid (famotidine) which appears to be the safest of all the OTC H2 blocker options out there. Then, gradually wean off the H2 blocker over the next several weeks.
- 1 Time September 7, 2017
- 2, 44 Midwestern Doctor Substack September 16, 2023
- 3 Therapeutic Advances in Gastroenterology 2018; 11: 1756284818777943
- 4 The Surgical Clinic. What Is GERD?
- 5 Nutrition Facts December 11, 2023
- 6 The Washington Post October 17, 2023 (Archived)
- 7 YouTube NutritionFacts December 11, 2023 1:38 minutes
- 8 YouTube NutritionFacts December 11, 2023 5:53 minutes
- 9 FDA Safety Alert May 25, 2010
- 10 YouTube NutritionFacts December 11, 2023 3:37 minutes
- 11 Calcif Tissue Int January 2009; 84(1): 13-19
- 12 StatPearls Relative Risk
- 13 Osteoporosis International January 2016; 27(1): 339-347
- 14 JAMA December 27, 2006; 296(24): 2947-2953
- 15, 20, 22 Front. Endocrinol. July 22, 2020
- 16, 17, 18, 19, 21 International Journal of Molecular Sciences September 2022; 23(18): 10733, Section 3
- 23 YouTube NutritionFacts December 11, 2023 4:21 minutes
- 24 YouTube NutritionFacts December 11, 2023 4:33 through 5:03 minutes
- 25 The Journal of the American Medical Association 2016;176(2):238
- 26 British Journal of Clinical Pharmacology, January 5, 2017, DOI: 10.1111/bcp.13205
- 27 PLOS ONE December 27, 2013, DOI: 10.1371/journal.pone.0084890
- 28 PLOS One June 10, 2015 DOI: 10.1371/journal.pone.0124653
- 29 Osteoarthritis Cartilage April 2022; 30(4): 559-569
- 30 JAMA Neurology February 15, 2016, doi: 10.1001/jamaneurol.2015.4791
- 31 Annals of Translational Medicine 2016;4(12):240
- 32 Journal of the American Medical Association 2016;73(4):410-416
- 33 Alzheimer’s Research & Therapy 2015;7:79
- 34 Health January 25, 2016
- 35 Everyday Roots, 15 Natural Remedies for Heartburn & Severe Acid Reflux
- 36, 40, 43 Medical News Today 6 Ways to Increase Stomach Acid
- 37, 41, 42 Integr Med February 2020; 19(1): 32-36
- 38 Drugwatch PI Alternatives
- 39 Phytomedicine June 2008; 15(6-7): 391-9
- 45 Journal of the American Medical Association Otolaryngology – Head & Neck Surgery September 7, 2017; doi: 10.1001/jamaoto.2017.1454
Eating Mistakes That Can Damage Your Kidneys
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/11/19/low-acid-meal-plan.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.
Analysis by Dr. Joseph Mercola November 19, 2023
STORY AT-A-GLANCE
- Your kidneys lower your body acid burden. As kidney failure progresses, acid tends to accumulate in your system, causing severe harm
- A high-acid diet can deteriorate your kidney function and accelerate the progression of kidney disease
- Any diet high in fruits and vegetables and low or devoid of processed foods and dairy products will be lower in acid
- Anything that helps improve diabetes will also improve kidney health. This includes fasting or time-restricted eating and exercise
- High-protein diets can also damage your kidneys, thanks to the ammonia generated. To protect your renal health when eating a high-protein diet, add in more fruits and vegetables to buffer the acid created
In this interview, Dr. Lynda Frassetto, a nephrologist and Professor Emeritus in the department of medicine at University of California San Francisco (UCSF), shares important information about how acid in your diet affects your kidney health and longevity.
“When I was in internal medicine training, I happened to have a really super mentor, Dr. Eli Friedman, at the State University of New York (SUNY) in Brooklyn,” Frassetto says. “He made nephrology sound really interesting.
And so, after I finished my residency and was a hospitalist for a couple of years, I decided to go back and do nephrology, because people who did nephrology just have a better understanding of physiology than most internists do.
I thought that would help make me a better doctor. After I finished my fellowship, I started working with Anthony Sebastian here at UCSF. He was interested in diet acid load in people who were relatively healthy.
The kidneys do a lot of things. One of the things they do is they get rid of acid. We know that as kidney failure progresses, you have trouble getting rid of the acid. It accumulates in your system and has a lot of bad side effects.
We also know that, as you get older, your kidneys tend not to work as well. What Tony was looking at was, in otherwise healthy, older people — whose kidneys just aren’t working as well as they did, let’s say, 40 or 50 years earlier — does eating a high-acid diet have any potential side effects?”
Low-Acid Diets as a Means to Protect Kidney Function
In the initial stages of their work, Frassetto and Sebastian worked on neutralizing acid in the diet using bicarbonate. Then, just over a decade ago, they started looking at low-acid diets. While all foods contain precursors that can be metabolized into acids, fruits and vegetables contain a lot of alkali precursors that are metabolized into bicarbonate, like citrate or malate.
Frassetto’s interest in low-acid diets began with the paleo diet, promoted by Loren Cordain, Ph.D. According to Cordain, many foods in our modern diet were unavailable to our ancestors, such as processed grains and sugars.
He believed a diet closer to our ancestral diet would be healthier, and one of the reasons for this is because any diet high in fruits and vegetables (and devoid of processed food) will be lower in acid. As explained by Frassetto:
“If you look at any large population, and you just look at the average kidney function over time, on average, everybody’s kidney function declines. But if you look at specific individuals, kidney function either declines much more slowly or may even level out.
The question is, ‘How related is that to eating a low-acid diet or doing things that wouldn’t bother your kidneys?’ This has actually been looked at by Dr. Donald Wesson, a nephrologist at University of Texas (UT) Southwestern.
He’s looked at both alkalized supplements and fruits and vegetable diets in people with Stage 2 kidney disease, with an estimated glomerular filtration rate (GFR) between 60 and 90, and Stage 3 chronic kidney disease (CKD), which has an estimated GFR from 30 to 60.
[GFR is] an estimate of kidney function. So, if you’re 50 years old, your GFR is about 90. If you’re 80 years old, your GFR is about 60. On average, people who are older are going to have … Stage 2 or Stage 3 CKD.
Wesson showed that in these people, if you either give them alkalized supplements like baking soda, or put them on a diet with more fruits and vegetables, that you could slow the rate of decline …
If you extrapolate that from people with kidney failure to just older people, the idea would be that, maybe, you can slow the rate of decline of your kidney function, even if you’re otherwise healthy and just getting older. That’s the idea.
Everything that you do, everything, is related to kidney function in some degree. Because the kidneys get rid of a lot of things. The worse the kidneys work, the worse everything works.”
Fasting Also Protects Kidney Function
According to Frassetto, most kidney disease in western countries is more advanced kidney disease caused by high blood pressure and Type 2 diabetes. Three-quarters of patients on dialysis are there due to high blood pressure and diabetes. So, ultimately, anything that helps improve diabetes and high blood pressure will also improve kidney health.
One strategy known to significantly lower your risk of Type 2 diabetes is fasting, including time-restricted eating. I’ve previously interviewed Dr. Jason Fung, a nephrologist in Canada, who uses fasting to reverse diabetes in his patients. Exercise is yet another strategy that will lower your risk of diabetes, and thus protect your kidney health.
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Acid Versus Protein Damage
Acid isn’t the only thing that can damage your kidneys. High-protein diets can also cause harm, thanks to the ammonia generated. As for which may ultimately be worse for you — high acid or high protein — Frassetto explains:
“All proteins contain acid precursors. If you’re eating a high protein load and you don’t have enough alkali to help the kidneys either buffer or get rid of the acid, then that’s ultimately bad for your kidneys. But you do need to eat a certain amount of protein, or you’re going to have problems building things too.
This is really a balance question. It’s not that protein is bad. It’s that, if you’re eating a lot of protein, you should also be eating a lot of alkali. That will help you not use the body systems to neutralize or buffer the acid in your system. The whole idea is that you want to maintain your blood pH within the range considered to be normal.
To do that, you either move the acid inside the cells, you break down the muscles to supply glutamine, ultimately to the kidneys, to excrete the acid as ammonium. You also break down your bone, which is calcium hydroxyapatite, which is the alkali.
Or, you have to decrease the amount of endogenous acids that you produce in order to be able to maintain your blood pH. Your body has a lot of ways of dealing with the acids that the kidney has to get rid of.
So, if you’re giving the body exogenous alkali, meaning you either take bicarbonate or you eat a lot of fruits and vegetables, you don’t need to break down your bones and muscles in order to be able to neutralize the acid in your system …
Hydrogen ions are balanced at the level of 10-9, which is a super-low level of free hydrogen ions in the body. And the changes that you can make to that without going outside the range of normal and becoming ill is not very big.
There are only a couple of things you can do here. Either you’re going to break down your body systems or you [need to] give your body exogenous alkali.”
Patients with advanced kidney disease will typically get exogenous alkali — usually a combination of sodium bicarbonate and sodium citrate — as it’s been shown to slow the advancement of the disease and delay the need for dialysis. The sodium citrate will also lower your risk of kidney stones.
Potassium bicarbonate should not be used when you have kidney disease. The reason for this is because, when you have kidney failure, potassium can accumulate to lethal levels. Controlling blood pressure and diabetes are also important when you have kidney disease, as is controlling proteinuria (damage to the glomerular barrier).
How Klotho Benefits Kidney Function
The protein klotho is helpful for ridding your body of phosphate, and phosphate is another acid that has to be excreted by your kidneys. Interestingly, transgenic animals that have been genetically edited to overexpress the klotho gene also live 10% to 40% longer.
Klotho is a membrane transporter and a soluble protein. When you eat a high-phosphate diet, you release fibroblast growth factor 23 (FGF23), which attaches to klotho as a cofactor and then goes to the kidneys, where it removes the transporters that allow your kidneys to reabsorb phosphate. This helps maintain a normal phosphate balance.
However, with age and declining kidney function, you need more and more FGF23 to get rid of the phosphate. FGF23 also prevents the actions of 1-alpha hydroxylase, an enzyme necessary for the activation of vitamin D, and vitamin D is necessary for the production of klotho.
So, as you get older and continue eating a high-phosphate diet (which is easy since phosphate is in most foods), your FGF23 goes up while your vitamin D and klotho levels go down. As a result, your kidneys start reabsorbing more phosphate, thus incurring more and more damage.
The answer, then, is not only a low-acid diet. You also want your diet to be relatively low in phosphate. What is a high-phosphate diet? Frassetto explains:
“First off, dairy products. All dairy products contain essentially four things: calcium, phosphorus, protein and fat … So, for kidney failure patients, we pretty much eliminate dairy products.
And then colas. They add phosphatidic acid to a lot of things, including soda. We try to get people not to drink stuff that has phosphatidic acid in it. And then there are some other specific foods, like chocolate and nuts that we tell people with advanced kidney failure to avoid … Beans are another high source of phosphate.”
Assessing Your Kidney Function
To get an idea of how well your kidneys are functioning, you’d typically start with a renal panel. This will give you your blood urea nitrogen level and serum creatinine. Your GFR is then calculated based on your gender, age, race and serum creatinine level. Based on the results of your renal panel, other tests may be prudent.
“In terms of just looking at kidney health, there are two things that we look at,” Frassetto says. “One is [the estimated] GFR number. Two is, ‘Do you have any protein in the urine?’ Those can be two separate problems. Protein in the urine, in and of itself, is bad for kidney function …
This was discovered many years ago by Dr. Barry Brenner. He did five/sixth nephrectomies in rats (so only a small part of one kidney remained) and showed that the remaining kidney, the so-called nephron remnant, had to hyperfilter to be able to clear all the blood. That hyperfiltration through the glomerular membrane was bad for the membrane, so the membrane started to leak protein, and the kidneys failed faster.
So, we now know that there are a number of kidney problems where the membrane is leaking protein. That causes the kidney to be more damaged.
If you had to do just two things just to see how healthy you are, the first would be to get a blood test to see where your kidney function is. The second is to get a urinalysis. Pretty much any time you go in for a primary care visit, those are the two tests that they usually do.”
Acidotic Stress
While most people are familiar with oxidative stress, acidotic stress is another type of stress that can take a significant toll on your health. Frassetto believes both are equally important, especially where kidney disease is concerned. Acidotic stress also plays a role in aging.
“A friend of mine named Dr. Elissa Epel has looked at the relationship between telomere length, telomerase activity and oxidative stress. [She] has shown people who are under a lot of psychological stress have shorter telomeres and abnormal telomerase function.
They have higher levels of oxidative stress. I happen to have done more research on [acidotic stress], but really, I think it’s a combination of both,” Frassetto says. “So, the whole idea would be to lower the amount of oxidative stress and lower the amount of acidotic stress, and therefore limit the damage to the body.”
More Information
To summarize, a low-acid diet is basically a diet high in fruits and vegetables, with a moderate amount of protein. Again, the more protein you eat, the more fruits and vegetables you need to maintain a healthy balance. A low-acid diet is also low in or devoid of dairy products.
Keep in mind that by the time most people are sent to a nephrologist, they’ve already lost three-quarters of their kidney function. So, to make a difference, you really want to start thinking about your kidney function early on. Get regular blood tests of your BUN and creatinine, and a urinalysis, and if they start revealing a problem, address it as soon as possible.
While the kidney transplant process has improved a great deal in recent years, the number of available donors is limited, so the number of patients on dialysis has steadily risen.
As noted by Frassetto, dialysis is extremely expensive, and just barely keeps you alive. Moreover, while end-stage renal disease is covered by Medicare in the U.S., it only really covers dialysis. It does not cover all needed medications, for example.
The take-home message is that you cannot count on sophisticated end-stage therapies. The answer is preventing the problem in the first place. The role of dietary acid is a fairly recent discovery that is not widely known, but that can make a big difference in your renal health.
Avoiding high-phosphate foods could go a long way toward improving and maintaining your kidney function as you get older. Cronometer, a free online nutrition tracker, is an easy way to track the amount of phosphorous is in your diet. The National Kidney Foundation’s website1 is another helpful resource.
Schizophrenia Is Chronic Encephalitis …and Niacin Cures It
Reproduced from original OMNS article (OrthoMolecular News Service):
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Orthomolecular Medicine News Service, October 12, 2023
by Thomas E. Levy, MD
OMNS (October 12, 2023) Orthomolecular medicine is based on the concept that most chronic diseases are ultimately initiated, and then sustained, by the chronic deficiency of one or more vitamins, minerals, nutrients, or other natural agents. When the deficiency can be lessened, the disease improves. Conversely, the worse the deficiency and the longer it persists in the body, the more advanced and entrenched the disease becomes. What often is unclear for both the public as well as many healthcare providers is that the clinical benefits of some nutrient supplements continue to increase as the doses are increased. These doses can vastly exceed the Recommended Dietary [or Daily] Allowance (RDA) disseminated by the Food and Nutrition Board, a committee established by the United States National Academy of Sciences. Since 1997, the term Dietary Reference Intake (DRI) has been in use to describe much the same information as the RDA. The DRI recommendations have not significantly deviated from the earlier RDA recommendations. [1]
While a few nutrients can rapidly become toxic with minimally excessive intake (calcium, copper, and iron), many nutrients have little toxicity at almost any dose. [2] In general, the doses of vitamins are difficult to push to the point of clinical toxicity. However, nearly all the nutrient minerals can readily be taken to excess and result in various presentations of toxicity. Toxicity in this context refers to definable physiological damage to the supplement taker, not occasional side effects such as nausea in a sensitive stomach (niacin) or osmotic diarrhea (vitamin C or magnesium) when too much is not efficiently absorbed but accumulates in the colon instead.
However, the concern about potential toxicity keeps supplements like niacin, vitamin C, and magnesium severely underdosed, resulting in a loss of the incredible benefits they offer when optimally dosed.
Vitamin C and Magnesium Supplementation
Vitamin C is the safest of all known nutrient supplements. In fact, there has never been established any dose of vitamin C above which toxicity will reliably ensue. This is consistent with the fact that vitamin C is the molecule on which the physiology of all cells runs, and the healthy function of the body relies on having large amounts of it both inside the cells as well as outside of them. Arguably, vitamin C is the safest consumable agent in existence. Rare individuals can experience minimal side effects, but this should not be confused with any degree of cell-damaging toxicity. By contrast, too much water intake is toxic and can even result in death. [3-5]
The vitamin C RDA for older children and adults ranges from 45 to 90 mg per day. However, many people maintain a much higher level of general health when multigram supplementation is taken regularly, on the order of 100 times the RDA. Furthermore, the administration of vitamin C in doses 1,000 times the RDA are frequently given intravenously around the world for the treatment of a wide range of infections and medical conditions, with excellent effect and unrivaled safety. [6-8]
Magnesium, like all minerals, can be pushed to toxic levels of intake. However, it is almost impossible to induce toxicity with ORAL magnesium intake, as the highest levels of intake will reliably induce an osmotic diarrhea from unabsorbed magnesium reaching the colon. But when given intravenously, enough magnesium will reliably lower even the most elevated of blood pressures to hypotensive levels. In some surgeries, sufficient magnesium is infused to deliberately keep blood pressure below normal levels to help achieve hemostasis and keep the surgical field from bleeding excessively. [9-11]
Such highly-dosed infusions should only be administered in a hospitalized setting. However, the addition of a few grams of magnesium can always be added to a therapeutic vitamin/mineral IV bag and be safely infused over an hour or so in the clinic setting. In fact, the appropriate administration of magnesium by IV infusion is the best way to help restore low body levels of magnesium, especially in patients who cannot take very much orally. [12,13] Some caution and dosage adjustments need to be made by the clinician when there is decreased kidney function.
Just like vitamin C, but much less dramatically so, oral magnesium supplementation of several grams daily can be taken as long as the osmotic diarrhea is not induced. With a magnesium RDA of roughly 300 to 400 mg daily, the amounts of supplementation to keep most adults out of a significant deficiency of magnesium will be in the range of 5-fold or more of this RDA. Furthermore, very few people can reach an optimal magnesium status with oral supplementation. Rather, the practical goal is to minimize the degree of magnesium deficiency. Nevertheless, as a significant magnesium deficiency causes some diseases and makes all diseases worse, taking as much magnesium supplementation as can be readily tolerated is always a good idea. [14]
Of the 13 essential vitamins (A, C, D, E, K, B1, B2, B3, B5, B6, B7, B9, B12), increased intake and/or increased blood levels have been associated with decreased all-cause mortality for 11 of them. [15-23] Studies clearly establishing the same associations with biotin (vitamin B7) and pantothenic acid (vitamin B5) were not found. For the most part, these studies only examined vitamin intakes in the range of the RDA or DRI values, further supporting their critical support of good health even when ingested in relatively small amounts. While toxic effects can be seen with vigorous dosing of vitamin A, vitamin D, or vitamin E, the rest have RDA or DRI values that can be greatly exceeded, resulting in only improved health and blood chemistries.
Niacin: Nomenclature and Physiology
Confusion can easily arise in sorting through the literature on niacin and its derivatives. Niacin is vitamin B3. It is also known as nicotinic acid. These are all synonyms for the chemically identical substance. Niacin, vitamin B3, and nicotinic acid are completely interchangeable terms. For completeness, niacin is also rarely referred to in the literature as “vitamin PP,” with the PP meaning “pellagra-preventive.” Pellagra is the clinical condition that results from a severe deficiency of niacin in the body. [24]
Niacin has several vitamers. Vitamers are derivatives or related chemical substances that fulfill the same specific vitamin functions despite not being chemically identical. Niacin derivatives that qualify as vitamers include niacinamide (also known as nicotinamide or nicotinic acid amide), nicotinamide riboside, and nicotinamide mononucleotide. Referring to nicotinamide as niacinamide decreases the possibility of niacin and its vitamers as being perceived by the public as having nicotine-like properties, which it does not. All these substances promote the biosynthesis of NAD (nicotinamide adenine dinucleotide) throughout the body, and they are the primary sources of NAD. [25,26]
Large amounts of NAD are essential for optimizing the electron supply in the first of the four steps of the electron transport chain (ETC). Located along the membranes of the mitochondria inside every cell, the ETC is responsible for the production of all the ATP (adenosine triphosphate) in the body. ATP is the most important energy-providing molecule in the body. Any compromises in its production results in a decline in the healthy function of all affected tissues and organs. When there is not enough NAD present at the beginning of the ETC, sufficient ATP simply cannot be generated.
Optimizing the production of NAD for ATP synthesis in the cells is the most important function of niacin and its vitamers.
Furthermore, greater deficiencies in available NAD results in even more pronounced declines in cellular function throughout the body. Nothing is more important for optimal health than maximal amounts of intracellular ATP. [27] Low NAD levels have been recognized as a sign of aging in not only humans, but in all living cells, including those in animals and insects. [28-34]
Niacin Supplementation
Names of forms of niacin supplementation that directly fuel NAD production in the body:
- Niacin
- Niacinamide
- Nicotinamide
- Nicotinamide riboside
- Nicotinamide mononucleotide
- Inositol hexaniacinate
- Inositol hexanicotinate
Of note, niacin has an additional important property that its vitamers do not have. Reported as early as 1955, niacin has been documented to lessen the abnormal lipid metabolism that promotes atherosclerosis. [35-37] It reduces triglycerides and the lipoproteins VLDL and LDL while raising HDL, the “good” lipoprotein. [38]
If well-tolerated, niacin is the best of the supplement forms itemized above to take, as it has both the positive impact on the lipids as well as on the NAD levels in the body. It also costs less. However, niacin causes a warm to hot flushing effect in many people who supplement it. While for many people this flushing effect is either minimal or even disappears after several doses, for some people it is not tolerable. The other supplement forms noted above are largely “flush-free,” and can be easily taken by nearly everyone. The downside is that the non-flushing forms do not have the positive lipid impact of unmodified niacin.
Niacin and all its vitamers profoundly impact ATP generation throughout the body, as noted above. However, like so many other powerful orthomolecular therapies, the niacin RDA and DRI is amazingly tiny, completely misleading the health seeker as to its importance and impact of much higher doses. The optimal energy-supporting doses of niacin can be 200- to 1,000-fold higher than these officially-advised doses. And other than nausea in a few individuals, side effects are decidedly uncommon. [39] Very high doses have been linked to liver toxicity, as reflected in significant liver enzyme elevation. However, minor enzyme elevation that typically resolves without discontinuation of the supplementation is not uncommon. Such enzyme increases are felt to represent a temporary increased metabolic activity in the liver cells and not inflammatory damage. [40]
In the toxin-laden, pro-oxidant environment in which we now all live, virtually everyone is deficient in the antioxidant impact provided by niacin supplementation and the NAD levels it supports. Everybody should take at least some niacin supplementation. There really does not exist a dietary regimen that can provide the NAD-producing benefits of even a minimal supplementation of niacin.
Niacin, Health, and Schizophrenia
Optimizing the production of ATP in the body is a very desirable goal. Many clinicians today regard chronic fatigue patients as having “mitochondrial dysfunction” or “mitochondrial fatigue.” While decreased ATP production is uniformly present in such patients, different patients can have different reasons for that decline in production. [41] However, except for individuals with genetic deficiencies that typically cannot be completely resolved, increasing the production of ATP not only can resolve the fatigue and associated symptoms, it can also infuse the needed energy into the dysfunctional metabolic pathways to completely resolve the biochemical abnormalities that decreased the ATP production in the first place. Quite literally, this results in cellular healing. Niacin supplementation has been shown to restore healthy NAD levels (which then increase ATP production), greatly improving muscular strength in patients with mitochondrial dysfunction. [42]
Ultimately, all such dysfunction inside the cytoplasm as well as inside the mitochondria comes from increased numbers of inactivated, oxidized biomolecules relative to the numbers of normal, reduced biomolecules. This is traditionally referred to simply as increased oxidative stress. Improvements in all pathological states can be anticipated with increased ATP production, although certain conditions, such as muscle fatigue from low ATP levels, can be expected to respond even more dramatically. The heart muscle in heart failure is a classic example of a tissue severely depleted of ATP, no longer able to respond to significant exercise with a sufficiently increased production of ATP. [43]
Endomyocardial biopsies have documented that heart muscle in congestive and hypertrophic cardiomyopathies have significantly depressed levels of both ATP and NAD. [44] Normal heart muscle has the highest NAD levels in the body. [45] In both congestive and hypertrophic cardiomyopathy impaired energy metabolism has been identified. [46] Consistent with these findings, the elevation of NAD levels in different studies has been shown to improve atherosclerosis as well as different forms of heart failure, including ischemic, hypertrophic, and congestive cardiomyopathies. [47,48] In an animal study, niacin has also been shown to lessen damage in myocardial infarction. [49] Studies in both animals and humans have shown that niacinamide can lower elevated blood pressures and decrease cardiac mortality. [50,51] In a mouse model of cardiac arrest, niacinamide administration was able to normalize NAD levels and improve survival. [52]
Niacin vitamer supplementation in humans has been clearly shown to dramatically increase blood levels of NAD. [53] Not surprisingly, NAD-increasing agents, with their strong support of ATP production, are also being increasingly appreciated as being useful for both anti-aging and overall good health. [54-59] In an animal study of sepsis, probably the most advanced and dire of medical conditions, a niacin vitamer was shown to increase survival and prevent the lung and heart injury otherwise seen. [60]
Some studies indicate that lower NAD and ATP levels are the primary abnormalities that result in cancer. [61-63] In one human study, it was shown the niacinamide supplementation was effective in reducing the appearance of new skin cancers. [64] This is consistent with the pellagra-associated skin inflammation (dermatitis) seen when niacin levels are very low. [65] Higher niacin intake has been linked to decreased all-cause mortality, indicating its importance in every cell in the body. [66,67]
The clinical effectiveness of daily multigram niacinamide dosing depends on how severely the affected tissues or organs in a disease are depleted of the NAD needed to make ATP. Heart failure, while not always responsive to increased NAD production, will often respond dramatically to an improved NAD status. A significant number of patients with congestive cardiomyopathy and low cardiac output have been spared heart transplantation after adequately-dosed Coenzyme Q10 (CoQ10), another agent capable of increasing ATP production via the ETC in the mitochondria. In many of those patients, ejection fractions have increased dramatically, and all-cause mortality decreased along with an improved exercise capacity. [68-74] Also, like niacinamide, CoQ10 also improves heart failure patients with preserved ejection fractions (hypertrophic cardiomyopathy with diastolic dysfunction). [75,76]
Niacinamide has also been shown to enhance acetyl-CoA production, which in turn enhances the biosynthesis of CoQ10.
This means that niacinamide supplementation can provide the substrates needed for both NAD and CoQ10 production, directly powering two of the four steps of the ATP-producing ETC. [77,78]
Like heart muscle, the brain and central nervous system (CNS) require very high levels of ATP for normal function relative to the rest of the body. As such, having inadequate building blocks for ATP production in the body will be reflected more often and more prominently as nervous system and psychiatric disorders than other medical conditions. Many studies have indicated that niacinamide is essential for the development, growth, and maintenance of the CNS. [79-81] Furthermore, niacinamide has been shown to readily pass the blood-brain barrier in both directions, supporting its supplementation as a simple and effective approach to treating various CNS conditions. [82] Also, oral niacinamide supplementation has been shown to be very well-absorbed. [83]
Animal studies have shown that niacinamide will protect against ischemia-induced (decreased blood supply) damage in the brain and CNS. Neuronal death is reduced, and the recovery of affected sensory and motor function is improved as well. [84-87]
Significant infection protection and resolution can be seen when NAD production is optimized with niacin and several other NAD-producing agents. Sepsis recovery is supported by increased niacin levels. COVID has also been shown to resolve more rapidly with agents that help to optimize cellular ATP levels. [88-91] Improved outcomes in COVID-related acute kidney injury have been seen with niacinamide therapy. [92] Niacinamide has also been shown to lessen inflammation-induced renal failure in an animal model. [93] It has a protective effect against the pro-inflammatory toxicity of paraquat in rats. [94]
Severe niacin deficiency results in a disease known as pellagra. This syndrome has been characterized by a triad of symptoms: delirium, dermatitis, and diarrhea. More accurately, the triad should be referred to more broadly as neurocognitive, dermatological, and gastrointestinal symptoms. A substantial variation in this symptom pattern can be seen, as the circumstances resulting in a deficiency of niacin can result in a variety of other significant nutrient and micronutrient deficiencies in a given patient. [95-97] Nevertheless, the complete restoration of niacin levels in the body, along with the micronutrients supplied by a balanced diet, reliably resolves the symptoms of pellagra, including those involving the CNS.
The neurocognitive symptoms in patients with severe niacin deficiency are always present, and they can be very pronounced clinically. Both Alzheimer’s disease and Parkinson’s disease typically have depleted NAD levels in the affected tissue, and some of their symptoms can be lessened with increased niacin intake. [98] Other CNS symptoms, including disorientation, memory loss, confusion, dementia, poor sleep, and even frank psychosis can be seen in the severely niacin-deficient patient. [99] Of note, the statistical risk of Parkinson’s disease is lessened in individuals having an increased consumption of niacin-containing foods. [100,101]
Schizophrenia is one of the most devastating of diseases, with enormous societal impact in addition to the symptoms endured along with the effective loss of a functional life in the patient. [102] Chronically increased oxidative stress defines a state of chronic inflammation in the brain (neuroinflammation). The presence of chronic inflammation in the brains of schizophrenic patients has been well-documented. [103,104] Studies have shown that schizophrenia in younger individuals can be initiated following exposure to the toxins, or pro-oxidants, encountered in prenatal exposures to infection. [105,106] Consistent with this, many cases of schizophrenia start early in life with toxin-induced abnormal neurodevelopment. [107,108]
The symptoms of schizophrenia are numerous and diverse, with some symptoms assuming a much more prominent role in one patient versus another. The bulk of the literature simply recounts the classical and well-known symptoms of schizophrenia that focus solely on brain dysfunction. Such symptoms include hallucinations, delusions with loss of contact with reality, difficulty thinking clearly, and social/emotional withdrawal, sometimes to the point of staying in a largely motionless, catatonic state. However, it has also been recognized that symptoms not directly referable to brain dysfunction are often present as well. These include the classical symptoms of pellagra, the potentially fatal condition secondary to severe niacin deficiency in the body.
The niacin deficiency in pellagra can result brain and CNS pathology manifesting as irritability, difficulty concentrating, some social withdrawal, depression and manic depression, insomnia, delirium, hallucinations, coma and even frank psychosis. Some authors have termed this “pellagroid encephalopathy.” [109] Furthermore, the psychosis with associated delusions that sometimes occurs in pellagra is indistinguishable from some cases of schizophrenia. [110] These symptoms all typically resolve with adequate restoration, and maintenance, of niacin levels in the body. [111] The effective use of niacin for psychiatric symptoms has also spawned the concept of “reversible dementia,” a remarkable term since dementia is generally considered to be progressive and non-resolving in nature, especially in older individuals. [112] Similarly, the close relationship between pellagra and brain dysfunction has spawned the term “niacin-respondent subset of schizophrenia.” [113]
The niacin deficiency in pellagra always has symptoms of brain dysfunction, and niacin restoration treats them very effectively.
Pellagra causes significant gastrointestinal problems and symptoms. This is significant in understanding the contribution and worsening that a pellagra-related leaky gut with a pathogen-overgrown microbiome does to diseases of the CNS (and elsewhere in the body). Alzheimer’s, Parkinson’s, amyotrophic lateral sclerosis (ALS), and schizophrenia have all been clearly documented to either have pathogens and/or their toxic metabolites present in the affected nervous tissue. [114-125] The damage that niacin deficiency (pellagra) does to the microbiome is a major factor in the associated neuropsychiatric problems and schizophrenia-like symptoms seen with it as well. Niacin deficiency not only results in decreased energy production in the brains of schizophrenics, it also results in the continued exposure of pathogens and/or their toxic metabolites from an abnormal gut microbiome to the CNS of those patients.
Schizophrenia most commonly appears in late adolescence or early adulthood. [126] But it can occur later in life as well. Increased intracellular oxidative stress, left unchecked, results in premature death of the affected cells. Brain volume studies have established that schizophrenic patients progressively lose gray matter and the actual physical mass of the brain over time, well beyond the deterioration seen with aging. [127-130] Microglia, the scavenger white cells of the brain, become activated in the inflammation seen in schizophrenia. [131-133] Pro-inflammatory cytokines and other inflammatory markers are also increased. [134-136] All this information leads to the following assertion:
Schizophrenia is chronic encephalitis.
Encephalitis is inflammation of the brain, typically occurring acutely in conjunction with a new viral infection precipitating widespread inflammation throughout the brain and CNS. In schizophrenia the chronically elevated inflammatory parameters indicate that ongoing inflammation is causing the signs and symptoms of schizophrenia. Schizophrenia = chronic brain inflammation = chronic encephalitis. [137] Many of the symptoms seen in acute encephalitis brain are also seen in the chronic encephalitis brain of the schizophrenic patient, including alterations in consciousness, confusion, hallucinations, and cognitive impairment. Some authors have descriptively referred to schizophrenia as “the shattered mind.” [138] The steady destruction of brain tissue by the chronic inflammation also explains why schizophrenia present for years responds less readily to any nutrient or drug regimen than schizophrenia of recent onset. The chronic inflammation slowly destroying brain tissue in schizophrenia is analogous to the patient with ongoing myocarditis and death of heart muscle eventually going into congestive heart failure. The later a positive therapy is started, the less effective it will be.
The effective clinical resolution of many schizophrenics is further complicated and even impaired by the common and severe side effects seen with the drugs commonly used in its treatment. Many of these side effects are indistinguishable from many of the symptoms for which the drugs are being given. Such symptoms include restlessness, brain fog, and social withdrawal with the loss of desire to interact with others. [139] Once a schizophrenic patient has received prescription drugs for a long enough period, it can become impossible to know when the condition itself is getting worse or a drug needs to be discontinued and/or decreased in dosage. As it is, the clinical picture of an unmedicated schizophrenic patient also spans a variety of symptoms present in many different combinations. [140]
The levels of niacin in schizophrenic patients are always low, oftentimes severely so. This also means that their cellular ATP levels are significantly depressed as well. It has been clearly shown that high doses (relative to RDA or DRI recommendations) of niacin or a niacin vitamer often completely resolves schizophrenia, even in its advanced stages. And when clinical resolution is not complete, significant improvement in the major symptoms of schizophrenia is nearly always seen.
In a group of 30 acute schizophrenia patients, one gram three times daily of niacin or niacinamide were given for only 30 days, and the patients were then followed for one year. 80% of the niacin-treated group recovered versus 33% of the placebo-treated group. [141] Recovery in acute or chronic schizophrenia was only considered to have been reached when the patient
- Had complete disappearance of disease-related symptoms and signs
- Was interacting normally with family members as well as members of the community
- Became gainfully employed
Vitamin C, a perfect treatment for any condition involving chronic inflammation, was often given in a dose of 1 to 10 grams daily as well. As the primary antioxidant (anti-inflammatory agent) in the body, vitamin C should always be used to help resolve the brain inflammation of schizophrenia. [142] Much higher doses will always help, and sometimes dramatically so, especially in schizophrenia of recent onset.
While not typical, acute schizophrenia can spontaneously resolve. Presumably, the factors provoking the inflammation in the brain of those patients eventually resolve, or become much less pronounced (e.g., infection, toxin, autoimmune reaction, micronutrient depletion).
Six more double-blind, randomized and controlled clinical trials confirmed the positive impact of niacin on the recovery of schizophrenic patients. [143,144] Many of the most chronic patients (with the most structural brain damage) required this therapy for five or more years to derive clear benefits. [145] For the niacin treatment of schizophrenia, the starting dose was 1,000 mg three times daily, with the dose slowly increased to as much as 4,500 to 18,000 mg daily, depending on clinical response. For those treated with niacinamide rather than niacin, the daily dose rarely exceeded 6,000 mg due to the increased problems with nausea and stomach sensitivity. [146-148]
Dr. Abram Hoffer treated over 5,000 schizophrenic patients with this niacin protocol. No deaths ever resulted from the administration of niacin. Furthermore, consistent with the wide-ranging positive effects of niacin on NAD levels throughout the body described above, Hoffer noted improvements in many symptoms not directly attributable to schizophrenia in his niacin-treated patients. [149] He also developed a more comprehensive orthomolecular approach to schizophrenia over the course of his years in clinical practice. [150] Currently, over 85% of chronic schizophrenic patients treated with traditional measures never resolve, even if some treatment benefits are realized. Instead, they remain sick and dysfunctional for the rest of their lives when niacin is not at least a part of their treatment program.
The following can be definitively asserted:
Niacin cures acute schizophrenia most of the time. And substantial clinical improvement is the rule even when a complete cure is not realized in acute or long-standing schizophrenia.
As covered above, schizophrenia, with its close connection to pellagra, is a condition precipitated and worsened by multiple factors. A quality diet and a wide array of vitamin and mineral nutrients are mandatory for an optimal clinical response in all these patients. Several reasons account for the varied (but positive) clinical responses of schizophrenia patients treated with niacin. [151] Nevertheless, monotherapy with niacinamide has completely resolved schizophrenia. [152] As an important and non-toxic nutrient vitamin, niacin should NEVER be denied to any patient with any brain disorder, much less schizophrenia. As Dr. Hoffer put it: “Apparently the worst sin in orthodox medicine is to see a recovery for the wrong reason.”
The production of ATP, the final physiological goal in the severely NAD-depleted brain (and body) of the schizophrenic patients is specifically nurtured and supported not only by niacin, but also by riboflavin, CoQ10, and methylene blue. These four agents directly power the different steps in the mitochondrial ETC needed to optimize ATP production, which directly accounts for all healing and good health. And when permanent brain damage is minimal and the symptoms are due to ongoing neuroinflammation, an excellent clinical response can be anticipated, even if a complete cure is not realized. Niacin, CoQ10, and riboflavin comprise a nutrient triad that has been shown to benefit the antioxidant status of breast cancer patients. [153-155] And even though vitamin B3 is important to everyone, its optimal dosing is achieved by few individuals. While it is literally good for everyone, it nevertheless needs to be clearly asserted that:
Everyone with any psychological or psychiatric condition should take niacin or one of its vitamers, and the dose should be maximized before considering such a condition permanent and/or unresponsive.
Currently, the standard of care in psychiatry does not include the routine administration of niacin or niacinamide for schizophrenia or any other mental or emotional disorder.
While the established standard of practice is usually sufficient to protect a physician from malpractice, deliberately avoiding the usage of niacin for schizophrenia after being exposed to much of the literature and information cited in this article nevertheless constitutes clear medical malpractice, even if it remains unadjudicated.
Healthcare practitioners have an obligation, albeit rarely-honored, to stay informed on the science of old, current, and new therapies. The benefit of niacin therapy in schizophrenia and most brain disorders is certainly not a new discovery. As with all other conditions that have been shown to clearly benefit from an orthomolecular approach to addressing vitamin, mineral, and other nutrient deficiencies, a healthcare practitioner should always be open to all legitimate scientific information that the patient might offer. If such a practitioner refuses to even review such information, and/or will not even discuss such information with the patient, it is time to find a new one.
You do not need a doctor to give you niacin, and there are no absolute contraindications to taking it. You can take it for yourself, and you can advise any friend or family member with a neurological or psychiatric condition that you have information indicating that it is often beneficial regardless of the precise diagnosis.
Recap
Niacin and its related compounds have a long history of improving the mental status of a wide variety of mental and emotional disorders. It has been shown to cure or greatly improve most cases of schizophrenia for which it is properly-dosed. These disorders are primarily caused by a severe deficiency of NAD in the ATP-generating mitochondria in all cells. The primary role of niacin is to increase NAD levels, resulting in an improved or normalized amount of cellular ATP, the most important energy-providing molecule in the body. While many other nutrients will be of benefit in schizophrenia, highly-dosed vitamin C and magnesium should always be given to further control and quell the ongoing neuroinflammation.
Pellagra, the disease established to occur after severe and long-standing niacin deficiency, typically presents with significant brain dysfunction, sometimes clinically identical to schizophrenia. Niacin administration often completely resolves such states of psychosis, further supporting the concept that NAD repletion leading to optimal ATP levels in the brain is the root cause of schizophrenia.
A chronic NAD deficiency always causes increased oxidative stress in the affected tissue. This means that schizophrenia is a chronic encephalitis, as chronic encephalitis simply means an ongoing state of neuroinflammation in the brain.
The variability in clinical response of schizophrenia to niacin therapy is primarily due to how many other nutrient deficiencies are present and whether they are properly restored. How long the schizophrenia has been present and how much irreversible brain damage (decreased brain mass) has occurred is also critical in determining how much clinical benefit is realized.
Even though the psychiatric standard of care does not include niacin therapy for schizophrenia, it can only be considered malpractice not to apply it, especially considering the enormous physical, mental, and societal impact of this dreaded disease. Opting not to use a toxic therapy that might only help a little for a relatively minor condition does not apply to niacin for schizophrenia. That reasoning is reserved for many pharmaceutical agents, not natural nutrients.
Dedicated to the work of Abram Hoffer, MD, PhD
(Dr. Thomas E Levy, an OMNS Contributing Editor, is a cardiologist, attorney, and author of 13 books. He can be reached at televymd@yahoo.com. A collection of all his OMNS articles can be easily accessed with the following link under the subheading of “Orthomolecular”: https://www.tomlevymd.com/health_ebytes.php )
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137. Bechter (2013) [Schizophrenia-a mild encephalitis?] Article in German. Fortschritte der Neurologie-Psychiatrie 81:250-259. PMID: https://pubmed.ncbi.nlm.nih.gov/23629631/
138. Osmond H, Hoffer A (1959) A small research in schizophrenia. Canadian Medical Association Journal 80:91-94. PMID: https://pubmed.ncbi.nlm.nih.gov/13618799/
139. Lahteenvuo M, Tiihonen J (2021) Antipsychotic polypharmacy for the management of schizophrenia: evidence and recommendations. Drugs 81:1273-1284. PMID: https://pubmed.ncbi.nlm.nih.gov/34196945/
140. Weller M (1987) The spectrum of schizophrenia. Postgraduate Medical Journal 63:1021-1024. PMID: https://pubmed.ncbi.nlm.nih.gov/3330234/
141. Hoffer A, Osmond H, Callbeck M, Kahan I (1957) Treatment of schizophrenia with nicotinic acid and nicotinamide. Journal of Clinical and Experimental Psychopathology 18:131-158. PMID: https://pubmed.ncbi.nlm.nih.gov/13439009/
142. Sandyk R, Kanofsky J (1993) Vitamin C in the treatment of schizophrenia. The International Journal of Neuroscience 68:67-71. PMID: https://pubmed.ncbi.nlm.nih.gov/8063516/
143. Hoffer A, Prousky J (2008) The proper treatment of schizophrenia requires optimal daily doses of vitamin B3. Journal of Orthomolecular Medicine 23:191-195. http://orthomolecular.org/library/jom/2008/pdf/2008-v23n04-p191.pdf
144. Hoffer A, Prousky J (2008) Successful treatment of schizophrenia requires optimal daily doses of vitamin B3. Alternative Medicine Review 13:287-291. PMID: https://pubmed.ncbi.nlm.nih.gov/19238764/
145. Hoffer A (1994) Chronic schizophrenic patients treated ten years or more. Journal of Orthomolecular Medicine 9:7-37.
146. Hoffer A, Osmond H (1964) Treatment of schizophrenia with nicotinic acid. A ten year follow-up. Acta Psychiatrica Scandinavica 40:171-189. PMID: https://pubmed.ncbi.nlm.nih.gov/14235254/
147. Hoffer A (1963) Nicotinic acid: an adjunct in the treatment of schizophrenia. The American Journal of Psychiatry 120:171-173. PMID: https://pubmed.ncbi.nlm.nih.gov/13963912/
148. Osmond H, Hoffer A (1962) Massive niacin treatment in schizophrenia: review of a nine-year study. Lancet 1:316-319. PMID: https://pubmed.ncbi.nlm.nih.gov/14482545/
149. Hoffer A, Saul A, Foster H (2023) Niacin: The Real Story. Nashville, TN: Basic Health Publications, Inc.
150. Hoffer A (2020) Light on Schizophrenia: Revealing causes and solutions from an orthomolecular perspective. Victoria, BC: Tellwell Publishing
151. Hoffer A (1971) Megavitamin B-3 therapy for schizophrenia. Canadian Psychiatric Association Journal 16:499-504. PMID: https://pubmed.ncbi.nlm.nih.gov/4947171/
152. Hoffer A (1973) A neurological form of schizophrenia. Canadian Medical Association Journal 108:186. PMID: https://pubmed.ncbi.nlm.nih.gov/4684627/
153. Premkumar V, Yuvaraj S, Vijayasarathy K et al. (2007) Effect of coenzyme Q10, riboflavin and niacin on serum CEA and CA 15-3 levels in breast cancer patients undergoing tamoxifen therapy. Biological & Pharmaceutical Bulletin 30:367-370. PMID: https://pubmed.ncbi.nlm.nih.gov/17268082/
154. Yuvaraj S, Premkumar V, Vijayasarathy K et al. (2008) Augmented antioxidant status in tamoxifen treated postmenopausal women with breast cancer on co-administration with coenzyme Q10, niacin and riboflavin. Cancer Chemotherapy and Pharmacology 61:933-941. PMID: https://pubmed.ncbi.nlm.nih.gov/17668211/
155. Premkumar V, Yuvaraj S, Sathish S et al. (2008) Anti-angiogenic potential of Coenzyme Q10, riboflavin and niacin in breast cancer patients undergoing tamoxifen therapy. Vascular Pharmacology 48:191-201. PMID: https://pubmed.ncbi.nlm.nih.gov/18407793/
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Why You Should Never Take Antacids for Digestive Reflux
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/09/27/never-take-antacids-for-digestive-reflux.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.
Analysis by Dr. Joseph Mercola Fact Checked September 27, 2023
STORY AT-A-GLANCE
- Proton pump inhibitors (PPIs) inhibit acid production in your stomach and are routinely used to treat acid reflux. An estimated 15% of the U.S. population are on PPIs. Antacids like Tums neutralize acid in your stomach but don’t block production. They’re the least harmful, as their effects are temporary. Be sure to read the ingredients list, however, as many acid neutralizing medications contain aluminum hydroxide, a toxic compound that impairs your body’s zeta potential
- If you regularly suffer from heartburn or acid reflux, inhibiting acid production is actually the last thing you want to do
- Acid reflux occurs when contents from your stomach back up into your esophagus, causing stomach acid to irritate the lining of your esophagus. However, excess acid is not the problem. Low acid is, because the lower esophageal sphincter (LES) is pH sensitive and only closes once sufficient acidity is present in the stomach
- Other causes of heartburn include hiatal hernia, medications and foods that relax the LES, foods that irritate the stomach, obesity, smoking and helicobacter pylori infection
- PPIs and antacids are inadvisable as none of the potential underlying causes involves excess stomach acid. What you need is more acid. Long term use of PPIs can compromise your health, as insufficient stomach acid has been linked to asthma, GI-related issues, skin diseases, depression, gallbladder disease, migraines, macular degeneration, osteoporosis and a variety of autoimmune conditions
Americans spend a whopping $13 billion a year on over-the-counter (OTC) antacids (acid neutralizers) and prescription proton pump inhibitors (PPIs), which are the most popular antireflux medications on the market.1 It’s estimated that over 27% of Americans are taking antacids, and more than 15% are on PPIs.2,3
PPI drugs like Nexium, Prevacid and Prilosec inhibit acid production in your stomach and are routinely used to treat acid reflux, a condition affecting about 20% of the U.S. population.4 Once prescribed, your doctor may keep you on a PPI drug for years, despite label warnings suggesting they be used only for short periods.
Antacids like Tums neutralize acid in your stomach but don’t block production. As such, they’re the least harmful, as their effects are temporary. That said, many acid neutralizing medications contain aluminum hydroxide, a toxic compound that impairs your body’s zeta potential,5 so be sure to read the ingredients.
If you regularly suffer from heartburn or acid reflux and are using prescription PPIs or OTC antacids, you’ll want to pay careful attention to this article, as inhibiting acid production is the last thing you want to do.
In a September 16, 2023, Substack article,6 A Midwestern Doctor took a deep dive into the problems caused by acid-suppressing medications, and how to properly address acid reflux.
As noted in that article, PPIs top the list of medications that are routinely prescribed despite providing minimal benefit and causing real harm. I’ll review some of the highlights from that article here, but if you want more, I highly recommend reading his article, “Stomach Acid Is Good For You,”7 in its entirety.
The Primary Cause of Acid Reflux
Acid reflux occurs when contents from your stomach back up into your esophagus, causing stomach acid to irritate the lining of your esophagus. Other common names for this condition include acid indigestion, acid regurgitation, heartburn and gastroesophageal reflux disease (GERD).
If you experience acid reflux symptoms more than twice a week, you very likely have reflux disease or GERD, which involves bloating, burning pain in your chest and gut discomfort.
Now, because stomach acid is involved, and the word “acid” connotes the idea of “burning,” it’s commonly believed that excess stomach acid is the problem. Indeed, the entire antacid industry is built around this idea.
Acid reflux occurs when contents from your stomach back up into your esophagus, causing stomach acid to irritate the lining of your esophagus. However, excess acid is not the problem. Low acid is, because the lower esophageal sphincter is pH sensitive and only closes once sufficient acidity is present in the stomach.
Unfortunately, that’s completely backward. Acid reflux is typically caused by a deficiency in stomach acid, not excess. How is this possible? It’s rather simple, actually. As explained by A Midwestern Doctor:8
“The lower esophageal sphincter is pH sensitive and only closes once sufficient acidity is present in the stomach (which makes sense since otherwise food would not be able to get to the stomach in the first place, but once it’s there, you need a way to keep it from getting back into the throat).”
Other Causes of Heartburn
When low acid is not the cause of heartburn, the culprit can any of the following:
| A hiatal hernia — The hernia basically forces the LES open, allowing gastric juices to back up into your throat9 | Helicobacter pylori infection10 — One 2012 study found 82.5% of GERD patients tested positive for H. pylori infection11 |
| Obesity12 | Smoking, by interfering with the LES function13 |
| Certain medications can relax the LES, including bronchodilators, calcium channel blockers (blood pressure meds), valium, nitroglycerine and opioids14 | Foods, including fats, chocolate, caffeinated beverages, peppermint and spearmint, sugar, onions and alcohol can also weaken the LES15 |
| Foods that irritate your stomach can trigger reflux. Common irritants include citrus fruits, tomato, spicy foods, carbonated beverages, coffee and high-lectin foods16 |
In all these cases, the solution is to address the underlying problem, which would be to fix the hernia, treat the H. pylori infection, lose weight, quit smoking, minimize use of the offending drug (be sure to discuss alternatives with your doctor) and not eat the foods that are causing your LES to relax or that irritate your stomach.
OTC antacids and PPIs are entirely the wrong approach, regardless of the underlying cause, because none of the underlying causes of acid reflux have anything to do with excess stomach acid.
These drugs will reduce what little acid you have, leaving less to be regurgitated, but they basically ensure you’ll never get better. What’s worse, over time, low acid can contribute to a whole host of other health problems.
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The Purpose of Stomach Acid
Stomach acid serves several important functions, such as breaking down proteins, killing ingested pathogens, ensuring optimal nutrient absorption and regulating the rest of the digestion process.
If you use acid blockers, you’re compromising your entire digestive system, which can have downstream effects. For example, poor protein digestion increases your risk of food allergies.17 As reported by A Midwestern Doctor, there are clear links between insufficient stomach acid and a variety of health conditions, the following in particular:18
| Asthma | GI-related issues |
| Skin diseases | Depression |
| Gallbladder disease | Migraines |
| Macular degeneration | Osteoporosis |
| Autoimmune conditions, including but not limited to Celiac disease, Type 1 juvenile diabetes, Grave’s disease (hyperthyroid), lupus, multiple sclerosis (MS), rheumatoid arthritis and ulcerative colitis |
Low stomach acid can also have a detrimental impact on your immune function by allowing harmful pathogens such as bacteria and viruses to enter your GI tract. For example, a 2021 systematic review19 found that patients taking PPIs had a 77% higher risk of dying from COVID infection than those who did not take these drugs.
Low stomach acid has also been linked to impaired nutrient absorption, an 80% increased risk of stomach cancer,20 19% increased risk of death,21 28% increased risk of a major cardiac event,22 74% increased risk of kidney disease23 (and a 142% increased risk of death for these patients), 37% increased risk for pneumonia24 and a 33% increased risk for dementia.25
So, one of the take-home messages from this is that acid reflux is also a warning sign that other bodily systems may be adversely impacted. The good news is that all these related conditions can be improved by addressing the acid reflux the right way, which is to increase the acidity of your stomach so that the pH-sensitive esophageal sphincter can close properly.
What Causes Stomach Acid Insufficiency?
Before we address how to increase stomach acid, let’s review why it happens in the first place. Stomach acid production is known to decrease with age, and diet likely plays an important role in that decline. Stomach acid is made from hydrogen and chloride, and processed foods frequently do not contain the dietary sources of these components.
Hydrogen-rich foods include fresh fruits, vegetables, proteins and whole grains,26 while high amounts of chloride are found in salt, seaweed, rye, tomatoes, lettuce, celery and olives.27
Certain autoimmune conditions can also attack acid producing cells in your stomach, causing production to decline. H. pylori infections in your stomach will lower acid production as well. Mitochondrial dysfunction may also be a major part of the puzzle. As explained by A Midwestern Doctor:
“Stomach acid production is an energy intensive process (hence the cells which make stomach acid having a large number of mitochondria), and I have long suspected that mitochondrial dysfunction … is partly responsible for declining stomach acid levels.”
Importantly, PPIs will shut down acid production, and the longer you’re on them, the less acid your body will produce. As a result, it can be extremely difficult to stop using these drugs.
As soon as you stop taking them, you’ll experience rebound, and the rebound won’t stop until your stomach acid level is normalized and the LES starts closing properly, which in some long-term use cases can take up to two years.28
Talk to Your Doctor About Getting Off PPIs
Considering the dangers posed by PPIs, you do need to get off these drugs though. The best and safest way to do that is to work with your doctor to lower the dose you’re taking while simultaneously implementing the following lifestyle modifications:
- Avoid reflux triggers and/or any food that irritates your stomach
- Avoid processed foods and sugar
- Eat a Mediterranean diet, focused on fruits, healthy fats, lean meats, nuts and vegetables. Research published in the Journal of the American Medical Association Otolaryngology — Head & Neck Surgery found a Mediterranean diet was as effective as PPIs in treating acid reflux symptoms29
- Reseed your gut with beneficial bacteria from traditionally fermented foods or a high-quality probiotic supplement
- Thoroughly chew each bite of food
Once you get down to the lowest dose of the PPI, you can start substituting with an over-the-counter H2 blocker like Pepcid (famotidine) which appears to be the safest of all the options out there. Then, gradually wean off the H2 blocker over the next several weeks.
Natural Remedies for Treating Occasional Reflux Problems
If you suffer from occasional heartburn, indigestion and other minor reflux symptoms, forgo the PPIs and OTC antacid medications and try one or more of the following nondrug alternatives instead:30,31,32,33,34
| Aloe juice — The juice of the aloe plant naturally helps reduce inflammation, which may ease symptoms of acid reflux. Drink about one-half cup of aloe juice before meals. To avoid its laxative effect, look for a brand in which the laxative component has been removed. |
| Apple cider vinegar (raw, unfiltered) — Take 1 tablespoon of raw unfiltered apple cider vinegar in a large glass of water before or directly after meals. |
| Astaxanthin — When compared to a placebo, this potent antioxidant was found to reduce symptoms of acid reflux, especially for individuals with pronounced H. pylori infection.35 The researchers concluded a daily dose of 40 mg of astaxanthin was effective for reflux reduction. |
| Baking soda — One-half to 1 teaspoon of baking soda (sodium bicarbonate) in an 8-ounce glass of water or orange juice will help neutralize your stomach acid and ease the burn of acid reflux. While I do not advise this as an ongoing remedy, it is effective on an “emergency” basis when you are in excruciating pain. |
| Ginger root — Ginger has a gastroprotective effect by suppressing H. pylori. It also accelerates gastric emptying which, when impaired, contributes to heartburn. Add two or three slices of fresh ginger root to 2 cups of hot water and let it steep for several minutes. Drink it about 20 minutes prior to your meal. |
| Sauerkraut — Consuming sauerkraut or cabbage juice will stimulate your body to produce stomach acid. |
| Glutamine — The amino acid glutamine has been shown to address gastrointestinal damage caused by H. pylori. Glutamine is found in many foods, including beef, chicken, dairy products, eggs, fish and selected fruits and vegetables. L-glutamine is widely available as a supplement. |
| Ripe papaya or a papain supplement — Papaya contains papain, an enzyme useful for breaking down both protein and carbohydrates. |
| Fresh pineapple or bromelain supplement — Bromelain is a proteolytic enzyme found in pineapple that helps digest proteins. |
| Pepsin supplement — Like bromelain, pepsin is a proteolytic enzyme involved in protein digestion.36 |
| Betaine HCI supplement — Betaine HCl is the hydrochloride salt of betaine, not to be confused with betaine or trimethylglycine (TMG). As noted in a 2020 review paper:37 “… the most common recommendation for the use of betaine HCl supplements is usually implemented using an empirical test for low stomach acid whereby increasing doses of betaine HCl are given during sequential meals until such time as an uncomfortable sensation is noticed by the patient.
Along with improvements in symptoms of dyspepsia (or laboratory analysis of improved protein digestion), the lack of side effects acts as an empirical confirmation that low gastric acid production was contributing to poor digestion and/or dyspeptic symptoms.” |
| Bitters — Bitters have a long history of use in herbal medicinal traditions to promote digestion and/or to relieve digestive complaints.38 |
| Slippery elm — Slippery elm coats and soothes your mouth, throat, stomach and intestines, and contains antioxidants that may help address inflammatory bowel conditions. Because it stimulates nerve endings in your gastrointestinal tract, it is useful for increasing mucus secretion, which has a protective effect against ulcers and excess acidity. |
| Vitamin D — Vitamin D is important for your gut health. Once your vitamin D levels are optimized, you will benefit from your body’s production of about 200 antimicrobial peptides that will help eradicate gut infections. |
| Zinc — Your stomach needs zinc to produce stomach acid, so make sure your body has the necessary raw ingredients. The recommended daily amount for adults is 8 to 11 mg. Zinc rich foods include oysters, lobster, beef, cashew nuts, beans and raw yogurt. A zinc supplement can be used if you rarely eat these foods.39 |
- 1 Time September 7, 2017
- 2, 5, 6, 7, 8, 9, 14, 15, 16, 18, 28 Midwestern Doctor Substack September 16, 2023
- 3 Therapeutic Advances in Gastroenterology 2018; 11: 1756284818777943
- 4 The Surgical Clinic. What Is GERD?
- 10 Acta Biomedica 2018; 89(Suppl 8): 40–43, H. pylori and reflux disease
- 11 JSLF April-June 2012; 16(2): 260–263
- 12 Acta Biomedica 2018; 89(Suppl 8): 40–43, Conclusion
- 13 Acta Biomedica 2018; 89(Suppl 8): 40–43, Reflux disease and esophagitis, definition and pathophysiology and Conclusion
- 17, 33, 37, 38 Integr Med February 2020; 19(1): 32-36
- 19 World Journal of Clinical Cases April 26, 2021; 9(12): 2763-2777
- 20 Cancers July 2022; 14(13): 3052
- 21 Gastroenterology June 30, 2022; 163(4): 852-861
- 22 International Journal of Cardiology August 10, 2013; 167(3):965-974
- 23 British Journal of Clinical Pharmacology December 23, 2020; 87(7): 2967-2976
- 24 Ann Pharmacother May 2022; 56(5):524-532
- 25 Neurology August 9, 2023 DOI: 10.1212/WNL.0000000000207747
- 26 Life Persona 10 Foods Containing Hydrogen
- 27 Mount Sinai Chloride in Diet
- 29 Journal of the American Medical Association Otolaryngology – Head & Neck Surgery September 7, 2017; doi: 10.1001/jamaoto.2017.1454
- 30 Health January 25, 2016
- 31 Everyday Roots, 15 Natural Remedies for Heartburn & Severe Acid Reflux
- 32, 36, 39 Medical News Today 6 Ways to Increase Stomach Acid
- 34 Drugwatch PI Alternatives
- 35 Phytomedicine June 2008; 15(6-7): 391-9
Blockbuster Skinny Pills Can Paralyze Your Stomach
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/08/25/semaglutide-gastroparesis.aspx
The original Mercola article may not remain on the original site, but I will endeavor to keep it on this site as long as I deem it to be appropriate.
Analysis by Dr. Joseph Mercola Fact Checked August 25, 2023
STORY AT-A-GLANCE
- Semaglutide, sold under brand names Ozempic and Wegovy, can lead to debilitating side effects, including delayed gastric emptying, also known as gastroparesis or stomach paralysis
- Gastroparesis slows or stops the movement of food from your stomach to your small intestine; this results in feeling full longer, which is one mechanism by which semaglutide results in weight loss
- Gastroparesis can also lead to debilitating nausea, vomiting and, in severe cases, dehydration and malnutrition
- Due to the delayed stomach emptying that occurs with semaglutide, the American Society of Anesthesiologists (ASA) released a warning that it could increase the risk of regurgitation and aspiration of food during general anesthesia
- Other risks of these trendy weight loss drugs include intestinal obstruction, pancreatic cancer, thyroid tumors, gallbladder disease and suicidal behavior
The demand for medications promising easy weight loss has skyrocketed, with prescriptions rising 2,082% from 2019 to 2022.1 Semaglutide, more popularly known as Ozempic, is leading the pack, with the hashtag #Ozempic having received 1.2 billion views on TikTok2 as of July 2023 — to give just some indication of its popularity.
Semaglutide is sold under the name Ozempic as a diabetes drug and, in a higher dose, under the name Wegovy as a weight loss drug. It touts weight loss of 14.9% among adults with obesity,3 but it comes at a steep price. Not only does Wegovy cost more than $1,000 a month,4 it can also lead to debilitating side effects, including stomach paralysis.
‘I Wish I Never Touched It’
Joanie Knight took Ozempic for about two years, when she became unable to swallow food. The reason? Her stomach was full of food. Violent vomiting and constant nausea followed, along with a diagnosis of severe gastroparesis, or delayed gastric emptying.5
“I wish I never touched it. I wish I’d never heard of it in my life,” Knight told CNN. “This medicine made my life hell. So much hell. It has cost me money. It cost me a lot of stress; it cost me days and nights and trips with my family. It’s cost me a lot, and it’s not worth it. The price is too high.”6
Gastroparesis slows or stops the movement of food from your stomach to your small intestine. This results in feeling full longer, which is one mechanism by which semaglutide results in weight loss. However, gastroparesis also leads to nausea, vomiting and, in severe cases, dehydration and malnutrition. Diabetes is the most commonly known cause of gastroparesis, due to nerve damage in the stomach.7
However, semaglutide and similar drugs are designed to delay gastric emptying, and nausea and vomiting — common symptoms of gastroparesis — are reported in many who take them. Even Novo Nordisk, which manufactures Ozempic and Wegovy, told CNN these side effects are listed on the label:8
“Gastrointestinal (GI) events are well-known side effects of the GLP-1 [glucagon-like peptide 1] class. For semaglutide, the majority of GI side effects are mild to moderate in severity and of short duration. GLP-1’s are known to cause a delay in gastric emptying, as noted in the label of each of our GLP-1 RA medications. Symptoms of delayed gastric emptying, nausea and vomiting are listed as side effects.”
GLP-1s Dramatically Slow Digestion
Semaglutide is a glucagon-like peptide 1 receptor agonists (GLP-1RAs). As a peptide hormone, GLP-1 is, among other things, part of a group of incretin hormones, which are released when you eat to regulate insulin, along with many other functions.9
Along with affecting insulin, GLP-1 may influence the nervous system, leading to an appetite-reducing response. However, one of their mechanisms is, in fact, delayed gastric emptying — an effect many who take it aren’t aware of. In 2021, Mayo Clinic researchers wrote that “their [GLP-1 agonists and analogs] effects are mediated, at least in part, by retardation of gastric emptying”10 — the hallmark of gastroparesis.
Meanwhile, in Wegovy clinical trials, 44% of those taking the drug experienced nausea while 24% had vomiting and 20% had abdominal pain,11 all common symptoms of gastroparesis. Mayo Clinic researchers also looked at the effects of another GLP-1 receptor agonist, called liraglutide, in adults with obesity.
They found the drug’s weight loss effects were associated with “delay in gastric emptying of solids,”12 and the longer food sat in the stomach, the greater the weight loss effects became. The delay in digestion was dramatic.
While food typically left the stomach in just four minutes among those in the placebo group, it took an average of 70 minutes in those who took liraglutide. For some, the delay was even more — up to 151 minutes. While this decreased somewhat by 16 weeks, with food leaving their stomachs in about 30 minutes, this was still much longer than the seven minutes in the placebo group.13
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WeightWatchers Plans to Promote Obesity Drugs
WeightWatchers is moving into the obesity drug market via its acquisition of telehealth platform Sequence. In a press release, WeightWatchers stated, “Sequence seamlessly integrates the patient and clinician experience for ongoing, clinical care and medication management while providing high-touch support in navigating the insurance approval process.”14
In other words, WeightWatchers members will be able to book a virtual consultation with a clinician and get a prescription for Wegovy or another GLP-1. In fact, Sequence’s program is entirely based around weight loss medications. One of their FAQs is “What if my clinician determines a prescription is not right for me?”15
The answer is you’ll take an intake quiz and have an initial consultation, but, “Your program only begins if your clinician determines that you’re a good fit.” In other words, you’re virtually guaranteed to get a prescription if you sign up.
Skepticism is wise in this case, as the number of significant side effects tied to the drugs continues to increase. On social media, many members were taken aback by the move, saying it “rubbed them the wrong way.”16 As Rolling Stone reported:17
“The move seems to be at odds with the longstanding tenets of the program. WeightWatchers, which was first started in 1963 and instituted in strip malls across America, has long been touted by its supporters (including Oprah Winfrey herself, who owns stake in the company) as an easier way to lose weight, while avoiding the stigma and temptation of crash diets and weight loss pills.
… Some Weight Watchers users feeling stuck or plateaued in their weight loss have welcomed the change, while a majority in online chat rooms on sites like Facebook and Reddit seem to have more questions than decisions.”
Case Reports Highlight Semaglutide-Induced Stomach Paralysis
Gastroparesis among those taking semaglutide isn’t unheard of. Case studies of two women who suffered from medication-induced gastroparesis were published in the Journal of Investigative Medicine in 2021.18
The first involved a 52-year-old woman who took semaglutide for one month before symptoms, including abdominal pain, bloating and nausea, began. Testing revealed delayed gastric emptying, which resolved after she stopped taking the drug. The second case involved a 57-year-old woman suffering from abdominal bloating, nausea and vomiting for a year.
She had started taking dulaglutide, brand name Trulicity, another GLP-1 receptor agonist, 15 months prior. Testing revealed she had severe delayed gastric emptying, which gradually resolved when the drug was stopped.
However, this isn’t always the case. In Knight’s case and another described by CNN, symptoms did not get better even after they stopped taking the drug. Knight ended up having stomach bypass surgery due to the severe gastroparesis, which left her able to “eat enough that I’m not malnourished.”19
Anesthesiologists Warn Not to Take Ozempic Before Surgery
Due to the delayed stomach emptying that occurs with semaglutide, the American Society of Anesthesiologists (ASA) released a warning for those taking the drugs before elective surgery.20
They suggest stopping this and other GLP-1 receptor agonists before the procedure, as they could increase the risk of complications associated with anesthesia — namely that you could regurgitate food that’s still sitting in your stomach, even if you’ve fasted appropriately.
As a result, they recommend not taking the medications for a day or a week prior to surgery, and possibly delaying the procedure if symptoms such as nausea, vomiting, abdominal pain or bloating are present. In a news release, Dr. Michael W. Champeau, ASA president, explained:21
“While there is currently a lack of scientific data on how GLP-1 receptor agonists affect patients having surgery and interact with anesthesia, we’ve received anecdotal reports that the delay in stomach emptying could be associated with an increased risk of regurgitation and aspiration of food into the airways and lungs during general anesthesia and deep sedation.
These complications can be serious, so we are providing guidance on when GLP-1 agonists should be stopped in advance of an elective procedure.”
The likelihood of those using semaglutide having a full stomach is so high that the ASA suggests using ultrasound to evaluate the stomach contents prior to surgery if a patient hasn’t withheld the drug, stating:22
“If the stomach is empty, proceed as usual. If the stomach is full or if the gastric ultrasound is inconclusive or not possible, consider delaying the procedure or proceed using full stomach precautions. Discuss the potential risk of regurgitation and aspiration of gastric contents with the proceduralist or surgeon and the patient.”
Intestinal Obstruction Risk Rises 3.5-Fold on Semaglutide
These trendy weight loss medications cause other significant risks as well and may even cause a potentially fatal intestinal obstruction. Diabetic patients who use the drugs have a 4.5 times higher risk of intestinal obstruction than those using other medications. A study of 25,617 people also found use of GLP-1Ras increases the rate of intestinal obstruction by 3.5-fold.23
The drugs were also found to increase the length and weight of the small intestine in animal studies, while in humans they may increase intestinal length and villus height; villi are the hairlike projections inside the small intestine that help absorb nutrients. Writing in Acta Pharmaceutica Sinica B, researchers explained how this could seriously affect intestinal function, increasing obstruction risk:24
“Because GLP-1RAs could cause continuous increases in the intestinal length and villus height, the small intestine may become as inelastic and fibrotic as a loose spring, leading to long-term upper intestinal obstruction …”
To date, clinical trials haven’t revealed such changes in the human gut, likely because it’s difficult to measure small intestine length. Further, the most common symptom of these changes is constipation, which can be attributed to many causes — not to mention, the team noted, studies typically aren’t long enough to reveal intestinal obstruction risks:25
“The risk of chronic intestinal obstruction in humans cumulates over time, with the highest occurrence appearing 1.6 years following GLP-1RA treatment. However, clinical trials on GLP-1RAs usually do not last for more than a year …”
Kidney, Cancer Risks Are Also Concerning
The long-term risks of semaglutide are unknown, but already the drug carries a black box warning because rodent studies found semaglutide causes thyroid C-cell tumors “at clinically relevant exposures.”26 Pancreatic cancer is another concern. One patient in the Sustain 5 trial developed metastatic pancreatic carcinoma about 65 days post-treatment.27
A pharmacovigilance study using the FDA Adverse Events Reporting System also looked into “increasing data on the potential risk of pancreatic carcinoma associated” with GLP-1Ras, including semaglutide, finding a clear association.28
“Based on this pharmacovigilance study, GLP-1RAs, except albiglutide, are associated with pancreatic carcinoma,” researchers noted, adding, “Based on the bibliometric investigation, cAMP/protein-kinase, Ca2+ channel, endoplasmic-reticulum stress, and oxidative stress are potential pathogenesis of pancreatic carcinoma resulting from GLP-1RAs.”29
The kidneys also seem to be negatively affected, with two case studies showing acute kidney injury in people taking semaglutide. Both patients had chronic kidney disease as a result of diabetes and “experienced rapid worsening of kidney function and increased proteinuria after being prescribed the GLP-1 receptor agonist semaglutide.”30 Wegovy’s prescribing information also has a sizeable list of warnings and precautions, including for:31
| Acute pancreatitis | Acute gallbladder disease |
| Hypoglycemia | Acute kidney injury |
| Hypersensitivity reactions, including anaphylactic reactions and angioedema | Diabetic retinopathy complications |
| Heart rate increase | Suicidal behavior and ideation |
Better Options for Weight Loss
It is my strong belief that we will never see the “miracle cure” drugs for weight loss in our lifetime. Using drugs to lose weight could lead to permanent, debilitating health problems — and if we do, it’s likely you’ll regain the weight if you ever stop taking them.
Fortunately, there are solutions that we know today that address the fundamental reason why most people gain weight, which is insulin resistance secondary to mitochondrial dysfunction from excess reductive stress. Excess linoleic acid (LA) from seed oils is the primary cause of mitochondrial reductive stress.
Participants in one study regained two-thirds of their prior weight loss, and most of the changes in cardiometabolic variables also reverted back to pretreatment levels one year after stopping semaglutide.32 Fortunately, there are better ways to lose weight that don’t put your health at risk. Top strategies include:
• Reducing your intake of seed oils while increasing your intake of healthy fats — Consuming too much linoleic acid is the primary factor driving the overweight and obesity epidemics. LA is a type of omega-6 fat found in seed oils like soybean, cottonseed, sunflower, rapeseed (canola), corn and safflower.33
Consider cutting LA down to below 5 grams per day, which is close to what our ancestors used to consume before chronic health conditions, including obesity, became widespread.
Ideally the actual amount though is better defined as a percentage of daily calories. LA should be less than 2% of your daily calories. I was able to get my percentage down to 0.8%. You don’t need expensive lab tests, as all you need to do is carefully enter your food data into Cronometer and it will tell you your percent.
• Avoiding nearly all ultraprocessed foods, fast foods and restaurant foods — Virtually all of them contain seed oils. The easiest way to do this is to prepare the majority of your food at home so you know what you are eating.
• Using time restricted eating (TRE) — Our ancient ancestors did not have access to food 24/7, so our genetics are optimized to having food at variable intervals, not every few hours. When you eat every few hours for months, years or decades, never missing a meal, your body forgets how to burn fat as a fuel.
Most people who practice TRE limit the time they consume food to eight to 10 hours or less on most days of each week. In one study, adults with obesity who used an eight-hour eating window lost more weight, and had better improvements in diastolic blood pressure and mood, than those who used a 12-hour or more eating window.34
Although TRE is an amazing tool initially for most people, once you regain insulin sensitivity you want to increase your food window to 10 to 12 hours.
- 1 Komodo Health February 17, 2023
- 2 TikTok, #ozempic
- 3 N Engl J Med 2021; 384:989-1002
- 4 Reuters July 11, 2023
- 5, 6, 8, 13, 19 CNN Health July 25, 2023
- 7 National Institute of Diabetes and Digestive and Kidney Diseases, Gastroparesis, Symptoms & Causes
- 9 Substack, Modern Discontent March 28, 2023
- 10 Adv Exp Med Biol. 2021;1307:171-192. doi: 10.1007/5584_2020_496
- 11 Wegovy Prescribing Information, Page 10
- 12 Lancet Gastroenterol Hepatol. 2017 Dec;2(12):890-899. doi: 10.1016/S2468-1253(17)30285-6. Epub 2017 Sep 27
- 14 Globe Newswire March 6, 2023
- 15 Sequence, FAQs
- 16, 17 Rolling Stone July 30, 2023
- 18 J Investig Med High Impact Case Rep. 2021 Jan-Dec; 9: 23247096211051919
- 20, 21, 22 American Society of Anesthesiologists June 29, 2023
- 23, 24, 25 Acta Pharmaceutica Sinica B May 2023, Volume 13, Issue 5, Pages 2291-2293
- 26 NovoMedLink.com Wegovy, Important Safety Information
- 27 J Investig Med. 2022 Jan; 70(1): 5–13., Precautions
- 28, 29 Int J Clin Pharm. 2023 Mar 28. doi: 10.1007/s11096-023-01556-2
- 30 Kidney Medicine March-April 2021, Volume 3, Issue 2, Pages 282-285
- 31 Wegovy Prescribing Information, Page 1
- 32 Diabetes, Obesity and Metabolism April 19, 2022
- 33 Int J Mol Sci. 2020 Feb; 21(3): 741
- 34 JAMA Internal Medicine August 8, 2022