What is the impact of underweight on self-reported health trajectories and mortality rates: a cohort study

Being thin is an ideal embedded in Western culture [1], but is it healthy? Being thin or underweight (i.e. BMI <18.5 kg/m²) is not necessarily a negative characteristic [2–4]. It constitutes a rather complex group, since people can have a low BMI for a number of reasons: It can be the result of healthy living (e.g. healthy diet and exercise), but it may also apply to individuals with eating disorders or be due to malnutrition or weight loss due to clinical or sub-clinical disease [5–7].

Underweight can potentially by itself lead to adverse health effects such as higher disease burden, it affects the outcome for several medical conditions, and it is a known risk factor for older people (>65 years) [8–15]. Weight loss is another factor known to have a potential negative effect on health [16–20]. Even a modest decline in body weight is a known risk of mortality in older adults [21]. It has been shown how body weight declines three to 5 years before cardiovascular deaths [22]. It is known that Individuals with eating disorders have significantly elevated mortality rates [23], and these conditions have a severe impact on the patient’s health-related quality of life [24]. However, it remains unanswered how these outcomes are affected by low BMI in a general population and whether this risk changes when people grow older.

Our intention was to examine how body mass affected two different aspects of health: Mortality, which concerns survival, and self-rated health (SRH), which is a person’s general assessment of his/her own health and health-related quality of life. SRH is associated with a broad range of objective health outcomes, including mortality [25], subclinical and clinical disease [26], and health service use [27]. Since being thin can also be beneficial for health, it is of interest to investigate whether the SRH benefits at some point in life outweigh the disadvantages of very low body mass. We thus wanted to examine the relationship between underweight (i.e. BMI <18.5 kg/m²), SRH and mortality.

Our aim was to estimate the independent effects of BMI on mortality and SRH from youth and estimate whether any independent effects change as people grow older. The design and comprehensive database of the Tromsø Study allowed us to examine the relationship between body weight and SRH throughout life in the general population, including the impact of a broad range of other health-related factors. The Tromsø Study (TS) consisted of six repeated population health examinations carried out in 1974 (TS1), 1979-80 (TS2), 1986-87 (TS3), 1994-95 (TS4), 2001 (TS5), and 2007-08 (TS6). The six surveys had the same general design. Based on the official population registry, residents of the municipality of Tromsø were invited to take part in the survey. The aim was to include large, representative samples of the Tromsø population, with the invitation of entire birth cohorts and random samples. The attendance rate was high (66-75%). In all surveys, a questionnaire was enclosed in the invitation. Over the years, the questionnaires were expanded to include questions about a wide range of diseases and symptoms, dietary habits, other lifestyle aspects, use of medication, sleeping patterns, socio-economic status, and use of health care services. The physical examination consisted of blood samples and measurements of blood pressure, height and weight [28]. SRH was introduced in 1986.

Variables

The participants completed well-validated questionnaires that included questions on a broad range of diseases, symptoms, health behavior, social conditions, education, and level of physical activity [28]. Outcomes of interest were SRH and all-cause mortality. SRH was reported by answering the survey question ‘What is your current state of health?’ in a range from Poor (1) to Very Good (4). Time of death was retrieved from the Norwegian National Causes of Death Registry. The degree of coverage of the registry is near-complete [30].

BMI and age were the independent variables of interest. The conceptual model was that BMI has an effect on SRH that is moderated by age (Fig. 1). The other variables were treated as confounders for the sake of the presentation. Age was registered at attendance. Specially trained personnel took non-fasting blood samples and measured blood pressure (SBP/DBP), resting heart rate (RHR), body weight and height. Comorbid diseases were self-reported specific medical conditions. We selected 13 symptomatic medical conditions reported in all panels. These were psoriasis, food allergies, chronic bronchitis, migraine, ulcer, asthma, thyroid disease, arthritis, myocardial infarction, cerebrovascular stroke, diabetes, osteoporosis, and angina, which all have a varied impact on SRH. We therefore utilized the Health Impact Index (HII) to measure the comorbid conditions. HII classifies patients with comorbid disease according to the impact that each condition has on SRH by assigning a weight to each condition. HII equals the total score of each condition of the participant. HII thus considers both the severity and joint effects of the conditions [31].

Mental distress was based on well validated self-report symptom inventories comprising questions representative of the symptom configurations of anxiety and depression commonly observed among outpatients. Each answer is scored from 1 to 4. The measurement is the average score. The mental health index (CONOR-MHI) was used at TS4. In the following surveys (TS5-6), the Hopkins Symptom Checklist (HSCL) was used [32]. The CONOR-MHI has been compared with the HSCL with reasonably good agreement. It was highly correlated with HSCL-10 (r = 0.8). A cut-off level of 2.15 for significant symptoms is equivalent to the 1.85 level in HSCL-10 [33]. We standardized the variable for better longitudinal comparison in the regression model. TS3 did not include any validated mental health measures and these were coded as missing.

Physical exercise in leisure time was measured by answers to ‘How often do you exercise?’, categorized as inactive (0), light (1), moderate (2-3), and intensive (3-7) physical activity. This scale has been widely used in Scandinavian studies, and physical activity levels have been correlated with physical fitness [34].

This study shows that SRH changed with increasing age, but age affected the thinnest subjects more than all others. Underweight was associated with a higher mortality risk, and weight change increased this risk. Several authors argue that the health consequences of being underweight might be more severe in terms of premature mortality and quality of life, compared to being overweight [8–10, 16–18, 36–38]. Although being thin is an ideal, and despite the general advice for obese people to lose weight, our study indicates that being thin could in itself represent a health risk later in life. Inverse probability weighting (IPW) showed that loss to follow-up did not significantly affect this result, which supports the causal claim that being thin drives the later decline. It is interesting that normalizing the weight resulted in fewer comorbid conditions and lower mortality rates, and yet, lower SRH. SRH is strongly associated with biological factors, however, it is also known to be sensitive to factors such as coping skills, as well as mental distress, and social context [39]. One plausible explanation could be that general health advice is focused on losing weight, while normalizing the weight for underweight persons will imply gaining weight. This study cannot answer questions regarding health beliefs, but this could be addressed using qualitative methods.

Previous studies have shown that persons with BMI of <18.5 kg/m² and ≥30 kg/m² report impaired quality of life and SRH [40, 41]. Our study shows that this depends on age. Having a BMI above 30 kg/m² was never beneficial for SRH as compared to the normal BMI range, while those with BMI below 18.5 kg/m² started out with more beneficial levels but had a far more negative SRH trajectory as age increased. For underweight subjects, we see a positive gap in SRH scores compared to the other categories, but they fell more rapidly with age. Consequently, a low BMI was slightly beneficial at a young age, but it represented an increasingly negative factor with age, passing below the reference category at age 38 and even below the trajectory of obese subjects at age 67 in the fully fitted model.

Previous studies have shown that subjects who reported being obese in young adulthood only or in both young and middle adulthood experienced mortality rates that were 40%–90% higher than those subjects who were non-obese at either time [42]. Our study showed a similar association, but even higher rates for those who were very thin, with a 69% higher all-cause death risk (1.69, 95% CI: 1.38-2.06) as compared to only 12% for obese subjects (1.12, 95% CI: 1.02-1.23). The estimate is based on the baseline BMI at study entry. It indicates that starting as thin represented a mortality risk even though the body weight may change later in life, and although reaching a normal weight was beneficial for them.

The most underweight subjects were females among the youngest (<30 years) and oldest (>70 years) subjects. This is consistent with the difference we found between the group that started out as underweight and those who ended up as underweight. A Swedish study concluded that persons aged 75-90 who were overweight had a lower mortality risk than old persons with a BMI below 25 [43]. This is consistent with our findings for persons aged >67. Our study further shows that underweight in young age also represented a risk, even though underweight in younger adults is more likely to be associated with other medical issues (e.g. % fat mass), while in older adults underweight BMI could be an indicator of sarcopenia [44], malnutrition or other clinical conditions [6, 12].

Our models examined how body mass affected two different aspects of health. Mortality concerns survival, while SRH reflects the quality of survival. Being underweight affected both mortality and SRH negatively, while gaining weight had a negative association with all-cause mortality but might be beneficial for SRH. Weight loss is known to have a potential negative effect on health [13, 16–19, 21, 22]. Hence, it is reasonable to ask if the findings of our study are more a question of becoming, rather than being, underweight. The negative trajectory is explained as a combination of within-subject effects (i.e. becoming underweight) and between-subject effects (i.e. being underweight). It implies that changing BMI category (i.e. adding weight for those who were underweight) can affect SRH. However, when examining the effect of weight change in individual subjects, we find that weight gain was associated with lower SRH levels, even for those with a very low body mass. Although we would advise overweight persons to lose weight towards the normal range, gaining weight as general advice for underweight persons does not necessarily lead to better SRH.

Mortality was not affected by weight change in the same manner. The baseline BMI predicted a 69% increased risk, and when we modeled weight change by updating BMI values, we found that the risk increased to 79%, while for those in the lower normal range, the risk increased from 14% to 19%. This is consistent with a previous study of the Tromsø study cohort that showed that weight loss and gain were associated with increased all-cause mortality for men and in the subgroup of women who reported no weight-loss attempts [20].

Our study suggests that there is a healthy and an unhealthy underweight group, and that thinness due to waste is a risk. It seems plausible to distinguish between those who were initially underweight and those who became underweight (e.g. due to malnutrition). There are studies of nutrition and BMI status among older persons [6], but there are no studies that identify subgroups at risk among younger subjects. Our models control for known physical diseases, but not for eating disorders. Further studies should try to identify subgroups at particular risk among underweight persons. Health-related behavior explained 17% of the variance in our data, while gender and age (21%), comorbidity (23%) and mental distress (28%) are therefore important factors for an understanding of the decline. Our study suggests following up particularly gender differences, smoking status, the effect of weight change and development of comorbid diseases later in life.

We find more persons who exercise among the underweight subjects. This is consistent with being thin as part of a healthy life, but at the same time we find more persons who lead active lives and more non-smokers among the obese than we find from <25 kg/m². It is timely to ask whether this might be an indication that health information is primarily targeting overweight subjects.

BMI affected SRH and all-cause mortality independently from comorbidity, mental health, other biological risk factors or health-related behaviors. Being underweight was associated with excess mortality as compared to all other weight categories, and age affected the thinnest subjects more than all others. Weight increase was beneficial for mortality but not for SRH among the underweight. The rapid decline of SRH with increasing age suggests that particular attention should be paid to underweight subjects after 38 years of age.