Kate Northstone

Prof. Kate Northstone


Research Focus & Metrics

Academic Career Length

27Years (2000-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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14 December 2005 in European Journal of Human Genetics
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Journal Article
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TTThe ALSPAC Study Team
The ALSPAC Study Team
MPMarcus E Pembrey
Marcus E Pembrey
LBLars Olov Bygren
Lars Olov Bygren
GKGunnar Kaati
Gunnar Kaati
SESören Edvinsson
Sören Edvinsson
JGJean Golding
Jean Golding
Transgenerational effects of maternal nutrition or other environmental ‘exposures’ are well recognised, but the possibility of exposure in the male influencing development and health in the next generation(s) is rarely considered. However, historical associations of longevity with paternal ancestors' food supply in the slow growth period (SGP) in mid childhood have been reported. Using the Avon Longitudinal Study of Parents and Children (ALSPAC), we identified 166 fathers who reported starting smoking before age 11 years and compared the growth of their offspring with those with a later paternal onset of smoking, after correcting for confounders. We analysed food supply effects on offspring and grandchild mortality risk ratios (RR) using 303 probands and their 1818 parents and grandparents from the 1890, 1905 and 1920 Överkalix cohorts, northern Sweden. After appropriate adjustment, early paternal smoking is associated with greater body mass index (BMI) at 9 years in sons, but not daughters. Sex-specific effects were also shown in the Överkalix data; paternal grandfather's food supply was only linked to the mortality RR of grandsons, while paternal grandmother's food supply was only associated with the granddaughters' mortality RR. These transgenerational effects were observed with exposure during the SGP (both grandparents) or fetal/infant life (grandmothers) but not during either grandparent's puberty. We conclude that sex-specific, male-line transgenerational responses exist in humans and hypothesise that these transmissions are mediated by the sex chromosomes, X and Y. Such responses add an entirely new dimension to the study of gene–environment interactions in development and health.

13 March 2003 in New England Journal of Medicine
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GLGideon Lack
Gideon Lack
DFDeborah Fox
Deborah Fox
KNKate Northstone
Kate Northstone
JGJean Golding
Jean Golding
The prevalence of peanut allergy appears to have increased in recent decades. Other than a family history of peanut allergy and the presence of atopy, there are no known risk factors.

14 March 2019 in Wellcome Open Research
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KNKate Northstone
Kate Northstone
MLMelanie Lewcock
Melanie Lewcock
AGAlix Groom
Alix Groom
ABAndy Boyd
Andy Boyd
JMJohn Macleod
John Macleod
NWNicholas Wells
Nicholas Wells
The Avon Longitudinal Study of Parents and Children (ALSPAC) is a prospective population-based study. Initial recruitment of pregnant women took place in 1990-1992 and the health and development of the index children from these pregnancies and their family members have been followed ever since. The eligible sampling frame was constructed retrospectively using linked recruitment and health service records. Additional offspring that were eligible to enrol in the study have been welcomed through major recruitment drives at the ages of 7 and 18 years; and through opportunistic contacts since the age of 7. This data note provides a status update on the recruitment of the index children since the age of 7 years with a focus on enrolment since the age of 18, which has not been previously described. A total of 913 additional G1 (the cohort of index children) participants have been enrolled in the study since the age of 7 years with 195 of these joining since the age of 18. This additional enrolment provides a baseline sample of 14,901 G1 participants who were alive at 1 year of age.

21 November 2010 in Nature Genetics
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CECathy E. Elks
Cathy E. Elks
JPJohn R.B. Perry
John R.B. Perry
PSPatrick Sulem
Patrick Sulem
DCDaniel I. Chasman
Daniel I. Chasman
NFNora Franceschini
Nora Franceschini
AMAnna Murray
Anna Murray

1 March 2011 in Journal of Allergy and Clinical Immunology
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Journal Article
Open access
SBSara J. Brown
Sara J. Brown
YAYuka Asai
Yuka Asai
HCHeather J. Cordell
Heather J. Cordell
LCLinda E. Campbell
Linda E. Campbell
YZYiwei Zhao
Yiwei Zhao
WMW. H. Irwin McLean
W. H. Irwin McLean
IgE-mediated peanut allergy is a complex trait with strong heritability, but its genetic basis is currently unknown. Loss-of-function mutations within the filaggrin gene are associated with atopic dermatitis and other atopic diseases; therefore, filaggrin is a candidate gene in the etiology of peanut allergy. To investigate the association between filaggrin loss-of-function mutations and peanut allergy. Case-control study of 71 English, Dutch, and Irish oral food challenge-positive patients with peanut allergy and 1000 non peanut-sensitized English population controls. Replication was tested in 390 white Canadian patients with peanut allergy (defined by food challenge, or clinical history and skin prick test wheal to peanut ≥ 8 mm and/or peanut-specific IgE ≥ 15 kUL(-1)) and 891 white Canadian population controls. The most prevalent filaggrin loss-of-function mutations were assayed in each population: R501X and 2282del4 in the Europeans, and R501X, 2282del4, R2447X, and S3247X in the Canadians. The Fisher exact test and logistic regression were used to test for association; covariate analysis controlled for coexistent atopic dermatitis. Filaggrin loss-of-function mutations showed a strong and significant association with peanut allergy in the food challenge-positive patients (P = 3.0 × 10(-6); odds ratio, 5.3; 95% CI, 2.8-10.2), and this association was replicated in the Canadian study (P = 5.4 × 10(-5); odds ratio, 1.9; 95% CI, 1.4-2.6). The association of filaggrin mutations with peanut allergy remains significant (P = .0008) after controlling for coexistent atopic dermatitis. Filaggrin mutations represent a significant risk factor for IgE-mediated peanut allergy, indicating a role for epithelial barrier dysfunction in the pathogenesis of this disease.

1 December 2015 in Appetite
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Journal Article
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CTCaroline Taylor
Caroline Taylor
SWSusan Wernimont
Susan Wernimont
KNKate Northstone
Kate Northstone
PEPauline Marion Emmett
Pauline Marion Emmett
Picky eating (also known as fussy, faddy or choosy eating) is usually classified as part of a spectrum of feeding difficulties. It is characterised by an unwillingness to eat familiar foods or to try new foods, as well as strong food preferences. The consequences may include poor dietary variety during early childhood. This, in turn, can lead to concern about the nutrient composition of the diet and thus possible adverse health-related outcomes. There is no single widely accepted definition of picky eating, and therefore there is little consensus on an appropriate assessment measure and a wide range of estimates of prevalence. In this review we first examine common definitions of picky eating used in research studies, and identify the methods that have been used to assess picky eating. These methods include the use of subscales in validated questionnaires, such as the Children's Eating Behaviour Questionnaire and the Child Feeding Questionnaire as well as study-specific question(s). Second, we review data on the prevalence of picky eating in published studies. For comparison we present prevalence data from the UK Avon Longitudinal Study of Parents and Children (ALSPAC) in children at four time points (24, 38, 54 and 65 months of age) using a study-specific question. Finally, published data on the effects of picky eating on dietary intakes (both variety and nutrient composition) are reviewed, and the need for more health-related data and longitudinal data is discussed.