The document discusses osteoporosis, a complex disorder marked by reduced bone mass, leading to fractures. It reviews various types, diagnostic methods, dietary impacts, and medical therapies associated with osteoporosis, emphasizing the importance of calcium, vitamin D, and other nutrients in bone health. The document also includes scientific studies on dietary influences and maternal factors affecting bone health in offspring.

1. OSTEOPOROSIS & DIET
By V.S. Deepika
M.Sc. I year (Applied nutrition)
Reg. No. 15MSAN16

2. Introduction
OSTEOPOROSIS = “porus bones”
Definition of osteoporosis
Osteoporosis is a multifactorial, complex disorder characterized by an
asymptomatic reduction in the quantity of bone mass per unit volume.
When bone mass becomes too low, structural integrity and mechanical
support are not maintained and fractures occur with minimal trauma.

3. Sites affected by Osteoporosis
Distal radius
vertebrae
humerus
pelvis
ribs

4. Types of Osteoporosis
There are various types of osteoporosis such as,
1. Idiopathic juvenile osteoporosis - pre-pubertal children
2. Idiopathic osteoporosis - young adults (30 to 50 years) with no obvious
cause
3. Age related osteoporosis - in people above 50 years etc.
most frequently seen in post menopausal women & elderly of both
sexes.
Normal spine at age 40 and
osteoporotic changes at ages 60
and 70. These changes can cause a
loss of as much as 6 to 9 inches in
height and result in so called
Dowager’s hump (far right) in the
upper thoracic vertebrae.

5. Bone Composition
Bone
Organic
30%
Cells,
collagen
(95%)
Non collagenous
proteins &
mucopolysaccharides
(5%)
Inorganic
70%
Hydroxyapatite
[Ca10(PO4)6OH2]

6. Bone Structure

7. Types of Bone & Bone cells

8. Bone modeling and remodeling
1. Activation step
2. Resorption phase
3. Reversal phase
4. Formation

9. Peak bone mass & Turn over
Age (years)
Attainment of Peak
Bone Mass
Consolidation Age Related Bone Loss
Men
Women
Menopause
0 10 20 30 40 50 60
Fracture
threshold
0.2 to 0.5% per
year
2 to 5% per year

10. Diagnosis of osteoporosis
BMC – bone accumulated before end of growth cessation
gm of mineral / cm of bone.
BMD – bone mass after development period is complete
gm of mineral / cm squared of bone.
Techniques for assessment :
1.Bone biochemical markers - can be measured in blood stream or urine.
Matrix markers – collagen molecules
Bone cell markers – enzymes alkaline phosphatase, serum PTH, 25 (OH) D.
2. Bone densitometry - single x- ray absorptiometry, DEXA, quantitative CT,
bone histomorphometry.

11. X-Rays Insensitive, Detect loss >30-50%
SPA / DPA Requires Radionuclide photon source
DEXA Gold standard
QCT
Spine & Peripheral sites, High
radiation
US
Cannot be used for diagnosis,
Used for assessment of # risk
MRI No direct information on BMD

12. T score – number of SDs a patient’s BMD deviates from a
reference population of normal young adults.
WHO, Guidelines for Preclinical Evaluation and Clinical Trials in Osteoporosis, 1998.

13. Osteoporosis association with Non- Dietary
factors
1. Age and Sex
2. Body weight and body composition – Body wt. α bone density
3. Race / ethnicity – e.g. Africans vs. Asians
4. Physical activity – weight bearing exercises
5. Reproductive history - high parity & long lactation periods
6. Genetics and Familial factors – genetic polymorphisms - BMD
7. Estrogen depletion – menopause, early oophorectomy
8. Other medical conditions – type- 1 DM, hyperthyroidism, CRF
9. Use of other medications – Al- antacids, tetracyclines,
anticonvulsants, exogenous thyroid etc.
10. Cigarette smoking- alterations in estrogen metabolism

14. Osteoporosis association with Dietary
factors
Calcium : -ve balance in osteoporosis
Ca balance depends on Ca content in diet, efficiency of Ca
absorption by intestine etc.
Pre menopausal women, post menopausal women –
Increase Ca intake decrease in rate of bone loss.
Phosphorous : P depletion occurs before the Ca is locally depleted
Osteoblast function is severely compromised
Indians usually meet RDA for phosphate so depletion is not common.
Vitamin D : commonest cause of osteoporosis.
Vit- D supplementation in elderly (800 IU/day) is beneficial for
optimal bone health and reduces the risk of fractures.

15. Contd…
Vitamin K : Vitamin K is a co- factor for gamma carboxylation of 3 bone
matrix proteins.
Osteocalcin is the best studied of these which is a bone specific protein.
Vitamin K may reduce urinary Ca loss in patients with Osteoporosis

16. Contd…
Vitamin C : Is necessary for collagen cross linking.
Leveille et al have found that the long term use of vit- C supplements - higher
BMD in women aged 55 to 64 yrs vs. those who had never used estrogen.
Vitamin A : Excess vitamin A seems to stimulate osteoclasts and suppress
osteoblasts.
Bone has receptors for vitamin A and vitamin D, hence high intakes of vit –A
interfere with vit – D activity.
Protein : Excess of purified protein- contributor of osteoporosis risk
Calciuric effect
Most protein rich foods contain many other nutrients that could counteract
Calciuric effect of protein.

17. Contd…
Fiber : It chelates Ca (and other minerals) in G.I tract.
High fiber diets (taken as staple foods) increase osteoporotic risk.
Other micronutrients : several dietary components affect dietary Ca
absorption. Manganese, copper, and znic are necessary cofactors for
enzymes involved in bone metabolism.
Some evidences showed their supplementation to have some benefit
when added to a supplementation regimen.
Alcohol : Moderate alcohol is beneficial.
Alcohol stimulates the conversion of androstenedione to estrone,
an estrogenic compound with bone preserving properties.
But,
Bone formation is decreased in patients who abuse alcohol.

18. Contd…
Phytoestrogens : confer estrogen like effects.
these have both estrogenic and anti – estrogenic activity and seem
to achieve these properties by binding to estrogen receptors.
e.g. present in sprouts, beans, and soybeans.
Isoflavones have most potent estrogenic activity when compared to other
phytoestrogens. – prevent bone loss.
Sodium and caffeine are also said to cause increase in Ca excretion.

19. Medical therapies for osteoporosis
1. ERT / HRT : Administration of estrogen molecules to replace the
menstrual hormone.
Approved by FDA. But now only used for treating menopausal
symptoms because of its adverse effects.
2. Biphosphonates : inhibition of bone resorption through a direct dose
related effect on osteoclasts. Approved by FDA.
3. Calcitonin: inhibits bone resorption.
salmon calcitonin is a more potent inhibitor of bone resorption
than human calcitonin.
4. Selective estrogen receptor modulator (SERM) : these act on estrogen
receptors in osteoblasts to promote the maintenance of bone
tissue.
5. Intermittent therapy of PTH : it is the first anabolic agent to be FDA
approved for the treatment of osteoporosis.

20. SCIENTIFIC REPORT – 1:
Chennaiah S, Vijayalakshmi V, Suresh C
Effect of supplementation of dietary rich phytoestrogens in
alternating the vitamin D levels in diet induced osteoporotic rat
model.
J Steroid Biochem Mol Biol.121:268-272, (1.F2.866), March 2010.
Aim of the study : was to elucidate whether supplementation of
Isoflavones (daidzein and genistein) rich Cow pea is capable of preventing
rapid bone loss occuring after diet induced OSP in rats.
Animals and conditions maintained:
Female weanling WNIN rats (30-35g) were selected and maintained
at an ambient temperature (20±20C) and relative humidity of 50 to 80%.
Rats were allowed for illumination 12 hour light and 12 hour dark.
It was approved by institute’s animal ethical committee.

21. Contd…
Study design and conduct: Total of 68 rats.
Firstly they are fed semisynthetic diet with low Ca (O.15%) & low
VD (0.1IU/day/rat) as proposed by suda et al.
In combination with low (10mg/kg) or high (25mg/kg)
concentration of PE’s derived from CPIF. The study groups are
1. Normal Ca (0.47%) & normal VD (25 IU/day/rat) - 6 rats – control diet.
2. Low Ca & low VD – 38 rats
3. Low Ca & low VD & low CPIF (10mg/kg diet) – 8 rats
4. Low Ca & low VD & high CPIF (25mg/kg diet) – 8 rats
5. Low Ca & Low VD & 17- β – estradiol (3.2mg/kg diet) – 8 rats
They had an access to deionized water and food intake was
recorded every alternative. Body weight was checked for every 4 days.
After as rats developed OSP after 6 weeks as indicated by BMD,
BMC and biochemical analysis, the group 2 was sub grouped into
SG 1 continued on low Ca & VD – 8 rats
SG 2 low CPIF – 8 rats
SG 3 high CPIF – 8 rats
SG 4 17- β – estradiol – 8 rats
SG 5 normal Ca & VD – 6 rats.

22. Contd…
After 90 days the rats were sacrificed and investigations were
carried out to find the protective and therapeutic effects of CP.
BMD and BMC noted by DEXA, serum 25 (OH) D- RIA, serum ALP-
Walter-schult-enzyme activity, serum Ca –atomic absorption
spectrophotometry.
Inference from the results:
• Improved BMD, BMC of whole body, Ca, P and ALP levels. In
addition 25-VD also found to play a role in partially reversing the
clinical manifestation of the osteoporotic situation in the rats.
• CPIF diet alone was not sufficient to reverse the loss in the whole
body BMD due to diet induced OSP but can provide additive effect
in terms of bone density; BMD was maintained normally in the
control diet group.
• Low BMD and BMC levels improved in SG 2, 3 & 5 of group 2, after
OSP + supplementation of CPIF.

23. Contd…
• Daidzein and genistein, improved BMD by suppressing the bone
turnover increase.
• CPIF might have suppressed osteoclastic activity through tyrosine
kinase inhibition and the bone loss preventive effects of IF
resulted from suppression in bone turnover increase and could
be due to mechanism similar to that of estrogens.
• IF inhibitory effects on osteoclasts as inhibitors of Ca- dependent
signaling molecules calmodulin and protein kinase which
antagonizes the reduction in osteoclast no. induced by these
compounds.
• 25 – VD levels were found to be altered in a significant way in SG
2, 3 and 5 of group 2 indicating the fact that CPIF and VD
metabolism involvement in bone mineralization.

24. Conclusion of the study
CPIF had a convincing effect in protecting the bone
mineralization in the critical situation like OSP in
terms of improving BMD, BMC, Ca, ALP and 25 VD
levels. It is inconclusive whether IF had a therapeutic
effect and needs to be further investigated.

25. SCIENTIFIC REPORT - 2:
Bharati kulkarni, Anjali Ganpule- Rao, Urmila Deshmukh and
Chittaranjan Yajnik.
Maternal influences on bone health in Indian children: Appraisal of
the evidence.
Asia- Pacific journal of endocrinology, 2009.
Aim of the study:
The study was on the impact of maternal factors on offspring bone health
review and it suggested that the “Developmental Origins of Health and
Disease” (DoHaD; or the life cycle) approach is the best available model to
curtail the epidemic of osteoporosis and related conditions.
Proving by the evidence from Pune maternal nutrition study – 1993 –
carried out in 6 villages near to Pune.
PMNS cohort was established to test and elaborate the fetal origins
hypothesis. That study data provided the data needed to prove the maternal
influence on offspring bone heath.

26. Contd…
Details of the study:
1. House to house study.
2. 1675 young women registered.
3. All aged < 35 years and not sterilized.
4. Menstrual dates were recorded every month.
5. Detailed anthropometry done for every 3 months.
6. Age of mother’s = 21.5 (+3.4) years, weight=
46.7(+6.5)kg, height= 1.52 (+0.05)m, BMI= 18.1
(+2.5)kg/m2.
7. All ate approximately 1700 kcal/day. 45 g of protein,
physically active worked both at home and farm.
8. During the study 824 women became preganant.
9. 770 women delivered single live baby.
10. LBW registered is 28%.

27. Contd…
Conduct of the study:
The PMNS collects data serially at different time points of study material
and from data we draw the developmental influences on offspring bone
health.
Maternal factors
Size and body
composition,
Dietary intake,
Physical activity,
supplements.
Fetal skeleton
development
Birth size
Lactation
Childhood
&
adolescent
growth
Peak bone
mass
Osteoporosis
Fracture risk
DoHaD concept of skeletal development,
Growth and its relationship to bone health
and Disease.

28. Contd…
Observations from the study:
1. They suggest that modifications in maternal nutritional factors may
influence bone health in offspring. Paternal influence might operate
through genetic mechanism or through a shared environment.
2. Preterm infants had lower total body BMC than term infants and are
at increased risk of osteopenia, rickets and fracture.
3. Impact of childhood nutrition on the accumulation of peak bone
mass may contribute to osteoporosis.
4. Suboptimal peak bone mass resulting from early life factors may be
difficult to compensate for by optimal nutrition in later years.
5. A beneficial effect of maternal calcium supplementation on neonatal
bone health has been reported from India.
Conclusion from the study:
This study report states that the available evidence to achieve
optimum offspring bone health points towards modifiable maternal factors
including nutrition and physical activity. The life style factors including
nutrition and environment during growing years also need equal attention.
The DoHaD model emphasizes the need to start early in life to
prevent the rising epidemic of osteoporosis.

29. Slide Title