A surprising number of Americans fall short of vitamin and mineral intake recommendations, and will never know it.

It’s a state we know as ‘inadequacy’—insufficient micronutrient intakes for optimum health.

It is really hard to know if you fall into this category. Unlike true vitamin and mineral deficiencies, that manifest as diseases like rickets or pellagra, there is often no telltale sign of a micronutrient inadequacy – many have non-specific symptoms or no symptoms at all.

Yet the scientific evidence suggests inadequacies are very real and have long-term consequences on our health and well-being.

As an example, we turn to vitamin E inadequacy taking from LPI’s own Dr. Maret Traber and her recent review on the subject.

Maret Traber with molecular model.
Maret Traber, PhD

In contrast to severe vitamin E deficiency that often shows in neurologic symptoms, like poor balance and coordination, nerve damage, muscle weakness, and damage to the eye, marginal vitamin E status is difficult to define as it has effects on neurological function are often subtle.  This is because the increased amounts of inflammation, susceptibility to infection, and oxidative damage are not severe enough to require hospitalization or specific enough to point to vitamin E as the only cause.

In other words, since many things can cause these types of problems in the body, you’re more likely to look elsewhere besides the amount of vitamin E you’re eating.

However, the consequences of inadequate vitamin E levels can be very real. Low vitamin E status has been implicated in an increased risk of cardiovascular disease, macular degeneration, and complications from type II diabetes – but these can take a lifetime to develop.

Vitamin E is also critical in brain development, and this should of particular interest to expectant mothers. When a pregnant woman has a vitamin E inadequacy, the fetus bears the brunt of this low-vitamin status. Again, with deficiencies the consequences are severe – with extremely low vitamin E levels the brain fails to develop and the fetus will not survive; the mother may never know she was pregnant. But milder cases vitamin E inadequacy in the mother, may allow the nervous system to develop with some abnormalities. Vitamin E inadequacy has also been implicated in low birth weight, as well as stunted growth and impaired cognitive function in infants.

PregnancyThe effects of vitamin E inadequacy, however, are not restricted to fetal development and infancy. Many children are at risk for low vitamin E status, possibly resulting in various neurological disorders, anemia, and increased risk for infections. Moreover, adults with inadequate vitamin E status may be at increased risk for Alzheimer’s disease or other age-related neurological and cognitive disorders.

The good news is that vitamin E inadequacies can be prevented by consuming the recommended levels of alpha-tocopherol (15 mg) each day in the form of nuts, seeds, and oils. However, this may not be an easy solution for some, as many Americans don’t get enough vitamin E.

Vitamin E is not a lone standout in our micronutrient inadequacies. The average American cbrain vitamin Eonsumes less than the recommended value of four or more vitamins and minerals each day. Again, we never know there’s a problem because symptoms of micronutrient inadequacies are mild or nonexistent, and the true effects of these inadequacies may not affect our lives until we are sick or older.

This is why the Linus Pauling Institute recommends a daily multivitamin/mineral supplement to ensure that you meet intake recommendations and increase your chance of a long and healthy life.

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4 thoughts on “Feelings of (Micronutrient) Inadequacy? Probably not.

  1. This question is only indirectly connected to this post, but I do not know where else to direct it.
    The Institute’s resource on Vitamin K states that
    “Replacing dietary saturated fats like butter and cheese with monounsaturated fats found in olive oil and canola oil will increase dietary vitamin K intake and may decrease the risk of cardiovascular disease.”
    However, it also states that
    “Most menaquinones are synthesized by human intestinal microbiota and found in fermented foods and in animal products. ”
    One can easily get large amounts of vitamin K1 from commonly eaten vegetable foods, without requiring the small amounts found in these oils. However, the main source of vitamin K2 in the western diet is fermented cheeses, and there is also vitamin K2 in grass-fed butter.
    Furthermore, cheese is NOT a “saturated fat” but a high protein food with a fat content (which includes a fair proportion of monounsaturated fat), whereas vegetable oils supply no protein in the diet.
    The question of whether saturated fat causes heart disease is a vexed one, all we can say at present is that saturated fat is not associated with heart attacks, even in cases of established coronary artery disease, in the vast majority of epidemiological studies. Whether the lipid hypothesis was true or a just tragic delusion, in this case it appears to have distorted valuable advice ostensibly related to the availability of vitamin K or other essential nutrients.

    • By ‘dietary saturated fats’ we are saying dietary sources of saturated fats (perhaps that should be clarified). Our recommendations should not be viewed as a “avoid saturated fat” mantra, but a recommendation to include unsaturated fats in the diet.
      Unfortunately, the current data is very limited on sources of K2, so our ability to comment on that subject is equally limited. Some cheeses and butters may have appreciable levels of K2, but the data gathered thus far suggests that the amount of K1 in the diet far exceeds levels of K2.

      • Thank you,

        that is a good response. However, recent re-analysis from Harvard of the epidemiological evidence regarding polyunsaturated fats and heart disease (fat choice has no effect on total mortality, only on CVD) shows that the benefit of replacing saturated fat with polyunsaturated fat is identical to that of replacing carbohydrate with polyunsaturated fat.
        This is confirmed by looking at the papers which show no correlation of saturated fat with CVD; these show much the same correlations for SFA, carbohydrate and MUFA.
        Monounsaturated fat shows no benefit in other analyses of this data, it is specific to polyunsaturates (but there is other evidence for a specific benefit of olive oil).

        Given that replacing carbohydrate appears to have the same CVD benefit as replacing saturated fat, and given that sugar, wheat flour and corn starch are highly refined carbohydrates of little nutritional value, consumed widely, while whole fat dairy and organ meats do have nutritional value, I submit that advice to replace carbohydrate with sources of unsaturated fat will be at least as beneficial as advice to replace sources of saturated fat with sources of unsaturated fat. All fats contain unsaturated fat, and all except coconut contain appreciable amounts.

        Vitamins K1 and K2 have different effects in the body, vitamin K2 inhibits arterial calcification and is required for brain sulfatide synthesis. Vutamin K2 can be made from vitamin K1 but the conversion is inhibited by statins and is clearly not optimal, as studies of vitamin K1 intake vs K2 do not show equal benefit in cardiovascular health. The authors of the papers cited in this review were able to find reliable data about the vitamin K2 content of animal foods, however the K2 studies cited were European. It may be that there are European nutritional databases that will provide more information on vitamin K2 than the USDA does.

        The vitamin K2 and brain sulfatide connection is fascinating and I summarized the research here a few years ago:


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