This study analyzed 127 573 subjects from the Korean NHIS database and found that degree of height loss was independently associated with an increased risk of MACCE, defined as cardiac death, non-fatal MI, unplanned hospitalization for HF, or stroke. Subgroups analyses of the elderly (age ≥ 60 years) and postmenopausal women (age ≥ 50 years), both of which have more height decline, also demonstrated this association (Online-Only eTables 1–4). Subjects with the most height decline (i.e., ≥ 0.6 cm/year) had significantly worse event-free survival for MACCE compared to subjects with lesser degrees of height loss. Height loss determinants included age, sex, menopausal status, and income level. These results are in parallel with the British data published approximately two decades ago and support the hypothesis that height loss is not simply a common aging process but is also independently correlated with CVD occurrences and may be a modifiable risk factor.
The Height Loss Mechanism and CVD Associations
The inverse relationship between adult height and CVD has been repeatedly reported in epidemiological investigations. However, a single theory cannot explain the mechanism for the phenomenon. We and others claimed that dyslipidemia, arterial stiffening represented by a higher pulse wave velocity or diastolic dysfunction of the heart would serve as a link between shortness and CVD occurrences and outcomes.13–17 Further, the association mechanism between height decreases and CVD is also unclear. However, it might differ from the theory that adult height is a risk CVD factor. An individual’s maximum height is genetically determined and a non-modifiable factor. Conversely, height loss resulting from senile bone, muscles, and joints changes, is affected by environmental and personal factors and might be modifiable. Pathophysiology for osteoporosis and sarcopenia is poorly understood and likely multifactorial, but some factors can be targeted for intervention, such as physical inactivity, alcoholism, tobacco use, vitamin D deficiency, or an unhealthy diet. Osteoporosis, characterized by a reduction of bone density and increased fracture risk, is the primary contributor to height loss by reducing vertebral body strength and inducing the loss of mineral content and trabecular connectivity. Notably, a decrease in stature from osteoporosis and fracture is often remarkable and is likely to reach several centimeters.10, 18 CVD and osteoporosis, which often coexist, are public health problems with multiple epidemiological links, pathophysiological mechanisms, and economic consequences.19–22 Studies have demonstrated that CVD and cardiovascular mortality are associated with reduced bone mineral density and bone fractures. Additionally, sarcopenia and poor muscle strength, occurring as part of the aging process, are associated with bone loss and diseased bone structure, eventually resulting in height loss. Osteoporosis and sarcopenia are known predictors of mortality and are preventable and treatable conditions, theoretically, with environmental modifications and medical interventions.9
Presumable Rationale of the Adverse Effect of Height Loss for CVD
The basis for mechanisms relating to height loss and subsequent CVD remains unclear. However, the effect of height loss, which is a predictor of vertebral fracture, on the respiratory and gastrointestinal systems is noteworthy. Vertebral fractures induce thoracic deformity and pain and disturb pulmonary function. Conversely, percutaneous vertebroplasty and kyphoplasty for vertebral fractures improve lung function. Further, lung capacity and gastrointestinal function decrease as height decline, potentially leading to less exercise, effort intolerance, early satiety, and poor nutritional status, resulting in sarcopenia and senile fragility.23–28 Weight loss and leanness, attributed to the loss of skeletal muscle mass in the elderly, are known risk factors for CVD (the so-called “obesity paradox”).29–32 Moreover, a musculoskeletal deformity has a significant effect on psychological problems, such as depression and anxiety and the quality of life. From that perspective, a height decline might play a causative role in CVD occurrence. However, bone loss and poor bone quality (important determinants of height decline) share common pathophysiological mechanisms with CVD, such as oxidative stress, inflammation, abnormal homocysteine levels, and metabolic risk factors (i.e., hypertension, diabetes, and dyslipidemia).33 Considering this, height loss would be a co-finding of CVD rather than a primary cause.
Study Strengths and Limitations
The current investigation was performed based on KCD-7. Thus, biomarkers that are known cardiovascular risk factors, such as laboratory findings, were not available for analysis. Further, data on each patients’ medication history was unavailable. The main contributor to height loss is osteoporosis, but we were unable to objectively assess each subject’s bone mass density beyond the KCD-7 code. However, the foremost strength of the current epidemiologic study using an anthropometric parameter is the large sample size. Our study sample homogeneity is also noteworthy as all data were gathered in one country in a relatively short time frame (ten years of height monitoring and two years of outcome surveillance), and the analysis included one ethnicity. Adult height and height loss are influenced by many factors. Thus, the effects of confounders, such as race and socioeconomic status, are minimized.