Diseases of the musculoskeletal system “rheumatic type”:
4 groups

1. Degenerative – non-inflammatory – disorders (e.g.b Arthrosis deformans)
2. Primary inflammatory diseases (e.g.b Rheumatoid arthritis, para- & post-infectious
   arthritis, paraneoplastic arthritis)
3. Metabolism-related (secondary) inflammatory diseases (e.g.b gout)
4. Soft tissue rheumatic, “non-inflammatory” complaints
   (e.g.b Fibromyalgia as a chronic painful muscle disease)

Main problems:

• Pain (chronification!)
• Restriction of mobility & quality of life
• Inability to work & early retirement

 

Non-drug measures & orthopedics

A) Nutrition

The relationship between joint diseases and nutrition exists since the time of Hippocrates. Biochemical research in recent years has been able to identify the inflammatory mediators of rheumatic diseases and show the connections with food
.

Recommended diet:

• with a high proportion of micronutrients
• Wholesome (Mediterranean or Asian-oriented), natural,
  fiber-rich food with a high proportion of fruit, vegetables, (fish)
  herbs and nuts, high-quality oils
• with favorable acid-base ratio; v.a Reduction of
  • Base-removing foods (sugar, white flour, industrially produced
    foods)
  • Acid donors such as animal protein & animal fats, alcohol, coffee and nicotine, certain grain products (e.g.b white bread, crispbread), certain vegetables (e.g.b Brussels sprouts, peas, artichokes), certain types of cheese (e.g.b processed cheese)

B) Healthy exercise

• (Exhalation of CO2 = CARBON ACID, sweating, increased oxygen supply)
  Influences overall metabolism and the aging process.
• Endurance-oriented sports (e.g.b Cycling, swimming, cross-country skiing)

C) Stress reduction, mental balance & relaxation ---> Relaxation exercises enable better processing of stress and pain

 

D) Important micronutrients in orthopedics & rheumatic diseases

 

Vitamin C

• Vitamin C is the most effective antioxidant in blood plasma
• Vitamin C is essential for collagen formation
• Vitamin C regenerates oxidized vitamin E and thereby protects the lipid membranes (cf. Niki et al., 1991)
• Hydrophilic compartments in which vitamin C has an antioxidant effect:
  • Cell plasma
  • Blood plasma
  • Synovial fluid (fluid in the cavities of movable joints)

 

Vitamin E

• Antioxidant in the cell membranes (lipid solubility!)
• Scavenges membrane-damaging oxygen radicals
• Inhibition of the activation of NF-κB - a protein that is important in the immune response and therefore the inflammatory process (cf. Miehle, Bad Aibling, Advances in Medicine 115, 1997, p.39-42)
• Inflammation-reducing and central analgesic effects (influencing pain perception and processing) with an increase in β-endorphins (are related to The most effective endorphins for pain suppression) (cf. Edmonds et al., Ann of the rheum.Diseases 56, 1997)
• Improved mobility and improved general well-being
• Lipophilic compartments in which vitamin E has an antioxidant effect: v.a Membranes
• Indications
  • Inflammatory & degenerative diseases of the musculoskeletal system
  • Rheumatoid arthritis & Bechterew's disease (inflammation of the spine) with pathological immune reactions in the joint
  • Activated arthrosis, spinal syndromes, Dupuytren's disease (disease of the connective tissue of the palm of the hand)
  • Saving on medications such as non-steroidal anti-inflammatory drugs (NSAIDs) & corticoids (such as Cortisone)
  • Reduction of side effects (42 patients with chronic polyarthritis were treated in a 3-week study under stationary conditions with either 1600 I.E
    Vitamin E or treated with 50 mg diclofenac (an NSAID) per day. Comparable, highly significant improvements in rheumatological findings such as grip strength, morning stiffness, pain, walking time and Ritchie joint indices were noted in both treatment groups. The results were not statistically separable (KOLARZ et al., 1990))
  • Increased vitamin E consumption in rheumatic patients
  • Decreased vitamin E concentrations in the synovial fluid of inflamed
    joints
  • Typical dosage: up to 2x600mg vitamin E/day and higher!

 

Omega-3 fatty acids

• have an anti-inflammatory effect --> Omega-3 fatty acids are antagonists of the inflammatory arachidonic acid (omega-6 fatty acid, especially.a contained in meat)
• Reduce collagen breakdown --> Inhibit the formation of messenger substances
  that cause collagen breakdown (TNFα + Interleukin-1α/-β)
• Omega-3 and Omega-6 fatty acids…
  • cannot be converted into one another
  • compete for the same enzyme pathways
  • inhibit each other
  • Intake recommendation: Omega 3 to Omega 6 in a ratio of 1:5
• These omega fatty acids have anti-inflammatory effects:
  • y-linolenic acid (omega-6 fatty acid, etc.a Contained in hemp seed oil or in the oil of evening primrose and black currant): displaces arachidonic acid from cyclooxygenase/cell membrane, increases PGE1 (Prostaglandins of groups 1 and 3 have an anti-inflammatory effect, those of group 2, on the other hand, have a pro-inflammatory effect ) and (low) eicosapentaenoic acid (EPA)
  • alpha-linolenic acid (omega-3 fatty acid, etc.a contained in hemp seed oil): acts as a nervous structural lipid, increases PGE3 (anti-inflammatory effect)
  • Fish/algae oils (contain EPA and DHA, with the EPA relevant for inflammatory processes i.dR is only present in high concentrations in fish oil):
    Displace arachidonic acid from cell walls, increase PGE3 (v.a EPA due to structural similarity to arachidonic acid), prevent eicosanoid & inflammatory mediator formation

 

 

PGE 2 from arachidonic acid

• 90% of arachidonic acid is incorporated into cell membranes when absorbed
• Arachidonic acid serves as a prostaglandin 2 (PGE 2) precursor
• PGE 2 …
  • Promotes local inflammatory activity in the joint
  • systemically inhibits lymphocyte proliferation
  • triggers pain
  • can be blocked by: NSAID/COX inhibitors, vitamin E, histidine,
    y-linolenic acid / dihomo-y-linolenic acid

 

PGE 1 & PGE 3 decrease Inflammatory activity

• PGE 1 from Ɣ-linolenic acid
• PGE 3 from long-chain omega-3 fatty acids (eicosapentaenoic acid (EPA) & docosahexaenoic acid (DHA))

 

Cartilage micronutrients: 4 cartilage building blocks

1. Collagen hydrolyzate
   As a scaffolding protein, collagen forms the supporting substance of cartilage

• Proline/glycine (contained in collagen hydrolyzate) are important protein building blocks for the formation of collagen
• can save on painkillers
• support the improvement of symptoms

 

• Crossover study (source: Adam M. Therapy Week 1991;41:2456-61.): Reduction in pain and analgesic consumption ≥50%
• • Duration: 2 months collagen hydrolyzate + 2 months break + 2 months placebo, n= 52
  • Dosage: 3-4 grams/day
  • Conclusion:
    • The half of the patients who took collagen hydrolyzate reported a 50% reduction in pain.
    • 69.2% of collagen hydrolyzate patients were able to reduce their painkiller intake by half

 

2. Glucosamine and chondroitin sulfate

• support cartilage metabolism, are building blocks of cartilage cells for building
  the cartilage components and the synovial fluid
• can be given in addition to painkillers and help save
  these
• support the improvement of symptoms (pain, stiffness of the joints, difficulty walking and everyday activities)
• EULAR recommendation (European League Against Rheumatism) 2003: Glucosamine and chondroitin sulfate were assessed with the (highest) level of evidence 1A; H. there are studies that meet the highest level of scientific validity; they are among the 10 most important recommendations
• Indication: mild to moderate osteoarthritis
• Effect: Inhibition of the progression of primary gonarthrosis, structural modification
  (cartilage degradation is stopped), improvement of symptoms (according to WOMAC à the “Western Ontario and McMaster Universities Osteoarthritis Index” is a self-assessment questionnaire and is used for Evaluation of the most important and everyday-relevant consequences of osteoarthritis)
• Possible side effects: hair loss, drowsiness, visual disturbances, drop in blood pressure, fainting (Source: Jordan KM, Arden NK, Doherty M, et al. EULAR Recommendations 2003: an evidence based approach to the management of knee osteoarthritis. Ann Rheum Dis 2003;62:1145-55)
• Combination of glucosamine and chondroitin sulfate is more effective than single substance

--> 20% improvement in WOMAC pain score (baseline vs 24 weeks)
(Source: Glucosamine/Chondroitin Intervention; Clegg DO et al ., New England Journal Med 2006; 354(8):795-808)

 

 

3. Hyaluronic acid

• Properties
  • pronounced ability to bind water
  • viscous = gel-like
• Determines the properties
  • of the aqueous humor (eye)
  • the lymphatic fluid
  • the synovial fluid
• Improves cartilage quality (long-term effect unclear)
• Indication: Pain in degenerative changes in joints
• Dose: 3-5-x intra/para-articular at intervals of 1 week - or subcutaneously or orally
  it is also possible
• Possible side effects: pain, feeling hot, swelling (rare)
• Studies:
  • Oral hyaluronic acid in horses with OCD (osteochondrosis dissecans); Source: Bergin BJ, et al. Equine Vet J 2006;38(4):375-8
  • Hyaluronic acid 50 mg orally, human study, placebo-controlled double-blind study (source: Ubia A. NutraCos 2007;July/August:21-2) à the increase in the “Bodily Pain” value by 11.2 (point value) corresponds to a significant pain reduction of 33% (p<0,05); n = 20

 

 

Amino acids in orthopedics

Amino acids are important in orthopedics for...

• Structure of the hyaline structures (hyaline cartilage is a form of cartilage tissue that is primarilya located in the articular cartilage) of the musculoskeletal system
• Regulation of bone and cartilage metabolism (“cartilage protectant”)
• Additionally direct effect on inflammation and pain

 

Examples of important amino acids

• Histidine
  • Inhibits the formation of pathogenic immune complexes (low histidine levels in rheumatoid arthritis!)
  • Influences prostaglandin metabolism (inhibits PGE2 synthesis)
• Tryptophan
  • Improves mobility, walking distance, pain
• Methionine / S-Adenosyl-Methionine (SAM)
  • Influences release of inflammatory mediators
  • Involved in glutathione synthesis (after conversion into cysteine)

 

Enzymes in orthopedics = mechanisms of action of proteases

• Proteases break down proteins
• Have anti-inflammatory activity
• Reduce proinflammatory cytokines (IL-1β, TNF-α) and adhesion molecules such asb CD44 (adhesion molecules are proteins on the surface of cells that mediate the binding of one cell to another cell; during inflammation, numerous cells migrate into the inflammatory area via adhesion molecules)
• Support antioxidant enzymes (superoxide dismutase (SOD), catalases, glutathione peroxidase)
• Immunomodulating effect
• Destruction of immune complexes (immune complexes made of antibodies/antigen are difficult to break down by the phagocytes and reach the surrounding tissue via the blood, where they trigger inflammatory processes)
• Analgesic effect (indirectly through the breakdown of pain mediators such as kinins and prostaglandins, as well as directly through the effect on the pain-receiving sensor (nociceptor))
• Degradation of cell fragments in degenerative joint processes
• Antiedematous effect

 

Mechanisms of action of proteases in orthopedics

 

 

Other micronutrients for bone and cartilage metabolism

• Vitamins of the B complex
  • Vitamin B6: Cofactor of the enzyme that crosslinks collagen
  • Positive influence on symptoms through vitamin B12, folic acid (vitamin B9), nicotinamide (vitamin B3)
• Boron
  • Anti-inflammatory, bone building, metabolism of steroid hormones
  • A dietary supplement with boron leads to a subjective improvement in activated osteoarthritis due to its anti-inflammatory properties. Boron develops its effect by reducing ROS (reactive oxygen species) and inhibiting cyclooxygenase (COX II) and lipoxygenase (LOX), which are mediators of the inflammatory cascade. There is an incidence of osteoarthritis in countries with boron-poor soils of 20 to 70% (Jamaica, Mauritius). Countries with boron-rich soils only have an incidence of 0 to 10% (Israel).
• Vitamin D
  • is indispensable for calcium absorption from the intestine as well as for calcium incorporation into the bones
• Vitamin K
  • Supports bone metabolism through osteocalcin formation à Osteocalclin is a protein that binds bone calcium
  • Vitamin K2 (MK-7) dose-dependently inhibits cyclooxygenase-2 (enzyme that oxidizes arachidonic acid to PGE 2) and the synthesis of PGE 2 (group 2 prostaglandins are pro-inflammatory)

 

 

 

Illness pictures in orthopedics & rheumatic diseases

A) Osteoarthritis

• Most common disease of the supporting and connective tissue: Affects ~80% of >60 year olds!
• Imbalance load – resilience
• Possible causes:
  • Genetic disposition (e.g.b Protein synthesis disorders with incorporation of cysteine ​​instead of arginine)
  • Incorrect loading & injuries/operations & overload, excess weight
  • Lack of exercise & protective postures, gender (women more often), age
  • Inflammation
  • Metabolic disorders (e.g.b Hyperuricemia, osteoporosis, hyperthyroidism, hyperacidity)
  • Chronic micronutrient deficiencies
• Pathogenesis:
  • Damage to the articular cartilage (“hyaline cartilage”, suspension and shock absorber function), v.a in the stress zones, with breakdown of proteoglycans (important components of cartilage tissue)
  • Change in the basic substance with unmasking & separation of the collagen fibers and roughening of the surface & increase in frictional resistance
  • Deformation of cartilage and bone structures
  • Complete destruction of the cartilage & reactive bone remodeling in the marginal zones (sclerotic bone as “articular surface” & bone defects)
  • Pain
  • Reduction of muscles (muscle protection of the joint!)
  • Less power
  • Restriction of mobility up to stiffness
• Complaints in osteoarthritis:
  • Pain
  • Joint stiffness
  • Limited mobility
  • Uncertainty and instability
  • Joint swelling
  • Joint noises

 

 

Micronutrients and typical dosage for osteoarthritis:

• Glucosamine sulfate: approx. 15-20mg/kg body weight per day; d.H 600-2000 mg per day divided into 3 doses (~ 3x 500 mg/day)
• Chondroitin sulfate: 400-1200 mg/day (e.g.b 3x 400mg/day)
• Methylsulfonylmethane (MSM): 2x2 capsules of 500 mg
• Methionine / SAM: 400-1200 mg
• Niacinamide (vitamin B3): 500-3000 mg (e.g.b 3x 500 mg/day)
• Vitamin K2 MK7: 100-200 µg (has an analgesic, anti-inflammatory effect; involved in the synthesis of osteocalcin (protein important for bone formation))
• Omega 3 fatty acids: 2000-3000 mg per day; important: high EPA content (v.a the case with fish oils)
• Collagen hydrolyzate: 2.5 grams up to 10 grams
• Vitamin C: 500-2000mg (initially also infusions with 7.5 -15g, 1.2x week): Antioxidant, immune system
• Vitamin E: 200-1000 I.E per day; Antioxidant, Energy & protein metabolism, connective tissue, bones
• Vitamin D3: 5000-20.000 IE daily; Bones & Teeth (Osteoporosis!)
• Folic acid: 0.4-5 mg
• Sufficient protein supply (0.8 grams per kg body weight)
• Vitamin B12: 50-1000 mcg
• Vitamin B6: 5-50 mg; especially in pain (analgesic, anti-inflammatory)
• Calcium: 600-1000mg (e.g.b calcium citrate); most important mineral component of
  bone
• Boron: 6-9 mg – arthritic complaints: A dietary supplement with boron leads to a subjective improvement in activated arthrosis due to its anti-inflammatory properties. Boron develops its effect by reducing ROS (reactive oxygen species) and inhibiting cyclooxygenase (COX II) and lipoxygenase (LOX), which are mediators of the inflammatory cascade. There is an incidence of osteoarthritis in countries with boron-poor soils of 20 to 70% (Jamaica, Mauritius). Countries with boron-rich soils only have an incidence of 0 to 10% (Israel).

 

 

 

 

B) Rheumatoid arthritis

• Most common primary inflammatory disease of the supporting and connective tissue
• Autoimmune reaction with unclear genesis, destructive inflammatory reaction
  against the body's own (connective tissue) structures
• Immunological process leads to
  • Stimulation of B & T lymphocytes
  • Release of arachidonic acid & its oxidation to Eicosanoids
  • Joint inflammation (modulated by prostaglandins)
• Consequences:
  • Pain & restriction of movement
  • Reduction in quality of life
  • Inability to work and early retirement (after 5 years of illness ~50% of patients are unable to work!)
  • Drug-related susceptibility to infection
  • Gastrointestinal complications caused by medication (shorten life expectancy by approx. 7 years)

 

• Therapy of Rheumatoid Arthritis / Rheumatism “natural remedies”
  • Whole food (lacto-vegetarian = plant-based food + dairy products and eggs), sometimes only a vegan diet is successful
  • Exercise, relaxation
  • Physical measures
    • Active, e.g.b Muscle strengthening
    • Passive, e.g.b classic massage therapy, electrotherapy
  • Heat & cold (e.g.b Rye pillow, hay bag, rheumatism bath)
  • y-linolenic acid (GLA) 150-600 mg, e.g. contained in hemp seed oil
  • Boswellic acids from frankincense have an inhibitory effect on lipoxygenase (enzyme that oxidizes unsaturated fatty acids in the presence of oxygen) and thus have an inhibitory effect on leukotrienes (inflammatory messenger substances released from immune cells)
• Typical dosages:
  • Omega 3 fatty acids (v.a EPA, contained in large quantities in fish oil): 2000-6000 mg, converted during metabolism into anti-inflammatory prostaglandin E1
  • Vitamin A and ß-carotene: 0.3 mg, inhibits conversion of arachidonic acid into inflammatory mediators
  • Vitamin C (important: high bioavailability through liposomal carrier molecules): 160 mg with Qidosha Bio+ system, otherwise 500-2000 mg (initially also infusions with 7.5 -15g, 1.2x week); Antioxidant with anti-inflammatory & pain relief
  • Vitamin E: approx. 1200 IE, fat-soluble antioxidant, inhibits eicosanoid synthesis (inhibition of 5-hydroxy-lipogenase activity and thus inhibition of the synthesis of inflammatory prostaglandin PGE2 and leukotrienes), central analgesic effect
  • Vitamin D: 10.000-20.000 IE (i.eH 10-20 drops of 1000 I.E), possibly. also significantly higher (cf. Coimbra Protocol)
  • Vitamin B12: 1.000 mcg
  • Vitamin B6: 50 mg, especially for pain, analgesic (pain-relieving) and anti-inflammatory (anti-inflammatory) effects
  • Selenium: 100-300 mcg, antioxidant, often insufficient in arthritis
  • Zinc: 10-100 mg, improves tissue tension, reduces inflammation, accelerates wound healing
  • Proteolytic enzymes (cleavage of proteins by peptidases) such as Papain and broelain: analgesic (direct effect on the nocireceptor), anti-inflammatory and decongestant effect
  • Boron: 6-9 mg; Boron develops its effect by reducing ROS (reactive oxygen species) and inhibiting cyclooxygenase (COX II) and lipoxygenase (LOX), which are mediators of the inflammatory cascade. These cause joint swelling, reduced joint mobility and other arthritic problems.
  • Magnesium: 150-300 mg; Magnesium intake correlates positively with bone density; With long-term therapy with PPIs (proton pump inhibitors / “stomach acid blockers”), the risk of magnesium deficiency, clostridial infection and osteoporotic fractures increases. US epidemiologists led by Benjamin Lazarus from the University of Baltimore have now been able to show that chronic kidney failure is also increasingly observed with long-term PPI use (JAMA Intern Med 2016, online 11. January).
  • Copper: 1-2 mg
  • Manganese: 2-20 mg
  • Folic acid (as folate): 0.4-5 mg
  • Sufficient protein supply: 0.8g per kg body weight
  • Calcium: 600-1000 mg (e.g.b Calcium citrate), calcium as the most important mineral component of bone
  • Resveratrol: 500 mg

 

 

C) Osteoporosis

• Type 1: Post-menopausal osteoporosis
  Sex hormone deficiency (estrogen, testosterone): Bone resorption (osteoclasts, whose activity is hormonally controlled, break down the bone tissue and, among other things,a Calcium released into the blood) > Bone formation, resulting in increased fracture rate
• Type 2: Senile Osteoporosis
  Reduced bone formation and reduced production of vitamin D3. Leads to loss of cortical (outer layer of bone) and trabecular (inner part of the bone) bone with increased risk of fractures of hip, long bones and vertebrae
• Type 3: Secondary osteoporosis:
  Increased bone loss due to medication (e.g.b Glucocorticoids) or other causes (e.g.b Malnutrition/micronutrient deficiency)

Normal bone:

Bones with osteoporosis:

• Osteoporosis risk increased in:
  • Aluminum (e.g.b in medicines to neutralize stomach acid (so-called “Antacids”), such as Maaloxan or Masigel)
  • Proton pump inhibitors (PPI)
  • Medicines for the treatment of epileptic seizures (so-called “Anticonvulsants”), such as Phenobarbital, Phenytoin
  • Cytotoxic drugs
  • Glucocorticosteroids and adrenocorticotropin (up to 10% bone loss in the first Year of therapy) (Source: Homic, Cochrane Library 2004, 5 randomized, controlled studies)
  • Immunosuppressants
  • Lithium
  • Long-term use of heparin (anticoagulant)
  • Supraphysiological (i.e.H doses of thyroxine
  that exceed physical requirements
  • Premenopausal use of tamoxifen (estrogen receptor modulator)
  • TPN (Total Parenteral Nutrition)
  • Selective serotonin reuptake inhibitors (SSRIs) (antidepressants that block serotonin transporters and thereby increase the concentration of serotonin in the brain's tissue fluid): Men who use SSRIs have significantly lower bone mineral density in the hip and lumbar vertebrae (in an area such as below chronic cortisone intake) as controls (does not apply to other antidepressants) (source: cross-sectional analysis of 5995 men (Osteoporotic Fractures in Men-Study) Haney EM et al. Association of low bone mineral density with selective serotonin reuptake inhibitor use by older men; Arch Intern Med 2007; 167: 1246-1251. Cauley JA et al.; Factors associated with the lumbar spine and proximal femur bone mineral density in older men. Osteoporos Int 2005; 16: 1526-1537)
  • Continuously high Vitamin A intake of > 1.5 mg / day (approx. 5000 IE), va all-trans-retinol, increases the risk of osteoporotic hip fractures. This does not apply to beta-carotene. (Source: Nurses Health Study, JAMA 287, 2002, 47-54, 102-103)
  • The intake of vitamin E, beta-carotene and selenium shows a significant inverse correlation with the risk of fractures.
  • Smoking (2564 participants; hang J; Antioxidant Intake and Risk of Osteoporotic Hip Fracture in Utah: An Effect Modified by Smoking Status; Am J Epidemiol; 2006; 163; 9-17)

 

Primary prevention in pre-menopause

• Diet: B. Rich in calcium (dairy products), low in phosphate (cola, sausage, meat), not too high in protein
• Sun exposure: Vitamin D synthesis in the skin (only possible from May to September in our latitudes, otherwise supplementation)
• Avoid/reduce stimulants: Nicotine, alcohol
• Exercise: Sport, leisure activities, gardening, fitness, strength training
• Elevated plasma levels of the amino acid homocysteine ​​(hyperhomocysteinemia) are a significant risk factor for osteoporosis. Homocysteine ​​lowering with vitamin B6, B12, folic acid (vitamin B9) should be carried out. (Source: Van Meurs; 2406 Pat.; Rotterdam study, Longitudinal Aging Study Amsterdam 2004, prospective, population-based cohort studies)
• With vitamin B12 concentrations of < 148 pmol, there is a significantly lower bone density in the hip in men and significantly lower in the spine in women. (Source: Tucker KL et al.; 2005: Inhibition of osteoblast activity in B12 deficiency)
• Seniors, who fall, have significantly lower folic acid levels. A high folic acid serum level turns out to be the only protective factor for reducing the risk of falls.
  For each nanogram/ml increase in folic acid concentration, the risk of falls decreases by 19%.
  (Source: Hahar D et al.; Nutritional Status in Relation to Balance and Falls in the Elderly; A Prelaminary Look at Serum Folate; Ann Nutr Metab 2009; 6; 59-66)

 

Calcium and osteoporosis

• Dosage: 1000 mg total daily amount incl. Food (“normal” food provides 650-900 mg)
• Absorption: 30-35%; particularly poor absorption in cases of anacidity (lack of stomach acid as a result of the use of proton pump inhibitors); Calcium citrates, gluconates and lactates are better absorbed
• Excretion: approx. 300-350 mg per day
• Calcium supplementation: Cardiovascular mortality increases with regularly very high calcium intake (Source: Dtsch Ärztebl 2013; 110(13): A-614 / B-546 / C-546)

 

Vitamin D and osteoporosis

• Increases calcium absorption and stabilizes calcium homeostasis
• Maintains bone density
• Influences neuromuscular function
• Dosage: 000-10.000 IE Vitamin D3 /day (depending on level)
• Sun – possible endogenous production up to 20.000 IE/Day; Requirement: full sun exposure without sunscreen

 

Vitamin C and osteoporosis

• Increases bone density
• Essential for collagen and bone matrix synthesis
• Even a small deficiency leads to bone loss
• In a cohort study with 994 older women, 500 mg vitamin C additionally consumed through food significantly increased bone density (stimulates procollagen formation and collagen synthesis as a precursor for bone matrix). Vitamin C works synergistically with estrogen. (Source: DJ Morton, San Diego, 29. American Society of Bone and Mineral Research Meeting; EZ 15.101997)
• Dosage: 2-4 x 500-1000 mg/day; For highly bioavailable liposomal vitamin C, 180-240 mg/day is sufficient

 

Magnesium and osteoporosis

• Activates enzymes of bone synthesis
• Partner of calcium (magnesium deficiency leads to calcium deficiency)
• Deficiency common in osteoporosis
• Dosage: 300-1.200 mg/day

Boron and osteoporosis

• Boric acid is involved as a hydroxyl group donor in the hydroxylation of 25-hydroxy-cholecalciferol to 1,25-dihydroxy-cholecalciferol (i.e.H the actual active form of vitamin D3) in the kidneys.
• Boron shows synergism with vitamin D, inhibits protein breakdown
• Boron reduces calcium excretion via urine
• Boron can prevent osteoporosis; In the event of a magnesium deficiency, boron replaces its
  function, increasing the boron concentration in the bone tissue.
• Boron has a positive effect on the metabolism of steroid hormones as a hydroxyl group donor. So it increases the 17-ß-estradiol and testosterone levels in the serum in women and thereby the effectiveness of estrogen. (Source: Journal of Dental Sciences Volume 11, Issue 3, September 2016, Pages 331-337; The effect of boron on alveolar bone loss in osteoporotic rats; Conclusion: Within limitations of this study, we conclude that boric acid may decrease alveolar bone loss in a rat model with periodontitis and osteoporosis.)

 

Silicon / silica and osteoporosis

• The positive effect of silicon on bone and various other tissues was first reported in Nature and Science over 30 years ago. Since then, studies on this have appeared again and again. (Sources: Carlisle EM. Silicon: a possible factor in bone calcification. Science 1970; 167: 279–80. Black K, Milne DB. Growth-promoting effects of silicon in rats. Nature 1972; 239: 333–4.)

 

Arginine & Lysine and Osteoporosis

The role of arginine and lysine in bone metabolism (e.g.a also to accelerate fracture healing)

* Osteocalcin (Synonym: "bone γ-carboxylglutamic acid-containing protein" or: "BGP", the
gene: BGLAP) is a peptide hormone. It is formed in bone by osteoblasts and in tooth
by odontoblasts and binds to hydroxyapatite and calcium.

 

Vitamin K and osteoporosis

• Vitamin K & calcium lead to an increase in the bone density of bones in the spine (so-called vertebral bone); Synergism vitamin K + calcium + vitamin D3
• Vitamin K is a coenzyme of the vitamin K-dependent γ-glutamylcarboxylase: controls conversions in various proteins such as:b in osteocalcin (binds bone calcium) and matrix Gla protein (inhibits the deposition of calcium in the artery wall). This carboxylation is important for protein functions because it allows their binding ability for calcium and their binding to phospholipids.
• Vitamin K2 (but not vitamin K1) also inhibits osteoclast activity: With vitamin K2 (45 mg), bone mass and the thickness of the femoral neck increase in postmenopausal women compared to placebo. The strength of the hip bone does not change during therapy, but decreases significantly under placebo (measurement with DXA). (Source: Randomized, placebo-controlled; 325 participants over 3 years; Knapen MH et al.; Vitamin K2 supplementation improves hip bone geometry and bone strength indices in postmenopausal women; Osteoporosis Int 2007; 18; 963-972)

 

 

Phytoestrogens and osteoporosis

• Secondary plant substances (structurally similar to estrogen)
• a. Isoflavones, lignans
• Occurrence e.g.b in soy, oilseeds or whole grains
• Societies in which soy is consumed regularly have:
  • Lower rates of breast and ovarian cancer
  • Less menopausal syndromes (< 25% vs. 80%)
  • Less cardiovascular disease
  • Less osteoporosis
• With administration of isoflavones (84 or 126 mg) there is a significant linear
  improvement in bone density in the lumbar spine and femoral neck compared to placebo. (Source: Randomized, placebo-controlled, single-blind; 90 participants over 6 months; Ye YB et al.; Soy isoflavones attenuate bone loss in early postmenopausal Chinese women: a single-blind randomized, placebo-controlled trial; Eur J Nutr 2006; 45; 327-334)
• Typical dosage: Isoflavones (incl. Genistein): approx. 50 mg/day (e.g.b 100 g tofu, 100 g soy germ)