THE LANCET
SCIENCE AND MEDICINE
Passive smoking changes lipid profiles in at-risk children of hyperlipidaemia and were not takhe authors of a US study of ing drugs that might affect lipid prochildren aged 2–18 report that files. More than 70% of passive smoking is assothe children had a famciated with a decrease ily history of premature in serum concentrations heart disease; nearly all of high-density-lipoprohad a family history of tein (HDL) cholesterol. hypercholesterolaemia. According to lead Mean serum HDLauthor Ellis Neufeld cholesterol values were (Children’s Hospital significantly lower in and Harvard Medical children who came School, Boston, MA, from households where USA) although previone or more members ous studies in children smoked than in those have shown a correlawho came from nontion between lower No thought to the future? smoking households HDL-cholesterol values (1·00 mmol/L vs 1·13 mmol/L, and passive smoking, “this is the first p=0·005). Before puberty, the study to take diet, obesity, exercise, population-average HDL-cholesterol and sociodemographic factors into value is 1·42 mmol/L. account” (Circulation 1997: 96: The higher an individual’s HDL 1403–07). cholesterol concentration is, the less The 103 children in the study likely that person is to have a heart attended a hyperlipidaemia clinic at attack. HDL is thought to promote the Children’s Hospital. All had an cholesterol transport from the arterial LDL cholesterol in the top fifth perwall back to the liver, explains centile but had no secondary causes
Neufeld, adding that the children in his study face a triple jeopardy: a family history of heart disease and high cholesterol; low HDL-cholesterol concentrations because family members smoke; and an increased chance of becoming smokers themselves because they come from smoking families. “This research is particularly relevant to the 3 million young people in the USA who have more than 5·17 mmol/L cholesterol, and indicates that removing people from smoke exposure may substantially increase their HDL cholesterol”, says Neufeld. Gilbert Thompson (MRC Lipoprotein Unit, Hammersmith Hospital, London, UK) adds that the ratio of HDL to LDL cholesterol determines outcome. These children already had high LDL-cholesterol concentrations, so anything that reduced HDL would compound the mischief, he explains.
Fungal problems in Kenya
How do prion proteins get to the brain?
News in brief
study carried out at the University of Nairobi, Kenya, indicates that commercial maize flour is heavily contaminated with toxigenic fungi and mycotoxins. These findings are crucial since maize is a staple food in sub-Saharan Africa. George Siboe and Gacheri Muriuki analysed 172 samples of maize flour from shops and supermarkets in Nairobi. 70% of the samples were contaminated with 16 fungal species of Aspergillus, Fusarium, and Penicillium. The samples were also heavily contaminated with aflatoxins and other mycotoxins. The number of fungal colonies in each flour sample increased with the moisture content, and “as the expiry date for the flour approached, the total number of fungal colonies increased, raising the levels of mycotoxins”, says Sibeo. The high prevalence of some human cancers in Transkei has been linked to eating maize contaminated with F moniliforme mycotoxins. Also, findings from Nigeria, Mozambique, and Liberia indicate that aflatoxin ingestion is responsible for some of the problems associated with kwashiorkor and marasmus.
N
Diet and endometrial cancer A new study provides evidence that women who eat food low in fat, high in fibre, and rich in legumes have a reduced endometrial cancer risk. The study is also the first to show an inverse relation between eating soy and uterine cancer risk (Am J Epidemiol 1997; 146: 294–306).
Anderson Wachira Kigotho
Jane Bradbury
Bubbles
T
A
718
ew data explaining how abnormal prion proteins get into the central nervous system may help researchers develop ways to block infection with prion proteins. An abnormal isoform of prion protein, PrPres, is believed to be the infectious agent in transmissible spongiform encephalopathies, and consumption of beef from cattle with bovine spongiform encephalopathy has been linked to new variant Creutzfeldt-Jakob disease in man. But how does PrPres get from the gut to the brain to cause disease? Adriano Aguzzi (University of Zurich, Switzerland) and colleagues report that, at least in mice, lymphohaemopoietic stem cells are the main site of prion replication after intraperitoneal or intravenous inoculation of scrapie prions (Nature 1997; 387: 69–73). However, these sites are not enough to produce a productive infection of the central nervous system and it seems likely that this requires a chain of tissues expressing endogenous prion proteins. The researchers speculate that the peripheral nervous system could be involved in this chain.
Peter Moore
Cot deaths increase The sudden infant death rate in England and Wales increased from 0·6 per thousand live births in 1995 to 0·7 in 1996. Responding to data released on Aug 27, the Foundation for the Study of Infant Deaths urged parents, carers, and health professionals to continue to follow all aspects of the Reduce the Risk campaign launched in 1991. Gene therapy advance University of Chicago researchers have found a way to limit the expression of genes to a single cell type, an important safety concern in gene therapy. Reporting in the Sept 1 issue of the Journal of Clinical Investigation, the scientists say that they restricted the expression of an introduced gene to smooth muscle cells.
Vol 350 • September 6, 1997