6 Reasons Why Countries Like Denmark, Norway And Sweden Are The Happiest In The World

Scandinavian countries like Denmark, Norway and Sweden are at the top of the UN’s annual World Happiness Report, year after year after year. We would suggest moving there, but these are countries where temperatures in winter drop to around -20˚C!

So alternatively, we thought we’d try to figure out why they’re so happy and healthy. According to the UN, Scandinavians are also leading in terms of health, with regards to diet and exercise.

Here are the secrets to their health and happiness.

1. They have the perfect work-life balance.

Scandinavian Way Of Life

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Working on weekends is unheard of in these countries, and the idea is that everyone should get to have dinner with their family. In Norway, the average work week is only 34 hours! Swedes have 15 minute breaks built into their working schedules twice a day, where they can have a chat, go for coffee, or just relax. The idea being that it will make them more productive. Danes are extremely protective of their private time, and are known to refuse breakfast meetings and after work drinks.

2. They’re kind to themselves.

Scandinavian Way Of Life

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People in Denmark have a tradition known as “hygge” (pronounced “hooga”), which is “the practising of wellbeing towards yourself and others”. The term was actually coined in order to describe the need to escape the harsh Danish winters, but it can also apply to something that a person really loves doing, whether it’s snuggling up with a good book or having a nice dinner with a friend. The only condition is that the activity cannot be inconsiderate to others in any way.

3. Their diet consists of plenty of fish, root vegetables and berries.

Scandinavian Way Of Life

via CarrotMuseum

While the Mediterranean diet is considered to be the best in the world for heart health, the Nordic diet is a close second. Studies show that following this diet can reduce cholesterol considerably, and even boost weight loss. So what exactly does the Nordic diet entail? It consists of foods that are typically eaten in these countries, like oily fish, which is loaded with omega-3 fatty acids and protein, root vegetables like carrots, radishes, potatoes, etc. and several types of berries. Scandinavians are not big on red meat and animal fat, which is another plus for them.

4. They’re trusting people.

Scandinavian Way Of Life

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According to the Prosperity Index of 2014, 74% of Norwegians said they felt like they could trust others, while 83% of Swedes said that they trust their government to do right by them. Amazing, isn’t it? Several studies document a strong link between trust and happiness, where trust triggers the release of oxytocin, the hormone associated with love, happiness and bonding.

5. They spend plenty of time with nature.

Scandinavian Way Of Life

via Giphy

Scandinavian countries have several public access laws, which give anyone and everyone the right to walk, ride, camp and enjoy all land freely. Citizens enjoy vast, green, public spaces, spending plenty of time with nature. Studies show that spending time with nature increases happiness, memory, learning, mental health and heart health.

6. They have amazing healthcare services.

Scandinavian Way Of Life

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In these countries, if you need to see a doctor, you will be given an appointment that same day. All forms of treatment are free, although they are paid for indirectly in the form of extremely high taxes. But still, it could be worth it, if you consider the amazing services they get. When a woman gives birth to a baby for example, she is given an entire boxful of supplies, clothes and toys for her child!

Prostate Tops List of Most Inheritable Cancers.

One legacy that most men could do without is an inherited risk for prostate cancer, but a massive cohort study shows that for some men, genetic history hints at oncologic destiny.

Data on both identical (monozygotic) and fraternal (dizygotic) twins from the comprehensive birth-to-death registries in Denmark, Finland, Norway, and Sweden show that a man whose monozygotic twin has prostate cancer has a 32% risk for the disease himself, whereas a dizygotic twin whose brother has prostate cancer has only a 16% risk, said Jaakko Kaprio, MD, PhD, professor of genetic epidemiology at the University of Helsinki.

The estimated heritability of prostate cancer — the degree to which genes contribute to risk — was 58% (95% confidence interval, 52 – 63), which is the highest for any malignancy studied, Dr. Kaprio reported here at the American Society of Human Genetics 63rd Annual Meeting.

“These estimates for common cancers are greater than previously estimated. For rare cancers, such as testicular cancer, the concordance risk was substantial. We believe it provides an accurate estimate of familial risk prediction,” Dr. Kaprio toldMedscape Medical News.

Table. Cancers With Significant Heritability

Cancer Type Heritability Estimate, % 95% Confidence Interval
Prostate 58 52–63
Testicular 36 2–95
Breast 28 12–52
Kidney 23 11–42
Lung 25 12–44
Melanoma 39 8–81
Ovarian 28 15–47
Stomach 24 5–65
Uterine 24 14–87
Colon 16 2–63

The magnitude of the genetic contribution to prostate cancer found in this study is higher than the estimated 42% seen in a previous study of Nordic twins (N Engl J Med. 2000;343:78-85). Dr. Kaprio explained that this difference can be attributed to the fact that his team expanded the original cohort to include data from Norway, had 10 additional years of follow-up data, and had an aging cohort, with a resultant increase in incident cancers.

Dr. Kaprio’s team looked at data on 133,689 monozygotic and dizygotic pairs as part of the Nordic Twin Registry of Cancer. They used time-to-event analysis to estimate heritability and familial cancer risk.

What’s Going On?

This study raises important questions about the interplay between genetics and environment in cancer, said Richard Stevens, PhD, professor of cancer epidemiology at the University of Connecticut Health Center in Farmington.

“It’s a very strong study. The exciting thing about this study with prostate cancer is that it’s certainly saying something about mechanism that we don’t get,” he explained.

The study supports the presence of genetic polymorphisms in prostate cancer, and to a lesser degree breast cancer, that can cumulatively contribute to risk, he said.

“The specific polymorphisms we’re aware of — familial syndromes — account for very little breast cancer or prostate cancer. There are other genes where allelic variation and risk is moderate. There must be a lot of those genes with moderate risk; you put them together and it makes you more susceptible,” Dr. Stevens said.

Norway uses waste as eco-friendly fuel

Forget coal, oil, shale gas, even nuclear. The bin bag – full of your household waste – is becoming one of Norway’s fuels of choice.

Try to imagine the smell when a bin lorry passes you on the street on a hot summer’s day. Breathe it in through your nostrils. Stinks, doesn’t it? Now multiply it by a thousand.

That’s what it is like inside the largest energy recovery facility in Norway, the Klemetsrud plant. A vast concrete hall of waste. Tens of thousands of tonnes of rubbish piled up. The conveyor belts clunk and clank as more pours in. Bin lorries reverse towards the chutes and tip out more plastic bags of waste.

A huge industrial claw swoops down, its pincers reaching round a tonne of rubbish, picking it up and transporting it to the other end of the hall, where it is dropped. A cloud of white dust builds, and soon fills the hall. It is not good to stay in here too long.

This is where the waste thrown out by millions of households from Norway, Britain and elsewhere is turned into heat and electricity for the city of Oslo.

Cheap heating

The rubbish is pre-sorted. Everything that can be recycled is meant to have been taken out, but even then they are still left with more than 300,000 tonnes a year.

They do not see it as waste here – they see it as energy.

“Four tonnes of waste has the same energy content as one tonne of fuel oil,” says the director of the waste-to-energy agency in Oslo, Pal Mikkelsen.

“That means a lot of energy, and we use very little energy to transport it.”

One tonne of fuel oil, Mr Mikkelsen says, could heat a house for half a year. In other words, take just part of an English bin lorry’s maximum load picked up on the streets of Leeds or Bristol, turn it into energy here – and you can heat a home in Oslo for half a year.

The process is simple. The waste, tonne by tonne of it, is dropped into an incinerator. It soars to 850 degrees. Peeking through a small porthole of toughened glass, the fire burns bright orange with a fierce roar of flames.

Bags of waste delivered to Klemetsrud
Most of the waste is burned, but some can be recycled

Greener schools

Not everything is burned. Old tin cans and some mattress springs are left. At the end of the process they are left with ash, metal -which is recycled – and a lot of heat.

The heat boils water. The steam drives a turbine, which produces electricity. And the scalding water is piped off from the plant, to houses and public schools across Oslo.

Which means at Bjoernholt School the technical manager, Agnar Andersen, does not have to worry about fuel deliveries during the harsh Norwegian winter any more.

“We don’t have to think about fuel oils or fossil fuels. They are phasing out the last school this year with fossil fuels.”

At full capacity the plant will provide all the heat and electricity for Oslo’s schools and heat for 56,000 homes.

An environmentalist’s dream, you might have thought. Not necessarily, cautions the chair of Friends of the Earth Norway, Lars Haltbrekken.

“The overall goal from an environmental perspective should be to reduce the amount of waste, reuse what we can reuse, recycle, and then the fourth option is to burn it and use the energy.

“We have created such an overcapacity in these power plants in Norway and Sweden. We have made ourselves dependent on producing more and more garbage.”

Send us your rubbish

Norway waste-to-energy plant at Klemetsrud
Norway burns rubbish to get energy – and avoids resorting to landfill

Supporters disagree, and point out that, used together, all of Europe’s current waste-to-energy plants could only consume about 5% of the continent’s total annual landfill. Norway – they say – is actually helping to dispose of some of that waste in the best way possible.

That is certainly true in the case of the English cities Leeds and Bristol. Both export waste to Oslo. Rather than pay for it to go into landfill after the recyclable bits have been removed, they actually pay Oslo to take it off their hands.

So, Oslo is paid to dispose of the rubbish, and gets energy out of it as well.

The waste-to-energy revolution can also be heard on the streets of the Norwegian capital, as the number 144 bus rumbles past.

It is powered by biogas, created from the city’s decaying organic matter. One kilogramme of food waste produces half a litre of fuel. Use all of the organic waste they have and they will be able to power 135 buses year-round in Oslo.

If this whole project were repeated across Europe, Pal Mikkelsen believes it would make a huge difference.

“I think it would mean we get a lot better level of self-sustainability when it comes to energy. If it’s done properly it would also mean a lot more materials recovery. And a sharp decrease in the landfill.”

With tight controls to clean up the gases from the burning, Oslo believes converting waste into energy will help it to halve its carbon dioxide (CO2) emissions within 20 years – making a city, whose wealth was built on oil, one of the greenest on the planet.

A randomized, open-label study of sirolimus versus cyclosporine in primary de novo renal allograft recipients. .

Despite a decreased incidence of acute rejection and early renal allograft loss due to calcineurin inhibitors (CNIs) in transplant recipients, nephrotoxicity associated with long-term CNI use remains an important issue. This study evaluated whether a CNI-free regimen, including sirolimus, mycophenolate mofetil, corticosteroids, and anti-interleukin-2 receptor antibody induction, results in improved long-term renal function.

METHODS: This open-label, randomized, parallel group, comparative study in primary de novo renal transplant recipients was planned for 48 months but terminated early because of high acute rejection rates in the sirolimus arm.
RESULTS: Enrollment was stopped after approximately 12 months, with 475 transplanted patients randomized (2:1) to sirolimus (n=314) or cyclosporine A (CsA) treatment (n=161). Mean length of follow-up after transplantation was 190 days; this article focuses on available data through 6 months. Mean+/-SD on-therapy Nankivell-calculated glomerular filtration rate was not significantly different between the sirolimus (69.1+/-18.7 mL/min) and CsA (66.0+/-15.2 mL/min) treatment groups. Occurrence and length of delayed graft function was not significantly different between groups. Patients in the sirolimus group experienced numerically lower survival rates (96.9% vs. 99.4%; P=0.14), with nine deaths reported with sirolimus and one with CsA; higher rates of biopsy-confirmed acute rejection (21.4% vs. 6.1%; P<0.001); and higher rates of discontinuations due to adverse events (17.4% vs. 6.8%; P=0.001).
CONCLUSION: A sirolimus-based, CNI-free immunosuppressive regimen, when used with mycophenolate mofetil, corticosteroids, and anti-interleukin-2 receptor antibody induction, was associated with high rates of biopsy-confirmed acute rejection compared with CsA-based immunosuppression and is not recommended.

Source: Transplantation.


Mortality and causes of death in Crohn`s disease: results from 20 years of follow-up in the IBSEN study.

Population-based studies have shown a slightly decreased life expectancy in patients with Crohn`s disease (CD). The primary aim of the present study was to evaluate mortality and causes of death 20 years after the diagnosis in a well defined population-based cohort of CD patients in Norway.
DESIGN: The Inflammatory Bowel South-Eastern Norway study has prospectively followed all patients diagnosed with CD in the period between 1 January 1990 and 31 December 1993 in four geographically well-defined areas. All patients (n=237) were age and sex matched with 25 persons from the same county selected at random from the general population. Data on death and causes of deaths were collected from the Norwegian Causes of Death Register. All causes and cause-specific mortality (gastrointestinal cancer, cancer and heart disease) were modelled with Cox regression model stratified by matched sets. Results are expressed as HRs with 95% CIs.
RESULTS: There was no significant difference between CD patients and controls in overall mortality (HR=1.35, 95% CI 0.94 to 1.94, p=0.10). Furthermore, there were no marked differences in deaths from gastrointestinal cancer, other cancers or cardiovascular diseases in the CD group compared with the controls. In the CD group, 13.9% had died compared with 12.7% in the control group (p=0.578).
CONCLUSIONS: In our population-based inception cohort followed for 20 years, there was no increased mortality or more deaths from cancer compared with the general population.

Source: Gut

Basal metabolic rate can evolve independently of morphological and behavioural traits.

Quantitative genetic analyses of basal metabolic rate (BMR) can inform us about the evolvability of the trait by providing estimates of heritability, and also of genetic correlations with other traits that may constrain the ability of BMR to respond to selection. Here, we studied a captive population of zebra finches (Taeniopygia guttata) in which selection lines for male courtship rate have been established. We measure BMR in these lines to see whether selection on male sexual activity would change BMR as a potentially correlated trait. We find that the genetic correlation between courtship rate and BMR is practically zero, indicating that the two traits can evolve independently of each other. Interestingly, we find that the heritability of BMR in our population (h2=0.45) is markedly higher than was previously reported for a captive zebra finch population from Norway. A comparison of the two studies shows that additive genetic variance in BMR has been largely depleted in the Norwegian population, especially the genetic variance in BMR that is independent of body mass. In our population, the slope of BMR increase with body mass differs not only between the sexes but also between the six selection lines, which we tentatively attribute to genetic drift and/or founder effects being strong in small populations. Our study therefore highlights two things. First, the evolvability of BMR may be less constrained by genetic correlations and lack of independent genetic variation than previously described. Second, genetic drift in small populations can rapidly lead to different evolvabilities across populations.

Source: http://www.nature.com

Improving antibiotic prescribing in acute respiratory tract infections: cluster randomised trial from Norwegian general practice (prescription peer academic detailing (Rx-PAD) study).


Objective To assess the effects of a multifaceted educational intervention in Norwegian general practice aiming to reduce antibiotic prescription rates for acute respiratory tract infections and to reduce the use of broad spectrum antibiotics.

Design Cluster randomised controlled study.

Setting Existing continuing medical education groups were recruited and randomised to intervention or control.

Participants 79 groups, comprising 382 general practitioners, completed the interventions and data extractions.

Interventions The intervention groups had two visits by peer academic detailers, the first presenting the national clinical guidelines for antibiotic use and recent research evidence on acute respiratory tract infections, the second based on feedback reports on each general practitioner’s antibiotic prescribing profile from the preceding year. Regional one day seminars were arranged as a supplement. The control arm received a different intervention targeting prescribing practice for older patients.

Main outcome measures Prescription rates and proportion of non-penicillin V antibiotics prescribed at the group level before and after the intervention, compared with corresponding data from the controls.

Results In an adjusted, multilevel model, the effect of the intervention on the 39 intervention groups (183 general practitioners) was a reduction (odds ratio 0.72, 95% confidence interval 0.61 to 0.84) in prescribing of antibiotics for acute respiratory tract infections compared with the controls (40 continuing medical education groups with 199 general practitioners). A corresponding reduction was seen in the odds (0.64, 0.49 to 0.82) for prescribing a non-penicillin V antibiotic when an antibiotic was issued. Prescriptions per 1000 listed patients increased from 80.3 to 84.6 in the intervention arm and from 80.9 to 89.0 in the control arm, but this reflects a greater incidence of infections (particularly pneumonia) that needed treating in the intervention arm.

Conclusions The intervention led to improved antibiotic prescribing for respiratory tract infections in a representative sample of Norwegian general practitioners, and the courses were feasible to the general practitioners.


The main effects of this study of a prescription peer academic detailing intervention (Rx-PAD) were a decrease in overall prescription rates for antibiotics for acute respiratory tract infections and, in particular, an increased use of the narrow spectrum agent penicillin V when an antibiotic was issued.

Whereas reductions were seen in the intervention arm, both prescription rates and proportions of non-penicillin V antibiotics increased in the control arm. The greater increase in the number of episodes of acute respiratory tract infections in the intervention arm after intervention compared with the control arm could have affected the prescription rates if the diagnostic drift mainly tended towards diagnoses with a low prescribing rate; however, we found no evidence of this. The general practitioners in the intervention arm would probably have had greater awareness of acute respiratory tract infection diagnoses as a consequence of the intervention and therefore have recorded them more often.

As measured by unadjusted means (table 2), the change in total antibiotic prescribing rate was relatively small and its clinical significance may be debatable. However, the reduction in prescribing of broad spectrum antibiotics was substantial and of clinical importance because of the reduction in promoting resistance. The adjusted outcome measures show a more consistent effect of the intervention, with odds ratios of 0.72 and 0.64, and are closer to the effect estimates of the study.

The larger effects on antibiotic treatment for acute bronchitis and acute sinusitis were intentional, as parts of the intervention focused on the overuse of antibiotics for these diagnoses. Another topic particularly covered in the intervention was the overuse of macrolides. A major part of the increase in the proportion of penicillin V can be explained by a decrease in use of this antibiotic group.

The control arm received another intervention, and the mere participation in a course could possibly have affected the outcome of antibiotic prescribing, although the topic of antibiotic use was not part of the control arm course. However, we found no indication of such effects when we compared the distribution of different prescribed antibiotics typically used for acute respiratory tract infections in the control arm with the total sales in Norway for the same period.

When we were planning this study, the hypothesis was that an improvement in prescription behaviour could be obtained in a group setting where the participants knew each other well and were used to discussing challenging topics related to their own clinical practices. In the continuing medical education group setting, each participant was confronted with, and had to reflect on, the baseline report on their own prescription practice. We believe that this was a key component for obtaining improved prescription habits.

We had an expectation of greater effects of the intervention among the general practitioners with the highest baseline prescribing rates, but this was not the case. Whether the effect of such an intervention would be higher in countries with high prescribing is not easy to predict from our data.

Source: BMJ

No Need for Screening Echocardiogram in Asymptomatic Adults, Study Confirms.

Echocardiographic screening for structural and valvular heart disease in the general population does not reduce mortality, according to a JAMA Internal Medicine study. The finding, the authors say, “supports existing guidelines that echocardiography is not recommended … in asymptomatic adults.”

In a population-based study, nearly 7000 middle-aged adults in Norway were randomized to screening echocardiography or usual care. About 9% of the screening group had abnormal echo results that required additional testing.

During 15 years’ follow-up, the primary endpoint — all-cause mortality — did not differ significantly between the groups. Secondary outcomes, including sudden death, death from heart disease, and myocardial infarction, also did not differ.

In a subgroup of participants with a family history of early MI, screening appeared to reduce all-cause mortality (number needed to screen to prevent 1 death, 21) — a novel finding that the authors say warrants confirmation.

Source: JAMA

Pre-eclampsia and the risk of kidney disease.

Worldwide, about 2—8% of pregnancies are complicated by pre-eclampsia, a disorder that is characterised by new-onset hypertension and proteinuria after 20 weeks of pregnancy.1 Pre-eclampsia is associated with risk of adverse fetal outcomes and can progress to severe pre-eclampsia, eclampsia, or death if not diagnosed and treated with delivery. Substantial progress in understanding the pathophysiological mechanisms of the disease has been made in recent years, and changes in concentrations of soluble fms-like tyrosine kinase 1 and other angiogenic factors seem to be key.2 However, mechanisms behind pre-eclampsia and development of acute kidney injury and chronic kidney disease in the mother are less well understood and warrant further discussion.


Although acute kidney injury caused by pre-eclampsia or eclampsia is rare in high-income countries, it complicates 2% of third-trimester pregnancies in India, for example, with pre-eclampsia accounting for 36% of cases (ie, pre-eclampsia associated with acute kidney injury might occur in one of 150 pregnancies).3 Dialysis might be required in up to 50% of cases, and when not available, acute kidney injury is a frequent cause of maternal death. Other major causes of acute kidney injury associated with pregnancy in developing countries include sepsis and major bleeding, whereas less common disorders such as primary renal disease, thrombotic thrombocytopenic microangiopathy, or acute fatty liver of pregnancy are probably relatively more common in developed countries. Although most women with acute kidney injury in pregnancy recover renal function, 7—29% do not fully recover, which can have serious long-term outcomes.34 However, few high-quality studies have assessed the cause, prevalence, and prognosis of acute kidney injury in pregnancy, and more studies are needed to inform strategies for prevention, treatment, and follow-up.

Despite several small studies showing recovery of renal function after so-called pure pre-eclampsia,4 a population-based study from Norway suggested that women who had had pre-eclampsia were at a four-to-five-times increased risk of development of end-stage renal disease during a follow-up of 35 years.5 The risk was significant after exclusion of women with known kidney disease, diabetes, hypertension, or rheumatic disease before pregnancy. Other studies67 showed that pre-eclampsia was a significant risk marker for development of kidney disease, requiring a diagnostic kidney biopsy, but that previous pre-eclampsia was not associated with rapid progression of established kidney disease to end-stage renal disease, suggesting that pre-eclampsia is more strongly associated with the development of kidney disease than with subsequent progression. A Taiwanese study8 also noted an increased risk of chronic kidney disease and end-stage renal disease in women with previous pre-eclampsia. In line with these findings, a meta-analysis concluded that women with previous pre-eclampsia had a four-times increased risk of microalbuminuria 5—10 years after a pre-eclamptic pregnancy compared with women without previous pre-eclampsia.9 This meta-analysis was, however, restricted by inclusion of small studies of variable quality and most of the women either had severe pre-eclampsia or underlying disease such as diabetes mellitus. Associations between pre-eclampsia and subsequent microalbuminuria, which suggest renal injury resulting from pre-eclampsia, need to be verified in large population-based studies.

How pre-eclampsia predisposes to an increased risk of renal disease is not well understood. The issue is complicated by the strong association between pre-eclampsia and cardiovascular risk factors, which also increase risk of kidney disease. That pre-eclampsia might induce primary renal injury is, however, supported by reports that the risk of kidney disease and microalbuminuria after pre-eclampsia seems to be greater than the risk of cardiovascular disease.5910 In addition, much the same increase in risk was noted for all types of kidney disease after pre-eclampsia,56 underscoring the hypothesis that a primary renal insult, possibly mediated by extensive endothelial or podocyte injury,11 induces nephron loss and contributes to progression of renal disease. The strong clinical similarity between pre-eclampsia and underlying kidney disease also complicates these studies, because the clinical presentations can be almost identical, especially in multiparous women.12

Developmental and genetic factors are also important determinants of pre-eclampsia risk (as discussed in the accompanying Series), and might themselves be independent risk factors for renal disease. Men and women born in pre-eclamptic pregnancies are at an increased risk of fathering or bearing pre-eclamptic pregnancies, respectively,13 and women born with low birthweight had a 1·5-fold increased risk of pre-eclampsia.14 This intergenerational transfer of risk might suggest genetic predisposition, perinatal programming, or socioeconomic factors, the last of which is an independent risk factor for pre-eclampsia, especially in developing countries.15

Pre-eclampsia is probably an important cause of acute kidney injury and an important risk marker for subsequent chronic kidney disease. Women with previous pre-eclampsia should receive long-term follow-up, especially with respect to hypertension, insulin resistance, and obesity. However, pre-eclampsia might also unmask underlying primary renal disease, and women with pre-eclampsia should be monitored for proteinuria and hypertension within 6—8 weeks of delivery and have a nephrological work-up if these disorders do not resolve.


1 Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-eclampsia. Lancet 2010; 376: 631-644. Summary | Full Text |PDF(865KB) | CrossRef | PubMed

2 Levine RJ, Maynard SE, Qian C, et al. Circulating angiogenic factors and the risk of preeclampsia. N Engl J Med 2004; 350: 672-683. CrossRef | PubMed

3 Prakash J, Niwas SS, Parekh A, et al. Acute kidney injury in late pregnancy in developing countries. Ren Fail 2010; 32: 309-313.CrossRef | PubMed

4 Sibai BM, Villar MA, Mabie BC. Acute renal failure in hypertensive disorders of pregnancy. Pregnancy outcome and remote prognosis in thirty-one consecutive cases. Am J Obstet Gynecol 1990; 162: 777-783. CrossRef | PubMed

5 Vikse BE, Irgens LM, Leivestad T, Skjaerven R, Iversen BM. Preeclampsia and the risk of end-stage renal disease. N Engl J Med2008; 359: 800-809. CrossRef | PubMed

6 Vikse BE, Irgens LM, Bostad L, Iversen BM. Adverse perinatal outcome and later kidney biopsy in the mother. J Am Soc Nephrol2006; 17: 837-845. CrossRef | PubMed

7 Vikse BE, Hallan S, Bostad L, Leivestad T, Iversen BM. Previous preeclampsia and risk for progression of biopsy-verified kidney disease to end-stage renal disease. Nephrol Dial Transplant 2010; 25: 3289-3296. CrossRef | PubMed

8 Wang IK, Muo CH, Chang YC, et al. Association between hypertensive disorders during pregnancy and end-stage renal disease: a population-based study. CMAJ 2013; 185: 207-213. CrossRef | PubMed

9 McDonald SD, Han Z, Walsh MW, Gerstein HC, Devereaux PJ. Kidney disease after preeclampsia: a systematic review and meta-analysis. Am J Kidney Dis 2010; 55: 1026-1039. CrossRef | PubMed

10 Bellamy L, Casas JP, Hingorani AD, Williams DJ. Pre-eclampsia and risk of cardiovascular disease and cancer in later life: systematic review and meta-analysis. BMJ 2007; 335: 974. CrossRef | PubMed

11 Garovic VD, Wagner SJ, Turner ST, et al. Urinary podocyte excretion as a marker for preeclampsia. Am J Obstet Gynecol 2007;196: 320. PubMed

12 Fisher KA, Luger A, Spargo BH, Lindheimer MD. Hypertension in pregnancy: clinical-pathological correlations and remote prognosis. Medicine (Baltimore) 1981; 60: 267-276. PubMed

13 Skjaerven R, Vatten LJ, Wilcox AJ, Ronning T, Irgens LM, Lie RT. Recurrence of pre-eclampsia across generations: exploring fetal and maternal genetic components in a population based cohort. BMJ 2005; 331: 877. CrossRef | PubMed

14 Rasmussen S, Irgens LM. Pregnancy-induced hypertension in women who were born small. Hypertension 2007; 49: 806-812.CrossRef | PubMed

15 Nanjundan P, Bagga R, Kalra JK, Thakur JS, Raveendran A. Risk factors for early onset severe pre-eclampsia and eclampsia among north Indian women. J Obstet Gynaecol 2011; 31: 384-389. CrossRef | PubMed

Source: Lancet

Mediators of the association between pre-eclampsia and cerebral palsy: population based cohort study.


Objective To test the hypothesis that pre-eclampsia is a risk factor for cerebral palsy mediated through preterm birth and being born small for gestational age.

Design Population based cohort study.

Setting Clinical data from the Norwegian Cerebral Palsy Registry were linked with perinatal data prospectively recorded by the Medical Birth Registry of Norway.

Participants All singleton babies who survived the neonatal period during 1996-2006 (849 children with cerebral palsy and 616 658 control children).

Main outcome measures Cerebral palsy and cerebral palsy subtypes.

Results Children exposed to pre-eclampsia had an excess risk of cerebral palsy (unadjusted odds ratio 2.5, 95% confidence interval 2.0 to 3.2) compared with unexposed children. Among children born at term (≥37 weeks), exposure to pre-eclampsia was not associated with an excess risk of cerebral palsy in babies not born small for gestational age (1.2, 0.7 to 2.0), whereas children exposed to pre-eclampsia and born small for gestational age had a significantly increased risk of cerebral palsy (3.2, 1.5 to 6.7). Non-small for gestational age babies born very preterm (<32 weeks) and exposed to pre-eclampsia had a reduced risk of cerebral palsy compared with unexposed children born at the same gestational age (0.5, 0.3 to 0.8), although the risk was not statistically significantly reduced among children exposed to pre-eclampsia and born small for gestational age (0.7, 0.4 to 1.3). Exposure to pre-eclampsia was not associated with a specific cerebral palsy subtype.

Conclusions Exposure to pre-eclampsia was associated with an increased risk of cerebral palsy, and this association was mediated through the children being born preterm or small for gestational age, or both. Among children born at term, pre-eclampsia was a risk factor for cerebral palsy only when the children were small for gestational age.


In this study we found that pre-eclampsia was associated with an increased risk of cerebral palsy and that the excess risk was mainly mediated through preterm birth, but also through being born small for gestational age. Exposed children born at term as non-small for gestational age did not have an excess risk of cerebral palsy and we did not find that a specific cerebral palsy subtype was more common in children exposed to pre-eclampsia than not exposed. Thus we were not able to find evidence for a direct effect of pre-eclampsia on the risk of cerebral palsy.

What is already known on this topic

  • Pre-eclampsia is a frequent cause of preterm birth and being born small for gestational age, both of which are known risk factors for cerebral palsy
  • Observational studies have shown conflicting results with respect to whether pre-eclampsia is a risk factor for cerebral palsy
  • Pre-eclampsia is a risk factor for cerebral palsy mainly mediated through preterm birth and being small for gestational age
  • Among term born children exposed to pre-eclampsia only those born small for gestational age had an excess risk of cerebral palsy
  • Pre-eclampsia was not associated with specific subtypes of cerebral palsy

What this study adds


Source: BMJ


Hydropower In Norway.