Human height represents a complex trait regulated by numerous physiological, genetic, and environmental factors. However, research is surprisingly sparse regarding the course of post-adolescent height increase after age 18, even as the health and economic consequences of inadequate adult height become clearer. This article provides an integrated framework to better understand the mechanisms, potential treatments, and health consequences of increased height growth in adulthood. Attained adult height is a classic quantitative genetic trait, the result of complex interactions among numerous genetic and environmental factors affecting height growth during development. Previous studies have illuminated the numerous mechanisms by which humans are able to increase height during late adolescence, primarily influenced by hormones and skeletal maturation. Yet overall somatic and appendicular proportions continue to change as late as the mid- to late-20s. Despite these clearly documented growth phenomena, the literature on height increase after age 18 beyond adolescence and early adulthood is sparse, and no previous single source has attempted a comprehensive mechanistic synthesis of the physiological processes that continue to govern height growth age limit far beyond the conclusion of skeletal maturation. The sparsity of the literature surrounding late-disproportional growth and the ethics of attempting medical interventions to increase adult height have been conspicuously absent from the literature. Prior to this, no major synthesis of the various phenomena around height and disproportionality has been attempted. This article provides an integrated framework, grounded in established mechanisms that continue to be influential far beyond skeletal maturity, to better understand the cultures and populations where adult height is likely to be increasingly tall, potential treatments, and improved growth practices to further increase the utility of elevated adult height beyond the normal range, and the health consequences of contextual shifts until what age does height grow.
Growth in height occurs in spite of the protective effects of sex steroid hormones on cartilage using the so-called growth plates, which are areas of cartilage present on the ends of long bones. These plates are responsible for providing length to the long bones, especially during childhood and adolescence when the sex hormones are absent or secreted in low amounts. After a period of heightening, growth in height stops because of the closure of these growth plates, which occurs at the end of adolescence. These growth plates close in a predictable pattern: first at small bones and later at bigger bones. Among the small bones, the toe bones are the first to stop increasing in length during adolescence, followed by the fingers and the wrist bones. Among the long bones of the body, the legs and the arms stop adding length around the same time, with the earlier closure of the humerus in males.
The whole path of development has typically six sequential stages, from fetus/embryo to the young adult. Each stage is characterized by the following step in the development of the bone and related tissues. First, the bulk of the cartilage is converted into weak, primary bone, which is too spongy to hold a shape. In the next three stages, this primary bone is strengthened by the addition of second bone-like material secreted from bone cells lying just outside the developing bone. After the growth plate stops adding length to the bone, it changes to a solid bone. This solid line can possibly be seen by using X-ray equipment, but is far more easily seen in the dissection of bones. Bone length is determined by genetics as well as attributable to the growth plate, as indicated by family studies and animal experiments. In addition to these basic biological factors, the end of epiphyseal development can also be influenced by factors affecting height growth that, alone or more often together, lead to the cessation of growth. Nutritional deficiencies, infections, and certain diseases, or in general, endocrine diseases, if they fall within the juvenile age, but sometimes specifically between ages 10 and 16, can negatively influence growth, halting the lengthening of the skeleton and effectively anticipating the phenomenon of epiphyseal closure. There are also rare genetic factors affecting height growth responsible for early skeletal fusion. At the opposite pole of reduced growth, there is the case of central precocious height growth after puberty in girls, which, by determining the early closure of the growth plates, causes premature entry into height growth after puberty.
Growth plates are layer-like tissues that can be found at the ends of a growing long bone, such as a femur, giving it the ability to elongate.
They are the site of both chondrogenesis and osteogenesis and consist of four zones:
(1) resting zone, (2) proliferation zone, (3) hypertrophic zone, and (4) ossification zone.
The prime zone is the zone of proliferation where a population of cells stays active, multiplying themselves to create new cells. The points begin to become inactive and instead begin to enlarge, due to the countless small vacuoles converging into larger ones. Consequently, it appears lighter and is referred to as the primary spongiosa. The process whereby a growth plate will elongate a long bone is referred to as endochondral ossification, and this process can be repeated hundreds of times, meaning that a long bone can continue getting longer even after birth. Growth plates can become ossified when an organism is mature.
This happens when the zones are as follows:
(1) a thin layer of cartilage on the physical end of the bone,
(2) inactive chondrocytes,
(3) ossifying cells forming a metaphyseal bracket,
(4) a plate of osteoblasts covering the area between the metaphysis and epiphyseal bone, also known as the binding phenomenon.
The growth plates do not close all at one time or age at the same time in both male and female individuals, especially when growth takes place over a broad life period and large amounts of height are accumulated in humans. Around the world, females reach adult heights earlier than males, although the ending time of growth prior to adulthood will be based on many factors affecting height growth and probably different for male and female individuals. In general, does height grow after 18 determined by his or her genetic potential will depend on physical influences such as nutrition and hormones. A delay in the age of epiphyseal closure may mean that a long bone will continue to elongate and could reach a longer length than average. Strong sports participation that leads to constant heavy wear and tear on the joint regions may negatively affect growth plate longevity. This is because growth plates, just like other cartilage, require excellent care and nutrition in order to stay healthy. If a growth plate is not healthy, it may ossify and close at an earlier age than it would have if it did not experience extreme use as a child or young adult. Eventually, no additional height gains are possible. Furthermore, because a growth plate is cartilage, disorders affecting other cartilage in the human body affect the normal longitudinal growth of the long bones in humans. Various injuries to the human skeleton can also lead to problems affecting height due to the negative effects of growth plates. Finally, diseases such as hormonal imbalances, localized pathologies, or genetic abnormalities may negatively affect the potential of a child to attain an adult’s final height. These disorders can also affect the time when all bone growth will end, when the growth plates will close and no focal growth will be possible.
Height is determined not only by genetic factors but is also influenced by environmental factors. In the general population, adult height is about 80% heritable, meaning that 80% of the variation in adult height is attributed to genetic factors. The heritability factors affecting height growth are complex because it is polygenic, meaning it is determined by a combination of multiple genes. Moreover, there are numerous non-genetic factors that interact within the gene framework, such as environmental, socio-economic, and health status, that have a direct or indirect effect on height. In summary, there is no doubt that genetics play a determining role in human height, but there are many environmental factors affecting height growth that can modulate the expression of growth and final height. In fact, improvements in living conditions and environment are associated with secular trends of increasing height.
Socioeconomic status and access to good healthcare services can impact a child’s physical growth. Lower income or poverty and underemployment make access to healthy food, healthcare, and safe environments to live and play difficult. Poor health may slow the growth process and decrease adult height. Although it is estimated that 80% of height is controlled by genetic factors, this also means environmental factors affecting height growth play a very significant role in determining the remaining 20% of height because there is an interaction between genes and the environment in determining phenotype. Nutrition, particularly vitamin A, vitamin D, zinc, and protein, is perhaps the most important non-genetic factor. Moreover, other dietary elements like calcium and sufficient omega-3 fatty acids can directly affect bone growth. Longitudinal growth is inversely related to the total content of n-6 fatty acids in the diet. Lifestyle choices such as sleep patterns and the quantity and type of physical activities and exercise can also affect growth. Children who do not get enough high-quality rest may grow less than children who get enough sleep.
Nutrition has long been considered critical in the process of growing tall. It is important from birth to adulthood, just as an infant’s nutrition has paramount importance for a child’s growth, which can persist into later years. A child’s growth is primarily influenced by the supply of energy and proteins, as well as adequate vitamins and minerals to ensure good body and, particularly, children’s bone development. Proteins and essential amino acids in the form of eggs and milk are principally important for good calcium absorption. Essential vitamins and minerals also support and regulate bone formation and many physiological processes in the body. Therefore, children should get proper nutrition throughout their growth years through a balanced diet. Nutrients particularly important for growth from infancy to age 18 include protein, calcium, phosphorus, vitamin D, and zinc. Low calcium intake is often associated with impaired bone mineralization and a lower risk of nutritional rickets. Vitamin D contributes to calcium absorption in the small intestine and bone homeostasis at any age. Additionally, vitamin D levels fluctuate seasonally, with the highest levels at the end of summer and the lowest levels at the end of winter. For this reason, prolonged deficiency during childhood increases the risk of preexisting rickets. Consumption of coffee and caffeine can decrease calcium absorption, but if the calcium intake is adequate, the effect of dietary intake of coffee and caffeine on calcium metabolism is minimal. Dietary habits in early life are not only huge health determinants but also form the basis for health in adulthood. A large number of studies have described the relation between malnutrition and delayed growth.
Nutrition has long been considered critical in the process of growing tall. It is important from birth to adulthood, just as an infant’s nutrition has paramount importance for a child’s growth, which can persist into later years. A child’s growth is primarily influenced by the supply of energy and proteins, as well as adequate vitamins and minerals to ensure good body and, particularly, children’s bone development. Proteins and essential amino acids in the form of eggs and milk are principally important for good calcium absorption. Essential vitamins and minerals also support and regulate bone formation and many physiological processes in the body. Therefore, children should get proper nutrition throughout their growth years through a balanced diet. Nutrients particularly important for growth from infancy to age 18 include protein, calcium, phosphorus, vitamin D, and zinc. Low calcium intake is often associated with impaired bone mineralization and a lower risk of nutritional rickets. Vitamin D contributes to calcium absorption in the small intestine and bone homeostasis at any age. Additionally, vitamin D levels fluctuate seasonally, with the highest levels at the end of summer and the lowest levels at the end of winter. For this reason, prolonged deficiency during childhood increases the risk of preexisting rickets. Consumption of coffee and caffeine can decrease calcium absorption, but if the calcium intake is adequate, the effect of dietary intake of coffee and caffeine on calcium metabolism is minimal. Dietary habits in early life are not only huge health determinants but also form the basis for health in adulthood. A large number of studies have described the relation between malnutrition and delayed growth.
In recent years, many adults show signs of growth that are traditionally associated with growth in the second decade. Bands of muscle fiber, visible in the femur, and the presence of simple bone marrow adipose tissue confirm this growth, along with the clinical observation of progressive growth in the extremities. Adults in the last decades have the growth spurt at age 20, or even 24 years, is something frequent and easy for the patient to perceive when they leave childhood and height growth after puberty. They are still growing. For clinicians with some experience in practice, increasing height through and into the twenties is easily proven by height measurements and confirmed by analyzing the calculated dates to which self-fitting to any curve applied to growth velocities they present.
Statistical concepts that explore and corroborate growth with S-shaped curve models, growth velocities, growth peaks, or phase contrasts, in the first, second, and third phases of growth, and the physiological basis for these concepts, have not yet been incorporated into clinical questionnaires and are not prioritized in any examination, including studies of physiopathology, therapeutic aspects, and follow-up protocols. As a result, reaching heights in the last quartile in young adults is still limited to the perception of the most experienced, who interpret the height growth age limit 20 to 24-year-old patients with ease, lacking precise clinical data and pathophysiological principles bringing growth to this age group. All this simple evidence, both clinical and physiological, and the methodical assessment of variability can provide important implications for customs, growth rules, attitudes, and expectations associated with the later stages of growth.
Currently, this phenomenon is known as “height growth in adulthood,” and it is possible to make effective interventions in adults to promote a gain of centimeters. But how is this phenomenon defined, and does height grow after 18? The definition of height growth in adulthood is totally based on the knowledge of the anatomical structure of bones. This knowledge is possible because bones are complex organs that contain numerous cells and tissues and have a very specific structure. With aging, the morphological properties of bones are extremely sensitive to internal and external signals, and these intrinsic characteristics can directly influence height. Height growth in adulthood is due to three processes that can act in isolation or consecutively: calcification time of the epiphysis and lower calcification average, disk regrowth rate, and trabecular thickness of the calcified bone.
Regarding the biological explanation of adult height growth age limit, it has been shown that what happens in the epiphyseal plate throughout the life of a human is very dynamic. Epiphyseal cartilages in adults receive signals such as an extracellular matrix and growth factors that can act on the proliferating zone, facilitating cell elongation and division. In addition, the presence of active mesenchymal cells can not only aid in these two processes but, when stimulated, produce new cartilage tissue, making the epiphyseal plate thicker. Through these new cells produced in this proliferating portion that equals the old values of the proliferative and hypertrophic zones, the epiphyseal plate can be re-differentiated into the growth zone. In this new growth zone, a new chondrocyte column can emerge and be quickly calcified, forming a new part of the epiphyseal region and increasing the height of the organism.
In conclusion, this overview of the multicellular processes that underpin preadult and adult growth emphasizes that the subject remains salient. Inter-individual differences in growth are profound, interpreted using a variety of methods. The importance of increased investigation into this process has recently been expressed, particularly in relation to health and nutrition, supporting our stance.
Based on our detailed analysis of the growth and development of human height, a number of key findings can be derived:
– Genetics is of paramount importance in determining how tall an individual grows and how quickly growth takes place.
– Nutrition is a primary driver of growth and late growth spurts that can lead to taller stature in adulthood beyond genetic expectations.
– Effective regulation and integration of growth-promoting processes, as well as the hormonal and biological signals on which they rely, play a significant role in a person’s ability to grow taller into adulthood and old age.
– At times, in the developmental stage, growth spurts may occur, with men often experiencing until what age does height grow around 18-19 years, resulting in their increasing height until their twenties.
– Exceptions can be observed, with individuals sometimes gaining height beyond their genetic potential throughout the third and sometimes fourth decades.
– Overall health, in particular nutritional status and the existence of disease, significantly influences an individual’s ability to grow in their current stage of life, which can be prolonged into late height growth after puberty and even adulthood if adequate health is achieved.
– Late growth spurts closer to adulthood (defined as being over 20 years of age) are significantly rarer than beliefs and anecdotal evidence suggest. However, there are significant gaps in current research knowledge, which goes some way towards explaining why the impact, extent, and influences on adult height growth are currently poorly understood. Available data is largely descriptive and offers little on the prevalence or molecular and genetic drives of abnormal stature development in the broadest adult lifespan, nor more subtle alterations that conspire across the lifespan to determine our final human height.
Recommendations for future research include:
– Studying or collating and analyzing cohort datasets with a broad age range, where reliable measures of accurate height and time points of this measurement are taken.
– Identifying influences and predictors of stature variance in later life, including nutrition, socio-economic status, and major chronic disease.
– Investigating correlations and interactions between the ability for and enriching stimuli to increase height postnatally and the incidence of conditions such as osteoarthritis and cardiovascular disease.
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