GLYVIA™ – NATURAL alternative sweetener also induces insulinogenic pharmacology!

GLYVIA™ deliciously and naturally sweetens foods and beverages without carbohydrate contribution; improves serum sugar clearance;  helps suppress appetite and carbohydrate cravings; helps manage dietary calorie balance.  Add  GLYVIA™ to Tea, Coffee, Oatmeal, Baking, Protein shakes and more! WHY NOT? The question we should ask ourselves more often than we ask ‘WHY’ is ‘WHY NOT?’ WHY NOT venture beyond convention; beyond the rules or standards or boundaries that are set by other human beings with the same human limitations you have. WHY NOT explore uninhibited human potential to discover what lies outside common perception. Fear not peer judgement; fear not ridicule; fear not failure! Just keep aiming with intellect-guided intuition at ‘WHAT COULD BE’, ‘WHAT SHOULD BE’ and ‘WHAT MUST BE’. BIOLOGIC Pharmamedical has been on a proven track record of repeated discovery because ‘WHY NOT’ has helped guide us to discover what others have been fearful of being judged by. GLYVIA™ is our latest discovery; a NATURAL carbohydrate-neutral alternative sweetener that also supports blood sugar management by way of multiple mechanisms:  1) insulinogenic pharmacology to induce pancreatic beta cells  –  similar activity to the common anti-diabetic drug, Glyburide;    2) reduces carbohydrate intake by deliciously sweetening beverages and foods without aftertaste and carbohydrate contribution;    3)  suppresses appetite and carbohydrate cravings. Avoid dietary carbs; fulfill sweet-tooth / cravings; improve serum glucose clearance. Ask us ( how you can leverage this newly discovered FUNCTIONAL ALTERNATIVE NATURAL SWEETENER with claims- to build your brand to the next level with the latest research to support human health; with what is expected to be one of the most profound ways.

Review of Amyotrophic Lateral Sclerosis, Parkinson’s and Alzheimer’s diseases helps further define pathology of the novel paradigm for Alzheimer’s with heavy metals as primary disease cause.

Review of Amyotrophic Lateral Sclerosis, Parkinson’s and Alzheimer’s diseases helps further define pathology of the novel paradigm for Alzheimer’s with heavy metals as primary disease cause.

Franco Cavaleri (as seen in Elsevier’s Medical Hypotheses) Faculty of Medicine, Department of Experimental Medicine, Brain Research Center, UBC Hospital, 2211 Wesbrook Mall, Vancouver, BC V6T 2B5, Canada Abstract Pathologies of neurological diseases are increasingly recognized to have common structural and molecular events that can fit, sometimes loosely, into a central pathological theme. A better understanding of the genetic, proteomic and metabolic similarities between three common neurodegenerative diseases – Amyotrophic Lateral Sclerosis (ALS), Parkinson’s disease (PD) and Alzheimer’s disease (AD) – and how these similarities relate to their unique pathological features may shed more light on the underlying pathology of each. These are complex multigenic neuroinflammatory diseases caused by a combined action by multiple genetic mutations, lifestyle factors and environmental elements including a proposed contribution by transition metals. This comprehensive dynamic makes disease decoding and treatment difficult.

Nullam rhoncus aliquam metus

Morbi a metus. Phasellus enim erat, vestibulum vel, aliquam a, posuere eu, velit. Nullam sapien sem, ornare ac, nonummy non, lobortis a, enim. Nunc tincidunt ante vitae massa. Duis ante orci, molestie vitae, vehicula venenatis, tincidunt ac, pede. Nulla accumsan, elit sit amet varius semper, nulla mauris mollis quam, tempor suscipit diam nulla vel leo. Etiam commodo dui eget wisi. Donec iaculis gravida nulla. Donec quis nibh at felis congue commodo. Etiam bibendum elit eget erat.

Mauris elementum mauris vitae tortor

Praesent in mauris eu tortor porttitor accumsan. Mauris suscipit, ligula sit amet pharetra semper, nibh ante cursus purus, vel sagittis velit mauris vel metus. Aenean fermentum risus id tortor. Integer imperdiet lectus quis justo. Integer tempor. Vivamus ac urna vel leo pretium faucibus. Mauris elementum mauris vitae tortor. In dapibus augue non sapien. Aliquam ante. Curabitur bibendum justo non orci.