Jaakko Tuomilehto
Southampton General Hospital
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Featured researches published by Jaakko Tuomilehto.
Hypertension | 2000
Johan G. Eriksson; Tom Forsén; Jaakko Tuomilehto; Clive Osmond; D. J. P. Barker
The association between low birth weight and raised blood pressure has been extensively replicated. Little is known about the way childhood growth modifies the effects of low birth weight. We report on the fetal and childhood growth of 1958 men and women who received treatment for hypertension and belong to a cohort of 7086 people born in Helsinki, Finland, during 1924–1933. As expected, the men and women who developed hypertension had low birth weight (P =0.002). They were also shorter in body length at birth (P =0.02). After birth they experienced accelerated growth, so that by 7 years their heights and weights were approximately average. In a simultaneous regression, both birth length and tall height had statistically significant although opposing effects on hypertension (P =0.003 for birth length and 0.009 for height at 7 years). Accelerated postnatal growth was associated with better childhood living conditions. Children who later developed both hypertension and type 2 diabetes, rather than hypertension alone, had small placental size as well as small body size at birth, and their accelerated postnatal growth continued beyond 7 years. We suggest that hypertension may originate through retarded growth in utero followed by accelerated postnatal growth as a result of good living conditions. Retarded fetal growth leads to permanently reduced cell numbers in the kidney and other tissues, and subsequent accelerated growth may lead to excessive metabolic demand on this limited cell mass.
Stroke | 2000
Johan G. Eriksson; Tom Forsén; Jaakko Tuomilehto; Clive Osmond; D. J. P. Barker
BACKGROUND AND PURPOSEnA number of studies have shown that reduced intrauterine growth and low birth weight are associated with raised rates of fatal and nonfatal stroke in adult life. Whether this increased risk of stroke is modified by growth in childhood or by socioeconomic status in adult life is not known.nnnMETHODSnWe studied hospital admissions and deaths from stroke among 3639 men who were born in Helsinki University Central Hospital during 1924 to 1933. They had detailed records of their body size at birth, their growth through childhood, and their social circumstances as adults. Three hundred thirty-one of the men had had a stroke.nnnRESULTSnHazard ratios for stroke were related to low birth weight in relation to head circumference (P=0.005) and to short length in relation to head circumference (P=0.02). These associations were stronger for hemorrhagic than for thrombotic stroke. Men who developed stroke still had below-average stature at 7 years (P=0.05), but after 7 years their height caught up through accelerated growth. As adults they had low incomes and low social class (P<0.0001).nnnCONCLUSIONSnStroke may originate through reduced fetal growth, with low body weight and short body length at birth but sparing of head growth. Other studies suggest that this pattern of growth is associated with persisting elevation of blood pressure and raised plasma fibrinogen concentrations, 2 known risk factors for stroke. The risk of stroke is increased by accelerated growth in height during childhood. Accelerated growth has previously been linked to the development of hypertension in adult life. Stroke risk is further increased by adverse influences linked to low income.
The Proceedings of the Nutrition Society | 2005
Jaana Lindström; Markku Peltonen; Jaakko Tuomilehto
Currently, in many European countries more than half the adult population is overweight; it hass become abnormal to be of normal weight. The risk of type 2 diabetes, CVD, hypertension and certain forms of cancer increase with increasing weight. Biological evolution has produced body-fat-regulating mechanisms that are more powerful in protecting against weight loss than against weight gain. The current environment offers constant availability of affordable palatable energy-rich foods, with no need to consume the energy through physical activity. The obesogenic environment is to some extent a political issue, but it has been shown that the healthcare system can also have a role in preventing obesity-related morbidity. The Finnish Diabetes Prevention Study was the first controlled randomised study to show that individualised lifestyle counselling of individuals with high risk of developing type 2 diabetes can influence diet, physical activity and body weight, and that type 2 diabetes can be prevented, or at least postponed. Most importantly, lifestyle changes do not have to be extreme. If the population would adopt a lifestyle in line with the official nutrition recommendations, the obesity and diabetes trend could at least be stabilised.
WOS | 2016
Jaakko Tuomilehto; Peter Schwarz
There are a number of arguments in support of early measures for the prevention of type 2 diabetes (T2D), as well as for concepts and strategies at later intervention stages. Diabetes prevention is achievable when implemented in a sustainable manner. Sustainability within a T2D prevention program is more important than the actual point in time or disease process at which prevention activities may start. The quality of intervention, as well as its intensity, should vary with the degree of the identified T2D risk. Nevertheless, preventive interventions should start as early as possible in order to allow a wide variety of relatively low- and moderate-intensity programs. The later the disease risk is identified, the more intensive the intervention should be. Public health interventions for diabetes prevention represent an optimal model for early intervention. Late interventions will be targeted at people who already have significant pathophysiological derangements that can be considered steps leading to the development of T2D. These derangements may be difficult to reverse, but the worsening of dysglycemia may be halted, and thus the clinical onset of T2D can be delayed.
WOS | 2013
Jaakko Tuomilehto; Peter Schwarz; Jaana Lindström
The potential to prevent type 2 diabetes in high-risk individuals by lifestyle intervention was established in several clinical trials. These studies had a strong focus on increased physical activity and dietary modification as well as weight reduction among overweight participants. The key issue seems to be a comprehensive approach to correct several risk factors simultaneously. Furthermore, long-term follow-up studies of lifestyle interventions lasting for a limited time period seem to have a long-lasting carry-over effect on risk factors and diabetes incidence (Table 1).nnView this table:nnTable 1 nLong-term effectiveness of diabetes prevention trialsnnnnThe research evidence has inspired national and local authorities and health care providers all over the world to start programs and activities to prevent type 2 diabetes and its complications. Based on the experiences from the clinical trials, as well as from the “real world” implementation programs, the IMAGE (Development and Implementation of a European Guideline and Training Standards for Diabetes Prevention) Study Group collated information in a systematic manner. The IMAGE deliverables include a European evidence-based guideline for the prevention of type 2 diabetes, a toolkit for the prevention of type 2 diabetes in Europe, and the quality indicators for the prevention of type 2 diabetes in Europe.nnWhat is needed now is political support to develop national action plans for diabetes prevention. The prerequisites for successful prevention activities include involvement of a number of stakeholders on the governmental and nongovernmental level as well as on different levels of health care. Furthermore, structures to identify high-risk individuals and manage intervention, follow-up, and evaluation have to be established.nnObservational studies have provided firm evidence that multiple lifestyle-related factors either increase or decrease the risk of type 2 diabetes. Thus, in type 2 diabetes prevention, it is important to pay attention not only to one single factor such as obesity but …
Archive | 2001
Jaakko Tuomilehto; Jaana Lindström; Johan G. Eriksson; Timo T. Valle; Helena Hämäläinen; Pirjo Ilanne-Parikka; S. Keinanan-kiukaanniemi; Markku Laakso; Anne Louheranta; Merja Rastas; Virpi Salminen; Matti Uusitupa
Archive | 2016
Soumitra Ghosh; Carl D. LANGEFELDt; Peter S. Chines; Gunther Birznieks; Hong-Shi Kaleti; Joyce Tannenbaum; William Eldridge; Shane Shapi; Jennie Chang; Ben Shurtleff; Rachel Porter; Jillian BLASCHAK-HARVANt; Eva Tuomilehto-Wolft; Jaakko Tuomilehto; Richard N. BERGMANtt; H R. Hauser; Timo T. Valle; Victoria L. Magnuson; Delphine S. Ally; Kimmo Kohtamäki; Anjene Musick; Catherine Te; Colin Martin; Alyson Witt; Alistair So; Stina Kudelko; Arun Unni; Leonid Segal; Tuula Tenkula; Gabriele Vidgren
Archive | 2014
Peter Schwarz; Jaakko Tuomilehto
Archive | 2008
Jaakko Tuomilehto; Jaana Lindström
Archive | 2005
Karen L. Mohlke; Andrew D. Skol; Laura J Scott; Timo T. Valle; Richard N. Bergman; Jaakko Tuomilehto; Michael Boehnke; Francis S. Collins