Diseases of the musculoskeletal system “rheumatic form circle”:
4 groups

1. Degenerative – non-inflammatory – disorders (e.g. arthrosis deformans)
2. Primary inflammatory diseases (e.g. rheumatoid arthritis, para- & post-infectious
   arthritis, paraneoplastic arthritis)
3. Metabolic (secondary) inflammatory diseases (e.g. gout)
4. Soft tissue rheumatic, "non-inflammatory" complaints
   (e.g. fibromyalgia as a chronic painful muscle disease)

Main problems:

• Pain (chronification!)
• limitation of mobility & quality of life
• Incapacity for Work & Early Retirement

Non-pharmacological measures & orthopedics

A) Nutrition

Relationship between joint diseases and nutrition have existed since the time of Hippocrates. Biochemical research in recent years has been able to identify the inflammatory mediators of rheumatic diseases and connections with food
point out.

Recommended diet:

• with a high content of micronutrients
• Full-fledged (Mediterranean or Asian oriented), natural,
  high-fiber diet with a high proportion of fruit, Vegetables, (Fish)
  herbs and nuts, high-quality oils
• with cheap acid-base ratio; especially reduction of
  • Alkaline-depleting foods (sugar, white flour, industrially manufactured
    Groceries)
  • Acid donors such as animal protein & animal fats, alcohol, coffee and nicotine, certain cereal products (e.g. white bread, crispbread), certain vegetables (e.g. Brussels sprouts, peas, artichokes), certain types of cheese (e.g. processed cheese)

B) Healthy exercise

• (Exhalation of CO2 = CARBON ACID, sweating, increased oxygen supply)
  Influences overall metabolism and aging process.
• Endurance-oriented sports (e.g. 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!)
• Captures membrane-damaging oxygen radicals
• Inhibition of the activation of NF-κB – a protein important in the immune response and therefore in the inflammatory process (cf. Miehle, Bad Aibling, Fortschritt der Medizin 115, 1997, p.39-42)
• Anti-inflammatory and central analgesic effects (influence on pain perception and processing) with an increase in β-endorphins (are the most effective endorphins in terms of pain suppression) (cf. Edmonds et al., Ann of the rheum.Diseases 56, 1997)
• Improved mobility and general well-being
• Lipophilic compartments in which vitamin E has an antioxidant effect: especially 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 inpatient conditions with either 1600 IU
    Vitamin E or 50 mg diclofenac (an NSAID) per day. In both treatment groups, comparable highly significant improvements in rheumatological findings such as grip strength, morning stiffness, pain, walking time and joint indices according to Ritchie were found. The results were not statistically separable (KOLARZ et al., 1990))
  • Increased vitamin E consumption in rheumatic patients
  • Reduced 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, mainly found in meat)
• reduce collagen degradation --> Inhibit the formation of messenger substances,
  that cause collagen degradation (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
  • Recommended intake: 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, found in hemp seed oil or evening primrose and black currant oil): displaces arachidonic acid from cyclooxygenase/cell membrane, increases PGE1 (Prostaglandins of groups 1 and 3 have an anti-inflammatory effect, while those of group 2 have a pro-inflammatory effect) and (low) eicosapentaenoic acid (EPA)
  • alpha-linolenic acid (Omega-3 fatty acid, contained in hemp seed oil): acts as a neural structural lipid, increases PGE3 (anti-inflammatory effect)
  • fish/algae oils (contain EPA and DHA, whereby EPA, which is relevant for inflammatory processes, is usually only present in high concentrations in fish oil):
    Displace arachidonic acid from cell walls, increase PGE3 (especiallyEPA due to structural similarity to arachidonic acid), prevent eicosanoid & inflammatory mediator formation

PGE 2 from arachidonic acid

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

Lower PGE 1 & PGE 3 inflammatory activity

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

Micronutrients of cartilage: 4 cartilage building blocks

1. collagen hydrolysate
   Collagen is a scaffold protein that forms the supporting substance of cartilage

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

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

2. glucosamine and chondroitin sulfate

• support cartilage metabolism, are building blocks of cartilage cells for the construction
  the cartilage components and the synovial fluid
• can be given in addition to painkillers and to save
  contribute to this
• support the improvement of symptoms (Pain, stiffness of the joints, difficulty walking and performing daily activities)
• EULAR recommendation (European League Against Rheumatism) 2003: Glucosamine and chondroitin sulfate were assessed with the (highest) evidence level 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 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 to evaluate the most important and everyday relevant consequences of osteoarthritis)
• Possible side effects: hair loss, dizziness, 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

• Characteristics
  • pronounced ability to bind water
  • viscous = gel-like
• Determines the properties
  • of the aqueous humor (eye)
  • the lymph fluid
  • the synovial fluid
• Improves cartilage quality (long-term effect unclear)
• Indication: Pain in degenerative changes of joints
• Dose: 3-5-x intra/para-articular at intervals of 1 week – or subcutaneously or orally is
  it is also possible
• Possible side effects: pain, feeling of heat, 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 value “Bodily Pain” by 11.2 (point value) corresponds to a significant pain reduction by 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 mainlyin the articular cartilage) of the musculoskeletal system
• Regulation of bone and cartilage metabolism (“cartilage protective agent”)
• Additionally direct effect on inflammation & 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 to 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 as 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 area of ​​inflammation via adhesion molecules)
• Support of antioxidant enzymes (superoxide dismutase (SOD), catalases, glutathione peroxidase)
• immunomodulatory effect
• Destruction of immune complexes (immune complexes consisting of antibodies/antigens are difficult to break down by the phagocytes and enter the surrounding tissue via the blood, where they trigger inflammatory processes)
• Analgesic effect (indirectly through splitting of pain mediators such as kinins & prostaglandins, as well as directly through action on the pain-receiving sensor (nociceptor))
• degradation of cell fragments in degenerative joint processes
• Anti-edematous effect

Mechanisms of action of proteases in orthopedics

Other micronutrients for bone and cartilage metabolism

• B-complex vitamins
  • Vitamin B6: cofactor of the enzyme that cross-links 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 of activated osteoarthritis due to its anti-inflammatory properties. Boron exerts its effect by reducing ROS (reactive oxygen species) and its Inhibition of cyclooxygenase (COX II) and lipoxygenase (LOX), which are mediators for the inflammatory cascade. There is an osteoarthritis incidence 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 essential for calcium absorption from the intestine as well as for calcium incorporation into the bones
• vitamin K
  • Supports bone metabolism through osteocalcin formation à Osteocalcin 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 thereby the synthesis of PGE 2 (group 2 prostaglandins are pro-inflammatory)

Clinical pictures in orthopedics & rheumatic diseases

A) Osteoarthritis

• Most common disease of the supporting and connective tissue: Affects ~80% of >60 year olds!
• imbalance between stress and resilience
• Possible causes:
  • Genetic predisposition (e.g. protein synthesis disorders with incorporation of cysteine ​​instead of arginine)
  • Incorrect loads & injuries/ operations & overload, overweight
  • Lack of exercise & protective postures, gender (women more often), age
  • inflammations
  • Metabolic disorders (e.g. hyperuricemia, osteoporosis, hyperthyroidism, hyperacidity)
  • Chronic micronutrient deficiencies
• Pathogenesis:
  • Damage to the articular cartilage (“hyaline cartilage”, suspension and shock absorber function), especially in the stress zones, with degradation of proteoglycans (important components of the cartilage tissue)
  • Change in the basic substance with demasking & 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!)
  • loss of strength
  • Restriction of mobility up to stiffness
• Symptoms of osteoarthritis:
  • Pains
  • 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; i.e. 600-2000 mg per day divided into 3 doses (~ 3x 500 mg/day)
• Chondroitin sulfate: 400-1200 mg/day (e.g. 3x 400mg/day)
• Methylsulfonylmethane (MSM): 2x2 capsules of 500 mg each
• Methionine / SAM: 400-1200 mg
• Niacinamide (vitamin B3): 500-3000 mg (e.g. 3x 500 mg/day)
• Vitamin K2 MK7: 100-200 µg (has analgesic, anti-inflammatory effects; involved in the synthesis of osteocalcin (a protein important for bone formation))
• Omega 3 fatty acids: 2000-3000 mg per day; important: high EPA content (especially the case with fish oils)
• Collagen hydrolysate: 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 IU per day; Antioxidant, energy & protein metabolism, connective tissue, bones
• Vitamin D3: 5000-20,000 IU daily; bones & teeth (osteoporosis!)
• Folic acid: 0.4-5 mg
• Adequate protein supply (0.8 grams per kg of body weight)
• Vitamin B12: 50-1000 mcg
• Vitamin B6: 5-50 mg; especially for pain (analgesic, anti-inflammatory)
• Calcium: 600-1000mg (e.g. 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 osteoarthritis due to its anti-inflammatory properties. Boron exerts its effect by reducing ROS (reactive oxygen species) and its Inhibition of cyclooxygenase (COX II) and lipoxygenase (LOX), which are mediators for the inflammatory cascade. There is an osteoarthritis incidence 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 destructive inflammatory reaction of unclear origin
  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 & Restricted Movement
  • reduction in quality of life
  • Incapacity for work and early retirement (after 5 years of illness, ~50% of patients are unable to work!)
  • Drug-induced susceptibility to infection
  • Gastrointestinal complications caused by medication (shorten life expectancy by about 7 years)

• Therapy Rheumatoid Arthritis / rheumatism "natural remedies"
  • Wholesome (lacto-vegetarian = plant-based food + dairy products and eggs) food, sometimes only a vegan diet is successful
  • exercise, relaxation
  • Physical measures
    • Active, e.g. muscle strengthening
    • Passive, e.g. classical massage therapy, electrotherapy
  • Heat & cold (e.g. rye pillow, hay bag, rheumatism bath)
  • y-linolenic acid (GLA) 150-600 mg, e.g. contained in hemp seed oil
  • Boswellic acids from frankincense inhibit lipoxygenase (enzyme that oxidizes unsaturated fatty acids in the presence of oxygen) and thus have an inhibitory effect on leukotrienes (inflammatory messengers released from immune cells)
• Typical dosages:
  • Omega 3 fatty acids (especiallyEPA, contained in fish oil in large quantities): 2000-6000 mg, converted in 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 IU, 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 IU (i.e. 10-20 drops of 1000 IU), possibly even much higher (see Coimbra Protocol)
  • Vitamin B12: 1,000 mcg
  • Vitamin B6: 50 mg, especially for pain, analgesic (pain-relieving) and antiphlogistic (anti-inflammatory) effect
  • Selenium: 100-300 mcg, antioxidant, often deficient 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 nociceptor), anti-inflammatory and decongestant effect
  • Boron: 6-9 mg; boron works by reducing ROS (reactive oxygen species) and inhibiting cyclooxygenase (COX II) and lipoxygenase (LOX), which mediate the inflammatory cascade that causes joint swelling, reduced joint mobility and other arthritic symptoms.
  • Magnesium: 150-300 mg; magnesium intake correlates positively with bone density; with long-term treatment 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 renal insufficiency is also increasingly observed with long-term PPI use (JAMA Intern Med 2016, online January 11).
  • Copper: 1-2 mg
  • Manganese: 2-20 mg
  • Folic acid (as folate): 0.4-5 mg
  • Adequate protein supply: 0.8g per kg body weight
  • Calcium: 600-1000 mg (e.g. calcium citrate), calcium as the most important mineral component of the 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 release calcium into the blood) > bone formation, thus 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 the hip, long bones and vertebrae
• Type 3: Secondary osteoporosis:
  Increased bone loss due to medications (eg glucocorticoids) or other causes (egmalnutrition/micronutrient deficiency)

Normal bone:

Bones with osteoporosis:

• Osteoporosis risk increased in:
  • Aluminium (e.g. in medicines to neutralise stomach acid (so-called “antacids”), such as Maaloxan or Masigel)
  • Proton pump inhibitors (PPIs)
  • 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 trials)
  • immunosuppressants
  • lithium
  • Long-term use of heparin (anticoagulant)
  • Supraphysiological (i.e. exceeding physical requirements) doses of thyroxine
  • Premenopausal use of tamoxifen (estrogen receptor modulator)
  • TPN (total parenteral nutrition)
  • Selective serotonin reuptake inhibitors (SSRIs) (antidepressants that block the serotonin transporters and thereby increase the concentration of serotonin in the tissue fluid of the brain): Men who use SSRIs have a significantly lower bone mineral density in the hip and lumbar vertebrae (in a range similar to that seen with chronic cortisone use) than 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)
  • Continuous high vitamin A intake of > 1.5 mg / day (approx. 5,000 IU), especially all-trans-retinol, increases the risk for 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 fracture risk.
  • smokers (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

• Nutrition: B. rich in calcium (dairy products), low in phosphate (cola, sausage, meat), not too rich 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
• Movement: Sports, leisure activities, gardening, fitness, strength training
• Increased plasma levels of the amino acid homocysteine ​​(hyperhomocysteinemia) are a significant risk factor for osteoporosis. Homocysteine ​​reduction with vitamin B6, B12, folic acid (vitamin B9) should be carried out. (Source: Van Meurs; 2406 patients.; Rotterdam Study, Longitudinal Aging Study Amsterdam 2004, prospective, population-based cohort studies)
• At vitamin B12-Concentrations of < 148 pmol result in significantly lower bone density in the hips in men and significantly lower bone density 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 serum folic acid level turns out to be the only protective factor for reducing the risk of falls.
  For every 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 including food (“normal” food provides 650-900 mg)
• Absorption: 30-35%; particularly poor absorption in cases of anacidity (lack of gastric 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 regular very high calcium intake (Source: Dtsch Arztebl 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 IU vitamin D3 / day (depending on the mirror)
• Sun – possible endogenous production of up to 20,000 IU/day; prerequisite: full sun exposure without sunscreen

Vitamin C and Osteoporosis

• Increases bone density
• Essential for collagen and bone matrix synthesis
• Even a slight deficiency leads to bone loss
• In a cohort study with 994 older women, additional dietary intake of 500 mg vitamin C the bone density significant (stimulates procollagen formation and collagen synthesis as precursors for bone matrix). Vitamin C acts synergistically with estrogen. (Source: DJ Morton, San Diego, 29th meeting of the American Society of Bone and Mineral Research; ÄZ 15.10.1997)
• 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 often occurs in osteoporosis
• Dosage: 300-1,200 mg/day

Boron and Osteoporosis

• Boric acid acts as a hydroxyl group donor in the hydroxylation of 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (i.e. the actual active form of vitamin D3) in the kidneys.
• Boron shows Synergism with vitamin D, inhibits protein degradation
• boron reduces calcium excretion via urine
• Boron can prevent osteoporosis; in case of magnesium deficiency, boron replaces its
  Function, whereby the boron concentration in the bone tissue is increased.
• Boron has a positive effect on the metabolism of steroid hormones as a hydroxyl group donor. it increases serum 17-ß-estradiol and testosterone levels in women and thereby increases 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

• More than 30 years ago, Nature and Science first reported on the positive effect of silicon on bones and various other tissues. Since then, studies have been published on this topic. (Sources: Carlisle EM. Silicon: a possible factor in bone calcification. Science 1970; 167: 279–80. Schwarz 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 (also to accelerate fracture healing)

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

Vitamin K and Osteoporosis

• Vitamin K & Calcium lead to an increase in bone density of the spine (so-called vertebral bone); Synergism Vitamin K + Calcium + Vitamin D3
• Vitamin K is a coenzyme of vitamin K-dependent γ-glutamylcarboxylase: it controls conversions in various proteins such as 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 Binding ability for calcium and their binding to phospholipids allows.
• Vitamin K2 (but not vitamin K1) also inhibits osteoclast activity: Vitamin K2 (45 mg) increases bone mass and the thickness of the femoral neck in postmenopausal women compared to placebo. The strength of the hip bone does not change during treatment, but decreases significantly under placebo (measured 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.in soy, oilseeds or whole grains
• Societies in which soya is regularly consumed have:
  • Lower rates of breast and ovarian cancer
  • Fewer menopausal syndromes (<25% vs. 80%)
  • Fewer cardiovascular diseases
  • Less osteoporosis
• With the administration of isoflavones (84 and 126 mg, respectively) there is a significant linear
  Improvement in bone density at 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 (including genistein): approx. 50 mg/day (e.g. 100 g tofu, 100 g soybeans)