Anemia
now browsing by category
Chronic Kidney Disease: A Hidden Threat to Your Heart
Story at-a-glance
- Chronic kidney disease often develops silently for years, but even early kidney damage sharply increases your risk of heart attack, stroke, heart failure, and dangerous heart rhythm problems
- Two common tests called eGFR and UACR reveal hidden kidney stress long before symptoms appear and provide an early warning sign that your cardiovascular system is already under strain
- Researchers discovered that damaged kidneys release microscopic particles into the bloodstream that directly injure heart muscle cells, weaken heart contractions, and disrupt the electrical timing of the heartbeat
- Chronic inflammation, fluid overload, high blood sugar, excess sodium retention and overactivation of the nervous system create a destructive cycle that damages both the kidneys and the heart simultaneously
- Daily habits that improve metabolic health, including stable blood sugar, regular movement, lower intake of seed oils, restorative sleep, and healthy circulation, help reduce long-term stress on both organs before irreversible damage develops
Your kidneys do far more than filter waste. They shape your blood pressure, your circulation, your fluid balance, and even the rhythm of your heartbeat. When they start to falter, the damage rarely announces itself. There’s no chest pain, no dramatic warning sign, no clear moment when something feels wrong. Instead, kidney function slips downward year after year while you continue to feel mostly fine, which is exactly what makes chronic kidney disease so dangerous.
Here’s what most people don’t realize: when kidneys start failing, the first organ to suffer often isn’t the kidneys. It’s the heart. Long before dialysis ever enters the conversation, injured kidneys begin reshaping the cardiovascular system. Most adults can recite their cholesterol number from memory, yet very few could tell you whether their kidneys are filtering normally or already under stress.
The tests that would reveal the answer are inexpensive, widely available, and often already sitting inside routine bloodwork, but the results rarely get explained in a way that connects them to heart attack, stroke, or heart failure risk. Recent research has uncovered something startling: damaged kidneys actively release particles into the bloodstream that travel to the heart and injure cardiac muscle cells directly.
The kidneys aren’t just failing alongside the heart; they’re actively damaging it. Understanding this connection gives you something powerful: the chance to intervene while the damage is still reversible.
2 Simple Kidney Tests Reveal Hidden Heart Danger
Harvard Health Publishing examined the growing evidence linking chronic kidney disease to cardiovascular disease and explained why doctors now view the kidneys and heart as deeply connected systems rather than separate organs.1 Dr. John Ostrominski from Harvard-affiliated Brigham and Women’s Hospital stressed that chronic kidney disease often goes unnoticed even though it affects about 1 in 7 U.S. adults.
Early chronic kidney disease often develops silently because the kidneys compensate for damage over long periods. You might feel normal while kidney function steadily declines. Once symptoms finally appear, they often include swelling in the legs or ankles, fatigue, trouble breathing, exercise intolerance, and changes in urination. By that stage, substantial damage has already occurred. This is exactly why early testing changes outcomes.
You gain a chance to slow progression before the disease starts affecting circulation, fluid balance, and heart function.
• Two screening tests give an early warning long before a medical emergency develops — The first test is estimated glomerular filtration rate, called eGFR, which measures how effectively your kidneys filter waste from your blood. A score of 90 or higher is considered normal, while values below 60 signal impaired kidney function.
The second test is the urine albumin-to-creatinine ratio, called UACR, which checks whether protein leaks into your urine. Healthy kidneys keep protein inside your bloodstream. Once albumin starts leaking into urine, it signals structural kidney damage.
• Protein leakage in urine strongly predicts future heart problems — Ostrominski explained that elevated UACR levels reveal cardiovascular strain and future heart risk. According to the report, both low eGFR scores and high UACR values are strongly linked with greater risk of heart attacks, strokes, heart failure, and atrial fibrillation, which is an irregular heartbeat rhythm. That means a simple urine test gives you an early look at whether your blood vessels and circulation are already under stress.
• High blood pressure and diabetes damage the kidneys through direct physical strain — Elevated blood pressure forces the body to hold onto more sodium and fluid, increasing pressure inside the tiny blood vessels within the kidneys. Over time, this chronic stress damages the filtration system itself.
Diabetes creates a second layer of injury because prolonged exposure to high blood sugar thickens and damages microscopic kidney blood vessels called capillaries. Once those delicate filters stiffen and narrow, waste removal slows and inflammation rises.
• The kidneys and heart create a feedback loop that worsens both diseases together — Healthy kidneys help regulate blood pressure, fluid levels, and mineral balance, all of which directly affect heart function. When kidney function declines, fluid builds up more easily, blood pressure rises further, and the heart works harder to move blood throughout your body.
That extra strain increases the likelihood of heart enlargement, rhythm disturbances, and heart failure. At the same time, weakened heart function reduces blood flow back to the kidneys, which accelerates additional kidney damage.
• Metabolic dysfunction sits at the center of this entire process — Cardiovascular-kidney-metabolic syndrome, often shortened to CKM syndrome, links obesity, diabetes, high blood pressure, kidney disease, and cardiovascular disease together because they share the same underlying metabolic drivers.2 Excess body fat, poor blood sugar regulation, chronic inflammation, and impaired energy production damage multiple organ systems simultaneously.
Tiny Kidney Particles Damage the Heart Directly
Research published in Circulation investigated why so many people with chronic kidney disease develop heart failure even when doctors aggressively manage blood pressure, diabetes, and cholesterol.3 Researchers studied blood samples from 35 patients with moderate to advanced kidney disease and compared them to healthy controls.
Instead of focusing only on conventional risk factors, the team examined microscopic particles called extracellular vesicles, tiny membrane-covered packages released by cells into the bloodstream.
Think of extracellular vesicles as microscopic mail packages sealed in membrane envelopes. Cells normally use them to send routine messages to other cells. But when kidneys are damaged, they start mailing toxic cargo — genetic instructions and stress signals — that travel through the bloodstream and get opened by heart muscle cells, which then begin shutting down.
These extracellular vesicles carried genetic material and stress signals from injured kidney tissue directly into circulation. Once these particles reached heart muscle cells, they triggered cell death and interfered with the heart’s ability to contract normally. Researchers repeatedly described the kidney-derived vesicles as “cardiotoxic,” meaning directly harmful to heart tissue itself. That changes the entire understanding of kidney disease because the kidneys actively send damaging signals throughout the body.
• The study found direct evidence of heart muscle injury — Researchers exposed healthy heart muscle cells to extracellular vesicles taken from patients with kidney disease. Those cells rapidly showed increased apoptosis, which is programmed cell death. The heart cells began shutting themselves down after exposure to these kidney-derived particles.
Healthy control vesicles didn’t create the same damage. That confirmed the harmful effect came specifically from the diseased kidneys rather than from normal circulation.
• Heart contraction strength also weakened significantly — The study examined how well heart muscle cells squeezed and relaxed after exposure to kidney-derived vesicles. Researchers found impaired contractility, meaning the heart cells struggled to pump efficiently.
Calcium handling inside the cells also became disrupted. Calcium acts like an electrical timing signal that tells heart muscle when to contract and relax. Once calcium balance breaks down, the heartbeat loses efficiency and stability. Over time, this creates the conditions for heart failure and rhythm disturbances.
• The harmful particles carried specific microRNAs linked to tissue damage — MicroRNAs are tiny genetic regulators that switch certain cellular programs on or off. They work like dimmer switches on your genes. Each one can turn down specific cellular activities, including the genes that tell heart muscle how to contract properly. When the wrong microRNAs flood into heart cells, they essentially dim the lights on the machinery that keeps your heartbeat strong.
The researchers identified distinct microRNAs inside the extracellular vesicles that directly interfered with genes responsible for healthy heart contraction. When researchers inserted these microRNAs into laboratory-grown human heart cells, the cells showed the same toxic effects seen earlier in the study. This gave scientists a clearer explanation for how kidney disease physically alters heart tissue at the molecular level.
• The kidney itself appeared to be the source of these toxic signals — Researchers traced the microRNAs back to injured kidney tissue rather than the liver, heart, or immune cells. The strongest signals came from specific kidney cells damaged during chronic disease progression.
That finding reinforced the idea that chronic kidney disease acts as an active driver of heart failure instead of simply existing alongside it. The more severe the kidney dysfunction became, the stronger the cardiovascular injury markers appeared.
• Removing these harmful particles improved heart function in early animal research — Researchers used mice with chronic kidney disease and pharmacologically reduced circulating extracellular vesicles. Heart function improved significantly after the vesicles were depleted. Researchers also observed improvement in heart failure progression. This suggests that reducing the biological stress signals released by damaged kidneys directly lowers strain on the heart.
Researchers described these kidney-derived microRNAs as promising biomarkers for earlier disease detection and future therapies. These microscopic signals could eventually help identify cardiovascular damage years before a major cardiac event occurs.
Tracking kidney function, improving metabolic health, lowering inflammation, and reducing long-term stress on circulation become much more meaningful once you understand that silent kidney injury physically reshapes heart tissue over time.
Kidney Disease Changes Your Entire Cardiovascular System
A 2023 review published in Cardiovascular Research by the European Renal and Cardiovascular Medicine Working Group examined the growing cardiovascular burden inside chronic kidney disease across all stages.4 Researchers explained that cardiovascular complications become the leading cause of death in people with advanced kidney disease and regular dialysis treatment.
The review also highlighted a striking reality: many people with progressive kidney disease die from heart complications before their kidneys fail completely. That means protecting your cardiovascular system early becomes just as important as preserving kidney function.
• Cardiovascular danger rises step-by-step as kidney function declines — Researchers cited a meta-analysis involving more than 1 million individuals showing that death risk climbed sharply as kidney filtration rates worsened.5 Compared to a healthy reference filtration rate, mortality risk increased 18% at moderate kidney impairment, 57% at more advanced decline, and more than tripled in severe kidney dysfunction. Protein leakage into urine independently raised cardiovascular death risk too.
• Heart enlargement begins surprisingly early in kidney disease — The review discussed left ventricular hypertrophy, often shortened to LVH, which means the main pumping chamber of the heart becomes enlarged and thickened from chronic strain. Researchers found LVH already appears in earlier kidney disease stages and affects roughly 70% to 80% of patients with kidney failure on dialysis.
An enlarged heart muscle becomes stiffer, less efficient, and more vulnerable to heart failure and rhythm problems over time.
• Fluid overload places continuous stress on the heart and blood vessels — Damaged kidneys struggle to remove excess sodium and water efficiently. As fluid accumulates, blood pressure rises and the heart must pump harder against greater resistance. Researchers emphasized that volume overload alone doubles death risk in dialysis patients, even independent of other cardiovascular risk factors.
• Inflammation emerged as one of the strongest hidden drivers of damage — The review explained that chronic low-grade inflammation becomes almost universal in advanced kidney disease. Oxidative stress, gut microbiome disruption, metabolic acidosis, and retained waste compounds called uremic toxins all fuel inflammatory signaling. Uremic toxins are waste products the kidneys normally remove.
Once these compounds accumulate, they damage blood vessels, impair nitric oxide production, and increase oxidative injury throughout the cardiovascular system. Researchers noted that inflammation predicted cardiovascular death more strongly than LDL cholesterol in some kidney disease populations.
• The nervous system also becomes trapped in a chronic stress state — Researchers found sympathetic nervous system activity rises dramatically in kidney disease patients and becomes extremely elevated during dialysis treatment. Your sympathetic nervous system controls your “fight-or-flight” response.
Once chronically activated, it raises heart rate, constricts blood vessels, and increases blood pressure around the clock. The review linked this excessive sympathetic activation to higher rates of heart enlargement, arrhythmias, and cardiovascular death.
• Anemia further weakens oxygen delivery and strains the heart — Failing kidneys produce less of a hormone that stimulates red blood cell production. As anemia develops, oxygen delivery throughout the body drops. To compensate, the heart works harder and pumps faster, gradually increasing workload and accelerating structural heart changes. Researchers linked anemia directly to left ventricular hypertrophy and cardiovascular hospitalization risk in kidney disease patients.
• Sedentary behavior sharply increased cardiovascular risk — The review found limited physical activity was extremely common in both kidney disease and dialysis populations because of fatigue, illness burden, and reduced exercise tolerance.
Yet researchers consistently observed that higher physical activity levels strongly associated with lower cardiovascular mortality and fewer hospitalizations. One walking-based intervention reduced hospitalization risk by 29% over 36 months in dialysis patients.6 Movement improves circulation, blood pressure regulation, metabolic health, and mitochondrial energy production all at once.
Lower the Stress Load on Your Kidneys and Heart
Your kidneys and heart respond to the environment you create every single day. Years of metabolic dysfunction, high blood pressure, excess blood sugar, inflammatory foods, poor circulation, and chronic stress gradually damage the tiny blood vessels that keep both organs alive.
Once kidney tissue becomes injured, the research showed those damaged kidneys begin sending harmful signals directly into the bloodstream that weaken heart function too. That means the earlier you reduce the stress load on your body, the better your chances of slowing this cycle before it gains momentum.
1. Track your kidney numbers like a personal health score — Many people track weight or cholesterol but ignore the numbers that reveal silent kidney stress. It’s important to keep track of your eGFR and UACR values the same way you do your blood pressure. Those two markers often change years before symptoms appear.
Create a simple habit tracker on your phone or calendar and record your blood pressure and kidney labs whenever you get bloodwork done. Watching those numbers improve gives you direct feedback that your daily habits are reducing strain on your circulation and filtration system instead of damaging them further.
2. Lower blood sugar spikes before they injure tiny blood vessels — Chronic high blood sugar acts like fine sandpaper on the microscopic blood vessels inside your kidneys, gradually scarring the delicate filters they depend on. That same damage weakens circulation throughout your entire cardiovascular system. Your body runs far more efficiently when blood sugar stays stable.
Build meals around high-quality protein, collagen-rich foods, fruit, root vegetables, and other healthy carbohydrates instead of ultraprocessed foods, like seed oils, and sugary snacks.
If your digestion is compromised, with regular bloating or irregular bowel movements, begin with easier-to-digest carb sources like whole fruit and white rice before introducing harder-to-digest starches. Most adults need about 250 grams of carbohydrates per day from whole-food sources. This steady fuel supply turns your mitochondria back on and keeps your metabolism resilient.
3. Remove the inflammatory oils that damage cellular energy production — Seed oils, including soybean, corn, sunflower, safflower, and canola oils, are high in the polyunsaturated fat linoleic acid (LA), which places enormous oxidative stress on blood vessels, mitochondria, and kidney tissue when consumed in excess. Restaurant foods, packaged snacks, salad dressings, sauces, and processed convenience meals flood your body with these unstable fats that accumulate in tissues over time.
Replace those oils with grass fed butter, ghee, or tallow. If you eat animal protein, prioritize lower-PUFA ruminant meats instead of conventionally raised chicken or pork. Small daily swaps create a measurable reduction in inflammatory stress over months and years.
4. Use movement to improve circulation and metabolic function every day — Both organs run on the same fuel: steady, healthy blood flow. Every hour you spend sitting, that flow slows — and both kidneys and heart pay the price. Focus less on exhausting workouts and more on daily movement consistency because your body responds best to repetition.
Start with 20 minutes of walking daily and build toward an hour, along with resistance training twice a week. Also work in regular daily activity, like yardwork and frequent standing instead of sitting.
5. Restore your circadian rhythm to reduce chronic stress signals — Poor sleep and artificial light exposure raise stress hormones, worsen blood sugar regulation, and increase blood pressure strain on your kidneys and heart. Morning sunlight exposure helps reset your body clock and improves cellular energy production. I recommend getting outside shortly after sunrise and again near solar noon when possible.
However, if your diet has been high in seed oils, avoid peak sun exposure (10 a.m. to 4 p.m.) until you have removed them for at least six months, as excess LA stored in tissues increases susceptibility to sunburn and oxidative stress. At night, lower blue light exposure from phones, tablets, and televisions to support melatonin production inside your mitochondria.
FAQs About Kidney Disease and Your Heart
Q: How do I know if my kidneys are affecting my heart?
A: Most people don’t feel symptoms early on. Hidden kidney stress often shows up first through abnormal eGFR and UACR test results, which reveal declining filtration function and protein leakage into urine. Research showed these changes strongly predict higher risk of heart attack, stroke, heart failure, and irregular heartbeat rhythms long before severe symptoms appear.
Q: What causes chronic kidney disease to damage the heart?
A: Damaged kidneys increase fluid retention, raise blood pressure, disrupt mineral balance, and trigger chronic inflammation. Research also found injured kidneys release microscopic particles into the bloodstream that directly damage heart muscle cells and weaken your heart’s ability to contract efficiently. Over time, this creates a feedback loop where kidney dysfunction and heart strain worsen each other simultaneously.
Q: What are the early warning signs of chronic kidney disease?
A: Early chronic kidney disease often stays silent for years. As damage progresses, common symptoms include swelling in the ankles or legs, fatigue, shortness of breath, exercise intolerance, muscle cramps, fluid retention, and changes in urination patterns. Many people discover kidney dysfunction only after routine blood or urine testing.
Q: What lifestyle changes help protect both the kidneys and the heart?
A: The most effective strategies focus on reducing the root causes driving metabolic and vascular stress. Stable blood sugar, lower blood pressure, regular movement, restorative sleep, and reducing inflammatory processed foods all lower strain on both organs. Daily walking, resistance training, whole-food carbohydrates, adequate protein, and avoiding seed oils help improve circulation, mitochondrial energy production, and long-term cardiovascular resilience.
Q: Why does inflammation matter so much in kidney disease?
A: Inflammation damages blood vessels, stiffens arteries, and increases oxidative stress throughout the cardiovascular system. Researchers found inflammation becomes extremely common as kidney function declines because waste compounds, called uremic toxins, begin accumulating in the bloodstream. Chronic inflammation also increases sympathetic nervous system activity, raises blood pressure, and accelerates heart enlargement and heart failure risk.
All About Phytic Acid and Phytates – Good and Bad
Reproduced from original article:
https://www.precisionnutrition.com/all-about-phytates-phytic-acid
By Ryan Andrews, MS, MA, RD, RYT, CSCS
Phytic acid – the storage form of phosphorus – is one of those pesky “anti-nutrients” the Paleo community keeps telling you to avoid.
It’s often considered an anti-nutrient because it binds minerals in the digestive tract, making them less available to our bodies.
Yet these same anti-nutrient properties can also help in the prevention of chronic disease.
What is phytic acid?
Seeds — such as nuts, edible seeds, beans/legumes, and grains — store phosphorus as phytic acid. When phytic acid is bound to a mineral in the seed, it’s known as phytate.
The tables below compare various seed types according to their phytic acid/phytate content.
Whole grains
Legumes
Nuts
Oil seeds
As you can see, phytic acid content varies greatly among plants. This is due to the type of seed, environmental condition, climate, soil quality, how phytate is measured in the lab, and so forth.
Roots, tubers, and other vegetables may also contain phytic acid, but usually in lower amounts.
The most concentrated sources tend to be whole grains and beans. Phytic acid is isolated in the aleurone layer in most grains, making it more concentrated in the bran. In legumes, it’s found in the cotyledon layer (where the protein is).
Phytate = phytic acid bound to a mineral
Phytates perform an essential role in plants, as they are an energy source for the sprouting seed. When a seed sprouts, phytase enzymes break down the stored phytates.
When we eat the plant, phytates are hydrolyzed during digestion to myo-inositol-1,2,3,4,5,6-hexkisphosphate (IP6) and lower inositol polyphosphates including IP1 through IP5 (these are phytate degradation products).
Who’s eating phytic acid?
Everyone who eats plants consumes some phytic acid. It’s all a question of degree.
As you can imagine, intake tends to be much higher among those who follow non-Westernized diets. In developing countries, plants are staple foods, which means people eat more of them, and therefore get more phytic acid.
In developed countries, plant-based or vegetarian eaters tend to consume more phytic acid than omnivores. Further, males usually consume more phytic acid than females, simply because they eat more food.
Phytate digestion
Most phytate (37-66%) is degraded in the stomach and small intestines.
Ordinarily, our bodies regulate phytate levels pretty well, adjusting uptake in the gut and excretion until body levels come into balance.
Vitamin D status in the body seems to influence how much phytate is actually retained. The more vitamin D, the more phytate retained; the less vitamin D, the less phytate retained.
Potential problems with phytic acid
Phytic acid can bind minerals in the gut before they are absorbed and influence digestive enzymes. Phytates also reduce the digestibility of starches, proteins, and fats.
Here’s an example.
Vegan eaters often consume more iron than omnivores. Yet, they also consume more anti-nutrients, including phytates, and these reduce the amount of iron available to their bodies. Consuming 5-10 mg of phytic acid can reduce iron absorption by 50%.
This is why vegetarian eaters should eat more iron than omnivores (33 mg for veg eaters vs. 18 mg for omnivores).
Daily iron loss for men & women
- Adult men lose ~1 mg of iron per day
- Adult menstruating women lose ~1.4 mg/day
- Postmenopausal women lose ~0.8 mg/day
- Lactating women lose ~1.1 mg/day
While in the intestines, phytic acid can bind the minerals iron, zinc, and manganese. Once bound, they are then excreted in waste.
This can be a good or bad thing, depending on the condition. It’s a bad thing if you’re having trouble building up iron stores in the body and have developed iron-deficiency anemia.
When is it a good thing? Keep reading – you’ll find potential benefits of phytic acid below.
Potential benefits of phytic acid
Despite its potential drawbacks, phytic acid is similar in some ways to a vitamin, and metabolites of phytic acid may have secondary messenger roles in cells.
Some experts even suggest that it’s the phytic acid in whole grains and beans that lends them their apparent protective properties against cardiovascular disease, cancer, and diabetes.
(Remember, the grains with little to no phytic acid are the refined ones.)
The supplement industry has caught on to this. Have you even seen a bottle of inositol hexaphosphate, or IP6? That’s simply a supplemental source of phytic acid.
When phytic acid binds minerals in the gut, it prevents the formation of free radicals, thus making it an antioxidant. Not only that, but it seems to bind heavy metals (e.g., cadmium, lead) helping to prevent their accumulation in the body
Phytic acid’s preventative properties
Cancer
Foods higher in phytic acid seem to enhance the activity of natural killer cells and inhibit tumor growth.
Those who consume more phytic acid are less likely to succumb to breast and prostate cancer. Exposing the colon to less iron seems to decrease the risk of colon cancer. And phytic acid might reduce the side effects of chemotherapy.
Cardiovascular disease
Phytic acid helps prevent hardening of the arteries and platelet formation.
Kidney stones
With some phytate being excreted in the urine, this may improve kidney health and prevent stones.
Insulin resistance
Phytic acid plays a role in pancreatic function and insulin secretion. And it may reduce the glycemic response from meals, meaning you feel full for longer.
Hemochromatosis
Hemochromatosis, or iron overload, is a common genetic disorder that phytic acid’s iron-binding properties can protect against or reduce.
In the balance
Is phytic acid worth worrying about? Maybe not, for most of us.
One study showed that subjects consuming a Mediterranean-style diet that included 1000-2000 mg of phytic acid per day did not suffer from reduced mineral bioavailability.
At the same time, certain people might have to be more wary.
In particular, iron intake and absorption can be critical for infants nearing six months of age. So when plants are added to infants’ diets, it may be important to adopt strategies to reduce phytic acid and enhance iron absorption.
Overcoming phytic acid as an antinutrient
Luckily, it’s possible to overcome the anti-nutrient effects of phytic acid in our foods while still getting the benefits of a plant-rich diet. Here are a few strategies that my be more or less helpful depending on the specific situation:
Heat
Heating foods can destroy small amounts of phytic acid. (Note: heat can also destroy phytase and vitamin C.)
Processing
Milling grains and removing the bran decreases phytic acid. Unfortunately, milling also tends to remove many of the minerals! Removing the bran and then enriching a food with minerals might allow for enhanced nutrient absorption in the body.
Soaking
Soaking beans and grains can reduce phytic acid (and other antinutrients).
Fermenting
Fermentation and bread leavening (using yeast) can help to break down phytic acid due to the activation of native phytase enzymes, reducing the number of phosphate groups.
This is big stuff since myo-inositol phosphates with fewer than five phosphate groups don’t inhibit zinc absorption (IP1 to IP4). And those with fewer than three phosphate groups don’t inhibit iron absorption (IP3 to IP2).
Also, some of the acids produced during fermentation might actually boost absorption of certain minerals.
Sprouting
Sprouting and malting enhances native phytase activity in plants and thus decreases phytic acid.
Vitamin C
Vitamin C appears strong enough to overcome phytic acid. In one study, adding 50 mg of vitamin C counteracted the phytic acid load of a meal. In another study, 80 mg of ascorbic acid (vitamin C) counteracted 25 mg of phytic acid.
Protein powders
During processing of plant-based protein powders, it’s possible to de-phytinize (via addition of microbial phytase). Also, protein isolates and concentrates can be treated with dialysis or ultrafiltration to remove phytic acid.
Seed breeding
Scientists are working on seed breeds containing less phytic acid. There are modern seed hybrids of grain and legume plants that contain less phytic acid.
Animal protein
Animal protein may enhance absorption of zinc, iron, and copper. Adding small amounts of animal protein might increase the absorption of these minerals in the body. (Well, except for dairy/casein, as it also seems to hinder iron and zinc absorption.)
Gut health
A low pH in the gut enhances iron absorption. Balancing the level of beneficial bacteria in the GI tract might help with this. See All About Probiotics.
Bonus: Can other animals digest phytic acid?
Ruminant animals (e.g., cattle, sheep, goats, buffalo) possess phytase producing flora for digesting phytic acid.
Non-ruminant animals (e.g., pigs, chickens, dogs, cats) don’t have phytase producing flora, so phytic acid passes through them undigested and makes its way into the soil.
Feeding livestock too much grain can inhibit mineral absorption and increase phosphorus excretion, leading to pollution. Ever heard of the Dead Zone in the Gulf of Mexico?
Summary and recommendations
In healthy people eating balanced diets, phytic acid’s effects on iron, zinc, and manganese status is minimal and it doesn’t seem to cause nutrient deficiencies.
To argue that some plant foods are “unhealthy” because of their phytic acid content seems mistaken, especially when phytic acid’s potential negative effects on mineral assimilation may be offset by its health benefits.
So we should aim to reduce phytic acid rather than eliminate it.
To reduce the anti-nutrient effects of phytic acid in foods, try the following:
- Soak, sprout, ferment, and cook plant foods.
- Consume vitamin C-rich foods with meals that contain phytic acid. Dense source of vitamin C include guava, bell pepper, kiwi, oranges, grapefruit, strawberries, Brussels sprouts, cantaloupe, papaya, broccoli, sweet potato, pineapple, cauliflower, kale, lemon juice, and parsley.
- Use vinegar in salad dressings and cooking to enhance mineral absorption and offset phytic acid.
- Supplement with phytase enzymes if necessary.
- Eat mineral fortified foods if necessary
- Supplement minerals if there is still a shortfall in your diet.
- If you’re eating a plant-based diet and have confirmed nutrient deficiencies, and you’ve tried all the above strategies with no success, adding small amounts of animal foods on occasion might boost stores of necessary minerals in your body.
The Silent Epidemic of Excess Iron
Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/03/10/high-iron.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 March 10, 2024
STORY AT-A-GLANCE
- High iron is an under-recognized health threat. There’s a general lack of awareness in the medical community regarding the potential health risks associated with high iron levels
- A ferritin level above 100 typically means you’re either inflamed, have high iron, or both. A level above 200 is considered pathological. The higher your ferritin level, the shorter your lifespan. You’re also more likely to die of a heart attack and cancer
- Left untreated, high iron levels can cause liver damage and an increased susceptibility to certain diseases, including infections and cancer
- Lab tests that can help diagnose iron-related conditions such as hemochromatosis include a full iron panel, a complete blood count (CBC) test, gamma-glutamyl transferase (GGT), and a comprehensive metabolic panel to ensure you have sufficient liver enzymes. Measuring your copper and ceruloplasmin levels can also be helpful
- The easiest way to lower your iron is to donate blood on a regular basis. Natural supplements such as curcumin, silymarin and alpha-lipoic acid can also help prevent from continuing to accumulate iron from your food
In this interview, Christy Sutton, D.C., reviews the dangers of excessive iron. While most doctors look for iron deficiency, few ever pay attention to elevated iron. Sutton is the author of two books, “Genetic Testing: Defining Your Path to a Personalized Health Plan: An Integrative Approach to Optimize Health,” and “The Iron Curse, Is Your Doctor Letting High Iron Destroy Your Health?”
Iron plays an important role in health, especially for children and young adults. Without sufficient iron, you’re not going to be able to form red blood cells and certain proteins in your mitochondria that are responsible for producing energy. On the flip-side, an excess of iron can cause significant damage.
A Silent Epidemic
Sutton’s interest in iron has been “lifelong” she says, as she struggled with low iron while her husband has a genetic anomaly that causes him to have elevated iron levels. So, she has personal experience with both ends of the spectrum.
“I have Crohn’s [disease], celiac, and lost part of my small intestine due to Crohn’s when I was 16,” she says. “Because of that, I have to take a bile sequestrant. Then, being menstruating female who’s had a child, low iron has been something that I have been watched very closely for and I had to take iron a lot.
Like a lot of clinicians, when I came into practice, I seemed to be more hyper-focused on people’s problems that were my own problems. I dealt with iron issues. So, I wanted to watch my patients’ iron levels closely. Then I realized, ‘Oh, not everybody is low. A lot of people actually have high iron.’
It wasn’t until I was writing my first book, ‘Genetic Testing: Defining Your Path to a Personalized Health Plan,’ that I discovered the hemochromatosis genes. I realized that my husband had a hemochromatosis gene, and I realized that that was why I kept telling him to donate blood.
His doctor would order iron labs, ferritin, CBC, and he would get elevated iron often, high ferritin. He was developing high liver enzymes and his red blood cells were getting high as well, which is a common issue with people that have too much iron …
He went to a gastroenterologist, because he was trying to figure out why his liver enzymes were high. I thought it was the high iron, but that was presented to the gastroenterologist and dismissed. So, they went down this rabbit hole of misdiagnosing him with autoimmune hepatitis.
Later we went to a hematologist where we figured out he had hereditary hemochromatosis. So, it’s not something that’s particularly difficult to treat. Removing blood, diet supplements, things like that can help.
But once I got really savvy about looking for the genes and the labs combined, I realized that this is a silent epidemic that is not really being talked about. I would tell people, ‘You have a problem with high iron,’ and then they would often go and get a second opinion.
Their second opinion would say, ‘You’re fine. Don’t worry about it,’ which is a common issue where people are getting high iron labs that should warrant more investigation and then they’re just getting dismissed.”
How to Lower Your Iron Level
I have beta thalassemia, a hemolytic anemia that results in a high turnover of red blood cells. My red blood cells only live about two months, rather than the normal three months. As a result, my iron tends to accumulate because of the rapid turnover. So, while I do not have the hemochromatosis gene, it results in similar problems. I inherited it from my father, who had a ferritin level close to 1,000 by the time he was diagnosed. Ideally, it should be below 40.
One of the supplements he tried was inositol, also referred to as hexaphosphate or IP-6, but it did nothing. I rapidly came to the conclusion that the supplements typically recommended for high iron are useless and potentially even dangerous, because they prevent you from doing what is really helpful, which is to remove iron through regular phlebotomies.
The most effective way to lower your iron is to donate blood two to four times a year. If losing 10% of your blood in one sitting is problematic for you, then you can remove blood in smaller amounts once a month on the schedule I have listed below. If you have congestive heart failure or severe COPD, you should discuss this with your doctor, but otherwise this is a fairly appropriate recommendation for most.
| Men | Postmenopausal Women | Premenopausal Women |
| 150 ml | 100 ml | 50 ml |
As it turns out, Sutton did not include IP-6 in her book, as she couldn’t find any research to back up the claims. She doesn’t dismiss all supplements, however. One of the most helpful, in her view, is curcumin.
“Clinically, I have seen curcumin’s ability to lower iron almost to a fault,” she says. “It’s annoying to me, because I can’t take curcumin for inflammation because it makes me low in iron. But for people that are high in iron or even inflamed with high iron, high ferritin, that’s a great place to start, because curcumin binds to iron.
It also has all of these other wonderful health promoting properties. It’s so good for your brain — it actually helps remove excess iron from the brain and other organs, the heart, liver, spleen.
So, unlike other iron chelators that might be used pharmaceutically, it doesn’t have all these possible negative side effects, but it works very effectively. I mean, I’ve seen it be used in hereditary hemochromatosis patients to lower iron without blood removal … Now, people that have really high iron might need 3 grams a day, which can create diarrhea. So, you have to look at other potentially limiting factors.”
She also recommends taking curcumin with an iron-rich meal, such as shellfish or red meat, to inhibit iron uptake. Other supplements that help bind iron include silymarin, (an extract from milk thistle). It too is very good for hemochromatosis patients, because it lowers iron and helps protect and repair the liver. Another thing that binds to and lowers iron is alpha-lipoic acid. It’s also great for protecting nerves and lowering blood sugar.
“I don’t think silymarin lowers iron quite as much as curcumin, but it’s still a significant way to lower iron,” she says. “The best way to take these — to lower iron — is take them with iron-rich meals. If you want to take them just for medicinal properties but not to lower iron, take them away from iron-rich meals.”
Download this Article Before it Disappears
Health Risks Associated With High Iron
The health risks of high iron are manifold and include an elevated risk of skin infections and skin cancer. I suspect high iron may actually be a catalyst when it comes to skin cancer, along with high linoleic acid (LA) intake. LA is oxidized by iron, creating something called lipofuscin, which is basically iron attached to oxidized LA.
A more common term for lipofuscin is liver spots. So, liver spots are a dermal representation of oxidative damage to LA by high iron. Similarly, skin cancer is likely driven by a combination of high LA and high iron. Ancestral LA levels were below 2%. Today, the average is around 25%. If you had normal ancestral levels, you could have higher iron yet not get as much damage.
Understanding Hemochromatosis
There are several potential diagnoses related to iron, including iron deficient anemia, copper deficient anemia, iron overload and hereditary hemochromatosis, and getting to the correct diagnosis can be tricky.
“The nice thing is that you can always fall back on labs,” Sutton says. “You don’t want to just use symptoms to guide you, because if you’re using symptoms, then this person is well far down a pathological path that you could have potentially stopped years ago, if not decades before.”
Starting with hereditary hemochromatosis, this is when you have inherited one of three hemochromatosis genes, which causes increased iron absorption by decreasing hepcidin, a liver protein. If you have the hemochromatosis gene, you don’t make as much hepcidin, causing you to absorb more iron.
That can become pathological, because over time, you just keep absorbing more and more iron, until your body finally runs out of places to put it. The first place that gets overloaded is your liver. After that, your body will store the iron in other organs, such as your heart, pancreas, brain, pituitary gland, gonads, ovaries, testes and skin.
Eventually, the iron will go everywhere because the human body has evolved to hold onto as much iron as possible. The only way, really, to lose iron is through blood loss. This is why menstruating women have a lower risk for high iron and a higher risk for low iron.
“Having said that, when you start looking at the hemochromatosis genes, all bets are off, because you’ll see females that have these hemochromatosis genes that develop high iron … you will even see children with the hemochromatosis genes that develop high iron,” Sutton says.
“I discovered that in my colleague’s 5-year-old, where predatory hemochromatosis was causing her to have severe neurological problems. That was a very difficult thing to get through because the hematologist didn’t really want to deal with it.
When you look at labs, hereditary hemochromatosis can look very similar to non-hereditary hemochromatosis, which is where you have high iron but you don’t have one of those hemochromatosis genes.
So, for you, you have more of a non-hereditary secondary hemochromatosis, because you have that thalassemia issue where your red blood cells are breaking and letting all this iron out and then you develop high iron with potentially low red blood cells.
That’s common with thalassemia. Some people, they don’t have a thalassemia gene and they develop high iron without hemochromatosis gene, because they’re just eating a lot of iron-rich foods and they’re not losing iron through menstruation. This is usually men.”
How to Diagnose Hemochromatosis
When it comes to lab work, Sutton recommends starting with a full iron panel, a complete blood count (CBC) test, gamma-glutamyl transferase (GGT), and a comprehensive metabolic panel to ensure you have sufficient liver enzymes. Measuring your copper and ceruloplasmin levels can also be helpful.
“The full iron panel has the ferritin, the TIBC [total iron-binding capacity], the UIBC [unsaturated iron-binding capacity], the serum iron and the iron saturation. With hereditary hemochromatosis, you develop high ferritin with a high iron saturation. That combination is hereditary hemochromatosis. So, over 45% iron saturation and high ferritin …
With hereditary hemochromatosis, you’ll see high iron, you’ll see the TIBC go low, the UIBC go low. The serum iron often goes high, and then that ferritin will go high. You’ll often see the liver enzymes go high and it’s common to see the red blood cells, hemoglobin, hematocrit go high.
But that doesn’t always happen. These days, so many are taking testosterone. So, you have to always ask, ‘Are you on testosterone?’ Because that can cause red blood cells, hemoglobin, hematocrit to go high as well …
I always get the GGT as a part of the labs that I order. Occasionally, I will see a high GGT when the AST and ALT, which are the other two liver enzymes, are normal. More often than not, I’ll see a high ALT or high AST. Usually, if they’re not drinking alcohol and they just have high iron, you’re going to see that high ALT.”
What’s the Ideal Ferritin Level?
Sutton recommends keeping ferritin below 100. Ferritin above 100 means you’re either inflamed, have high iron, or both. Studies referenced in her book suggest that anything over 200 is pathological. The higher your ferritin level, the shorter your lifespan. You’re also more likely to die of a heart attack and cancer.
“I feel like 100 is high enough that I’m not swooping everybody in, but low enough that I’m not leaving stragglers out,” she says. “Now, if somebody has a ferritin over 100 with an iron saturation that is in the 40s or higher, then I’m highly suspicious of a hemochromatosis gene and I immediately want to get those hemochromatosis genes tested.
If they have a hemochromatosis gene, then we know why they’re high on iron and we know where this story is going — and it’s not going to be a pretty picture most likely. Then it’s time to refer to a hematologist … and talk to them about how to get iron lower …
The key is, if you don’t have a hemochromatosis gene, then you need to figure out ‘Why does this person have high iron? Do they have a thalassemia gene? Are they just eating a lot of iron?’ And then, ‘Do they have hemolysis for some unknown reason?’ That’s a non-hereditary hemochromatosis situation.
The treatment is basically the same, other than you want to use more of the supplements, go really heavy on the supplements to lower iron. If you have plenty of red blood cells and hemoglobin, then therapeutic phlebotomy is a wonderful place to start.
A lot of times people don’t because they either have a thalassemia issue where their red blood cells are getting chewed up too quickly, or they have lost so much blood so quickly because their doctors are just trying to get the iron down that they become low in hemoglobin or red blood cells. Rather than waiting for months for that to recover, you could be doing the supplements to lower the iron.”
The Link Between High Iron and Cushing’s Disease
Sutton’s husband also developed a pituitary tumor that was causing him to have high cortisol (Cushing’s disease). “Ultimately, I think the high iron created a lot of oxidative stress on his pituitary gland,” Sutton says. The only reason he was diagnosed early enough to save him was that they’d been checking his cortisol and DHEA on a regular basis.
“Periodically, they would jump up and then go back down. Then when the hemochromatosis got properly treated and the DHEA was still high, we were like, ‘Why is this happening?’ So we went to the endocrinologist and I said, ‘I’m worried my husband has Cushing’s.’ She was like, ‘He doesn’t have Cushing’s. He doesn’t look like somebody with Cushing’s. His hemoglobin A1C is normal.’
Five months later, he’s having surgery to remove the pituitary tumor. The reason I say that is because for years, he was told, ‘You just need to exercise and lose weight.’ His problem was not exercise. He had a pituitary tumor and hemochromatosis. Hemochromatosis was destroying his liver and his brain and his heart and everything else, and the pituitary tumor was causing him to have high cortisol, which made him look overweight.”
I believe progesterone may be one of the best ways to treat Cushing’s disease, as it very effectively blocks cortisol. Other natural substances that will inhibit cortisol include aspirin, DHEA, pregnenolone, emodin, vitamins A and D, gelatin or glycine, and niacinamide.1
The normal dose for progesterone is 25 to 50 milligrams. For Cushing’s, I would recommend about 300 mg. It’s virtually impossible to overdose on progesterone and there are no downsides to it. One caveat is that you need to administer it correctly to gain the optimal effects.
Avoid creams, pills and suppositories. Instead, mix pharmaceutical grade progesterone with the contents of one natural vitamin E capsule. Mix it with a paperclip or tiny spoon until all the powder is dissolved, then rub it on your gums. Vitamin E is the only natural compound that dissolves progesterone completely. For guidance on how to pick a good vitamin E supplement, see “The Four Hormones Most Adults Need More Of.”
Understanding Iron-Deficient Anemia
As explained by Sutton, iron deficient anemia is a serious issue. Children born of women with iron-deficient anemia have significantly higher risk of low IQ, ADD, ADHD and other neurological issues that often do not go away with age.
“Many kids suffer from low iron, because they eat a lot of calcium rich foods. Calcium binds to iron, and then you get low in the iron. Maybe they’re picky eaters, they’re growing rapidly. So many kids are not being checked for their iron levels and they’re being diagnosed with ADHD when their problem is actually just low iron, because if you don’t have enough iron, you can’t make dopamine. So, low iron is a serious issue.”
People with iron-deficient anemia will typically have high TIBC and UIBC, as their bodies are trying to mobilize more iron. Serum iron and iron saturation will be low and ferritin will typically be below 30.
“Now, iron deficient anemia is more complicated in many ways because the question is, why are you low in iron?” Sutton says. “There’s so many reasons that you can be low in iron. Are you just not eating enough? Are you not absorbing it? I think the most common reasons that people develop low iron is because they have a GI bleed. They have intestinal malabsorption issues, maybe undiagnosed celiac disease.
There is a gene that can cause you to be more likely to have low iron. I have that gene and that gene actually causes you to make more hepcidin. With iron-deficient anemia you’ll also see low red blood cells sometimes, low hemoglobin and low hematocrit. MCH [mean corpuscular hemoglobin] might get low, MCV [mean corpuscular volume] might get low.”
Copper Deficiency Can Cause Both Low and High Iron
One common cause for iron-deficient anemia is a deficiency in copper. Paradoxically, lack of copper is also a common cause for iron overload. Sutton explains:
“The reason for that is because copper is necessary for two key enzymes. The first one is called hephaestin and the second one is called ceruloplasmin. Hephaestin is in the lining of the gut, the intestinal lining. Copper is necessary for iron to be absorbed in the gut lining. So, without copper, you will not absorb iron and you will develop iron deficient anemia.
Once iron has been absorbed in the gut lining by hephaestin, it passes it off to ceruloplasmin, which is the second copper-rich enzyme. Ceruloplasmin basically then allows that copper to transfer in and then move throughout the body. So, without ceruloplasmin, iron gets stuck in the tissues. It’ll get stuck in the digestive system, it’ll get stuck in the retina, it’ll get stuck in the brain, it’ll get stuck in the liver.
So, you develop iron overload in the tissues. But eventually, if you’re low in copper long enough, you might then become low in iron, and then you don’t end up with all this extra iron in the tissues. The solution is take copper to fix that problem. That’s the way you solve copper-deficient anemia.
Copper-deficient anemia looks very similar to iron-deficient anemia if you’re looking at the iron panel. You’ll have a high TIBC, high UIBC, low serum iron, low iron saturation, low ferritin. You’ll also potentially see low neutrophils and low white blood cells, because you need copper to have normal immune function as well. So, you might be more at risk for infections.
Then of course you can look at the ceruloplasmin. I don’t find ceruloplasmin to be the easiest lab to look at, because it’s an inflammatory marker … If you’re taking hormones like estrogen or birth control or you’re pregnant or you’re just inflamed or have an infection, ceruloplasmin can jump around and go high.
If you have a low or low-normal ceruloplasmin, and then you take copper and ceruloplasmin goes up, that’s a good sign that you didn’t have enough copper.”
How to Get More Iron Into Your Diet
The best way to get iron is through your diet. Shellfish and beef are iron-rich foods with highly absorbable iron. That’s key, because there are two types of iron: heme iron and non-heme iron, the latter of which is not very absorbable. Heme iron is found in animal products while non-heme iron is found in vegetables such as spinach.
“If you’re not eating iron-rich foods like red meat, then you’re more likely to get low in iron if that is something that you struggle with,” Sutton says. “If you struggle with being high in iron, maybe you don’t want to eat as many of those things or maybe you just want to remove blood and supplement accordingly, so that you continue to eat those things.
The form that I like if I’m going to go to a supplement is ferrous peptonate, which I found to be the gentlest on my gut but also get the iron levels up. I really don’t like ferrous sulfate, which is the most common given iron. I don’t think it works very well, and it tends to create a lot of stomach pain. I always have to take my iron with food and sometimes I’ll add copper or vitamin C to it. If I don’t take it with food, it’s really going to upset my stomach.”
More Information
To learn more, check out Sutton’s books, “Genetic Testing: Defining Your Path to a Personalized Health Plan: An Integrative Approach to Optimize Health,” and “The Iron Curse, Is Your Doctor Letting High Iron Destroy Your Health?”