Biostructural Medicine Cell membrane stability and receptivity
- Biostructural Medicine Development
- Pathophysiology - Degenerative Disease
- Biostructural Medicine Concept
Biostructural Medicine Development
For ten years, Biomedica Laboratories, a Canadian nutraceutical company, has focused on the development of the health science Biostructural® Medicine. Biomedica Laboratories has researched and studied the age-related changes that occur to cell structure and function.
Biostructural® Medicine goes beyond simply suppressing symptoms; it implements both a proactive and reactive approach to address tissue trauma and inflammation. Biostructural® Medicine is a cell structure-oriented health science designed to address the pathogenic factors of degenerative and inflammatory conditions by improving cell membrane stability and receptivity.
By implementing the principles of Biostructural® Medicine, veterinarians, now have an additional therapeutic advantage to manage conditions associated with inflammation and soft tissue breakdown by increasing cell stability and receptivity.
Over the last ten years, Biomedica Laboratories has focused research on the comparison of normal cell membrane and extracellular matrix (ECM) structure to the negative changes that occur in conditions such as inflammation, trauma and age-related decline; these investigations have lead to a potentially groundbreaking development in health science called Biostructural® Medicine, which has further lead to the development of a potential natural disease modifying anti-catabolic (dmac) Nutricol® (Recovery®SA).
Biostructural® Medicine and the disease modifying anti-catabolic (dmac) Recovery®EQ provide veterinarians with a different perspective in the type of treatment, that he/she may choose for their patient, to increase cell stability and receptivity.
Pathophysiology - Degenerative Disease
When oxygen is utilized by the body, damaging "exhaust" called reactive oxygen species (ROS) are released. ROS include hydroxyl radicals, superoxides, hypochlorite and hydrogen peroxide, to name a few. ROS, in smaller quantities, play necessary roles in metabolic processes, however, when ROS production increases and the ability to neutralize ROS decreases, the overall effect on tissues is destructive. (1-4)
Increased cellular production of ROS are linked to most degenerative conditions including heart disease, arthritis, cancer, periodontal disease, liver disease, cataracts, macular degeneration, diabetes, gastrointestinal inflammatory diseases, autoimmune diseases and asthma. (5-7)
ROS react with cellular components initiating destructive chain reactions that result in degeneration of tissue and disease causing potential inflammation and pain. (1,3)
Antioxidants, such as coenzyme Q10 (CoQ10), alpha lipoic acid and NADH (nicotinamide adenine dinucleotide) and anti-catabolic enzymes, such as glutathione peroxidase, superoxide dismutase and catalase minimize the damaging effects of ROS. Researchers at Biomedica Laboratories believe that younger healthy cells produce much larger quantities of these antioxidants and anti-catabolic enzymes. (3,5)
Aging and disease results in diminished cellular production of the above stated protective compounds, which leads to increased damage to the membrane structures; inevitably, damage to membrane structures diminishes cellular ability to repair traumatized tissue. (1,7)
Damage to membrane and extracellular matrix (ECM) structure leads to decreased ideal first-intention healing involving parenchymal elements. (8-10)
This results in:
1.Decreased production of long chain glycosaminoglycans with a compensatory increase in shorter chain glycosaminoglycans, which leads to dehydration of tissue and decreased membrane receptivity (9,11,12)
2.Decreased cellular ability to receive growth factors (somatomedins, insulin, etc.), which are necessary for cellular repair, maintenance, protection and communication * (13-15,41)
3.Deposition of heavily glycosylated, compact and inflexible collagen types V and VI (12,16-22)
4.Increased granulomatous second intention healing involving stromal elements (i.e. development of scar tissue), which leads to loss of cellular/tissue function (9,42)
Consequences:
Loss of cellular and tissue function results in further inability to repair damage, leading to increased tendency to bruising, excessive inflammation, spasm, joint stiffness, digestive abnormalities, respiratory distress. (7,9,15,20,21,23,24)
* Insulin normally acts as a shuttle to drive amino acids, glucose, fatty acids, glucosamine and other precursor biochemicals into the cell so that the cell may synthesize required structures for tissue repair.
Biostructural® Medicine Concept
The establishment of a more youthful and healthy state of membrane and ECM structure leads to more effective tissue responsiveness and healing.
The goal of medicines developed from this medical concept is to increase cell regenerative and communicative capacity and to limit sub-optimal repair (granulomatous tissue) and unnecessary cell necrosis associated with aging, trauma and disease.
Increasing cell membrane stability and improving the stability and hydration of extracellular glycoprotein structures within epithelial and connective tissue has the potential to:
1.Decrease pathological micro-vascular permeability, therefore, decreasing edema 2.Inhibit the cascade of cell necrosis and/or damage, in other words, halting the domino effect - necrosis or damage in one cell resulting in the resultant necrosis or damage of many
Prior to the development of Recovery®EQ, the first natural product developed that follows the principles of Biostructural® Medicine, researchers of Biostructural® Medicine theorized that accelerated catabolism and declining cellular production of certain glycoproteins were rate-limiting factors in the healthy construction and maintenance of tissue. Biostructural® Medicine researchers believe that a sub-optimal production of these same glycoproteins would affect the formation of normal extracellular aldimine reducible cross-linking at repair sites, which may lead to an increased production of glycosylated cross-linking (compact type V and VI collagens, as are abundant in granulomatous tissue) and inadequate extracellular spacing that could further affect cellular nutrient, hormone and waste exchange. In other words, it is possible that sub-optimal cellular production of these glycoproteins and the resultant lack of extracellular collagen spacing, may inevitably result in dehydration and lack of cellular function at affected tissue sites.
Biostructural® Medicine researchers believe that by inhibiting oxidative damage (via increasing cell membrane stability), that cellular necrosis, excessive platelet adhesiveness and altered cellular function would dramatically decrease, thereby decreasing the size of the affected zone of degeneration. In other words, protecting cells via increasing the stability of cell membrane structures and decreasing cell membrane exposure to damaging compounds is a method of inhibiting the excessive initial activation of the pro-inflammatory phase; accomplished via two routes of action:
1.Increased stability of the extracellular protective glycoprotein matrix to prevent reactive oxygen species (ROS) induced damage to cell membrane structures
Mechanism: Increased anabolism and decreased catabolism of certain glycoprotein structures within the ECM

Cell Membrane and ECM Biostructure
2.Increased stability of cell membrane fatty acids to inhibit excessive cell membrane oxidation and subsequent excessive release of inflammatory mediators such as prostaglandins, leukotrienes, histamines, thromboxanes and platelet activating factor (PAF)
Mechanism: Embed substances within cell membrane structures that neutralize potentially damaging substances
Due to the above two routes of action, compounds associated with excessive inflammatory reactions and cell necrosis are inhibited (e.g. cyclo-oxygenase 2 that increases formation of prostaglandins of the 2 series and lipoxygenase which increases formation of leukotrienes, which are powerful potentiators of abnormal inflammatory reactions and tissue destruction in surrounding structures)
Recovery®SA - Biostructural® Medicine
The development of the first potential natural disease modifying anti-catabolic (dmac) Biostructural® Medicine, Recovery®SA is paving new grounds in the successful management of chronic degenerative conditions associated with pain, inflammation and tissue damage. Biomedica Laboratories researchers compiled many journal references regarding the pathology of connective tissue and reviewed rate-limiting biochemicals that are orally bioavailable, which has led to the development of the potential natural disease modifying anti-catabolic (dmac) ingredient Nutricol® and Recovery®SA