Abstract

Aims

The aim of this study was to assess the relationship between short stature and coronary heart disease (CHD) morbidity and mortality.

Methods and results

We performed a systematic search from MEDLINE, PREMEDLINE, and All EBM Reviews as well as from a reference list of relevant articles. We used SPICO (Study design, Patient, Intervention, Control-intervention, Outcome) criteria. The methodological quality of studies was analysed by modified Borghoust criteria. From a total of 1907 articles, we selected 52 studies comprising population-based follow-up studies and patient cohorts followed after a CHD event, as well as case-control studies with height either as a continuous or categorical variable, totalling 3 012 747 individuals. The short ones were below 160.5 cm and tall ones over 173.9 cm on average. Among the shortest height category, the relative risks were 1.35 (95% CI 1.25–1.44) for all-cause mortality, 1.55 (1.37–1.74) for all cardiovascular disease (CVD) mortality, 1.49 (1.33–1.67) for CHD, and 1.52 (1.28–1.81) for myocardial infarction when compared with those within the highest height category. The mean relative risk was 1.46 (1.37–1.55). Short stature was associated with increased cardiovascular morbidity and mortality in both genders.

Conclusion

The relationship between short stature and CVD appears to be a real one. On the basis of comparison, adults within the shortest category had an ∼50% higher risk of CHD morbidity and mortality than tall individuals.

See page 1674 for the editorial comment on this article (doi:10.1093/eurheartj/ehq183)

Introduction

History

The first report on the inverse association between coronary heart disease (CHD) and height was published in 1951.1 It was found that the average height of males hospitalized for myocardial infarction (MI) prior to the age of 40 was 5.08 cm lower (170.2 cm) than the average height of the non-hospitalized control group (175.3 cm). Since then, the association between short stature and cardiovascular diseases (CVDs) has been dealt with in more than 1900 papers according to database search. Many reports agree with Gertler et al.,2–12 but this association was also considered a misconception, as several large epidemiologic follow-up studies3,13–15 showed no association between height and CHD risk. It has even been suggested16,17 that racial factors may determine the outcome, e.g. the shorter populations such as southern Europeans have lower death rates from CHD and all causes compared with, for example, the taller northern Europeans. Although seven reviews have been published,16–22 no systematic meta-analysis has been done on this topic.

The reasons for a systematic review

In this paper, we have performed, for the first time, a systematic review of studies reporting on the association between adult height and CHD events. What makes it difficult to investigate this association is that the literature deals with various populations and outcomes as well as different height criteria within various study designs. Some studies start with healthy people and follow their outcome in relation to their height, whereas other studies follow patients by stature after a CHD event. Thirdly, there are case-control studies that comprise coronary artery disease patients and healthy controls defined by height, with varying outcomes and treatments. These studies also differ in the way they take the effect of known CHD risk factors into account, such as age, sex, smoking, lipid disorders, and diabetes—or whether they include any of these as confounding factors in their analyses. This is important, since in many papers the association between height and CHD often disappears when adjusted for all other factors. The most striking obstacle was, however, the use of various height categories.

Article quality was assessed by Quality of Reporting of Meta-analysis criteria. The hypothesis of this study was that short height is associated with increased CHD risk. We decided to compare the shortest group to the tallest group instead of using a fixed height limit and calculated average heights for combined risk values from the meta-analysis.

Objectives

This systematic review addresses whether short height shows an inverse association with variable CHD endpoints, and what the magnitude of the possible risk is. The meta-analysis will also address the effect of gender on the risk of different endpoints.

Criteria for considering studies for this review

Types of studies, participants, interventions, and outcome measures

According to the SPICO (Study design, Patient, Intervention, Control-intervention, Outcome) criteria, the original study design had to be a systematic review, meta-analysis, randomized clinical trial, clinical trial, and cohort or case-control setting and feature a number of subjects over 200 in total. Patients had to be either healthy at the beginning or already having symptomatic CHD. The patient setting was considered quite helpful if there was division into men vs. women. Intervention and control intervention had to be continuous, with the mean height and standard deviation given to be dichotomized as short vs. tall ones or classified and, if classified, there had to be at least two classes. Outcome had to be defined as diagnosis of angina pectoris, ischaemic heart disease (IHD) or heart disease without MI, acute MI, or history of MI, coronary artery occlusion equal to or more than 50%, revascularization or percutaneous transluminal coronary angioplasty (PTCA), as well as all-cause mortality, CVD mortality, or CHD mortality, or in clinical trials and cohort studies, any of the previous after at least 2 years of follow-up.

An article was excluded if the previously mentioned SPICO criteria were not fulfilled, or the information was insufficient for quality assessment or further conclusions, or height was only mentioned as a confounding factor.

Search strategy for identification of studies

We aimed to identify all articles that investigated height and CHD association by performing a systematic literature search from MEDLINE, PreMEDLINE, and All EBM Reviews, search ending 6 April 2007. The detailed search strategy is included as a Supplementary material online. This systematic search from the sources above yielded a total of 1907 articles. On 3 December 2007, we checked that there were no new articles to include.

Two reviewer authors (T.A.P. and N.K.J.O.) independently assessed the studies for eligibility without consideration of the results. In cases of distributed opinions, a third evaluator was used (P.J.K.).

We included an article if predefined SPICO criteria were fulfilled in title and abstract. A total of 68 articles were reviewed as full-text versions. Next, we excluded articles that did not report adult height but birth height (five rejected on this ground) and articles that did not use English language (three rejected on this ground). Sixty articles remained after these additional restrictions.

After the database search, we screened the reference lists of included articles, which yielded 22 new articles. Excluding reviews and overlapping cohorts at this point, the number of eligible articles narrowed from 82 to 52, from which the final synthesis was made.

These articles comprised various racial and socioeconomic groups and samples from both genders separately totalling 3 012 747 individuals comprising population-based follow-up studies of initially healthy people, patient cohorts followed after a CHD event, and case-control studies with adequately defined classification of height either as a continuous or categorical variable. Figure 1 summarizes the systematic forwarding of the search.

Figure 1

The Quality of Reporting of Meta-analysis flow diagram.

Figure 1

The Quality of Reporting of Meta-analysis flow diagram.

Methods

One author (T.A.P) extracted data from a previously designed Excel database see (Supplementary material online, Table S1). Completed data forms were checked for discrepancies by two authors (N.K.J.O. and P.J.K.).

Systematic review

We decided to do subgroup analyses by first extracting the data of those articles that reported risk ratios (RRs). If RRs were reported for the tallest group, we changed them to represent RRs for the shortest group. If RRs were not reported, but cross-tabulation for RR calculation was possible, we used the tallest group as the reference group and calculated RRs for the shortest group.

When odds ratio (OR) was reported for the tallest group, we used the following calculation: RR = OR/[1 − pc(1−OR)], in which pc is the event rate for the control group.23 When possible, we extracted the gender-specific data because gender is one known confounding factor.

We also used ORs, hazard ratios (HRs), and other variables separately when it was impossible to calculate RRs due to the total number of individuals lacking. Thus, all 52 articles included are also evaluated in this systematic review results.

Meta-analysis

Meta-analysis was accomplished using statistical StatsDirect software. To examine the heterogeneity of the results and summarize results across various articles, we used methods suggested by DerSimonian and Laird.24–26 The I2 test showed 72.1% inconsistency (95% CI 62.8–78.2%). Though we found significant within-trials and between-trials heterogeneity for the articles included in the meta-analysis, we present summary estimates based on a random effects model instead of a fixed effect model. We did not remove any of the selected studies based on heterogeneity. The Z-test for overall effect was 12.1 with P < 0.0001. According to bias analysis (Figure 2), our analysis was unbiased (Begg–Mazumdar: Kendall's τ = 0.147449, P = 0.1175 and Egger: bias = 0.724877 (95% CI =− 0.172388–1.622143), P = 0.111).

Figure 2

Bias test.

Figure 2

Bias test.

Description of studies

Supplementary material online, Table S1, presents the most important descriptive information for the 52 studies included in our analysis. The total number of participants included in our systematic review was 3 012 747. In the meta-analysis, it was possible to include 22 studies see (Supplementary material online, Table S2). From a total of 30 studies, it was not possible to extract RRs and they were analysed in the text see (Supplementary material online, Table S3).

Methodological quality of included studies

Criteria for the assessment of the quality of studies were modified from Borghoust et al.27 see (Supplementary material online, Table S4). The quality of the studies included in the systematic review varied from 7 to 15 see (Supplementary material online, Table S1). The quality score was commonly low because the subcriteria of the study size (5c, 5b) or the amount of dropouts/loss to follow-up (8a) were too small, or information provided from dropouts/loss to follow-up (8b) was insufficient. There was no association between quality score and bias assessment plot scattering (data not shown).

Results

Studies included in meta-analysis

Of the 52 studies, 224,5,7,11,28–45 provided adequate data for a meta-analysis based on RRs see (Figure 3, Supplementary material online, Table S2). Meta-analysis shows that risks for different kinds of cardiovascular endpoints are higher within the shortest ones when compared with the tallest height categories. The combined RR was 1.46 (95% CI 1.37–1.55). On average, the short ones were below 160.5 cm and tall ones over 173.9 cm, so the average height cut-off for short ones was 13.4 cm lower than the average height cut-off for the tall ones. When men and women were considered independently on average, short men were below 165.4 cm and short women below 153.0 cm, tall men over 177.5 cm and tall women over 166.4 cm. Height cut-offs were available for 21 articles. Only one article33 failed to report height cut-offs and was not taken into the calculations. Additional meta-analysis information is provided in Supplementary material online, Table S2.

Figure 3

Meta-analysis of 22 articles.

Figure 3

Meta-analysis of 22 articles.

The combined RR for all-cause mortality for short men was 1.37 (1.29–1.46) and for short women 1.55 (1.41–1.70) see (Supplementary material online, Figures S1 and S2). On average, the short ones were defined to be below 161.1 cm and the tall ones over 176.0 cm and short men below 165.5 cm and short women below 153.3 cm, tall men over 178.9 cm and tall women over 163.7 cm see (Supplementary material online, Figure S3).

Similarly, the combined risk for all types of cardiovascular (CVD) deaths among men and women was 1.55 (95% CI 1.37–1.74) see (Supplementary material online, Figure S4). In line, the risk for combined CHD mortality and morbidity brought by short stature among men was 1.49 (1.33–1.67), varying between 1.10 and 4.55. In these studies, men with a height of <166.1 cm were considered short and men >176.2 cm tall. There were only three studies in women reporting a risk varying from 1.10 to 2.08 for short ones (<153.1 cm) compared with the risk among tall ones (>165.6 cm) see (Supplementary material online, Figure S5).

The risk of MI incidence associated with short stature was 1.52 (95% CI 1.28–1.81) for all. In these studies, the mean reported height cut-off for short males was 14.4 cm lower (164.0 cm) than the average height cut-off of tall men (178.4 cm). Similarly, there was a 14.5 cm difference between reported cut-offs for short (153.7 cm) and tall women (168.2 cm) see (Supplementary material online, Figure S7).

Meta-analysis subgroup results see (Supplementary material online, Figures 1–8) show a more detailed interpretation.

Studies not included in the meta-analysis

There were 30 studies fulfilling the SPICO criteria but not included in the meta-analysis2,3,6,8–10,12–15,46–65 because it was impossible to calculate RRs for absolute height cut-offs see (Supplementary material online, Table S3). Of these, seven studies reported RRs by variable increments of height without data on measured height.8,13,15,47,51,61,64 From these seven studies, we can conclude that a 5–10 cm height increase is usually linked with a reduction of RR for all-cause death or CHD by 10–15% and a 30 cm decrease of height may double the risk.

Additionally, six studies reported ORs from which RRs could not be calculated.3,50,52,53,56,65 Incidence of non-fatal MI and CHD as well as coronary lesions ≥50% were inversely associated with height, but 30-day or operative mortality after isolated coronary artery bypass grafting did not show significant association with height.

Furthermore, three studies reported HRs by quartiles14,60,63 and as with ORs, some researchers also used staircase increments of height when reporting HRs.6,49,55,59 An inverse association for CHD was found when height was used as a continuous variable in every study; in a twin study, discordant for height was found not only between twin individuals but also within twin pairs. Per 5 or 10 or 15 cm increase HR was inversely associated with height for fatal CVD and for fatal CHD and for all-cause mortality.

There were four studies2,9,10,48 reporting only statistically significant P-values to support statements of height being an important factor for risk of CHD.

Six studies could not be grouped at all, based on the used endpoints.12,46,54,57,58,62 However, reported endpoints such as operative mortality percentage after coronary artery bypass grafting (CABG), advanced coronary lesions in an autopsy study, incidence of IHD, estimated CHD mortality ratio, all-cause mortality ratio, and affirmative answer about symptoms implying coronary or peripheral atherosclerotic disease were all inversely associated with height in these studies.

Discussion

In this paper, we have addressed two questions: Is adult short stature really a risk factor for CHD events and, if it is, how big a factor is it? Our systematic review and meta-analysis show that adult short stature poses ∼1.5 times higher risk for CHD morbidity and mortality than being a tall individual. This appears to be true both for men and women and for different kinds of endpoints. Although it has been previously hypothesized that height may possess a greater risk for men, shorter women may pose an even higher risk when other confounding factors are not taken into consideration.

Due to the heterogeneity of studies, we cannot reliably answer the question on the critical absolute height. The height cut-off points did not only differ between the articles but also between men and women and between ethnic groups. This is why we used the shortest-vs.-tallest group setting. Our strategy thereby reduced the study population pool. Based on the bias analysis, we used the random effect model, assuming that the true height value varies in different study populations. The advantage of the use of random effect model was that we did not have to remove any of the selected studies based on the variability mentioned above. We believe that this heterogeneity only strengthens the association found.

According to our modified Borghoust criteria list, the methodological quality of the articles appeared to be reasonably good on average to be used for the assessment of height as a risk factor, though most of them were originally designed for other purposes. Two of the most common methodological shortcomings appeared to be the missing number of individuals with outcome and lack of information provided for dropouts/loss to follow-up. More than half the included studies failed to fulfil these criteria.

Our systematic review has some limitations. Meta-analyses are also prone to different kinds of biases and confounding factors that are inherent to the original studies. The possibility of missing published studies also remains, though we used a large set of keywords for databases and standardized the search flow in accordance with the guidelines. Furthermore, we searched only for studies which were published in indexed journals or found from reference lists, so unpublished studies and non-indexed journals may have been partly missed. Positive results are more easily published, but in this systematic review, height was usually not the main topic of the original paper but rather was given as a demographic variable. This is why we believe that our results were not biased by positive publication bias. Only a few studies were focused to identify height as a prognostic factor.

We excluded only three studies out of the total of 1907 articles because they were not published in English. This language limit would hardly have changed the result because in these abstracts the results were parallel.

The reason(s) for short stature being a risk factor for CHD remain open for hypotheses. Most commonly, in previous studies it has been suggested that the reason behind this association could be low socioeconomic background with associated risk factors such as poor nutrition and infections resulting in poor foetal or early-life growth.39,66

Nwasokva et al.56 found that short men have not only a higher prevalence of coronary disease, but also a greater severity of coronary disease than tall men.56 Also, Kortelainen and Särkioja12 found that short stature was associated with more advanced coronary lesions.

In Physicians Health Study, there was a significant association between height and MI, but not between height and cardiovascular death.67 Similarly, the Framingham Heart Study found no association between short stature and increased risk for all-cause or cardiovascular mortality in either sex, although shorter women had increased risk for MI.33

In the Coronary Artery Surgery Study (CASS), surgical mortality was inversely related to the average diameter of the grafted coronary arteries in both men and women.68 It was therefore hypothesized that the physical size of the patient, including coronary artery diameter, may predict operative mortality.68 In recent studies using angiographic measurements, the coronary artery diameter was correlated with height and body weight.69,70 It could be hypothesized that smaller coronary arteries may be occluded earlier in life under similar risk conditions.

Conclusions

The relationship between short stature and CVD seems to be a real one. Adults within the shortest category had a ∼50% higher risk of CHD morbidity and mortality compared with tall individuals. The possible pathophysiological, environmental, and genetic background of this peculiar association is not known.

Implications for practice

Height is used to calculate body mass index (BMI), which is a widely used quantity risk of CHD. The value of BMI has been recently questioned by reports showing that BMI may not associate with the severity of CHD in angina patients with chronic kidney disease71 or may even be inversely associated.72,73 This has been discussed as the obesity paradox. The results of this meta-analysis suggest that height may be considered as a possible independent factor to be used in CHD risk calculations.

Implications for research

It would be interesting to explore—e.g. in autopsy series—the possibility that short stature is connected with the risk of CHD and MI through the effect of smaller coronary artery diameter, and that smaller coronary arteries may be occluded earlier in life under similar risk conditions. Recent findings on the genetic background of body height74 suggest that inherited factors rather than speculative early-life poor nutrition or birth weight may explain the association between small stature and later-life increased risk for CHD events.

Contributions

T.A.P., N.K.J.O., P.J.K., and P.K. designed the present study. T.A.P. analysed and interpreted the data, and drafted the article. N.K.J.O., P.J.K., and P.K. interpreted and organized the data, critically revised the article and contributed to the final version.

Supplementary material

Supplementary material is available at European Heart Journal online.

Funding

This study was supported by grants from the Pirkanmaa Regional Fund of the Finnish Cultural Foundation, the Medical Research Fund of Tampere University Hospital, the Aarno Koskelo Foundation, and the Finnish Foundation for Cardiovascular Research.

Conflicts of interest: none declared.

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Supplementary data

Comments

4 Comments
A contrary report on height and coronary heart disease
19 July 2010
Thomas T. Samaras

I have researched over 5000 papers on the health ramifications of human height and published 31 papers in professional journals and books.1- 5 However, my conclusions on height and coronary heart disease (CHD) differ from the impressive paper by Paajanen et al.6

Our conflict relates to several variables that obscure the relation between height and heart disease; e.g., low birth weight combined with catch-up growth increases adulthood CHD. Also, childhood diseases that retard growth impact adult mortality. Another problem is that taller people tend to be in higher economic classes. In addition, shorter people tend to have stockier builds, which correlate with higher CHD.

Many findings indicate that short height is correlated with low CHD.1 -5 A few examples follow.

Numerous short populations (e.g., males: 153 to 163 cm) have low or no CHD,2,5 but not one tall Western population is free of CHD.1 However, not long ago Western populations, including the elderly, had low CHD due to different dietary patterns.7 For example, since 1900, CHD increased dramatically along with increased animal protein intake and greater height.

Since 1985, a progressive decline in CHD was found for decreasing height of five US ethnic groups (8 million male deaths).1 In addition, a 70-year study of 1.3 million Spaniards found shorter men lived longer.8 A similar pattern was found in Sardinia.1 Chan et al. concluded that short and slender people are more likely to become centenarians.2,5,9 It's unlikely that short people can outlive taller people if they suffer from CHD.

Okinawans have lower CHD compared to mainland Japan and the US.1 US males had ~500% higher mortality and taller mainland Japanese males had a 54% higher mortality vs. Okinawans. Another study showed that six populations with the lowest CHD mortality were shorter than the six tallest populations.2 The tallest populations had 136% higher mortality.

Osika and Montgomery2 found that taller men had a 21% lower risk of heart disease vs. short men. However, when they evaluated men in low income brackets, tall men had a 71% higher risk than short men.

A study of 350,000 dogs found smaller dogs have much less heart failure compared to bigger dogs.10 They also live longer;5 e.g., miniature poodles live 25% longer than standard poodles.

Several biological mechanisms suggest that being short is good for the heart. Shorter people of the same body proportions have lower BP, BMIs, atrial fibrillation, left ventricular hypertrophy, and CHD risk parameters, such as C-reactive protein, cystatin C, and creatinine. Their smaller hearts also have higher pumping efficiencies.1,11,12,13

Western nutrition and increased growth are tied to CHD.7,14,15 A comprehensive review concluded that red meat intake should be minimized and processed meats eliminated entirely to reduce the risk of chronic diseases.7

In conclusion, short people are not biologically at risk for CHD.1- 5.16 The good news is that short and tall individuals can avoid CHD if they follow a healthful diet and lifestyle, preferrably starting in childhood. (Samarastt@aol.com)

References

1. Samaras TT. Role of height in cancer and cardiovascular disease. J Chinese Clin Med, 2010; 5: 87-99.

2. Samaras TT. Are 20th-century recommendations for growth and height correct? A review. S Afr J Clin Nutr, 2009; 22: 171-176.

3. Samaras TT. Should we be concerned over increasing body height and weight? Exp Gerontol 2009; 44: 83-92.

4. Samaras TT, Elrick H, Storms LH. Is short height really a risk factor for coronary heart disease and stroke mortality? a review. Med Sci Monit 2004; 10: RA63-76.

5. Samaras TT. Body height and its relation to chronic disease and longevity. In Samaras, T (Ed), Human Body Size and the Laws of Scaling: Physiological, Performance, Growth, Longevity and Ecological Ramifications. New York: Nova Science Publishers, 2007, 63-112.

6. Paajanen TA, Oksala NKJ, Kuukasjarvi P, Karhunen PJ. Short stature is associated with coronary heart disease: a systematic review of the literature and a meta-analysis. Eur Heart J, 2010, doi:10.1093/eurheartj/ehq155

7. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity and the Prevention of Cancer: a Global Perspective. AICR: Washington, DC, USA, 2007, pp 7, 352, 373

8. Holzenberger M, Martin-Crespo RM, Vicent D, Ruiz-Torres A. Decelerated growth and longevity in men. Arch Gerontol Geriatr, 1991, 13: 89-101. doi: 10.1093/aje/kwk096

9. Chan Y-C, Suzuki M, Yamamoto S. A comparison of anthropometry, biochemical variables and plasma amino acids among centenarians, elderly and young subjects. J Am Coll Nutr 1999; 18: 358-365.

10. Egenvall A, Bonnett BN, Hedhammar A, Olson P. Mortality in over 350,000 insured Swedish dogs from 1995-2000: breed-specific age and survival patterns and relative risk for causes of death. Acta Vet Scan 2005; 46:121 -136.

11. de Simone G, Devereux RB, Daniels SR, Mureddu GF, Roman MJ, Kimball TR, et al. Stroke volume and cardiac output in normotensive children and adults. Circulation 1997; 95: 1837-1843.

12. Hanna IR, Heeke B, Bush H, Brosius I, King-Hageman D, Beshai JF, Langenberg JJ. The relationship between stature and the prevalence of atrial fibrillation in patients with left ventricular dysfunction. J Am Coll Cardiol 2005; 47: 1683-1688.

13. Samaras TT. BMI and weight: their relation to diabetes, CVD, Cancer and all-cause mortality. In Samaras, T (Ed), Human Body Size and the Laws of Scaling: Physiological, Performance, Growth, Longevity and Ecological Ramifications. New York: Nova Science Publishers, 2007, 113- 146.

14. Campbell, TC, Campbell, TM. The China Study. Benbella Books: Dallas, Texas, USA, 2006: p 102-103.

15. Silventoinen K. First author replies. Am J Epidem 2007; 165: 114.

16. Tuomilehto J. Tall is beautiful and heart healthy? Eur Heart J 2010,

doi:10.1093/eurheartj/ehq183.

Conflict of Interest:

None declared

Submitted on 19/07/2010 8:00 PM GMT
Re:A contrary report on height and coronary heart disease
7 May 2013
thomas t samaras

Since I responded to the review on heart disease, I have had a new paper on heart disease and height published in 2013.

The paper presents a review of over 30 international studies found that shorter people have lower coronary heart disease compared to taller ones. The study, published by the Cardiological Society of India in the Indian Heart Journal, finds that shorter people have an inherently lower risk of coronary heart disease because of a variety of biological factors. The article is titled: Shorter height is related to lower cardiovascular disease risk--a narrative review. http://www.indianheartjournal.net/article/S0019-4832(12)00317-3/fulltext

The study found that populations with the zero coronary heart disease are short (men 4'8" to less than 5'5"). Examples, based on 20th century studies, include Solomon and Cook Islands, Papua New Guinea, Kalahari bushmen and Congo pygmies. No country of tall people in the Western world could meet this record. Shorter people with lower heart disease included the US mainland and Hawaii, China, India, Sweden, Sardinia, and Japan.

Shorter people benefit from several biological mechanisms that lower the risk of heart disease. One advantage is a greater potential for cell doublings in later life. Because bigger bodies require the creation and maintenance of more cells, cells run out of the ability to reproduce themselves with age because they have a fixed number of times that they can duplicate themselves. There are many harmful effects from the reduced potential for cell replication, including damage to the cardiovascular system.

If we compare short and tall people of similar body proportions and lifestyle, other advantages of smaller bodies include lower blood pressure, lower DNA damage, fewer free radicals, greater heart pumping efficiency, lower work load on the heart, lower risk of blood clots, and lower atrial fibrillation.

The human findings in this study are consistent with the very low heart failure in small dogs compared to large dogs. In addition, the findings complement over 100 studies involving short height and lower mortality from all-causes, cardiovascular disease and cancer. Centenarians tend to be quite short and light and it is unlikely that they would reach 100 years of age if they had heart problems.

I agree that many studies conflict with my findings. However, these studies are corrupted by many factors outside of height that can bias the findings. For example, poor people tend to be more obese and shorter than higher income people who tend to be taller and eat healthier. It's interesting to note that early in the 1900s, coronary heart disease was rare compared to today. Yet, people were a few inches shorter in 1900. Before the 1970s, higher income, taller men had more heart disease than shorter working class men in the US. Another problem for the "taller have less heart disease" supporters is that coronary heart disease was rare before the industrial revolution when people were shorter than in the 20th and the 21st centuries.

Regardless of whether one is short or tall, avoiding heart problems is mostly related to following a healthful diet and lifestyle. For example, a plant-based diet, regular exercise, low weight for height, good medical care, not smoking, higher socioeconomic status, social networks, and effective stress management are more important than one's height.

More information on height and longevity available from: http://www.humanbodysize.com

Conflict of Interest:

None declared

Submitted on 07/05/2013 8:00 PM GMT
Meinander (former Paajanen) et Karhunen replies
14 May 2013
Tuula A. Meinander (with Pekka J. Karhunen, Professor of Forensic Medicine)

We are grateful to Mr. Samaras for his comments and interest (1) (2) in our work published in European Heart Journal (3). In this paper we made a meta-analysis comprising all published papers fulfilling following inclusion criteria: the original study design had to be a systematic review, a meta-analysis, a randomized clinical trial, a clinical trial, or represent a cohort or case-control setting. The study should comprise subjects at least 200 in total, and if patients they had to be either healthy at the beginning or already having symptomatic CHD. Height had to be a continuous measure with the mean height and standard deviation given to be dichotomized as short vs. tall ones or classified and, if classified, there had to be at least two classes. Outcome had to be defined as diagnosis of angina pectoris, ischaemic heart disease (IHD) or heart disease without MI, acute MI, or history of MI, coronary artery occlusion equal to or more than 50%, revascularization or percutaneous transluminal coronary angioplasty (PTCA), as well as all-cause mortality, CVD mortality, or CHD mortality, or in clinical trials and cohort studies, any of the previous after at least 2 years of follow-up.

We are very well aware about Mr. Samaras publications but based on the criteria above they were not included in the meta-analysis because they did not reach the criteria. An article was excluded if the previously mentioned inclusion criteria were not fulfilled, or the information was insufficient for quality assessment or further conclusions, or height was only mentioned as a confounding factor.

Studies by Page et al (4), Lindeberg et al (5) and (6), Poulain et al (7) and Evans et al (8) to which Mr. Samaras referred to, presented demographic data from which it can be concluded that populations in those studies with low coronary heart disease morbidity were on average short. They did test many correlations, but any of them height was associated with atherosclerosis. Page et al. suggested that the observed phenomenon might be due lower blood pressure due to low salt intake or possible differences in dietary habits. Evans et al and Lindeberg et al. speculated that different (non-western) diet might be one explanatory factor, others possibly being leanness, low diastolic blood pressure and lower serum cholesterol. Poulain et al suggested that besides biological/genetic factors, the behavioral factors including life style, demographic behavior, family support and community characteristics may play an important role.

We agree that it is interesting to compare height and CHD mortality between various populations and continents, but when analyzing the association between height and risk of coronary heart disease (CHD), it should be done within one population at a time. The reason is that stature (adult body height) and body mass index (BMI) have a strong genetic component explaining observed variation across human populations (9). Estimates of heritability are as high as 90 %. Recent genome-wide association studies of height have discovered over 180 common variants associated with height. Although common variants are associated with height at the extremes of height as well as across the population, additional factors become more prominent at the shorter extreme (10).

Adult height has been continuously increased through history. Therefore it is tempting to think that increased mortality and morbidity associated with CHD has something to do with the increase of mean height. The concept of CHD being a modern disease due to Western lifestyle and diet has recently challenged by evidence obtained from whole body CT scans of mummies from four different geographical regions or populations spanning more than 4000 years (11). Atherosclerosis was common already in preindustrial populations including pre-agricultural hunter-gatherers that had died below 40 years of age. The estimated height several thousand years ago did not commonly exceed 160 cm (12).

However, height has something to do with the risk of CHD. Our current hypothesis is that individuals with short stature may have smaller-sized coronary arteries which may be earlier occluded by atherosclerosis. We are currently studying this hypothesis.

References

1. Samaras TT. A contrary report on height and coronary heart disease. European Heart Journal. 2010.

2. Samaras TT. Shorter height is related to lower cardiovascular disease risk - A narrative review. Indian Heart J. Cardiological Society of India; 2013. p. 66-71.

3. Paajanen TA, Oksala NKJ, Kuukasj?rvi P, Karhunen PJ. Short stature is associated with coronary heart disease: a systematic review of the literature and a meta-analysis. European Heart Journal. 2010;31:1802-1809.

4. Page LBL, Damon AA, Moellering RCR. Antecedents of cardiovascular disease in six Solomon Islands societies. Circulation. 1974;49:1132-1146.

5. Lindeberg S, LUNDH B. Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava. J Intern Med. Blackwell Publishing Ltd; 1993;233:269-275.

6. Lindeberg S, Nilsson-Ehle P, Terent A, Vessby B, Schersten B. Cardiovascular risk factors in a Melanesian population apparently free from stroke and ischaemic heart disease: the Kitava study. J Intern Med. 1994;236:331-340.

7. Poulain MM, Pes GG, Salaris LL. A population where men live as long as women: villagrande strisaili, sardinia. J Aging Res. 2010;2011:153756- 153756.

8. Evans AE, Ruidavets JB, McCrum EE, Cambou JP, McClean R, Douste-Blazy P, McMaster D, Bingham A, Patterson CC, Richard JL, Mathewson ZM, Cambien F. Autres pays, autres coeurs? Dietary patterns, risk factors and ischaemic heart disease in Belfast and Toulouse. QJM. 1995;88:469-477.

9. Sammalisto S, Hiekkalinna T, Schwander K, Kardia S, Weder AB, Rodriguez BL, Doria A, Kelly JA, Bruner GR, Harley JB, Redline S, Larkin EK, Patel SR, Ewan AJH, Weber JL, Perola M, Peltonen L. Genome-wide linkage screen for stature and body mass index in 3.032 families: evidence for sex- and population-specific genetic effects. Eur J Hum Genet. 2009;17:258-266.

10. Chan YY, Holmen OLO, Dauber AA, Vatten LL, Havulinna ASA, Skorpen FF, Kval?y KK, Silander KK, Nguyen TTT, Willer CC, Boehnke MM, Perola MM, Palotie AA, Salomaa VV, Hveem KK, Frayling TMT, Hirschhorn JNJ, Weedon MNM. Common variants show predicted polygenic effects on height in the tails of the distribution, except in extremely short individuals. PLoS Genet. 2011;7:e1002439-e1002439.

11. Thompson RC, Allam AH, Lombardi GP, Wann LS, Sutherland ML, Sutherland JD, Soliman MA-T, Frohlich B, Mininberg DT, Monge JM, Vallodolid CM, Cox SL, Abd el-Maksoud G, Badr I, Miyamoto MI, el-Halim Nur el-Din A, Narula J, Finch CE, Thomas GS. Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations. The Lancet. Elsevier Ltd; 2013;381:1211-1222.

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Conflict of Interest:

None declared

Submitted on 14/05/2013 8:00 PM GMT
Re:Meinander (former Paajanen) et Karhunen replies
3 June 2013
Thomas T. Samaras

Samaras replies on Shorter height is related to lower cardiovascular disease

Thank you for your reply to my comments (1)(2).

I agree that some people in the past suffered from atherosclerosis and other chronic diseases (2). However, numerous reports have been published indicating that the explosion in atherosclerosis and coronary heart disease (CHD) is a recent phenomenon. For example, the 2007 World Cancer Research Fund reported: that along with urban living and industrialization, we have grown taller, heavier and CHD has increased (3). In addition, the World Health Organization reported that early in the 1900s, Europe and the US had very little CHD (4). Burkitt (5) reviewed data from almost 1000 hospitals in non-developed populations, and found that CHD and other chronic diseases were rare. Harvard, other institutions and researchers Walter Willett, Barry Popkin, Urban Jonsson, David Barker, ARP Walker, and Colin Campbell reported the same results. During the Korean and Vietnam wars, autopsies of Korean and Vietnamese soldiers found no evidence of atherosclerosis. However, US soldiers had substantial amounts of artery clogging. Fontana (6) found long-term caloric restriction was a powerful protector against atherosclerosis in humans.

My confidence in the findings of the preceding reports is supported by current trends in countries where CHD is becoming a problem due to deviations from traditional diets and increased height and weight. These include China, Greece, S. Korea, Singapore and India; e.g., young and middle aged Indians are experiencing an epidemic of CHD (7).

I appreciate that you had to establish criteria for selecting various studies in your impressive paper (8). However, studies not included in your paper still have value. In fact, many of these studies can provide a perspective that allows a better focus on CHD etiology. For example, the US government collects death certificates from all states and provides a summary of mortality rates for various causes, including heart disease throughout all age groups. These data are categorized by the major US ethnic groups. I found that the shortest ethnic group, male Asians, had an age-adjusted mortality rate of 198/100,000 population compared to Whites who had a mortality of 333/100,000 (9). Blacks were about the same height as Whites but had a mortality of 408/100,000 (before 1925, Blacks were shorter and had lower CHD vs. Whites). Native Americans were shorter than Whites and Blacks and had a mortality of 220/100,00. Hispanics were about the same height as Native Americans and had a mortality of 214/100,000. The pattern for females was similar with Asian females having a mortality of 121 vs. 218/100,000 for White females. These data covered the period of 1985-1999 and involved about 8 million deaths. This finding concurs with California data covered in the Indian Heart Journal (7). Researchers need to be aware of these findings to provide a balanced perspective.

Another observation that can help balance the picture is a comparison of CHD mortality among developed states. Levi et al. (9) provided age- adjusted CHD on about 50 developed populations. When I compared males in the six top populations in terms of the lowest CHD morality to the six tallest populations, I found that the six tallest populations had a 236% higher mortality. The tallest females had a 227% higher mortality. The six lowest mortality populations were relatively short: Japan, Hong Kong, France, Portugal, Spain and Italy. The tallest populations were Scandinavia, Finland the Netherlands and Germany.

The preceding examples illustrate that taller height is not the primary factor for taller people having lower CHD. In addition, we were shorter in the 1900s when CHD was quite rare compared to the later part of the 20th century. Tuomilehto and Silventoinen also reported that the Western diet was correlated with both greater height and cardiovascular disease (CVD) (7)

It is true that studies by Page, Lindeberg, etc. did not test for a correlation between height and CHD, although Page did report that the subjects of six tribes were free of atherosclerosis based on clinical evaluations. I don't see how Lindeberg could report the absence of CHD and stroke in Kitava and Papua New Guinea unless these populations were relatively free of atherosclerosis. The facts are that the males averaged 161 cm (7) or less and were free of CHD and atherothrombotic stroke which tells us that being short per se is not harmful. In addition, Bartke (10) reported that short individuals with Laron and related dwarfing syndromes have little atherosclerosis.

Animal studies cannot be ignored as well. I reported on research (7) that found large dogs had much higher rates of heart failure compared to small dogs over a 5-year period. This study was based on 350,000 dogs and 20 breeds. The researchers also found that Great Danes had 70 times the risk of heart failure as miniature Dachshunds. The regular size Dachshund have 3 times the death rate from heart failure as the miniature Dachshund.

As you stated, a possible advantage of being tall is having larger diameter blood vessels which may avoid blockaged from the buildup of plaque due to the Western diet. This makes sense to me but the dog study seems to negate it. For example, if small blood vessels were a problem, then how does the previously mentioned Dachshund have such a low rate of heart failure? Women are smaller than men and have smaller blood vessels but they also have substantially lower CVD.

Another problem I have with correlation studies showing shorter people have higher levels of CHD is that the biological mechanisms favor shorter people having less heart disease. For example, Maier, van Heemst and Westendorp (7) found shorter people tend to have longer telomeres. The reason for this is that taller, bigger bodies require more cell replications (and consequently shorter telomeres) to create and maintain a bigger body. We lose about 60 billion cells a day, depending on our size and other factors. Many studies have found that shorter telomeres are related to higher CVD (11).

A number of studies show that increased left ventricular mass (LVM) increases with increased height (12), and Bouzas (13) reported that LVM promotes CVD independent of other risk factors. In addition, shorter people have lower blood pressure, higher heart pumping efficiency, lower atrial fibrillation and blood clots, and lower DNA damage. Levels of many biological parameters also favor reduced CVD risk (7). In contrast, free radical damage to the heart, which is related to protein and energy intake (14). Protein and energy intake not only increase free radicals, they also promote insulin-like growth factor-1 and greater height.

In conclusion, my research shows that many populations of short people are free or nearly free of CHD to the extent that taller Western populations cannot duplicate. Once we recognize that short height per se is not the cause of CVD, we can focus on why shorter people within our society tend to have higher death rates than taller people. I have given some explanations in my paper (7). Thank you for the research covered in your excellent paper. About 40 of my papers and books on height, health, longevity and physical performance are listed at http://www.humanbodysize.com

1. Samaras TT. A contrary report on height and coronary heart disease. European Heart Journal. 2010 & 2013.

2. Meinander (former Paajanen and Karhunen replies. European Heart Journal. 2013.

3. World Cancer Research Fund/American Institute for Cancer Research. Food, Nutrition, Physical Activity and the Prevention of Cancer: A Global Perspective, vol. 5. Washington, DC: AICR; 2007:5.

4. WHO Study Group. Diet, nutrition, and the prevention of chronic diseases. Technical Report 797. Geneva, World Health Organization , 1990, p. 54.

5. Burkitt DP. The emergence of a concept. p.8: In: Temple NJ and Burkitt DP (eds): Western Diseases-Their Dietary Prevention and Reversibility. Humana Press, Totowa, New Jersey. 1994.

6. Fontana L, Meyer TE, Klein S, Holloszy JO. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proceedings of the National Academy of Science, USA. 2004; 101, 6659-6663.

7. Samaras TT. Shorter height is related to lower cardiovascular disease risk - A narrative review. Indian Heart J. Cardiological Society of India; 2013. p. 66-71.

8. Paajanen TA, Oksala NKJ, Kuukasjarvi P, Karhunen PJ. Short stature is associated with coronary heart disease: a systematic review of the literature and a meta-analysis. European Heart Journal. 2010;31:1802- 1809.

9. Samaras TT. Should we be concerned over increasing body height and weight? Exp Gerontol. 2009;44:83-92.

10. Bartke A. Healthy aging: is smaller better?-a mini-review. Gerontology. 2012;58:337-343.

11. Salpea KD, Humphries SE. Telomere length in atherosclerosis and diabetes. Atherosclerosis. 2010; 209: 35-38.

12. Rider OJ, Francis JM, Ali MK, Byrne J, Clarke K, Neubauer S, et al. Determinants of left ventricular mass in obesity; a cardiovascular magnetic resonance study. J Cardiov Mag Reson. 2009; 11:9 doi:10.1186/1532 -429X-11-9.

13. Bouzas-Mosquera A, Broull?n FJ, ?lvarez-Garc?a N, Peteiro J, Mosquera VX, et al. (2012) Association of Left Ventricular Mass with All- Cause Mortality, Myocardial Infarction and Stroke. PLoS ONE 7(9): e45570. doi:10.1371/journal.pone.0045570

14. Misra MK, Sarwat M, Bhakuni P, Tutja R, Tueja N. Oxidative stress and ischemic myocardial syndromes. Med Sci Monit. 2009;15:RA 209eRA 219.

Conflict of Interest:

None declared

Submitted on 03/06/2013 8:00 PM GMT