Every weekend, 93-year-old Bob Williams walks into his local dollar store in Long Grove, Iowa, and buys a box of Herseys. Not those small, regular-sized candy bars… but the really big ones.
Bob, however, typically doesn’t enjoy them himself. He gives one to the cashier, and then to the person waiting behind him in line. And then he walks the downtown area handing them out to everyone he sees… …young, old, men, women, happy, sad… …everyone. He has been doing this for the past 11 years and he’s known as “The Candy Bar guy.”
It’s estimated that over the years, Bob has handed out about 6,000 chocolate bars.
So why does Bob do it? Because it puts a smile on everyone’s face. And THAT’S always worth it.
(Tom: Here’s a man making a positive difference in people’s lives!
Not many of us cannot do something this simple.
Doesn’t take an iron will, superhuman strength or millions of dollars. Just a bit of money, time, care and the intention to make the world a better place.
And if you want to start with zero dollars down, here’s a great quote I saw yesterday:
“You cannot add to the peace and goodwill of the world if you fail to create an atmosphere of harmony and love right where you live and work.” – Thomas Dreier
So, on your list of things to do today, what are you going to add that makes the world better than it was yesterday? Here are some suggestions.
Smile more. Especially when you first make eye contact and answering the phone.
Hold a door open.
Let someone merge into your lane when driving.
Smile and wave or say thank you when someone lets you cut in or is otherwise polite to you.
Pay more attention when someone is talking to you.
When the fuel from the food you eat cannot efficiently be burned and converted to energy (ATP), it’s typically diverted and stored as fat. So, the primary cause of obesity is the inability to efficiently metabolize food, typically glucose in the mitochondria, into energy
The inefficient burning of fuel (metabolizing of food) is why people who are obese typically also struggle with other health issues, such as low energy, fatigue, an inability to maintain focus, digestive problems and poor immune function
Mitochondrial dysfunction, psychological stress, oxidative stress (reductive stress), heavy metals, endotoxin, lack of sleep and certain nutritional deficiencies can flip your metabolism into fat burning, which then impedes the metabolism of glucose and converts the glucose into fat rather than energy
High energy production equates to high metabolism, so part of the solution for obesity and most other conditions is to raise your metabolic rate
A key strategy to optimize your mitochondrial energy production is to remove blocks in the electron transport chain. Endotoxin and other bacterial toxins are among the biggest culprits, as they can directly impair electron transport. Another effective blocker of mitochondrial energy production is polyunsaturated fat (PUFA)
In the “GET LEAN Eat Clean” podcast above, personal health and wellness coach Brian Gryn interviews Jay Feldman — a health coach and independent health researcher who is extremely knowledgeable in the work of the late Ray Peat — about the underlying causes of obesity and how to optimize mitochondrial energy. I am also scheduled to interview Jay in the near future.
Feldman is the founder of Jay Feldman Wellness and hosts the Energy Balance podcast. A key concept he presents is that when the fuel from your food you eat cannot be efficiently metabolized and converted to energy (ATP), it’s instead typically diverted and stored as fat. In my view, he is the best teacher of Ray Peat’s work. You can view the first seven episodes of his podcast to develop a foundational understanding of bioenergetic medicine.
Another key concept is that high energy production equates to high metabolism, so part of the solution for obesity is to raise your metabolic rate. Unlike conventional wisdom which suggests calorie restriction is associated with longevity, a high metabolic rate slows aging and helps you remain more youthful — at least biologically speaking — as you age.
Lack of Energy Is a Foundational Problem in Obesity
The inefficient burning of fuel (metabolizing of food) is why people who are obese typically also struggle with other health issues, such as low energy, fatigue, an inability to maintain focus, digestive problems and poor immune function.
As noted by Feldman, these all result from a lack of energy production in your mitochondria. So, the primary problem in obesity is that your body cannot efficiently convert the food you eat into energy. Instead, it gets converted into fat. As a result, you end up with obesity, low energy and perpetual hunger, which leads to overeating. Feldman explains:
“I … come from the bioenergetic view of health … the idea that energy, the energy that’s produced in our mitochondria, is the main driver of our health, and a lack of that energy is what leads to dysfunction …
I would say obesity is an energy problem, and endocrine problems are superimposed, happening on the energetic front. So, it’s really helpful to look at hormones … like cortisol … thyroid hormones … the reproductive hormones …
Those things are really helpful when we’re trying to get a gauge on where somebody’s at because you can’t always see what’s happening in the cells and the mitochondria. So, we can look at hormones as a proxy there, but those hormones are just signals and messengers that are being produced or inhibited in response to what’s going on in terms of the energetic state.”
Glucose Metabolism Is Easily Hindered
As noted by Feldman, your metabolism is a sensitive system, especially when it comes to glucose metabolism. Things like mitochondrial dysfunction, psychological stress, oxidative stress (reductive stress), heavy metals, endotoxin, lack of sleep and certain nutritional deficiencies can flip your metabolism into fat burning, which then impedes the metabolism of glucose and converts the glucose into fat rather than energy.
“This is why we want to be looking at food choices in terms of how they affect our energy production,” Feldman says. The conventional view is that fuel equates to energy, which is why obesity is thought of as an energy excess and all you need to do is eat less and exercise more. But that’s not accurate.
“That [view] is something I think we definitely want to work ourselves away from and instead focus on how well we’re using the food that’s coming in, and what types of foods are better used, considering our human physiology,” Feldman says. “That’s really where we want to focus, as opposed to eating less or exercising more.”
Lack of Fat Burning Is Not the Problem
Many, myself included, used to believe that optimizing fat burning was the solution not only to obesity but most other health problems as well, but we’re now starting to realize that this is borne out of a misconception. As explained by Feldman:
“I think what’s happened is we’ve come into this with preconceived notions that people are overweight and have excess body fat, so there must be a fat burning problem. And that is an assumption that I would say is definitely not true …
There have been clear metabolic studies where they see that you can be on a low-carb diet and you can be burning more fat with lower insulin, and having more fat released from the fat stores, and still be losing less body fat because there’s also more fat coming into the fat stores.
And on the flip side, you can be on a higher carb diet, burning less body fat, and still losing more body fat because in that case you’re storing less body fat. So, we’ve just focused in on this one piece of the equation — how much fat are we burning — when it doesn’t acknowledge the whole flow in and out of of the fat stores …
I used to think that … everyone was oxidizing carbs and the problem was that we needed to become better fat burners, but when you actually look at what’s going on in these states, fat burning is part of the problem. That is what happens when things are problematic.
There is one caveat here that’s important, which is that burning carbohydrates doesn’t always mean the same thing. We can oxidize glucose through oxidative processes, meaning we go through glycolysis, and then we go through the Krebs cycle, and then we go through the electron transport chain …
The glucose gets oxidized and we end up with a decent amount of energy. When we are in a degenerated state, in addition to burning more fat, we also run through glycolysis more, and glycolysis is the first step … of glucose burning.
Because there are blocks farther down, we can’t use the glucose all the way, and that’s a problem … but that is not caused by the sugar, it’s not caused by the carbohydrates, it’s not caused by carb burning.
That’s caused by mitochondrial dysfunction caused by our ability to produce energy. So, we’re stuck in a very inefficient glucose burning along with fat burning, and that’s not a great state to be in. But that is not the same thing as fully oxidizing glucose in a healthy metabolic state.”
How Your Body Produces Energy
I like to use graphics when explaining this, so let me restate what Feldman is saying, along with a couple of images. In summary, your body can use two fuels for energy: glucose and fat. If you eat any type of sugar or complex carbohydrate, it’s metabolized to glucose. Glucose is then broken down to pyruvate.
At that point in the process, there’s a “switch,” known as the Randle Cycle. The pyruvate can either enter the glycolysis pathway and turn into lactate, or it can be metabolized into acetyl-CoA through aerobic respiration, as shown in the image below.
Provided your fat intake is below 30% or so (this is merely a best-guess at this point, as no one knows exactly what the threshold is), the glucose you consume will be shuttled into acetyl-CoA. When it goes to acetyl-CoA, it goes into the electron transport chain in the mitochondria.
Free fatty acids can also be metabolized into acetyl-CoA through beta-oxidation in the mitochondria, and there’s a competition that occurs there with glucose, which is why your fat intake needs to be low enough for glucose to enter this pathway.
Aerobic respiration uses oxygen in the mitochondria, whereas glycolysis, which occurs in the cytosol, does not use oxygen and is very inefficient. Glycolysis only generates two ATP molecules for each molecule of glucose, whereas aerobic respiration, which occurs in the mitochondria, generates 36 to 38 ATPs per molecule of glucose.
Ultimately, you want to burn glucose in your mitochondria. That’s the most efficient, allowing you to generate the most energy, while simultaneously producing the least amount of harmful “exhaust” in the form of reactive oxygen species (ROS).
And, again, the only way to ensure that is to keep your dietary fat content below 30% of your total calories. If you’re insulin resistant, which means you’re metabolically inflexible, that threshold may be closer to 20% or even 10%. So, if you’re insulin resistant, you’ll want to significantly lower your fat intake until your insulin resistance is resolved. Then you can increase it to 30%.
Endotoxin and PUFAs Decimate Mitochondrial Energy Production
Next, Feldman discusses a key strategy to optimize your mitochondrial energy production, which is to remove blocks in the electron transport chain so that electrons can move smoothly forward, without accumulating and backing up.
“We don’t need to focus on doing extra things to stimulate [mitochondrial energy production],” Feldman says. “Our mitochondria will work perfectly well if they have the right fuel and nutrients, and they aren’t being inhibited or blocked.”
According to Feldman, endotoxin (lipopolysaccharide or LPS) and other bacterial toxins are among the biggest culprits when it comes to things that hinder mitochondrial energy production. These toxins can directly impair electron transport through the complexes of the electron transport chain. They can also impair certain enzymes in the Krebs cycle.
Poor digestion is frequently associated with negative gram bacteria in your gut that produce endotoxin, and this will inhibit your ability to convert food to energy, resulting in increased body fat. So, it’s important to reduce your endotoxin load. Aside from poor digestion, excess endotoxin is also a common culprit in degenerative conditions, metabolic syndrome, diabetes and fatty liver. To reduce your endotoxin load:
Rebalance your gut microbiome by reintroducing beneficial bacteria (probiotics and prebiotics). One of the best and least expensive ways to do this is to eat a serving of fermented vegetables each day.
Temporarily go on a low-fiber diet and avoid fiber supplements as it can feed undesirable bacteria. Cook your vegetables thoroughly rather than eating them raw, and if your condition is serious, limit fruits for a time too.
Eat a low-carb ketogenic diet and/or fast until the problem is resolved. As noted by Feldman, “This is one of the main places where low-carb diets, ketogenic diets, fasting, carnivore [diets] are really helpful, as they provide relief from the feeding of bacteria that are producing a lot of endotoxin.” Foods to avoid include most grains, legumes, nuts, and seeds.
Avoid resistant starches, as they feed LPS-producing bacteria.
Once your microbiome is balanced and symptoms of poor gut function have resolved, you can slowly reintroduce whole fruits, vegetables, roots and tubers, and other foods. Another effective blocker of mitochondrial energy production is polyunsaturated fat (PUFA).
These are your processed seed oils, canola oil being among the worst of the worst. Seed oils are loaded with linoleic acid, an omega-6 PUFA, which appears to be one of the primary drivers of chronic diseases, in part due to its detrimental impact on your mitochondrial function and energy production.
The Expensive Tissue Hypothesis
After a short discussion about ancestral diets and the likelihood that such diets were generally high in carbs, Feldman and Gryn review the “expensive tissue hypothesis,” which is the idea that the less energy you waste on hard to digest, fibrous foods, the more energy is available for your brain.
“… that’s also a reason to be consuming a lot of carbohydrates and not excess protein, because the conversion from protein to glucose and then to energy is very inefficient,” Feldman says.
“It’s about 30% less efficient than just using glucose. So, if we consider the … expensive tissue hypothesis, we shouldn’t be consuming excess protein beyond our needs and trying to use that for energy, because … that leaves less energy for our immune function, our brain function, for reproductive function and and on …
Coming back to weight loss, there’s the constrained model of energy expenditure, which is very related here, which basically says that you can’t just expend more and more calories from, let’s say, exercise, without it coming at a cost.
So, if you exercise 1,000 calories’ worth and before you were burning 2,000 calories, that doesn’t mean that you just burned 3,000. What actually happens is, you start to cut into your own basal metabolic rate, and you start to cut into your bodily function.
So, your reproduction is turned down, your immune function is turned down … Extrapolated, it really also gets at the problem with the ‘eat less exercise more’ advice for weight loss.”
Endotoxin, Not Fructose, Causes Fatty Liver Disease
Feldman also debunks the argument that fructose, unlike what is being promoted by Drs, Robert Lustig, Richard Johnson and David Perlmutter, causes nonalcoholic fatty liver disease (NAFLD). He reminds listeners that both dietary fat and fructose can be converted into fat, and fructose isn’t automatically destined to end up as liver fat.
“In fact, very little fructose gets converted to fat,” he says, because “there are all sorts of of routes for it to go before it’s getting converted to fat … Fructose does go to the liver and it gets picked up by the liver immediately, whereas glucose will go out into the bloodstream and can be picked up by the muscles.
But our livers have developed to handle massive amounts of fructose. Most of the research that is looking at what happens to fructose … is going on in rats. And there are a few differences, there are a few problems there. One is that rat livers are very different from human livers in their capacity for fructose handling.
Our livers have an incredible capacity for handling fructose. Hundreds and hundreds of grams can be stored as glycogen, can be converted to glucose or lactate and sent out to be stored elsewhere, or used elsewhere, and then can also be oxidized.
So, when we consume excess fructose in a normal context, in a healthy liver, very little is going to be going to fat. It takes huge amounts of carbohydrates before you’re … producing much fat in the liver through de novo lipogenesis. And that’s because our livers have this incredible capacity for handling it …”
Feldman also remarks that many fructose studies are flawed in that they’re looking at fructose-only sources, which rarely ever exists in our food supply as it is virtually always accompanied with glucose. Results from such studies therefore do not tell you much about how natural, whole food-based fructose, say from fruit or honey, acts in the body.
“Whether you’re consuming fruit or honey or anything else, the fructose to glucose ratio is always near 1-to-1,” he says. “Sometimes there’s a slight bit more fructose [than] glucose, but even in high fructose corn syrup … it’s about 55% fructose and 45% glucose. We’re really not talking about major differences here.
And that’s important because our intestines don’t absorb pure fructose. If there’s glucose present, we absorb it very well. But if there’s no glucose present … you can’t really absorb it very well.
So, what happens is a lot of it doesn’t get absorbed in our small intestine. [It] continues down to the large intestine where it feeds bacteria. Those bacteria produce endotoxin, and that is what leads to things like fatty liver production [and] fatty liver disease.”
How to Gauge Your Metabolic Rate
According to the rate-of-living theory, the higher your metabolic rate — which means the quicker the electrons move from food toward oxygen, which is the final acceptor of electrons — the faster you’ll age because there’ll be higher oxidative stress.
However, deeper analysis reveals the exact opposite. The truth is, the higher your metabolic rate, the slower you age, because a high metabolism creates fewer ROS that can damage your tissues.
Your metabolism is high when electrons move rapidly and easily through the mitochondrial electron transport chain, which results in optimal energy production. When electrons are impeded from moving forward, they can back up, leak through the mitochondrial membrane and start moving backward, where they combine with oxygen to create excessive ROS.
So, for optimal health, you want high energy production and that means a high metabolic rate. As explained by Feldman, you can gauge your metabolic rate using your pulse and body temperature.
“If you’re not hitting 98.6 [degrees Fahrenheit] later in the day, if you’re not hitting 97.8 or 98.0°F when you’re waking up, that can be a sign of a hypometabolic state,” he says.
“If your [resting] pulse [first thing in the morning] is particularly low, if you’re not getting into the mid-70s or potentially low-80s, depending on your fitness state, that can also be a sign of a low metabolic rate.
The caveat is that the more cardiovascularly fit you are, the lower your pulse rate will be, independent of metabolic state. That’s because your stroke volume increases. The stroke volume is the amount of blood your heart pumps with each beat. So you can have fewer beats and still pump the same amount of blood … You can also look at temperature and pulse before and after a meal.
If … somebody wakes up at temperature 98.4°F. and then they have their breakfast and it drops to 97.5°F., that is a situation of a drop in stress hormones, where someone was waking up in a stress state, their sleep’s probably not optimal, they’re probably not optimal metabolically, then they’re consuming some carbohydrates and their stress hormones drop.
If you’re seeing that happen after a meal, it’s a pretty good sign that that’s what’s happening.
Another good way to do it is just seeing how many calories you can consume while maintaining your weight … If, with your activity and everything else, you should be burning 3,000 calories a day, but you’re maintaining your weight on 2,200 calories a day, that’s a sign that you’re pretty hypometabolic.”
Conversely, if you can maintain your weight when you add more calories, your metabolic rate is likely high, and the extra food will oftentimes improve your sleep, relaxation, energy and recovery.
Methylene Blue — A Useful Rescue Remedy
While there are no magic pills to fix slow metabolism or low energy production, there are some that can help. I’ve previously written about the usefulness of niacinamide, for example. Another helpful one is methylene blue. As explained by Feldman:
“As a supplement, it’s got a number of interesting effects. For one, it’s antimicrobial … but it also has some pretty interesting mitochondrial or energetic effects, where it is able to work as an electron acceptor and donor.
So, if things are not working well in the electron transport chain, the main site where we produce ATP, [if] something’s blocked, let’s say by endotoxin or polyunsaturated fats, whatever it is, methyl blue can help us bypass those issues and allow us to continue to produce energy despite those things.
It also lowers nitric oxide, which is another inhibitor of mitochondrial respiration. So, it’s got a number of benefits. I will say, like any other supplement, there’s a place for it and there’s also a place where it can be problematic, and it’s never the first thing I would go to.
We always want to work at those foundations first — get diet on point, eat consistently, get enough carbs and fats in, make sure we’re getting the nutrients we need, trying to work on our sleep hygiene, our movement …
But I do think there’s a place for methylene blue to help with either those microbial issues or for getting the metabolism going in certain instances. It also, in particular, has some benefits neurologically, because of these stimulating effects on respiration … So, yeah, I like it. Again, it’s not magic in that it is going to fix the problems, but it can be helpful along the way.”
Constructing the Ideal Diet to Maximize Energy
While it’s nearly impossible to come up with a diet that is ideal for everyone, general guidelines can be provided. After that, it’s up to you to experiment and note what works and what doesn’t. For example, some are outfitted with genes that can handle dietary fats better than others, while some may have had their gallbladder removed and can’t handle much fat at all. Following are some general principles for devising your ideal diet:
•Protein — Most adults need about 0.6 to 0.8 grams of protein per pound of lean body mass. As an example, if your body fat mass is 20%, your lean mass is 80% of your total body weight. Ideally, stick to animal-based protein such as clean seafood and low-LA animals like beef, bison, lamb and other ruminant game animals, raw grass fed dairy and organic pastured eggs.
Avoid chicken and pork as, even if pasture-raised and organically fed, they are given grains and other foods that are high in LA so they will increase your LA levels. Many plant-based proteins, including nuts and seeds (with the exception of macadamia nuts), are also high in PUFAs.
•Carbs — Avoid hard-to-digest carbs like most grains, including brown rice, and legumes, unless they’re soaked, properly cooked, sprouted or fermented. Good options include raw authentic honey, maple syrup, white rice, ripe and dried fruit, and well-cooked (preferentially pressure cooked) tubers like red potatoes, sweet potatoes and parsnip.
•Fats — Avoid seed oils, which are loaded with PUFAs like LA. Good options include butter, tallow, ghee, coconut oil and avocados.
If you’ve been on a low-carb, high-fat diet, slowly add in more carbs while simultaneously lowering your fat intake. As mentioned earlier, your fat intake probably needs to be somewhere around 30% or lower to allow for efficient glucose metabolism.
Feldman typically recommends a range of 20% to 40%, with the upper limit being for more physically active people with greater muscle mass. With fats at 30%, carbs would then be in the range of 55% to 60%, with protein making up the remaining 10% to 15%.
Increase Your Metabolism to Slow Your Aging
As mentioned earlier, high metabolism is the key to slowing down aging. And the slower you age, the more youthful and resilient you’ll be. As noted by Feldman:
“When we’re in our 20s, let’s say, or late teens, we can kind of eat whatever, our metabolic rate’s really, [we have] high libido’s, sleep is never an issue … digestion is really good; things don’t bother you. That’s the state … we want to be getting to. And I would say the key difference there is, where is our metabolic rate at?
Over time, metabolic rate slows, mitochondrial respiration slows. If you take aged mitochondria from someone who’s above the age of let’s say 60 or 70, there’s a dramatic reduction in energy production … So, the solution is to get back to that young metabolism. And I think it’s totally doable.
It’s just a matter of eating the things that are designed for optimal function, that allow for maximal energy production, [and] avoiding the things that interfere with that — avoiding the polyunsaturated fats, lowering endotoxin, having good, consistent sleep, consistent movement.
It’s a complex, right? It’s never as simple as ‘Just eat this one thing,’ or ‘just take this one pill.’ [It’s] having that perspective of trying to think of speeding things up, as opposed to slowing things down.”
More evidence they lied. “The lipid nanoparticles stay at the injection site.” they said. They lied.
“Of 13 lactating women receiving the vaccine (20 exposures), trace mRNA amounts were detected in 10 exposures up to 45 h post-vaccination. Our findings suggest that the COVID-19 vaccine mRNA administered to lactating mothers can spread systemically to the [breast milk] in the first two days after maternal vaccination. Initially, it was thought that the vaccine mRNA encapsulated in LNPs would remain localized at the injection site and quickly degrade. However, several reports suggest that the LNPs/mRNA can enter the bloodstream and accumulate in distant tissues.”
For two years since nations agreed to develop a Pandemic Treaty that allows the WHO to dictate “potential” emergencies, controlling lockdowns, vaccinations, and mobility restrictions, you and I have fought to keep any new powers away from the WHO.
Thanks to our efforts, the radical globalist leaders and leftist organisations pulling the strings behind the scenes at the UN are panicking!
The fear of not securing a global agreement within their timeline is starting to set in for them. In short, they’re feeling your pressure.
So much so, that the UN has unexpectedly called for an emergency high-level meeting to be included in the agenda of this month’s General Assembly on September 20th, to fabricate a sense of urgency to reignite interest in the proposed Pandemic Treaty.
The WHO is against the clock… They are moving twice as fast, to get things back on track. There’s no better time than now to step up the pressure and bury this treaty once and for all.
Sign the petition urging the Australian delegation — headed by Australia’s Ambassador to the UN, James Larsen — to oppose the dangerous centralisation of global governance during the upcoming negotiations of the WHO Pandemic Treaty at the UN General Assembly.
A group of 12 women were at a seminar on how to live in a loving relationship with their husbands. The women were asked, “How many of you love your husband?” All the women raised their hands.
Then they were asked, “When was the last time you told your husband you loved him?” Some women answered today, a few yesterday, and some couldn’t remember.
The women were then told to take out their cell phones and text their husband “I love you, sweetheart.”
Next the women were instructed to exchange phones with another woman and read aloud the text message they received in response to their message.
Below are the 12 actual replies from their husbands. If you have been married for quite a while, you understand that these replies are a sign of true love. Who else would reply in such a succinct and honest way?
Who the hell is this?
Hey, mother of my children, are you sick or what?
Yeah, and I love you too. ….. What’s wrong?
What now? Did you wreck the car again?
I don’t understand what you mean?
What the hell did you do now?
Are you sure this is for me?
Don’t beat about the bush, just tell me how much you need?
Am I dreaming?
If you don’t tell me who this message is actually for, someone will die
I thought we agreed you wouldn’t drink during the day.
Vitamin K1 (phylloquinone) is found in green leafy plants and is best known for the role it plays in blood clotting. Vitamin K2 (menaquinones) comes in several forms, the most common of which are MK-4, found in animal foods, and MK-7, found in fermented foods. Vitamin K2 plays important roles in bone and cardiovascular health
Research has found that people with the highest intakes of both types of vitamin K have significantly lower risks of atherosclerosis-related heart disease. Those with the highest intakes of vitamin K1 had a 21% lower risk of being hospitalized with atherosclerosis-related heart disease and those with the highest intakes of vitamin K2 had a 14% lower risk. Those with high vitamin K2 intake also had a 34% lower risk of peripheral artery disease
One of the primary ways in which vitamin K2 protects your cardiovascular health is by activating matrix Gla protein (MGP), which is a potent inhibitor of arterial calcification. Vitamin K2 can have a direct blood pressure lowering effect in some individuals
Low vitamin K status also raises the risk of frailty, impaired mobility and disability in elderly individuals
Statin drugs can deplete your body of vitamin K2 by inhibiting MK-4 synthesis. As a consequence, statins may contribute not only to age-related frailty but also insulin resistance, because MK-4 synthesis requires the same enzymes that synthesize cholesterol
Vitamin K is a fat-soluble vitamin that has a significant influence on your bone, heart and cardiovascular health. Vitamin K1 (phylloquinone) is found in green leafy plants and is best known for the role that it plays in blood clotting.
Vitamin K2 (menaquinones) comes in several forms, the most common of which are menaquinone-4 (MK-4) and MK-7, which play important roles in bone and cardiovascular health. While vitamin K1 has been found to moderately reduce the risk of bone fractures,1 MK-7 is more effective than vitamin K1 at reaching and protecting your bones.2,3
MK-4 is a short-chain form of vitamin K2 found in animal products such as meat, eggs, liver and dairy.4,5 The source matters, however. For example, animal products from factory-farmed animals are not high in MK-4 and should be avoided. Only grass-fed animals (not grain-fed) will develop naturally high levels.
MK-4 has a short biological half-life, making it a poor candidate as a dietary supplement. However, MK-4 from food is important for good health as it plays a role in gene expression. For example, research6 has found it may lower your risk of liver cancer.
MK-7 is a longer-chained vitamin K2 found in fermented foods such as sauerkraut, certain cheeses and natto (a fermented soy product).7 It’s produced by specific bacteria during the fermentation process. However, not all strains of bacteria make it,8 so not all fermented foods will provide it.
Most commercial yogurts, for example, provide little to no vitamin K2, and while certain types of cheeses, such as Gouda, Brie and Edam, are high in K2, others are not. MK-7 is what you’ll want to look for in supplements, as this form is extracted from real food and has a longer half-life.9
Vitamin K-Rich Diets Lower Atherosclerosis Risk
A 2022 study by Edith Cowan University, in which patients were followed for 23 years, found that people with the highest intakes of both types of vitamin K had significantly lower risks of atherosclerosis-related heart disease.10
Those with the highest intake of vitamin K1 had a 21% lower risk of being hospitalized with atherosclerosis-related heart disease and those with the highest intake of vitamin K2 had a 14% lower risk. Those with high vitamin K2 intake also had a 34% lower risk of peripheral artery disease. As noted by senior author Nicola Bondonno:11
“Current dietary guidelines for the consumption of vitamin K are generally only based on the amount of vitamin K1 a person should consume to ensure that their blood can coagulate.
However, there is growing evidence that intakes of vitamin K above the current guidelines can afford further protection against the development of other diseases, such as atherosclerosis.
Although more research is needed to fully understand the process, we believe that vitamin K works by protecting against the calcium build-up in the major arteries of the body leading to vascular calcification.”
How Vitamin K Protects Your Cardiovascular System
One of the primary ways in which vitamin K2 protects your cardiovascular health is by activating matrix Gla protein (MGP), which is a potent inhibitor of arterial calcification.
As explained in a 2019 study,12,13 “Stiffening and calcification of the large arteries are forerunners of cardiovascular complications,” and by improving your vitamin K2 status, you can significantly reduce arterial stiffness14 and improve blood pressure. Other investigations have also found that vitamin K2 can have a direct blood pressure lowering effect in some individuals.15
Vitamin K Status Also Plays a Role in Frailty
Vitamin K has also been shown to play an important role in frailty. As reported by Science News:16
“Reduced levels of circulating vitamin K are linked to an increased risk of mobility limitation and disability in older adults, according to a study published in the Journals of Gerontology: Series A17 …
‘Low vitamin K status has been associated with the onset of chronic diseases that lead to disability …’ said Dr. Kyla Shea, a nutrition scientist in the Vitamin K Laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts University.
‘Here, we’re building on previous studies that found that low levels of circulating vitamin K are associated with slower gait speed and a higher risk of osteoarthritis.’ Dr. Shea and colleagues examined two biomarkers: circulating levels of vitamin K and a functional measure of vitamin K (plasma ucMGP).
They used data from 635 men and 688 women ages 70-79 years old, who participated in the Health, Aging, and Body Composition Study (Health ABC). Mobility was assessed every six months for 6 to 10 years through annual clinic visits and phone interviews in the intervening time.
For the analysis, the researchers defined mobility limitation as two consecutive semi-annual reports of having any amount of difficulty either with walking a quarter of a mile or climbing 10 steps without resting, and mobility disability as two consecutive semi-annual reports of having a lot of difficulty or inability to walk or climb the same amount.
They found that older adults with low levels of circulating vitamin K were more likely to develop mobility limitation and disability. The other biomarker, plasma ucMGP, did not show clear associations with mobility limitation and disability.
Specifically, older adults with low circulating vitamin K levels were nearly 1.5 times more likely to develop mobility limitation and nearly twice as likely to develop mobility disability compared to those with sufficient levels. This was true for both men and women.”
Statin Drugs Deplete Vitamin K2
A factor that many overlook is the impact of statins (cholesterol-lowering drugs). In addition to depleting your body of Coenzyme Q10, which can adversely impact your heart health as it’s crucial for mitochondrial ATP production and healthy contraction of the heart muscle, statin drugs can also deplete your body of vitamin K2 by inhibiting MK-4 synthesis.18
Consequently, statins may contribute not only to age-related frailty but also insulin resistance, because MK-4 synthesis requires the same enzymes that synthesize cholesterol. As noted in a 2020 study:19,20
“There is emerging data to suggest that by inhibiting the production of intermediates of cholesterol synthesis, statins also inhibit the mevalonate pathway and impede the production of vitamin K2 in peripheral tissues.
There is growing evidence to suggest that vitamin K2 plays a key role in glucose homeostasis as well as vascular calcification. On this background, we hypothesized that statin use would be associated with both insulin resistance and vascular calcification in community-dwelling participants of a large longitudinal study of osteoporosis.”
As predicted, statin users did have higher indices of insulin resistance, which the authors stressed “could be relevant in healthy aging.” In conclusion, they recommended that individuals who have risk factors for diabetes should avoid lipophilic statins21 such as atorvastatin, simvastatin, lovastatin, fluvastatin, cerivastatin and pitavastatin.
Safer alternatives, according to this study, would be nonlipophilic statins (i.e., hydrophilic statins, which are only distributed to the liver), with the exception of rosuvasatin, a high-potency hydrophilic statin. Doing this “may provide the intended cardiovascular protection without the increased incidence of insulin resistance,” the authors said.
General Dosing Suggestions
To optimize your vitamin K status, the ideal solution is to eat plenty of vitamin K-rich foods. K1-rich sources include green leafy veggies like collard and turnip greens, kale, spinach, broccoli, Brussels sprouts, cabbage and lettuces.22
K2 MK-4 is found in organic, grass fed and pastured animal foods like eggs, liver, meat, and dairy,23,24 while MK-7 is found in fermented foods such as natto, sauerkraut, and cheeses such as Gouda, Brie and Edam.25
If you opt for an oral K2 supplement, it’s best taken with your evening meal, along with any vitamin D and/or calcium and magnesium you may be taking. As explained in previous articles, anytime you take a vitamin D supplement, you also need to be mindful of taking extra vitamin K2 and magnesium.
The K2 is needed to prevent arterial calcification while magnesium is required for vitamin D conversion. If you take large doses of vitamin D, you may inadvertently deplete magnesium, as it’s required in the conversion of vitamin D into its active form.
Research26 has shown you need 146% more vitamin D to achieve a blood level of 40 ng/ml (100 nmol/L) if you do not take supplemental magnesium, compared to taking your vitamin D with at least 400 mg of magnesium per day.
Combined intake of magnesium and vitamin K2 has an even greater effect. You need 244% more oral vitamin D if you’re not concomitantly taking magnesium and vitamin K2. What this means in practical terms is that if you take all three supplements in combination, you need far less oral vitamin D to achieve a healthy vitamin D level.
Unfortunately, the ideal ratio of vitamin K2 to D is still undetermined, so there are no hard and fast rules here. Some experts suggest 200 micrograms of vitamin K2 per day will meet the needs of the “average” healthy person,27 but if you’re taking high-dose vitamin D, you may need a bit more.
Also, if you’re going to use a vitamin K2 supplement, it is best to use MK-7, since MK-4 has a short biological half-life. One caveat: While nontoxic, people who are taking vitamin K antagonists, i.e., drugs that reduce blood clotting by reducing the action of vitamin K, are advised to avoid vitamin K2 (MK-7) supplements.