Subject: vitamin overdose vs. vitamin deficiency

Submitted by: Simon Dankel, Bergen, Norway

Since your recommendation for vitamin A intake approaches about 3 times that of the government's Upper Level (30,000IU versus 10,000IU), I would like to know your evidence (and share it with a skeptical professor, who thinks your recommendation questions your credibility). I am aware that excess vitamin A is associated with birth defects, and that the UL is set to prevent this. You may therefore exclude pregnant women from your recommendation?

A 1989 report also suggests that there may be adverse effects of long-term vitamin A supplementation:

"Our study suggests that elderly people should limit their intake of supplemental vitamin A particularly over the long term. Our data may also indirectly support a lowering ofthe RDA for vitamin A. It was suggested that hepatic stores of vitamin A are maintained with lower intakes ofthe vitamin (14). Daily intakes throughout life of vitamin A at RDA levels may result in an accumulation of hepatic vitamin A stores over time so that the capacity to store vitamin A in later life is reduced. Consequently, the margin of safety for vitamin A intake may be decreased in elderly people predisposing them to hypervitaminosis A."

(Krasinski SD et al 1989 Relationship of vitamin A and vitamin E intake to fasting plasma retinol, retinol-binding protein, retinyl esters, carotene, alpha- tocopherol, and cholesterol among elderly people and young adults: increased plasma retinyl esters among vitamin A-supplement users.)

Also, the following study seems to indicate that vitamin A can have an adverse effect on bone: Melhus H, Michaelsson K, Kindmark A, et al. Excessive dietary intake of vitamin A is associated with reduced bone mineral density and increased risk for hip fracture. Ann Intern Med 1998;129:770-778. What about liver abnormalities?

I am personally inclined to think that we are well adapted to eat relatively large amounts of vitamin A through liver, though I am less convinced of long-term consistent vitamin A supplementation. Why do you recommend at least 5000IU of vitamin A daily, and why may up to 30,000IU be more optimal?

 

Thank you for your letter, Simon. I see you are deeply engaged in your nutrition studies at the university. The first principle that I profess, which my professors professed to me, is that knowledge does not exist without critical thinking. Because of the massive amounts of data circulating, you need critical thinking to discern what's true, what's false, what's accurate, and what's not. Therefore, a school that teaches thinking is superior for learning about nutrition than a school that teaches "nutrition."

There'll always be professors within a school, or between schools, whose views clash or are at variance with each other. You can't learn from studying one side of a controversy. Nutrition is a subject where it's difficult to find consensus, because there are varying conceptions of nutrition. Some individuals conceive of it mainly in terms of preventing "a deficiency," while others may be more prone to ask what is the ideal amount to prevent development of degenerative disease.

 

Because of the massive amounts of data circulating, you need critical thinking to discern what's true, what's false, what's accurate, and what's not.

 

Regarding the 1989 study you cited, "liver damage" is more prevalent among the elderly than the young; the question is whether a causal connection exists between the liver damage noted in elderly subjects and vitamin A supplementation. I question both the authors' definition of liver damage, and the purported correlation between liver damage and supplemental vitamin A intake. The study was performed at a USDA center, and you can accord to that fact whatever relevance you wish. Assuming for the sake of argument that supplemental vitamin A contributed to liver damage in the elderly subjects of the study, we must then weigh that negative against the positive effects produced by the supplementation regimen, with a view toward evidence indicating a role for vitamin A in cancer prevention and resistance to infection.

The 1998 study you cited is a food intake study, and there are many potential confounding factors. Of the experimental protocols, double-blind, placebo-controlled studies are regarded as the most reliable (and often are in conflict with each other depending on who's sponsoring the study or interpreting the data); and self-reported food intake questionnaires tend to be less reliable. The question of correlation vs. causation is never more prominently showcased than when using this type of data to try to show that a particular nutrient causes or helps prevent a disease.

The published research and anecdotal reports of natural medicine practitioners who regularly prescribe vitamin A supplementation at dosages much higher than 5000 i.u. show benefits not detriments. The richest source of vitamin A is organ meat, particularly liver and kidney; and the richest sources of carotene-derived vitamin A is dark green leafy vegetables, like spinach and collards, and orange vegetables like yams and squash – all of which we in modern society tend to shun in favor of carbohydrate-dense, nutrient-deplete processed foods. If you want to do an interesting and enlightening food intake study, add-up how much vitamin A the diet of the Ancient Warriors (see NHE Ch. 5) contained. I believe you'll find it unlikely that a meat-eating Paleolithic man or woman could've regularly consumed less than 5000 i.u. of vitamin A daily, especially if they were also consuming unprocessed green or orange plants. The consequences of the shortfall between the vitamin A content of modern man's diet and that of his ancient ancestors is an issue I hope you and your professors will take up.



It isn't easy for a young student with a different view to gain attention, especially not when skepticism towards a Paleolithic way of eating amounts to the "extreme".
 

Extremely unreasonable it seems to me. Whether you use the terms "Paleolithic" or "ancient warrior" isn't important. These are representations designed to point to alterations in the human diet over time. Viewed objectively, it's impossible to disclaim the fundamental changes that have occurred to the food supply since the industrial revolution, and more dramatically, since food became a multi-billion dollar business. This view is not new, though "paleolithic nutrition" has come into vogue in recent years as the study of dietary anthropology has attracted greater interest. In 1975, in a bulletin titled, "Diet, Theory of a Natural Diet" L. Ron Hubbard asked: "what does the human body require, what is the natural diet?" I believe any serious and substantive nutritional curriculum should begin with this inquiry, and proceed forth from it. Otherwise the analytical framework is flawed, and you're more likely to arrive at wrong answers to basic questions.

 

The researcher who reacted to your vitamin A recommendation is among the more open I've met. When I told her about my diet she was impressed and became interested to read NHE. Indeed, she's now giving the NHE Eating Plan a go! Like you, she encouraged critical thought. In particular, she argued that it's critically important to consider potentially relevant nuances. Here are some points that were raised in one of our conversations:

Contained in food matrix versus contained in pills. The molecule may be (virtually) the same, but how does matrix affect absorption and utilization? It seems plausible that 20,000IU of vitamin A taken in via 150 grams of chicken liver results in lesser absorption than 20,000 IU of a pure vitamin A extract. Could food matrix have other effects?

 

The significance of delivery method relative to absorption is an acknowledged fact, though its nuances have not been fully delineated. In some cases might not absorption be higher from food given that food contains other nutritional components that may act as digestive cofactors or otherwise enhance bioavailability? (for example, certain nutrients enhance uptake of other nutrients while others compete for absorption). While this is a practically significant line of inquiry, it does not displace the harsh reality that most people aren't getting enough nutrition, even as caloric intake and the prevalence of food-borne toxins and "anti-nutrients" have increased. Rather than focusing on the largely academic question of how much nutrition is too much, we should focus on the critical question of how to get enough. When you compare the number of people who are suffering from vitamin overdose with the number of people developing diabetes, osteoporosis, heart disease, or cancer partly because of chronic sub-optimal provision of nutrients intrinsic to health, you can't help but wonder why we're wasting so much time discussing the former.

 

. . . most people aren't getting enough nutrition, even as caloric intake and the prevalence of food-borne toxins and "anti-nutrients" have increased. Rather than focusing on the largely academic question of how much nutrition is too much, we should focus on the critical question of how to get enough.

 

Source is precursor pigment versus source is retinol. The intestine regulates the conversion of vitamin A precursors to retinol, whereas large doses of retinol are potentially more toxic.

Retinol is, in fact, one of the more toxic vitamins - and the least toxic drug is approximately as toxic as the most toxic vitamin. A 1995 article published in the New England Journal of Medicine concluded that 10,000 i.u. intake per day of retinol increases the risk of birth defects. But when you read the study and see how the authors arrived at this conclusion, the presumed causal relationship is tenuous. A single study doesn't establish anything in any case, and in this case is directly contradicted by a 1997 study published in the American Journal of Obstetrics and Gynecology that found no increased risk of birth defects in pregnant women taking 10,000 i.u. of vitamin A per day.

Low vitamin A status among pregnant women has been linked to low fetal birth weight/preterm delivery and increased maternal mortality. In young children, vitamin A deficiency is one of the more prevalent vitamin deficiencies, especially in socioeconomically disadvantaged areas. It has devastating effects on growth and immune function, increasing susceptibility to infectious diseases. An article published in the New York Times (March 3, 2006) reports that "rampant malnutrition. . . is stunting the development of more than 100 million children worldwide" and "lack of food is usually not the main cause of child malnutrition." Considering no vitamin is more important for healthy growth hormone production in children, and vitamin A deficiency is the primary cause of growth-hormone-deficiency-related small stature (stunted growth), I wouldn't be surprised to discover that a large percentage of the 100 million stunted children worldwide are stunted as a direct consequence of inadequate intake of vitamin A (and zinc). The Times article uses the term "stunting" to refer both to small stature and cognitive retardation. Furthermore, the article states that by two years of age, it's too late - the damage is irreversible. It would certainly seem prudent, therefore, for pregnant and lactating women to take vitamin A supplements in order to help secure the early-life advantage of proper physical and mental development and strong immunity - and to avoid the potentially severe consequences of vitamin A deficiency. Accidental ingestion of a single dose of up to 300,000 i.u. of retinol produces acute toxicity in children, causing vomiting, severe headache, joint pain, and disorientation. In all such cases that have been reported, symptoms subside upon withdrawal of the vitamin resulting in complete recovery.

 

 

A Paleolithic diet presumably contained more precursors than retinol?

 

The "paleolithic diet" encompassed both hunting and gathering modes of food procurement. Considering 4 ounces of beef liver contains approximately 40,000 i.u. of retinol, I hesitate to endorse the generalization that "a Paleolithic diet contained more precursors than retinol."

 

 

A larger share of the vitamin A intake in the form of precursors may be better tolerated (or, more optimal?) than a larger share in the form of retinol? (i.e. the amount of vitamin A per se contained in the source needs not reflect the actual health effects).

 

Carotenoid precursors of vitamin A are non-toxic - except that ultra-high megadosages can cause your skin to exhibit a redish-yellow or orangish tint, which goes away after such intake is discontinued. If you've ever seen ads for "sunless tanning pills" it's usually a carotenoid called canthaxanthin. Most people have to ingest outrageously high dosages of it to get the "tanning effect," and even at that level serious side effects are rare (though there are reports of retinal damage resulting from prolonged use at a dosage level sufficient to change the visible color of the skin). I recommend getting vitamin A from both retinol and precursors, as a means of maintaining healthy vitamin A status without overloading on retinol - and get a suntan from sunshine not from a pill bottle.

The larger underlying issue is the way nutrient studies are structured, whereby the findings to have only tangential relevance to the pursuit of optimal nutrition. The study of particular nutrients in relation to specific health/disease parameters is a flawed carryover of the medical standard in which select toxic and overpriced drugs are associated with discrete disorders. This notion of magic bullets to treat artificially demarcated conditions is chiefly a selling mechanism to promote chemical treatment of organic disorders. The drug paradigm has no appropriate application to nutrition and, in fact, the opposite paradigm applies. This paradigm, which defines my nutritional outlook, views all nutrients ingested daily as constituting a singular entity or cognizable "data sheet." My nutritional approach is founded on an appreciation of nutrient interaction and synergy.

Practically, this translates to nutrient ratios that foster complementary interaction and facilitate maximal synergy. This is the untapped frontier in nutrition, capable of producing results well beyond what has been generated by the single-nutrient trials that dominate experimental protocol, limit therapeutic efficacy, and promote "false positive" outcomes in toxicity testing. It's easier to test one nutrient only, because you limit the number of variables that can potentially confound the findings. But the results generated from such studies have little application outside of the academy, and are sometimes cited to downplay the benefits of nutritional supplements or deter their beneficial use in favor of encouraging drug use.