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Posted by: | Posted on: April 7, 2024

‘Long Vax’ Finally Enters Lexicon


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/04/05/covid-vaccine-long-vax.aspx

Analysis by Dr. Joseph Mercola     April 05, 2024

covid vaccine long vax

Story at-a-glance

  • Dr. Pierre Kory and Dr. Paul Marik are trying to get the word out that long vax is not only real but has disabled many Americans who were at the peak of health prior to getting a COVID jab
  • At Kory’s long COVID clinic, 70% of the patients actually have long vax and reported their symptoms began “minutes, hours, days or several weeks” after receiving a COVID-19 shot
  • Long vax symptoms are nearly identical to those of long COVID — the difference being that the long vax patients tend to be sicker, with more frequent small fiber neuropathy and dysautonomia
  • A study by Yale scientists detailed long vax, which they called chronic post-vaccination syndrome, in 241 people
  • Top reported symptoms include exercise intolerance, excessive fatigue, numbness, brain fog and neuropathy

An estimated 6.4% of U.S. adults have experienced symptoms of long COVID, a term used to describe a complex disorder that persists for three or more months after contracting COVID-19.1 While long COVID has been extensively covered in the media, millions more suffer from long vax — a condition with nearly identical symptoms to long COVID, but often even more severe.

New York pulmonologist Dr. Pierre Kory and Dr. Paul Marik, a critical care doctor formerly with Sentara Norfolk General Hospital in East Virginia, are part of the Front Line COVID-19 Critical Care Working Group (FLCCC). They’re trying to get the word out that long vax is not only real but has disabled many Americans who were at the peak of health prior to getting a COVID jab.2

At Long COVID Clinic, 70% of Patients Have Long Vax

Kory opened a tele-health practice that specializes in treating COVID disease, including long COVID. Kory says:3

“Long COVID, although a new name, is not a new disease. It meets the diagnostic criteria for a decades-old condition called myalgic encephalitis/chronic fatigue syndrome (ME/CFS).

The three symptom ‘pillars’ which lead to the diagnosis are fatigue, post-exertional malaise (PEM), and ‘brain fog’ (i.e. cognitive deficits ranging from word finding difficulties, short term memory loss, inability to focus/comprehend, and more rarely confusion or disorientation).

Although this triad is present in nearly every patient I see (rarely brain fog is missing), the patients also present with a ‘side menu’ of problems which can include sensory neuropathies, dysautonomia/POTS, motor neuropathies, abdominal issues, musculoskeletal complaints, and cranial symptoms (i.e tinnitus, vertigo, headaches, vision, hearing loss, smell loss, taste loss).

Many of my patients are debilitated and meet criteria for disability, despite the majority reporting being in the peak of health and functioning prior to the pandemic.”

Yet, Kory and colleagues quickly noticed that most of their patients reported their symptoms began “minutes, hours, days or several weeks”4 after receiving a COVID-19 shot. While many had also had COVID-19, only a small number tied their symptoms to the viral infection.

While the team initially called the condition post-COVID vaccine injury syndrome, they changed the diagnosis to “long vax” because the symptoms were so close to long COVID — the difference being that the long vax patients tended to be sicker, with more frequent small fiber neuropathy and dysautonomia, Kory said.5

Research Details Neuropathic Symptoms Following COVID-19 Jabs

Scientific studies detailing long vax symptoms continue to emerge. In one study from early in the pandemic, more than two-thirds of those reporting long COVID symptoms had negative antibody tests, suggesting at least some of them didn’t even have COVID-19.6 Meanwhile, many COVID jab recipients report long COVID-like symptoms.

As reported by Science magazine in 2022, “In rare cases, coronavirus vaccines may cause long COVID-like symptoms,”7 which can include (but is not limited to) brain fog, memory problems, headaches, blurred vision, loss of smell, nerve pain, heart rate fluctuations, dramatic blood pressure swings and muscle weakness. The feeling of “internal electric shocks” are also reported.

Also in 2022, a preprint study from the U.S. National Institutes of Health reported new neuropathic symptoms that began in 23 adults within one month of receiving a COVID-19 shot.8 All of the patients felt severe tingling or numbness in their faces or limbs, and 61% also experienced dizziness when standing up, intolerance to heat and heart palpitations.

When 12 of the patients had their nerve function tested, seven had less sweating in their hands and feet than normal, while six had a condition where their heart beats too fast when they stand up.9

The researchers also took skin samples from the lower legs of 16 patients. Among them, 31% showed signs that the small nerves in the skin were not as dense as they should be, which can indicate nerve damage. Another 13% were on the border of being considered damaged, and 19% had swollen nerve fibers. When five of the samples were evaluated more closely, signs of an immune reaction in the blood vessels were detected.10

Further, while electrical tests on the nerves were normal for most participants, 52% showed clear signs of damage to the small nerves that can be felt but not easily seen. The study shows that after getting the COVID-19 shot, a range of symptoms related to nerve damage is possible, which might be caused by an immune system reaction.

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Yale Scientists Detail Long Vax Symptoms

A study by Yale scientists, including Dr. Harlan Krumholz of Yale School of Medicine in New Haven, Connecticut, also shed light on long vax, which they described as chronic post-vaccination syndrome, or PVS.11 In a study of 241 people who reported PVS after an mRNA COVID-19 shot, the median time from the jab to the onset of symptoms was three days, with symptoms continuing for 595 days. The five most common symptoms included:12

  • Exercise intolerance (71%)
  • Excessive fatigue (69%)
  • Numbness (63%)
  • Brain fog (63%)
  • Neuropathy (63%)

In the week before the survey was completed, patients reported a range of additional symptoms highlighting the mental toll the condition takes. The symptoms required a median of 20 interventions for treatment and included:13

Feeling unease (93%) Fearfulness (82%)
Overwhelmed by worries (81%) Feelings of helplessness (80%)
Anxiety (76%) Depression (76%)
Hopelessness (72%) Worthlessness (49%)

“In this study,” the researchers explained, “individuals who reported PVS after COVID-19 vaccination had low health status, high symptom burden, and high psychosocial stress despite trying many treatments. There is a need for continued investigation to understand and treat this condition.”14

Even a 2021 study reported a series of patients who experienced new autoimmune conditions — or flare-ups of existing autoimmune disease — following mRNA COVID-19 shots,15 highlighting the importance of careful research into the ongoing health risks.

Will Long Vax Be Censored?

It’s hopeful that scientific on long vax is reaching medical journals and getting some media coverage.16 But Kory and Marik are concerned it could reach a similar fate as other COVID shot coverage during the pandemic.

“The concern is that our findings, Krumholz’s study, and any reports of adverse events from COVID-19 vaccination, will be subject to the same institutional censorship we saw throughout the pandemic. Suppressing this information risks creating an even bigger disaster,” they told The Hill,17 referring to a potential epidemic of autoimmune diseases that could occur as a result.

“America’s health agencies need to snap into action to help study this problem so we can better understand and treat these conditions. Unfortunately, there doesn’t seem to be much hope of this happening,” Kory and Marik wrote. “The National Institutes of Health is fixated on studying the effect of Paxlovid, an antiviral COVID treatment, to treat long COVID and long vax, despite it having no proven effect on autoimmune disease.”18

Further, Kory explains that while major medical centers and hospitals across the U.S. have opened long COVID clinics, the treatments they offer are largely ineffective, and they often gas-lit long vax patients who tried to get help:19

“[F]or most of 2022 into 2023, those centers consistently gas-lit the Long Vax patients who presented to those clinics. Gaslighting of medical injuries is the well-described inability for physicians to recognize or accept when their own treatments (i.e the mRNA vaccines) cause harm …

The stories my patients would tell me of the care they received included what I would describe as abuse or insults from the treating physicians when the patients tried to convince them that the vaccines were the cause. These stories still make my blood boil and have estranged many of my patients from ‘the system.’ I believe the gaslighting responses have lessened somewhat but I don’t really know how much.

What angered me even further is that the health agencies only directed funding at long COVID and the medical literature and media only referred to sufferers as having long COVID. The contribution of the gene therapy vaccines are consistently ignored.”

Is Long Vax Behind the Explosion of Disability Claims?

Kory believes that long vax, and to a lesser extent long COVID, are behind the explosion of disability claims that have occurred since COVID-19 shots rolled out.20

Data compiled by former BlackRock analyst and fund manager Edward Dowd revealed a sobering glimpse into the true carnage that occurred at the hands of the COVID-19 shot campaign,21 and its results are striking. It revealed the following estimated human and economic costs:22

Human cost:

  • 26.6 million injuries
  • 1.36 million disabilities
  • 300,000 excess deaths

Economic cost:

  • Total: $147.8 billion
  • Injuries: $89.9 billion
  • Disabilities: $52.2 billion
  • Excess deaths: $5.6 billion

What’s more, this data is from the employed population, aged 16 to 64 — a typically healthy crowd. To put this into perspective, John Leake writes on Courageous Discourse, “Note that this death count in one year is 5.2 times the number of men killed in ten years of combat in Vietnam.”23

Help for Long Vax Symptoms

As long vax and its symptoms become increasingly recognized, it will hopefully lead to increased access to effective treatments. If you’re experiencing symptoms, it’s important to find a holistic health care practitioner who’s familiar with long vax and how to treat it. You can also access FLCCC’s I-RECOVER24 guide,25 which offers step-by-step instructions on how to treat reactions from COVID-19 injections.26

I also summarized strategies to optimize mitochondrial health if you’re suffering from long COVID or long vax, with a focus on boosting mitochondrial health. To allow your body to heal you’ll want to minimize EMF exposure as much as possible. Your diet also matters, as the cristae of the inner membrane of the mitochondria contains a fat called cardiolipin, the function of which is dependent on the type of fat you get from your diet.

The type of dietary fat that promotes healthy cardiolipin is omega-3 fat, and the type that destroys it is omega-6, especially linoleic acid (LA), which is highly susceptible to oxidation. So, to optimize your mitochondrial function, you want to avoid LA as much as possible and increase your intake of omega-3s.

Primary sources of LA include seed oils used in cooking, processed foods and restaurant foods made with seed oils, condiments, seeds and nuts, most olive oils and avocado oils (due to the high prevalence of adulteration with cheaper seed oils). Animal foods raised on grains, such as conventional chicken and pork, are also high in LA.

Another major culprit that destroys mitochondrial function is excess iron — and almost everyone has too much iron. You can learn more about the health risks of excess iron in my interview with Christy Sutton, D.C. The most effective way to lower your iron is to donate blood two to four times a year.

Copper is also important for energy metabolism, detoxification and mitochondrial function, and copper deficiency is common. Other strategies include sun exposure and near-infrared light therapy, NAD+ optimizers and methylene blue, which can be a valuable rescue remedy. By improving your mitochondrial function and restoring the energy supply to your cells, you’ll significantly increase your odds of reversing the problems caused by the jab or the virus.

Posted in Coronavirus, Corruption, Infrared, Iron, Linoleic Acid, Methylene Blue, Minerals, Mitochondria, NAD+, Omega-3, Omega-6, Sunlight, Supplements | No Comments »

Posted by: | Posted on: March 26, 2024

Prunes or Plums — Which Has More Benefits?


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/03/22/prunes-or-plums.aspx

Analysis by Dr. Joseph Mercola     March 22, 2024

prunes or plums

STORY AT-A-GLANCE

  • Once known as prunes, dried plums are now the more palatable name for the fruit that, whether fresh or dried, contains numerous compounds that impart amazing health advantages
  • Studies show that a single serving or about five dried plums may help prevent bone loss in older, osteopenic postmenopausal women
  • Plums are loaded with flavonoid polyphenolic antioxidants, primarily lutein and cryptoxanthin, as well as neochlorogenic and chlorogenic acid, but the nutrients are highly concentrated in the dried fruits
  • The vitamin C is destroyed when plums are dried, but they become significantly higher in other antioxidants and contain significantly higher concentrations of most of the other nutrients found in the fresh fruit

If you know anyone with osteoporosis, you may be familiar with some of the more overt signs, such as broken bones, weak grip strength or back pain. People with this condition may develop a “stooped” posture or even become shorter because their bones are literally being compressed.

There’s good news, though, as a study revealed dramatic and positive effects from dried plums. Scientists found that “dried plum not only protects against but more importantly reverses bone loss in two separate models of osteopenia,” another name for bone loss and the forerunner of osteoporosis.

Osteoporosis affects both males and females, although more women than men. One study describes it as a “debilitating disorder” exacerbated by age:

“As the demographic shift to a more aged population continues, a growing number of men and women will be afflicted with osteoporosis and a search for potential non-pharmacological alternative therapies for osteoporosis is of prime interest.

Aside from existing drug therapies, certain lifestyle and nutritional factors are known to reduce the risk of osteoporosis.

Our [three]-month clinical trial indicated that the consumption of dried plum daily by postmenopausal women significantly increased serum markers of bone formation, total alkaline phosphatase, bone-specific alkaline phosphatase and insulin-like growth factor-I by 12, 6, and 17%, respectively.”1

Ironically, several drugs taken for osteoporosis taken for five years or more have been shown to actually cause esophageal cancer, according to an Oxford study.2 However, in exploring non-pharmacological alternative therapies, researchers discovered dried plums may not only protect against, but reverse, the condition.

Researcher Bahram H. Arjmandi, Ph.D., from Florida State University, said that over his entire career, he’d examined many fruits, including figs, dates, strawberries and raisins, but none of them come close to having the effe

ct on bone density that dried plums or prunes have.

He added that in terms of bone health, this particular food is exceptional.3 Studies show that a single serving of dried plums may help prevent bone loss in older, osteopenic postmenopausal women as well as the previous recommendation of two servings, equating 100 grams or eight to 10 dried plums.4

Plum History and Description

Closely related to apricots, peaches and almonds, plums are an ancient fruit that experts believe may have originated in China, but were cultivated by Alexander the Great in Mediterranean regions by around 65 B.C.

Plums are about the size of limes, but that’s the only similarity. They’re dark purple (some have a golden tinge) with smooth, rather dull skins and sweet, delectable flesh inside, wrapped around a single, large pit, the main criteria for a drupe. Prunes are simply dried plums, the latter name thought to be more palatable.

All prunes are plums, but the reverse is not always the case. The high sugar content in plums allows them to be dried without fermentation. Further, like all dried fruit, dried plums are dehydrated by natural-drying, sun-drying and the use of dehydrators. Medical Daily clarifies:

“So if dried plums are just plums with the water taken out of them, why do they lower our colon cancer risk while fresh plums don’t? Not only does dried plum retain both soluble and insoluble fiber from its original form, but it also contains more sorbitol than fresh plums.”5

Far more than just a tasty snack, these juicy little fruits are loaded with flavonoid polyphenolic antioxidants, primarily lutein and cryptoxanthin, as well as neochlorogenic and chlorogenic acid, which can help prevent cell damage from oxidation of lipid molecules.

All cell membranes, including those in your brain, are mainly composed of fat-containing lipids, found to inhibit LDL cholesterol oxidation and making them a significant factor in helping prevent chronic disease.6

A Comparison of Nutritional Attributes Between Plums and Prunes

Plums contain 26% of the reference dietary intake (RDI) in vitamin C; 13% in vitamin K; and 11% in vitamin A, or retinol, as well as iron, potassium, thiamine, riboflavin and calcium, plus vitamin B6 and niacin to metabolize one of their most serious drawbacks: high natural sugar and carbohydrate content.

As for prunes, a 1-cup serving gives you 87% of the RDI of vitamin K. The Guardian notes that soluble fiber helps slow down the absorption of glucose, which stabilizes blood sugar levels.7

Because prunes are a concentrated source of the nutrients and phytonutrients found in plums, their antioxidant potential is six times that of the fresh fruit. Prunes are also significantly higher in antioxidants than many other dried or fresh fruits or vegetables. Comparing the two, Healthy Eating observes:

“Although most of the vitamin C in plums is destroyed during the drying process, prunes contain significantly higher concentrations of most of the other nutrients found in the fresh fruit.

One cup of pitted prunes provides 129 percent, 36 percent, 27 percent and 9 percent of the daily recommendations for vitamin K, potassium, vitamin A and iron, respectively. Vitamin K is vital to the function of several proteins involved in blood coagulation, and vitamin A promotes healthy vision.”8

These vitamins, minerals and phytonutrients have several benefits throughout your entire body, including your skin and improved vision due to the high iron, of which a deficiency can cause hair loss.

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Fiber: Good for Gut Health and Colorectal Cancer Prevention

Bone health isn’t the only benefit of this oft-neglected fruit, though. Studies indicate dried plums can lower your risk of colon cancer.

One factor that helps give plums and prunes such high marks in this category is fiber, crucial for moving food along smoothly through your colon for elimination, but also the natural chemicals sorbitol and isatin, both helpful for relieving constipation. These three ingredients are why prunes have the (earned) reputation as a laxative. Media outlet Chatelaine notes that fiber:

“Helps to … [optimize] cholesterol by soaking up excess bile in the intestine and then excreting it. Bile is made from cholesterol in the liver in order to digest fat.

When the body excretes bile along with the fiber from prunes and plums, the liver must use cholesterol in the body to make more bile thereby lowering the amount in circulation in the body. Soluble fiber may also inhibit the amount of cholesterol manufactured by the liver in the first place.”9

Plums contain 2 grams of fiber in a 1-cup serving, which also helps produce beneficial gut microbiota. One of the big differences between fresh and dried plums is that the dried version contains 12 grams of fiber, which, compared to fresh plums, is about half of the RDI needed for an entire day (although I believe about 50 grams per 1,000 calories consumed is ideal).

According to Alimentary Pharmacology and Therapeutics, prunes are even more effective than psyllium as a laxative.10 Plus, the sorbitol pulls moisture into your digestive tract to help bring about a bowel movement.11 That’s where its effectiveness as a colorectal cancer preventive comes in.

More Benefits From Plums and Prunes

An online resource called Colon Cleansing and Constipation recommends stewed prunes to alleviate constipation, or infrequent bowel movements. Eating them regularly can help prevent subsequent stomach pain and hemorrhoids. All of these can become serious enough to necessitate surgery.

Aside from skin cancers, colorectal cancer is the third most common cancer in the U.S. It encompasses both rectal and colon cancer, which together have stricken around 140,000 people in the U.S., and more than 50,000 die from it every year, according to the American Society for Gastrointestinal Endoscopy.12

Medical Daily mentioned one study that found eating dried plums can help lower your risk for colon cancer by maintaining good gut bacteria in your colon, adding that “a diet high in [certain] red meats can increase colon cancer risk while a diet high in fruits … [and] vegetables … can reduce colon cancer risk.”13

A FASEB Journal study backed up the gut bacteria benefit, noting that their data supported their initial hypothesis:

“Diet is known to alter metabolism and composition of colon microbiota, which has major implications for disease prevention and treatment … The hypothesis tested by this experiment was that consumption of dried plums would promote retention of beneficial microbiota and patterns of microbial metabolism throughout the colon, and that by doing so would reduce colon cancer incidence.”14

Fructose in Plums and Prunes

It takes around 4 pounds of fresh plums to produce 1 pound of dried plums, and both are very versatile. You can chop them up to add to raw grass fed yogurt, blend them in smoothies and shakes and add them to salads and vegetable dishes. In fact, just about anything you use raisins for, prunes are a tasty, healthy alternative.

Eating plums and prunes may also help alleviate problems related to obesity, heart disease and diabetes. However, whether it’s fresh plums or dried prunes you crave, make sure you consume these in moderation, as they both contain high amounts of sugar. Nutritionist Anshul Jaibharat cautions:

“Prunes are high in natural sugar, so too many may not be good for people watching their weight. After all, excess of anything is stored as fat in your body. Prunes have such high nutritional values ensuring that you can eat just one piece and still gain measurable nutrients.”15

However, the sorbitol, which is a sugar alcohol, is not a source of ethanol, the substance found in alcoholic beverages. It’s a natural substance found in many fruits and vegetables, and is about 50% as sweet as sugar.16

Plums are often used to make the French form of Armagnac, a quickly distilled version of cognac with a raw, earthy body. They also end up soaked in brandy for several desserts, including brûlée. The sugar (and, for the former, alcohol) content in these, however, is considerable and outweighs the nutritional benefits that the fruit provides.

Additionally, prune juice is often loaded with high-fructose corn syrup and, even if it’s not, will still be a significant source of fructose without the fiber benefits, so be aware that consuming the whole fruit is preferable.

Posted in Cancer, Cholesterol, Fibre, Food, Fructose, Hair, Iron, Sugar, Vitamins | No Comments »

Posted by: | Posted on: March 10, 2024

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.”

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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?”

– Sources and References

Posted in Anemia, Copper, Ferritin, Hormones, Iron, Supplements | No Comments »

Posted by: | Posted on: January 19, 2024

What’s the Best Predictor of Heart Disease?


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/01/18/predictors-atherosclerosis.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 18, 2024

STORY AT-A-GLANCE

  • High total cholesterol and/or elevated low-density lipoprotein (LDL) cholesterol do not cause atherosclerosis
  • Low levels of high-density lipoprotein (HDL) cholesterol are associated with both atherosclerosis and insulin resistance, and insulin resistance appears to be the foundational cause of heart disease. As such, the fasting insulin test is one of the best predictors of atherosclerosis
  • Insulin resistance is primarily driven by excessive consumption of the omega-6 fat linoleic acid (LA). High LA intake is also associated with elevated levels of oxidized LDL — found in atherosclerosis plaque — further confirming this link
  • One theory is that oxidized LDL protects your body from oxidative damage by sacrificing itself. If true, it may be beneficial to have higher, rather than lower, LDL levels
  • The apoB test can also be helpful in assessing your atherosclerosis risk. As mentioned above, apoB is the primary carrier for LDL, and research over the past decade shows it’s an accurate predictor of cardiovascular risk when apoB is high and LDL is normal

Is high total cholesterol and/or elevated low-density lipoprotein (LDL) cholesterol indicative of elevated heart disease risk? According to Dr. Paul Saladino, the answer is no. With regard to total cholesterol, as far back as 1977, with the publication of the Framingham Study,1 no correlation between heart disease and total cholesterol could be found.

Low levels of high-density lipoprotein (HDL) cholesterol was associated with coronary heart disease, but not high LDLs or total cholesterol. However, as noted by Saladino, low HDL is also associated with insulin resistance, and he believes this is part of the confusion.

Saladino suspects that what has been blamed on LDL (atherosclerosis) is due to insulin resistance, i.e., metabolic dysfunction. Insulin resistance/metabolic dysfunction, in turn, is primarily driven by excessive consumption of the omega-6 fat linoleic acid (LA).

High LA intake also raises your levels of oxidized LDL, which are what you find in atherosclerosis plaque. In the video above, Saladino and Dr. Nadir Ali specifically discuss the role of oxidized LDL, and why it is not a direct cause of atherosclerosis, as commonly thought.

Summary of Available LDL Tests

But before I summarize Saladino’s and Ali’s discussion, let’s take a look at the available LDL-related tests, as there’s more to LDLs than the total amount.

  • A regular LDL cholesterol blood test (LDL-C), which measures the total amount of LDL cholesterol in your blood
  • A nuclear magnetic resonance lipoprofile (NMR lipoprofile) test, which measures the size of the LDL particles (LDL-P), which is thought to be more predictive of your cardiovascular risk, even if you have low total cholesterol2
  • Oxidized LDL (oxLDL) test, which measures the level of LDLs that have been damaged by oxidation
  • The apolipoprotein B (apoB) test, which measures the number of apoB particles in your blood. ApoB is a protein involved in the metabolism of lipids and the primary carrier for LDL. This test is a good predictor of cardiovascular risk, and does so far more accurately than the standard cholesterol panel
  • Advanced lipid testing, which measures the amounts of large-buoyant LDLs (lbLDL) and small-dense LDLs (sdLDL), with the sdLDLs being associated with insulin resistance and heart disease3

High LDL Does Not Cause Atherosclerosis

When it comes to LDL cholesterol, the most important factor is the level of oxidized LDL, as oxLDLs are primarily what you find in atherosclerosis plaque.4 Unfortunately, most doctors will simply prescribe a statin drug or PCSK9 inhibitor if LDLs are high, to reduce the total LDL.

As noted by Ali in the short video above, this is a serious mistake. The primary question that needs to be asked is why is LDL oxidized in the first place, and how can you prevent that oxidation from taking place?

“Is the oxidized LDL a bad player?” Ali asks, “[or] is it there to protect us from oxidative injury? Rather than letting the important cells get oxidized, is the LDL sacrificing itself in protecting the body? Then, your whole paradigm changes …

LDL is not a bad player — it’s trying to protect us. What I need to figure out is how do I prevent this oxidative injury in the first place, and an argument that should surface is that, maybe I should have more LDL around so that oxidative injury can be … prevented, rather than having less LDL? These are the kinds of fundamental questions that science should be asking.”

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Oxidized LDL May Be a Protective Mechanism

Saladino agrees, saying that LDL “is probably a repository for oxidized phospholipids,” much like lipoprotein(a) (Lp(a)). He cites research showing that the more polyunsaturated fats (PUFAs) you consume — such as LA — the higher your Lp(a) and oxidized LDL.

So, your LDL may in fact have a protective rather than injurious role. It may protect you from the harmful effects of LA and other PUFAs. What this means, then, is that high oxidized LDL may be a marker of high PUFA consumption, and it’s the PUFAs, LA in particular, that are driving the atherosclerotic disease process.

The primary way to prevent atherosclerosis, then, is to radically reduce your LA intake by eliminating seed oils from your cooking, and avoiding processed foods (which are loaded with seed oils) and restaurant foods (as most are cooked in seed oils).

When it comes to measuring your oxLDL, the Boston Heart test called oxidized phospholipids on APO-B (OxPL/apoB) appears to be a better choice than the traditional oxLDL. The oxLDL tends to be inaccurate because it’s just a proxy for APO-B and the LDL number, while the OxPL/apoB test gives you a truer measure of your oxidized LDLs.

The ApoB Test

Aside from oxLDL, the apoB test can also be helpful in assessing your atherosclerosis risk. As mentioned above, apoB is the primary carrier for LDL, and research over the past decade shows it’s an accurate predictor of cardiovascular risk when apoB is high and LDL is normal. As reported by The Washington Post:5

“The standard cholesterol panel calculates the total quantity or concentration of ‘bad’ cholesterol or LDL in the blood, in milligrams per deciliter (technically, LDL-C). Because cholesterol is a fatty substance and thus not water-soluble, it must be carried around in little particles known as lipoproteins.

Testing for apoB, a protein on the outside of LDL-carrying particles, counts the number of these lipoprotein particles in the blood. In addition to LDL, it also captures other types of cholesterol such as IDL (intermediate-density lipoproteins) and VLDL (very low-density lipoproteins), which carry triglycerides.

Why is this important? As our understanding of heart disease improves, scientists are recognizing that apoB particles are more likely to become lodged in the arterial wall and cause it to thicken and eventually form atherosclerotic plaques. Thus, the total number of apoB particles matters more than the overall quantity of cholesterol that they carry.

In a majority of people, apoB and LDL-C track fairly closely, says Allan Sniderman, a professor of cardiology at McGill University in Montreal. But some people have a ‘normal’ amount of LDL-C, but a high concentration of apoB particles — a condition called ‘discordance,’ which means they are at greater risk.”

sdLDL — Another Helpful Predictor of Atherosclerosis

Measuring your sdLDL-C can also be helpful, as explained by Dr. Eric Berg, a chiropractor, in the video above. The small-dense type of LDLs are indicative of inflammation inside your arteries, which is a hallmark of atherosclerosis. As noted by Berg, potential causes of this inflammation include:

  • Seed oils
  • Processed foods and junk foods
  • Smoking
  • Low vitamin E
  • High glucose levels

Unfortunately, Berg lumps high-carb diets into these risk factors and recommends a ketogenic diet to avoid elevated sdLDL, but as I’ve explained in previous articles, high glucose levels are not necessarily a sign that you’re eating too many (healthy) carbs.

In summary, when you consume significantly more than 30% fat, a metabolic switch called the Randle Cycle switches from burning glucose in your mitochondria to burning fat instead. As a result, glucose backs up into your bloodstream, thereby raising your blood sugar.

Glucose is actually a cleaner and far more efficient fuel than dietary fats, provided it’s metabolized in your mitochondria and not through glycolysis. For a refresher, refer back to “Crucial Facts About Your Metabolism” and “Important Information About Low Carb, Cortisol and Glucose.”

Atherosclerosis Is a Consequence of Metabolic Dysfunction

In the video directly above, Saladino debates LDL cholesterol with Dr. Mohammed Alo, a cardiologist and personal trainer. While Alo argues for the conventional LDL-atherosclerosis connection, Saladino highlights evidence showing that it’s not LDL per se that is the cause, but rather insulin resistance in combination with high oxLDL, both of which are caused by high LA intake.

For this reason, Saladino believes one of the best assessments of your heart disease risk is a fasting insulin test, as your insulin sensitivity is such a foundational factor of your metabolic function. The OxPL/apoB test mentioned earlier would be a good complement.

If you have high fasting insulin, you are insulin resistant and hence have some degree of metabolic dysfunction (and, of course, mitochondrial dysfunction). Ideally, you want a fasting insulin level of 3 mcg/mL or less.

Most definitely, do not go by the “normal” ranges offered by labs in this case. Many will list levels as high as 24 mcg/mL as normal, when in fact that’s a clear sign of serious insulin resistance and metabolic dysfunction.

If you’re already eating a healthy diet, exercising, and all of your metabolic parameters look good, yet you have an insulin level of 7 or 8, the core culprit may be stress, because when cortisol goes up, insulin rises with it. Cortisol release is a rescue mechanism to ensure you don’t die from low blood sugar.

To assess whether stress is at play, keep an eye on your white blood cell count. Chronically depleted white blood cells are often a sign of chronic stress and high cortisol.

You can also get an AM cortisol test after fasting for 12 to 16 hours. You don’t want to fast longer than that because, after 16 hours of fasting, cortisol will naturally start to rise. An ideal AM cortisol range is between 15 and 17. If your fasting AM cortisol is below 15, it’s a sign you’ve become stuck in a long-term stress response.

High LA Intake Promotes Atherosclerosis

So, to summarize, Saladino argues that insulin resistance is the primary root cause for atherosclerosis — not elevated LDL or total cholesterol — and the primary driver of insulin resistance is excessive LA intake from seed oils. Lowering your LA intake is the foundational strategy to embrace.6

Low levels of high-density lipoprotein (HDL) is a proxy for insulin resistance, and if you have low HDL, then LDL tracks well with cardiovascular disease. But if you have normal HDL (65 to 85 mg/dL), then you typically have good insulin sensitivity and the correlation with LDL and atherosclerosis vanishes.

The Keto Trial Match Analysis7 presented in mid-December 2023 (video below) confirms this, as they found no relationship between elevated LDL levels and arthrosclerosis plaque.

Other Tests to Assess Your Metabolic Health

In addition to the tests already mentioned, other blood tests that can help you assess your metabolic health include the following. Additional information about these and other lab tests can be found in my interviews with Dr. Nasha Winters and Dr. Bryan Walsh.

• Fasting glucose — The ideal range is between 82 and 88 milligrams per deciliter (mg/dL), based on the available literature, while nonfasting glucose should ideally be between 82 and 130 mg/dL.

• Gamma-glutamyl transferase (GGT), a powerful predictor of mortality, also should not be above 20 U/L. GGT is a liver enzyme involved in glutathione metabolism and the transport of amino acids and peptides.

Not only will the GGT test tell you if you have liver damage, it can also be used as a screening marker for excess free iron and is a great indicator of your sudden cardiac death risk.

GGT is highly interactive with iron. Excessive iron will tend to raise GGT, and when both your serum ferritin and GGT are high, you are at significantly increased risk of chronic health problems, because then you have a combination of free iron, which is highly toxic, and iron storage to keep that toxicity going.

Cysteinylglycine is liberated from glutathione via GGT. That, in the presence of iron or copper, initiates the Fenton reaction. That’s when you get massive oxidative stress.

• The Intermountain health risk score is a mortality risk score created based on the basic blood chemistry markers of tens of thousands of patients in a hospital setting, including complete blood count (CBC), sodium, potassium bicarbonate, mean platelet volume and other basics. Based on these markers, you end up with a 30-day, a one-year and a five-year mortality risk.

A risk score calculator is freely available on the Intermountain website, where you can also find more information about this score.8 Simply enter your variables and it will calculate your score for you.

• Coronary artery calcium (CAC) scan — This test provides images of your coronary arteries. Existing calcium deposits, an early sign of coronary artery disease, will show up on these images, and can therefore reveal your risk of heart disease before other warning signs become apparent.9

For even more information about cholesterol, and why high cholesterol and/or high LDL are not risk factors for heart disease, check out the video below by Dr. Ken Berry.

Posted in Cardiovascular, Cholesterol, Ferritin, Glucose, Heart, Iron, Oils, Omega-3, Omega-6, Processed Food, Sugar, Vitamins | One Comment »

Posted by: | Posted on: January 8, 2024

Serum Ferritin and GGT — Two Potent Health Indicators You Need to Know


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2024/01/04/monitoring-serum-ferritin-and-ggt.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 04, 2024

monitoring serum ferritin and ggt

STORY AT-A-GLANCE

  • By monitoring your serum ferritin (stored iron) and GGT levels and taking steps to lower them if they’re too high, you can avoid serious health problems
  • Virtually all adult men and postmenopausal women are at risk for iron overload due to inefficient iron excretion. Left untreated, it can contribute to cancer, heart disease, neurodegenerative diseases and other chronic health problems
  • GGT is a liver enzyme involved in glutathione metabolism and the transport of amino acids. GGT can be used as a screening marker for excess free iron and is a potent predictor of mortality

While many health screens and lab tests are overrated or unnecessary, there are a few that are vitally important, such as vitamin D. I recommend checking your vitamin D level at least twice a year.

Two other really important tests are serum ferritin (which measures stored iron) and gamma-glutamyl transpeptidase or sometimes called gamma-glutamyltransferase (GGT; a liver enzyme correlated with iron toxicity, disease risk and all-cause mortality). By monitoring your serum ferritin and GGT levels and taking steps to lower them if they’re too high, you can avoid serious health problems.

For adults, I strongly recommend getting a serum ferritin test and GGT on an annual basis. When it comes to iron overload, I believe it can be every bit as dangerous to your health as vitamin D deficiency. In this interview, Gerry Koenig,1 former chairman of the Iron Disorders Institute and the Hemochromatosis Foundation, explains the value of these two tests.

Iron Overload Is More Common Than Iron Deficiency

Iron is one of the most common nutritional supplements. Not only can you get it as an isolated supplement, but it’s also added to most multivitamins. Many processed foods are also fortified with iron. While iron is necessary for biological function, when you get too much, it can do tremendous harm.

Unfortunately, the first thing people think about when they hear “iron” is anemia, or iron deficiency, not realizing that iron overload is actually a more common problem, and far more dangerous. Many doctors don’t understand or appreciate the importance of checking for iron overload.

Virtually all adult men and postmenopausal women are at risk for iron overload due to inefficient iron excretion, since they do not lose blood on a regular basis. Blood loss is the primary way to lower excess iron, as the body has no active excretion mechanisms. Another common cause of excess iron is the regular consumption of alcohol, which will increase the absorption of any iron in your diet.

For instance, if you drink wine with your steak, you will likely absorb more iron than you need. There’s also an inherited disease, hemochromatosis, which causes your body to accumulate excessive and dangerously damaging levels of iron.

If left untreated, high iron can contribute to cancer, heart disease, diabetes, neurodegenerative diseases and many other health problems, including gouty arthritis. In one small study,2 100% of the patients achieved marked reduction in attacks or complete remission after phlebotomy was used to remove iron and maintain an iron level at near-iron deficiency — “the lowest body iron store compatible with normal erythropoiesis and therefore absence of anemia.”

Iron causes all this harm by catalyzing a reaction within the inner mitochondrial membrane. When iron reacts with hydrogen peroxide, hydroxyl free radicals are formed. These are among the most damaging free radicals known, causing severe mitochondrial dysfunction, which in turn is at the heart of most chronic degenerative diseases.

GGT Is a Potent Predictor of Mortality

Download Interview Transcript | Video Link

GGT is a liver enzyme involved in glutathione metabolism and the transport of amino acids and peptides. Not only will the GGT test tell you if you have liver damage, it can also be used as a screening marker for excess free iron and is a great indicator of your sudden cardiac death risk.

In fairly recent years, scientists have discovered GGT is highly interactive with iron, and when both your serum ferritin and GGT are high, you are at significantly increased risk of chronic health problems, because then you have a combination of free iron, which is highly toxic, and iron storage to keep that toxicity going.3

“Recently, [GGT] was proven by the life insurance industry as the single measure that is most predictive of early mortality,”4,5 Koenig says. “In other epidemiological studies, it’s linked to pretty much every cause of death,6 because it provides those free radicals and hydroxyl radicals …

I believe that … people born after World War II are now at greater risk because of the environmental toxicants we face … Basically, reduction in glutathione levels — your body’s most important antioxidant — is indicated by an increase in GGT …

[G]lyphosate, excess iron, all of the substances in the environment — whether you take it in as food or it’s in the air — that utilize your body’s toxic waste disposal system in some way [will] reduce your antioxidants, whether it’s vitamin D, cholesterol, vitamin E or vitamin A. A reduction of those makes you more vulnerable to disease, particularly chronic disease and autoimmune diseases across the board.”

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Ideal GGT and Iron Levels

As with many other lab tests, the “normal” ranges for GGT and serum ferritin are far from ideal.7 If you’re in the “normal” range, you’re virtually guaranteed to develop some sort of health problem. Based on Gerry’s recommendation I had my GGT tested last month and it was 17, which is healthy especially since my ferritin level is 37. You really need both tests to confirm lack of iron toxicity as he explains in the full interview.

Ideal GGT Level, units per liter (U/L) Average level, above which your risk for chronic disease increases significantly “Normal” GGT Level8
Men Less than 16 U/L 25 U/L Up to 70 U/L
Women Less than 9 U/L 18 U/L Up to 45 U/L

According to Koenig, women with a GGT above 30 U/L have a higher risk of cancer and autoimmune disease. Interestingly, while for most other tests the range between what’s healthy and what’s risky tends to be quite broad, in the case of GGT, the range between health and disease is in the single digits.

“Part of it is dependent on body weight,” Koenig says. “Strangely enough, the most recent indications are that people who are too thin (whatever their level of GGT is), it could be harmful if [their GGT is] relatively high.9 For instance, for a thin woman with a GGT … in the range of the second quartile, which is going to be generally 14 to 18 today it can be dangerous if she’s expecting to have children and has a very low BMI.”10

When it comes to serum ferritin, a level of 200 to 300 nanograms per milliliter (ng/mL) falls within the normal range for women and men respectively, which is FAR too high for optimal health. An ideal level for adult men and non-menstruating women is somewhere between 30 and 60 ng/mL.

You do not want to be below 20 ng/mL or above 80 ng/mL. The most commonly used threshold for iron deficiency in clinical studies is 12 to 15 ng/mL.11 Maintaining a healthy iron level is also important during pregnancy. Having a level of 60 or 70 ng/mL is associated with greater odds of poor pregnancy outcomes.12 That said, iron deficiency during pregnancy is equally problematic, so make sure you get tested.

Last but not least, since the ferritin and GGT are interactive, low GGT tends to be protective against higher ferritin. So, if your GGT is low, you’re largely protected even if your ferritin is a bit higher than ideal. Still, it would be wise to take steps to lower your ferritin to a more ideal level nonetheless. On the other hand, even if your ferritin is low, having elevated GGT levels is cause for concern, and needs to be addressed.

When Might a Transferrin Saturation Test Be Useful?

If you are thin, with a body mass index (BMI) below 22 or 23, Koenig suggests getting a transferrin test as well, which gives you a percentage saturation level. A level of 25% to 35% is typically considered healthy. In the 1970s, the transferrin saturation test was used as a marker for early death. Having a transferrin saturation percentage of over 55 indicated a 60% increased risk for premature death.

At that time, an estimated 2.6% of the U.S. population had transferrin saturation percentages that high. Today, it’s down to half of that, in large part because of the increase in obesity, which “dilutes” your saturation percentage, and the transferrin test is no longer used as a marker for early death. However, if you are very thin, it can still be a useful test.

“Anything between 25 and 35 is safe. If you’re unusually thin, I would get that test because there you could have unsuspectingly high transferrin saturation, particularly if you’re malnourished … Anorexia nervosa has severe effects on the brain when you’re that thin and your BMI is at 14 or 15,” Koenig says.

Why Excess Iron Is so Dangerous

Your body creates energy by passing the electrons from carbs and fats you eat as fuel to oxygen through the electron transport chain in your mitochondria to produce adenosine triphosphate (ATP). Ninety-five percent of the time, the oxygen is converted to water. But 0.5% to 5% of the time, reactive oxygen species (ROS) are created. ROS are not all bad as they are important biological signaling molecules, but excessive ROS leads to mitochondrial damage and dysfunction.

Iron can react with hydrogen peroxide in the inner mitochondrial membrane. This is a normal part of cellular aerobic respiration. But when you have excessive iron, it catalyzes the formation of excessive hydroxyl free radicals from the peroxide, which decimate your mitochondrial DNA, mitochondrial electron transport proteins and cellular membranes. This is how iron overload accelerates chronic disease.

If you eat excessive net carbs (total carbs minus fiber) the situation is further exacerbated, as burning carbs as your primary fuel can add another 30% to 40% more ROS on top of the hydroxyl free radicals generated by the presence of high iron.

Unfortunately, most people reading this are burning carbs as their primary fuel. If you struggle with any kind of chronic health problem and have high iron and eat a standard American diet that is high in net carbs, normalizing your iron level (explained below) and implementing a ketogenic diet as described in my book, “Fat for Fuel,” can go a long way toward improving your health.

Taking extra antioxidants to suppress ROS generated by high iron alone or in combination with a high-sugar diet is inadvisable, as ROS also act as important signaling molecules. They’re not all bad. They cause harm only when produced in excess.

Your best bet is to lower the production of ROS. One of the easiest and most effective ways to do that is to eat a diet high in healthy fats, adequate in protein and low in net carbs. Eating healthy fats can make a bigger difference than you might think, especially if you have high iron.

How to Lower Your Iron

The good news is it’s easy to lower your iron level if it’s too high. One of the easiest ways is simply to donate blood two or three times a year. If you have severe overload you may need to do more regular phlebotomies. Two years ago, my ferritin was 150 ng/mL. I implemented self-phlebotomy where I would take out anywhere from 2 to 6 ounces of blood every few weeks, which brought me below 100 ng/mL.

I stopped the phlebotomy when I started a comprehensive detoxification strategy involving near and far infrared sauna, and interestingly, despite the fact I was no longer removing blood, my ferritin continued to drop over the next nine months. Now, it’s down to 37 — far lower than I was ever able to get down to with therapeutic phlebotomies, and as I mentioned earlier I have a healthy GGT level of 17.

As it turns out, an effective detoxification program can lower iron as well. While this was a surprise to me, Koenig confirms that this has indeed been documented by Dr. F.S. Facchini in some of his research on iron. While I’ve long recommended donating blood as the solution to iron overload, I now believe a balanced approach using phlebotomy, detoxification and reducing dietary iron, especially meat, is the best way to go about it.

Keep in mind that trying to control high iron through your diet alone can be risky, as you will also forgo many valuable nutrients. That said, to avoid maximizing iron absorption, avoid eating iron-rich foods in combination with vitamin C-rich foods or beverages, as the vitamin C will increase iron absorption. If needed, you could also take a curcumin supplement. Curcumin acts as a potent chelator of iron and can be a useful supplement if your iron is elevated.

How to Lower Your GGT

GGT is inversely related to glutathione, a potent antioxidant produced in your body. As your GGT level rises, your glutathione goes down. This is part of the equation explaining how elevated GGT harms your health. By elevating your glutathione level, you will therefore lower your GGT. The amino acid cysteine, found in whey protein, poultry and eggs, plays an important role in your body’s production of glutathione.

Red meat, which does not contain cysteine, will tend to raise GGT, as will alcohol, so both should be avoided.13 Research also suggests eating at least 10 servings of fruits and vegetables rich in in vitamin C, fiber, beta-carotene, anthocyanins and folate per week can help reduce GGT.14,15 Examples include carrots, romaine lettuce, spinach, sweet potatoes, apricots and tomatoes.

Also, be aware that certain medications can raise your GGT. If this is the case, please confer with your doctor to determine whether you might be able to stop the medication or switch to something else, and avoid over-the-counter medicines, including ibuprofen and aspirin, both of which can damage your liver.

General detoxification is another important component if your GGT is high, as your liver’s job is to remove toxins from your body. The fact that your GGT is elevated means your liver is under stress.

The Protein-Iron-GGT Connection

I personally typically eat only 2 to 4 ounces of meat per week. Americans tend to overeat meat in general, and most of it is dangerous CAFO meat loaded with toxins. Additionally, while the meat supplies you with more iron than you likely need, excess protein can also cause problems. Another little-known fact is that giving iron to a person who is malnourished and cannot process protein properly can be extremely dangerous. Koenig explains:

“I’ve been studying malnutrition for several years now, mainly kwashiorkor (also known as protein-calorie malnutrition), which is a typical malnutrition disease, along with marasmus in developing countries. There you have a situation where the children, particularly in kwashiorkor, cannot synthesize important proteins because of essential amino acid deficiencies …

[When] giving iron too early in a recovering child with kwashiorkor, or an adult for that matter, the measure that skyrockets early on, in that particular case, happens to be GGT.

High amounts of free iron [are dangerous] because they don’t have the proteins to safely contain that iron into either transferrin, which is the protein that protects the body from the iron in the bloodstream, or ceruloplasmin, which is necessary for copper transport.

To get iron safely into the brain, it needs to be complexed with ceruloplasmin. Those can’t be synthesized in a malnourished person. [So, giving] iron to a malnourished person is highly toxic.”

African and Chinese Research Confirm GGT’s Relation to Chronic Disease

Koenig found a few African studies showing the importance of GGT. In the 1990s, when GGT was tested broadly in the U.S. as part of the National Health and Nutrition Examination Survey III (NHANES III, 1988 to 1994), results revealed that African-Americans had higher levels of both serum ferritin and GGT than Caucasians and Hispanics.

“Back then, those measurements were compared to measurements in Zimbabwe. In [Zimbabweans] who were not exposed to spraying for mosquitoes … the [ferritin and GGT measurements] were roughly half.

They had obviously been on a native diet … But I found, through several papers recently submitted in South Africa, that those measurements now are very high. They’re catching up and probably surpassing the American Blacks’ measurements, and they’re suffering the [same] chronic diseases …”

More recent studies from South Africa depict increasing GGT levels are associated with insulin resistance and cardiometabolic disease risk.16 Moreover, a Chinese study showed that while having a GGT level above the midpoint raised the risk of chronic kidney disease, when combined with high serum ferritin, that risk increased nearly fivefold.17 Other common diseases associated with high iron and GGT include diabetes, heart disease and cancer.

Blood Donations Lead to Radical Reduction in Disease

A number of epidemiological studies have also documented a significant reduction in chronic diseases among those who donate blood two or three times a year — findings that support the notion that iron overload is prevalent, and contributes to chronic disease. In some, heart disease and cancer were reduced by as much as 50%, Koenig notes.

Unfortunately, many doctors are still unaware of the importance of checking for iron overload (based on ideal levels and not what’s considered normal), and may overlook the GGT test as well.

“One of the reasons it’s difficult to get doctors to order GGT tests is they’re discouraged because they know some prescription drugs increase [GGT]. Although the overall effect may be protective, it’s not a happy situation to see a measure of disease increase just by taking a drug. There’s resistance in that area of getting tested. But it’s a pretty simple test. It would be recommended. And blood donation basically keeps one healthy,” Koenig says.

In summary, if you’re concerned about maintaining your health and preventing chronic disease, I would strongly encourage you to get a ferritin and a GGT test regularly, and if needed, implement the strategies discussed above to get them into their optimal ranges.

Serum ferritin and GGT are markers for iron toxicity, which is a major mostly unrecognized contributor to heart disease, cancer, diabetes, nonalcoholic fatty liver disease and many other chronic diseases.

High iron even increases your risk of infections. As noted by Koenig, you really don’t want to check into a hospital with high iron, as your risk of contracting a hospital-acquired infection will be that much greater. The good news is, it’s so easy to turn around, thereby dramatically reducing your risk.

More Information

To learn more, I recommend visiting HealtheIron.com, where you can also order your serum ferritin and GGT tests or either of their special FeGGT-LifePRO™ test panels. If either serum ferritin or GGT is elevated, you need to take action. The treatment couldn’t be simpler. Unless you’re a menstruating woman, simply donate blood two to three times a year. If you do not qualify to donate blood, ask your doctor to write you a prescription for therapeutic phlebotomy.

Posted in Blood, Ferritin, Iron, Mortality, Testing | One Comment »

Posted by: | Posted on: September 18, 2023

Why Checking Your Iron Level Is so Crucial for Optimal Health


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/09/17/iron-overload-disorder.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 17, 2023

STORY AT-A-GLANCE

  • Iron overload is incredibly common and likely as dangerous to your health as vitamin D deficiency, as it creates excessive free radicals that damage your mitochondrial DNA, cell membranes and electron transport proteins
  • Iron overload is easily diagnosed by measuring your serum ferritin. Lab normal levels are correct and should be between 20 and 80 ng/ml; between 40 and 60 ng/ml is the sweet spot
  • Iron overload is easy and inexpensive to treat. Most adult men and non-menstruating women would benefit by donating blood two to three times per year to keep their mitochondria healthy

Editor’s Note: This article is a reprint. It was originally published June 12, 2016.

One in 3 reading this likely has a serious overload of a mineral that may be more dangerous to your health than lack of vitamin D. That mineral is iron.

Making matters worse, few physicians fully appreciate the danger of excess iron, which Gerry Koenig, former chairman of the Iron Disorders Institute and the Hemochromatosis Foundation,1 discusses in this interview. Koenig’s personal story is a powerful illustration of what can happen to someone with excess iron.

Approaching his 50th birthday, he’d lost a lot of weight, worked out, and felt healthy. By age 55, he was in good shape, but he did drink more than recommended. Eventually, during a physical exam, he found out his liver enzymes were high.

“The doctor recommended I stop drinking,” Koenig says. “I stopped drinking. But I got sick again … Turned out I had hemolytic anemia. My red blood cells were breaking down.

I didn’t know what that meant, nor, apparently, did my doctor. They never tested my iron … Finally I had an episode where I went to the hospital. I had encephalopathy, a pretty serious condition … They said I would need a new liver.

I didn’t get an iron test until the eve of my liver transplant in 2005 … By chance I ran across a Scientific American article. It described something called hemochromatosis, which I didn’t know anything about. I decided I would have the test.

As it turns out, I have a single gene for one of the variants for hemochromatosis — C282Y. Because of that, I decided to look into it more and started researching it … I’ve been doing that for the last 11 years.”

Are You at High Risk for Iron Overload?

Most all adult men and non-menstruating women have damaging levels of iron. However, there is a genetic disorder called hemochromatosis which causes your body to accumulate excessive and dangerously damaging levels of iron.

If left untreated, it can damage your organs and contribute to cancer, heart disease, diabetes, neurodegenerative diseases and many other disorders.

The good news is iron overload is easy and inexpensive to treat. By monitoring your serum ferritin and/or gamma-glutamyl transpeptidase (GGT) levels, avoiding iron supplements and donating blood on a regular basis, you can avoid serious health problems.

Sadly, many doctors are severely underinformed about iron overload. Hence the problem tends to go undetected.

How High Is Too High?

The serum ferritin test measures your stored iron. I strongly recommend all adults to get your iron tested (serum ferritin test) on an annual basis. I believe iron overload is every bit as dangerous to your health as vitamin D deficiency.

Just don’t make the mistake of going by what’s considered “normal.”2 In some labs, a level of 395 nanograms per milliliter (ng/ml) falls within the normal range, which is FAR too high for optimal health. In reality, you’re virtually guaranteed to develop disease at that level.

Ideally, your serum ferritin should be somewhere between 20 and 80 ng/ml, certainly no higher than that. As a general rule, somewhere between 40 and 60 ng/ml is the sweet spot for adult men and non-menstruating women.

Unfortunately, few besides children, premenopausal women who lose blood through monthly menstruation, and those with acute blood loss like a bleeding ulcer, have these ideal levels.

“Even some premenopausal women (if they’re not under control) will go up to 60 or 70, which is dangerous if they get pregnant. There’s a greater chance of poor outcomes in the pregnancy.

The U.S. is 35th in the world in infant survival. It’s a terrible situation when you look at the numbers. There’s no reason for this. There’s no reason for us to have a population that’s so unhealthy given the access to medical care that we have,” Koenig says.

Again, if your iron level is high, the solution is to simply donate your blood. If you’re an adult male, you’ll want to donate blood two to three times a year once your levels are normal. If ferritin levels are over 200 ng/ml, a more aggressive phlebotomy schedule is recommended.

Although your local blood bank may not realize this, U.S. legislation allows all blood banks to perform therapeutic phlebotomy for hemochromatosis or iron overload. All you need is a doctor’s order.

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Recommended Lab Tests

While a full iron panel that checks serum iron, iron-binding capacity and ferritin can be helpful, you really only need the serum ferritin test. It’s fairly inexpensive — typically less than $40. Your doctor can write you a prescription for the ferritin test, as well as a gamma-glutamyl transferase (GGT) test.

GGT measures liver enzymes, which can tell you if you have liver damage. It can also be used as a screening marker for excess iron. The free iron measured by GGT is also great indicator of sudden cardiac death.

“If you only took that marker (GGT), you have an indication of iron that’s not well-bound. When you have iron in the serum, it’s generally bound by transferrin, which carries two iron atoms through the serum.

Ferritin can hold 4,000 to 4,500 iron molecules and put those inside the cells. If those measures are high, they’re risky, because you don’t know how well your body is going to hold on to that iron when the cells fall apart over time hemolysis or catabolism.

Our diet is the biggest factor today that’s really causing this problem. It’s not so much that we’re eating too much iron; it’s that the iron we have in our body effectively can harm us. That’s where the GGT comes in. It’s a surrogate measure of free iron.”

For women, a healthy GGT level is around 9 U/L, whereas the high end of “normal” GGT lab ranges are generally 40 to 45 U/L for women. For men, Koenig recommends a level of 16 U/L (normal lab ranges for men is 65 to 70 U/L).3

“Women with GGT above 30 U/L have higher risk of cancers — breast cancer, all kinds of cancers — and they will have high risk of autoimmune disease,” Koenig warns.

What Causes Excess Iron Buildup?

Besides having one or both genes for hemochromatosis, you may also end up with high iron levels for the simple fact that most people don’t excrete iron very well. So what’s the biology behind iron loading?

Ninety percent of the energy your body creates is by burning carbs or fat with oxygen in your mitochondria to produce adenosine triphosphate (ATP). You need oxygen to burn the fuel because it goes through the Krebs cycle. Ninety-five percent of the time, oxygen is converted to water.

But anywhere from 0.5 to 5% of the time, you’re going to develop what’s called a reactive oxygen species (ROS). The first one is superoxide, which then transforms to the next ROS, which is hydrogen peroxide.

Here’s the key: when you have excess iron in your blood, the chemical reaction (Fenton’s reaction) doesn’t produce water. Instead, the excessive iron catalyzes the formation of hydroxyl free radicals, which are the most potent and destructive free radicals known to man. They will decimate your mitochondrial DNA, mitochondrial electron transport proteins and cellular membranes.

This is how iron overload accelerates every major disease we know of. That’s how it causes the pathologies, especially in liver and cardiovascular disease. Believe me, very few health care professionals understand the molecular biology of this reaction, which is why virtually no one is sounding the alarm about excessive iron levels. This is why you need to share this article with your friends and family as you can literally save many of their lives.

It is absolutely vital to confirm that you have safe iron levels, and once they are in a safe range, continue to monitor them so they don’t rise. Remember, you don’t have to have hemochromatosis to be affected. According to Koenig, iron levels have literally DOUBLED in the general population over the past four decades.

“Serum ferritin was not measured for the first National Health and Nutrition Examination Survey (NHANES I,4 1971 to 1974) was done. But during NHANES II5 (1976 to 1980), they measured ferritin. The male serum ferritin was under 100 nanograms per milliliter (ng/ml). Now the median is close to 200 ng/ml. In some minorities, it’s a lot higher …

If you look at the scales of premature death and infant mortality in African-Americans versus whites, that big difference can be accounted for by this one element. Hispanic-Americans live longer than white Americans. They also handle the iron a little bit better,” Koenig says.

Beware of High Iron, High-Carb Diet Combination

If you eat a lot of net carbs (total carbs minus fiber), the situation is exacerbated. Unfortunately, most reading this are burning carbs as their primary fuel, which adds another 30 to 40% more ROS on top of the hydroxyl free radicals generated by the presence of high iron.

“What people generally have when they eat better, in terms of slowing those little fires down before they become a raging fire, are antioxidants,” Koenig says. “The most important one is glutathione. If you don’t have good cellular health, including glutathione, those fires (inflammation) will just self-ignite and you’ll have a chain reaction of effects that go on until you’re really sick.

That happened to me. I got peripheral neuropathy. They try to say it’s a diabetic problem, and I never had diabetes. Both of my legs were on fire. The pain was unbelievable. You wind up going to a specialist for that, a neurologist. But when the membranes on your neurological system essentially flare up and melt, the pain is unbearable. But nobody connected that to the iron.”

Hemochromatosis, Another Iron-Damaging Disease

About 1 in 3.5 or an estimated 100 million people in the U.S. have the single gene for hemochromatosis. But not all of them get sick with an iron overload disorder. If you have both genes for hemochromatosis, then your risk of developing iron overload and associated health problems rises significantly.

Approximately 1 million people have the double gene variant (C282Y/C282Y), which is considered the genotype most predictive of liver disease complications. However, this only becomes a serious problem if significant iron overload occurs before a diagnosis is achieved and proper treatment can be administered.

Each year there are roughly 56,585 deaths from liver diseases;6 and in 2021 there were 9,234 liver transplants in the U.S.7 Most all of these cases are affected by excess iron, whether or not they have a hemochromatosis genotype.

The primary cause for liver transplantation and liver death is nonalcoholic fatty liver disease (NAFLD), a condition that can advance to nonalcoholic steatohepatitis (NASH) and cirrhosis. Excess dietary fructose is likely a primary contributor or initiator to NAFLD these days (especially in children and young adults), but high iron is another major culprit that triggers insulin resistance and disease progression.

Certainly, if you combine a high-sugar diet with excess iron, you’re asking for trouble. That will create a powerfully poisonous, deadly synergy that will accelerate just about any pathology. If you’ve read this far, you probably know more about this problem than your physician. High iron simply isn’t brought to their attention in the medical literature. The reason I know about it is because I’ve been personally affected.

My dad had beta-thalassemia and he gave me the gene, which is a form of hemolytic anemia (similar to sickle cell anemia). As a result of that, my red blood cells die faster than normal, and I’m prone to excess iron. My dad had a ferritin level of 800 when I diagnosed him 20 years ago.

He would have died if we hadn’t taken measures to correct it. When he was 90 he was hospitalized with pneumonia. His doctor did an iron test, which came back “low,” despite being well over 200 ng/ml! They were about to give him an iron injection when my sister intervened and stopped them. Had she not been there, he might have ended up another medical error statistic.

Key Treatment Points

To reiterate, the three keys to control this situation are:

  1. Lower your net carb intake and increase your consumption of healthy fats, including animal-based omega-3, to switch over to fat-burning mode and protect your mitochondria. This will help to radically reduce reactive oxygen species (ROS) and secondary free radical production.
  2. Regularly screen for iron overload with a serum ferritin or GGT level to confirm that you don’t have excess iron, and if you do, donate blood to lower your levels.
  3. If you are an adult male or non-menstruating woman, make sure that you donate your blood at least twice a year.

Relying on antioxidants to indiscriminately suppress ROS can backfire, as ROS also act as important signaling molecules. They’re not all bad. They cause harm only when produced in excess. You’re better off lowering the production of them rather than squelching them after they’re produced.

So optimize your ROS levels biologically rather than relying on vitamins and supplements. Eating healthy fats can make a bigger difference than you might think, especially if you have high iron. Koenig explains:

“There was a very interesting group of studies on captive U.S. Navy dolphins. The dolphins had metabolic syndrome. Very, very high ferritin (serum iron). They were unhealthy. Metabolic syndrome in any population is a sign of potential risk of going from diabetes to heart disease. They cured it by providing them good fish to have plenty of fats, where they had been getting fish with poor fats …

If anybody remembers the film ‘Lorenzo’s Oil,’ that’s where children have brain damage as a result of having this metabolism that doesn’t create a good mixture of fatty acids in the cell linings. If the cell linings are damaged, particularly if it happens in the brain … you’re going to get hurt …

… If you have leakage of iron from subcells, lysosomes, and/or red blood cells (hemolysis) … it will shoot the ferritin level up high as an indication of risk. That’s when action should be taken. But it’s hard to find specialists. We need a couple of thousand general practitioners who know about this.”

Be Mindful of Food Combos That Promote Iron Retention

Here are a few other tips and suggestions regarding diet. Eating vitamin C-rich food with a meal that has iron will increase iron absorption. If you’re anemic, this might be a good thing, but if you struggle with high iron, avoid combining foods high in vitamin C and iron. On the other hand, calcium will bind to iron, limiting absorption.

It impairs iron, so to speak, so if your iron is high, consider eating iron-rich foods with foods high in calcium. Interestingly, curcumin (derived from turmeric) acts as a potent chelator of iron and can be a useful supplement if your iron is elevated.

“For most people that works well. Your body is designed to not over-absorb non-heme iron, which is elemental iron. That’s the iron inside vegetables and fruits. If you do something to enhance that absorption, the body will take it in.

The iron from meats you can’t control very well. We’re the only country in the developed world, together with Canada, to put 44 parts per million of elemental iron in our grains and flours. The other one is the U.K. They put 16.5 parts per million. That’s a lot of iron, and [many] don’t need it,” Koenig says.

More Information

After testing, if either serum ferritin or GGT is elevated, you need to take action. The treatment couldn’t be simpler. Unless you’re a menstruating woman, simply donate blood two to three times a year. If you cannot donate blood due to restrictions for hemochromatosis, get your doctor to write you a prescription for therapeutic phlebotomy.

Every blood bank can do that for you and many will do it free of charge, so shop around. Otherwise, a typical charge ranges from $30 to $90, which is still fairly inexpensive considering the health benefits. Most people with moderate iron overload will require no more than two or three such treatments a year to keep this risk under control.

There’s also a really informative book called “Dumping Iron: How to Ditch This Secret Killer and Reclaim Your Health,” which is a well written and easy to understand resource. Remember, high iron may not only be as common, or more, than low iron. It’s also more dangerous, and may actually be a factor in a significant number of diabetes, heart disease and cancer cases.

Unfortunately, nearly every physician is still clueless about this, and so you need to be your own advocate if you suspect (or know) your iron is too high.

I believe correcting elevated iron levels may be just as important, if not more so, than optimizing your vitamin D. If you have high iron, you definitely have the pedal to the metal when it comes to speeding up disease and aging. Koenig is a perfect example. He ended up needing a liver transplant as a result of iron overload. In conclusion, Koenig notes:

“If your doctor tells you that you have fatty liver disease, you probably have high iron, high ferritin. He probably will not test you for that. Get the test. You can see some benefit by donating blood, or changing your diet. On my website, I have about 700 publications. If you want to dig into it, it’s a section. Find out how to reduce [your iron] by diet alone. It’s been done and done successfully.”

Posted in Blood, Ferritin, Iron | No Comments »

Posted by: | Posted on: July 23, 2023

A Critical Look at ‘The China Study’ and Other Food Plans


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/07/22/the-china-study-and-other-nutrition-plans.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     July 22, 2023

STORY AT-A-GLANCE

  • Although veganism has some health benefits, it is also loaded with many disadvantages and is unsuitable for many, especially if you have certain genetic polymorphisms predisposing you to poor beta-carotene conversion
  • People with polymorphisms causing poor conversion of beta-carotene are at high risk for reproductive problems, skin and eye problems and poor dental health
  • The blood type diet, detailed in “Eat Right 4 Your Type,” often works well for those with blood type O, as those recommendations are consistent with a healthy diet. It typically does not work well for the other blood types
  • Nutrient cycling (cycling between higher and lower amounts of fat, net carbs and protein) and cycling between high and low calorie intakes (fasting and feasting) appear to be foundational criteria for optimal biological functioning
  • If you’re on a ketogenic diet, it’s important to cycle high and low amounts of net carbs once your body is able to efficiently burn fat for fuel in order to optimize your metabolism. Cyclical fasting is also recommended

Editor’s Note: This article is a reprint. It was originally published July 8, 2018.

Denise Minger is perhaps most noted for her comprehensive rebuttal of “The China Study” some eight years ago. She’s heavily vested in the vegan versus omnivore battle, having cycled through vegetarianism and raw veganism, finally coming full circle to being an omnivore.

Minger took to vegetarianism when she was just 7 years old. “I was eating steak one night at dinner and almost choked on it. I developed some kind of phobia surrounding things with meat textures and went vegetarian overnight,” she explains.

Raw Veganism Took a Toll on Health

However, during the 10 years she remained a vegetarian, she began developing food allergies, including wheat and dairy allergies. “By the time I was a teenager, I was really health-conscious,” she says. “I had to get into that whole scene just to stay healthy.”

At age 15, she discovered the raw vegan movement and got on the 80/10/10 diet, promoted by Dr. Douglas Graham. The diet is based on the hypothesis that we should eat what other primates eat, particularly frugivorous chimpanzees and bonobos.

“I was reading about it online at the age of 15 without having any background in human biology, physiology or anthropology … I fell into this trap of logic, that humans are the only animals that cook our food. We’re the only animals that eat this species-inappropriate diet, [so] I went raw vegan overnight,” she says. “For one year straight, [I ate] nothing but fruits, vegetables and some nuts — all uncooked.

I did great for the first month, as most people do when they stop eating crappy foods. After that, I started losing weight and muscle. My hair was falling out. My energy levels were fluctuating like crazy.

I was in high school at the time, taking the Scholastic Assessment Test (SAT). My brain fog got so bad at one point that when I was taking the SAT, I would read the question and by the time I got to the end I couldn’t remember what the first part said …

The kicker for me, because I’ve always taken great care of my teeth, was at the end of this period of raw veganism I had 16 cavities in my mouth, after a lifetime of what had previously been perfect dental health … It was actually the dental health issue that really turned my mind around … At that point, I had to let go of the vegan philosophy. I had to start questioning things …

That’s when I came across things like the Weston A. Price Foundation, which [details] what humans have been eating that has supported health in the past. I learned about the paleo movement — different forms of health-conscious omnivory. That’s where I ended up. It was a process.”

Debunking ‘The China Study’

As mentioned, Minger produced a very comprehensive critique of “The China Study” which is the scientific justification for many vegan positions. Her analysis — which some suspected to be funded by the meat industry — was actually undertaken while recovering from an accident. At the age of 22, she was hit by a car while riding her bicycle and shattered her elbow. Her convalescence afforded her the time to work on this project.

“I got a huge book of the raw ‘China Study’ data. I love numbers. I have fun with correlations. I have fun looking at patterns. My brain gets happy. I spent about two or three months poring over the data. I needed a project, because I had nothing else to do.

I was poring over the data and that’s when I realized I needed to write a critique of the book. So much of what [author T. Colin] Campbell said was not supported by his own data. I just felt like if there’s anything I needed to do in life, it was going to be this.

I didn’t expect anyone to read it. I had a little blog. I like to say I had six readers, five of which were my mother on different computers. I didn’t realize at the time how much interest the critique would gather; how much interest there was in that book itself. I hadn’t really seen the rivalry upfront between the vegan and the paleo worlds. When I released this critique, I didn’t know it was going to be that influential,” she says.

Minger developed quite a bit of notoriety as a result of that critique, especially in the vegan community. She’s been vilified by many, including Campbell, who wrote personal rebuttals to her commentary on his work. Some have gone so far as to characterize her as someone who’s promoting processed food.

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The Case for Lowering Protein Intake

For all its drawbacks, there are benefits to veganism. The biggest one, from my perspective, is that vegans have — compared to those who eat the standard American diet — a significantly lower protein intake. I think there are valuable insights that can be drawn from that, which can be integrated into a low-carb paleo approach. Minger agrees, saying:

“For the protein issue, what I find interesting is that whenever we look at the actual China Study, for example, when you look at their food intake, it’s much different in terms of the types of animal parts they consume than what we see in America.

The protein issue is complicated, but I will say that high methionine intake — for example from muscle meat — [needs to be balanced with] glycine. You get that by eating the entire animal, the skin, tendons, connective tissue — all the stuff that Americans typically discard …

In the China Study, you don’t see them eating steaks and chicken breasts at every meal. Even the lower animal product-consuming societies, a lot of them eat insects. A lot of them eat the weird parts of the animal. I think that’s imperative for staying healthy on an omnivorous diet. Because the way we eat meat in America is pathogenic. It’s not healthy. But it’s not necessarily because animal products are bad for you …

What was amusing to me, because it was completely left out of ‘The China Study’ book, was that the healthiest populations were the seafood eaters … They had the best health outcomes. The only disease that they had more of was liver cancer. That was because they were living in humid areas where aflatoxin was more prevalent … But it wasn’t because of the animal protein. It wasn’t because of the fish.”

This makes sense considering the importance of long-chained omega-3 fats: eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). Those who restrict themselves to a plant-based diet are only getting alpha-linolenic acid (ALA) which, while being a precursor for EPA and DHA cannot be converted at significant, therapeutic levels.

Protein Cycling

Clearly, the composition of the animal protein is a significant issue. We don’t want processed foods. We don’t want meat from factory farms that is contaminated with glyphosate (due to contaminated grain feed). But there’s also the issue of the amount. Many are simply eating far too much protein, which (when consumed in excess) activates mTOR, a pathway involved in both aging and cancer. Pulsing higher and lower amounts of protein also seems a wise strategy.

“When we look at historical groups of humans, the animal food intake was generally on the lean side. We don’t have year-round access to these big fatty animals … It’s going to be seasonal when it occurs at all,” Minger says. “I’m reminded of a study on Australian aborigines. They put people out in the wild to try to acquire foods from their environment and survive on that …

Their fat intake ended up being something like 8% to 12%, because the animals were so lean and the lean protein intake was consequently much higher. I have trouble believing that animal protein itself is going to be a problem. I think what might be a problem is this consistency thing — the idea that eating the same foods year-round, without any fluctuation in the composition of the diet, is healthy. I don’t think that’s the case …

I think things like protein cycling might be therapeutic for humans. I think that even carb cycling and going through different periods of different macronutrient intakes instead of always being low-fat or always being low-carb [is a good idea]. That’s probably what the human body is best adapted to.”

Macronutrient Cycling — An Overlooked Component

In deconstructing and assessing the low-carb, high-fat approach, Minger concluded the lack of high and low nutrient cycling was one of the main problems, especially long-term, and particularly for women. “I do one-on-one consulting with people,” she says.

“A large group that I have come in contact with are women who’ve done low-carb. Their thyroid function is tanking. They’re gaining weight. They feel terrible. Their hair is falling out. It happens with men too sometimes, but I think women, hormonally, are more sensitive to the lack of carbohydrates.”

She’s also found evidence suggesting chronic lack of carbohydrates may be having an adverse effect on your gut microbiome. In his commentary, “Sorry Low Carbers, Your Microbiome Is Just Not That Into You,”1 Jeff Leach with the Human Food Project details the likely shifts found in the gut microbiome composition of people who consume low-carbohydrate diets. Whether or not those shifts are wholly detrimental or not is still unknown, but it’s worth keeping an eye on.

Minger is equally ambivalent about long-term, chronic high-fat consumption, as some of the evidence suggests it may increase gut permeability and the transport of endotoxin from gram-negative bacteria into the bloodstream, which increases chronic inflammation and related health problems.

“On one hand, we see people switching away from the standard American diet to low-carb. Yeah, they’re going to feel great. Yeah, they’re going to lose weight. There’s going to be this initial honeymoon period, just like I had with raw veganism. My question is what happens over the course of many years on a large scale … I’m wondering what the bulk of the evidence is going to show. I don’t know if we really know that yet.”

From my perspective, I think there are compelling reasons to suspect one might run into problems, for many of the reasons Minger cites. It appears nutrient cycling (i.e., cycling between higher and lower amounts of fat, net carbs and protein), and also cycling between high and low calorie intakes (fasting and feasting), are foundational criteria for optimal biological functioning.

The challenge is to find that happy balance. When writing “Fat for Fuel: A Revolutionary Diet to Combat Cancer, Boost Brain Power, and Increase Your Energy,” I dove deep into the scientific literature looking at this aspect of health.

Cyclical Ketogenic Diet Combined With Cyclical Fasting

First of all, the late Dr. Joseph Kraft showed that using sensitive oral glucose loading and testing insulin levels that insulin resistance is pervasive. Based on a more refined definition of insulin resistance, at least 80% of the population have diabetes in situ,2,3 which means they’re insulin resistant even though their fasting glucose is normal.

This is where low-carb can be really useful, yet it alone will still not be enough for many. A lot of people need to get even more aggressive and do fasting. Once you’ve done that for a while and resolve the insulin resistance, you need to cycle net carbs (total carbs minus fiber) back in.

“Low-carbohydrate eating … is a great tool to lose weight, and lose fat around the organs. You start improving insulin sensitivity because of that weight loss, and because of the reduction in the energy surplus that many people are constantly surrounded with. But I use the analogy of a [broken] refrigerator.

Your refrigerator breaks. You can do one of two things. You can say, ‘OK, I’m never going to buy any perishable food again. Everything I’m going to buy is going to be dry goods as long as the freezer or the refrigerator is broken.’ Or, you can fix the refrigerator.

Low-carbohydrate diets are like saying, ‘Let’s not use our refrigerator anymore.’ Let’s not use our carbohydrate metabolism pathways anymore. Let’s just avoid those. It’s not actually fixing the issue. As anyone who knows who’s been low-carb, you go low-carb for a while, and then you reintroduce carbohydrates and, whoa, it’s terrible.

Your blood sugar goes crazy. You feel awful. It’s like, ‘Wow. The carbohydrates are terrible.’ No. It’s because your body is no longer working to metabolize them efficiently.”

The converse can also occur. If you suppress insulin for too long, your blood sugar will tend to rise from hepatic gluconeogenesis. If you reintroduce carbohydrates at that point, it will raise insulin and lower your blood sugar. You can also eat too much fat; since fat is high in calories, the excess calories alone can lead to weight gain. As mentioned above, protein intake also needs to be regulated to avoid mTOR activation.

Traditional paleo is frequently high-protein, high-fat, similar to the Atkins approach. But you’re not going to get all the benefits unless you restrict protein. As a general rule, I recommend limiting protein to half a gram per pound of lean body weight, to ensure you’re getting the protein you need for muscle maintenance and repair. The answer is not to cut protein out altogether. You do need some, just not the enormous amounts most Americans are used to eating.

Focus on Nutrient Density

When asked what the best animal food composition might be, Minger stresses the importance of nutrient density over any specific dosage recommendations, as the ideal amount will depend on the type of meat you’re eating. “For my own diet, I focus on organ meats and shellfish,” she says. “Those are the primary foods I eat that are of animal origin. Oysters are my favorite. Nutritionally, if you look at liver and oysters, oysters are kind of like the liver of the ocean.”

People who shun animal foods due to ethical concerns about eating something that is highly sentient can also take heart in the fact that oysters lack the central nervous system “that would make them equivalent to a cow.” “There’s a bivalve vegan movement, where people are vegan with the inclusion of certain shellfish. I think that can go a long way for people to balance out a vegan diet,” she says.

As for cooking, Minger recommends using gentle methods to avoid the creation of carcinogens associated with high-temperature cooking. These byproducts “seem to be driving the correlation between meat consumption and different cancers that we see in observational studies,” she says.

“Whenever you look at a study that actually controls for the cooking method, typically once you take away the high-heat kind of strategies for cooking your meat, the correlations with various diseases start to diminish, if not disappear completely.” Byproducts created during grilling and frying include heterocyclic amines and polyaromatic hydrocarbons that form carcinogens. So, don’t overcook your meat, and balance muscle meat (steaks) with organ meat and other animal parts.

How Minger’s Diet Has Changed Over the Years

When asked how her diet has changed over the past seven years, and what insights changed her approach to eating the most, Minger replies:

“I started out really fruit-based from my raw vegan history. I would eat a ton of fruit in the morning; smoothies … In learning more about the gut microbiome, learning about digestive-resistant starch; different forms of fiber and their effect on the body, I’ve been incorporating more legumes, lentils and potatoes that have been heated and cooled [to increase] the resistant starch content. I think that has helped a lot.

I’ve also flipped my diet in terms of staggering macronutrients throughout the day. I used to start with a lot of carbohydrate and not much else (in the form of fruit). Now, I usually start with a lot of protein and vegetables, and have my high-carb meals at the end of the day. I find that helps with sleep, energy levels [and] focus.”

It’s worth noting that legumes may not be ideal for everyone, especially if you have autoimmune issues. Minger, who does a lot of work with autoimmunity, agrees lectins can be problematic if you are susceptible to autoimmune problems, whether caused by genetics, lifestyle, antibiotic use or gut microbiome issues. “At that point, the lectin problem can be real,” she says.

“There can be a legitimate reason to avoid foods that are high in certain lectins, especially the ones that are individually triggering autoimmune responses. But for people with a healthy gut microbiome, I don’t see that being necessarily bad, because if you look at human history … the lectin content of wild foods is generally pretty high.

There’s going to be a long adaptation period for us to learn how to coexist with those lectins in our diet. I think [the larger issue] is that the modern environment is creating a really unhealthy microbiome that’s making it so some people cannot handle what should be a natural lectin load. That’s my takeaway right now, subject to revision.”

Critiquing the Blood Type Diet

In preparing for this interview, I watched some of Minger’s latest material on YouTube. One of her more recent videos was a Weston A. Price Foundation presentation in which she critiqued Dr. Peter D’Adamo’s blood type diet, detailed in his book, “Eat Right 4 Your Type.”

I tried this diet back in the ’90s and had to quit because it made me diabetic. My personal take on it is that while his recommendations for blood type O, which is about half the population, is consistent with what I believe is a healthy diet, it doesn’t seem to work well for the other blood types. According to Minger:

“The fundamental issue with everything he’s saying is that it’s all wrong. The premise of his diet — that foods have different lectins [that] interact with what’s expressed on our blood cells to cause issues within the blood, which then causes inflammation and disease — there’s absolutely no mechanistic evidence showing that we can obtain high enough levels of lectins from certain foods, and that those foods will specifically interact with our specific blood type to create these problems.

That evidence just isn’t there … [He may have had] a lab, but there are problems with the research actually being published. It certainly hasn’t been replicated by other researchers. It’s more of a, ‘This is what I found. You have to take my word for it, because I wrote a book and I have a [medical] degree.’ There’s a certain, ‘Just trust me. I’m a scientist,’ behind that. If there’s anything I don’t like, it’s that …

What fascinated me … [was that] our ABO blood group can actually influence the composition of our gut microbiome for people who are secretors — people who secrete their blood type antigens on the surface of mucous cells throughout the body, the saliva and the gut, the gut in particular.

Let’s say you’re a blood type A and you’re secreting the A antigen on different cells within the gut. There are going to be certain bacteria that use that antigen as a food source and as an attachment site.

Those specific bacteria are going to be more attracted to your microbiome. They’re going to set up camp there, in a way that they might not be doing to somebody who’s a blood type O. You’re actually going to start shifting the proportion of different bacteria because of your blood type.

Tied into this is the idea of being a secretor versus a non-secretor. Most people are secretors. They will express their blood type antigens on the surface of different cells throughout the body. About 20% of the population are non-secretors.

For this group, regardless of what their actual blood type is, they have a much higher risk of a lot of digestive diseases, a lot of different health conditions in general, related to the fact that their microbiome is fundamentally different. It’s providing a lack of attachment sites for different bacteria. So, there is an influence of blood type on different things going on in the body. It’s just not through D’Adamo’s theory.”

Awesome Omnivore

After taking a professional hiatus, Minger is now working on a few new projects, including an e-book called “Awesome Omnivore.”

The book is a how-to guide for eating animal products in a way that minimizes potential risks and maximizes nutrition, including guidance on balancing methionine and glycine, differences in A1 versus A2 dairy, how to prepare meat to reduce carcinogen exposure, how to modify your animal food consumption based on genetics, and how to combine meat with other foods to reduce the absorption of heme iron to lower your risk of intestinal cancer and other health problems related to excessive iron.

High iron increases oxidative stress and can cause serious mitochondrial dysfunction. I have a genetic condition called thalassemia, which predisposes me to high iron levels. I have to be really vigilant about keeping my iron level low for these reasons.

As explained by Minger, because the molecular structure of heme is so similar to chlorophyll, if you eat lots of green leafy vegetables with your steak, the chlorophyll will inhibit absorption of some of the iron. “That alone is going to make that meal probably, on the whole, healthier for you,” she says.

“There’s this kind of dichotomy — you have the vegetable eaters and the meat eaters. The meat eaters are not usually eating enough vegetables to offset the heme issue. But if you look at studies that actually adjust for that one variable, the link with meat’s problems tends to disappear.

It’s, again, veggies to the rescue. But it doesn’t mean that you can’t eat meat too. Anyway, the book is going to be a collection of things people can do to ensure that the meat they’re consuming, the eggs and the dairy products (if they’re doing that), are as healthy as possible.”

Plant-Based Paleo

Minger is also working on a book about plant-based paleo, designed for people who are committed to avoiding animal products, for whatever reason. The aim of this book is to provide strategies to help you stay as healthy as possible for as long as possible within the limitations of a plant-based diet.

“There are vegans who have survived a long time on their diet. It’s not impossible. The human body is incredibly adaptable. But we need to understand what’s working for those people.

We need to understand that there are a lot of genetic components that go into being able to convert plant-based nutrients into their active forms. Take beta-carotene, for example. People who have really good conversion of beta-carotene into retinol, they’re probably not going to run into reproductive issues, teeth issues, skin issues or eye issues, like I did.

But for about 45% of the population, there are mutations with the BCMO1 gene that prevent that conversion from being efficient. If you have two very common polymorphisms, your conversion rate is going to drop by almost 70%.

Another less common mutation will tank your conversion by 90%. If you’re a vegan, you’re not eating any preformed vitamin A, and if you have some of those mutations, you’re going to have problems pretty quickly. How do we work with people’s genetics? How do we work with their dietary limitations?

Supplements would be good. I’d love for people to take cod liver oil if they can get over that one issue. But you need to be really aware of your specific conditions … I have those BCMO1 mutations. My vitamin A conversion is terrible. That’s part of the reason that eating liver was a huge boon for my diet. It’s my first concentrated source of vitamin A that I had in a decade, more than a decade.”

Lifelong Learning Is Key to Staying Ahead

As nutritional science keeps moving forward, we’re bound to learn new things about what we currently think of as factual. For example, Minger touches on evidence suggesting really low-fat intake may actually improve carbohydrate metabolism.

“We have the Randle Cycle. There’s competition between free fatty acids and glucose in the bloodstream for use as fuel. I think we have enough evidence to say pretty clearly that when you combine fat and carbohydrate within the same meal, if you’re a healthy person — you’re going to see a reduced blood-glucose response, but you’re going to see the same amount of insulin secretion.

Fat doesn’t decrease the insulin needs of your body when you’re eating carbohydrate. It kind of amplifies it. There have been studies where they’ll take a potato, feed it to a diabetic, then repeat the study with butter added … The more butter added to the potato, the more insulin the diabetic needs to use to deal with that meal. There’s an interactive effect, even within the span of one meal, between fat and carbohydrate …

I don’t believe in staying at one [end of the spectrum, i.e., high-carb or high-fat] forever. Obviously, you need fat-soluble nutrients. You’re going to need some fatty foods that are highly nutritious too. At the same time, you’re going to need to cycle in more carbohydrate to deal with the long-term consequences of ketogenic diets …

I believe there’s a way to integrate everything. What it comes back to is all the warring diet communities need to let go of the ego and communicate with each other. Stop saying, ‘We own the truth.’ Start listening to the other side and be curious about why things are working for them.

For me, that’s the way I’ve learned best — by challenging what I believe. Because if what I believe can be dismantled, then it’s not a good belief to hold. You need to constantly revise your theory about the world, about nutrition, about everything. It needs to be in a state of flux.”

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Posted by: | Posted on: April 3, 2023

Strategies to Optimize Mitochondrial Health in Long COVID


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2023/04/02/optimize-mitochondrial-health-long-covid.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     April 02, 2023

STORY AT-A-GLANCE

  • Mitochondrial dysfunction is at the root of most all chronic diseases, and it also plays a crucial role in conditions such as long COVID, which is becoming quite common. It’s also a root factor that must be addressed in COVID jab injuries, regardless of symptoms or severity
  • One of the most foundational lifestyle components that can make or break your mitochondrial health is electromagnetic field (EMF) exposure. To allow your body to heal, you’ll want to minimize EMF exposure as much as possible
  • The cristae of the inner membrane of the mitochondria contains a fat called cardiolipin, the function of which is dependent on the type of fat you get from your diet. Cardiolipin is important because, if cardiolipin is damaged, mitochondrial energy production will be impaired. The most damaging fat is omega-6 linoleic acid, found in seed oils
  • Another major culprit that destroys mitochondrial function is excess iron, and almost everyone has too much iron. Copper is also important for energy metabolism, detoxification and mitochondrial function, and copper deficiency is common. Copper is also required for proper iron recycling, and low ferritin is typically a sign of copper insufficiency
  • Other strategies reviewed include sun exposure and near-infrared light therapy, time-restricted eating, NAD+ optimizers and methylene blue, which can be a valuable rescue remedy

The video above features a recent lecture I gave to the American College for Advancement in Medicine (ACAM) on how to optimize your mitochondrial health and function.

Mitochondrial dysfunction is at the root of most all chronic diseases, and it also plays a crucial role in conditions such as long COVID, which is becoming quite common. It’s also a root factor that must be addressed in COVID jab injuries, regardless of symptoms or severity.

Features of the post-jab injuries we see point to severe mitochondrial dysfunction, which in turn causes energy failure. The same goes for long COVID in people who struggle with unrelenting fatigue and other symptoms for months after they’ve recovered from COVID-19 infection.

If you can improve your mitochondrial function and restore energy supply to your cells, you’re going to massively increase your odds of reversing the problems caused by the jab or the virus.

US Life Expectancy Falls in Historic Decline

Allopathic medicine has been a leading cause of death in the U.S. for over two decades. In 1998, researchers concluded that properly prescribed and correctly taken pharmaceutical drugs were the fourth leading cause of death in the U.S.

Two years later, in 2000, Dr. Barbara Starfield published her groundbreaking paper, “Is US Health Really the Best in the World?”1 in which she provided data showing that medical errors by doctors were the third leading cause of death. Little has changed since then.

In 2016, Johns Hopkins patient safety experts calculated that more than 250,000 patients died each year from medical errors, again pegging it as the third leading cause of death.2

In July 2022, the National Institutes of Health concluded the annual death toll from medical errors could be as high as 440,000 — and possibly even more because of lack of reporting — making it, still, the third leading cause of death.3

In future years, I believe the medical intervention sold as “COVID vaccines” will prove to be the No. 1 killer of Americans, and we’re already seeing that trend. Something extraordinarily odd happened in 2020 and 2021, something that shaved nearly three years off the life expectancy in the U.S.4

Even a tenth or two-tenths of a year mean decline in life expectancy on a population level is a big deal, as it means a lot more people are dying prematurely than they really should be. A three-year drop is simply unheard of.

While media blame this drop on COVID-19 infection, that makes no sense because the average age of those who died from COVID was about 85, well over the life expectancy in 2019. No, this massive drop in life expectancy is due to younger people dying decades earlier than they should, and the only factor that can account for that is the mass injection of people with an experimental bioweapon.

Limit Your EMF Exposure

One of the most foundational lifestyle components that can make or break your mitochondrial health is electromagnetic field (EMF) exposure. To allow your body to heal, you’ll want to minimize EMF exposure as much as possible. The World Health Organization classified cell phone radiation as a 2B carcinogen in May 2011.

However, as I detail in my 2020 book, “EMF*D,” it’s actually a Class 2A carcinogen. To minimize your EMF exposure, which includes electric fields, magnetic fields and radiofrequencies:

  • Keep your cell phone in airplane mode whenever you’re not actively using it
  • Do not sleep with it near your bed
  • At night, be sure to turn off your Wi-Fi
  • Turn the breakers off to your bedroom, as the electrical wiring in most homes also emit dirty electricity
  • Alternatively, sleep in an EMF-shielding tent, which is what I use whenever I travel and have no control over the EMF exposure in my room

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Dietary Fat Choices Influence Energy Production

You have about 40 quadrillion to 100 quadrillion mitochondria throughout the cells of your body. In my lecture, I show a picture of the structure of your mitochondria. The cristae of the inner membrane of the mitochondria contains a fat called cardiolipin,5 the function of which is dependent on the type of fat you get from your diet.

Cardiolipin is important, because it influences the structure of the cristae inside your mitochondria, which is the area where energy production occurs. If cardiolipin is damaged, then the complexes will not be close enough together to form supercomplexes and thus the mitochondrial energy production will be impaired.

Cardiolipin also works like a cellular alarm system that triggers apoptosis (cell death) by signaling caspase-3 when something goes wrong with the cell. If the cardiolipin is damaged from oxidative stress due to having too much LA, it cannot signal caspase-3, and hence apoptosis does not occur. As a result, dysfunctional cells are allowed to continue to grow, which can turn into a cancerous cell.

The type of dietary fat that promotes healthy cardiolipin is omega-3 fat, and the type that destroys it is omega-6, especially linoleic acid (LA), which is highly susceptible to oxidation. So, to optimize your mitochondrial function, you want to avoid LA as much as possible, and increase your intake of omega-3s.

Primary sources of LA include seed oils used in cooking, processed foods and restaurant foods made with seed oils, condiments, seeds and nuts, most olive oils and avocado oils (due to the high prevalence of adulteration with cheaper seed oils), and animal foods raised on grains such as conventional chicken and pork.

Ideally, consider cutting LA down to below 7 grams per day, which is close to what our ancestors used to get. If you’re not sure how much you’re eating, enter your food intake into Cronometer — a free online nutrition tracker — and it will provide you with your total LA intake.

Cronometer will tell you how much omega-6 you’re getting from your food down to the tenth of a gram, and you can assume 90% of that is LA. Anything over 10 grams of LA is likely to cause problems. Healthy fat replacements include tallow, butter or ghee, all of which are excellent for cooking.

Address Iron Excess and Copper Insufficiency

Another major culprit that destroys mitochondrial function is excess iron, and almost everyone, with the exception of menstruating women and those with large blood losses, have too much iron. On the other side of this coin is copper, which most people are deficient in.

Iron and copper are highly interdependent and need to be considered together. Low ferritin is rarely indicative of low iron. In most cases, it’s a sign that copper insufficiency is preventing proper iron recycling. Copper is also crucial for energy metabolism, detoxification and mitochondrial function.6 You can learn more about this in “The Poorly-Understood Role of Copper in Anemia.”

To increase your copper level, you can either take 4 to 10 milligrams of copper bisglycinate per day, or eat more copper-rich foods, such as bee pollen, grass fed beef liver and acerola cherry. (Acerola cherry is very high in vitamin C, which contains the copper-rich tyrosinase enzyme.)

The other side of the equation is to lower your iron, which is easily done through regular blood donations. One way is to simply donate blood two to four times a year. If losing 10% of your blood in one sitting is problematic, 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 150 ml
Postmenopausal Women 100 ml
Premenopausal Women 50 ml

The Importance of Sun Exposure

A third leading contributor to mitochondrial dysfunction is lack of sun exposure. Getting regular sun exposure is crucial for several different reasons:

1.UVB triggers vitamin D production in your skin — In addition to playing an important role in infections, vitamin D is also necessary for mitochondrial function and cell health in general.7,8 The ideal source of vitamin D is sun exposure, so if you live in an area with plenty of year-round sunshine, aim to expose as much bare skin as possible for about an hour during solar noon.

If you live in an area that doesn’t get enough sunshine during parts of the year, you’ll want to take a vitamin D3 supplement, along with magnesium and vitamin K2.

You need 244% more oral vitamin D if you’re not also taking magnesium and vitamin K2,9 so taking them together means you need far less vitamin D in order to achieve a healthy vitamin D level, which is between 60 ng/mL and 80 ng/mL (150 nmol/L to 200 nmol/L).

2.Near-infrared rays in sunlight shining on your bare skin trigger melatonin production in your mitochondria10 — The vast majority of the melatonin your body produces (95%) is made inside your mitochondria in response to near-infrared radiation from the sun. Only 5% of melatonin is produced in your pineal gland.

Melatonin is a master hormone,11 a potent antioxidant12 and antioxidant recycler,13 a master regulator of inflammation and cell death,14 and an important anticancer molecule.15

Melatonin has also been shown to be an important part of COVID treatment, reducing incidence of thrombosis and sepsis16 and lowering mortality,17,18 and is a known cytoprotector with neuroprotective properties that can potentially reduce the neurological sequelae documented in patients infected with COVID-19.19

When your mitochondria produce ATP (the energy currency of your cells), reactive oxygen species (ROS) are created as a byproduct. ROS are responsible for oxidative stress, and excessive amounts of ROS will damage your mitochondria, contributing to suboptimal health, inflammation and thrombosis (blood clots).

Melatonin production in your mitochondria is your body’s built-in mechanism to counteract this damage, but in order for this invaluable system to work, you must expose your body to near-infrared light. While you can raise your vitamin D level using a supplement, this cannot be done with melatonin.

Oral melatonin supplements do not wind up in your mitochondria where they are needed most to quench the damage from oxidative stress produced in the electron transport chain. An alternative to sun exposure would be to use a near-infrared sauna, described in “Near-Infrared Sauna Therapy — A Key Biohack for Health.”

3.Near-infrared light also:

  1. Increases mitochondrial ATP production
  2. Increases autophagy
  3. Increases heat shock proteins, which help proteins maintain their three-dimensional structure and refold misfolded proteins
  4. Reduces inflammation
  5. Triggers the conversion of retinol (vitamin A) to retinoids, which are crucial for immune function
  6. Structures the water in your body — Structured water acts like a storage battery that stores energy in your body in your blood, and helps push blood cells through your capillaries

Restore Metabolic Function With Time-Restricted Eating

The vast majority of people eat across 12 hours or more, which is a recipe for metabolic disaster. Health statistics bear this out. In July 2022, the Journal of the American College of Cardiology20 posted an update on the metabolic fitness or flexibility of the American population.

Metabolic fitness includes things like blood glucose and blood sugar, blood pressure and weight, and metabolic flexibility refers to your body’s ability to seamlessly transition between burning fat and carbohydrates as your primary fuel.

TRE is one of the easiest yet most powerful interventions for restoring metabolic flexibility and optimizing your mitochondrial function, which is key for recovery from any illness or disease.
In 2016, 12.2% of Americans were considered metabolically fit.21 Two years later, in 2018, only 6.8% of U.S. adults had optimal cardiometabolic health.22 That was four years ago so, today, that ratio is probably even lower, especially if you consider the number of people who are now struggling with mitochondrial dysfunction as a result of the COVID jab.

TRE is one of the easiest yet most powerful interventions for restoring metabolic flexibility and optimizing your mitochondrial function, which is key for recovery from any illness or disease.

As a general rule, I recommend compressing your eating window to between six and eight hours, and fasting for the remaining 14 to 16 hours each day. The timing of that eating window is important though.

You want to avoid eating first thing in the morning (wait at least two or three hours) and you want to avoid eating right before bed. Ideally, have your last meal at least three hours or more before bedtime. So, to give you an example, you could eat all your meals between 10 a.m. and 6 p.m., or 11 a.m. and 5 p.m.

Optimize NAD+

Boosting nicotinamide adenine dinucleotide (NAD+) is, I believe, another crucial component when treating COVID jab injuries and long COVID. NAD+ is a crucial signaling molecule believed to play an important role in mitochondrial function and longevity.

NAD is used up by DNA repair enzymes and enzymes involved in inflammation and immunity, such that chronic inflammation or acute illness can rapidly result in depletion. To learn more about the role of NAD+ in health, see my interview with Nichola Conlon, Ph.D., a molecular biologist, featured in “The Crucial Role of NAD+ in Optimal Health.” There are a number of ways to boost NAD+ without resorting to expensive supplements, including:

  • Circadian rhythm optimization
  • TRE and other forms of intermittent fasting
  • Low-dose niacinamide (not niacin), taken at a dose of 50 mg three times a day. More is not better as it will impair the function of your longevity proteins (sirtuins)
  • Intense exercise in a fasted state

Mitochondrial Rescuer: Methylene Blue

Methylene blue can be particularly useful for addressing the fatigue and neurological problems that are common in long COVID and COVID jab injuries, as it works as an electron cycler. It basically acts like a battery, but unlike other compounds that do the same thing, it doesn’t cause damaging oxidation in the process.

If anything interferes with oxygenation or cellular respiration, methylene blue is able to bypass that point of interference through electron cycling, thus allowing mitochondrial respiration, oxygen consumption and energy production to function as it normally would.

Methylene blue can also be helpful in instances where you have impaired blood flow that prevents the delivery of oxygenated hemoglobin to the tissues. In this case, methylene blue helps counteract the reduced blood flow by optimizing the efficiency of mitochondrial respiration.

Methylene blue also activates the Nrf2 pathway. Nrf2 is a transcription factor that, when activated, goes into the cell’s nucleus and binds to the antioxidant response element (AREs) in the DNA. It then induces the transcription of further cytoprotective enzymes such as glutathione, superoxide dismutase catalase, glutathione peroxidase, phase II enzymes, heme-1 oxygenase and many others.

Methylene blue’s action on mitochondrial respiration is also coupled with biochemical upregulation of your oxygen consumption machinery in general. This upregulation remains even after the methylene blue is expelled from your system, and over time, it can actually increase the number of mitochondria.

For neurological conditions, consider using methylene blue in combination with near-infrared sauna therapy. A 2020 paper23 in Translational Neurodegeneration reviews the benefits of this combination, specifically as it refers to neuroprotection.

Methylene Blue Dosages and Quality Considerations

Methylene blue is a hormetic, so low dosages have the opposite effect of high dosages. While every possible dose response has not been tested, as a general guideline, the benefits mentioned here are based on lower dosages, ranging from 0.5 mg per kilogram of bodyweight to 4 mg per kg at most. For brain health and nootropic effects, a dosage between 0.5 mg to 1 mg per kg per day is recommended.

Selecting the correct product is of crucial importance. There are three basic types of methylene blue: industrial, chemical and pharmaceutical-grade. The only version you’ll want to use medicinally is pharmaceutical-grade, which is 99%+ pure. Lower grades will contain varying levels of heavy metals and other contaminants.

Pharmaceutical grade will be marked USP, which stands for United States Pharmacopeia. Taking it with some ascorbic acid (vitamin C) facilitates absorption. To learn more, see “The Surprising Health Benefits of Methylene Blue,” in which I interview Francisco Gonzalez-Lima, Ph.D., who has spent many years studying this drug.

Posted in Coronavirus, EMF, Ferritin, Iron, Melatonin, Mortality, NAD+, Omega-3, Supplements | No Comments »

Posted by: | Posted on: November 28, 2022

The Dangers of Copper Deficiency and Iron Overload


Reproduced from original article:
https://articles.mercola.com/sites/articles/archive/2022/11/27/dangers-of-iron-overload-copper-deficiency.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     November 27, 2022

STORY AT-A-GLANCE

  • Iron and copper are highly interdependent and need to be considered together. Low ferritin is rarely indicative of low iron. In most cases, it’s a sign that copper insufficiency is preventing proper iron recycling
  • Copper deficiency will down-regulate several genes, including aldose reductase-1 (which plays a crucial role in glucose and fructose metabolism), glutathione peroxidase (a master antioxidant enzyme), mitochondrial aconitase (involved in iron metabolism in the mitochondria) and transferrin (which mediates the transport of iron)
  • Iron deficiency virtually doesn’t exist outside of acute blood loss that is unrelated to menstruation. Unless you have a history of acute blood loss, you are likely dealing with iron recycling dysfunction due to copper deficiency
  • The best way to lower excessive iron is to donate blood. Most adult men and postmenopausal women have high iron and could benefit from regular blood donation, as high iron is extremely toxic and destroys health
  • To raise your copper level, you could use a copper bisglycinate supplement, or foods like grass fed beef liver, bee pollen and whole food vitamin C

Here, I interview repeat guest Morley Robbins, MBA, CHC,1 founder of the Magnesium Advocacy Group and author of “Cu-RE Your Fatigue: The Root Cause and How to Fix It on Your Own.”

While we’ve discussed the topic of iron and copper before, the percentage of doctors and natural medical clinicians who understand his work is probably about 1% or less, so it’s well worth revisiting. Besides, it’s near-impossible to learn this information in a single interview without repeated review of these vital principles.

Iron is often viewed as a universal panacea that most need more of, but nothing could be further from the truth. The reality is that almost everyone, with the exception of menstruating women, or those with large blood losses, have too much iron.

Conversely, copper is often considered toxic, yet most people are deficient and actually need more in order for their iron metabolism to function properly. Without copper, your iron will not recycle properly, resulting in what appears to be a low iron level upon testing.

The real problem, however, is not low iron but low copper. Adding iron will only worsen the situation as excess iron is extremely damaging to your cardiovascular system. Iron rusts, and that’s basically what happens in your blood vessels as well.

Effects of Copper Deficiency

Robbins cites animal research2 from 2009 that looked at what happens to genes (which are responsible for encoding proteins) when rats are denied copper. As it turns out, six genes (and subsequent proteins) are down-regulated or turned off, while one gene in particular, transferrin, is upregulated, as follows:

  1. Beta-enolase (ENO3)
  2. Carbonic anhydrase, which increases carbon dioxide access, assisting rapid inter-conversion of carbon dioxide and water into carbonic acid, protons and bicarbonate ions. Carbonic anhydrase is billed as a zinc enzyme but it’s actually a copper enzyme
  3. Aldose reductase-1, which plays a crucial role in glucose and fructose metabolism
  4. Glutathione peroxidase (GPX), one of your master antioxidant enzymes, which is copper dependent
  5. Muscle creatine kinase, which your muscles need to function as it plays an important role in energy production
  6. Mitochondrial aconitase, which is involved in iron metabolism in the mitochondria
  7. Transferrin, which binds to and mediates the transport of iron through blood plasma, is upregulated, among others, in a state of copper deficiency

If you’re copper deficient, none of these genes will function properly, and beyond these, there are at least 300 other genes that are also copper-dependent. Your mitochondria also need copper for optimal function, and mitochondrial dysfunction is a driver of virtually all chronic disease and ill health.

The Importance of Copper for Mitochondrial Function

Copper and its master protein, ceruloplasmin, are instrumental for mitochondrial function. Ceruloplasmin is what drives the copper into the mitochondria, and each mitochondrion needs about 50,000 atoms of copper to do its work.

There are five cytochrome complexes embedded in your inner mitochondrial membranes. Their purpose is to shuttle electrons created from the food you eat that is ultimately converted to acetyl-CoA to produce ATP. If these complexes are deficient in key minerals you will not be able to generate enough cellular energy.

The enzymes of the mitochondrial respiratory chain are called mitochondrial respiratory complexes. Complexes 1, 3, 4 and 5 are copper-dependent. Complexes 1, 3 and 4 create what is called “the respirasome,” and they work together as a unit to stimulate NADH dehydrogenase activity. (NADH dehydrogenase is an enzyme that converts NAD from its reduced form, NADH, into its oxidized form NAD+, which is important for mitochondrial function and healthy muscle mass.)

Complexes 1, 3, 4 (acting as the respirasome) are hooked up to cardiolipin, a unique fat found only in the mitochondrial membrane that supports copper and enables the dynamics of the electron transport to take place. Retinol (vitamin A) is also crucial for moving electrons from complex 3 to complex 4.

The Type of Fat You Eat Matters

Now, the composition of fatty acids, such as cardiolipin, is completely dependent on what you are eating. If you’re like most Americans and 20% to 30% of the fat you eat is omega-6 linoleic acid, a high percentage of the fatty acids in the cardiolipin is going to consist of linoleic acid. If you eat a lot of saturated fat, or mono-unsaturated fat, then it’s going to be made up of that.

Why is that important? Because unsaturated fats like linoleic acid are predisposed to oxidation. And when you have oxidation in cardiolipin, you are destroying the structure of your mitochondria and decimating the ability of the mitochondria to function well. They can’t transfer electrons as efficiently when cardiolipin is oxidized.

The only place cardiolipin is found in your body is in the cristae of your inner mitochondrial membrane of your mitochondria. This is where most of your cytochrome complexes are embedded. If cardiolipin is damaged then the complexes will not be close together to form supercomplexes and thus they will not be able to generate as much mitochondrial energy. It’s also important to know what the match causing the oxidation is, and that’s iron.

“When people are told they have low iron in the blood, the practitioner doesn’t know that iron is high in the tissue, and then they give them more iron, and what’s the iron going to do? It’s going to find its way to the cell, and then it’s going to find its way to the mitochondria, and then, there’s this collapse in energy production,” Robbins explains.

Understanding Iron Testing

The confusion that pervades the iron issue is how to actually measure it. Seventy percent of the iron in your body is stored in the hemoglobin in your red blood cells, 10% is found in intercellular protein, and only one-tenth of 1% of the iron is serum iron, attached to transferrin.

The key detail here is that your red blood cells are not in your blood but actually float in the watery serum portion of the blood that gets measured when you do a blood test. So, when you’re measuring serum ferritin, you are not actually getting a true measure of your iron stores. Low ferritin is typically interpreted as low iron, but that is a major clinical mistake.

You need to look at all of the containers of iron — hemoglobin, serum iron and ferritin. You also need to look at non-iron markers such as zinc, copper and ceruloplasmin, as well as vitamin A and vitamin D because they influence the bioavailability of copper. This holistic evaluation is the focus of Robbins’ “Root Cause” protocol.

What’s the Problem if You Have Low Ferritin?

According to Robbins, when someone is told they have low iron because their ferritin is low, 99.9% of the time the real problem is iron recycling dysfunction related to copper deficiency. This contradicts almost every medical “expert” in the world, so it’s a major claim, but understanding it can have a significant impact on your health.

Basically, “iron deficiency” virtually doesn’t exist outside of acute blood loss that is unrelated to menstruation. Unless you have a history of acute blood loss, say due to an injury, you are likely dealing with iron recycling dysfunction due to copper deficiency.

“We have the myth of iron deficiency. We have the myth that iron regulates itself. It does not. It is entirely copper dependent. When you get into the real deep research, you’re going to find that copper is the General, iron is the foot soldier. Now try to picture the Battle of the Bulge without Patton. Very different story there.

The third is this idea that, ‘Well I feel so much better when I take iron.’ Dr. Robert E. Hodges in 1978 did a masterful job of explaining the deception of iron supplementation. It offers a six-week hit. Hemoglobin does go up, people are going to feel a little bit better. But it’s only going to last for six weeks.

He was able to document it meticulously in the three-year study that he did with humans. He was able to show exactly why they respond. The key is that any heavy metal, and iron is a heavy metal … is going to force increased red blood cells. There is this dynamic of heavy metals driving more red blood cells, [likely] to deliver more oxygen to deal with the toxicity.

But the increase of iron and the feeling better is short-lived and deceptive. When did all of the blood marker dynamics change in Dr. Hodge’s study? When he introduced retinol, which makes copper bioavailable.”

High Ferritin Is Often a Sign of Liver Dysfunction

On the flip-side we have high ferritin. This is routinely interpreted as having normal (or high) iron stores, but that’s not accurate either. Importantly, when you have high ferritin, it’s oftentimes a sign of liver dysfunction. The ferritin is spilling out of the liver into the bloodstream because the recycling center of the hepatocyte is not working.

The liver’s recycling center is called the lysosome. This is where ferritin is turned over to make iron available for use. When that lysosome isn’t working right, iron will accumulate in the liver, causing ferritin to be secreted into the cell. The key to proper iron recycling in the liver is, again, copper. The loading of iron in ferritin that takes place inside the cell, and the recycling of ferritin inside the cell, is entirely copper-dependent. Robbins explains:

“Copper goes into the ferritin as a result of ferroxidase enzyme function, which is copper driven. And then, copper is needed to recycle that ferritin protein, break it down and let the iron out. It’s a copper-dependent process.

People don’t realize the role that copper chaperones are playing to move that iron where it’s needed in the body. And the principle chaperone for iron in the blood, the serum iron, is transferrin.”

As mentioned earlier, the gene that encodes transferrin is upregulated when copper is deficient. So, transferrin rises counterintuitively, due to copper insufficiency, iron gets sequestered into the RES macrophages, and thus iron is not recycled and distributed properly. Robbins continues:

“There was a different [study in which] they were using rodents, denying [them] copper. They were looking at 13 different genes. The only gene that fired up in the face of copper deficiency was the ferritin light chain (FTL) gene. It’s very different than ferritin heavy chain (FTH), which is copper-dependent, because it, again, relies on the ferroxidase enzyme.

And where is ferritin light chain found? It’s found in the liver, and iron builds up in the liver in a copper-deficient body. We’ve known that since 1928 … (Hart et al., 1928)

I think what’s important, the big macro for everyone in this conversation, is to see the profound interaction that copper and iron have in our metabolism, and that there is no iron metabolism, there’s only copper-iron metabolism, and you can’t make conclusions on iron status, by measuring just serum ferritin status.”

How Much Iron Do You Need?

As mentioned, unless you’re losing a lot of blood, your iron will (most likely) be high. The reason for this is because your body has no way of eliminating iron, other than blood loss.

High iron, due to its corrosive nature, can cause tremendous damage inside your body. You only need 25 milligrams of iron in your body for red blood cell maintenance, and 24 of those 25 mg come from the recycling system (provided you have enough copper to make it work as it should).

So, you need very little iron from your diet — only 1 mg per day. The problem is that the optimal amount of iron needed is about 5,000 mg. Older people can have closer to 25,000 or 30,000 mg, thanks to excessive intake over the course of their lives.

“What’s happening is there’s total silence about iron recycling,” Robbins says. “Because we live in this copper deficient environment, the recycling system is not as efficient. The serum iron is going to show low under those conditions. The doctor is going to react with, ‘You need more iron,’ when in fact what you need is more copper. The recycling system is dependent upon one iron egress doorway.

It’s called ferroportin (iron doorway) and ferroportin entirely depends on a copper enzyme. It’s called hephaestin. It’s a copper protein that expresses the exact same enzyme as ceruloplasmin, called ferroxidase.

What hephaestin does is make sure that the iron gets out of the recycling macrophages as soon as possible — 2.5 times faster than if copper’s not present — and ensures it’s loaded onto transferrin to take that iron to the bone marrow [where red blood cells are created 2.5 million times per second].

That recycling system that’s occurring all day and all night is never factored into the clinician’s interpretation of blood work. They’re just seeing low numbers and they’re not thinking recycling, they’re only thinking replacement.

I think that would be a really important takeaway for people — to question your doctor’s assertion that more iron is needed, ‘Could it be that my iron recycling system isn’t working right, as opposed to my need for new iron?’”

Optimize Your Health by Donating Blood and Boosting Copper

The good news is that lowering your iron, which has many health benefits and can improve your life span, is easy to do. All you need to do is donate blood two to four times a year. As explained by Robbins:

“Blood loss is the only way to bring iron levels down in the human body. We’ve been trained to think we’re anemic and we’ve been trained to think we need to replace the iron, when in fact the missing piece of the puzzle is bioavailable copper — which is copper in the presence of retinol — so that the enzymes get properly loaded and can properly function.”

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 150 ml
Postmenopausal Women 100 ml
Premenopausal Women 50 ml

Lowering iron is one side of the equation. The other is increasing copper and retinol. For copper augmentation, Robbins recommends taking up to 3 to 4 mg of copper bisglycinate per day, or eating copper-rich foods, such as bee pollen, grass fed beef liver and acerola cherry. (Acerola cherry is very high in vitamin C, which contains copper-rich tyrosinase enzyme.)

Retinol is found in beef liver and beef organs, so if you eat that, you may not need any kind of supplement. Absent that, cod liver oil is a recognized source of real retinol.

More Information

In the interview, we also review a recent case study of a woman with persistent low ferritin, despite doing everything Robbins recommended, and what it took to resolve this case. So, for more details, be sure to listen to the whole interview.

We discuss the negative influence the stress hormone cortisol has on bioavailable copper (which can result in stubbornly low ferritin levels), and how addressing emotional knots using the Emotional Freedom Technique (EFT) can be instrumental in healing cases where stress and emotional turmoil play a part.

Robbins also reviews how dysfunctional iron metabolism and copper insufficiency affects conditions such as schizophrenia, obesity, ulcerative colitis and Crohn’s disease.

To learn more, be sure to visit Robbins’ website, RCP123.org, where you’ll find hundreds of YouTube videos and articles. There you can also access Robbins’ Root Cause Protocol, as well as his online RCP Institute training program, which is a 16-week course. Of course, you can also learn more from his book, “Cu-RE Your Fatigue: The Root Cause and How to Fix It on Your Own.”

Posted in Ferritin, Iron, Liver, Minerals, Mitochondria, Supplements | One Comment »

Posted by: | Posted on: September 12, 2022

The Poorly-Understood Role of Copper in Anemia

Reproduced from original article.
Dr Mercola’s web site has been moved to https://mercola.substack.com.

Analysis by Dr. Joseph Mercola     Fact Checked     September 11, 2022

STORY AT-A-GLANCE

  • Iron and copper are highly interdependent and need to be considered together. If you don’t have enough copper in your diet, hemoglobin production becomes impaired, along with many other aspects of iron metabolism
  • Being anemic does not automatically mean that you’re iron deficient. Anemia typically relates to impaired iron recycling, not deficiency, and impaired iron recycling is caused by copper and retinol deficiency
  • The best way to lower excess iron is to donate blood, one to four times a year. Most adult men and postmenopausal women have high iron and could benefit from regular blood donation, as high iron is extremely toxic and destroys health. An even better strategy is to remove smaller amounts of blood every month
  • To raise your copper level, you could use a copper supplement, but foods like grass-fed beef liver, bee pollen and whole food vitamin C are better
  • If you’re a farmer or grow your own food, the best way to put copper back into the soil, to get it into the food, is to add copper sulfate. Before you plant, simply spray the soil with copper sulfate, 10 to 15 pounds per acre, or use a copper sulfate foliage spray

Morley Robbins, MBA, CHC,1 a repeat guest, is the founder of the Magnesium Advocacy Group. He’s best known as the Magnesium Man, and is the author of “Cu-RE Your Fatigue: The Root Cause and How to Fix It on Your Own,” in which he explains the roles of magnesium, copper, iron, vitamins A and D and other essential nutrients.

His Root Cause Protocol2 is the implementation of that information. We’re currently planning to write a book together, which will focus on the little-understood importance of copper and its interaction with iron.

As explained by Robbins, if copper is lacking in your diet, iron will build up in your liver, which changes its physiology and immunoproperties. Liver metabolism is highly dependent on copper and retinol, and there’s not a lot of awareness of that.

“It’s a very sophisticated process of interaction between copper and iron, and if that interaction doesn’t go well, iron is going to start to accumulate in the tissues. It’s going to start in the liver, but it’s going to go elsewhere too,” he says.

“I think that is kind of the takeaway of these conversations — to make sure people know that iron does accumulate, and that iron can be reduced through blood donations. Especially as you get into your 50s, 60s, 70s, it needs to be a regular part of your health routine.”

Three Ways to Measure Iron Status

The clinical term for excess iron in the liver is hemosiderosis, and it’s so pervasive as to be near-universal. But where does the excess iron actually come from? And why is it that many with high iron stores have low serum ferritin?

As Robbins explains, oftentimes, low serum ferritin is not at all a sign of iron deficiency, but rather a deficiency in copper and retinol. The deficiency in copper basically locks iron in the liver and prevents it from being recycled as it should:

“It’s important for practitioners to not measure iron status with just one marker. I think a lot of practitioners are falling into that trap of just using serum ferritin. There are three key ways to measure iron status: Hemoglobin, serum iron and serum ferritin.

The biggest concentration of iron in the body is in our hemoglobin; 70% of the iron is in our red blood cells … Hemoglobin is essential to understand what is going on with the biggest bulk of iron.

The second marker that I really focus on is called serum iron. It’s less than 1% of the iron, but it’s a very important measure of iron because it’s really getting at the iron recycling program. Every second of every day, we have to turn over 2.5 million red blood cells. That’s a lot of activity. In the course of 24 hours it’s 200 billion red blood cells that need to be turned over.

But what’s a surprise is to learn that only 25 milligrams (mg) of iron are needed to support that 24-hour cycle, but 24 of those 25 milligrams, 95% of the iron, is coming from this recycling program. So, it’s a very significant understanding that the serum iron only represents a small percent, but it represents the efficiency of the iron recycling.”

Ideally, hemoglobin should be between 12.5 and 13.5 for women, 14.5 to 15.5 for men. Serum iron should ideally be about 100 for women and 120 for men. The closer serum iron is to these, the more efficient your recycling is.

What You Need to Know About Serum Ferritin

The third iron measure is serum ferritin. There are four different types of ferritin in your body, broadly categorized as heavy chain and light chain. Heavy chain ferritin refers to ferritin protein inside cells and mitochondria that require copper to work properly. Serum ferritin refers to ferritin in your plasma, is outside the cell — and also outside the red blood cells, the hemoglobin.

“What is not well-known is that this ferritin that shows up in the blood is very iron-poor. It doesn’t have iron in it. The iron has been discharged in the liver and then the protein gets secreted out … So, serum ferritin is not representative of iron per se. The iron was discharged in the liver …

I would never use ferritin only as an indication of iron status. You need to see hemoglobin, serum iron, and serum ferritin. You need to see them in relationship to each other …

[When] serum ferritin starts to get high, it’s highly correlated with inflammation or an infection. And again, it makes sense. The liver is taking it on the chin. Iron is not being metabolized properly. Pathogens might be involved. And so, the body starts to secrete the ferritin in a more significant way …

Serum ferritin should be between 20 and 50. That seems to be a nice sweet spot for people. When the serum ferritin begins to get up in the hundreds, there’s a significant likelihood that there’s pathology in the liver that’s causing that …

For women, the serum ferritin red flag goes up at 150. For men, the red flag goes up at 300. It can go up into the 5,000s and even higher, with severe chronic disease and inflammation …

Low ferritin is an indication of metabolic breakdown in the spleen … it’s some kind of parasitic dynamic that’s affecting protein production. The ferritin protein is not getting transcribed properly …

So, low ferritin … means low recycling. Something in the iron recycling system is out of balance and needs attention. I would argue that, almost without exception, it’s a lack of bioavailable copper. The spleen organ is intensely copper dependent. The liver intensely copper dependent. That’s not well known in clinical circles.”

So, to summarize, one of the most common errors doctors will make is to prescribe iron pills when serum ferritin is low. More than likely, what’s needed is copper, retinol and other factors to support iron recycling. Unfortunately, articles and textbooks on iron metabolism rarely if ever mention the copper side, even though copper plays a far more important role in the recycling of iron.

Why Blood Donation Is so Important

Most all men and non-menstruating women have excess iron. The reason for this is because many foods are fortified with iron, and your body has no excretory system for iron besides blood loss. So, it accumulates, and if the recycling mechanism doesn’t work properly, the iron gets lodged in tissues.

This is why regular blood donations are so important. Less iron means less oxidative stress, which is going to create less metabolic dysfunction, which results in fewer health problems and less tissue damage.

Every day you’re alive, your body accumulates about 1 mg of iron. Add up 1 mg of iron for every day of your life, and you’ll realize you won’t be able to eliminate all of it even if you tried. When you take out one unit of blood (500 cc), you remove about 250 mg of iron.

If donating a full pint (half a liter, 500 ml or about 8 ounces) of blood three to four times a year is problematic, you can remove blood in smaller amounts once a month on the schedule listed below.

Men 150 ml
Postmenopausal Women 100 ml
Premenopausal Women 50 ml

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. I personally remove 60 cc or 2 ounces of blood once a week, which is about 7 pints per year. This is a large amount but because it is done slowly it is far better tolerated. Robbins adds:

“I think what’s amazing is the sheer simplicity of doing a blood donation, and what it does to revitalize the body. When you have that blood loss, it trips a wire for erythropoietin, a very important hormone that triggers the production of new red blood cells.

And the beauty is it actually has two signals. The second signal is, let go of the iron in the tissue. It has a very powerful effect of releasing the iron to get it back down to the bone marrow, where it’s needed to make the new red blood cells.”

Hepcidin and Hemosiderin

To fully understand iron metabolism, you also need to understand the roles of hepcidin and hemosiderin. A ferritin protein can hold as many as 4,500 atoms of iron. Each iron atom has four unpaired electrons, which causes oxidative stress. Hemosiderin, an iron-storage complex composed of partially digested ferritin and lysosomes, can hold 10 times more iron than ferritin.

This also means it holds 10 times more unpaired electrons. When hemosiderin builds up in your tissue, that’s when you start having serious issues with iron regulation.

“What’s wildly confusing is hepcidin, [which is encoded by] the HAMP gene,” Robbins says. “Hepcidin is an antimicrobial peptide. So, it’s got some connection to pathogens. And what’s it trying to do? Hepcidin is trying to get iron out of the circulation, to get it away from the pathogens. But it’s a bit of a slippery fish because it reacts to iron status. It reacts to inflammation status. It reacts to hormonal status.

Estrogen and testosterone have significant influence over hepcidin. It’s reacting to copper status … Elevated levels of active hormone D [vitamin D] can suppress hepcidin. Retinol deficiency can increase hepcidin …

The key is understanding that this constant recycling system of the red blood cells, the iron doorway, is being opened by a copper doorman. And if copper isn’t doing its job, we’re going to have a problem. And what is hepcidin’s job?

Hepcidin shuts down the iron doorway. So, we have this significant dynamic between this very important iron egress that needs bioavailable copper, and if bioavailable copper’s not there, this hepcidin protein is going to shut it down.

That’s where a lot of the confusion is because the true anemia that exists on the planet isn’t one of iron deficiency. It’s one of copper deficiency not allowing for proper iron recycling. That’s a very important nuance.

And the misunderstanding is that iron may look low in the blood, ferritin looks low or hemoglobin looks low, serum iron looks low, but it’s high in the tissue. There’s no blood test that measures iron status in the tissue.”

Excess Iron Can Cause Dysfunction in Many Organs

A colleague of Robbins in Miami, Florida, has developed a way to measure iron in the liver and brain using a Tesla 2 MRI and a novel scoring technique. This technique was catalyzed by my previous interview with Robbins, because the doctor in question was initially skeptical, but after measuring his own liver iron, he was shocked at the amount stored in there.

But iron is also stored in other organs, including your heart, which can have serious consequences. Robbins explains:

“Jerry Sullivan, a pathologist — his real focus was on cardiology — developed what became known as the iron heart hypothesis. It’s not a very popular thesis with cardiologists, but he was able to prove that it was accumulation of iron in the heart muscle cells that were causing the wide spectrum of all the issues, whether it’s atrial fibrillation, enlarged heart, any kind of myocardial infarct.

He was able to link it back to the accumulation of iron, and what that was doing to kill energy production in that incredibly important organ in our body. So, the accumulation of iron in our organs is very significant, because these organs are supposed to be producing energy to do their function …

Too much iron syncs up with the symptoms that are laid out in the Merck Manual. You can trace just almost every one of them back to this iron-copper dysregulation, because copper’s supposed to be regulating the iron. And when it doesn’t do that, it starts to accumulate … and then cause dysfunction and dysregulation in the body.”

Food Supply Nearly Devoid of Copper

As mentioned, iron recycling depends on copper and retinol, both of which are lacking in our food supply, thanks to depleted soils. Copper is further eliminated through processing and refining. Making matters worse, our food supply is chockful of iron, sugar and seed oils (which are loaded with linoleic acid) and this triad suppresses copper and retinol function.

For these reasons, copper supplementation can be a good idea, especially if you’re anemic, in addition, of course, to reducing or eliminating iron, sugar and seed oils.

“My new phrase, and I don’t know whether it’s going to get traction or not, but I’m coming to the opinion that sugar is white iron,” Robbins says. “People don’t realize how glucose metabolism influences iron metabolism, especially accumulation of iron, and it’s absolutely staggering when you get into it.

So, I think it’s important for people to just be aware that sugar isn’t just bad, it’s really bad. And I think the coupling with the linoleic acid, it’s out of control.”

Facts About Retinol

Retinol is vitamin A, which is not the same as beta carotene. They are two different distinct molecules, not to be confused, although nutrition labels get away with conflating beta carotene with vitamin A. Vitamin A also should not be confused with retinyl palmitate.

What people believe is “vitamin A toxicity” is actually a sign of iron toxicity in the liver, caused by copper deficiency. What happens is, when you get vitamin A from your diet, be it cod liver oil, beef liver or free range eggs, the retinol is turned into retinyl palmitate and gets stored in the stellate cells in your liver.

To function properly, the retinyl palmitate then needs to be turned back into retinol, so it can be transported on the transthyretin (TTR) protein, composed of T4 and retinol. Without the retinol, TTR becomes destructive. While Robbins cannot prove it yet, he’s convinced that copper is required for the conversion of retinyl palmitate to retinol.

“And while we’re talking about retinol, it’s probably important for people to know [that] retinol as a key component of the movement of electrons from complex 3 to complex 4. The electron actually rides the back of the retinol structure. That alone is mind blowing to think about that.

If retinol is not in our diet, then it’s not in our electron transport chain, then it’s not able to support the optimal generation of energy. So think of retinol as an energy-focused nutrient. It’s very unusual, because most of its [known benefits are] around immune system or vision.”

Retinol is best obtained through whole foods, such as cod liver oil, beef liver, free range egg yolks (the deeper orange the yolk, the more retinol it contains), cacao and hot cocoa, and organic grass fed butter, ghee and heavy cream.

More on Copper

Copper also plays an interesting role in energy production. Your mitochondria produce melatonin in response to natural sunlight, and melatonin in turn catalyzes and upregulates glutathione, which is important for energy production, antioxidant protection against free radical damage and more.

As explained by Robbins, glutathione is also the “greeter” of copper in the cell’s cytoplasm. There are two metabolic steps to make glutathione, and one of the steps involve cysteine, which has a very tight relationship with copper.

Furthermore, a copper-dependent enzyme is required to convert serotonin into melatonin. Copper is also instrumental in regulating immune function. All of these functions are yet more reasons to make sure your copper level is optimal.

How to Optimize Your Copper Level

As for raising your copper intake, it’s best to get your copper from food and not a supplement. Good sources include bee pollen, grass fed beef liver and other organ meats. You also want plenty of saturated fats in your diet, as copper is a fat-soluble mineral. If you don’t have fat in your diet, your ability to absorb copper plummets.

If you do opt for an oral supplement, Robbins suggests 3 to 4 mg of copper bisglycinate per day, taken with a fatty food (as it’s a fat-soluble mineral). The upper tolerable limit is 10 mg. This is so good because it has no charge on the molecule and readily penetrates cell membranes.

If you’re a farmer or grow your own food, you can put copper back into the soil, to get it into the food, by adding copper sulfate. Before you plant, simply spray the soil with copper sulfate, 10 to 15 pounds per acre. Alternatively, use a copper sulfate foliar spray, which is what I do.

Most farmers merely use NPK (nitrogen, phosphorous and potassium) fertilizer and NPK actually blocks copper uptake in the plants, which was highlighted by Andre Voisin, Ph.D., in his 1957 classic (which, sadly, is now out of print): “Soil, Grass & Cancer.”

Vitamin C Can Help Augment Copper Level

Whole food vitamin C can also boost your copper level, as vitamin C contains an enzyme called tyrosinase, which has 2 atoms of copper in it. Acerola cherry is one excellent source. A single acerola cherry contains about 80 mg of whole food vitamin C. Ascorbic acid is prooxidant, while vitamin C complex is actually an antioxidant. Anything that has copper is going to be antioxidant.

Do not make the mistake of taking ascorbic acid, however, as it is NOT the same as whole food vitamin C. If you were to compare the two to a car, vitamin C would be the whole car, fully functional, and the engine is an enzyme called tyrosinase, while ascorbic acid is the car frame, with no moving parts.

Importantly, ascorbic acid chelates copper out of tyrosinase, which is exactly what proton pump inhibitors do. It’s my view that ascorbic acid is a “pharmacomimetic.” While it’s a natural molecule, it has drug-like effects. It acts differently from vitamin C because it’s been taken out of the vitamin C complex. For example, ascorbic acid does not prevent or treat scurvy. Only whole food vitamin C does.

Ascorbic acid was identified by two scientists who also discovered ceruloplasmin, the major copper-carrying protein in your blood, and ascorbic acid can affect the structure and the copper composition of this crucial copper protein too.

The ideal ratio of copper to ceruloplasmin is copper around 100, and ceruloplasmin at 30, giving us a ratio of 3.33. If that ratio starts to rise or fall, then you likely have some kind of pathology going on.

A ratio in the fours and fives is often indicative of inflammation or an infection of some sort. When it starts to drop precipitously, it’s a clear sign that there isn’t adequate copper to fuel the function of ceruloplasma protein. So, to summarize the key take-home, if you’re going to take vitamin C, use whole food vitamin C, not ascorbic acid.

More Information

If you missed our last interview, where we went deep into iron metabolism and recycling, you can find it here. You can also learn more on Robbins’ website, RCP123.org, which stands for Root Cause Protocol.

“We have an RCP community that you can join, where every other week we have Q&As. People get to ask questions and we do our best to answer them. And then we offer training through the RCP Institute. We’re about halfway through the class now. Historically, we’ve had 20 or 30 students in each class.

It started to creep up, and this class is 220 students. So, word is getting out. And it’s a very switched on group of people. I’m absolutely blown away by the caliber. But we have intakes and the classes are in the beginning of the year and then the second half of the year, for 16 weeks.”

– Sources and References

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