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Introduction
Obesity and diabetes are becoming more prevalent across all age groups in the United
States, and these diseases could affect an adolescent’s health both short and long-term into
adulthood. This group is more susceptible to developing poor body image, risky eating
behaviors, insulin resistance just to name a few. Adolescence is a crucial time in their life
because this is the point where they gain stature and start to develop a strong skeletal frame
that will support them throughout life. Calcium is one of the minerals that play a role in the
ossification and resorption of the skeletal frame. This remodeling process involves bone cells
secreting enzymes to break down the calcium while simultaneously replacing calcium to build
stronger bones. When osteoclasts break down bone faster than it is being rebuilt, the bones can
become fragile, and porous. This imbalance puts a person at risk for osteoporosis, which can
lead to a loss of height, a weak skeleton, and bone fractures. Foods and soft drinks that are
empty-calorie, high in fat and sugar, and low in nutrients, are some of the key factors that
correlate with being obese and developing type 2 diabetes. These foods and beverages are
sweet, rich in flavor, and leave little room for nutrients like calcium that are essential for
adequate bone growth in adolescents. As the rates of metabolic diseases like obesity and
diabetes increase across all ages, science is starting to investigate how these diseases can
Current research
Factors like genetics, environment, a sedentary lifestyle, and economic issues contribute
to obesity being a multi-faceted problem. The treatment plan for obesity is to prevent future
weight gain, lose weight, and maintain a healthy weight. Since obesity is becoming such a
problem in the United States, research is being conducted looking specifically at how obesity
can affect bone health. Bones need a stimulus such as mechanical stress in order to build more
bone. When a bone is put under stress or force, this causes the bone to become weaker with
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microtears. Osteoblasts are turned on, migrate to the affected area, and secrete a matrix to help
repair the bone. Body weight and other forces like weight-bearing exercise can help bones
become stronger. People who are overweight or obese should have stronger bones due to the
extra amount of stress being put on the bones. A study was conducted on Finnish women for
three generations and it found that an increase in body weight and fat decreases the strength of
their bones, but this is not the case for children.1 The possible explanation could be due to a
term called skeletal unloading. If an individual is sedentary or immobile, the bones will be under
minimal stress, and more fat cells will proliferate while osteoblastogenesis will decrease.1 The
individual will be not repairing or making new bone, so their bones could possibly become
weaker. A prospective cross-sectional study used convenience sampling of 2213 children aged
two to seventeen and categorized their BMIs.2 They came to the conclusion that obese children
were not at risk for fractures in their extremities.2 The study hints that a possible explanation
could be due to the relationship between bone mineral density and the odds of a fracture.2 It
could be possible that overweight and obese children have higher bone mineral densities which
put them at less risk for fractures. Researchers cannot seem to agree who is at risk for fractures
and who is not. Discrepancies in research such as the study group, factors such as male verse
The kind of fat and the location of the fat in the body could be another indication of your
bone health. Visceral fat is more harmful than subcutaneous because it covers vital organs and
could possibly disrupt their natural processes like hormones. One common issue we see with
obesity is a disruption of hormones. Hormones need ideal conditions in order to carry out their
functions properly. When the specific pathway is interrupted, hormone cycles can become
erratic and many processes can be distorted. Obese individuals have higher levels of estrogen
which is produced by white adipose tissue and this may increase bone loss in obese post-
menopausal women.1 CT and MRI scans can measure visceral and subcutaneous fat. Visceral
fat was found to be correlated with reduced bone mass while subcutaneous fat was found to be
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more beneficial to protecting bones.1 So possibly visceral fat is messing up the synchronism of
hormones but subcutaneous is helping to put more stress on the bones. After menopause
estrogen levels decrease for women. Women who are post-menopausal and obese have been
found to have lower osteocalcin levels which are responsible for bone formation.1 Therefore, an
increase in visceral fat can potentially increase the estrogen that is circulating around in the
body. Hormones are complex and sensitive so any changes in the pathway could lead to
The mesenchymal cell is responsible for creating and directing adipocytes and
osteoblasts.4 This is a complex process that involves pathways with specific receptors and
enzymes. Cytokines are cells that are responsible for communicating signals to other cells
regarding things like inflammation, repair, infection, etc. They are like the policeman who is
directing traffic and communicating with drivers on where to drive. When infection takes place in
a cell, these cytokines communicate to other cells and eventually, macrophages come and
engulf the bacteria. In obese people, cytokines are elevated, and this leads to an increase in
inflammation. The hypothesis is that cytokines create instability in the mesenchymal cell and
somehow modify the receptor which turns on osteoclasts leading to bone resoprtion.4
Cytokines can be triggered by parathyroid hormone (PTH). PTH is responsible for increasing
the absorption of calcium. If calcium in the blood is too low, PTH will stimulate bone resorption,
stimulate calcium absorption in the kidneys and activate vitamin D. This allows for the intestine
to get ready to absorb calcium. This process is also affected by fat mass and is also responsible
for releasing cytokines.1 The processes that happen in the body are intricate and intertwined so
a change in the system can directly affect the body in many ways.
Type one diabetes sometimes known as juvenile diabetes is when the pancreas either
makes little or no insulin. Insulin is the hormone that is released by the pancreas when blood
sugar is high, and insulin helps facilitate sugar or glucose into the cell. When there is little, or no
insulin produced by the pancreas this results in hyperglycemia. Since this disease is most likely
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noticed during adolescence, blood sugar levels can remain unchecked until a symptom occurs.
In type one, insulin growth like factor one and hyperglycemia may disrupt bone growth during
adolescence and lead to a lower bone mass later in adulthood.4 As we age, our bones stop
absorbing minerals and we start to lose bone mass usually in our forties. If bones do not
achieve an adequate amount of reserves during adolescence, this will put them at risk for
osteoporosis and bone fractures as they age. Another interesting point to consider is that
hyperglycemia can affect vitamin D and calcium absorption.4 These two nutrients are important
when it comes to bone ossification. Adolescents have become a prime target for food
advertising, especially fast food. Most of the time, the food is low in calcium and vitamin D and
adolescents prefer sugar and caffeinated drinks. Many adolescents are not consuming enough
of these vital nutrients appropriate for peak bone growth. Now add impaired absorption of
vitamin D and calcium and you have the perfect recipe for low bone mineral density. If
adolescents have problems with eating disorders or malabsorption this may not be easily
detected.4 If these symptoms are not well defined it can be hard to diagnose someone and help
treat the condition early on. This can lead to a lack of nutrition, low bone mineral density, and a
low body weight. If this happens in adolescence, this will directly affect bone quality, bone
density, and could possibly lead to osteoporosis and other bone-related diseases.
Most of the time people with diabetes also suffer from other complications like kidney
disease, damage to blood vessels, which could potentially put them at a higher risk for fractures.
The kidneys cannot function correctly and excrete more calcium than usual into the urine
diminishing bone mineral density. In order to test this hypothesis, a case study was conducted
to see if diabetes and the complications of diabetes put a person at risk for fractures. After
adjusting for the complications of diabetes, they found that there is little difference in overall
fractures for type one and type two diabetes.5 The only difference was that type one is more
susceptible to hip fractures due to diabetic kidney disease.5 This led to the conclusion that high
blood sugar levels could be the culprit for an increase in fractures compared to the
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complications of other diseases from diabetes. Type one diabetes may require a different
treatment plan when it comes to bone health compared to type two diabetes.
Type two diabetes is when your pancreas secretes insulin, but cells become resistant
resulting in hyperglycemia and hyperinsulinemia. In type two, insulin growth like factor is
elevated and this increases bone formation. Obese people with type two have a higher BMD
possibly due to the elevated levels of insulin, estrogen, and mechanical loading.4 Yet they are
still at risk for fractures. Science is hypothesizing that the bone quality is somehow
compromised so the skeletal frame does not have the adequate amount of minerals making it
and measured the hard (cortical) and spongey (trabecular) components of their nondominant
forearm and leg.6 They found that fractures could be due to resistance to bending due to the
shift of less intracortical bone compared to the increase in the trabecular part of the bone.6 The
cortical part of the bone is important because it’s the outer hard surface that helps the bone in
weight-bearing and during bending. If the cortical portion of the bone is weak and cannot
support force or stress than it could fracture more easily. If this theory is correct, people with
type two diabetes are at risk for bone diseases like osteoporosis which can be detrimental to
their bone health and potentially put them at risk for fractures.
Conclusion
Diabetes and obesity are increasing dramatically and can be very detrimental to
adolescents. These diseases are becoming more prevalent due to high caloric, high fat and
sugar, food, soft drinks and a sedentary lifestyle. Obesity and type two diabetes are diseases
that can be prevented through healthy eating habits, and an active lifestyle. Despite the
obesity affecting bone health especially when it comes to adolescents. If adolescents miss the
window for peak bone mass this could put them at a disadvantage as their age into adulthood.
Many people are going under the knife and getting Bariatric surgery to help them achieve a
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healthy weight. But certain procedures can disrupt calcium and vitamin D absorption and can
lead to the weakening of bones putting someone with diabetes even more at risk for bone
complications. Research in this field and its effects on bones is complex and inconclusive.
Researchers are finding contradicting results and future research is crucial in an attempt to find
a possible correlation. Diabetes and obesity are complex issues in which many systems and
processes are intertwined. These diseases already cost the United States millions of dollars and
if we dismiss the new research, we only are adding to the cost of healthcare spending.
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Work Cited
1. Shapses SA, Claudia Pop L, Wang Y. Obesity is a concern for bone health with aging.
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2. Sabhaney V, et la. Bone fractures in children: Is there an association with obesity? The
PMID: 24836073
3. Cao JJ. Effects of obesity on bone metabolism. Journal of Orthopedic Surgery and
relationship with risk of fractures in type 1 and 2 diabetes. Calci ed Tissue International
6. Burghardt AJ, Issever AS, Schwartz AV. High-resolution peripheral quantitative computed
tomographic imaging of cortical and trabecular bone microarchitecture in patients with type