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Sunshine and Cod Liver Oil: How Ancient Folklore Led to a Modern Diagnosis

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Title: Sunshine and Cod Liver Oil: How Ancient Folklore Led to a Modern Diagnosis


1
Sunshine and Cod Liver Oil How Ancient Folklore
Led to a Modern Diagnosis
  • Elisabeth Goldwater, MD
  • Texas Tech Health Sciences Center
  • Department of Pediatrics
  • Lubbock, Texas

2
Abstract
  • Rickets is a disease of Vitamin D
    deficiency that plagued children for centuries
    yet perplexed all who investigated its cause. In
    the early 20th century, rickets was widespread
    among children living in the northern cities of
    the United States and Europe. It had been
    observed that the addition of cod liver oil to
    the diet had the ability to heal this mysterious
    ailment. At the same time, scientists noted the
    curative effects of sunshine on these bony
    deformities. The fact that both diet and
    environment played a role in this disease was
    puzzling. Advances in research led to the
    discovery of Vitamin D, the elusive factor
    present in cod liver oil that was responsible for
    these therapeutic benefits. Further studies in
    the early 1920s determined that sunlight
    mediated the cutaneous synthesis of Vitamin D.
    The connection between the dietary and
    photosynthesized sources of Vitamin D provided
    the knowledge to eradicate rickets. The public
    health initiatives to prevent rickets have been
    extremely successful, yet children today continue
    to be afflicted with this disease. A modern
    awareness of this disorder is crucial. This case
    presentation illustrates how a seemingly historic
    disease can still have a contemporary emphasis.

3
Background/Objectives
  • Looking retrospectively at rickets illustrates
    the great historical advances that have been made
    in preventing and curing this disease.
  • This case illustrates the classic clinical
    findings of rickets.
  • It highlights the fact that general pediatricians
    may be confronted by this disease and serves as a
    reminder to be vigilant in current medical
    practices.
  • It points out the vulnerability of certain
    populations to rickets, particularly in infants
    that are exclusively breastfed, African American
    infants, and infants residing in northern
    latitudes.
  • It provides overwhelming evidence of the
    importance of public health campaigns in the
    prevention and eradication of disease.

4
Case Presentation
5
History of Present Illness
  • Chief Complaint
  • falls down a lot
  • History of Present Illness
  • 23 month-old African American female with a six
    month history of difficulty walking
  • Initially started walking more slowly, now
    stumbles frequently and is unable to fully extend
    legs
  • Mom also noticed swelling of the patients
    wrists, knees, and ankles over the past 4 months
  • Occasionally points to knees/wrists and says they
    hurt

6
Review of Systems
  • General afebrile, no weight loss, normal
    activity level, no fatigue stumbling frequently
  • Skin no rashes or lesions
  • HEENT no concerns about vision or hearing
    nasal congestion/rhinorrhea itchy watery eyes
  • Respiratory no cough, no increased work of
    breathing
  • CV no history of heart murmur
  • GI normal appetite no vomiting no diarrhea
  • Musculoskeletal as per HPI
  • Neuro no weakness no motor/sensory deficits

7
Past Medical History
  • Birth Hx Term C-Section BW 610oz normal
    newborn nursery course no complications
  • Past Hx Allergic rhinitis no previous ER visits
    or hospitalizations
  • Past Surgical Hx born with supernumerary digit
    on left hand which was surgically removed at 10
    months of age

8
Social History
  • Lives in West Texas with mother and grandmother
  • No siblings
  • Mother is a 3rd year law student, employed by a
    local law firm Grandmother is retired and serves
    as the daytime caretaker
  • No pets
  • No one in the household uses tobacco products
  • No daycare

9
Diet History
  • Breastfed until 18 months of age
  • Whole milk introduced at 15 months of age (one 4
    oz serving/day) along with one serving of juice
    per day and several servings of water
  • Rice cereal introduced at 6 months of age
  • Baby foods introduced at 7 months of age
  • Currently eats table foods- meat, vegetables, and
    fruit
  • Picky eater according to mom

10
More History
  • Medications Zyrtec
  • Allergies NKDA
  • Family Hx Grandmother with HTN otherwise
    negative
  • Development
  • Sit alone without support 6 months
  • Pull self to standing position 9 months
  • Walking 12 months
  • Language and fine motor development were WNL
  • For the past few months she has had increasing
    difficulty running climbing stairs

11
Physical Exam
  • General slightly fussy but cooperative female
    infant
  • Vitals T 98.4 P120 R28
    BP 98/70
  • Weight 10.4 kg (10) Length 80 cm (5-10)
  • HEENT frontal bossing noted, EOMI, PERRL, TMs
    clear B Oropharynx moist normal-appearing
    dentition
  • Neck supple, no lymphadenopathy
  • CV RRR no murmur
  • Lungs CTA B good air movement throughout
  • Chest firm, palpable rounded prominences at the
    end of each rib that are apparent on visual
    inspection of the thorax

12
Physical Exam
  • Abdomen soft, nondistended, normal active bowel
    sounds no masses, no hepatosplenomegaly
  • GU Tanner Stage 1 female normal external female
    genitalia
  • Neuro DTRs 2, motor and sensory intact Gait
    walked slowly with knees slightly flexed
  • Ext enlarged wrists, knees, and ankles by
    inspection and palpation. 1-2 inch section of
    widening across the wrist joint. Slightly
    decreased range of motion in wrists, knees, and
    ankles. Unable to fully extend legs from the
    knees. No pain noted with passive or active
    motion. No joint warmth, erythema, or tenderness
    noted with palpation. Slightly bowing of the legs
    when standing.
  • Skin no rashes or lesions present

13
Rachitic Rosary
14
Enlargement of Wrists
15
(No Transcript)
16
Differential Diagnosis- Rickets
  • Inadequate Synthesis/Dietary Deficiency of
    Vitamin D
  • Inadequate exposure to sunlight/Dark skin
    pigmentation
  • Limited dietary intake of fortified foods
  • Poor maternal nutrition
  • Decreased absorption of Fat-Soluble Vitamin D
  • Cholestatic liver disease
  • Pancreatic insufficiency
  • Biliary tract obstruction
  • Celiac sprue
  • Extensive small bowel disease

17
Differential Diagnosis- Rickets
  • Problems with Vitamin D Metabolism
  • Increased degradation of Vitamin D and 25 (OH) D
    (exmeds)
  • Phenytoin
  • Phenobarbital
  • Rifampin
  • Impaired synthesis of 25 (OH) D
  • Diffuse Liver Disease
  • Decreased synthesis of 1,25 (OH)2 D
  • Advanced Renal Disease
  • Vitamin D dependent rickets Type 1
    (deficiency of renal
    a1-hydroxylase)

18
Differential Diagnosis-Rickets
  • End-Organ resistance to 1,25 (OH)2 D
  • Vitamin D Dependent Rickets Type 2
    (inherited absence/defective receptors)
  • Phosphate Depletion
  • Chronic antacid use (aluminum hydroxide binds
    phosphate leading to poor absorption)
  • X-linked hypophosphatemic rickets/ Familial
    Hypophosphatemia/ Vitamin D resistant rickets
    (excess renal tubule excretion of phosphate)

19
Diagnosis- Rickets
  • This patient had several risk factors for
    developing a Vitamin D deficiency from inadequate
    intake/synthesis.
  • Dietary Breastfed until 18 months of age.
    Vitamin D-fortified milk (only 120 ml/day) was
    not introduced until 15 months.
  • Breastmilk contains a Vitamin D concentration of
    25 IU/L.
  • The recommended adequate intake of vitamin D is
    200 IU/day.
  • Therefore the patient was not getting the
    recommended amount of Vitamin D for normal bone
    metabolism.
  • Darker skin pigmentation limited the cutaneous
    synthesis of Vitamin D in this patient.
  • Mom reports that the patient received very little
    sun exposure and spent most of her time indoors.

20
Laboratory Investigation
  • Laboratory Workup
  • Typical Lab findings in Vitamin D deficiency
  • Calcium can be normal or low
  • Phosphorus is usually low but can be normal (as
    in this patient who was receiving a limited
    amount of Vitamin D)
  • PTH is increased
  • 25 (OH) D is low
  • 1-25 (OH)2 D can be low, normal, or high (This
    wide variation is due to upregulation of renal 1
    a-hydroxylase due to hypophosphatemia and
    hyperparathyroidism)
  • Alkaline Phosphatase will be high

88
Calcium 9.7 (normal) Phosphorus 3.5
(normal) Alkaline Phosphatase 1118 (high) 1-25
(OH)2 D 95 (normal)
21
Radiographic Findings
-Fraying of the metaphysis -loss of the
normally sharp border -Cupping of the
metaphysis- edge becomes concave rather than flat
or convex -Widening of the distal end of the
metaphysis -Thickening of the growth plate
secondary to decreased calcification -Line of
healing evident at metaphysis secondary to the
introduction of 4 oz whole milk/day at 15 months
(a small source of Vitamin D)
This patients X-rays at time of diagnosis
22
Radiographic Findings One Year after Diagnosis
and Treatment
  • The patient was started on daily high dose
    Vitamin D therapy for 4 weeks
  • This was followed by daily Vitamin D
    supplementation of 200 IU
  • Dietary adjustments were made to provide more
    Vitamin D-rich foods
  • These changes resulted in dramatic improvements
  • At a follow-up appointment one year later, the
    bony deformities were healed and the patient
    showed no clinical signs of rickets

This patients X-ray 1 year after diagnosis and
treatment
23
Clinical features of Rickets
  • Rickets is a disease of growing bone due to
    unmineralized matrix at the growth plates
  • Vitamin D mediates calcium absorption and is a
    crucial factor in the progression of bone
    mineralization
  • Some of the clinical features present in rickets
    include
  • Rachitic rosary widening of the costochondral
    junctions
  • Enlargement of wrists/ankles widening of the
    growth plates
  • Craniotabes softening of the cranial bones
  • Harrison groove horizontal depression along the
    lower anterior chest due to pulling of the ribs
    by the diaphragm during inspiration
  • Valgus or varus deformities/Anterior bowing of
    the tibia and femur softening of the bones

24
Rickets Throughout History
  • Recorded in medical writings as early as the
    1st-2nd century AD
  • Soranus, a Roman physician of the time, noted
    bony deformities were more common among infants
    in Rome than in Greece
  • Rickets was endemic in England in the mid-17th
    century
  • Turn of the 20th century, it was rampant among
    poor children living in the northern cities of
    the United States and Europe
  • 1909 among infants lt18 mo who had died, Schmorl
    et al found that 96 had histopathological
    evidence of rickets at autopsy

25
Rickets Throughout History
  • Francis Glisson, a Cambridge physician,
    published this statement regarding rickets in
    1650
  • We affirm therefore, that this disease doth
    rarely invade children presently at birth, or
    before they are 6 months old (yea perhaps before
    the ninth month) but after that time it beginneth
    little and little daily to rage more and more to
    the period of eighteen months

26
Suggested Cures for Rickets
  • As found in Glissons De Rachitide
  • Cautery
  • Incisions to draw out bad humors
  • Blistering
  • Ligature of soft wool around the limb to retard
    the return of blood
  • Splinting and artificial suspension of infant

27
The Value of Cod Liver Oil
  • 1861- Trousseau of France ventured that cod liver
    oil could cure rickets.
  • 1889- Bland Sutton observed rickets among lion
    cubs at the London Zoo. Addition of cod liver oil
    to their diets helped the cubs recover
    completely.
  • 1918- Sir Edward Mellanby cured rickets in dogs
    by feeding them cod liver oil. He suggested that
    there was an anti-rachitic factor present in
    cod liver oil that was either Vitamin A or a
    substance similar to it.
  • Cod liver oil was recommended for rickets, yet
    its scientific basis was not understood.

28
The Value of Sunshine
  • 1890- Palm noted that despite a better diet,
    infants living in Britain were more at risk for
    rickets than infants living in the tropics.
  • After studying the geographical distribution of
    rickets, he concluded that rickets was caused by
    a lack of exposure to sunlight.
  • As a result of his research, he recommended
    systematic use of sun-baths as a preventative
    and therapeutic measure in rickets.

29
Advances in Nutritional Biochemistry
  • 1920- researchers discover that irradiating
    certain foods destroyed fat-soluble Vitamin A.
  • 1922- Edward McCollum irradiated cod liver oil
    but noted that it still retained a substance that
    was protective against rickets.
  • He concluded that this substance was distinct
    from fat-soluble Vitamin A, and the purpose of
    this substance involved the metabolism of bones.
  • This newly discovered substance was the fourth
    vitamin discovered, therefore it was called
    Vitamin D
  • 1931- Askew determined the chemical makeup of
    Vitamin D found in food.
  • Continuing research further delineated the
    properties of Vitamin D and its importance in
    diet and bone metabolism.

30
Making the Vitamin D Connection
  • 1919- K. Huldschinsky conducted a study where he
    cured children with rickets by using ultraviolet
    light
  • 1919-1922- Dr. Harriette Chick studied the
    treatment of rickets in Vienna and demonstrated
    by radiographic evidence that bone healing was
    equally achieved by ultraviolet light or cod
    liver oil.
  • 1936- Windaus determines the chemical structure
    of Vitamin D synthesized in the skin via
    sunlight.
  • This body of research allowed scientists to
    determine the relationship between the Vitamin D
    found in foods and the one produced in the skin
    and their collective role in bone metabolism and
    rickets.

31
Vitamin D deficiency
  • Vitamin D deficiency remains the most common
    cause of rickets worldwide.
  • Breast milk is a poor source of Vitamin D
  • Infants that are exclusively breast-fed rely on
    cutaneous synthesis of Vitamin D
  • Cutaneous synthesis is affected by increased skin
    pigmentation, as well as the ineffectiveness of
    the winter sun in promoting Vitamin D synthesis.

32
Infants at highest risk for Rickets
  • African American infants that are exclusively
    breastfed
  • Infants living in northern industrialized cities
  • Infants where cultural practices include covering
    of the majority of skin or limited sun exposure
  • Infants whose mothers are deficient in Vitamin D,
    thus lessening the amount of transplacental
    Vitamin D or reducing the content of Vitamin D in
    breastmilk
  • Infants who have unconventional dietary
    practices, such as vegan diets or unfortified
    milk

33
Public Health Initiatives
  • Few foods are naturally rich in Vitamin D
  • Dietary sources with high Vitamin D content
    include fish liver oils, fatty fish, egg yolks
  • 1930s Awareness brought about the fortification
    of milk with Vitamin D
  • Baby formulas are also fortified with Vitamin D
  • Experts began promoting sensible sunbathing
    for emphasis on Vitamin D

34
Treatment for Nutritional Rickets
  • Treatment
  • Daily, high dose Vitamin D ranging from
    2,000-5,000 IU/day over 4-6 weeks
  • Alternative 300,000-600,000 IU of Vitamin D
    administered orally/intramuscularly as 2-4 doses
    over 1 day
  • This should be followed by daily Vitamin D
    supplementation of 200 IU/day (given as
    multivitamin)
  • Confirm that the child is getting adequate
    calcium/ phosphorus in their diet

35
Prevention of Nutritional Rickets
  • The following groups should receive 200 IU
    Vitamin D supplementation per day
  • All breastfed infants (unless they consume at
    least 500 ml per day of vitamin D-fortified
    formula or milk). Supplementation should begin in
    the first 2 months of life.
  • All nonbreastfed infants who take less than 500
    ml per day of vitamin D-fortified formula or
    milk.
  • Children/Adolescents who do not have regular
    sunlight exposure or do not take at least 500 ml
    per day of vitamin D-fortified milk.

36
Conclusions
  • Nutritional rickets is a very real disease that
    still exists in an era of greater knowledge and
    understanding about its source.
  • Scientists historically faced many challenges in
    determining the etiology of this mysterious
    disease.
  • As pediatricians, we should be aware of
    populations susceptible to vitamin D deficiency
    and continue these historic efforts to prevent
    rickets.

French advertisement promoting Cod Liver Oil
37
References
  • Kliegman R, Behrman R, Jenson H. Nelson Textbook
    of Pediatrics 18th Edition. Philadelphia
    Elsevier Science, 2007. Pages 253-262
  • Gartner L, Greer F. Prevention of Rickets and
    Vitamin D Deficiency New Guidelines for Vitamin
    D Intake. Pediatrics 2003 111(4) 908-910
  • Rajakumar K. Vitamin D, Cod-Liver Oil, Sunlight,
    and Rickets A Historical Perspective. Pediatrics
    2003 112 e132-e135
  • Thomas S, Rajakumar K. Reemerging Nutritional
    Rickets. Archives of Pediatrics and Adolescent
    Medicine 2005 159 335-341
  • Nield L, Mahajan P, Joshi A, Kamat D. Rickets
    Not a Disease of the Past. American Family
    Physician 2006 74(4) 619-626
  • Dawodu A, Wagner C. Mother-child vitamin D
    deficiency an international perspective.
    Archives of Diseases in Childhood 2007 92
    737-740
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