Thread: Minerals

What Copper Does for Us

Speaking of sneezing, one of copper's roles is to help us get rid of histamine. Histamine is what makes us sneeze or itch in response to allergies. In the brain, histamine keeps us awake and alert, but too much contributes to anxiety and panic attacks. Histamine helps us make stomach acid, which is needed to digest our food, but too much can cause acid reflux and heartburn.

Some foods contain histamine. The worst offenders are semi-hard or hard cheese, canned anchovies, smoked fish, all shellfish, deli meats, curry, mustard, soy sauce, yeast, avocados, bananas, dried fruit, dried nuts, lemons, mandarins, and pineapples. The histamine in these foods can can cause diarrhea as well allergy symptoms, acid reflux, or anxiety. This is called "histamine intolerance."

Since copper helps us get rid of histamine, getting enough of it can help prevent or fix any of the histamine-related symptoms described above.

Remember from previous lessons, methylation also helps get rid of histamine, which requires choline, folate, and B12. When copper does this, it cooperates with vitamin B6 and vitamin C to get the job done.

Copper, in fact, cooperates with vitamin C in many other areas as well:

They strengthen collagen, which protects against osteoporosis, makes our bones strong, and prevents all the signs of scurvy described in the vitamin C lesson.
Our adrenals use them to make noradrenaline and adrenaline, also known as norepinephrine and epinephrine. These help us to respond to stress with the "fight-or-flight" response. Norepinephrine also helps us explore our options and focus when we find the right one.
We use them to make melanin, the main pigment that colors our skin, eyes, and hair.
They even make the signals within the brain that communicate the need for adrenal hormones and melanin.
They also play many interacting roles together in making us high-powered revved up sex machines: They make the oxytocin that produces the affectionate response to getting close, and they also make the signals to make sex hormones like estrogen and testosterone.
They also make the brain signal that tells our thyroid gland to make thyroid hormone, and that's what keeps the whole system running at top speed.
They make other signals that prevent us from peeing too much, especially at night when we should be sleeping, and prevent us from eating too much.
Copper also does some things on its own:

It allows us to use iron. This prevents anemia and allows iron to fulfill many other roles that we will discuss in the iron lesson.
It helps us make platelets, which clot the blood when we've been wounded, and white blood cells, especially neutrophils, key parts of our immune system that defend us against infection.
Copper helps us get rid of excess serotonin, our brain's key stress-coping chemical. Although we need some serotonin to handle stress, too much serotonin over time can cause us to run away from our fears instead of facing them, and can weaken our grip on reality, possibly contributing to schizophrenia. When we get too much serotonin all at once, it can cause sweating, irritation, tremors, and diarrhea.
Copper also helps us make dopamine, our brain's key motivation chemical, and helps us regulate dopamine in a way that keeps us motivated and prevents us from getting too easily distracted.
Along with most of the B vitamins, copper is directly involved in extracting energy from the food we eat.
Like vitamins E and C and several of the B vitamins, copper protects us from oxidative stress. This is the wear and tear on our tissues that occurs as we age. It accelerates in disease states and with exposure to toxins.
Copper Deficiency

The biggest things that stand out in severe copper deficiency are anemia, low white blood cells, and, in people who are rapidly growing, osteoporosis. Arthritis, loss of color in the skin, graying hair, and heart disease also occur. One study suggested high cholesterol and high blood sugar can also occur.

Based on everything we discussed at the beginning of this lesson, we might also expect copper deficiency to cause worsened allergies, histamine intolerance, insomnia, anxiety, acid reflux, brain fog, low sex drive, fatigue, poor stress-coping, overeating, hypothyroidism, waking up in the middle of the night to pee or peeing too much in general, poor motivation, easy distraction, excessive fear avoidance, and faster aging.

How Much Copper Do We Need?

The RDA for copper is 0.9 milligrams per day (mg/d) for adult men and women. On average, we absorb 50% of the copper in food, but we regulate how much we hold on to based on how much we need. As a result, anything between 0.8 and 2.4 mg/d can give us the amount of copper we need.

The RDA adjusts the copper requirement downward according to bodyweight for children. I recommend adjusting it based on energy intake instead: have the kids get 0.4-1.4 mg copper for every 1000 Calories.

The RDA for pregnancy was set at 1 mg/d based on the amount of copper that accumulates in the fetus. The RDA for lactation was set at 1.3 mg/d based on the amount of copper that a mom releases into her milk.

Copper in Food

So, how do we get these amounts from food?

We could obtain 1 mg copper, satisfying the RDA for all adults except nursing moms, from the following foods:

10 grams of (g) beef liver
12.5 g oysters (less than one oyster) or goose liver
14 g lamb liver
17 g dried spirulina or duck liver
20 g shiitake mushrooms
25 g sesame seeds or cocoa powder
If you eat chocolate, the copper content will be diluted by the sugar and milk. For example, you'd need 36 grams of 70% chocolate to hit the 1-mg target.

Most shellfish besides oysters, mushrooms besides shiitake, seaweed besides spirulina, whole grains, legumes, and potatoes are decent sources of copper that will help you hit the 1-mg target in larger amounts.

Muscle meats can be rich in copper but are often very low in copper and shouldn't be relied on. Milk can be a decent source of copper, but is also often very low and shouldn't be relied on. Eggs are very low in copper.

As a result, plant foods are on average richer in copper than animal foods, and vegetarians and vegans have the highest copper intakes. Omnivores and carnivores can level the playing field with a little liver or oysters.

Variation in Food Copper

There is tremendous variation in the copper content of foods, depending on the amount of copper in the soil. Unfortunately, the distribution of soil copper is rather random, and there are no easy rules of thumb to go by. Kidney, salmon, shrimp, and some vegetables vary only 2-fold or less, but milk varies 88-fold, muscle meat varies 18- to 100-fold, potatoes vary 32-fold, and oysters vary 48-fold. Unfortunately many of the top foods, such as liver, cocoa, mushrooms, and spirulina have not been adequately tested for variability.

The best thing to do is include a few of the richest foods in a rotation, and eat a broadly diverse diet in the background. This will ensure you don't put all your eggs in any one basket and risk relying on a food that is a poorer source of copper than you expect.

Other Causes of Deficiency

A few other things can cause deficiency besides poor diet:

Zinc supplements can cause copper deficiency when over 50 mg/d and not matched with at least 1 mg copper for every 2-15 mg zinc.

proton pump inhibitors and antacids

digestive disorders including celiac

gastric bypass surgery

dialysis, a treatment for kidney disease

severe burns

rare genetic defects may manifest as copper deficiency or toxicity

Copper Toxicity

Although copper deficiency causes many problems, too much copper is toxic. It can worsen oxidative stress, causing wear and tear on the tissues, and damage the liver, eyes, and brain, possibly contributing to age-related dementia. 10 mg/d is considered the limit of what is safe.

Severe copper toxicity is extremely rare. There exists only one case report of a 26-year-old male who took 30 mg/d for two years and 60 mg/d for another year. He damaged his liver so bad he needed a transplant.

Fortunately, it's almost impossible to get copper toxicity from foods unless we go overboard with the superfoods. For example, eating four ounces of liver every day could put you in danger, and I recommend limiting liver to 4-8 ounces per week. Even in copper-polluted areas, plants and animals limit their accumulation of copper and never get high enough to surprise you with toxic amounts.

The copper content of water varies 2000-fold before it flows through any pipes, and can reach 1 mg per liter (mg/L). If the water flows through corroded copper pipes, it can carry up to 30 mg/L. Fortunately, there are some warning signs. At 1 mg/L, the water will stain your laundry, sinks, and toilets blue. At 2.5 mg/L, the water tastes bitter and is likely to nauseate you if you drink much of it. If you do have copper-contaminated water, you should get a water filter or find an alternative source of water. As a quick fix, running the water for one minute before using it can dramatically reduce the amount of copper it contains.

Copper, Birth Control, and HRT

Copper IUDs used as birth control are usually considered safe, but some models sometimes raise copper levels.

All estrogen-based birth control and hormone replacement therapy (HRT) should warrant caution. During pregnancy, chronic exposure to estrogen increases copper absorption from food and the transport of copper across the placenta to the fetus. With birth control or HRT, the estrogen increases copper absorption but there is no fetus to give it to.

Estrogen can double copper levels, and this isn't necessarily a problem because usually the liver responds by making proteins to shield the copper and protect it from causing harm. However, if the increased copper levels exceed the liver's ability to do that, then copper can run amok and cause problems.

As a precaution, I would suggest women using supplemental estrogen limit their total copper intake from foods and supplements to no more than 5 mg/d, and avoid taking any supplements that contain more than 1 mg/d.

Copper Supplements

Copper supplements on the market may come as copper sulfate, or copper bound to an amino acid such as copper glycinate. All of these supplements contain copper in a different form than found in food, and there is some data from animal experiments suggesting supplemental copper is not used as effectively as food copper and might be more likely to cause harm.

The exception is a product called MitoSynergy, which has food-form copper bound to a small amount of niacin. If you wish to use supplemental copper as an insurance policy, I recommend using 2 capsules of the MitoSynergy MitoActivator Extra Strength to yield 1 mg/d copper.

Other forms of copper are much cheaper, and do serve to correct copper deficiencies quickly. For example, 7 mg/d copper sulfate corrected copper-deficiency anemia in a patient with celiac disease within two months. I don't recommend using cheap forms of copper long-term, however, and I would not supplement with more than 1 mg/d copper unless correcting a deficiency.

Copper supplements should never be given to infants, because they can't regulate how much they absorb.

Wrapping Up

So, wrapping up:

Copper deficiency causes anemia, low white blood cells, osteoporosis, gray hair, loss of color in the skin, heart disease, and maybe high cholesterol and high blood sugar.

Copper protects against allergies, histamine intolerance, insomnia, anxiety, acid reflux, brain fog, low sex drive, fatigue, poor stress-coping, overeating, hypothyroidism, waking up in the middle of the night to pee or peeing too much in general, poor motivation, easy distraction, excessive fear avoidance, and faster aging.

Copper toxicity damages the liver, eyes, and brain, and may contribute to age-related dementia.

Small amounts of liver, oysters, shiitake mushrooms, spirulina, or chocolate are the best sources of copper, but the copper content of foods varies widely.

Avoid zinc supplements over 50 mg/d and use a zinc-to-copper ratio between 2:1 and 15:1 if supplementing.

Digestive disorders, antacids, proton pump inhibitors, gastric bypass surgery, dialysis, and severe burns can all cause copper deficiency.

Use up to 7 mg/d of any copper supplement for 2 months to correct a severe deficiency.

As an insurance policy, try 1 mg/d of copper from MitoSynergy MitoActivator Extra Strength, if you wish to take a long-term supplement.

If you are a woman on supplemental estrogen, keep total copper under 5 mg/d and copper supplements to a maximum of 1 mg/d.

Filter your water if it's contaminated with copper, or find another source.

Be cautious about copper IUDs as birth control.

Antagonism Between Omega-6 and Omega-3

In yesterday's lesson on omega-6, we covered essential fatty acid (EFA) deficiency in its classical form, which was a deficiency of arachidonic acid that could be cured by arachidonic acid itself, found mainly in liver and egg yolks, or by its precursor, linoleic acid, found mainly in plant oils but also in animal products.

Omega-3 fatty acids did two obvious things to the EFA deficient rats:

They lessened the rapid weight loss and death.
They made the skin condition worse.
This can be explained rather easily:

Some minimum amount of PUFA in general, whether omega-6 or omega-3, is needed to allow us to extract energy properly from food. If we can't, we lose weight and die.
Omega-3s have the ability to interfere with omega-6 function, so they could make everything else in the deficiency, all of which is a specific result of omega-6 deficiency, worse.
For almost 50 years after the initial discovery of EFA deficiency in 1929, researchers dismissed the importance of omega-3 fatty acids. While they had the ability to make certain aspects of EFA deficiency a little better, omega-6 fatty acids had the ability to completely cure it all on their own. So, omega-3? Why bother?

A Six-Year-Old Girl Shot in the Stomach: The Ultimate Plot Twist

Things all changed in 1982 when a poor six-year-old girl suffered a gunshot wound to her abdomen. She required repeated rounds of surgery and couldn't eat anything for five months. When a patient can't eat anything, doctors will inject all their essential nutrients right into their veins. This is called total parenteral nutrition (TPN).

Through most of the 1970s, TPN had always been fat-free. However, TPN patients would often get eczema. Since the eczema looked a lot like EFA deficiency, researchers in the late 1970s argued that vegetable oil should be added to the TPN. The case for EFA deficiency was never strong. The TPN at that time was deficient in multiple nutrients, including vitamin K, iron, zinc, other less well understood minerals, and choline. Zinc, in particular, is now known to produce patches of dry skin as its earliest sign of deficiency. Leading up to the addition of vegetable oil to TPN, the fatty acid researchers published one report where topical corn oil did nothing to the eczema, and another report where they cured it with vegetable oil and zinc. But they never showed they could cure it with just vegetable oil. Nevertheless, in the early 1980s, vegetable oils were added to TPN.

So the six-year-old girl with the abdominal gunshot wound was fed for five months on TPN, which included intravenous safflower oil. She started experiencing periods of numbness, tingling, weakness, inability to walk, psychological disturbances, and blurred vision. Nothing like this had EVER happened on fat-free TPN.

Then they switched her to soybean oil. What happened? All of the problems disappeared. Poof! Like magic.

Here, we finally saw a mirror image of what had happened to the EFA-deficient rats that highlighted the critical importance of omega-3 fatty acids:

Omega-3 fatty acids can worsen the scaly skin of omega-6-deficient rats.
Omega-6 fatty acids can bring on the neurological problems of omega-3-deficient humans.
ALA, EPA, and DHA

In order to put these into the context of what we know now, let's look at the specific fatty acids involved.

Alpha-linolenic acid (ALA) is the omega-3 version of linoleic acid, and is found in plant oils.

Docosohexaenoic acid (DHA) is the omega-3 version of arachidonic acid, and is found mainly in fish, liver, and egg yolk.

Just like we and other animals convert linoleic acid to arachidonic acid, so we convert ALA to DHA. Just like arachidonic acid is the form that must be in the body to prevent the scaly skin, dandruff, hair loss, infertility, and hormonal problems of omega-6-deficiency, DHA is the form that must be in the body to prevent the neurological problems of omega-3 deficiency.

This conversion pathway leads us to look at a third fatty acid:

Eicosapentaenoic acid (EPA) is an intermediate along the way from ALA to DHA. In fish, it is essential and will always be found. By contrast, mammals that are very good at making the conversion from ALA to DHA can have zero EPA in their tissues and have nothing wrong with their health.

How Omega-6 and Omega-3 Can Each Each Cause the Other to Become Deficient

Linoleic acid (omega-6) and ALA (omega-3) both share the same machinery to be converted to the fatty acids we need. If one is provided in great excess of the other, it can hog the conversion machinery. Worse, an abundance of PUFA tricks our body into thinking we have enough of all of them, so it actually makes less of that machinery. Too much of one, then, causes a deficiency of the other.

So, ALA made the scaly skin worse in EFA-deficient rats because it hurt their ability to convert the linoleic acid in their own fat stores to arachidonic acid. No one fed fat-free TPN ever developed neurological problems. But the poor girl given intravenous safflower oil developed terrible neurological problems because the omega-6 in the oil prevented her from converting ALA in her own fat stores to DHA. Soybean oil has a nice balance between omega-6 and omega-3, so it made the problem disappear.

Omega-3's and omega-6's can interact in a second way: EPA is roughly the same size and shape as arachidonic acid. While DHA takes its own place in cell membranes, EPA steals the place that belongs to arachidonic acid. Then, when the activation machinery goes after the arachidonic acid, it uses the EPA instead, making inactive byproducts.

The "Anti-Inflammatory" Effects of EPA

In the 1990s, it became popular to see this as a beneficial anti-inflammatory effect of EPA. This made sense at the time, because we knew that arachidonic acid lit the flame of inflammation, and we thought that the flame just fizzled out on its own once it ran out of fuel. So, using EPA to dampen the lighting of the flame made sense.

Inflammation Resolution is an Active Process Requiring Arachidonic Acid and DHA

We now know that the flame never fizzles out. Our immune system puts it out when it decides that it is ready. DHA, like arachidonic acid, like vitamins A and D, and like the MK-4 form of vitamin K, plays a role in cellular decision-making. When the immune system decides to ramp up an attack against a bad microbe, it uses arachidonic acid to help it make the decision. When it decides to clean up the mess, pack up, and go home, it uses both arachidonic acid and DHA to make the decision. This process is called the "resolution" of inflammation.

EPA is never used in inflammation resolution *except* when you take aspirin. And this is a highly specific effect of aspirin. Natural anti-inflammatories in food don't count. Other NSAIDs don't count. Acetaminophen doesn't count. Just aspirin. While the right combination of EPA and aspirin might help jumpstart the resolution of inflammation, exactly how to combine them hasn't been well studied.

It makes more sense in most cases to focus on giving your body the DHA it needs.

Other Benefits of DHA

In addition to its role in cellular decision-making that helps us resolve inflammation, DHA is critical to two other processes. These are important throughout our bodies but are far more important in our nervous system than anywhere else:

In those oily membranes that enclose our cells and all their internal compartments, proteins move around fluidly. These proteins, made from the protein we eat in foods like meat and beans, help cells carry out many functions and often need to be docked in one place so they can interact with other proteins or with things in the cell's environment. DHA helps them dock.
As a PUFA, DHA is easily damaged by oxidative stress. When that happens, it acts as a red flag to the cell, causing the cell to ramp up its antioxidant defenses.
DHA and the Nervous System

Both of these roles are far more important in the nervous system than anywhere else, which is why the girl with the gunshot wound had neurological problems when she was made deficient.

The retina is the part of the eye where vitamin A is used to generate vision. The retina is actually part of the central nervous system, along with the brain. DHA is extremely important there, and losing it causes loss of visual acuity, making it harder for you distinguish fine detail when you are looking at things.

Omega-3s, Psychiatric Disorders, and Heart Disease

The importance of DHA to the nervous system suggests that people with many psychiatric disorders could benefit from improving their DHA status. Since ALA is converted to both EPA and DHA, and since EPA is converted to DHA, it is difficult when looking at the studies to tell which one of these fatty acids is most important, especially since supplements often contain EPA and DHA together. Generally speaking, supplementation with omega-3 fatty acids improves ADHD, autism, aging-associated memory loss, migraines, and depression.

EPA might be more effective than DHA for depression, suggesting it might be acting more like an anti-inflammatory drug than as a nutrient.

There is an enormous number of studies testing whether fish oil prevents heart disease. It probably doesn't, though it may protect against atrial fibrillation, a condition where the heart beats irregularly.

However, high doses of EPA lower levels of triglycerides in the blood, which might lower the risk of heart disease in certain people. Triglycerides are large molecules made of three fatty acids attached to a backbone. They are the main form of fat we eat in the diet. When we eat lots of carbs, we turn some of them into triglycerides. This is especially true if we are insulin resistant, as in the case of type 2 diabetes or people who are on their way toward type 2 diabetes. Insulin resistant people have trouble clearing triglycerides from their blood, so if they make even a small amount their blood levels can go quite high. High doses of EPA will stop the conversion of carbohydrate to fat, which makes them effective at lowering triglycerides in people who have a hard time clearing them from the blood.

So how much omega-3 do we need? This is a difficult question to untangle. Let's consider a few things:

There is a critical window to enrich the brain with DHA. In humans, this occurs during pregnancy and the first few years of life.
Outside of this critical window, fat-free diets do not produce any obvious omega-3 deficiency. This requires feeding omega-6-rich plant oils.
We can get DHA through conversion from ALA or EPA, but that requires good genetics, healthy insulin function, a low total PUFA intake, and enough B6, biotin, carbs, calories, protein, calcium, and zinc. In the general population, PUFA intakes are high from vegetable oils, insulin resistance is common, many people fail to get enough vitamins and minerals, and some of us just have bad genetics.
As with arachidonic acid, growing, fueling the growth of a baby, or having a disease state will increase needs for DHA. So, babies and growing kids, pregnant and nursing moms, bodybuilders in a gaining phase, people recovering from injury or illness, and people with chronic diseases may all need a little extra.
We can say this about the dose:

Healthy adults seem to need about 150 milligrams per day (mg/d) of DHA to maintain healthy amounts within their bodies.
If you rely on conversion from ALA and/or EPA, you could need a lot more.
2 grams per day of EPA and DHA together might be needed to improve neurological and psychiatric problems, and 4 grams per day of EPA are needed to lower triglycerides.
In one very impressive study, moms who took cod liver oil yielding 1.2 g/d DHA and 0.8 g/d EPA while pregnant and nursing increased the children's IQ at age four. This more than tripled the DHA content of the breast milk. A baby consuming 800 milliliters per day of this milk would get over 11 grams of DHA and almost 3 grams of EPA.
Putting this altogether, the following recommendations emerge:

Pregnant and nursing moms should aim for 2 grams per day of EPA and DHA, with an emphasis on DHA.

Kids should be breast-fed as long as practical, and should be weaned on to a diet containing as much fatty fish as they're willing to eat, up to age 4.

Most adults should be fine with 150 mg/d DHA, which can be obtained from five pasture-raised egg yolks per day or from one serving of fatty fish per week.

In the cases of ADHD, autism, age-associated memory loss, migraines, depression, or atrial fibrillation, 2 grams of EPA and DHA may be warranted. In most cases, err on the side of getting more DHA, but with depression try getting more EPA.

In the case of stubbornly high triglycerides, 4 grams per day of EPA may be warranted.

Fish oil or cod liver oil can be used to meet these requirements. They vary in their DHA and EPA content, so check the label. Cod liver oil has the benefit of extra A and D.

Vegans present a special case. Most of the talk on the internet about the omega-6-to-omega-3 ratio doesn't apply to people who are getting arachidonic acid and DHA, because the ratio mainly affects the ability to get these fatty acids from plant oils. Vegans who rely entirely on plant oils should aim for an omega-6-to-omega-3 ratio of no more than 4:1, and ideally close to 1:1. This still doesn't fix the poor conversion problem, however. Vegans are better off hitting the targets with arachidonic acid supplements from the fungus Mortierella alpina and with DHA supplements from algal oil.

As with omega-6, since all PUFA raise the need for vitamin E yet cannot be fully protected by it, you should never eat more omega-3 than you come across by way of seeking other vitamins and minerals from natural foods, or than you need to resolve signs and symptoms that appear to be related to deficiency.

Classical Essential Fatty Acid Deficiency

These are the types of things that happen to lab rats when they are deficient in the essential fatty acids. This is what happened to the poor rats:

They developed irritated, sore, and scaly skin, dandruff, and hair loss.
Their tails were inflamed, swollen, scaled and ridged, and were hemorrhaging in certain spots.
Their kidneys got hurt and they started peeing blood.
They drank what seemed like way too much water, yet didn't pee any more than usual because the water just evaporated from their skin.
The males lost interest in sex, stopped producing sperm, and their testosterone tanked.
The females stopped ovulating, couldn't get pregnant, and their levels of both estrogen and progesterone tanked.
The females developed enlarged adrenals, giving them an exaggerated response to stress.
The adrenals of the males shrunk, making them unable to mount any response to stress.
They ate more food, but gained less weight. Sounds nice at first! Eventually, though, they lost so much weight they died.
EFA Deficiency Required Refined Diets High in Sugar

To make these animals so deficient, they had to do a LOT. The earliest attempts to feed rats fat-free diets simply produced very healthy rats. No problems. It was only when they started making diets from highly purified ingredients that they stumbled into essential fatty acid (EFA) deficiency.

The early fat-free diets that produced healthy rats were made from meat residue and starch, with yeast and alfalfa for vitamins. The diets that produced EFA deficiency were made from milk protein and sugar that had undergone repeated rounds of purification, with yeast and fat-free extracts of cod liver oil and wheat germ for vitamins.

None of the known vitamins could cure the deficiency, nor could coconut oil. Butter cured it in very large amounts. Cod liver oil helped a handful of the symptoms but left many uncured. Lard, corn oil, flax oil, and olive oil all proved fully curative in relatively modest amounts.

But the KING was...

Liver!

Arachidonic Acid Is What's Missing

It turned out that EFA deficiency could also be cured with two specific fatty acids.

Fatty acids are the building blocks of larger molecules that make up the oil and fat we eat. Oils like olive oil and fats like butter are almost pure fat. Virtually all foods, though, contain at least some fat, and the foods with more fat have richer tastes and textures.

As we discussed in the lesson on vitamin E, there are three types of fatty acids:

Saturated, richest in fats that are solid at room temperature.
Monounsaturated, richest in oils that are liquid at room temperature but solid in the refrigerator.
Polyunsaturated, richest in oils that stay liquid in the refrigerator.
In the lesson on vitamin E, we discussed how the polyunsaturated fatty acids (PUFAs) are uniquely vulnerable to damage, and how vitamin E has just one job: to protect them. While vulnerable, it is these PUFAs that are essential.

There are many fatty acids within the PUFA class, but they can be broken down into two families: the omega-3s and the omega-6s Although many people think of omega-3s as "good fats" and omega-6s as "bad fats," it is the omega-6s, not the omega-3s, that cure the classical syndrome of EFA deficiency that we have been talking about. Linoleic acid, found mainly in plant oils, and arachidonic acid, found mainly in liver and egg yolks, are the two omega-6 PUFAs that cure the deficiency.

Arachidonic Acid is the Animal Form of EFAs

Just like carotenoids, the plant form of vitamin A, have to be turned into retinol, the animal form, and just like pyridoxine, the plant form of B6, has to be turned into pyridoxal, the animal form, linoleic acid has to be turned into arachidonic acid to cure essential fatty acid deficiency. The conversion is a three-step process requiring vitamin B6 and biotin.

Purified linoleic acid cured EFA deficiency at just over two percent of calories, but purified arachidonic acid was effective at only one-third the amount. Purifying individual fatty acids for these lab experiments damaged them in ways that increased the requirement, and foods were more effective. Lard cured EFA deficiency when it supplied 0.4% of calories as linoleic acid. Liver cured it when it supplied only 0.06% of calories as arachidonic acid!

Biotin and B6 Help Cure Deficiency

Why is liver such a boss? About half of its PUFA is arachidonic acid, unlike lard, which has mostly linoleic acid, AND it supplies boatloads of biotin and lots of B6 to help the conversion.

In fact, just giving rats extra B6 could often cure EFA deficiency. This is because they had plenty of linoleic acid stored in their own fat tissue. They could dig into those stores, and with enough B6 they could convert the linoleic acid into arachidonic acid.

Arachidonic Acid is Needed for Cellular Decision-Making

Like vitamins A and D, and the MK-4 form of vitamin K, arachidonic acid helps with cellular decision-making.

Arachidonic acid is first stored in the oily membranes that enclose our cells and all of their internal compartments. When needed, we release it from the membrane, and then activate it by converting it into one of a number of different possible byproducts that all help with cellular decision-making in their own unique way.

One of the effects these byproducts have is to allow cells to create bridges between one another that allow them to cooperate, and to create barriers that seal the spaces between each other to prevent things from slipping through. This helps water-proof the skin, prevents things from sliding right through the skin that should be kept out, and keeps food particles from getting into your blood before you have the chance to fully digest them.

However, while omega-3 fatty acids tended to make most of those problems worse, they actually helped with the weight loss and early death. The reason the poor rats ate so much and kept losing weight is because the energy-production machinery within the membranes of their mitochondria, those powerhouses of the cell, got jammed up. Just like PUFAs keep an oil liquid even in the refrigerator, any PUFA, whether it is omega-3 or omega-6, will help keep cellular membranes nice and fluid. It appears we need some minimum amount of fluidity in our membranes to keep energy production running smoothly.

Stomach Health, Immune Health, Balancing Inflammation, Confidence, Anxiety, and Exploration

We now know that these decision-facilitating byproducts of arachidonic acid do a number of other things:

They keep the lining of the stomach strong, preventing ulcers.
They teach the immune system to tolerate foods, preventing allergies and food intolerances.
They can dilate blood vessels or cause the blood to clot.
They initiate inflammation, protecting against infection, and help get rid of inflammation once the need for it has passed.
In the brain, arachidonic acid is used to make calming chemicals that decrease anxiety, increase confidence, and increase the degree to which we will reach out of our comfort zone to explore the possibilities that life has to offer us.
The Dangers of Anti-Inflammatories

Unfortunately, despite all the good things it can do, the ability of arachidonic acid to light the fire of inflammation, so critical to our defense against infection, means that it can also cause lots of discomfort:

headaches
menstrual cramps
almost any other type of pain
itching
redness
swelling
This has led to the development of a huge and wildly popular set of drugs that stop us from taking arachidonic acid out of our membranes and activating it into the byproducts that help with cellular decision-making.

These are the nonsteroidal anti-inflammatory drugs (NSAIDs). They include aspirin, ibuprofen (Motrin, Advil), and naproxen. Acetaminophen (Tylenol) is not considered an NSAID, but it does have a similar effect. Many natural foods and herbs contain salicylates, which are aspirin-like substances that act similarly to NSAIDs. EPA, an omega-3 fatty acid found in fish and fish oil, also acts like an NSAID. It is well known that NSAIDs can cause damage to the stomach, including ulcers.

We also have some studies in laboratory animals suggesting that while they do reduce peak inflammation, they prevent us from ever fully resolving inflammation, leaving us with chronic, persistent, low-level inflammation. Chronic inflammation is thought to play a role in many different diseases.

Although we have no direct evidence of this, we should be suspicious that excessive use of anti-inflammatories could also contribute to dandruff, skin problems, hair loss, infertility, low sex drive, a dysfunctional stress response, or any of the other features of EFA deficiency.

How Much Do We Need?

So, how much do we need? Under most circumstances, not too much.

Let's consider what it took to give rats EFA deficiency:

Lots of sugar. Sugar promotes oxidative stress, which both destroys PUFA in general and also hurts the conversion of linoleic acid to arachidonic acid.
An active state of growth. Young growing rats, pregnant rats, and rats that refeed after an extended period of starvation can all become EFA deficient. Adult rats that aren't growing cannot.
Mediocre nutrition. For example, the fact that B6 could cure EFA deficiency shows that the rats weren't getting enough B6.
Now let's consider how much was needed, even in the context of growing rats fed enormous amounts of sugar with mediocre vitamin status. Extrapolating from the rat studies, a human eating 2000 Calories per day would require one gram of linoleic acid or 133 milligrams of arachidonic acid.

It has been very hard to show EFA deficiency in humans, and there is no reason to suggest we need more than those rats. The only attempt to induce EFA deficiency in an adult human ever performed was in 1938 when a biochemist volunteered. He consumed three quarts of defatted milk, a quart of cottage cheese made from it, sugar, potato starch, orange juice, and some vitamin and mineral supplements. Rather than experiencing adverse effects, he experienced a marked absence of fatigue, a normalization of his high blood pressure, and the complete disappearance of the migraines he had suffered from since childhood.

EFA deficiency has been observed in human infants fed formula made mostly from corn syrup with a little bit of skim milk. They suffered from poor growth, increased infections, and scaly skin. They cured it with butter or with isolated linoleic acid, using the same doses that would have cured the rats.

So, let's go with our original calculation from the more detailed experiments with rats: one gram of linoleic acid or 133 milligrams of arachidonic acid for every 2000 Calories.

Even 2000 Calories of enriched, white flour has over two grams of linoleic acid. 2000 Calories of potatoes has over one gram. 2000 Calories of coconut oil, the lowest-PUFA oil on the market, provides at least 4 grams of linoleic acid.

There are two foods with zero EFAs: sugar, and fully hydrogenated oils. Hydrogenation is a process that converts unsaturated fats into saturated fats. Partial hydrogenation has been more common than full hydrogenation, and this produces both saturated fats and trans fats. Partially hydrogenated oils actually have plenty of linoleic acid, but they are currently being phased out of our food supply because of the unhealthy effects of trans fats. It is fully hydrogenated oils that completely eliminate EFAs, and these are found in some processed foods. 2000 Calories of sugar, fully hydrogenated oil, or some combination of the two, would fail to provide even one gram of linoleic acid.

Obviously any diet composed mostly of natural, whole foods, will provide more than one gram of linoleic acid. I have shown you the extreme of low-fat (flour, potatoes) and low-PUFA (coconut oil). Including higher-fat foods such as any animal products, nuts, seeds, avocados, olives, or any added fats or oils, will provide more, and will even help you make up for including some sugar in your diet.

Poor Conversion or Activation is Far More Common Than Absolute Deficiency

While few if any of us need to worry about not getting enough linoleic acid, many of us will need to worry about two things:

Poor conversion of linoleic acid to arachidonic acid.

Poor conversion of arachidonic acid to its byproducts that help with cellular decision-making.

Let's tackle these one at a time. We'll start with poor conversion of linoleic acid to arachidonic acid.

As mentioned before, biotin and B6 are needed for the conversion. As discussed in the lesson on B6, riboflavin is needed to get B6 from plant foods. This might explain why all three B vitamin deficiencies share inflamed, scaly skin as a common symptom with EFA deficiency.
Sugar hurts the conversion. Watch your sweet tooth!
Reheated vegetable oils hurt the conversion. Stay away from the deep fried foods in restaurants!
Calories, protein, and carbs boost the conversion. Eat enough of each.
Insulin boosts the conversion. Diabetics either don't have enough (type 1) or are resistant (type 2).
Calcium deficiency hurts the conversion.
Zinc deficiency might also hurt the conversion.
Some people have poor conversion because of their genetics.
Since so many things hurt the conversion, it makes sense to shoot for at least 133 milligrams of arachidonic acid for every 2000 Calories. You can get this from 2 large egg yolks or 100 grams of liver.

Vegan Arachidonic Acid Supplements?

Vegans, or those who cannot or will not eat liver and eggs, can use arachidonic acid supplements derived from the fungus Mortierella Alpina. Vegans should check with the manufacturer to ensure the entire production process is vegan.

Who Should Worry?

Who should be worried about meeting this requirement?

Growing children
Pregnant or nursing women
People recovering from injury
Bodybuilders in a gaining phase
Anyone suffering from a disease
Most of these people are growing. The pregnant and nursing mothers are fueling growth. Disease states often involve inflammation or oxidative stress, which deplete EFAs.

While 133 mg arachidonic acid for every 2000 Calories is a good starting place, you can try more if you have any signs or symptoms of EFA deficiency, and keep your intake higher if it helps.

Anti-Inflammatories and Poor Activation

The second problem is poor conversion of arachidonic acid to the byproducts responsible for curing EFA deficiency. To avoid confusion with the first conversion problem, let's call this "activation."

As mentioned before, activation is hurt by NSAIDs, acetaminophen, most natural anti-inflammatories in foods and herbs, and the EPA in fish and fish oil. We can add calcium deficiency to this list. In this case, the problem could apply to anyone, regardless of whether they are growing or suffering from a disease state. And the solution would not be to get extra arachidonic acid, but rather to remove the thing that's hurting its activation.

Is There a Toxic Dose?

Although there is no clearly defined toxic dose of any of the EFAs, we covered a good reason to avoid getting more than you need in the lesson on vitamin E: they are vulnerable to oxidative damage and raise the need for vitamin E, but vitamin E cannot fully protect them. Therefore, it makes sense to limit these fatty acids to what you would get when you pursue your other essential nutrients from whole foods, and whatever extra you may have to add to resolve signs of deficiency.

Wrapping Up

To wrap up:

EFA deficiency causes dandruff; inflamed, scaly skin; hair loss; low sex drive and infertility; low sex hormones; a blunted stress response in males and an exaggerated stress response in females.

EFA deficiency is cured by linoleic acid or arachidonic acid, both of which are omega-6 PUFAs.

Arachidonic acid is what's needed. Linoleic acid is just a precursor.

Arachidonic acid is also needed for stomach health, to prevent food intolerances, defense against infection, resolution of chronic inflammation, and the confidence to explore the world without anxiety.

EFA deficiency is mainly a concern for growing children, pregnant or nursing mothers, bodybuilders in a gaining phase, and those dealing with chronic diseases or recovering from disease or injury.

One gram of linoleic acid or 133 mg arachidonic acid for every 2000 Calories are sufficient in most cases.

Any diet of natural, whole foods will provide one gram of linoleic acid, but 133 mg arachidonic acid requires 2 egg yolks or 100 grams of liver. Fungi-derived supplements might be vegan.

Meeting the target for arachidonic acid is an insurance policy against poor conversion from linoleic acid.

Poor conversion can be caused by genetics; diabetes; insulin resistance; inadequate protein, calories, or carbs; inadequate biotin, B6, riboflavin, calcium, or zinc; sugar; or reheated vegetable oils.

Activation of arachidonic acid can be hurt by NSAIDs, acetaminophen, natural anti-inflammatories from foods or herbs, or EPA from fish or fish oil.

Anyone at any life stage should be concerned with activation and the solution is to reduce the things impairing activation.

Adjust your approach for increasing intakes of linoleic acid or arachidonic acid, or removing factors that impair the activation of arachidonic acid, according to what helps improve anything that seems like EFA deficiency symptoms. Don't use more than you need.

EFA’s are an essential part of my supplement daily program.

Max

Vitamin K and Blood Clotting

Vitamin K stands for "koagulation."

This is when your blood clots, or clumps together. The biochemist who first named it was Danish and spoke German, and although coagulation begins with a C in English, it begins with a K in German. The new vitamin he discovered was kritical for koagulation, so he kalled it "K."

Although clotting in the wrong context can contribute to a heart attack, stroke, or other serious or even fatal problems, clotting is necessary to stop us from bleeding to death when we get injured. In fact, even when we're fine our blood has a certain amount of clotting going on just to keep our blood from breaking through the blood vessel walls and gushing everywhere. When vitamin K runs deficient, one thing we might notice is that we bruise more easily. That's because bruises form when we bleed just under the surface of the skin. When K runs SEVERELY deficient, the bleeding can become serious, known as a hemorrhage, and the blood can gush throughout our internal organs.

Although you need vitamin K to clot your blood, vitamin K doesn't actually make your blood clot. It just gives you what you need to control clotting properly. So getting more K than you need doesn't increase your clotting above normal. You don't have to worry about too much K causing your blood to clot too much.

There is a class of drugs known as 4-hydroxycoumarins. The most popular brand name of drugs in this class is Coumadin. Coumadin and related drugs prevent blood clotting by preventing us from recycling vitamin K after it's been used. These drugs are given to people whose blood clots too much for reasons unrelated to K. They stop it from clotting too much by lowering the person's vitamin K status. Since their clotting is kept in control by keeping K status low, getting extra K will bring their K status closer to normal and cause their blood to clot more. But this is the exception to the rule: a healthy person does not get more clotting when K intake runs high.

Calcium Metabolism, Hormonal Health, Exercise Performance, and Cancer

Although vitamin K is named after its role in coagulation, it actually does lots of other cool things:

It prevents calcium from going into all the wrong places and makes sure it gets into all the right places. For example, it keeps calcium out of your kidneys, where it would cause kidney stones; it keeps it out of your blood vessels, where it would cause heart disease; it keeps it from depositing in cartilage, which could stop children from growing too soon or contribute to arthritis in adults; but it helps it to get into your bones and teeth, making your bones strong and your teeth resistant to cavities. In other words, it prevents calcium from going into the soft tissues (such as kidneys, blood vessels, and cartilage) and shuttles it into the hard tissues (bones and teeth).

In the first of the three lessons on vitamin D, calcium, and phosphorus, we talked about vitamin D doing the same thing, and said it "prevents soft tissue calcification." Remember the role of vitamin D? We said: "When vitamin D directs those minerals into your bones and teeth and away from your soft tissues, it partners up with vitamins A and K."

This is how they work together:

Our cells use vitamins A and D to decide how much to make of certain proteins that prevent soft tissue calcification.
Vitamin K activates those proteins.
Vitamin K does more:

It helps you make insulin and remain very sensitive to insulin. Insulin is a hormone that keeps your blood sugar stable. It's what gets out of control in diabetes, where we either don't have enough (type 1) or have too much and aren't sensitive to it (type 2). This means vitamin K helps stabilize your blood sugar and protects against diabetes.

Vitamin K promotes sexual health by helping you optimize your sex hormones. For example, it increases testosterone and fertility in males, and it helps bring the high levels of male hormones found in women with polycystic ovarian syndrome (PCOS) back down to normal. (PCOS can involve irregular periods, acne, male-like hair patterns, and infertility.)

It helps improve exercise performance by enhancing your ability to utilize energy during bouts of physical activity.

It protects against cancer by helping cells make the right decisions about how they spend their energy.

The Many Forms of Vitamin K

Vitamin K can be confusing because it comes in so many forms.

"Vitamin K" refers to a collection of different forms that we can group in two different ways.

The first way is to split them up into K1 and K2:

Vitamin K1 is found in plant foods.
Vitamin K2 is found in animal foods, or in fermented foods, regardless of whether the fermented foods are from animal or plant origin.
The second way is to split up the many different forms of vitamin K2. While K1 just refers to a single form, K2 actually refers to a collection of different forms that are all named MK-n, where "n" can be various different numbers, anywhere from MK-4 through MK-13. MK-4 is the form found in animal foods. Fermented foods contain the full spectrum of MKs.

A second thing that's confusing about K is that these different forms are kind of the same but they're kind of different.

Vitamin K fulfills its best-understood functions in two ways:

It activates certain proteins that carry out key functions.
Like vitamins A and D, it can also be used to help the cell make important decisions about what things to make.
When it does this, it's acting like the "mirror" we talked about in lessons 1 and 12. Remember what we said about A and D?

"It's a tool our cells use to know they are creating the right thing and putting them all in the right places. They use it like we use mirrors. The mirror doesn't make your lips red, but try putting lipstick on without one and you might look a little silly. "

The first role, activating proteins, is done by any form of K. But the different forms of vitamin K are better at reaching different parts of our body after we eat them. For example, some reach the liver more effectively, where proteins that control blood clotting are activated, and others reach bone more effectively, where a protein that controls sex hormones and insulin is activated.

The second role, helping the cell decide what to make, is only done by MK-4. This role is how vitamin K protects against cancer, making cancer protection a specific effect of MK-4. And, although protein activation within bone helps support hormonal health, MK-4 also acts directly within our sex organs to help boost hormone production by supporting cellular decision-making.

In fact, MK-4 is so important to have in our bodies that we, and all other animals, will convert any other form of vitamin K into it. That's why MK-4 is the main form of vitamin K found in animal foods. However, much like the conversion of carotenoids (the plant form of vitamin A) to retinol (the animal form of vitamin A) discussed in lesson one, many of us are bad at making the conversion.

In fact, we know a lot less about the factors that affect our ability to make this conversion than the ones that affect our ability to get vitamin A from plant foods. That makes it even less reliable. There are a few things we do know about it, however:

Humans seem to be bad at it, on average, and we vary in our ability to make it happen based on genetics.
Statin drugs, used to lower cholesterol, and bisphosphonate drugs, used to treat osteoporosis, hurt the conversion.
So it makes sense to get some MK-4 in our diets directly as an insurance policy against the possibility of poor conversion.

Lots of research has been done on K1, MK-4, and MK-7, with very little research on the other forms. Here is what we can say about these three:

Vitamin K1 travels to our livers more effectively than it does to our bones or blood vessels. The liver is where we use vitamin K to make the proteins involved in blood clotting, so vitamin K1 is better at supporting blood clotting than it is at providing other health benefits.
MK-7 is much more effective than K1 at reaching bone. This doesn’t just make it good for bones: our bones use vitamin K to produce a hormone known as osteocalcin, which improves metabolic and hormonal health and increases exercise performance. So, MK-7 better supports these health benefits than K1. The portion of MK-7 that reaches the liver, moreover, stays active in the liver much longer than K1 before being broken down; as a result, MK-7 is even better than K1 at supporting blood clotting.
MK-4 seems to be less effective than MK-7 at reaching liver and bone but more effective at reaching most other tissues.
This would make it less effective at supporting clotting but better at protecting those tissues from calcium deposits and cancer development and better at supporting sex hormone production through its direct actions within our sex organs.

How Much Vitamin K Do We Need?

How much do we need?

The Institute of Medicine set an "adequate intake" for vitamin K in 2001 at 120 micrograms per day (mcg/d) for men, 90 for women, and less for children. These numbers were based on average intakes, and 2001 was before most of the research on the health benefits of vitamin K2 was done.

Research done since then suggests that:

We should get at least 100 mcg/d of K2, with some additional benefit of getting 200 mcg/d.
At least a portion of that should be MK-4, but it's not clear how much.
There's no clear advantage of specifically getting K1, especially if you're getting plenty of MK-7, which is very good at supporting blood clotting.
Since we still have so much to learn about how the different forms of vitamin K impact our health, I recommend aiming for the full spectrum of K vitamins by including plant foods, animal foods, and fermented foods.

Consuming one or two servings of dark green vegetables per day will provide an abundance of K1, as well as many other benefits, and this is a good background against which to seek other foods rich in K2.

For K2, I recommend consuming at least 100 mcg/d. If you feel great on this, it may be enough. If you feel like any of the listed benefits of K2 are things you could use help with, try shooting for 200 mcg/d. To get 100 mcg/d K2, you want just under 34 ug/meal if you eat 3 meals a day.

Vitamin K in Foods

The following foods provide that amount. You'd need to consume three items from this list (or triple the dose of any one item) to hit the 100 mcg/d target, and you'd need to double that to hit 200 mcg/d.

3 grams of (g) natto, a fermented soy food.

4 g natto made from black beans

8 g emu oil

9 g goose liver

28 g free-range duck fat

32 g beef liver

45 g hard cheese

2.5 egg yolks

57 g dark chicken meat

60 g soft cheese

97 g ghee from pasture-raised cows

110 g goose leg

160 g butter or lard

225 g chicken liver or heart

425 g soured whole milk, light chicken meat, and many cuts of other meats.

An honorable mention has to be given to pork. Pork is extremely rich in MK-10. In fact, 100 grams of grilled kielbasa has over 500 mcg of MK-10! Unfortunately, very little research has been done on MK-10, and there are some indications that we might not be able to use it very well. Until we have more research on MK-10, I recommend not relying on pork for vitamin K2.

I'll give you a link to a database of K2 in foods I made at the end of this lesson if you'd like a more detailed look. But let's go simple for now. Clearly the simplest way to get enough K2 is to eat a half ounce of natto or an ounce of goose liver. Dark chicken meat, cheese, and egg yolks can allow you to hit the target if you use them in larger amounts.

Carnivore, Vegan, Moms, Kidney Disease, Warfarin, Statins, Osteoporosis Drugs

Let's look at how to get enough through the lens of several dietary patterns like carnivore and vegan, and special populations, like pregnant and breast feeding moms and people with kidney disease, and people on various drugs that impact vitamin K metabolism.

CARNIVORE

For most people, the amounts of vitamin K in most animal foods is very low compared to our needs. On a carnivore diet, they could become significant. For example, 2000 Cal medium-fat ground beef provides 64 mcg K2. 2000 Cal dark chicken meat would provide over 1000 mcg of K2. A carnivore diet that was 95% Cal from medium-fat ground beef and 5% from dark chicken meat would hit the 100 mcg target, and raising the dark chicken meat to 15% hits the 200 mcg target.

The only downside to this approach is that all the K2 is MK-4, which may not be that great at supporting blood clotting. Including some fermented foods (60-day aged hard cheese would be a good option if avoiding lactose, and meat itself can be fermented) or organ meats would help diversify the forms of K2.

VEGAN

Vegans, as long as they eat lots of greens, are likely to have very high intakes of K1. Natto is perfectly vegan, and this can meet the K2 target in as little as 1/3 of an ounce for 100 mcg or 2/3 of an ounce for 200 mcg. The high intake of K between greens and natto may yield a significant and perhaps adequate amount of MK-4 if the vegans are good converters.

But what if they're not? We don't yet have the tools to know whether we are good converters, and no vegan foods are rich in MK-4. I recommend vegans take a supplement with synthetic MK-4 if they have any health problems that seem related to low MK-4 status, such as cancer, hormonal problems, or soft tissue calcification.

PREGNANT AND BREAST-FEEDING MOMS

Mothers pass vitamin K to their unborn babies through the placenta, and to their babies through breast milk. Most moms don't get enough vitamin K, though, so babies tend to run deficient. A tiny number of these babies start hemorrhaging. This is only one baby out of every 10,000, but when it happens it's serious. It can cause hemorrhaging inside the head, chest, or intestines, and it can be fatal.

We know that infants are at greater risk if they don't consume enough milk, or if they have disorders of the liver, gall bladder, or pancreas that hurt vitamin K absorption. But for the most part, we don't know what makes an infant vulnerable.

Newborns are usually given injections of vitamin K1 to prevent this. Although oral supplements will protect most infants, they fail to protect infants whose vitamin K absorption isn't up to par.

50 mcg/d added to infant formula also protects all infants capable of absorbing dietary vitamin K. In order to get that much into her milk, a nursing mother has to consume 2 milligrams per day (mg/d) of K1. To get that from natural foods, she'd have to consume lots of greens. For example, measured after cooking:

2 cups of (c) collard greens, spinach, or parsley

2.5 c lambsquarters, mustard greens, or turnip greens

3 c dandelion greens or swiss chard

In adults, MK-7 is five times more effective at supporting blood clotting than K1. This would seem to suggest that mothers could simply get 400 mcg/d MK-7 from 36 grams of natto. Unfortunately, this hasn't been studied directly.

About 70% of fully breastfed infants who don't get any vitamin K injections or supplements become at least slightly deficient in the first week of life. Mothers consuming K-rich diets during pregnancy and while nursing would likely prevent this in most cases. But hemorrhaging only occurs in one out of 10,000 babies. It's a rare but unpredictable risk, and the injections appear to be a safe way to rule it out.

KIDNEY DISEASE

Patients with chronic kidney disease need at least 480 mcg/d, and it's possible that they need up to 3-4 mg/d. These patients are often on low-phosphorus diets that would prevent them from consuming cheese and dark chicken meat. Only natto could provide these amounts. 3-4 milligrams would require supplements in most cases.

The reason the needs are so high in kidney disease is that the kidneys fail to remove enough phosphorus from the body and the elevated phosphorus causes soft tissue calcification. The increased soft tissue calcification requires increased protection from vitamin K. Although it hasn't been studied directly, 3-4 mg/d might be the best dose for people with heart disease or other problems involving soft tissue calcification.

COUMADIN & RELATED DRUGS

The most commonly prescribed anticoagulants (drugs that prevent blood clots) are 4-hydroxycoumarins. These include warfarin, which is marketed under Coumadin and other brand names. These drugs prevent blood clots by blocking your body's ability to recycle vitamin K after it's been used. While on these drugs, a person's vitamin K intake should be low, because high intakes require higher doses of the drug. More importantly, it needs to be consistent from day to day. The dose of the drug can be adjusted to any given intake of vitamin K, but cannot accurately accommodate a widely fluctuating K intake.

Unfortunately, these drugs compromise all of the functions of vitamin K equally, including its protection against soft tissue calcification. Since MK-4 is likely to be far worse at supporting clotting compared to K1 or MK-7, but better at protecting against soft tissue calcification, it makes sense to include 50-100 mcg/d of MK-4 in the diet. It is absolutely critical, though, that you inform the prescribing physician about any changes you wish to make to your vitamin K intake and get your physician's OK.

STATINS AND BISPHOSPHONATES

Cholesterol-lowering statin drugs and bisphosphonates such as Fosamax, used to treat osteoporosis and several other disorders, impair the conversion of other forms of vitamin K to MK-4. It makes sense to aim to get 100-200 mcg/d specifically of MK-4 while on these drugs.

Other Things That Hurt Vitamin K Status

There are a few other things that impact your vitamin K status:

Because vitamin K is fat-soluble, any disorders that compromise fat absorption could hurt vitamin K status, and very low-fat diets might increase the amount you need.

The recycling of vitamin K requires thiamin, riboflavin, and niacin. Deficiencies of these nutrients could hurt vitamin K status.

The B vitamins help recycle vitamin K using energy taken from glucose, the main carbohydrate in our bodies. Although it has not been studied, it is possible that very low carbohydrate intakes could hurt vitamin K status.

Recycling vitamin K requires two important enzymes. One is glucose 6-phosphate dehydrogenase. About 8 percent of the world's population is deficient in this enzyme. The other is VKOR. Many people have reduced activity of this enzyme, and if you get a 23andMe report it would show up as "increased sensitivity to warfarin."

Unfortunately, we don't know exactly how much more K people with these conditions need. It makes sense to shoot for higher intakes, and, if you continue to have problems that could be explained by poor vitamin K status, take a supplement.

Vitamin K Supplements

Since vitamin K is fat-soluble, supplements should always be taken with a meal. If your fat intake varies a lot from meal to meal, take it with your highest-fat meal. If not, take it with your biggest meal.

Although there is no clear evidence of harm at any dose, excess vitamin K may contribute to oxidative stress and may deplete levels of the other three fat-soluble vitamins (vitamins A, D, and E). I recommend limiting vitamin K supplements to one mg/d (1000 mcg/d) unless you have a good reason to use more. Established heart disease or kidney disease may warrant 3-4 mg/d, and genetic factors or absorption problems may also warrant doses this high as well.

45 mg/d MK-4 is used to treat osteoporosis and sometimes to prevent liver cancer, but at this dose, the vitamin K is a drug, not a nutritional supplement.

Vitamin K supplements come in several forms.

VITAMIN K1 (PHYLLOQUINONE)

This is the plant form. It supports clotting better than any other function, though not as well as MK-7 supports clotting.

MENAQUINONE-7 (MK-7)

This can be synthetic or naturally derived from fermented soybeans or chickpeas. Look for the products labeled as natural, since the synthetic versions have lower activity. This form supports clotting better than K1, and may reach bone better than MK-4, giving it advantages for supporting insulin, certain aspects of hormonal health, and energy utilization during exercise.

MENAQUINONE-4 (MK-4)

This is synthetic, even if it says it is derived from a plant source (it is synthesized from a precursor in plants). It is identical to the natural form as far as we know. This is the least effective form to support blood clotting but has unique effects in cancer protection and hormonal health. Although not well studied, it may be the best form for preventing soft tissue calcification.

EMU OIL

Emu oil is a food-based supplement that contains the highest known concentration of MK-4 of any natural food. As a supplement, 5 capsules supplies 20 mcg MK-4, which is meaningful as a partial contribution to the diet, but is far from the target of 100 mcg/d. This is the currently the only supplement rich in naturally occurring MK-4.

I recommend seeking a supplement that contains a blend of forms that best matches what is missing from your diet. For example, if you do not eat many greens, it should contain K1. If you don't eat natto, it should contain MK-7. If you don't eat goose liver, dark chicken meat, or beef by the pound, it should contain MK-4.

Balancing the Fat-Soluble Vitamins

We should end with a final note on balancing fat-soluble vitamins, now that we've discussed all four.

Vitamins A, D, E, and K, can be broken down and removed from the body using common cellular machinery. Since they share breakdown pathways, consuming lots of one may increase the breakdown of the others.

For example, if you get too much K, your body has to break it down, so it makes more of the machinery that breaks down all four vitamins. Since the other three are in short supply, increasing the breakdown machinery causes them to run deficient.

A, D, and K partner together for many things, especially for protection against soft tissue calcification. So if you take too much K for that very reason, you could be shooting yourself in the foot. Vitamin E doesn't directly partner up with A, D, or K, but too much of any one of those could cause E to run deficient and hurt your antioxidant protection.

The best thing to do, then, is to stay within similar multiples of the requirements for all four vitamins. For example, we talked about getting these numbers as good baselines:

3,000 IU of vitamin A as retinol, plus lots of colorful veggies.

3,000 IU of vitamin D from all sources including sunshine (optimal sunshine practices in the summer should provide about this much)

20 IU of alpha-tocopherol plus a mixed background of the other forms of vitamin E

100-200 mcg/d K2 with one or two servings of greens in the background supplying K1

So if you start megadosing with one of these, consider going up similar multiples of the others to stay balanced. For example, 10,000 IU of vitamins A or D might warrant tripling the others. There may be specific cases where this doesn't apply. For example, maybe your genetics have really slammed your vitamin K recycling in a way that doesn't impact your requirement for the others. Still, as a default, balancing them is a good rule of thumb.

Vitamin E Prevents Damage to Cellular Membranes and Other Cellular Components

You and I are made of cells. Each of our cells is enclosed in an oily membrane. Inside our cells lie many specialized compartments. Each of those is also enclosed in a similar membrane. These oily membranes are what allow cells to protect themselves and to control what comes in and goes out, and what stays in and stays out. Controlling which things are found where is how our cells maintain their productivity, just like you keep different things in your bedroom, your kitchen, your living room, and your office if you have one. This allows you to sleep effectively in one place, cook effectively in another, relax effectively in another, and work effectively in another.

These oily membranes are made of many small pieces of fat known as "fatty acids." The fatty acids can be a lot like dominoes when they are exposed to harmful substances known as oxidants. The oxidants damage one fatty acid by oxidizing it. Then that fatty acid itself turns into an oxidant!

It oxidizes the next one

And the next one....

And the next one....

And the next one....

And the next one....

And the next one....

...if something doesn't stop this train...

...sooner or later they all fall down.

They all get damaged. Oxidized. Kaput. Washed up, wiped out, swimming with the fishes.

Vitamin E's only well established role is to stop this from happening.

When the fatty acids in the cell membrane oxidize, many of them shatter into smaller pieces. These little pieces of broken fatty acids are very much like shards of broken glass. They become a danger to everything else around them. (Not something you want to step on!) They can start damaging everything in your cell, including proteins and DNA. That makes vitamin E directly responsible for protecting the fatty acids in your cell membranes, and indirectly responsible for protecting everything else in the cell.

Vitamin E Deficiency

So what happens when we don't get enough?

The scientific word for vitamin E is "tocopherol," which comes from the Greek meaning "to carry a pregnancy to term." It was known as the "fertility vitamin" in the early days of its discovery. This is because lab animals with severe deficiencies became infertile.

In humans, severe deficiency results in neurological problems. This is because the brain is very oily and uses a lot of energy, which generates oxidants in the process. The neurological problems involve loss of coordination, difficulty walking, visual problems resulting from damage to the retina, and pain, weakness, numbness, or tingling in the hands and feet.

Deficiency also results in hemolytic anemia, a form of anemia where red blood cells get destroyed because their membranes fall apart.

Moderate deficits are not well studied, but they are likely to have the following effects:

Increased damage or poor healing in the gut, skin, and lungs.
Increased vulnerability to thyroid disorders and infections.
Increased wear and tear on the tissues more generally, worsening the risk of most chronic, degenerative diseases like heart disease and cancer.
Vitamin E Is Fat-Soluble

Notice that we keep taking about the role of vitamin E protecting the oily parts of our cells. Vitamin E is the third of the four fat-soluble vitamins we've discussed. That means it is found in the fatty portions of foods, is absorbed best with a large meal that contains fat, and will become deficient in diseases that impair our ability to digest and absorb fat.

Vitamin E is a "Chain-Breaking Antioxidant"

The domino effect of oxidation that occurs in cell membranes is called a chain reaction, and vitamin E is known as a "chain-breaking antioxidant." In fact, it is widely rumored within the classic rock underground that Fleetwood Mac's 1977 song, The Chain, in which they boldly stated, "you would never break the chain," was issued as a challenge to vitamin E.

Challenge... accepted!

Since vitamin E protects our cell membranes from oxidation, it is an "antioxidant" and is part of the "antioxidant system." Vitamin E relies on the larger system to get its job done. When an oxidized fatty acid is looking for the next domino to knock over within the membrane, vitamin E steps up and says, "pick meeeeeeeee!" After it takes one for the team, it needs to be rejuvenated. Vitamin E gets rejuvenated by vitamin C. In fact, this accounts for most if not all of vitamin C's contribution to the antioxidant system. Vitamin C gets its healing power from glucose, the main carbohydrate in our bodies, using the help of niacin, riboflavin, and thiamin in the process.

PUFAs are Uniquely Vulnerable to Oxidation

Now, get this. Inside our membranes, not all fatty acids are equal.

There are three types of fatty acids:

Saturated
Monounsaturated
Polyunsaturated
In fact, you'll see these three types listed on the label of packaged foods. These fatty acids are the main thing found in the fat we eat. When we eat fats and oils like butter or olive oil, these are mostly fat. When we eat other foods, smaller amounts of fat contribute to rich tastes and creamy textures. All foods contain all three types of fatty acids, but they contain them in different combinations.

Saturated fatty acids are most abundant in fats that are solid at room temperature, such as butter, coconut oil, or beef fat. Monounsaturated fatty acids are most abundant in oils that are liquid at room temperature but harden in the refrigerator, like olive oil. Polyunsaturated fatty acids are most abundant in oils that stay liquid even in the refrigerator.

To make it less of a mouthful, we will call polyunsaturated fatty acids "PUFAs" (POO-fuzz) from now on.

The oils richest in PUFAs are canola, soybean (often called "vegetable oil"), sunflower and safflower (if not labeled as "high-oleic"), corn, and cottonseed.

Within cell membranes, it is *only* PUFAs that oxidize. PUFAs are necessary in small amounts, and we will talk about that in the lesson on essential fatty acids. But they are vulnerable to oxidation in any amount. Vitamin E's only well established role, then, is to protect PUFAs from oxidation within our bodies.

Now, vitamin E plays the exact same role in plants and other animals. As a result, foods with higher PUFA content tend to have higher vitamin E content as well. This is important, because if the only need for vitamin E is to protect PUFAs, then the more PUFAs we get, the more E we need.

And yet, the ratios of vitamin E to PUFA in various foods are wildly different.

This is for a few different reasons:

Heat increases the rate of any chemical reaction, including the harmful reactions that lead to the oxidation of PUFAs. Unlike us warm-blooded animals, plants and cold-blooded or bloodless animals need more vitamin E for a given amount of PUFA in warmer environments and less E per PUFA in cooler environments.
Metabolic activity (breaking things down and building them up) generates oxidants. As a result, parts of an animal or plant that are very metabolically active (muscles, leaves) will have more vitamin E for a given amount of PUFA than less metabolically active parts (bones, seeds).
Among all forms of metabolism, photosynthesis is most dangerous. This is the process whereby plants take energy from sunlight and atoms from oxygen and water, and put them together to make glucose. Sunlight and oxygen both increase the rate of oxidation (in fact, oxidation is named after oxygen!), so the tremendous amount of these two factors involved in photosynthesis dramatically increase the need for E for a given amount of PUFA.
If we look at foods, then, we will notice a few things about the vitamin E-to-PUFA ratio:

It is low in fish, because fish are cold-blooded and need lots of PUFA to avoid becoming hardened in the cold water, yet don't need as much E because of that cold water.
It is very high in some tropical oils, such as palm oil, because of the warm environment. Coconut oil has very little vitamin E, though. This is because it has very little PUFA, and because the toughness of the meat and the hard shell slow the movement of oxygen and light through the coconut.
Green leaves have extremely high ratios, and seeds have very low ratios. Here I'm using the broad sense of "seed," anything you could plant in the ground and grow something with, including grains.
This is why grass-fed beef is anywhere from 1.3-fold to 5.4 fold higher in vitamin E than grain-fed beef. Although other animal products haven't been studied as much as beef has, generally meat, milk, and eggs from grass-fed animals are always higher in vitamin E than the same products from grain-fed animals.

If we look at the absolute amount of vitamin E in foods, wheat germ oil appears to have the most, with corn oil having half as much, palm oil a little bit less than corn oil, and butter and olive oil having practically none. But if we look at the vitamin E-to-PUFA ratio, things look very different. Palm oil is by far the winner, and wheat germ oil, olive oil, grass-fed butter, and corn oil are all similar.

Should We Use the Vitamin E Amount or the Ratio to PUFA?

The Institute of Medicine set the RDA for vitamin E in 2000, at the same time they set the RDA for vitamin C. Although they didn't express the RDA as a ratio between vitamin E and PUFA, they wrote that "high PUFA intakes should certainly be accompanied by increased vitamin E intakes."

Rarely do scientists use the word "certainly."

In fact, the principle that the more PUFA we get, the more E we need, is far more certain than the number given for the RDA.

The RDA is based on a single study where they tried inducing vulnerability of red blood cells to hemolysis on a low-vitamin E diet. They tried and tried, but they got nowhere until they started feeding "tocopherol-stripped corn oil."

Hemolysis is the process of red blood cells breaking apart, and it's what happens during hemolytic anemia. But in this study, they weren't inducing anemia. They were taking the red blood cells out of the people, then pouring hydrogen peroxide on them. Hydrogen peroxide is an oxidant, so vitamin E-depleted red blood cells will break apart in test tubes if you pour enough hydrogen peroxide on them. Tocopherol-stripped corn oil is corn oil that has been heated until all the vitamin E is destroyed. The heat doesn't just destroy the vitamin E, it also oxidizes the fatty acids, so the oil is full of extra oxidants just waiting to rip apart your cell membranes, wreck your proteins, and gum up your DNA.

So the RDA for vitamin E is the amount of vitamin E that will protect your red blood cells from falling apart when they've been taken out of your body and had hydrogen peroxide dumped on them, while you've been chronically eating the most toxic oil imaginable. However bad the average person's diet is, it isn't anywhere near as bad as the toxic diet used in this study, so vitamin E needs are probably lower than the RDA.

Even the people who made the RDA admit the data is pretty bad. In the following quote, the word "biomarker" means something we can measure to understand whether someone has enough vitamin E or needs more. α-Tocopherol is the main form of vitamin E.

"It is recognized that there are great uncertainties in the data utilized to set the α-tocopherol requirements. However, in the absence of other scientifically sound data, hydrogen peroxide-induced hemolysis is the best marker at the present time. It should be emphasized that research is urgently needed to explore the use of other biomarkers to assess vitamin E requirements."

That "urgent" need for research was identified 19 years ago. No changes yet.

Notice that when referring to the RDA itself, they wrote about "great uncertainties." But when they discussed the effect of PUFA, they wrote, "high PUFA intakes should certainly be accompanied by increased vitamin E intakes."

So, to summarize:

We are "greatly uncertain" about the absolute amount we need, but it's probably lower than the RDA.

We are certain that we need more E when we get more PUFA.

So, it follows that we should largely ignore the absolute amounts of E in our diet and instead seek a high E-to-PUFA ratio.

Vitamin E Cannot Completely Protect PUFA From Oxidation

There's just one catch: Vitamin E can't perfectly protect against high PUFA intakes. Remember how we called it a "chain-breaking antioxidant"? The "chain" starts when the first domino hits the second one, not when your finger hits the first one. In other words, vitamin E will never stop the first fatty acid from oxidizing. It will only stop the chain reaction from moving forward after this point. So if you eat a very large amount of PUFA and have a high exposure to oxidants from acute infection, chronic disease, metabolic problems, or toxin exposure, you will wind up with more fatty acids oxidized even if you have a very high intake of E.

Dietary Targets for PUFA and Vitamin E

So what we actually want to seek is:

A high vitamin-E-to-PUFA ratio.
A PUFA intake that isn't any higher than we need to get all of our nutrients in.
Whole foods like nuts and seeds are rich in PUFA, but also rich in many valuable nutrients. For example, we talked in past lessons about almonds being rich in B2, peanuts in B3, sunflower seeds in B5, and whole sesame seeds with the hull being rich in calcium. These foods have quite a lot of PUFA, but plenty of other nutrients. Their oils, by contrast, mainly just supply PUFA.

As a foundation for the diet, then, I would recommend the following:

Use high-PUFA foods like fatty fish, nuts, and seeds to meet your requirements of vitamins and minerals, but no more than needed for this.

Avoid high-PUFA oils like canola, soybean, corn, cottonseed, and sunflower or safflower oils that are not labeled as "high-oleic."

Use grass-fed animal products whenever possible (look for "grass-finished" labels, meaning they ate grass through the last few months of their life as well as earlier).

If your diet is more than 40% of Calories as fat, get the excess over 40% from oils that are very low in PUFA, such as butter, coconut oil, or the fat of red meat animals.

If you feel like you might need more E for skin, gut, lung, or brain health, or to lower the risk of chronic diseases like heart disease and cancer, work in red palm oil into your diet. As discussed in the first lesson palm oil is also a great source of vitamin A. The harvesting of palm oil often involves cruelty to orangutans, so look for sources that document cruelty-free practices.

Other Causes of Vitamin E Deficiency

Diet isn't the only thing that impacts vitamin E status:

Any intestinal disorders that hurt the digestion and absorption of fat can cause vitamin E deficiency.

There is a very rare genetic defect in a vitamin E transporter that requires extremely high doses of vitamin E to treat.

Vitamin E Supplements

Because vitamin E is fat-soluble, supplements should always be taken with a meal. If your meals are similar in fat content, take an E supplement with your largest meal. If they vary a lot in fat content, take it with your highest-fat meal.

Vitamin E supplements come in several forms.

SYNTHETIC ALPHA-TOCOPHEROL

Synthetic alpha-tocopherol is often called "all-rac" tocopherol. This consists of one form that is identical to natural vitamin E, and 7 forms that are not found naturally and have less, little, or no function. This is used only because it's cheap, and should be avoided.

D-ALPHA TOCOPHEROL

D-alpha-tocopherol is often labeled as "all-natural" or "RRR." This is the natural, fully functioning form. Alpha-tocopherol is, indeed, the most powerful and the most important form of vitamin E. However, it is one of only eight forms. High doses can flush out the other seven forms, so it isn't wise to take a supplement that only has this form unless it is a low dose, such as 15 mg or 20 IU.

MIXED TOCOPHEROLS

Natural vitamin E comes in eight forms, four tocopherols and four tocotrienols. Tocopherols are far more abundant in most foods than tocotrienols, so a supplement with "mixed tocopherols" is usually taken from a natural food that has a high tocopherol but low tocotrienol content.

It's important to recognize that, while the other tocopherols likely are important, alpha-tocopherol is still the best studied, most powerful, and most important form of vitamin E. If you use a mixed tocopherol supplement, make sure the label displays the alpha-tocopherol content and that it provides about 15 mg or 20 IU of this form.

MIXED TOCOTRIENOLS

There are four tocotrienols that make up the other half of the vitamin E spectrum. These are less studied than tocopherols, but they may have unique benefits by penetrating certain tissues better than tocopherols. High doses also lower cholesterol levels by acting similarly to the statin drugs that so many people are on. Tocotrienols are far less common in the food supply than tocopherols, found mainly in rice bran oil and palm oil.

Supplement Recommendations

As a means of ensuring some extra vitamin E, it is best to use a supplement that contains about 15 mg or 20 IU of alpha-tocopherol and also contains a mix of tocopherols or tocotrienols. One example is Jarrow Toco-Sorb.

However, if you feel like you have symptoms related to poor vitamin E status and a mixed tocopherol/tocotrienol supplement doesn't seem to help, it makes sense to experiment with a low-dose natural alpha-tocopherol, since it is the best studied and most important form. An example would be one drop of Now E-Oil per day, which provides 30 IU.

Switching from High-PUFA to Low-PUFA Oils

There's one clear case that warrants supplementation: if you consume PUFA-rich oils for a period of four years or more, your vitamin E requirement stays elevated for four years after you stop consuming them. If you switch, for example, from corn oil to coconut oil, the coconut oil will give you very little vitamin E, but your vitamin E requirement is actually calibrated to the amount in the corn oil.

In that case I would use one capsule of Jarrow Toco-Sorb or one drop of Now E-Oil per day.

High-Dose Vitamin E Supplements

There are some studies suggesting high doses of vitamin E may benefit immune function, heart disease, fatty liver, and age-related cognitive decline, cataracts, age-related macular degeneration, diabetes, and certain cancers. However, the studies are inconsistent, and some suggest high doses worsen the risk of diabetes and certain cancers.

High doses may also cause deficiencies of other fat-soluble vitamins, especially vitamin K. As a result, I do not recommend using high doses of vitamin E in most cases.

The only cases where high doses are clearly warranted are the rare genetic disorder of vitamin E transport, and intestinal problems that hurt fat absorption.

There may be reasons to use high doses of other fat-soluble vitamins, however, and in those cases using a proportional amount of vitamin E may be necessary to avoid causing imbalances. We will return to this topic after we cover the last fat-soluble vitamin, vitamin K, in the next lesson.

Wrapping Up

To wrap up:

Vitamin E is needed to protect our tissues from wear and tear as we age. It is especially important to our brain health and our fertility, and helps protect us from chronic, degenerative diseases like heart disease and cancer.

The ratio of vitamin E to PUFA is more important than the absolute amount of vitamin E.

We should seek a high ratio and avoid excess total PUFA regardless of E.

High-PUFA whole foods are good when they supply needed nutrients but the oils should be avoided.

Grass-fed animal products and fresh whole plant foods should be the foundation of the diet. Cruelty-free red palm oil is the best source of additional E.

Most people don't need a vitamin E supplement, but if you switch from high-PUFA oils to low-PUFA oils, it would be wise to supplement for about four years.

The best default supplement is one that provides close to 15 mg or 20 IU of alpha-tocopherol in a background of mixed tocopherols and tocotrienols.

Try a low-dose natural alpha-tocopherol without the other forms if the default does not give you the results you are looking for.

Higher doses are only warranted when treating rare disorders that cause severe vitamin E deficiency.

How Much Calcium Do We Need?

The RDA is 1000 milligrams per day (mg/d) for most people over the age of 3. It increases to 1300 for children aged 9-18 to account for increased growth, and to 1200 for women over the age of 50 and men over the age of 70. The RDA is 200 mg/d during the first six months of life, 260 during the next six, and 700 mg between the ages of 1-3.

While not without controversy, the calcium RDAs are among the best supported by large amounts of evidence. Many people object that the only way to get the RDA is to drink milk, and many human societies have thrived without using milk. But there are many other sources of calcium. In the Arctic, for example, where there are no cows and plant foods are limited, the natives ate dried, pulverized fish bones. In Africa, a group of hunter-gatherers known as the Hadza consume large amounts of baobab. This is a plant with more calcium than milk, is considered a "food group," and makes up over 20 percent of their diet. Similarly, the Native Americans of the Northern Plains ate stinging nettles, which is much higher in calcium than milk. Each culture found prized sources of calcium-rich foods and made them critical parts of their traditional diets. Ours is dairy, and if we leave dairy behind we need to find another.

Calcium Absorption From Different Foods

Most foods have some calcium in them, and many besides milk have a lot.

But then... there is absorption.

We absorb calcium from food much better when we get enough vitamin D. Nevertheless, for a given amount of vitamin D, the absorbability of calcium differs greatly among different foods:

A little over 30% of the calcium in milk is absorbed. Edible bones have not been tested but they are probably similar.
40-60% of the calcium in most cruciferous vegetables is absorbed. These are foods like broccoli, kale, and bok choy.
20-25% of the calcium in legumes is absorbed.
Rhubarb (9%) and spinach (5%) have very poor absorbability.
Unfortunately, there are a tremendous number of foods where we don't know for sure how absorbable the calcium is. Let's start by looking at foods where it's been directly measured, then make some guesses about the rest of the foods we eat.

To meet the RDA, children up to 3 years old need the equivalent of two 8-ounce glasses of milk. Most adults need three glasses, while children and adolescents 9-18, women over 50, and men over 70 need four glasses. This would provide everyone with calcium within 100 milligrams of the target, which would be filled in by the other foods they consume.

For foods where the absorption has been directly measured in humans, these are each the equivalent of one 8-ounce glass of milk (or the same amount of yogurt or kefir). The veggies are measured after cooking:

40 grams of (g) cheddar cheese
90 g napa cabbage
100 g Chinese mustard greens
190 g bok choy
270 g kale
290 g Chinese spinach
320 g broccoli
430 g white beans
700 g pinto beans
790 g rhubarb
1.4 kilograms of (kg) spinach
1.6 kg sweet potatoes
1.7 kg red beans
Of the plant foods, the most practical to use is Chinese mustard greens. 100 g is a little over two-thirds of a cup. It would require just over 2 cups, measured after cooking, to yield the equivalent of 3 cups of milk. Close behind is napa cabbage. 90 g is three-quarters of a cup. Just under 2.3 cups yields the equivalent of 3-milks-a-day. 190 g boy choy is a little over one cup. 3.4 cups of it will meet the target.

Going further down the list starts to become impractical. For example, it would take over 6 cups of kale or broccoli to meet the target.

One of the most common traditional sources of calcium in dairy-free cultures has been bones. You can gnaw the ends off the small bones in a roast chicken. You can eat the bones in canned sardines or canned salmon. As mentioned before, the natives of the Arctic would dry and pulverize fish bones to get their calcium. Although no one has directly measured how much calcium humans absorb from edible bones, we have good reason to think that it is similar to milk. First, most calcium is present in bone bound to phosphate. The absorption of calcium phosphate has been tested in humans, and it's about 25%, a little less than the 32% we absorb from milk. Second, in lab animals, the proteins found in bone increase the absorption of the calcium. So we humans probably absorb the calcium from bone at least as well as we do from milk. We can obtain our three-milks-a-day target from bone, then, by consuming just over two-thirds of a teaspoon of powdered bone. If you eat canned fish, count each 30% of the daily value for calcium as one glass of milk.

Putting this altogether, your best bet is to mix and match three of any of the following foods each day:

One cup of milk, yogurt, or kefir.

One serving of canned fish providing 30% of the daily value of calcium.

One cup of Chinese mustard greens, napa cabbage, or bok choy.

So far we have been limiting our scope to the foods where the absorption has been directly measured.

We can broaden our scope by making some reasonable guesses about how much we absorb from other foods. The most important inhibitor of calcium absorption in plants is oxalate. This is the same oxalate that we talked about causing kidney stones in part 1. Let's assume that most low-oxalate vegetables have similar calcium absorbability. Let's also assume that most nuts, seeds, and beans have similar absorbability as the beans that have been measured.

The following foods should be equivalent to one cup of milk:

100 g sesame seeds, hull included
150 g chia seeds
180 g flax seeds
200 g typical tahini
270 g almonds
290 g Brazil nuts
These options, while helpful, are quite impractical to rely on because of the amount of calories they supply. Calories (Cal) are units of energy, and too many will make you fat! Plus you can only fit so many in your tummy at a time. A cup of full-fat milk has 146 Cal and low-fat milk has even less. 150 g chia seeds has 729 Cal and 200 g of tahini has 1190 Cal!

This brings us back to our original conclusions: mix-and-match dairy, bones, or the top three greens (Chinese mustard, napa cabbage, or bok choy) to get your calcium. If you have space for the calories, you can replace one of those with some of the nuts and seeds. If you have space for the volume, you can replace one of those with some of the other vegetables.

Calcium in Mineral Water

Before we talk supplements, let's talk about one thing that's not really a food or a supplement: mineral water. The minerals in mineral water are fully dissolved, and are likely very well absorbed. For example, Gerolsteiner and Ferrarelle have more than a cup of milk's worth of calcium per liter. Perrier, Uliveto, San Pellegrino, and Lete have a little under half that.

Calcium Supplements: Safety Concerns

Calcium supplements are a mostly safe and effective way to bring your intake up to the target.

There are a few special concerns, however:

In supplemental form, calcium might enter your system too quickly and promote soft tissue calcification.
Calcium supplements sometimes cause "calcium-alkali syndrome."
This syndrome can make you unusually thirsty and pee too much. It can make your heart beat more slowly, skip a beat, or flutter. It may make you confused, weak, or depressed.

Typically the person who develops this syndrome fits these criteria:

She is a woman who is elderly, pregnant, or bulimic.
She is also taking antacids, nonsteroidal anti-inflammatory drugs (NSAIDs, such as aspirin or Advil) or medications to manage blood pressure and swelling.
Her calcium supplement is calcium carbonate, oxide, or hydroxide.
We can avoid the risk of soft tissue calcification and calcium-alkali syndrome by sticking to some easy rules:

Use calcium supplements to help you meet the RDA when you cannot do so with food alone. Don't use supplements to exceed the RDA.

They will hit your system more slowly, like food, if you mix them into your food. If you don't want to mix it, take it at the end of your meal.

Always spread your calcium evenly across 3-4 meals.

Don't use carbonate, oxide, or hydroxide.

If you fit the other criteria for calcium-alkali syndrome, keep your total intake under 1000 mg/d and discuss your supplement with your doctor.

Calcium Supplements: Which Forms Are Best?

There are an incredible number of forms that calcium supplements come in, so rather than discuss every single one in detail, we'll cover them in groups.

BONE MEAL / MCHC / MCHA

This form is a traditional food, like the pulverized fish bones the natives of the Arctic used. Bone can be contaminated with lead, so look for manufacturers that test and disclose the contaminants. This is a good default for most people. It contains many proteins and traces of non-calcium non-phosphorus minerals that support bone health. Bone meal might be poorly absorbed in those with low stomach acid, and it is too high in phosphorus for people who need to avoid it. It is rich in collagen, which supports healthy hair, skin, and nails. Most people could use more of it. However, people who develop calcium oxalate kidney stones may benefit from avoiding collagen. MCHC and MCHA are other names for bone meal.

CALCIUM PHOSPHATE

Examples include tricalcium phosphate and dicalcium phosphate dihydrate. These are similar to the calcium in bone meal, but without the protein and extra minerals. They are less nourishing as a result, and they still can't be used by people who need to avoid phosphorus, but they would be better than bone meal for people who need to avoid collagen.

CALCIUM CITRATE, MALATE, LACTATE, GLUCONATE, GLUBIONATE, SULFATE, & GLYCEROPHOSPHATE

All of these forms are highly absorbable, and all of them except glycerophosphate are good for people who need to avoid phosphorus. Calcium citrate is better studied and more popular than the others, giving it a good safety record. The citrate is helpful for kidney stone prevention.

CALCIUM CARBONATE, HYDROXIDE, AND OXIDE

These are popular because they are cheap, especially calcium carbonate. They lack phosphorus and collagen, which can be advantageous for some people, but they account for most reports of calcium-alkali syndrome, suggesting they are less safe than other forms.

OYSTER SHELL, EGG SHELL, CORAL CALCIUM, DOLOMITE

These are all mostly calcium carbonate. Since they are natural, they have the advantage of proteins (except dolomite) and other minerals, and the disadvantage of possible contaminants. Since they contain calcium carbonate, they may carry the same risk of calcium-alkali syndrome.

The bottom line:

Use a bone meal if you have no need to avoid collagen or phosphorus. Choose a product where the contaminants are measured and disclosed.

Use calcium citrate if you need to avoid collagen or phosphorus, especially if you are at high risk of kidney stones.

How Much Phosphorus Do We Need?

Phosphorus is a simpler discussion. Most people actually get too much. In part one, we pointed out how only 1% of our calcium but a full 15% of our phosphorus is found outside of our bones. This much wider distribution of phosphorus means it's found in far more foods, is much easier to obtain, and far less likely to run deficient.

The RDA for phosphorus for all adults is 700 mg/d. For children older than one and for adolescents, the RDA is adjusted according to their needs for growth and age-related differences in how well they absorb phosphorus from food. It is 460 mg/d for children 1-3, 500 mg/d for children 4-8, and 1250 mg/d for adolescents 9-18. For infants, there wasn't enough evidence for an RDA, so they set an "everyone-is-doing-it-so-it-must-be-ok," also known as an "adequate intake (AI)," of 100 mg/d for the first six months of life and 275 mg/d for the next six months. This is based on what infants were consuming in milk and baby food.

It's Hard to Become Deficient in Phosphorus

When consuming natural foods, it is nearly impossible to become deficient in phosphorus. For simplicity, let's consider the adult target of 700 mg/d.

These are what you'd get if you ate 2,000 Calories (typical for an average daily intake) of a single food group all on its own:

Dairy: 2,600 mg.
Eggs: 2,100 mg.
Meat, poultry, or fish: 1700 mg.
Legumes, nuts, or seeds: 1600 mg.
Veggies 1100 mg.
Grains: 1050 mg.
Fruits: 608 mg.
What do Fruitarians, Refined Flour-Heads, and Keto-Carnivores Have in Common?

Ok, so strict fruitarians might be at risk. But the least of a fruitarian's problems will be phosphorus. In fact, their phosphorus intake would be amazing compared to their calcium intake.

A more dangerous dietary pattern would be the fat-bomber. 2000 Calories of fat only provides about 150 mg of phosphorus.

Keto dieters can get plenty from animal products and low-carb veggies. Carnivores can get plenty from meat. The potential problem would be with keto carnivores. The phosphorus requirement could be met with 550 Calories of dairy, 670 Calories of eggs, or 850 Calories of meat, poultry, or fish. But just animal fat wouldn't cut it.

In theory, someone could develop a moderate phosphorus deficiency from relying exclusively on refined flour. 2000 Calories of white flour only provides 593 mg of phosphorus. As with fruitarianism, though, the phosphorus actually looks really good on that diet compared to many other nutrients, including calcium. As we will see soon, though, most white flour products are full of hidden phosphorus.

Starvation, Refeeding, and Hungry Bones

There is one way to become deficient in phosphorus: don't eat. Starvation and eating disorders can lead to extended periods of time with little or no phosphorus consumed, and breakdown of lean mass that allows stored phosphorus to be lost in the urine. Rapid refeeding, especially with poor-quality food, causes phosphorus to get sucked up into the muscles, which causes blood levels to drop to dangerous levels. This is called "refeeding syndrome" and it can also affect magnesium and potassium. The best way to keep phosphorus levels up is to eat lots of meat and eggs.

Something similar happens after medical correction of a disorder causing bone loss. Phosphorus, calcium, and magnesium all get swept up into bones, and the blood levels drop. This is called "hungry bone syndrome" and dairy products are the best remedy.

Meat and eggs are the best match for refeeding syndrome because the phosphorus is going into the muscles where it doesn't need calcium, and meat and eggs provide phosphorus without calcium. Dairy is the best match for hungry bone syndrome, because the phosphorus is going into the bones where it does need calcium, and dairy provides both minerals.

Hidden Phosphorus Additives in Processed Foods

Overwhelmingly, most of us are likely to get too much phosphorus, not too little. The average intake in the United States is almost twice the RDA. Nearly 500 mg/d come from unlabeled food additives!

Phosphorus is added in large amounts to cola, anything with baking powder, and processed, parmesan, or American cheese.

Phosphorus is usually added to the following products:

anything with baker's yeast
cocoa powder
non-perishable fruit juice
vegetable spreads for bread
cold cuts, hot dogs, and sausages
Phosphorus is sometimes added to these:

frozen meat
canned seafood
many cheeses
yoghurt
chocolate
beer
instant coffee
These additives are very often unlabeled. Worse, studies suggest that ONLY these hidden additives hurt bone health. Meat seems neutral and dairy beneficial.

So the end result:

We can get enough phosphorus by eating a mix of natural whole foods.

We can avoid too much phosphorus by avoiding processed foods.

There's no need for supplements. Just meat and eggs for refeeding syndrome, and dairy for hungry bone syndrome.

Wrapping It All Up

All right, let's wrap up our three-part series on vitamin D, calcium, and phosphorus:

Deficiencies of vitamin D, calcium, or phosphorus contribute to rickets and osteomalacia.

Deficiencies of calcium or vitamin D contribute to tetany.

Toxicities of all three cause soft tissue calcification.

Toxicities of vitamin D or phosphorus cause weak, porous bones; calcium toxicity causes hard, brittle bones.

Most of us lie in the middle where calcium and vitamin D are on one team and phosphorus is on the other.

In this middle area, calcium and vitamin D protect against osteopenia and osteoporosis; phosphorus makes these diseases worse.

We also want "team calcium and vitamin D" for blood pressure, asthma, allergies, colds and flu, autoimmunity, insomnia, hormones, heart disease, and cancer.

Our best sources of vitamin D are sunshine, pastured egg yolks, cod liver oil, certain fish, or certain mushrooms (the mushrooms contain D2, possibly less effective than D3).

Sunshine is best mid-day, and this matters most outside of the summer and far from the equator.

The darker your skin, the more time you need in the sun, or the more you should focus on exposing more skin and lying down.

The best sources of calcium are dairy, bones, napa cabbage, Chinese mustard greens, bok choy, and high-calcium mineral water. Mix and match two for young kids, three for most adults, or four for women over 50, men over 70, or adolescents.

Try to meet your targets with food first, and use supplements to fill the gaps. Bone meal from a lead-tested product is the best by default. Calcium citrate is best for those who need to avoid phosphorus or collagen, or who are at high-risk of kidney stones.

Phosphorus deficiency is mainly a risk of mostly fat diets, starvation, anorexia, or eating disorders.

Keto carnivore is at the greatest risk of deficiency but can avoid it with enough dairy, eggs, or meat. Regular keto can use veggies too.

Phosphorus levels drop in refeeding syndrome or hungry bone syndrome. Meat and eggs are great for refeeding and dairy is great for hungry bone.

We can avoid getting too much phosphorus by avoiding processed foods.

Remember that vitamin D requirements go down when you get enough calcium and go up when you get too much phosphorus. Before concluding you need more D than recommended in the lessons, check your calcium/phosphorus balance.

Very informative posts! I read them all

Max

Originally Posted by maxmuscle1

Very informative posts! I read them all

Max

Thanks Professor. That’s my name for you if you don’t mind

Originally Posted by thebear

Thanks Professor. That’s my name for you if you don’t mind

Sounds appropriate, like Professor Hyde!!

Max