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Vitamin A: Low Hemoglobin, Iron Overload & Neurodegeneration

Friday, February 16, 2018

Low hemoglobin levels leading to fatigue, loss of energy, difficulty concentrating, dizziness, and poor health is one of the most important public health problems in developing and developed countries, according to the World Health Organization. It affects many children, women of reproductive age, and older people.

The etiology of low hemoglobin levels is multifactorial and could be associated with iron deficiency, infections, genetic defects of folate or cobalamin, and vitamin A deficiency, which is suggested to impair iron mobilization, with consequent iron accumulation in neural tissues considered central in neurodegeneration during the aging process.

Because of its numerous functions, biomarkers of vitamin A status are diverse. Historically, signs of xerophthalmia were used to determine vitamin A deficiency. Before overt clinical damage to the eye, people who suffer from vitamin A deficiency are plagued by night blindness and longer dark adaptation times. 


Assessment of liver reserves of vitamin A retinol was soon considered the gold standard, because the liver is the major vitamin A storage organ.

Fortunately and unfortunately, serum retinol concentrations are homeostatically controlled until liver reserves become dangerously low. Therefore, other biochemical testing methods that respond to vitamin A liver reserves in the marginal category have been developed. These included dose-response tests and isotope dilution assays.

Enter a University of Brazil post-graduate program in human nutrition systematic review and meta-analysis 

The aim of the review recently published in Critical Reviews in Food Science and Nutrition was to assess and estimate the effect of vitamin A supplementation (VAS) on iron-status biomarkers in humans. 

Six databases, including Cochrane, EMBASE, LILACS, Pubmed, Scopus, and Web of Science were searched for clinical trials and cohort studies that investigated the effect of VAS alone on iron status and low hemoglobin symptomology, without time restriction.

The search yielded 23 eligible studies, 21 clinical trials and two cohort studies, with children, teenagers, and pregnant or lactating women. The meta-analysis of the clinical trials showed VAS reduces the risk of low hemoglobin symptomology by 26 percent and raises hemoglobin levels, compared to the non-treated group, independent of age.

All of the baseline studies that evaluated vitamin A deficiency (VAD) prevalence, showed a decrease in deficiency after supplementation. Among the 20 studies that evaluated serum levels after vitamin A supplementation, only two studies did not observe any difference in this biomarker.

Among the 11 studies that estimated the low hemoglobin level prevalence, most of them showed a reduction in the number of cases in the VAS group compared to baseline, except for one study that did not observe any difference.

In order to estimate the effect of VAS on low hemoglobin risk, a meta-analysis was conducted considering the 10 clinical trials that presented the data about cases of low hemoglobin.

In summary, this systematic review and meta-analysis suggests that supplementation with vitamin A alone may reduce the risk of ill health by improving hemoglobin and ferritin levels in individuals with low serum retinal levels.

This study brings more scientific evidence and suggests the development of further studies in order to precisely estimate the prevalence of health issues in aging also caused by vitamin A deficiency and emphasizes the vital importance of evaluating vitamin A status prior the implementation of iron supplementation in public health policies, particularly for older people.

The recommended daily intake of preformed vitamin A is 3,000 IU per day for men and slightly less for women. The daily safe upper limit (UL) is still 10,000 IU per day. 

Ellen Troyer, with Spencer Thornton, MD, David Amess and the Biosyntrx staff


Optimal vitamin A preformed, animal-based retinol absorption is somewhat dependent on other vitamins and minerals, including vitamins C, D, K, and minerals zinc, and magnesium. Unfortunately, vitamin K is rarely included in multiple vitamin formulations recommended for people over the age of 60 at this point, given the large number of people who regularly take prescription blood thinners or daily aspirin to prevent inappropriate clotting. 

Plant-based, pro-formed vitamin A carotenoids must be metabolically converted by our bodies to retinol for absorption. Unfortunately our body’s ability to convert beta carotene carotenoids into a bioavailable form of retinol is diet and age dependent. Beta carotene conversion to retinol is particularly difficult for those on a low-fat diet, those with diabetes, and for many older people.

Of the three hundred or more identified plant-based carotenoids, beta carotene is the only one with meaningful ability to convert to retinol. Lutein and zeaxanthin do not convert to vitamin A in the body. 

It is the policy of the Biosyntrx science team to not include hydro- carbon beta carotene in our formulations as a source of pro-formed vitamin A because it can interfere with the absorption of the macula pigment-specific xanthophyll carotenoids, lutein and zeaxanthin. 


As an aside: Our Biosyntrx co-founder, Spencer Thornton, MD, was the first to publish on the relationship between defects in dark adaption and vitamin A deficiency, liver disease, retinal degenerative changes, and the development of a relatively simple and accurate test of dark adaptation. This work was published in the June 1977 Annals of Ophthalmology.

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