Monday, December 28, 2009

Lactate as cause of secondary damage in acute ischemic stroke

Atherosclerosis of the carotid arteries is a leading cause of ischemic stroke. Increased carotid artery intima-media thickness (IMT) is a marker of atherosclerosis and also a predictor for ischemic stroke that represents more than 80% of strokes, with the remainder due to hemorrhage.
Recent study involving 187 patients with acute ischemic stroke or transient ischemic attack (1) have indicated that lactate in cerebrospinal fluid, but not in blood, is a reliable marker for the metabolic crisis in acute ischemic stroke and a possible cause of secondary neuronal damage in cortical infarction resulting in unfavourable evolution in the sub acute phase of stroke and poor long-term outcome.
However, some researchers believe that whole blood lactate, as measured in this study, unlike serum lactate, is an unreliable measure of systemic lactate (2).
It is interesting to note that a study from 2004 found ischemic stroke acidosis-mediated activation of acid-sensing ion channels may play a role to ischemic damage of brain tissue (3).
Most interesting is that cardiac glycosides, besides its anti-atherosclerotic effects as discussed recently in this blog (4, 5), also can provide cerebral neuroprotection in front of ischemic stroke and in prevention of its occurrence (6).

1) Evaluation of lactate as a marker of metabolic stress and cause of secondary damage in acute ischemic stroke or TIA, Brouns R, Sheorajpanday R, Wauters A, Surgeloose DD, Mariën P, DE Deyn PP. Clinica Chimica Acta 397 (2008) 27–31
2) The Lactic Acid Response to Alkalosis in Panic Disorder: An Integrative Review Richard J. Maddock, M.D.J Neuropsychiatry Clin Neurosci 13:1, Winter 2001. Full free paper at
3) Huang Y, McNamara JO. 2004. "Ischemic Stroke: “Acidotoxicity” Is a Perpetrator", Cell, Volume 118, Issue 6 , 17 September, Pages 665-666
4) The anti-atherosclerotic effects of cardiac glycosides, Carlos Monteiro at
5) Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at
6) Cardiac Glycosides in Prevention of Stroke, Carlos Monteiro, ICP, July 10, 2006, Full text at

Tuesday, December 15, 2009

Stress, lactic acid, hypertension, atherosclerosis and hair loss

The last weekend I have read an article in New York Times Journal, entitled “The Claim: High Blood Pressure Will Increase People’s Risk of Losing Their Hair.” (, which caught my attention.
NYT have discussed the results and linked to some of the studies suggesting that hair loss may indicate an increased risk of high blood pressure and heart disease.
Curious about this information I have searched at Pubmed were I found a recent paper linking hair loss also to atherosclerosis, with the conclusion by the authors that severe vertex pattern of androgenetic alopecia should be considered to have an increased risk of subclinical atherosclerosis (1).
Going deeper I have found a postulation made in 1997 by Marino Salin, from Italy, telling if there is excess adrenergic tone in the metabolic system, then there is also vasoconstriction, ischemia and hypoxia and if there is hypoxia, glycolysis leads to lactic acid that causes caustic damage to the inner sheath and this sheath seems to be raised above the hair cuticle (2).
This postulation coincides with our thoughts about the acidity theory of atherosclerosis (3).
1) Dogramaci AC et al,Is androgenetic alopecia a risk for atherosclerosis? J Eur Acad Dermatol Venereol. 2009 Jun;23(6):673-7.
2) Marino Salin e Andrea Marliani, EDIZIONI ELETTRONICHE “TricoItalia” (Firenze) marzo 1997, BOLLETTINO della Società Italiana di Tricologia, La Teoria e la Clinica delle “INCIDENZE” nelle Alopecie. Full paper in Italian language at
3)Carlos ETB Monteiro, Acidic environment evoked by chronic stress: A novel mechanism to explain atherogenesis. Available from Infarct Combat Project, January 28, 2008 at