Should older osteoarthritic patients- who mostly have high risk of all the common major degenerative diseases of aging and premature mortality- be fobbed off with non-steroidal anti-inflammatory drug – NSAIDs?


    This University of London study  on  confirms what has long been obvious- that it is foolish if not negligence to poison the body by noncurative-and potentially fatal – shotgun therapy eg oral  anti-inflammatories,  or intramuscular diclofenac, when self- inunction can do better.
              However, the report is surely an unnecessary punt for ibuprufen cream, and seriously misleading if not dangerous  on major scores including long term cost  for the older population
          1.  There is no need to use synthetic designer NSAIDs-  which inherently have  higher risk of eg sensitiziation;
       when either  selfmassage of the relevant sore point with any anti-inflammatory , even teatree oil or ung meth sal,
        or  appropriate targeted injection of the relevant tendon, ligament or joint with a few ml of local anaesthetic +- depot corticosteroid, may be more effective,  often speedily curative  and totally safe.

And     2.  the BBC report says  “the most common cause of  pain in the knee is osteoarthritis – a condition caused by abnormal wearing of the cartilage… an estimated third of over 50s suffer from knee pain…  in half of those the problem is classed as severe.” 

         The common causes of pain in the knees in the older  are many; but assuming that the clinical condition  indeed points to knee  “osteoarthritis”- a heterogenous multifactorial basket – (and not eg simple external ligament strain or bursitis-   it  is proven that while a chondro-glucosamine CGS combination has little analgesic effect, such a biological  oral combination  actually restores lost cartilage by millimeters over months to years, so that many people sentenced (usually by surgeons)  to eg bilateral knee replacement for destructive painful OA knees may recover completely without surgery  and are  walking normally within months and a decade later.


      Let alone analgesics masking if not   if not allowing more cartilage damage, it is dubious –indeed impossible-  that diffusely painful  overloaded osteoarthritic knees will  respond enough during the pain phase to just topical  analgesic anti-inflammatory massage therapy.


  And 3. The BBC report gives no details of the patients and the duration of the reported  trial. This topical cream approach was debunked by a metanlysis in the BMJ in 2004;


          4. older osteoarthritic patients are at high risk of all the chronic degenerative diseases of aging- hip, spinal  disc, hypertensive, atheromatous etc.
      So oral chondroglucosamine is simply combined with a combination of  natural safe effective  lowcost oral analgesic  anti-inflammatory antioxidant  weight-reducing  and anabolic  supplements (eg  fish oil 4gm/day  plus cat’s claw, MSM, bromelain, boswelia, curcumin, proline, GABA  and some vitamins and minerals), for progressive reversal of both pain, inflammation and the causative overweight and cartilage loss.

      The analgesic but risky  NSAIDs can be weaned off in due course while  the CGS continues as longterm protection.


More important still, the aging and overweight homo erectus is especially prone to pain and disability from degeneration and prolapse of the 23 intervertebral fibrocartillage discs  so well shown on

         In 2003 van Blitterswijk ea at the Netherlands Cancer Institute reported a man with a  lumbar disc prolapse (on MRI scan  with longstanding  lumbar pain,  which healed completely over 2 years on CGS.  They review the cartilagenous nature of the intervertebral discs with their hygroscopic sponge nuclei composed of proteoglycans including CGS, 

 and  fed by capillaries  from the periphery.

They noted that GCS is anti-inflammatory and anti-catabolic.  They concluded: “oral CGS can pass the gastrointestinal tract and can indeed reach articular cartilage, probably also intervertebral discs, where it may have at  least a chondroprotective effect  and, quite possibly, a regenerative effect. Contrary to NSAIDs, no significant adverse  clinical, hematological, hemostatic or other side effects were found in any  clinical study using CGS supplementation.

Contrary to degenerated cartilage, these dietary supplements had  no apparent effects on normal cartilage metabolism This may suggest a tropism of these agents for cartilage in the reactive  state, characterized by enhanced proteoglycan turnover.

GS/CS does not contribute to insulin resistance in  diabetics, probably because the pharmacokinetics and tissue distribution of GS/CS and glucose are different“. 


       In 2006  Grunhagen ea at Oxford University again noted that the avascular disc cells need the low concentration of blood oxygen and glucose that reaches them from the periphery.
         In 2007 Ulrich ea at UCSF showed that repeated disc injury (during healing) causes persistent inflammation, probably enhancing disc degeneration.


        But it is not just multiple joints that  warrant the protective benefit of long term CGS:
In 1979  Nakazawa ea in a German journal reported that CS for over 5 years lowered mortality and thrombosis in the elderly.
In 1985 Corsa ea in Italy showed significant improvement in peripheral vascular disease and lipidemia with high-dose glycosaminoglycan.
In 1997 McCarty in San Diego proposed that  GS may like heparan protection against atherogenesis. 
In 1998 Nowak ea in  Poland  showed that GS levels are raised in ischemic diabetics,and fall with exercise or other control of hyperglycemia.
In 2001 Talpur ea in Washington DC showed that CGS in rats had no adverse effects in IGR rats, and lowered systolic BP.
In 2002 Coccheri ea in Italy and in 2005 Lauver ea in Michigan  showed that glycosaminoglycan healed varicose ulcers and peripheral arterial and coronary ischemia, lowers fibrinogen and is lipolytic.
In 2005 Duan ea  in USA  showed that GS significantly reverses atherosclerosis, and
in 2006 Tannock ea in US that GS reduces longterm arteriosclerosis although it promotes it short term. .
 n 2007 in USA, Champattanachai ea  showed that  rise in endogenous NacetylGS is  an endogenous stress-activated response that improves cell survival;

                  and Fulop ea  propose the molecular basis for this;

and finally in 2008 Jones ea in USA conclude that “GS signalling represents a unique endogenously recruitable mechanism of cardioprotection“.


     Then there is the major body of evidence to support nutriceutical supplements not just for minimising  atheroma and osteoarthritis but also against overweight, (pre) diabetes, hypertension, osteoporosis, lipidemia, osteoporosis, cancer and dementia- with nitric oxide donor, antihomocysteine, antioxidant, insulin sensitizer  and anabolic supplements.


       So rather than dismissing the painful arthritic patient with some NSAID cream, the BBC report should have focussed on the golden opportunity- opportunistic screening-  that every consultation presents – to assess quickly the aging risks- simply a history questionnaire, BMI and waist measurement, arm  and ankle bloodpressure (ankle-brachial gradient)- and counselling  the patient both about the cardinal role of sensible exercise diet and lifestyle, and about taking the evidence-based lowcost combination of fish oil and a blend of up to threescore vitamins, minerals and biologicals  including CGS (and where appropriate- in most older people- appropriate non-oral balanced human hormone replacement HRT)..


 refs available on Pubmed.






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