Diseases Caused by

Dietary Problems
Diseases Caused by
Dietary Problems

Mary E. Miller
Diseases Caused by Dietary Problems
Copyright © Momentum Press®, LLC, 2018.

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 Abstract
The importance of meeting the dietary needs of individuals is critical
for good health. This requires the education of individuals so that they
understand how to best obtain important nutrients and that quality food
rich in these nutrients are accessible to the increasing world population.
Many diseases can arise from nutrient deficiencies and toxicities, includ-
ing rickets, scurvy, and spina bifida, resulting from deficiencies in vita-
mins D, C, and B, respectively. It is also possible to ingest materials in the
diet that can cause disease, such as lead which results in lead poisoning. In
each case, the imbalance of appropriate nutrients leads to an imbalance of
vitamin and minerals, causing defects in critical enzyme function in the
body. In some cases, the uptake of nutrients is healthy, but the body is
unable to breakdown or utilize the nutrients. When the body has access to
the appropriate nutrients, but is unable to break them down, then these
diseases can be influenced by genetic factors. These imbalances result in
unique symptoms for each disease that are directly related to the function
of these nutrients in the body. These diseases are avoidable and, when
recognized early, can be treated. These very serious diseases continue to be
a major health concern, particularly for individuals with restricted food
resources.

Keywords
calcium; lead; lead poisoning; phosphorous; rickets; scurvy; spina bifida;
vitamin B; vitamin C; vitamin D
 Contents
Acknowledgments....................................................................................ix
Introduction...........................................................................................xi
Chapter 1: Symptoms and Diagnosis...................................................1
Chapter 2: Causes and Contributing Factors.....................................11
Chapter 3: Treatment and Therapy....................................................25
Chapter 4: Future Prospects...............................................................31

Conclusion............................................................................................33
Bibliography..........................................................................................35
Glossary................................................................................................39
About the Author...................................................................................41
Index....................................................................................................43
 Acknowledgments
I would like to thank Malcolm Campbell for the opportunity to make
contributions to this book series. His forward approach to science and
scientific pedagogy is inspiring. I thank my husband David and daughter
Mallory for their patience and support of these efforts. I am fortunate to
work at Rhodes College, which has supported my professional and intel-
lectual development. I take pride that I have worked with outstanding
students and thank them for inspiring my passion for science education.
My outstanding mentors, colleagues, and collaborators have made it pos-
sible to carry out rigorous research and forward high-impact educational
practices. Specifically, I thank Mitch Smith, Dan Engel, Jeff Becker, Fred
Cross, and Pam Hanson, whose advice and influence have shaped my
professional success. The editorial staff at Momentum Press have been
supportive and kind, and I appreciate their work in the production of this
book. I hope that some aspect of this work is helpful for individuals work-
ing to better understand or manage these devastating diseases.
 Introduction
In some cases, very serious diseases can be entirely preventable by modi-
fications in diet. These nutritional diseases are dependent on a person’s
access to specific nutrients through natural biosynthetic processes in the
body or food that they eat. Appropriate access to food can prevent and
cure many life-threatening diseases. When considering worldwide access
to food, and how this access impacts human health, understanding clear
nutritional deficiencies and toxicity is critical in diagnosing, treating, and
curing nutritional diseases. We will consider four human health problems
(rickets, scurvy, spina bifida, and lead poisoning) that are related to
nutritional diseases or toxicity. In the case of rickets, scurvy, and spina
bifida, vitamin deficiencies trigger disease onset. In the case of lead poi-
soning, the ingestion of the heavy metal lead can cause disease.
Vitamins are small chemical molecules that can be obtained from our
diet. Humans generally need 13 different types of vitamins. Vitamin A,
D, E, and K are all fat soluble and therefore they are best absorbed by our
bodies when ingested with some form of fats consumed during a meal.
The other nine vitamins are water soluble and include vitamin C and
eight types of B vitamins. B vitamins include B1 (thiamine), B2 (ribofla-
vin), B3 (niacin), B5 (pantothenic acid), B6, B9 (folate), and B12. The B
vitamins are grouped because they all help similar sets of enzymes func-
tion in the cells of our body. Vitamins are generally produced by plants,
but can be obtained by consuming animal products because the animals
are capable of making the minerals or they eat plants that originally made
the vitamins. Since human cells cannot synthesize all of these vitamins,
we are frequently dependent on our diet to obtain and maintain high
enough levels of vitamins to maintain healthy physiological functions.
Vitamins contain carbon atoms and so they are considered organic
molecules. The carbon atoms in vitamins can react with or be incorpo-
rated into new chemical bonds with other molecules. In these reactions,
vitamins must physically interact with other molecules, so a vitamin’s
xii INTRODUCTION

shape is critical for its function. Heat can change the shape of a vitamin
enough so that it no longer functions. This is why fruits and vegetables are
more nutritious raw than cooked. Vitamins have very different chemical
structures than minerals. Dietary minerals such as calcium and phos-
phorous do not contain carbon, so are called inorganic, and are more
difficult to break into pieces or react with in nature. Therefore, dietary
minerals are not usually destroyed when food is cooked. With this in
mind, we normally associate vitamins with living organisms—we get our
vitamins by eating plants or animals because these living systems create
the vitamins. We associate minerals with our environment—found in the
water we drink or the soil where plants grow. Minerals can accumulate
in plants and animals that we eat because they take up the minerals from
their environment. Both vitamins and minerals are vitally important to
human health. Vitamins and minerals frequently rely on each other for
function, and depletion of one can cause the depletion of the other. For
this reason, nutritional deficiencies that we associated with a lack of vita-
mins in our diet can be tied to dietary deficiencies in minerals.
Vitamins and minerals are frequently associated with the function
of special proteins in the body called enzymes. Generally, proteins are
composed of amino acid chains, and each amino acid has chemical and
structural properties that determine the protein’s overall shape and thus
its function. The shape and structural characteristics of an enzyme protein
dictate how it interacts with other molecules and how an enzyme can
produce structural changes in other molecules. Enzymes are associated
with cellular metabolism—the synthesis and breakdown of the materi-
als inside living cells. For example, some enzymes add a hydroxyl group
to another protein; a hydroxyl group is composed of one oxygen atom
chemically bound to one hydrogen atom. When a protein is modified
by the addition of a hydroxyl group, it is very likely that the modified
protein has an altered three-dimensional shape that can produce a new
function in the modified protein. Many nutritional diseases cause defects
in critical enzyme function, and therefore many nutritional diseases pro-
duce a metabolic dysfunction in the body. Not all proteins interact with
vitamins are enzymes. Other types of proteins influenced directly by
vitamins are responsible for intercellular communication. For example,
some proteins called receptors are located on the surface of a cell and
 INTRODUCTION
xiii

bind (physically interact) with molecules found outside of the cell. Some

­receptors can interact with signaling molecules called hormones, and
when this occurs a signal transduction cascade is triggered that can bring
about many changes inside of the cell. Some vitamins are modified to
function as hormones. Therefore, vitamins can have profound impacts on
overall cellular function since vitamins can affect mineral levels, enzyme
function, and signal transduction. It should not be surprising that vitamin
deficiencies can produce detrimental physiological effects such as diseases.
All 10 trillion of our cells contain complex network of interactions
in the human body to ensure healthy growth and development of many
organs and tissues, and a subset of these interactions are influenced by
vitamins. For this reason, many symptoms of a specific vitamin deficiency
are well documented, even though how a vitamin deficiency is producing
its symptoms at the cellular or tissue level is not understood fully. Numer-
ous human diseases are caused by vitamin deficiency that changes mineral
levels in the body. For example, calcium levels are sensitive to vitamin
D, C, B9, and lead concentrations—and so the mineral calcium contrib-
utes to symptoms of rickets, scurvy, spina bifida, and lead poisoning. The
interplay between vitamin and mineral levels in the body can produce
complex problems throughout the body. When the underlying cause of
mineral depletion is understood to be a vitamin deficiency, changes in
diet can be used as an effective preventative measure or a treatment to
reverse symptoms.
 CHAPTER 1

Symptoms and Diagnosis

Symptoms and Diagnosis of Rickets

Rickets is a disease where the growth of new bone is impaired. Most
­commonly, rickets is associated with defects in the metabolism of vita-
min D (Figure 1.1), and for this reason most common types of rickets
are called vitamin D–dependent rickets (VDDR). VDDR is thought
to impact approximately 50 percent of the population worldwide. Vita-
min D can be made by our bodies, but only when we have been exposed
to sunlight. Early reports of rickets correlate to the industrial revolution
where pollution restricted access to sunlight, and for this reason rickets
is a candidate disease for one of the first to be caused by environmental
pollution. When VDDR is thought to result primarily from deficiency of
vitamin D in the diet (rather than a problem with using the vitamin D
that is in the body), it is called nutritional rickets (NR). While NR is a
serious disease, it is preventable with appropriate diet changes. Currently,
reports suggest that the global incidence of rickets is rising, particularly in
dark skinned immigrant populations as compared to native populations,
though the prevalence of the disease worldwide is not well recorded.
Rickets is characterized by symptoms of defective bone growth. Both
calcium and phosphorous are important minerals found in bone and are
responsible for the bone stiffness. Absorption of these minerals depends
upon vitamin D, so low levels of vitamin D can lead to osteomalacia, or
“softening” of the bone. Because most bone growth occurs during child-
hood, rickets frequently is first observed during infancy or childhood.
General symptoms include pain or tenderness in the bone; tendency to
fracture bones; and deformities in areas such as wrists, ribs, knees, or
elbows. Rickets can also cause curvature of the legs because the bones
2 DISEASES CAUSED BY DIETARY PROBLEMS

Figure 1.1  The chemical structure of vitamin D3

Source: By Sbrools [GFDL (http://www.gnu.org/copyleft/fdl.html), CC-BY-SA-3.0 (http://
creativecommons.org/licenses/by-sa/3.0/), or CC BY-SA 2.5 (https://creativecommons.org/
licenses/by-sa/2.5)], modified from Wikimedia Commons. J. Org. Chem. (1976) 41, 3476–8.

are too weak to bear weight, as well as large forehead, abnormally shaped
ribs, abnormally curved spine, large abdomen, stunted growth, and teeth
abnormalities. In rare cases of VDDR, hair loss can also occur; at times,
to the extent that the patient has no body hair at all. Calcium and phos-
phorous can also be important for neuromuscular function too, so varied
 Symptoms and Diagnosis 3

symptoms may include defects in muscle function, leading to muscle

weakness, at times accompanied by seizures.
Rickets can also cause an increase in the amount of parathyroid hor-
mone (PTH), which plays a role in maintaining calcium levels in the
body. Changes in PTH can lead to a condition called secondary para-
hyperthryoidism, which causes the parathyroid glands to become larger
than normal. Usually the parathyroid are four small glands, each about
the size of a grain of rice, located in the neck. Parathyroid glands control
calcium levels in the body by several mechanisms. If blood calcium levels
drop, parathyroid glands release PTH into the body. PTH stimulates the
release of calcium by regulating the breakdown of bone and increased
absorption of calcium in the intestines. PTH also lowers the excretion of
calcium in urine by altering kidney function. In this sense, PTH helps
maintain the proper balance of calcium available in the body.
If symptoms of rickets are noted, both x-rays of bone structure and
blood tests can be used to diagnose the patient. Blood tests are used to
detect the amount of the vitamin D, specifically a modified version of
vitamin D called 25-hydroxyvitamin D (25OHD). The 25OHD form
of vitamin D is freely circulating in the blood stream and is thought
to be a good indicator of vitamin D levels for diagnostic tests that
can give an early indication of rickets. Specifically, deficiency would be
a serum 25OHD concentration less than 12 ng/mL (or 30 nmol/L),
and insufficiency would be 12 to 20 ng/mL (30 to 50 nmol/L). The
U.S. Institute of Medicine has recently recommended that an indi-
vidual also be described as being vitamin D insufficient if 25OHD
levels fall between 21 and 29 ng/mL. The blood test for 25OHD can
also be used to screen for rickets in those cases where children have
other bone diseases or are on medications that might interfere with
vitamin D production or absorption. The diagnosis of rickets can also
include x-rays to detect atypical bone formation and areas of calcium
or bone density loss. Although the method is rarely used, bone biopsies
can confirm a rickets diagnosis. Phosphate levels are also influenced by
vitamin D, so low phosphate levels, hypophosphatemia, can occur in
rickets patients. Vitamin D resistant forms of hypophosphatemic rick-
ets can occur, where phosphate levels are too low but for reasons other
than vitamin D metabolism.
4 DISEASES CAUSED BY DIETARY PROBLEMS

Other conditions can be associated with healthy levels of vitamin D in

the body. Since vitamin D is a fat-soluble vitamin that acts as a steroid hor-
mone, it potentially can influence physiology of many cell types and tissues.
Correlations between healthy vitamin D levels and varying health condi-
tions have been identified including anti-inflammatory defects and reduc-
tion of colon cancer risk. One study found that patients with lower vitamin
D levels were at 60 percent higher risk of heart disease. The third National
Health and Nutrition Examination Survey (NHANES-III) found that high
blood pressure was also associated with lower vitamin D levels. Increased
vitamin D intake is associated with reduced diabetes progression, and in
some populations vitamin D intake is correlated with reduction in symp-
toms of depression. Other nonskeletal diseases associated with vitamin D
include polycystic ovary syndrome, thyroid disease, and new-onset Graves
disease. A person with rickets may or may not also have these diseases.

Symptoms and Diagnosis of Scurvy

Scurvy is a serious health concern that results from a nutritional defi-
ciency of vitamin C, also known by its chemical name ascorbic acid
­(Figure 1.2). Scurvy was originally described by Dr. James Lind in 1753
as treatable with citrus fruits, and scurvy was likely the cause of recorded
disease as early as the 1500s. Although scurvy’s significance is mostly his-
torical, some resurgence of scurvy can be observed in areas of the world
where nutritional access is restricted, or dietary habits do not include
sources of ascorbic acid. The Centers for Disease Control and Prevention
(CDC) published a study in 2009 finding that 10 to 17 percent of low-
income people in the United States suffer from scurvy-level vitamin C
deficiency. Scurvy can occur at any age, to any population of individuals
with nutritional deficiencies.
The initial symptoms of scurvy can be subtle, making diagnosis at
early stages of disease progression more difficult. Initially symptoms
may include general weakness, fatigue, and aching limbs. As the disease
progresses, the symptoms can include anemia, myalgia (muscle pain),
bone pain, easy bruising, swelling, petechiae (skin bleeding), perifollicu-
lar hemorrhages (bleeding around the edges of hair follicles), corkscrew
hairs, gum disease, poor wound healing, mood changes, and depression.
 Symptoms and Diagnosis 5

Figure 1.2  Chemical structure of ascorbic acid

Source: By Ben Mills [Public domain], from Wikimedia Commons. https://upload.wikimedia.org/
wikipedia/commons/c/ca/Ascorbic-acid-from-xtal-1997-3D-balls.png

More advanced symptoms include the accumulation of fluids in body tis-

sues (edema), excess levels of the pigment bilirubin (jaundice), bursting of
blood cells, (hemolysis), acute spontaneous bleeding, neuropathy (nerve
dysfunction), fever, convulsions, and eventually death.
Early symptoms of scurvy can be observed in a patient after approxi-
mately 8 to 12 weeks of insufficient vitamin C intake, when the body’s
reserves of vitamin C drop from the standard total body content of 1,500
mg to the pathological threshold of 350 mg. Symptoms will progress as
vitamin C levels continue to drop in the patient. This drop in vitamin
C levels can be associated with intake below 60 mg of vitamin C per
day. Diagnosis usually occurs with physical examination and the deter-
mination that the patient has a history of insufficient vitamin C intake.
Broad symptoms consistent with the breakdown of blood vessel function,
such as hematologic abnormalities, ulcerative gum disease (gingivitis), or
blood clotting in deep veins (deep vein thrombosis) can be consistent
with scurvy. Since the disease can impact many different organ systems,
diagnosis is complicated because it can be confused with other disorders.
Despite similarities with other causative disorders, only scurvy can be
­resolved by increasing dietary consumption of vitamin C.
6 DISEASES CAUSED BY DIETARY PROBLEMS

Symptoms and Diagnosis of Spina Bifida

Spina bifida is a group of diseases characterized by defects in the brain,
spine, spinal cord, or the meninges (a protective layer of tissue that sur-
rounds the brain and spinal cord). In the United States, the Center for
Disease Control and Prevention (CDC) estimates that approximately
1,500 to 2,000 babies are born with spina bifida each year. The National
Institute of Neurological Disorders and Stroke of the National Institutes
of Health (NIH) report that there are an estimated 166,000 individuals
living with spina bifida in the United States. Symptoms vary in intensity
and manifestation among different individuals and include absence of
segments of the brain/skull/scalp (anencephaly), accumulation of fluid in
the brain (hydrocephaly), asymmetry of the spine or joints, loss of bladder
control, malformation of the spine or spinal cord (myelomeningocele), or
fatty deposits called lipomas that typically are harmless and non-­cancerous
despite a term that sounds cancerous. Spina bifida is characterized as one
of four types including occulta, closed neural tube defects, meningocele,
and myelomeningocele. These different forms of the disease are charac-
terized by different types of formations of the neural tissue and they dif-
fer in severity. Spina bifida occulta (SBO, also called closed spina bifida)
describes the form of spina bifida where the openings or malformations
in the vertebra are covered by layers of other tissues, such as skin. Occulta
gets its name from Latin meaning “secret or hidden.” Closed neural tube
defects of the spinal cord contain malformed fat, bone, or meninges. In
this case, there can be a range of symptoms from none to partial paralysis/
urinary tract/bowel problems. In some cases, a dimple or tuft of hair on
the spine can be observed. In the case of meningocele spina bifida, a sack
of fluid protrudes through an opening on the back and can be observed
externally. However, the spinal cord does not move through this opening
in meningocele spina bifida. Myelomeningocele is the most severe form
of the disease, and in this case the spinal column, specifically the bone
of the spinal column, does not form completely. In myelomeningocele,
some part of the spinal cord or tissues associated with the spinal cord
bulge out of the opening on the back of the patient. ­Additional symptoms
can include partial or full paralysis below the spinal column, bowel or
urinary problems, and hydrocephalus.
 Symptoms and Diagnosis 7

The diagnosis of spina bifida usually occurs before birth, though mild
cases might not be diagnosed until after birth. Screening can occur during
weeks 16 to 18 of pregnancy, using blood tests of the mother to d ­ etect
maternal serum alpha fetoprotein (MSAFP). Alpha fetoprotein is made
naturally by the fetus and placenta and can enter the mother’s blood
stream. Elevated levels of this protein indicate that the fetus might have
a neural tube defect which can lead to serious forms of spina bifida. The
MSAFP test is only a first pass screen so that if a mother tested positive
for high levels of MSAFP, the doctor would do further tests to determine
if spina bifida is in fact present in the fetus. One probable follow up
test might be an ultrasound, where sound waves are used to visualize the
shape of the fetus to identify any malformations. Samples from the fluid
of the amniotic sac (amniocentesis) can also be tested to detect high levels
of alpha fetoprotein. Tests for spina bifida can be carried out later in preg-
nancy, along with broader panels of tests to identify other potential birth
defects. Diagnosis after birth would include physical examination of the
infant to detect weakness in feet, hips, or legs with associated deformities.
Imaging techniques after birth such as x-rays, CT scans, or MRI can give
a more clear view of the spinal cord and brain to diagnose one of the four
types of spina bifida.

Symptoms and Diagnosis of Lead Poisoning

Lead poisoning occurs when lead enters our bodies from the environ-
ment. Lead is a metallic chemical element that can be burned when
incorporated into fuel (Figure 1.3). Lead also can be combined with
other metals to make alloys. Lead alloys are used in a variety of manu-
facturing, construction, and mining industries, which means exposure

Figure 1.3  The element lead is represented by the symbol “Pb,” has
the atomic number 82 with a standard atomic weight of 207.2
8 DISEASES CAUSED BY DIETARY PROBLEMS

to lead frequently happens in these workplaces. However, it is a common

misconception that pencil lead contains the chemical lead; there is no
­elemental lead in pencils and thus not toxic. Lead can enter the human
body by inhalation, absorption, or ingestion of materials containing lead.
The levels of lead that can be taken into the body are the highest when
inhaled. Once lead has gained access to the body, the symptoms are simi-
lar no matter the route of entry. If a person is exposed to very high levels
of lead for a short time, symptoms can include fatigue, irritability, loss of
appetite, abdominal pain, constipation, pain/tingling in the hands/feet,
memory loss, and weakness (Figure 1.4). These symptoms can be subtle
and onset slowly, but can lead to death. Lead exposure can also cause ane-
mia and kidney or brain damage. In some cases, exposure to lead occurs
over long periods of time. Symptoms of longer-term exposure to lead can
include abdominal pain, constipation, irritability, forgetfulness, depres-
sion, distraction, and nausea. Prolonged lead exposure also increases the
risk of infertility, high blood pressure, heart disease, and kidney disease.
Studies from the Department of Health and Human Services (DHHS),
Environmental Protection Agency (EPA), and the International Agency
for Research on Cancer (IARC) also show that lead exposure increases the
risk of cancer. If exposed to high enough levels of lead in a short period
of time, death can occur quickly due to seizures, coma, and cardiorespira-
tory arrest.
Very low levels of lead exposure can cause symptoms of reduced cog-
nition in children, so great concern is placed on preventing lead exposure
in children and fetuses. Unfortunately, lead can cross the placental bar-
rier, so that maternal exposure can also poison the unborn child while
the fetus is developing inside the mother. Exposures during fetal develop-
ment can cause damage to the nervous system of the baby. It is possible
that lead exposure can lead to death of the unborn child. In children and
adults, symptoms of lead poisoning can be subtle and progress slowly,
so lead poisoning can be easy to misdiagnose. In cases where ingestion
of materials containing lead is suspected within the previous 24 to 36
hours, x-ray examination of the abdomen can reveal larger pieces of
lead—though x-ray visualization alone would not be enough to diagnose
lead poisoning.
 Symptoms and Diagnosis 9

Figure 1.4  Symptoms of lead poisoning can impact throughout

the body
Source: Modified from Wikimedia Commons; By Mikael Häggström [CC0]. https://upload
.wikimedia.org/wikipedia/commons/0/0d/Symptoms_of_lead_poisoning_%28raster%29.png
10 DISEASES CAUSED BY DIETARY PROBLEMS

Lead accumulates throughout the body, including the blood. Th

­ erefore,
lead poisoning can be diagnosed by a blood test, where the blood lead
level (BLL) is measured and determined in micrograms of lead per deci-
liter of blood (μg/dL). In 2015, the lead poisoning prevention subcom-
mittee to the board of scientific counselors (BSC) was created to inform
public health policies as related to lead poisoning. In 2017, the lead poi-
soning prevention subcommittee recommended mandatory reporting of
BLL levels when present above a set reference point and suggested that the
threshold point be lower than the currently acceptable amount in humans.
The suggested concentration was 5 to 3.5 μg/dL BLL, whereas the current
reference point is 10 μg/dL. Detection of BLL is an important diagnostic
measure for diagnosing lead poisoning.
 Index
Adult Blood Lead Epidemiology EPA. See Environmental Protection
Surveillance (ABLES) Agency
Program, 23 Environmental Protection Agency
Alpha fetoprotein, 7 (EPA), 8
American Association of Epiphyseal line, 11
Pediatricians, 25
Amniocentesis, 7 Folate, 18
Ascorbic acid, 4, 16 genetic defects associated, 20
chemical structure of, 5 Folic acid, 18
chemical structure of, 20
BLL. See Blood lead level Free radicals, 17
Blood lead level (BLL), 10, 22
Blood vessel function, breakdown Genome, 20
of, 5 Glucose-6-phosphate dehydrogenase, 27
Board of scientific counselors (BSC), 10
Breastmilk, 25 Haptoglobin, 18
British anti-Lewisite (BAL). See HNRNPC gene, 15
Dimercaprol Hormone, 13
BSC. See Board of scientific Human plasma protein haptoglobin
counselors (Hp2), 18
Hypocalcemia, 13
Calcipenic rickets, 15 Hypophosphatemia, 3, 15
Calcitriol, 13
CaNa2EDTA, 28 IARC. See International Agency for
Carnitine, 16, 17 Research on Cancer
CDC. See Centers for Disease Control Institute of Medicine, 3
and Prevention International Agency for Research on
Centers for Disease Control and Cancer (IARC), 8
Prevention (CDC), 4, 6 Iron metabolism, 18
Chelation therapy, 27
Closed spina bifida. See Spina bifida Lead poisoning
occulta causes and contributing factors of,
Collagen, 16, 17 21–23
CYP27B1 gene, 15 future prospects, 31–32
CYP2R1 gene, 15 symptoms and diagnosis of, 7–10
treatments and therapies for, 27–29
Department of Health and Human L-gluconolactone oxidase, 16
Services (DHHS), 8 Lind, James, 4
DHHS. See Department of Health Lipomas, 6
and Human Services
Dimercaprol, 27 Maternal serum alpha fetoprotein
D-penicillamine, 28 (MSAFP), 7
44 INDEX
MSAFP. See Maternal serum alpha
fetoprotein
Myelomeningocele, 6, 26–27
National Health and Nutrition
Examination Survey
(NHANES-III), 4
National Institute for Occupational
Safety and Health
(NIOSH), 22
National Institute of Child Health
and Human Development
(NICHD), 31
National Institute of Neurological
Disorders, 6
National Lead Poisoning Prevention, 32
Neural tube, 18
Norepinephrine, 16, 17
Nutritional rickets (NR), 1
Occulta, 18
Occupational Safety and Health
Administration (OSHA) Lead
Standards, 22
1-alpha-hydroxylase, 13
Ossification, 11
Osteoclastogenesis, 15
Osteomalacia, 1, 11
Parathyroid hormone (PTH), 3
Permissible Exposure Limit (PEL), 22
Phosphopenic rickets, 15
Physis line, 11
PTH. See Parathyroid hormone
Recommended Exposure Limit
(REL), 22
REL. See Recommended Exposure
Limit
Rickets
causes and contributing factors of,
11–16
future prospects, 31–32
symptoms and diagnosis of, 1–4
treatments and therapies for, 25–26
SBO. See Spina bifida occulta
Scurvy
causes and contributing factors of,
16–18
future prospects, 31–32
symptoms and diagnosis of, 4–5
treatments and therapies for, 26
Secondary parahyperthryoidism, 3
Spina bifida
causes and contributing factors of,
18–21
future prospects, 31–32
symptoms and diagnosis of, 6
treatments and therapies for, 26–27
Spina bifida occulta (SBO), 6
Stroke of the National Institutes of
Health (NIH), 6
SVCT1/SVCT2 transporters, 16
Tethered cord syndrome, 27
25-hyroxyvitamin D3 (25OHD), 3,
13
Type 1A (VDDR1A), 15
Type 1B (VDDR1B), 15
Type 2A (VDDR2A), 15
Type 2B (VDDR2B), 15
VDDR. See Vitamin D–dependent
rickets
VDR, 13
Vitamin C replacement therapy, 26
Vitamin D, 4
Vitamin D 25-hydroxylase, 13
Vitamin D deficiency, 11
Vitamin D3, chemical structure of, 2
Vitamin D–dependent rickets
(VDDR), 1
Vitamin international units, 25
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• Breast Cancer: Medical Treatment, Side Effects, and Complementary Therapies
by K.V. Ramani, Hemalatha Ramani, B.S. Ajaikumar, and Riri G. Trivedi
• Acquired Immunodeficiency Syndrome (AIDS) Caused by HIV by Mary E. Miller
• Down Syndrome: One Smart Cookie by Todd T. Eckahl
• Diseases Spread by Insects or Ticks by Mary E. Miller
• Autism Spectrum Disorder: He Prefers to Play Alone by Todd T. Eckahl
• Cancer by Mary E. Miller
• Muscular Dystrophy: I’m Grateful I’ve Proved Them Wrong by Todd T. Eckahl

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