Title: Selenium and the Environment

Key words: selenium, soil analysis, dietary selenium, hard wheat, Finland, supplementation, selenoproteins

Date: July 2000

Category: 5. Nutrition and the Environment

Type: Article

Author: Dr M Draper

 

Selenium and the Environment

A Personal View by Dr Mark Draper

Introduction

My interest in selenium began in November 1997 when I heard Dr Margaret Rayman being interviewed about her BMJ Editorial 'Dietary selenium: time to act' (1). At the time I knew little about selenium or its role in human health. However, several weeks later I was shown the soil analysis data from a farm near Henley in Arden (see appendix one) after prompting a friend to investigate the trace element status, prior to implementing organic farming methods. This prompted my own research.

Sources of dietary selenium

We mainly obtain this essential trace element from bread and cereals, meats (fish, poultry and red meats) and milk. In the U.K. the estimated daily intake of selenium fell from 60 microgms/person to 43 in 1988 and 34 microgms in 1994 (range of 29-39) primarily due to reduction in the import of Canadian flour (high selenium or hard wheat) but more recently, perhaps, due to further soil depletion. Generally, live stock farmers have attempted to improve trace element intakes by treating the animal directly with injections, drenches or mineral licks. This is in contrast to the more effective and enduring method of correcting the balance of trace elements for ruminants. This involves replenishing the elements directly to the soils and pastures, a technique which ensures that ruminants, plants and all the soil microflorae are treated.

In Finland daily intakes averaged 25 microgms when all the grain was home produced and 40-50 microgms when the harvest was bad and imported wheat was used. In 1984, selenium supplementation was made compulsory - to all grassland fertilisers at 6mg/kg, and to all grain phosphate fertilisers at 16mg/kg (reduced to 6mg/kg in 1994) (2). The aim of this was to increase the selenium content of grain from 10 to 100 microgms/kg. The levels in beef subsequently rose ten fold to 600 microgms/kg and in dairy products from 30 to 175-225 microgms/kg. The high local mortality from coronary heart disease has decreased, at least in part due to this rise in selenium intake.

What are the various functions of selenium in humans ?

The essential role of selenium is via the selenoproteins. These utilise selenocysteine that has been produced by the cells’ genes (The UGA Codon in messenger RNA produces selenocysteine which is then incorporated into proteins). There are about 35 selenoproteins and I would like to consider three which appear to have special relevance to the evolving picture about the nutritional functions of selenium.

Firstly, the antioxidant Glutathione Peroxidases. These are enzymes that stops lipid peroxidation and convert hydrogen peroxide to water. These enzymes, therefore, protect the phospholipids in cell membranes and appear to protect the cell from mutagenic peroxides formed from DNA and nucleotides. They appear to help maintain the integrity of red blood cells and to help white cells to kill bacteria. The mitochondria of macrophages appear to be particularly subject to free radical damage and this enzyme, plus mitochondrial superoxide dismutase (a Manganese dependent enzyme) help macrophages to function effectively. This forms an important part of the body’s immune response.

Secondly, the Iodothryonine de-iodinases are selenium dependent enzymes which are responsible for the conversion of thyroxine (T4) to trioiodothyronine (T3) which is six times more metabolically active. Low selenium would contribute to hypothyroidism and I have seen several cases of borderline thyroid function return to normal after appropriate selenium supplementation (2 microgms/kg/day).

The final selenoprotein I wish to detail is that found in the mitochodrial capsule which makes up the mid section of the human sperm tail. Early in spermatogenesis, this protects the developing sperm from oxidative damage and later polymerises into a structural protein that is required for sperm stability and motility.

What could be the significance of low levels of selenium in the U.K.?

I would like to consider examples from the Keshan region of China (3) where the first selenium deficiency syndrome was first described . Mothers there gave birth to children who died from a cardiomyopathy. At post mortem, the heart muscle was white and wasted. A similiar condition existed in the domestic animals in this region. The average daily intake was estimated at 11 microgms and the condition could be prevented by giving pregnant women selenium supplementation.

Keshan disease did not exist in areas where the the mean intake for a 60 kg man was 19.1 microgms or more per day. The population minimum mean intake (Se basal Pl min) was estimated to be 21 microgms per day.(4).

The data used by the WHO to derive normative requirements for selenium are taken from a Chinese experimental study in Keshan by Yang et al. (5)of the relationship between plasma glutathione peroxidase activity and selenium intake in adult men (aged between18-42 years old).

A daily dietary supplement of at least 30 microgms of DL-selenomethionine was necessary to saturate plasma glutathione peroxidase activity fully (equivalent to 41 microgms per day for a 65 kg man). However, at higher intakes the cell will produce more of the saturated enzyme, which may explain the protective value of having higher selenium intakes in reducing cancer (eg the inverse linear relationship in breast cancer mortality (6) and heart disease (cited in (7)).

The UK daily intake (29-39 microgms) of selenium would now appear to be less than normative (44 microgms in a 70 kg man). In pregnancy and lactation, when requirements are higher, the intakes move closer to the basal minimum levels at which syndromes of deficiency may start to appear, especially if dietary restrictions reduced the intake of wheat, meat or milk. The selenium in the diet is usually about 80% absorbed across the intestine (less from tuna fish - 45%) and appears not to be under homoeostatic control. Dietary selenium intake , therefore, determines tissue selenium levels. This explains why reductions in intake tend to be followed by a proportional reduction in blood levels and also why toxicity can occur when dietary intakes are high (well above 500 microgms per day).

Finally to summarise : A selenium deficient person may have:

(a) less resistance to infections (especially viral) and may be more susceptible to the harmful effects of toxins.

(b) reproductive difficulties with low sperm count and motility in men and miscarriage, unexplained infertility and perhaps malpresentations in labour

(c) an increased risk of cancer, heart disease, endocrine dysfunction and post viral fatigue syndromes.

 

References

  1. Dr Rayman MP. in BMJ Editorial 'Dietary selenium : time to act ' BMJ 1997; 314-387.
  2. Tolonnen M. 'Finnish studies on antioxidants with special reference to cancer, cardiovascular disease and aging ' Int. Clin Nutr Rev 1989; 9: 68-75.
  3. Yang GQ. et al ' Selenium- related endemic disease and the daily selenium requirements of humans.' World reviewof nutrition and diet, 1988; 55: 98-152
  4. World Health Organisation 'Trace elements in human nutrition and health' WHO publications Geneva 1996; ISBN 924-156-1734
  5. Yang GQ et al. ' Human selenium reqirements in China.' in Combs GF et al., eds. Selenium in biology and Medicine. New York, 1987; 589-607.
  6. Schrauzer G, White D and Schneider C.. Bioinorganic Chemistry 1977; vol 7 p36.
  7. Passwater RA ' Selenium as food and medicine ' 1980, Keats Connecticut, ISBN 0-87983-229-0.