Tuesday, October 5, 2010

Even the common cold hyperstimulates our immune system

Jennifer Ackerman reports in the New York Times that  when we come down with the common cold,
the symptoms are caused not by the virus but by its host — by the body’s inflammatory response. Chemical agents manufactured by our immune system inflame our cells and tissues, causing our nose to run and our throat to swell. The enemy is us.
Multiple viruses, including the HIV, other than the rhinoviruses that initiate the common cold act in a similar fashion. This hyperactivity can be ameliorated by the administration of 5-HTP in conjunction with levodopa.

Thursday, August 19, 2010

semagacestat fails to treat Alzheimer's

Yesterday, Gina Kolata in the NYT wrote that a large PHARMA is abandoning its drug semagacestat that decreases the production of amyloid in patients with Alzheimer's. IMHO I believe that this was a failed concept from the start.  Alll neurodegenerative diseases (multiple sclerosis, ALS, Huntington's, Parkinson's and many many more) occur when the central nervous system is stressed and reacts excessively. The answer for all these conditions is the same, rein in this excessive response. Treat these conditions at the source..I wrote this about Parkinson's years ago. I think PURSOR could work equally as well on other neurodegenerative disorders. It is at least worth a try.

Elsewhere, researchers at NIH have declared that mood altering drugs appear to partially protect the brain against neurodegenerative diseases  I am glad to see that mainstream medicine is coming around to this axiom.

All mood altering drugs influence the immune system (immunomodulate)

Thursday, August 5, 2010

The monoamines dopamine and serotonin v. glucocorticoids as the first regulators of stress

Sapolsky in this superb article discusses the damage that uncontrolled stress can do. He promotes the mainline hypothesis that corticosteroids are the primal regulators. I think there is a far more primitive reciprocal regulatory system:
  • The structures of both levodopa and serotonin are far simpler than glucocorticoids. 
  • The metabolite pathways for both monoamines are far simpler; both are only 2 steps from essential amino acids. 
  • Both TYRosine and TRYptophan are first hydroxylated and then decarboxylated to achieve their endpoints, DA and 5-HT. 
  • The enzymes for both are either identical (L-aromatic amino acid decarboxylase) or were identical in the past. 

Saturday, June 12, 2010

Sleep Apnea: An immune disorder

The conventional wisdom is that sleep apnea (SA), a condition that more than 5% of the American population and is associated with markedly increased risk of heart attacks and strokes, is a mechanical disease. Those with it are frequently overweight with short and thick necks. However, there is increasing evidence that SA is another immune disorder associated with inflammation. Inflammation and sleep apnea I strongly believe that PURSOR would remit SA. Do look at this review: serotonin rx of same

Wednesday, June 2, 2010

Severe allergies and celiac disease respond to treatment and didn't come back

This a recent review of celiac disease immunology. I have found that the combination of dopamine and serotonin precursors utilizing the PURSOR protocol has astounding therapeutic capabilities. Dopamine and 5-HT have reciprocal action, the former promotes Th1 and reigns in Th2 and the latter does the contrary. The PURSOR protocol seems to have the ability to restore Th1/Th2 balance. A patient with celiac disease did respond. Interestingly, she presented with life-threatening idiopathic anaphylaxis which not only also had total recovery but has been in remission for more than 10 years. Apparently, celiac and immediate hypersensitivity disorders do coexist.
In simpler words. Immune diseases are divided into allergies and autoimmune. Celiac disease is an autoimmune. Severe allergies lead to allergic disasters (anaphylaxis). This patient had both types of illness, responded to treatment and has never had a recurrence.
Could TH1 and TH2 diseases coexist? Evaluation of asthma incidence in children with coeliac disease, type 1 diabetes, or rheumatoid arthritis: a register study

Wednesday, March 17, 2010

Mechanisms of Glucocorticoid Receptor Action in Noninflammatory and Inflammatory Cells

Glucocorticoids differ from serotonin. The latter suppresses the inflammatory response (Th1 driven) but augments Th2. Glucocorticoids suppress either or both responses. Therefore, if you wish to manage an immune condition, the use of PURSORTM is far more specific than using the GLU sledgehammer. This is an extremely well-written article and, therefore, deserves a Frank McLynn award.
"Glucocorticoids exert profound and diverse physiological effects on a wide range of cell types. Produced and released from the adrenal cortex in response to stress, levels of glucocorticoids are under the control of the hypothalamic–pituitary–adrenal axis.
Glucocorticoids participate in numerous physiological processes such as glucose homeostasis; protein, lipid, and carbohydrate metabolism; development; neuorobiology; and programmed cell death. Glucocorticoids exert potent immunosuppressive and anti-inflammatory actions in a cell type–specific manner largely through the interruption of cytokine-mediated pathways. These anti-inflammatory actions are also complemented by the ability of glucocorticoids to induce apoptosis in many cells including thymocytes, blood monocytes, and peripheral T cells.

As a class of drugs, glucocorticoids are among the most widely prescribed in the world for the treatment of immune and inflammatory diseases, including asthma, rheumatoid arthritis, ulcerative colitis, and allergic rhinitis. They are also a component of many chemotherapy regimens for the treatment of leukemias, lymphomas, and myelomas because of their role in the induction of apoptosis. However, long-term use of glucocorticoids has been limited by adverse side effects ranging from suppression of the hypothalamic–pituitary axis and growth retardation to osteoporosis, in addition to the development of glucocorticoid resistance. These undesired side effects of glucocorticoids are hypothesized to occur mainly through activation of gene transcription, whereas the beneficial anti-inflammatory effects of glucocorticoids involve mainly mechanisms of gene repression.

Understanding the molecular basis of glucocorticoid-induced side effects requires an understanding of their actions on homeostatic signaling processes in all cell types. In this review, we discuss the basic cellular and molecular signaling mechanisms of glucocorticoid action during noninflammatory and inflammatory situations."

Mechanisms of Glucocorticoid Receptor Action in Noninflammatory and Inflammatory Cells -- Necela and Cidlowski 1 (3): 239 -- Proceedings of the American Thoracic Society: