musculoskeletal system disease: part 1 · nutritional treatment of specific musculoskeletal...

© Endeavour College of Natural Health endeavour.edu.au 1

NMDC221 Session 24:

Musculoskeletal System Disease

Part I


Reommended reading

Mahan, L.K., & Raymond, J.L. (2016). Krause’s food & the

nutrition care process (14th ed.). Pp. 790-811 St.

Louis, MO: Elsevier. (prescribed text).


Topic Summary

Musculoskeletal System Disease: Part I

o Principles and considerations in nutritional medicine

management of the musculoskeletal system

o Review anatomy & physiology of the musculoskeletal

system

Nutritional treatment of specific musculoskeletal conditions

and consideration of drug-nutrient interactions

o Osteoarthritis

o Gout

o Osteoporosis



Functions of the Skeletal System

o Support

o Protection

o Body Movement

o Haematopoesis

o Mineral Storage

o There are two types of bone; spongy and compact bone

tissues.

(Tortora & Derrickson, 2009)



o Bone maintenance is under hormonal control, and

nutrients play a major role in this

• Parathyroid Hormone

• 1,25-Dihydroxyvitamin D3

• Negative Feedback Control of Calcium and

Phosphate Balance

• Calcitonin

(Tortora & Derrickson 2009)



Osteoarthritis, viewed 24th Oct 2007

http://www.prism.gatech.edu/~gt7704b/images/osteoarthritis.gif


Osteoarthritis


Osteoarthritis

Synovial joints present with cartilage loss and significant

inflammation to articular and peri-articular structures.

o Morning stiffness (better for movement)

o Grinding of joints (crepitus)

o Loss of mobility, range of movement

o Pain after prolonged activity

o Pain relieved by rest

o Muscle contractures and spasms

o In advanced OA, redness, heat,

swelling, enlargement of joint,

bone spur formation. (Rona, 2000)


Osteoarthritis

Predisposing factors;

o Obesity

o Heredity

o Gender

o Biochemical abnormalities

o Previous trauma or inflammation

Investigations

o Blood tests (ESR & CRP)

o X-ray, ultrasound & MRI

(Kumar & Clarke 2009; Tortora & Derrickson 2009)


OsteoarthritisTreatment Aims

o Support pain management and anti-inflammatory action

o Maintaining adequate microcirculation to the joints

o Minimize load bearing exacerbation (obesity) while still

encouraging / sustaining activity of the joints while

supporting appropriate muscular articulation and

preventing further joint injuries

o Nutritional support for proteoglycan synthesis and

cartilage reconstruction

o Remineralisation of the calcified cartilage / bone junction

o Adjust the diet to have a less acidic load

(Sarris & Wardle, 2010; Mills & Bone, 2005, p.249)


Osteoarthritis

Nutrient Dosage Therapeutic Actions

Proline 500-1000mg Mucopolysaccharide component – major amino acid

combined with collagen

Lysine 300-3000mg Required for collagen synthesis & elastine

Vitamin C 250-

10,000mg

Collagen, elastin & proteoglycan production, deficiency

presents with unstable helix structures

Copper 2-5mg Controls expression of inflammation, recovery of

proteoglycan synthesis in inflammatory states

Manganese 2-50mg Co-factor in cartilage production

Omega 3 1-12gms Encourage the production of anti-inflammatory

cytokines

(Pasqualicchio et al 1996; Setty & Sigal, 2005; Osiecki, 2006; Lokireddy et al. 2008; Braun

& Cohen, 2010)


Osteoarthritis


Methyl-

sulfonyl-

methane

3000-6000mg MSM significantly decreased pain, swelling and

increased movement in damaged joints

Glucosamine 600-3000mg Proteoglycan component stimulating cartilage

formation, reduce pro-inflammatory cytokine

production

Chondroiton 1500mg Proteoglycan stimulate cartilage formation (RNA

synthesis by chondrocytes, partially inhibits

leukocyte elastase, overcomes dietary deficiency

of sulphur-containing amino acids.”

Calcium

Magnesium

1000-2000mg

300-1000mg

Bone formation, muscle contractibility

(Usha & Naidu, 2004; Osiecki, 2006; Anandacoomarasamy & March, 2010; Braun & Cohen, 2010)


Osteoarthritis

Drug Action Side Effects Interactions

Non-Opioid

Analgesics:

Paracetamol

Inhibits

prostaglandin &

some COX

production

within the CNS

(no anti-

inflammatory

benefits).

Analgesic &

antipyretic.

Used in

osteoarthritis

for symptomatic

relief

Skin rash &

nausea

Overdose (10-

15gms or 20-30

tablets) will

cause severe

liver damage

due to depletion

of glutathione,

and possibly

lead to death.

Alcohol: greater potential to cause liver damage when taken togetherVitamin C: prolong the amount of time paracetamol stays in the bodyBeta-CaroteneReduces toxic effectsQuercetin, Taurine and thioproline, Oleanolic acid, OPCs (Grape seed), N-acetyl cysteine, methionine and SAMe: reduce liver damage from toxicity by stimulating glutathione production

(Bullock et.al. 2007; Braun & Cohen, 2010; Bryant & Knights, 2011)


Osteoarthritis


Non-

Steroidal

Anti-

inflammatory

Drugs

(NSAID’s):

ibuprofen,

asprin,

diclofenac,

indomethacin,

piroxicam

Anti-

inflammatory

inhibits PG,

reduced cyclo-

oxygenase

enzymes

(aspirin,

ibuprofen,

paracetamol).

Used for

symptomatic

relief in

Osteoarthritis

Nausea,

vomiting,

diarrhoea/

constipation,

gastritis as

inhibits

mucous

productive PG.

Paracetamol

can present

with acute liver

failure if taken

in overdose.

Vitamin E & fish oil , turmeric,

garlic: additive pain relief

Garlic, Ginger, Grapeseed,

Turmeric: increased blood thinning

when used with aspirin.

Glutathione, Capsaicin, Colostrum

& Phosphatidylcholine: reduce

gastric mucosa effects & reduce

aspirin-induced damage.

Calcium, Folic acid, Iron,

Potassium, Zinc, Glutathione,

Vitamin A, Vitamin C: Alters

absorption or depletes these

nutrients

(Kumar Clark, 2005; Bullock et.al, 2007; Bryant & Knights, 2011)


Osteoarthritis


Corticosteroids

Intra-articular

Inhibits

phospholipase A &

cyclo-oxygenase to

reduce

inflammation.

Side effects include

pain &/ or infection at

injection site, post-

injection joint pain,

tendon damage, loss

of bone mass (long

term therapy).

None listed

(Bullock et.al. 2007; Bryant & Knights, 2011)


Gout


Gout

o Gout is an inflammatory arthritis associated with

hyperuricaemia (raised urate levels in the blood).

o Increased action of xanthine oxidase. This increases the

clearance of purines, however, a failure of the kidneys to

effectively clear the generated metabolite results in the

compound continuing to circulate throughout the body.

o This leads to deposition in joints

(Kumar & Clark 2009; Tortora & Derrickson, 2009)


Gout

Investigations

o joint fluid microscopy

o serum uric acid levels

o serum urea and creatinine

clearance to monitor renal

function

(Haslett et al. 2002; Kumar

& Clark 2009)

http://www.healthline.com/blogs/outdoor_health/uploaded_images/gout-738309.gif

http://www.healthline.com/blogs/outdoor_health/uploaded_images/gout-738309.gif


Gout geriatricsyllabus.com, 2007


Gout

Therapeutic Actions

Vitamin C

Huang et al. (2005) found that the incidences of

hyperuricaemia were higher in males and those that

suffered chronic illness.

The study found that ;

“Supplementation with 500mg/d of vitamin C for 2 months

reduces serum uric acid, suggesting that vitamin C might

be beneficial in the prevention and management of gout

and other urate-related diseases”. (pp. 1845)


Gout

Therapeutic Actions

Anthocyanidins & Pro-anthocyanidins

o Consuming 200gms of fresh or canned cherries per day has been shown to be very effective in lowering uric acid levels.

o Cherries, hawthorn berries, blueberries and other dark red-blue berries are rich sources of anthocyanidins and pro-anthocyanidins which supports collagen structures.

(Haslett et al. 2002; Jacob, 2003)


Gout

Nutritional Considerations

Alcohol

o Alcohol increases uric acid production by accelerating

purine nucleotide degradation and reduces uric acid

excretion by increasing lactate production which impairs

kidney function

(Lyu et al. 2003; Pizzorno & Murray 2006)

o It has been found that groups with gout have double the

alcohol intake of healthy controls

(Sharpe, 1984 too old!)


Gout


Refined sugars

o Hyon et al. (2008) found in a longitudinal study of males

with no history of gout that consumption of sugar

sweetened soft drink and fructose rich fruit drinks

increased the incidence of gout.

o The increased presentation was four times that of the

normal distribution of disease incidence.


Gout


Folate, Vitamin C, Fibre and Obesity

o Lyu et al (2003) found that “food sources rich in dietary

fibre, folate, and vitamin C, such as fruit and vegetables,

protect against gout. Waist-to-height ratio, which

indicates central obesity, has a significant linear effect on

gout occurrence, independent of body mass index.” (pp.

699)


Gout

Nutritional Treatment

o Eat low purine foods (purine rich foods include yeast,

shellfish, organ meats & offal) while eliminating refined

sugar in drinks, food & alcohol

o Consumption of fibre, folate, vitamin C rich foods &

coffee was associated with a lower risk & lowered rate of

flare-ups.

o High essential fatty acid intakes & drinking a minimum of

2 litres /day of filtered water is beneficial

o Reduce an unhealthy waist-to-height independent of

body mass index

(Lyu et al. 2003; Pizzorno & Murray, 2006; Jasvinder et al.

2010)


Gout


Folic acid 10000-12000mcg Inhibits xanthine oxidase. Low in gout clients

Vitamin E 200-800mg Inhibits the production of leukotrienes,

Antioxidant

Omega 3 1-12gms Limits the production of leukotrienes

Ginger Gingerols & diarylhepatanoids inhibits

Prostaglandin and leukotriene synthesis.

Bromelain &

Quercetin

750-1000mg COX – 2 Inhibitor Bradykinin inhibitor proteolytic

enzyme

Alanine

Aspartic acid

Glutamine

Glycine

200-600mg

1500-2000mg

500-3000mg

4-30mg

Reduced resorption of uric acid in the renal

tubules

(Kiuchi 1992; Gaspani L, 2002; Lyu et al, 2003; Setty & Sigal, 2005; Pizzorno & Murray 2006)


Gout


Xanthine

Oxidase

Inhibitor:

Allopurinol

Reduces the

synthesis of uric

acid (inhibits

xanthine oxidase).

This increases

xanthine’s use in

nucleic acid

synthesis which in

turn inhibits purine

synthesis. Useful for

urate deposits in the

joints (Gout) & urate

kidney stone

formation

Skin irritation

(itch, rash,

dermatitis,

alopecia),

abdominal

irritation

(diarrhoea,

vomiting),

Liver toxicity,

kidney

damage

Iron: Concurrent usage can lead

to excessive storage of iron in

the liver

Tryptophan: Allopurinol

decreases tryptophan

breakdown. Concurrent usage

can aid depression and help pain

management.

Vitamin D: Allopurinol has been

found to elevate serum vitamin D

levels. Monitor for vitamin D

toxicity signs with concurrent

administration

(Stargrove et al. 2008; Bryant & Knights, 2011)


Gout


Colchicine Plant alkaloid

used in the

acute attacks

to reduce

inflammation.

No

preventative

effect.

Diarrhoea,

nausea, vomiting,

abdominal pain,

anorexia &

alopecia (long

term use)

Narrow therapeutic

window – used

with caution in

individuals with

liver or kidney

impairment

Beta-carotene, Vitamin A:

Blocks the absorption of beta-

carotene and vitamin A from the

GIT. Blocks release of retinol

binding proteins.

Calcium: depletion & bone loss,

Magnesium, Potassium: reduced

absorption

Folate levels have been found to

be decreased.

Vitamin B12 absorption &

metabolism has been found to be

inhibited.

(Bryant & Knights, 2011)


Gout


Probenecid Competitively

inhibits urate

reabsorption

in the

kidneys,

increasing

excretion.

Headaches

Abdominal irritation

(anorexia, nausea,

vomiting)

Skin irritation

(dermatitis)

Kidney irritation

(haematuria,

increased

frequency, stone

formation, kidney

damage)

Anaemia,

leukopenia

Vitamin B2: Impairing

absorption, inhibiting urinary

excretion. Concurrent usage

has been found to reduce drug

side effects.

Niacin: Doses of vitamin B3

(above 50mg/day) have been

found to reduce uric acid

excretion.

Ascorbic Acid: combined use

has been found to increase uric

acid excretion. Higher doses of

ascorbic acid have been found

to cause gout attacks.

(Stargrove et al. 2008; Bryants & Knights, 2011)


Osteoporosis


Osteoporosis

o A generalised, progressive loss of bone density, causing

skeletal weakness, although the ratio of mineral to

organic elements is unchanged.

o Bones become porous, brittle and less dense as a result

of a loss of bone mass due to osteoclast dominance

(Kumar & Clark 2009; Tortora & Derrickson 2009; Vardaxis, 2010)


Osteoporosis

o Bone mass peaks in the middle of the 20’s and plateaus

for about 10 years.

o Turnover of bone is constant, with bone formation

approximately equalling bone resorption.

o Menopause and andropause causes accelerated bone

loss (may be increased tenfold at the rate of 3 to

5%/year)

o The movement of calcium and phosphorous in and out of

bone is under the control of Parathyroid hormone (PTH),

1,25 Vitamin D3 (calcitriol), Calcitonin

o Gonadal hormones also play a major regulatory role.

(Haslett et al. 2002; Vardaxis, 2010)


Osteoporosis

Bone Loss Associated factors:

o Cushing's syndrome

o Hyper parathyroid

o Anorexia nervosa

o High intake of alcohol

o Smoking

o Drug usage (corticosteroids, progesterone,

anticonvulsants, thyroid hormones, methotrexate,

cyclosporin, non-thiazide diuretics, aluminum antacids,

anti-coagulants and high dose vitamin A and vitamin D)

(Vardaxis, 2010)


Osteoporosis

Symptoms:

o Usually asymptomatic until severe backache

o Common in postmenopausal women

o Fractures to hips and vertebra

o Decrease in height

o Demineralization of the spine and pelvis

(Haslett et al. 2002; Pizzorno & Murray 2006)


Osteoporosis

Therapeutic Actions

Insoluble Fibre

o Robefroid (2000) found that “…a high concentration of

short-chain carboxylic acids resulting from the colonic

fermentation of the non digestible carbohydrates

facilitates the colonic absorption of minerals, particularly

Ca2+ and Mg2+.”

o Insoluble fibre fractions such as inulin can increase in

water retention in the bowel allowing minerals to dissolve

and increase in concentration. This encourages passive

diffusion and subsequent increased absorption.


Osteoporosis

Therapeutic Actions

Vitamin D, Calcium and Garlic oil

o Rasheed et al. (2009) found that animal trials

supplemented with “…vitamin D , calcium and oil extract

of garlic could effectively restore the reduced calcium

level, correct the high rate of bone turnover, elevate the

reduced serum estradiol level and improve both BMC

and BMD after ovariectomy. This effect was better in the

group co-administered with the three components”.


Osteoporosis

Therapeutic Actions

Calcium and BMI

o Varenna et al. (2007) found that “…the negative effect of

a low dietary calcium intake on BMD values in the first

years after menopause can be attenuated by a greater

BMI found in women with a low calcium intake.”


Osteoporosis

Therapeutic Actions

Soy Isoflavones

o Scheiber et al (2001) conducted a study to determine the

effects of dietary inclusion of soy foods on clinical

markers for cardiovascular disease (CVD) and

osteoporosis in normal postmenopausal women.

o The conclusion was that “dietary soy foods containing

60mg/day of isoflavones results in significant increases

in serum levels of phytoestrogens and a subsequent

reduction in clinical risk factors for CVD and

osteoporosis.”


OsteoporosisSoy

o Beneficial effects of soy on bone density have been reported in

epidemiological studies.

o One study gave 200 women 66mg of isofalnones or a soy protein

supplement/day (equivalent to an Asian diet intake) for six months.

o The researchers investigated changes in the women's bone activity by

measuring certain proteins (βCTX and P1NP) in their blood (responsible

for bone breakdown) & found that the women on the soy diet with

isoflavones had significantly lower levels of βCTX than the women on

soy alone, suggesting that their rate of bone loss & risk of developing

osteoporosis was reduced.

o Women taking soy protein with isoflavones were also found to have

decreased risk of cardiovascular disease than those taking soy alone.

o Conclusion - soy protein and isoflavones are an effective option for

improving bone health in women during early menopause. The actions of

soy appear to mimic that of conventional osteoporosis drugs

(Society for endocrinology 2015)


Osteoporosis

Nutritional Treatment

o Eliminate soft drinks (high in phosphates)

o Increase dietary and supplementary calcium intake

o Consumption of leafy green vegetables (vitamin K ,

boron and calcium)

o Increase intake of foods high in Vitamin D and ensure

exposure to sunlight

o Reduce fat intake, eliminate refined sugar, avoid

smoking & drink alcohol in moderation

o Participate in weight bearing exercise daily & maintain

ideal body weight

(Kohlmeier, 2003; Pizzorno & Murray 2006; Schlenker & Long 2007; Straub 2007; Rasheed

et al. 2009)


Osteoporosis

Preventative Strategies include:

o Maximizing peak bone mass (peak bone mass achieved

at age 30 years)

o Avoidance or modification of lifestyle and environmental

factors that cause bone loss

o Use of treatments such as oestrogens to prevent

postmenopausal bone loss

o Maintenance of postural stability and prevention of falls

(Haslett et al. 2002; Kumar & Clark 2009)


Osteoporosis

Treatment Aims

o In patients with established osteoporosis, the aim of all

treatment strategies (nutritional, dietary and

pharmaceutical) is very similar. These include;

o Alleviate the patient's symptoms (e.g. pain) if applicable

o Reduce the risk of fracture

o Improve bone mass

o Treat, any underlying or contributing causes such as

thyroid dysfunction, diabetes, achlorhydria, drug

therapies e.g. corticosteroids

(Haslett et al. 2002; Kumar & Clark 2009)


Osteoporosis


Calcium 1200-2000mg Major mineral in bone deposition, deficiencies present

with bone loss

Vitamin D 10-40mcg Deficiencies present with impaired calcium absorption,

secondary hyperparathyroidism, bone loss, and

osteoporosis

Silica 5-10mg Cross-linking collagen strands for the strength &

integrity of connective tissue matrix of bone.

Recalcification in bone modeling

Boron 2-7mg Accelerate bone and cartilage healing, improves

growth, mineralization and mineral retension in bone

(Kohlmeier 2003; Pizzorno & Murray 2006; Straub 2007)


Osteoporosis


Vitamin K 2-5mg Stimulates osteocalcin, matrix Gla protein and protein

S for bone mineralization

Magnesium 300-1000mg Improvement in bone density

Omega 3 1-12gms Decreases bone resorption by reducing excessive

inflammatory prostaglandin production

Vitamin B6

Vitamin B12

Folate

1.5-3mg Collagen cross linking.

Metabolism of Homocysteine

Vitamin C Essential for collagen formation, deficiency presents

with reduced osteoid tissue and ground substance.

(Kohlmeier 2003; Pizzorno & Murray 2006; Straub 2007; Sarris & Wardle 2010; Vardaxis 2010)


Osteoporosis


Bisphosphonates

Alendronate

Bind to bone

hydroxyapatite

crystals, becoming

a permanent part

of bone. This new

matrix is resistant

to enzymatic

degradation and

inhibits osteoclast

activity.

Gastrointestinal irritation (dyspepsia, nausea, vomiting, oesophagealirritation, gastritis, abdominal pain, diarrhoea)Osteomalacia, hypocalcaemiaMusculoskeletal pain, arthralgia, headache

Calcium, Magnesium,

Iron, Zinc: reduces drug

absorption, separate by

2 hours. Ca & Mg Is

required to stabilize

condition.

Vitamin D

Calcium absorption

requires the presence of

vitamin D. Concurrent

usage with

Bisphosphonates is

warranted.

(Bullock et al. 2007; Stargrove et al. 2008; Braun & Cohen, 2010; Bryant & Knights 2011)


Osteoporosis


Calcitonin Thyroid hormone that

inhibits osteoclast bone

resorption by blocking

the PTH action on

these cells. Most

effective in early

menopause.

Gastrointestinal upset

(nausea, vomiting)

Dizziness

Inflammation and pain

at injection site

Calcium & Vitamin D

Adequate levels of

calcium and vitamin D

are required to sustain

the bone-sparing effect

of calcitonin

(Bullock et al. 2007; Stargrove et al. 2008; Mahan & Escott-Stump 2008)


Osteoporosis


Hormone

Replacement

Therapy

Synthetic

oestrogen (&

progesterone)

reduces bone

turnover & loss,

increases calcium

absorption,

retention &

increases

calcitriol

concentrations.

Increased

risk of

coronary

heart

disease,

breast

cancer,

stroke and

pulmonary

embolism

Chromium: Inhibits IL-6

(increases bone resorption)

Calcium & Vitamin D:

Increases bone mineralization

Boron: elevates oestradiol levels,

l(limits calcium losses & supports

bone mineralization).

Vitamin E: minimizes HRT

induced thrombosis

Zinc & Vitamin B6: depleted by

HRT

Magnesium: HRT increases bone

delivery

(Dimitris et al. 1998; Stargrove et al. 2008; Braun & Cohen 2010; Bryant & Knights 2011)


Osteoporosis


Selective

Oestrogen

Receptor

Modulators:

Raloxifene

Tamoxifen

Stimulate oestrogen

receptors in bone tissue

& not glandular tissue.

Decrease bone

resorption & increase

bone mineral density.

Common: hot flushes (usually subsides after 6 months) & leg cramps.Retinal vascular occlusion

Calcium & Vitamin D:

Beneficial effect on

bone mineralization.

Concurrent usage

warranted.

Androgen

Replacement

Therapy

Testosterone

replacement maintains

bone mass & prevent

fractures.

Prostate growth Boron: Can elevate

testosterone levels,

limiting calcium losses

and supporting bone

mineralization

(Mahan & Escott-Stump 2008; Stargrove et al. 2008; Braun & Cohen 2010; Bryant & Knights 2011)


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