“Collagen abnormalities may cause mucosal lesions, altering tissue integrity and increasing the chance of larger proteins crossing the mucosal barrier and creating an immunogenic response.”
Archive for August, 2009
Medical: HORMONAL ASPECTS OF HYPERMOBILITY
August 5, 2009Dr. Bird, a leading expert on hypermobility has written about the ‘Hormonal Aspects of Hypermobility.” As always, we will only be quoting excerpts from this article, even though it is now available online (see link below)
“Although oestrogen tends to stabilise collagen, progestogens loosen it. Many hypermobile patients, though not all, noticed a worsening in symptoms, more pain in the joints, clumsiness or a greater tendency to dislocate in the five days leading up to menstruation and in the few days after menstruation. This is exactly the time when the progesterone compounds far exceed the stabilising oestrogen compounds…. ”
Women who have increased pain during menstruation usually notice this after their period has become irregular which means that the estrogen/progesterone ratio may be off.
His suggestion?
Avoid progesterone only pills or “progesterone depo contraception preparations or … mechanical devices impregnated with progesterone.“ But he also points out that this is not a one size fits all answer. Some women cannot take estrogen contraceptives, in which case he suggests trying a different kind of progesterone. More importantly, you need to discuss the pluses and minuses of your contraceptive choices with your doctor. Handing your doctor a copy of Dr Bird’s article would be a good start. If you live in the UK, the article is part of the Hypermobility Leaflet Pack.
And what about post-menopause when estrogen vanishes and the potential for pain increases? Will hormone therapy help in spite of the risks? “Since the oestrogen amount [during HRT] is very small…..[it] is often not enough to provide a protective effect for the joints.”
more here
Medical: Tiny rifts create fragility in collagen
August 5, 2009“Researchers at the Massachusetts Institute of Technology (MIT) have for the first time carried out a multi-scale analysis to shed light on how bone’s material flaws lead to brittle bone disease.
The researchers say that the weak tendons and fragile bones characteristic of osteogenesis imperfecta, or brittle bone disease, stem from a genetic mutation that causes the incorrect substitution of a single amino acid in the chain of thousands of amino acids making up a collagen molecule, the basic building block of bone and tendon.
They add that that minuscule encoding error creates a defective collagen molecule that, at the site of the amino acid substitution, repels rather than attracts the collagen molecule alongside it.
According to them, this creates a tiny rift in the tissue, which when repeated in many molecules, leads to brittle tissue, broken bones, deformity and, in the most severe form of the disease, death. For example, if healthy collagen tissue looked like a sheet of paper, diseased collagen tissue would look more like a sheet of paper full of tiny perforations. At each of these perforations, the sheet would be considerably more prone to tearing. “
