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Is foetal alcohol syndrome in children as old as alcohol consumption?

Foetal alcohol syndrome (FAS) is the leading cause of preventable intellectual disability in the world, according to the World Health Organization,1 and the true prevalence is almost certainly underestimated. As long as alcohol is present in our everyday lives, FAS will continue to challenge families, communities and countries. In this issue of Acta Paediatrica, Dr Feldmann suggests that a historical study of children living in a 1930s German wine-producing community showed widespread FAS.2 We believe that FAS and foetal alcohol spectrum disorder (FASD) have been around for as long as alcohol has been available, and not at all restricted to times and places where alcohol has been used as reward or payment for work. Pulque, a fermented agave juice with 4%-7% alcohol, can be traced back thousands of years to native Meso America. Ancient Aztecs ritualised Pulque and strictly limited its use, but it was still widely used when water was scarce. By the 1500s, Pulque had become so popular that it was temporarily prohibited to quell the devastating health and social problems it wrought on native Mexicans. It is still extensively consumed in poorer rural communities and pregnant women are encouraged to drink it due to its nutrient content and beliefs about its lactogenic effects. It has been suggested that heavy and early Pulque use in pregnancy adversely effects offspring growth and development.3 The College of Physicians suggested that excessive gin drinking in early 18th century, London, after distilling restrictions were lifted, caused ‘weak, feeble and distempered’ children.4 In 1889 and 1895, the French Psychiatrist Maurice Legrain linked alcohol to intrauterine and neurological problems and grave mental issues. More than 40% of inmates in his asylum were diagnosed ‘hereditary insane’, due to their parents' alcoholism.4 In the early 1900s, emerging research showed hereditary effects, direct teratogenic effects on the foetus, including structural dysmorphia, and other physical defects in animal models.4 A presentation at the Fourth International Congress against Alcohol Abuse in The Hague, in 1892, stated that alcohol was a toxic agent and alcohol abuse could poison the foetus in utero. Blastotoxie occurred when one partner was drunk during conception and blastophtorie was when one parent was a chronic alcoholic whose germ plasma had been seriously poisoned by alcohol.5 Literary works by authors such as Charles Dickens suggest that the general public were also aware of the deleterious effects that maternal alcohol use had on offspring. Many physicians of that time took an ambivalent stance, as alcohol was used as an anaesthetic, with few alternatives, and when premature labour was threatened. Some practitioners continued to believe the placenta was impervious to alcohol.4 When American prohibition arrived in the 1920s, it dampened enthusiasm for new studies, and scientists eschewed the pre-prohibition toxicological research, viewing it as tainted by moralistic tones. It was not until Lemoine's rediscovery of FAS in the 1960s 6 that interest and research were revived. The lives of women and children in ancient Meso America, 18th century London and 19th century France, may have been very different to life in a 1930s German wine region, but for Kaiserstuhl children, the implications of regular parental drinking were the same. Even so, we should avoid unfairly judging past research against today's standards and we were cautious when drawing inferences as we only had Feldman's essay to go on.2 Given the lack of interest in alcohol and human development in the 1950s, the Kaiserstuhl paper was probably novel. It might even have been a stand-out study, but for the author's conclusion that daily alcohol use by children and parents had no negative impact on their growth. What's more, it seemed to have been met with little scholarly opposition; the documented studies, suspicions and theories raised in the previous century were apparently insufficient to spur on a challenge by the medico-scientific community.2 Feldmann suggests that because Fischer did not connect the children's facial features to maternal alcohol consumption, he did not report any sub-group analyses.2 This may have been because the Kaiserstuhl children routinely drank wine, but their growth and gross motor skills appeared normal, even superior, to other groups. A more recent South African study also showed no detectable deficiencies in gross motor skills among FAS children in a wine-producing area compared with controls.7 As for the Kaiserstuhl children's normal height and weight, there may have been compounding differences in nutritional status between them and the control population in urban Freiburg, which was very badly affected by World War I. It is plausible that rural Kaiserstuhl had better access to nutritious food. Perhaps the wine also provided a source of nutrition in an otherwise limited diet. It is unfortunate, but understandable, that the Fisher study lacked reliable measures of cognitive function. Fisher used a Norwegian 60-m timed run as his key measure. The Kaiserstuhl children showed good running speeds, probably because they were unusually fit from


Is foetal alcohol syndrome in children as old as alcohol consumption?
Foetal alcohol syndrome (FAS) is the leading cause of preventable intellectual disability in the world, according to the World Health Organization, 1 and the true prevalence is almost certainly underestimated. As long as alcohol is present in our everyday lives, FAS will continue to challenge families, communities and countries.
In this issue of Acta Paediatrica, Dr Feldmann suggests that a historical study of children living in a 1930s German wine-producing community showed widespread FAS. 2 We believe that FAS and foetal alcohol spectrum disorder (FASD) have been around for as long as alcohol has been available, and not at all restricted to times and places where alcohol has been used as reward or payment for work.
Pulque, a fermented agave juice with 4%-7% alcohol, can be traced back thousands of years to native Meso America. Ancient Aztecs ritualised Pulque and strictly limited its use, but it was still widely used when water was scarce. By the 1500s, Pulque had become so popular that it was temporarily prohibited to quell the devastating health and social problems it wrought on native Mexicans. It is still extensively consumed in poorer rural communities and pregnant women are encouraged to drink it due to its nutrient content and beliefs about its lactogenic effects. It has been suggested that heavy and early Pulque use in pregnancy adversely effects offspring growth and development. 3 The College of Physicians suggested that excessive gin drinking in early 18th century, London, after distilling restrictions were lifted, caused 'weak, feeble and distempered' children. 4 In 1889 and 1895, the French Psychiatrist Maurice Legrain linked alcohol to intrauterine and neurological problems and grave mental issues. More than 40% of inmates in his asylum were diagnosed 'hereditary insane', due to their parents' alcoholism. 4 In the early 1900s, emerging research showed hereditary effects, direct teratogenic effects on the foetus, including structural dysmorphia, and other physical defects in animal models. 4 A presentation at the Fourth International Congress against Alcohol Abuse in The Hague, in 1892, stated that alcohol was a toxic agent and alcohol abuse could poison the foetus in utero. Blastotoxie occurred when one partner was drunk during conception and blastophtorie was when one parent was a chronic alcoholic whose germ plasma had been seriously poisoned by alcohol. 5 Literary works by authors such as Charles Dickens suggest that the general public were also aware of the deleterious effects that maternal alcohol use had on offspring. Many physicians of that time took an ambivalent stance, as alcohol was used as an anaesthetic, with few alternatives, and when premature labour was threatened.
Some practitioners continued to believe the placenta was impervious to alcohol. 4  Even so, we should avoid unfairly judging past research against today's standards and we were cautious when drawing inferences as we only had Feldman's essay to go on. 2 Given the lack of interest in alcohol and human development in the 1950s, the Kaiserstuhl paper was probably novel. It might even have been a stand-out study, but for the author's conclusion that daily alcohol use by children and parents had no negative impact on their growth. What's more, it seemed to have been met with little scholarly opposition; the documented studies, suspicions and theories raised in the previous century were apparently insufficient to spur on a challenge by the medico-scientific community. 2 Feldmann suggests that because Fischer did not connect the children's facial features to maternal alcohol consumption, he did not report any sub-group analyses. 2 This may have been because the Kaiserstuhl children routinely drank wine, but their growth and gross motor skills appeared normal, even superior, to other groups. A more recent South African study also showed no detectable deficiencies in gross motor skills among FAS children in a wine-producing area compared with controls. 7 As for the Kaiserstuhl children's normal height and weight, there may have been compounding differences in nutritional status between them and the control population in urban Freiburg, which was very badly affected by World War I. It is plausible that rural Kaiserstuhl had better access to nutritious food.
Perhaps the wine also provided a source of nutrition in an otherwise limited diet.
It is unfortunate, but understandable, that the Fisher study lacked reliable measures of cognitive function. Fisher used a Norwegian 60-m timed run as his key measure. The Kaiserstuhl children showed good running speeds, probably because they were unusually fit from