Because the epiphyseal plates (the end of long bones) are sealed
due to the effect of estrogen, by the end of adolescence, it?s hard to
see how an adult can increase her height. As a woman matures, bones do
become thicker and denser, but not longer.
I found scant reliable information on an adult gaining height! I
very briefly considered acromegaly or Sotos syndrome, but your
symptoms do not fit, and surely you would have been diagnosed during
your teen years. I thought of foot swelling or a foot arch oddity. I
even considered barometric pressure causing a change in your height. I
could find no information however to support these thoughts.
One is somewhat taller in the morning, as the spine becomes
?decompressed? as we sleep. Perhaps your vertebral disks retain more
fluid, longer, for some reason. Bone is constantly breaking down and
rebuilding. Perhaps your bones built a little extra! It may even be
possible that you had a decrease in estrogen during puberty and
adolescence, delaying your bone epiphysises from sealing, and that
they ?caught up? later and life? allowing your bones to continue
Some speculate that GH (Growth hormone) may have caused this
?spurt?, but once the bones are sealed, even GH will not increase
height. Adults DO need GH, but for different reasons than bone growth.
Adults need GH for muscle growth and maintenance, and normal brain
function. All of the above will be discussed further down in my
I have done an exhaustive search and am able to find only what I
have posted here. Please check each web site for additional
?Question: An acquaintance (female, age 35) has grown 1.5 inches in
the past twelve months. This is her first "growth spurt" since she was
14 years old. Isn't this very unusual? Why would she start growing
taller now, as an adult?
Answer: Adults usually stop growing due to fusion of their growth
plates to the associated bones. This usually occurs around menarche
for girls and about 25 for boys. Growth after this point is very rare,
although it could demonstrate excess growth hormone, which is a
medical condition that should be investigated.?
About Growth Hormone:
?Growth hormone (GH) is a protein hormone made by the pituitary, a
hormone producing gland located at the base of the skull. The
pituitary gland not only produces GH, but releases (secretes) GH into
the bloodstream. After entering the bloodstream, GH attaches to
certain tissues, especially bones, and results in height increase in
children. Damage to the pituitary gland in children results in low GH
secretion in children, resulting in poor growth and resultant short
stature. GH can be given to children to restore their normal growth
Over the last ten years, it has been discovered that adults need GH
too. Like children, adults can be given this hormone if deficient. The
approval by the FDA to give GH to deficient adults has been in place
for the last two years. Since adults have already achieved their
genetically determined height, loss of GH does not impact height, but
it does affect the body in many other ways. If adults have a
deficiency of GH, major changes to the composition of the body
results. These changes include loss of muscle, accumulation of fat,
especially in the abdomen, and a decrease in the density (but not the
length) of bones. Because GH is also necessary for normal brain
function, adults without this hormone have psychological changes in
addition. This article will focus on describing the GH deficiency
syndrome as it applies to adults, and how it is currently diagnosed
?The inhibition of estrogen synthesis delayed bone maturation.
These findings indicates that an increase in adult height can be
attained in growing adolescent boys or even adults who have open
growth plates by inhibiting of estrogen action.
Therefore, the pubertal growth rate of young adults can be blocked
thereby preventing bone maturation and increasing final height
?This study was conducted to analyse the effect of childhood-onset
diabetes mellitus on adult height. The height at time of diagnosis of
35 children with insulin-dependent diabetes mellitus (IDDM) was
compared with growth reference data. Predictions of the adult height
were made at the time of diagnosis using the target height and the
Tanner-Whitehouse II method. The adult height was compared with both
the predicted values and the height of healthy adults. The height at
time of diagnosis of the prepubertal children was increased compared
with growth reference data, in contrast to pubertal children who had
normal heights. Only the prepubertal boys were taller at time of
diagnosis. The adult height of the prepubertal patients was taller
than growth reference data. The mean adult height in all patients did
not differ significantly from the predicted heights. In conclusion,
the increased height at the start of IDDM in prepubertal children
persists until adulthood.?
?Bones grow in length at the epiphyseal plate by a process that is
similar to endochondral ossification. The cartilage in the region of
the epiphyseal plate next to the epiphysis continues to grow by
mitosis. The chondrocytes, in the region next to the diaphysis, age
and degenerate. Osteoblasts move in and ossify the matrix to form
bone. This process continues throughout childhood and the adolescent
years until the cartilage growth slows and finally stops. When
cartilage growth ceases, usually in the early twenties, the epiphyseal
plate completely ossifies so that only a thin epiphyseal line remains
and the bones can no longer grow in length. Bone growth is under the
influence of growth hormone from the anterior pituitary gland and sex
hormones from the ovaries and testes.?
?Estrogens have been used to reduce the height of unusually tall
girls since the 1950s1?4 based upon the concept that, during normal
puberty, increased estrogen levels lead to epiphyseal fusion in the
?In long bones, the growth and elongation (lengthening) continue
from birth through adolescence. Elongation is achieved by the activity
of two cartilage plates, called epiphyseal plates, located between the
shaft (the diaphysis) and the heads (epiphyses) of the bones (Figure
5). These plates expand, forming new cells, and increasing the length
of the shaft. In this manner, the length of the shaft increases at
both ends, and each head of the bone moves progressively apart. As
growth proceeds, the thickness of the epiphyseal plates gradually
decreases and this bone lengthening process ends. In humans, different
bones stop lengthening at different ages, but ossification is fully
complete by about age 25. During this lengthening period, the stresses
of physical activity result in the strengthening of bone tissue.?
?Bone development is influenced by a number of factors, including
nutrition, exposure to sunlight, hormonal secretions, and physical
exercise. For example, exposure of skin to the ultraviolet portion of
sunlight is favorable to bone development, because the skin can
produce vitamin D when it is exposed to such radiation. Vitamin D is
necessary for the proper absorption of calcium in the small intestine.
In the absence of this vitamin, calcium is poorly absorbed, the bone
matrix is deficient in calcium, and the bones are likely to be
deformed or very weak. Vitamins A and C also are needed for normal
bone growth and development.?
?When a low blood calcium condition exists, the parathyroid glands
respond by releasing parathyroid hormone (PTH). This hormone
stimulates osteoclasts to break down bone tissue, and as a result,
calcium salts are released into the blood. On the other hand, if the
blood calcium level is excessively high, the thyroid gland responds by
releasing a hormone called calcitonin. Its effect is opposite that of
parathyroid hormone; it inhibits osteoclast activity allowing
osteoblasts to form bone tissue. As a result, the excessive calcium is
stored in bone matrix. The actions of these hormones are both
excellent examples of some important negative feedback loops present
in our bodies (Figure 7). Without adequate supplies of these important
chemicals, the bones will not develop or grow normally.?
?When a force is applied to any material, such as bone, it deforms.
The amount of deformation in the material relative to its original
length, is the strain. When a material is pushed together, the
material shortens (compressive strain). When pulled, it gets longer
(tensile strain). Shear strain arises when layers of a material slide
against another, as might occur with torsion or bending. The strain
can be expressed as a percentage (100 x change in length/original
length). When your muscle contracts, the tendon can strain as much as
5% in tension during intense activities. Compressive strains in bone
during peak activities only rise to about 0.3% strain, and bone begins
to fail at 0.7% strain (7000 microstrain).? There are some good
explanatory illustrations on this page.
?Ordinary activity causes microscopic cracks in the bone, and these
are dissolved and replaced with new bone. Remodeling also allows bone
to respond to changes in mechanical forces. Thus, living bone is
totally different from the skeleton in the closet.? This page has an
animated illustration of the epiphyseal growth plate.
?The epiphyseal growth plate is made up of three tissue types: the
cartilage component divided into distinct zones (Fig. 2), the bony
tissue of the metaphysis and the fibrous tissue that surrounds the
growth plate. The vascular supply to the growth plate is illustrated
in Fig. 1. The secondary ossification centre is supplied by the
epiphyseal artery, branches of which end in the proliferating
cartilage zone. The metaphysis is supplied mainly by the nutrient
artery, with the periphery having an additional supply from
metaphyseal vessels (Chung, 1976). Terminal branches of these arteries
end in capillary loops below intact cartilage septae that delineate
the end of the cartilage zone. These capillaries drain into the large
central vein of the diaphysis. Since there are no branches from
metaphyseal or epiphyseal arteries to the hypertrophic zone, this
region of the growth plate is avascular. Only the proliferative zone
has an abundant blood supply.?
?A person's height also varies over the course of the day, by an
average of 19 mm (¾ in), gradually shrinking as the spine compresses
over the course of a day, and stretching back out overnight (Tyrrell,
et al. 1985).?
Receiving LH-releasing hormone (LH is leutinizing hormone) ?One of
the strategies to optimize GH therapy during adolescence is to delay
epiphyseal fusion with a LH-releasing hormone (LHRH) analog.
Administration of such analogs to children with central precocious
puberty has caused a regression of their clinical signs of puberty, a
slowing of their rate of bone age maturation (5), and an increase in
their final height (6, 7, 8, 9). Moreover, patients with GH deficiency
associated with hypogonadotropic hypogonadism have a mean final height
greater than that observed in patients with isolated GH deficiency (3,
10). This suggests that delaying sex steroid exposure in these
patients may enhance final height.?
?Do not believe those who tell you that you cannot grow any taller
after puberty. Young adults can grow a few inches taller even after
the bones in the lower body become ossified. This is because besides
the length of the bones in lower body, the length of spinal column in
the upper body also alters height. The bone segment in the spinal
column known as vertebra is held together by ligaments. Out of 33
vertebrae only the lowest 9 are fused into two immovable bones,
forming the back of pelvis. All the other 24 vertebrae are permanently
movable and thus never get fused. There are cartilaginous pad called
discs between these vertebrae, the thickness of which determines the
length of spinal column. There are totally 25 discs, their combined
length accounts for a part of the total height. Since these discs are
non-fusible cartilages, they can grow thicker under stimulation. The
thicker the discs are the longer becomes the spinal column and taller
the person grows.?
Your ?growth spurt? may have been due to the time of day you were measured:
?? I will confirm that it is true that many people, especially
people blessed with youth, are taller after they wake up. The same
phenomenon happens to astronauts when they're zinging around in outer
?When you're asleep in your bed, the disks that separate the vertebrae
in your spinal column expand just a bit. This separation can give your
height a little boost, but it all goes away during the day. According
to NASA, astronauts get to enjoy the extra height that "microgravity"
bequeaths them until they come home to Earth.?
?Researchers in Australia are in the midst of a six-month experiment
measuring a man and a woman every day to learn more about this very
subject. They told me they're finding that people are indeed taller
after lying down. This works any time of the day, they say. So
theoretically, you could lie down on the couch for a nap, and wake up
taller. Sitting and standing compact our vertebral column, especially
the intervertebral disks. It's also possible that the muscles holding
us up might get tired, because the more strenuous your daily
activities, the more height you lose.?
?We are about 1 cm taller in the morning than in the evening.
Layers of cartilage in the joints gets compressed during the day.?
?Compression testing is one of the most common tests performed on
spinal segments. This is because when we stand, the spine can feel
compression forces up to three times the weight of our trunk. What is
being tested in most cases is the compression of the spine on a daily
basis. As we lie down, the deformation from gravitational forces is
released and the spine elongates. This is why we are taller in the
morning than we are at night!
The goal of this experiment is to show that deformation
decreases as the spine ages due to an increased Young?s modulus in the
nucleus. This corresponds to decreased water content of the nucleus,
causing it to become stiffer. The stresses felt in the nucleus will
increase during this same aging. Also important in aging is the idea
that the collagen content is changing in the discs. Type I and type
II collagen have been identified as present in the annulus and
nucleus; the ratio of these two type of collagen is representative of
the age of the disc. More type I will be found in the annulus and
more type II in the nucleus when the disc is young and healthy.?
?Compression is not a native conception to Yoga students. Even if a
student senses a ?natural limitation? in their movements they will not
use the word ?compression? to describe it. The closest they will come
is ?I don?t bend that way.? Time and again I have seen students unable
to tilt his pelvis forward in a forward bending posture because the
trochanter of their femur is compressed. When I ask them where they
feel the restriction they are not sure what to say because they don?t
feel a ?stretch? in their groin or hamstrings. They are not in pain.
Pushing on them doesn?t bother them much. They just ?can?t do down?.?
?During loading the disc deforms and loses height. The endplate and
annulus bulge, increasing the tension on these structures, and the
pressure of the nucleus consequently rises. The degree of deformation
of the disc depends on the rate at which it is loaded. The disc can
deform considerably, compressing or extending by 30 to 60% during
flexion and extension. Distances between adjacent spinal processes can
increase by over 300%. If a load is removed within a few seconds, the
disc quickly returns to its former state, but if the load is
maintained, the disc continues to lose height. This ?creep? results
from the continuing deformation of the disc structures and also from
fluid loss, because discs lose fluid as a result of the increased
pressure. Between 10 and 25% of the disc's fluid is slowly lost during
daily activities, when the disc is under much greater pressures, and
regained when lying down at rest. This loss of water can lead to a
decrease in an individual's height of 1 to 2 cm from morning to
evening among dayworkers.
As the disc changes its composition because of ageing or degeneration,
the response of the disc to mechanical loads also changes. With a loss
of proteoglycan and thus water content, the nucleus can no longer
respond as efficiently. This change results in uneven stresses across
the endplate and the annulus fibres, and, in severe cases of
degeneration, the inner fibres may bulge inward when the disc is
loaded, which, in turn, may lead to abnormal stresses on other disc
structures, eventually causing their failure. The rate of creep is
also increased in degenerated discs, which thus lose height faster
than normal discs under the same load. Narrowing of the disc space
affects other spinal structures, such as muscles and ligaments, and,
in particular, leads to an increase in pressure on the facet joints,
which may be the cause of the degenerative changes seen in the facet
joints of spines with abnormal discs.?
Water is the major component of the disc and rigidity of the tissue is
maintained by the hydrophilic properties of the proteoglycans. With
initial loss of water, the disc becomes more flaccid and deformable as
the collagen network relaxes. However, once the disc has lost a
significant fraction of water, its mechanical properties change
drastically; the tissue behaves more like a solid than a composite
under load. Water also provides the medium through which nutrients and
wastes are exchanged between the disc and the surrounding blood
"Growth and development of the long bones of the skeleton are
influenced by numerous epigenetic factors, including both local and
systemic growth factors and hormones, as well as mechanical stimuli.
In the long bones, growth in bone length and girth occur via two
distinct processes. Growth in girth or cross section is accomplished
by direct bone apposition and resorption, whereas growth in bone
length occurs via endochondral ossification whereby cartilage is
replaced by bone. Numerous experimental investigations have
demonstrated that appositional bone growth is largely driven by the
changing mechanical stimulus that parallels the increase in body mass
of a growing individual. In contrast, while mechanical loading plays a
role in endochondral growth and ossification, experimental evidence
suggest that longitudinal bone growth is largely controlled by local
and systemic biochemical factors. Changes in mechanical stimuli
associated with altered physical activity have a minimal effect on
longitudinal bone growth unless those changes are extremely severe."
Perhaps the cartilage at the end of your long bones may have
increased in thickness!
"Figure 2. a) Features of an adult long bone end; b) Finite element
model used to predict the progression of osteoarthritis.
In this model (Fig. 2, b), each element represents a region of
cartilage or bone. In our computer simulations, we predict changes in
cartilage thickness and bone density as the bone develops and ages.
The simulations begin very early in development, when the bone end is
chiefly cartilaginous. Within the model, cartilage is assumed to
mature based on a combination of mechanical and genetic factors.
Mature cartilage is subsequently replaced by bone. Bone density is
increased in areas of high stress and decreased in areas of low
stress. These computer models are run repeatedly to simulate the
passage of time and aging. Our preliminary models predict early
development and endochondral ossification of long bones very well.
These models are now being applied over longer time periods to predict
the influence of bone geometry and loading conditions on the
progression of osteoarthritis."
Can an adult grow taller?
?It is all in the 'genes'. Good nutrition and habits (sleep, etc) can
certainly help, but in terms of height your genetic make-up will
determine most of it. For persons with a documented absence of growth
hormone, administration of this hormone can help them to acheive
'normal' stature, but this is indicated only for persons clearly way
below normal growth curves and a documented (by lab tests) deficiency.
Growth hormone given after bones have stopped growing (for example at
22) would be more likely to induce acromegaly. This is a disease seen
in persons that secrete too much growth hormone. The symptoms are
significant corsening of facial features, hyperplasia of joints and
Body growth, hence final height, is determined largely by the growth
in length of the long bones. At birth, the ends of most long bones
still consist of cartilage. Gradually, these begin to ossify, but a
plate of growing cartilage remains at the bone ends. This is called
the epiphysial, or growth, plate, and continues to produce new
cartilage, which increases the length of the bone, before this too
ossifies. At the end of the growing period, division of cartilage
cells within the plate ceases, and the plate itself ossifies, and
normal bone growth stops.
The rate and duration of growth is determined by many factors -
genetic, nutritional, and hormonal, and it should come as no surprise
that there is a growth spurt around puberty, when many of the
responsible hormones are very active. Growth then tails off
dramatically after puberty, and ceases around the late teens to early
Two more thoughts: Are you sure you were always barefoot when being
measured for height? Is it possible the measuring device was not
I hope this has helped you out. Please request an Answer
Clarification, if anything is unclear, and allow me to respond, before
you rate. I?ll do what I can to clarify my answer to your
delayed epiphyseal maturation + adult women
increased height + adult + genetic
long bone growth + adult
vertebral discs swelling
increased arch + foot
foot swelling + increased height
aromatase + height
thyroid + height