Health & Fitness

Dr. Mercola Interviews the Experts

This article is part of a weekly series in which Dr. Mercola interviews various experts on a variety of health issues. To see more expert interviews, click here.

Boyd Haley, Ph.D., is a chemist specializing in the development of chemicals to chelate toxic metals, both from the environment and the human body. I had the opportunity to interview Haley (above) at the 2018 Academy of Comprehensive Integrative Medicine (ACIM) conference in Orlando.

Haley has a Ph.D. in chemistry and biochemistry and conducted research funded by the National Institutes of Health (NIH) for 25 years at the University of Wyoming and at the University of Kentucky. Early in his career, he developed a biochemical detection system called nucleotide photoaffinity labeling and has published studies on its usage.¹ Haley explains:

"I took ATP and made it radioactive, which isn't a big feat. But then I attached to that a molecule that would explode when it hit a photon of light. When it exploded, it made a very reactive intermediate that had a half-life of something like 10-12 or 10-13 seconds.

If ATP was bound to a protein, such as sodium potassium ATP [and] … you hit it with light, it would form a covalent bond at the binding site of ATP on the enzyme it was interacting with …

You could use these kinds of probes to see the difference between the ATP, guanosine diphosphate (GDP), cyclic adenosine monophosphate (AMP) and nicotinamide adenine dinucleotide (NADH) — all these binding proteins, to see how the energetics of the cell was changing."

Haley's Alzheimer's Research

He later took a position with the Alzheimer's Center, a research center for Alzheimer's disease, where he collaborated with a former graduate student of his. The NIH funded their research for five years, which used Haley's technology to assess the differences of ATP, GDP and cyclic AMP binding proteins in normal brains versus those with Alzheimer's disease.

"There were dramatic differences," he says. For example, the enzyme creatine kinase, which is a fundamental enzyme, is 98 percent inhibited in Alzheimer's patients. They also discovered that tubulin — a major brain protein that holds an axon in its extended form and controls the growth direction of axons and dendrites — is inhibited by more than 80 percent.

In 1989, he published the paper² "Aberrant guanosine triphosphate-beta-tubulin interaction in Alzheimer's disease" in the Annals of Neurology, stating that "These results support the hypothesis that microtubule formation is abnormal in brains affected by Alzheimer's disease."

Haley goes on to recount the story of how he got into trouble with the NIH when he decided to investigate the influence of heavy metals on Alzheimer's susceptibility. A popular theory at the time was that Alzheimer's was caused by aluminum toxicity.

Using his technology, he was able to show that mercury was the only heavy metal capable of causing a normal brain to develop the same biochemical abnormalities — including abnormal tubulin — that you find in Alzheimer's disease.

Haley claims his research has since been replicated and confirmed. According to Haley, mercury causes the synaptic clefts to disappear and triggers the formation of neurofibrillary tangles, a major diagnostic hallmark of Alzheimer's, by causing abnormal hyperphosphorylation of tau.

He also published a paper³ in the respected medical journal Proceedings of the National Academy of Sciences in 1992, detailing how the presence of glutamine synthetase in the cerebrospinal fluid may be a potential diagnostic biochemical marker of Alzheimer's disease, as well as more than 100 other studies,⁴ including a review of the relationship between mercury and autism,⁵ and research showing how the chelating agent he developed, emeramide (NBMI), protects against the cytotoxicity of mercury.⁶

All Biochemical Abnormalities and Hallmarks of Alzheimer's Are Stimulated by Mercury

Beta-amyloid, which many associate with Alzheimer's, is not the actual cause of the disease. It's just a marker; it's a result of the disease. However, you can cause beta-amyloid buildup in the brain by treating neurons with mercury.

"What happens is mercury inhibits the expression of neprilysin, which is the main protease in the brain used to chew up beta-amyloid. Mercury doesn't affect beta-amyloid, but what it does do is it keeps the protease, the cleanup enzyme, from being expressed," he explains.

"If you give mercury at low levels, very low levels, to tissues that are going to live for a while, you'll see a buildup of beta-amyloid protein. The bottom line is: 6 out of 6 of the major biochemical abnormalities and pathological hallmarks of Alzheimer's disease can be stimulated by adding mercury.

I can tell you that was something that NIH, or the people who run NIH at the very top, did not want to hear … They said beta-amyloid is the cause of Alzheimer's disease. That made them heroes — they found the cause, so now they would find the cure …

But they don't want to look at it being something simple. There's no money to be made if you tell people, 'If you don't want to get Alzheimer's disease, don't expose yourself to mercury.'

Mercury is not the only cause. I would never say that, and I never did say that. I said, 'Mercury is the major exacerbating factor⁷ because we put dental amalgams in our mouth, and the major exposure, the source of mercury in our body, comes from them [sic] amalgams, according to the World Health Organization (WHO).'"

The Transformation of a Skeptic

It's interesting to note that Haley was in fact highly skeptical of the idea that dental amalgam released mercury before he started studying the matter. Like so many others, he assumed the U.S. Food and Drug Administration (FDA) and the American Dental Association would never allow something truly toxic to be placed in people's mouths.

His scientific investigations eventually convinced him that amalgams are a major source of mercury exposure that can indeed exacerbate and trigger chronic illness — something he details in his 2014 paper,⁸ "Evidence Supporting a Link Between Dental Amalgams and Chronic Illness, Fatigue, Depression, Anxiety and Suicide."

Haley also recounts the twists and turns in his life that brought him to investigate the links between mercury toxicity and autism, and how vaccines can be a source of toxic mercury exposure. While thimerosal (mercury-based preservative) has been removed from many childhood vaccines, it's still used in some.

One tipoff that thimerosal was bad news came from a 1977 report from Toronto Hospital, where 10 of 13 infants died after having their umbilical region treated with merthiolate (thimerosal) to kill bacterial infection. Merthiolate is no longer in use, as it was discovered that these infants died from mercury toxicity.

This report revealed that thimerosal turned into ethyl mercury, which the infant body cannot eliminate. Despite that, a mere decade later, in 1988, the U.S. Centers for Disease Control and Prevention (CDC) decided thimerosal was an appropriate preservative for use in vaccines given to newborn babies and infants.

How Genetics Influence Your Mercury-Elimination Capacity and Therefore Alzheimer's Risk

Haley completed his Alzheimer's research in 1988, just over 30 years ago, yet he's never been invited to an Alzheimer's conference to present his work. He has also published a book in which he proposed a mechanism for why having two copies of the ApoE2 gene renders you more or less immune to Alzheimer's.

The ApoE2 gene has two cysteine molecules on the surface, whereas ApoE4 — which is a major risk factor for Alzheimer's — has two tyrosine molecules. These are amino acids on the structure. The cysteine amino acid on E2 binds effectively to mercury, whereas the tyrosine on E4 cannot bind to mercury at all.

As a result, having two copies of the ApoE4 gene places you at a significant disadvantage, as your brain cannot eliminate mercury naturally, whereas having two copies of ApoE2 is highly protective because your brain has the ability to clear out mercury.

It is also helpful to note that Dr. Dale Bredesen who wrote the book "The End of Alzheimer's," believes the ApoE4 allele may actually protect against Alzheimer's if you are metabolically flexible and regularly engage in intermittent or partial fasting.

Therapeutic Interventions to Address Mercury Toxicity

Alzheimer's disease is associated with oxidative stress. While mercury is not a redox metal, meaning it cannot create hydroxyl free radicals, mercury does displace iron and kaempferol, and when mercury displaces iron it stops ATP production in that electron transport system.

By displacing iron from the iron sulfur centers mercury also blocks the cytochromes, as cytochromes require iron to work. "There are publications now showing that mercury exposure totally screws up the metabolism of iron in the body," Haley says.

The chelating compound he developed, called emeramide or NBMI,⁹ tightly binds to both mercury and free iron, which is also highly toxic. As such, emeramide can also be used in the treatment of hemochromatosis, a genetic disease that causes chronic iron overload.

Drawbacks of Most Popular Chelating Agents for Mercury

Haley also discusses the drawbacks of using dimercaptosuccinic acid (DMSA) or 2,3-dimercapto-1-propanesulfonic acid (DMPS) to detoxify mercury — the two most commonly used chemical chelators. According to Haley, they are in fact not true chelators. Rather they form a "sandwich complex" where each molecule of mercury will have two DMSA molecules attached to it, opposed to just one.

A significant problem is their ability to translocate mercury from the blood and other organs and concentrating it in the kidneys, thereby causing renal failure. What's more, most of the mercury is not in your blood but rather in your cells, and neither DMPS nor DMSA can enter the cell, Haley claims. They only remove mercury from your blood.

"I initially developed the idea that I had to have a hydrophobic chelator that would get into the mitochondria, into the DNA … Mercury is hydrophobic. It's uncharged. It's a gas. It goes through the biomembrane. You have to have a chelator that does the same thing.

[The mercury] starts out as a gas. It goes in as Hg0 when you breathe mercury vapor [from your mercury dental fillings], and then it goes wherever it wants. [If you're eating fish], then it will be methyl mercury, but it's the same thing. Methyl mercury is also membrane-permeable.

It goes right through membranes because it binds. It's CH3Hg+. But if it's in the blood, there's a high level of chloride, and chloride binds that negative charge, so you end up with some of the Hg methyl mercury in the chloride form that can go right through the membrane because it's uncharged. That's the reason it gets through the brain so effectively," Haley says.

"[T]hen, in the brain or in any tissue, it gets converted into Hg2+ by an enzyme called catalase … and then it becomes very toxic; it's charged, and then it won't go out [of the cell]."

Haley's Decision to Develop a Better Chelator

Haley's decision to develop a better chelating agent for mercury was the result of failed attempts to alert health authorities to the very real dangers of thimerosal in vaccines.

"One night I was sitting at home. I have a daughter who has a Ph.D. in molecular biology and toxicology. She called me up when she was writing her Ph.D. thesis. She said she found a website that mentioned me, and it wasn't very complimentary, to say the least.

She was kind of sad and teary. It made me angry that I just let those people go and say those things … I remember that night [in 2002] very vividly. I sat down with a glass of red wine … and said, 'How do I win? I can't out-PR these guys. You cannot out-PR the CDC' … That was the night I decided, 'I'm a chemist. I make things. I'm going to make a better chelator.' That's the way I went.

I wrote a grant. I got some funding to try and make the chelators that would enter the cells … If you're going to use a chelator, the first thing it has to be is nontoxic itself … It had to be hydrophobic [to] pass the blood-brain barrier and get in the cells …"

Haley recounts the history of how emeramide was developed— and describes the differences between it and DMPS and DMSA. Importantly, emeramide is nontoxic and binds very tightly to mercury. It's also a very potent antioxidant, with two glutathione "arms." (Glutathione is a powerful antioxidant produced in your body that is instrumental in detoxifying mercury and other toxins.)

Haley believes its antioxidant power comes from the glutathione components, which scavenge hydroxyl free radicals. Other testing showed each molecule of emeramide scavenges three hydroxyl free radicals. While it stops the toxicity, it does not repair any of the damage already done, which will need to be addressed through other means.

Why Was Haley's Initial Product Shut Down by the FDA?

Haley's first product, developed in 2006 and sold between 2008 and 2010 under the name Oxidative Stress Relief (OSR), was shut down by the FDA in 2010 after a complaint was filed. Haley explains the circumstances:

"When they shut me down, [my attorney, an FDA expert] told me, 'Dr. Haley, this is silly. The compound has in-structure, dicarboxyl benzoate, which is found in cranberries and cystamine, which is on the terminal end of coenzyme A. It's just cysteine without the carboxylic acid group. It's a natural product.

Two natural products [combined], just like slow-release niacin and n-acetyl cysteine … It can be [sold as] a natural product and a supplement if it contains any one of a natural product or any combination of two' …

That's what [the FDA rules] said. And then they changed that. We call it the Boyd Haley rule now. [The FDA] said, 'Not if you put [two natural products] together chemically' …"

In essence, Haley was targeted, and the FDA changed the rules to make their targeting stick. In the end, Haley chose not to fight the FDA in court. "I don't have that kind of money," he says. He closed down his business and no penalties or formal legal action were ever taken by the FDA.

Haley's attorney told him he would need to develop a chemical chelator that doesn't exist naturally, and go through drug approval. This is the route he took with emeramide.

Emeramide Phase I Studies

Emeramide is the active pharmaceutical ingredient (API). The drug itself is called Irminix, and it is designated as an orphan drug for use as a mercury chelator in both the U.S. and the European Union, because neither the FDA nor the European Medicines Agency (EMA) have an official treatment for mercury toxicity.

"We got it started and we took it through all animal trials that they requested we do. You have to get incredibly high levels to have an effect on an animal — 100 times more than you would ever give a human being. We use 4 to 5 milligrams (mg) per kilogram of body weight to treat a person for mercury toxicity.

We were giving these animals a minimum of 290 mg per kilogram of body weight to make them sick. Some animals don't get sick at all. Humans don't. I mean it's different. But there's nothing in there that's not reversible. It's something that you stop and it goes away. It's totally safe …

We did all that, and then we got permission to do a Phase I study in Sweden. That's when you give the drug in single doses for a period of time and go up higher and higher, and then you give multiple doses for a week …

We got up to 600 mg a day for two weeks in a Phase I study in humans with no adverse effects at all. I mean nothing happened; 600 mg is way more than you and I may ever need to take; 300 mg would be a good amount …

It peaks in your blood within two hours. About 60 to 80 percent … is absorbed … In test animals, we showed that it did the same thing and that it concentrates and it peaks in all tissues of the body at the same time. It gets in the brain. You get more of it in the kidney and the liver than you will get in the brain, but it does get into the brain. It crosses the blood-brain barrier and is effective in eliminating the iron out of the brain [as well] …"

Phase II Studies

Phase II studies were done on Ecuadorian gold miners, who use mercury during the refining and purification process, showing it decreased the mercury level in 10 of 11 miners. "Their urinary mercury levels dropped dramatically. Their blood levels went down also," Haley says.

"It was the people at the EMA advisory group who told us to go to South America or Africa or someplace where mining gold is thrust on those people. The adverse effects [of the mercury exposure] — stomachaches, headaches and diarrhea — were [also] dramatically improved in those who took the drug.

Mercury does all of this and some other toxic side effects. The problem with mercury is there's no endpoint that you can point at that the FDA will say they'll accept as a proof that you've done it."

Once you've taken the emeramide, the mercury is excreted through your stool. And, contrary to most other chelators, you are not required to use a binder to get it safely out. Haley adds:

"We've looked at the cytochrome P450 (CYP) enzymes or the P450 system and the mercury NBMI complex, which when it binds to it, it never lets go … The toxicity is eliminated very quickly when you take NBMI … [In] about a month, most of it is out … [after] just one dose."

The applications, of course, include not only those with mercury dental fillings, but also autistic children who have mercury toxicity, and people with neurodegenerative diseases such as Alzheimer's, ALS, Parkinson's, Huntington's and others. To hear anecdotal reports of improvements and recovery for some these conditions, please listen to the interview in its entirety.

Haley has himself been taking about 200 to 300 mg of emeramide daily since 2006, as a preventive measure. He's now 78 years old, and claims the compound has helped him maintain his cognition. He also has the blood glutathione level of a teenager.

It may also help people who struggle with chronic obstructive pulmonary disease (COPD) due to smoking, which exposes you to high amounts of toxic metals. A Phase II study has also been performed on COPD patients to make sure it's not toxic for this groups of patients.

More Information

Emeramid is still under drug development but can be obtained via expanded access, named patient use, compassionate use or special use, depending on the country you're in. An early access application and prescription, required by the EMA, is available on the company's website, EmeraMed.com, along with more details by country.

If you have questions about the company itself, which is based in Ireland, you may request an information packet via email at Info@EmeraMed.com. While the product is given away for free to those who qualify for early access, a two-week treatment package costs about $600 for Irish medical board fees, insurance and mailing.

OSR used to sell for $30 for a month's worth of treatment and was sold as a dietary antioxidant. "When you make it a drug, it's a lot more expensive," Haley says. It's still unclear exactly how much Irminix will sell for.

"I mean it's definitely not going to be anything like ($600)," Haley says. "The real slowdown here is that if you're going to get it drug-approved, you have to show it's nontoxic. You have to do the Phase I study. And then you have to do the Phase II study and the Phase III study. Those are efficacy (tests) to show your drug works.

How do you show that your drug is binding mercury in a group of Americans in which none of them — according to the FDA or to science or the NIH — are mercury-toxic? Because you have to be [at a certain level] in your urine level to be [considered] mercury-toxic.

That is scientifically incorrect because the people who don't excrete mercury have very low urinary and blood levels. They build it up in their cells, and that's what goes down [when using Irminix] …

We now have found a [test] group in Colombia, South America — A young boy found a jar of liquid mercury. He took it to his school, shared it with his friends. The process of all that made about 125 people very mercury-toxic, and they're not gold miners, so they're not being [continuously] exposed. We initiated a study in Colombia on those people, because they … do have very high levels. That'll be able to show [that emeramide works]."

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Blood Flow Restriction Training for Muscle Mass Maintenance

Blood flow restriction (BFR) training is, without a doubt, the most exciting innovation in exercise training I’ve encountered in my 50 years of exercise. To help us walk through how it’s done, and its many health benefits, is Dr. Jim Stray-Gundersen — an expert in BFR who has trained many elite and professional athletes.

BFR training was developed by Dr. Yoshiaki Sato in Japan in the mid-60s, where it’s known as KAATSU training. Stray-Gundersen met Sato and worked with his organization, KAATSU Global, for a while. Stray-Gundersen explains the history and origins of this breakthrough system:

“Sato had an epiphany in 1966. He was busy attending a funeral service. He ended up having to sit in a certain position where we would say our legs fell asleep. When he tried to get up, his legs didn’t work very well. This reminded him of when he would exhaust himself with heavy weightlifting. That just kind of stuck in his mind …

In 1973, he had a ski accident. He ended up in a full-length leg cast. As most physicians know, these full-length leg casts produce lots of atrophy. He had been, in a way, just playing around with this idea of BFR, but this was an occasion where he could try this out for himself.

He took a judo belt and wrapped it several times around the top of his thigh, above the cast. And then he did isometric exercises in the cast. In those days, the cast were routinely changed at six weeks, because there typically had been so much atrophy that the cast was now loose and really wouldn’t hold a fracture in the proper location.

When he reported to the physicians to change the cast, it turned out he really didn’t have much atrophy at all. His ankle fracture and his knee injury were now not tender. Instead of getting another cast put on for another six weeks, he basically just walked out of the clinic. That was the point for him to say, ‘Hey there’s really something here.’”

The Early Days of BFR

Over the next 30 years, Sato experimented on himself and his fellow bodybuilders, trying to understand the ins and outs of what they were calling occlusion training at the time. One thing he discovered was that he needed to use a relatively narrow elastic band.

He also realized he could control the pressure using a pneumatic bladder. Sato published his first paper in the English literature in 1998. Another paper was published in 2000, in which his team conclusively demonstrated BFR effectively increased muscle strength and hypertrophy. Since then, many more articles have been published on BFR by Sato¹ and others.

“In my particular case, I’ve had a career in human performance and elite performance,” Stray-Gundersen says. “I’ve worked with Winter Olympians from cross-country skiers, alpine skiers, speed skaters and hockey players. In the Sumer Olympics, runners, swimmers, cyclists, triathletes, manly focused on endurance sports, but also soccer to a large extent.

My day job was a professor at the med school at the University of Texas Southwestern in Dallas. Through all these years, I always had my eyes out for things that could improve athletes’ performance, as well as be very useful for the population in general.

In 2011, I happened to run into a colleague at the American College of Sports Medicine Annual Meeting, who told me about KAATSU … My colleague told me how great this was and that you could get improvements in strength in as little as two weeks. I was quite skeptical at first … To make significant gains in strength and muscle size you need about six weeks.

The short story is checked it out and ended up contacting KAATSU Global and Steve Munatones. From there, [I got to] spend some time with Dr. Sato learning the ins and outs of KAATSU … It’s actually quite fantastic. It’s really a big paradigm shift in how we think about training and how to think about antiaging medicine, or using exercise as a medicine for health and fitness.”

Preventing and Treating Sarcopenia With BFR

It’s important to realize that without resistance training, your muscles will atrophy and lose mass. Age-related loss of muscle mass is known as sarcopenia, and if you don’t do anything to stop it you can expect to lose about 15% of your muscle mass between your 30s and your 80s.²

An estimated 10% to 25% of seniors under the age of 70 have it and up to half of those over the age of 80 are impaired with it.³ One of my biggest regrets in life is not knowing about BFR before my parents passed away.

They both had severe sarcopenia. I really believe they could have survived longer had I been able to teach them this technique earlier in their life. Sarcopenia is not just cosmetic, and it’s not just about frailty. Your muscle tissue is a metabolic organ, an endocrine organ.

Your muscle tissue makes cytokines and anti-inflammatory myokines, and is a sink for glucose. That’s the primary reason I’m so interested in BFR. It has the ability to prevent and widely treat sarcopenia like no other type of training.

BFR Training Is Excellent for the Elderly

There are several reasons for why BFR is so superior to conventional types of resistance training. Importantly, it allows you to use very light weights, which makes it suitable for the elderly and those who are already frail or recovering from an injury. And, since you’re using very light weights, you don’t damage the muscle and therefore don’t need to recover as long. As explained by Stray-Gundersen:

“Succinctly, what KAATSU does … is it allows you to get the same benefits you get from heavy standard lifting with very light weights — 20% to 30% of one rep max...

What we’re doing is we’re limiting the venous outflow out of an extremity, creating a situation in the working muscle where it’s not getting enough oxygen to sustain or to rebuild the energy stores that are used up in the course of that work. So, you set up this metabolic crisis where you’re not making enough ATP to replace the ATP that you’re using.

The consequence of that is you get a disturbance of homeostasis, which is just like the disturbance of homeostasis you get with very heavy lifting. The difference is that we’re doing it by modulating and impeding the blood flow as opposed to doing very hard work, which actually does damage to the tissue at the same time.

One of the reasons why you get these effects much sooner than typical is because we have altered the time scale by not doing the damage. Therefore, we’re getting the benefits of this exercise in very short order. Really, we’ve tapped into starting to understand what the real adaptation to exercise is.

It’s creating that stress or that disturbance of homeostasis that the body then reacts to in a systemic way … At the same time, it has to repair the damage that was done during the course of the exercise …

What’s really nice about [BFR], which I would generically characterize as an elastic, pneumatic, relatively narrow BFR[-band] training, is that we provide an anabolic stimulus very early on through this systemic effect.

One of the things that other papers have shown is it’s not just the muscle that’s getting better. It’s the bone. It’s the blood vessels. There’s even a study showing that the neural transmission from a motor nerve to a motor fiber is improved by BFR training.

We know that regular exercise helps us maintain as much function as we can. But as we age, we become unable to do those same kinds of workouts that it took to recreate this stuff in the first place. Now, with BFR we have the ability to do this with very light, easy exercises that anybody can do, and therefore, get the benefits of this anti-aging medicine.”

Elderly Need BFR Even if They’re Fit

While most elderly cannot engage in high-intensity exercise or heavy weight lifting, even extraordinarily fit individuals in their 60s, 70s and 80s who can do conventional training will be limited by their physiology in terms of the benefits they can achieve. The reason for this is because your microcirculation tends to decrease with age.

Your capillary growth is diminished, and capillary blood flow is essential to supply blood to your stem cells, specifically the fast twitch Type II muscle fiber stem cells. If they don’t have enough blood flow — even though they’re getting the signal from the conventional strength training — they’re not going to grow. You’re not going to get muscle hypertrophy and strength.

BFR, because of the local hypoxia that is created, stimulates hypoxia-inducible factor-1 alpha (HIF1A), and secondarily, vascular endothelial growth factor (VEGF), which acts as “fertilizer” for your blood vessels. VEGF allows your stem cells to function the way they were designed to when they were younger.

This is part and parcel of what makes BFR such a phenomenal exercise. What’s more, the hypoxia also triggers vascular endothelial growth factor, which enhances the capillarization of the muscle and likely the veins in the arteries as well.

“What’s really exciting about that is that now all of a sudden, we have something that can repair and build endothelium,” Stray-Gundersen says. “And the endothelium is the first order of business when we’re talking about the ravages of atherosclerosis.

One of the big applications in Japan is with cardiac rehabilitation and stroke patients. They do BFR training with these people, because they can. Even if they have some hemiparetic problem or difficulty walking, they can always do some sort of exercise that stimulates the fibers that are still intact.

This whole thing is a way to recruit as many motor units as possible in a body or a human. That, in turn, is a very powerful stimulus for reversing sarcopenia or building muscle and better blood vessels. All of these things are related.”

Essentially, BFR has a systemic or crossover training effect. While you’re only restricting blood flow to your extremities, once you release the bands, the metabolic variables created by the hypoxia flow into your blood — lactate and VEGF being two of them — thereby spreading this “metabolic magic” throughout your entire system.

Systemic Benefits of BFR

For this reason, BFR can be a powerful way to not only treat strokes but also preventing Alzheimer’s and heart disease. As noted by Stray-Gundersen, BFR can be likened to “Drano for the arteries,” and you’re only as young as your arteries.

What’s more, lactate, far from being just a waste product, is also viewed as a pseudohormone with powerful benefits. For example, lactate can cross your blood-brain barrier through a monocarboxylate transporter and stimulate brain-derived neurotrophic factor (BDNF). Stray-Gundersen explains:

“There’s a whole series of things that are produced when you disturb the homeostasis in a working fiber. One of them is lactate. We tend to think of these things as local mechanisms, whether it’s lactate or the hypoxia or a drop in pH. These things stimulate local protein synthesis.

We’re already doing stuff to build more and better blood vessels. But in addition, these factors can go to other cells in the area and help them. But the big deal is that we recognize this disturbance of homeostasis in our brains. Our brains end up saying, ‘Wow. Our muscles are feeling fatigued or they’re running out of gas’ …

We use that same sensory system to see how it’s going with BFR training. The ultimate message is that our muscles are in trouble. They’re not getting enough oxygen. They’re not regenerating the amount of ATP that they need to do this.

This is happening now in all the fibers — the Type I fibers at the beginning, but they drop out, and then they recruit the Type II, and let’s say the Type IIx, and stimulate the stem cells to differentiate into satellite cells and build new muscle fibers.

But now this message has gotten into the brain and the brain reacts to it by putting out a neurohumoral systemic response. This has been well characterized by an increase in circulating growth hormone in the 15 to 30 minutes after an effective BFR session.”

Growth Hormone Amplifies Protein Synthesis

Growth hormone stimulates insulin growth factor 1 (IGF-1) in your liver, which is an anabolic hormone. Being lipolytic, the growth hormone also goes to fat cells where it breaks down fat to produce substrates. It also plays a role in protein synthesis, along with lactate.

The take-home message is you end up getting adaptation everywhere, not just in the muscles used in the exercise. Stray-Gundersen explains:

“A way to think of this is that there’s a systemic process. For example, let’s say we’re doing bench presses. We’re using our triceps, for example, that may be distal to the band. But we’re also using our pectoralis major muscles.

Their blood flow is normal because the bands don’t get in the way of it. But they also get the benefit ... Both muscles, proximal and distal to the bands, end up benefiting …

One of the things that happens — one of these local reactions — is self-surface receptors for growth hormone and for insulin and for a variety of anabolic hormones are upregulated, so there’s an increase in receptor density on the surface of cells used in the course of this exercise, for example the pecs and the triceps.

Growth hormone comes along and binds into these receptors, and that stimulates the mTOR pathway to upregulate protein synthesis. That’s where you get this amplification effect. It’s not that the growth hormone is stimulating mTOR.

It’s just that the hypoxia and the acidosis and the lactate acidosis in the cells have stimulated not only protein synthesis locally, but also the cell membrane receptors so that there’s a greater receptor density, and whatever growth hormone comes along ends up getting bound, amplifying the effect.”

Proper Occlusion Technique Is Imperative

To avoid injury, it’s important to use the appropriate type of occlusion bands, and to use the bands correctly. At present, there are essentially two different camps — the KAATSU camp, which uses very narrow elastic bands to control the pressure, and a more physical-therapy based camp that uses wider surgical occlusion bands.

The width of the cuffs and the ratio of occlusion are two important factors, as the only way to really hurt yourself with BFR is to occlude arterial flow. The risk of blocking arterial blood flow is high if you’re using wide and/or rigid bands. You want to slightly occlude venous flow only, not the arterial flow.

“All serious complications with BFR training happen if you happen to occlude the arterial inflow into an extremity,” Stray-Gundersen says. “The wider the cuff or the band, the easier it is to do that. If the cuff is rigid, as opposed to elastic, the easier it is to do that. Those are the two main factors.

These groups who have tried to use surgical tourniquets or blood pressure cuffs to do this, they first read Sato’s paper and were very excited but couldn’t get a hold of the KAATSU equipment at the time. As a result of that, they just picked up something they thought would do the same thing. Unfortunately, they didn’t quite understand what Sato was up to …

There’s a very narrow band of pressure or flow that is safe and effective. When you’re using something that is relatively narrow and elastic, then you have a much bigger window in which you can get enough blood flow restriction to be effective and still be safe throughout the time period you’re doing [the exercise] …

One of the really important things [is] what we call the muscle pump. Anytime you do any exercise, the working muscles contract; they get stiffer and a bigger … and that forces the blood out through the venous channels past through the venous blockade.

So, you’ve changed the venous flow from one in which you can think of as a lazy river where the venous flow was continually going back towards the heart, to one in which there are intermittent obstructions or occlusions of that venous flow with periodic pulsatile, high flow states. This ends up equaling the arterial inflow.

Usually, when you get into this kind of sweet spot of the right amount of BFR, you have decreased arterial inflow a little bit. But really, the big thing is you’ve changed the character or the venous outflow. You really can’t do that as well with a rigid system as you can with an elastic system, because when you have the muscles pumping this big amount of blood past the venous obstruction, if there’s a rigid outer casing, there’s just nowhere to go.

The muscles are getting thicker. It takes a tremendous amount of pressure to push any blood past this venous obstruction. If you have an elastic situation, now that elasticity can accommodate the increase in cross-sectional area and this increasing amount of venous flow.

While the rigid, wide systems can be made to work, there’s a very narrow window where they’re both safe and effective. On the other hand, with the elastic, relatively narrow ones, there’s a much larger window to get the pressures right.”

How to Find the Sweet Spot

So, how do you find that sweet spot, where venous flow is restricted, while arterial inflow is not? One way to make sure your arterial inflow is preserved is to feel for your pulse distal to the band. If the band is on your arm, you’d check the pulse in your wrist. If you have trouble feeling your pulse, you can check your blood flow by pushing hard on your hypothenar eminence and then release it.

The hypothenar eminence is the meaty portion on the palm-side of your hand at the base of your thumb. If the skin goes from white to reddish or pinkish in a couple of seconds, you know your arteries are open. If it takes several seconds for the skin tone to come back, your band is likely too tight.

General Training Guidance

The traditional recommendation is to do three sets of repetitions with 30 reps in the first set, 25 in the second and 20 reps in the third set. The main thing you’re trying to do is create fatigue in the working muscle. Three or four sets of any given exercise will do that.

“We want that first set to last somewhere around 30 to 45 seconds,” Stray-Gundersen says. “Then we want what we call 30 to 45 seconds of pseudo-rest. The muscle pump is pushing blood past the venous obstruction when you’re exercising. That increases the flow through the system.

When you’re resting or pseudo-resting, now you don’t have that muscle pump to help you with the flow, so the actual environment in the working muscle fibers deteriorates even more.

That’s why we generally use three or four sets with a specific amount of recovery in between, where the person thinks they’re recovering or resting, but really, the situation, the metabolic situation is getting worse in the fiber. It’s all about creating this disturbance of homeostasis and this fatigue feeling.

And so, we have a number of variables to play with. We have the pressure in the bands. We have the kind of exercises that we’re doing. We have the weight load, which generally we’d want to keep very low. And we have the number of reps in a particular set, and then the number of sets for a given exercise … Generally, that takes, for arms and legs, somewhere around 30 minutes.”

As for placement, on your arms, you want to place the bands up high on the arm, on the top of the bicep at the base of the deltoid. On your legs, you’ll place the bands as high as possible, close to your crotch.

How Often Can You Do BFR?

Again, because you’re not damaging your muscle with heavy weights, your recovery time is quite short. If I stick to the 20% to 30% one-rep max weight, I can easily do it every day. According to Stray-Gundersen a younger athlete may be able to do it twice a day. Some injured athletes end up doing three workouts per day.

“Generally, the 20 to 40 crowd can tolerate five [BFR] workouts a week. Generally, the 40 to 60 can tolerate three workouts a week. The greater than 60 ends up being twice a week,” Stray-Gundersen says.

Markers of a Good Session

The disturbance of homeostasis caused by the occlusion will trigger serious sweating, which can be used as a gauge that everything is working correctly. As mentioned growth hormone is triggered, which activates your sympathetic nervous system.

Sympathetic nervous system activation causes you to sweat and breathe harder. It also causes your blood pressure and heart rate to rise. All of these signs are markers of a good fatigue signal in the muscle.

“We look for increased sweating and inappropriately heavy breathing, that sort of thing,” Stray-Gundersen says. “When you have those things, you know you have had a good session.”

KAATSU Walking

Another workout strategy recommended in KAATSU is KAATSU walking, where you simply walk for 20 to 40 minutes wearing the occlusion bands on your legs. For example, you can wear all four bands while rowing, cross-country skiing, cycling or jogging. After 15 to 30 minutes, most will be too fatigued to continue.

“In the case of running, it decreases the amount of pounding you get in return for getting in shape,” Stray-Gundersen says. “We also use this in the water.”

Hypertensive Response and Other Risks

If you have high blood pressure, conventional exercise could potentially trigger a stroke. Some of the literature suggests BFR may have a similar effect. However, Stray-Gundersen emphasizes that this risk is an artifact of using the wrong types of bands, not BFR in general. He explains:

“Deep vein thrombosis (DVT) or blood clots in the veins in the extremity can be deadly … But Dr. Rudolf Virchow back in the 1800s, [found] there were three conditions that were necessary [for DVT to occur]. One was venous stasis. If you don’t have arterial occlusion, you don’t get venous stasis.

If you’re doing the exercises where the muscle pump is pushing the venous blood past and the arterial is backfilling into this space, then you never get stasis. One of the things about being safe is to never occlude the arteries. That way, you never get venous stasis.

That way, you don’t get deep venous thrombosis. The other aspect or another one-third of the Virchow’s triad is endothelial damage … With normal BFR training, you don’t injure those vessels at all. You also don’t get this endothelial damage that can start a clotting cascade …

The same cannot be said for these wide, rigid systems … [similar to] what are used in the operating room and basically have a pretty high incidence of DVTs associated with them. The other thing was hypertension … It is a real and important consideration when you’re using the wide, rigid systems.

Also, the wide, rigid systems, when the muscles contract, as I said before, there’s nowhere to go. That induces ischemia and potentially damage to the exercising muscle. This causes a reflex exercise pressure response that can manifest as increasing hypertension.

One of my sons who’s doing a Ph.D. at University of Texas at Austin just did a thesis on the difference in hypertensive response to walking with narrow, elastic bands versus wide, rigid tourniquet system. He found that the wide, rigid cuffs ended up causing a very robust hypertensive response …

When he used the narrow, elastic bands, [the hypertensive response] ended up being no different. In fact, slightly less than just walking on the treadmill by itself without any bands on it. I think it relates to this idea of a relatively narrow elastic setup that doesn’t elicit this kind hypertensive risk that the wider systems and rigid systems do.”

BFR Training Is Ideal for Most

I really think BFR is one of the most important components of an effective anti-aging strategy. Stray-Gundersen agrees, noting he’s seen dramatic improvements in fitness and function in people of all ages.

“I think the big contribution, when you get right down to it, is that this provides exercises that pretty much anybody can do,” he says. Frail individuals can even get significant improvement simply by using BFR bands while doing activities of daily living, such as rising and sitting down in a chair, or reaching for a high shelf using no weights at all.

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