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Want to be fit at forty? Don’t have a baby early!

Having a family early may not be good for your health later on. That was the conclusion of a team of researchers at the ESRC International centre for Lifecourse Studies when they looked at the interplay between the work and family lives of men and women, whose lives have been tracked over time in the 1958 Birth Cohort Study. But was it the same story for people born earlier and has it been the same for people who were born later? Dr Rebecca Lacey, who led the research, has been looking at the lives of thousands of adults in three Birth Cohort Studies to see whether the way their work and family lives intertwine impacts on the likelihood of them becoming overweight or obese later on.

In a recent blog for WorkLife, my colleague Anne McMunn outlined some of our research showing that, for both men and women, having children early, especially as a teenager, was closely linked with poorer health once they got into their forties.

Not only did the people we looked at for that piece of research have bigger waists, but they also had a great deal more fat circulating in their blood and less ‘good’ cholesterol, both of which are linked with a heightened risk of heart disease and diabetes.

Those findings stayed strong, even for young parents who had a job and were married, a clear indication that having children early on, with all the associated stresses and strains, seems to take a heavy toll on health over the life course.

For that piece of research, we looked only at people who had taken part in the National Child Development Study, also known as the 1958 Birth Cohort. For this research we looked, in addition at thousands more people, born in 1946 (National Survey of Health and Development) and another group born in 1970 (the British Cohort Study) whose lives had been tracked since birth.

Across cohorts

The reason for looking across cohorts was to see whether changes across generations in how we combine work and family (having children later, more cohabitation and less marriage, more women working etc.) have contributed in some way towards poorer health for some.

As with the earlier research, we made use of 12 specially created lifecourse types covering information on employment, partnerships and parenthood, such as ‘Work, Later family’ ‘Later family, Work break’, ‘Teen parent’.

Each individual in each birth cohort was ascribed a lifecourse type and this was then linked to their Body Mass Index (BMI) and how that changed over time. We went on to see how those figures differed between lifecourse types within and across the three cohorts. We used the World Health Organisation’s (WHO) definition of overweight (BMI greater than or equal to 25) and obesity (BMI greater than or equal to 30).

In addition, we took a host of other factors including our participants’ socio-economic background, prior health and educational attainment into consideration.

We anticipated that, as our earlier research had shown, that people who worked less and had children earlier would show steeper increases in BMI and that across the three cohorts, those increases would become more pronounced.

Changing attitudes and behaviours

The distribution of lifecourse types across the three cohorts reflected, as we thought it would, changing attitudes and behaviours across generations, with increasingly more women in employment and early parenthood becoming less and less common.

In the 1946 cohort, the average BMI of a very small group of men who were ‘Teen parents’ increased from 20.3 to 26.76 between age 16-42, significantly more than any other work-family combination. The same was true for male teen parents in the 1958 cohort and also for those who worked and had a family early. In the 1970 cohort, men who had no children or had children later had BMI that increased significantly less than those who became parents earlier. The only exception to this was a group of men with no family and unstable work.

Another notable finding across all three cohorts was that average BMIs for men at age 42 in all of the work-family groups were higher than the WHO threshold for overweight. The only exception was men who had children later or no children at all.

For women in the 1946 study, there was no real difference between the groups when we looked at how their BMI increased between the ages of 16 and 42. The average BMI of the 1958 cohort women who had children early increased significantly more than that of women who had them later. Women in the 1970 cohort who did not work and had children early had the biggest BMI rise (6.69) with teen parents (6.31) close behind. The average BMI of the 42 year-old women in these two groups was on the WHO obesity threshold (30), with the average BMI for the remaining work-family groups all falling under the WHO definition of overweight (25 and above).

Other interesting things to emerge included:

  • BMI increased more for male teen parents than female in the 1970 cohort
  • Marriage seems to have particular health benefits for men
  • Divorce has greater negative health effects for men than women

Negative impact

This research reinforces what we found earlier, which is that for both men and women having children early (especially in your teens) no matter what your background, is likely to have a negative impact on your health in mid life, especially if you don’t have a job or if your work is irregular or unstable. Looking across three cohorts, we can also see that those differences have become more pronounced.

How to explain and better understand how all this plays out in the day to day lives of younger parents is a challenge. Having children early may disrupt someone’s education or career. Younger parents may also be more likely to smoke and drink and exercise less than their older counterparts, unhealthy behaviours which can become established early and set in across adulthood.

Whatever the context and the reasons, there are some important messages here for young people, prospective parents, health and education professionals as well as for Government; not least that decisions about how to combine work and family life, especially when to become a parent, may have long lasting ramifications for your health.

This research adds to a growing body of evidence which makes it clear that, as far as obesity is concerned, early intervention is key and that we need to consider the complex way in which our biological and social lives intertwine over time.

Further information

Work-family life courses and BMI trajectories in three British birth cohorts is research by Rebecca Lacey, Amanda Sacker, Steven Bell, Meena Kumari, Diana Worts, Peggy McDonough, Diana Kuh, and Anne McMunn. It is published in the International Journal of Obesity.

Photo credit: Baby Fingers, Thomas

Can unemployment kill – Podcast

Our first blog showcased recent research from the team at ESRC International Centre for Lifecourse Studies about the links between long term unemployment and stress markers linked to killer diseases. If you were interested in that, you can also listen on Soundcloud to researcher Amanda Hughes discussing the research for the ICLS Podcast.

Can unemployment kill?

At the height of the recent recession around 2.7 million people were unemployed, and youth unemployment accounted for nearly 40 per cent of that total. Given growing evidence that unemployment is linked to long term illness and increased mortality, we can expect health implications for those affected. In a week when unemployment rose for the first time in over a year, Amanda Hughes presents new evidence from the ESRC International Centre for Lifecourse Studies on the links between unemployment and killer diseases such as heart disease.

In 1984 a study was published which had linked census data to mortality records and found that men unemployed in the week of the 1971 census were 36 per cent more likely to have since died than men of the same age who had been in work. Accounting for differences in social background only explained part of the excess, raising the question: can unemployment kill, and if so how?

That unemployment might damage health was not a new idea. Marie Jahoda’s research on unemployment in the 1930s had shown that the non-financial benefits of work, such as defining aspects of status and identity and providing regular social contact, are for many people crucial to mental wellbeing. And since job loss usually brings a sharp drop in income, it is intuitive that unemployment could affect physical health by reducing quality of diet or opportunities for exercise.

But there tends to be more scepticism as to whether serious physical illness or mortality could be causally influenced by the undoubtedly stressful experience of unemployment. Might those unemployed men have developed serious illness when employed, lost their jobs as a result, and then died from their illness? Or might their increased mortality simply be caused by unemployed people smoking and drinking more? In neither case could it be claimed that unemployment itself has caused any deaths.

New approach

Since the 1980s, the tools available to scientists researching the health impacts of social conditions have moved on considerably. One new approach involves molecules called ‘inflammatory markers’ which circulate in the bloodstream and appear to be influenced by stressful experiences.

Elevated concentrations have been found in the recently bereaved and caregivers; inflammatory markers are also typically higher for people of disadvantaged socioeconomic position as measured by income or occupational social class. Crucially, raised concentrations of these molecules are linked to atherosclerosis and predict heart disease, presenting a possible causal pathway between a stressful social environment and increased mortality.

It was for this reason that we wanted to see if two inflammatory markers – C-reactive protein and fibrinogen – were elevated in jobseekers compared to employed counterparts.

We used the Health Survey for England and Scottish Health Survey, annual government surveys used to track changes in the health of both countries’ populations. To isolate elevations in these molecules due to unemployment-related stress, we considered a number of additional factors beyond participants’ age and gender.

To rule out elevations due to serious illness predating job loss, we considered whether participants had a long-term illness of any type. To rule out elevations caused by disadvantaged socioeconomic position more generally, we took into account housing tenure and occupational social class from current or most recent job.

Finally, to test whether elevations might be explained by worse health-related behaviours of jobseekers, we took into account participants’ smoking, alcohol consumption and body mass index.

Stress markers

In our sample of over 23,000 men and women of working age, unemployed people had elevated circulating levels of both molecules even after consideration of these factors. These differences were moreover clinically relevant, since unemployed participants were 40 per cent more likely to have C-reactive protein over 3mg/L, the level at which cardiovascular risk becomes elevated.

Effects were not uniform across the population. Firstly, older jobseekers (48-64) were more affected than younger jobseekers. This might indicate that unemployment is more stressful for jobseekers facing age discrimination, or equipped with outdated skills.

Since older jobseekers will have accumulated more unemployment over their lifetimes than younger counterparts, it could alternatively indicate that long-term or repeated unemployment is especially damaging to this aspect of health.

Secondly, we found substantial differences in results by country, with much greater elevations in both molecules for jobseekers in Scotland than in England. Data from the Labour Force Survey and the British Household Panel Study show that during the years of data collection (1998-2010) unemployment was higher in Scotland than England, and unemployment spells on average longer, which suggests two possible explanations.

Firstly, the jobseekers in Scotland may have been unemployed for longer, or had more recent unemployment spells, than English counterparts. Secondly, unemployment could be more stressful in times and places where the background rate is higher, since jobseekers will rationally perceive their prospects for re-employment as worse.

Since these surveys only collect information from people at one point in time, it was not possible in this analysis to investigate effects in the context of people’s employment histories. But unpicking these explanations will be crucial if we are to better understand the conditions under which unemployment is most likely to damage health, and which groups are most at risk.

Crucially, given last week’s news of a 21,000 rise in unemployment for the first time in a year  to 1.7 million people, policy makers interested in the long term health of the population should not divert their gaze from its wider consequences.

Photo credit: Kate Hiscock

Further information

Amanda Hughes is a Senior Research Officer at the Institute for Social and Economic Research at the University of Essex.

Elevated inflammatory biomarkers during unemployment: modification by age and country in the UK is research by Amanda Hughes, Anne McMunn, Mel Bartley and Meena Kumari and is published in the Journal of Epidemiology and Community Health.

References

Unemployment and mortality in the OPCS Longitudinal study is research by K.A Moser, A.J Fox, and D.R. Jones, and is published in the Lancet.

Unemployment durations: evidence from the British Household Panel Survey is research by K. Long and is published in Economic & Labour Market Review.