The symptoms of ‘Type 1’ decline of Norway spruce ( Picea abies (L.) Karst.) and silver fir ( Abies alba Mill.) in mountainous areas of central Europe result directly from foliar magnesium (Mg) deficiency. This produces chlorosis of older needles, reduced photosynthesis and carbohydrate translocation. These changes result in lower rates of root growth and wood development as well as increased sensitivity of chlorotic needles to fungal pathogens, drought and cold stress. Foliar Mg deficiency results primarily from low rates of Mg uptake due to the low availability of Mg in some acid soils in central Europe. The Mg content of needles, xylem sap and roots have been linearly correlated with exchangeable and soil solution Mg. The symptoms have been reproduced in the laboratory by growing Norway spruce in sand culture supplied with all nutrients except Mg and in low-Mg forest soils under high light. This is not a ‘new-type’ of decline as the symptoms, and corrective measures based on Mg-fertilization, were known to occur in localized areas of the Black Forest in the 1960s. However, it is clear that the symptoms now occur over a wider area. This is probably because losses of Mg into biomass over a single forest rotation and through leaching by acid deposition, greatly exceeded exchangeable reserves plus atmospheric Mg inputs. In soils of deficient stands, release of Mg by weathering could not compensate for these losses. Indeed, there is limited evidence that soil pH and exchangeable soil Mg have decreased in some Norway spruce stands in recent decades. Mg uptake may be further reduced due to low Mg/Al ratios in soil solution. These soils are under higher leaching pressures than elsewhere in Europe judging from the levels of sulphate and nitrate in outputs. Better growth of trees, possibly due to increasing N inputs, has also increased demands on soil Mg. Leaching has reached the point where at least as much Mg is removed as by tree harvesting. Part of the increase in Mg deficiency between 1976 and 1983 was due to a transient stress. This was probably the dry summers of 1975/76 and 1981/84 as the Mg status of many stands improved in the wetter summers of 1986/88. Studies on Mg-deficient soils in New Zealand showed low rates of litter mineralization and root uptake during drought. Recent information, although incomplete, suggests that direct effects of gaseous pollutants and acid mist on the needles played only a minor role in the recent expansion of Mg deficiency. The uniform chlorotic symptoms cannot be reproduced in the laboratory by exposure to sulphur dioxide, ozone or acid mist. The anatomical and physiological changes in chlorotic needles are characteristic of Mg deficiency and have not been reproduced by direct exposure to pollutants. Magnesium cycling studies in deficient Norway spruce stands indicate that <10 per cent of Mg in the crown is removed by foliar leaching each year. Recent laboratory studies indicate that the effects of ozone on leaching are minimal. Acid mist accelerates foliar leaching, but Mg resorption/translocation was sufficient to prevent induction of deficiency symptoms. The improved nutritional status of chlorotic grafts attached to healthy trees indicates that limited Mg availability uptake was more important than foliar leaching. Magnesium deficiency has not appeared in the forests of countries along the maritime seaboard of northern Europe, because the rate of Mg deposition in precipitation is much greater than in central Europe. Consequently, Mg deficiency symptoms have not been seen in the UK or Norway, even in areas of high acid deposition, nor do coniferous forests in these regions respond to Mg fertilization.