Statin Adverse Effects: Evidence for a Mitochondrial Mechanism

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849981/?tool=pmcentrez




Statin Adverse Effects: A Review of the Literature and Evidence for a Mitochondrial Mechanism
 
In the case of statins, a potential basis for opposing effects occurring in muscle and in other organs can be identified. Evidence supports the proposition that antioxidant effects of statins underlie (or contribute to) many fundamental statin benefits – including benefits to flow and oxygen delivery46-48 and inflammation.49, 50 These effects may participate in improved walking distance in patients on statins, including benefits to muscle/walking in persons with and without peripheral artery disease.29 Yet a subset of people reproducibly exhibit increases in markers of oxidation on statins,51 and the occurrence of this increase has been tied to muscle pain on statins.52, 53
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A range of cases have now been reported in which statin use has “uncovered” previously clinically silent or clinically tolerated conditions, ranging from McArdle disease159, 160 to myotonic dystrophy159 to acid maltase deficiency161 to possible Kennedy disease.159 Statins have also exacerbated known muscle conditions, such as myasthenia gravis.78 In the case of mitochondrial myopathies, the relative degree to which statins have unmasked vs induced disease may not always be clear.159, 162
...

Several widely used statins – atorvastatin, simvastatin, and lovastatin (and previously cerivastatin, now off the market) – are metabolized by the cytochrome P450 (CYP)3A4 pathway.^318
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While a medley of potential mechanisms may cause or contribute to statin AEs (and these merit more full review in another venue), mitochondrial mechanisms have been repeatedly implicated in muscle AEs. Mitochondrial defects predispose to problems on statins (as shown in the second to last entry of Table IV, ‘Genetic mutations associated with mitochondrial dysfunction’). Additionally, statins predispose to mitochondrial defects (Table V,^{22 31, 32, 112, 155, 158, 162, 397, 406-414}) – in all users and, to a greater degree, in vulnerable individuals. Dose-dependent reductions in coenzyme Q10^20-22 can reduce cell energy, promote oxidation,^{362, 415} promote apoptosis, and unmask silent mitochondrial defects.^{23-25, 362, 415-418} The mevalonate pathway, which statins inhibit, also produces heme-A, which has it own central involvement in mitochondrial electron transport.^419
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 For instance, mitochondrial encephalomyopathy resulting from heritable coenzyme Q10 deficiency classically produces fatigue, muscle symptoms, and cognitive problems,⁴⁴⁰ although the cases referred for analysis are often relatively severe.^{429, 441} Gastrointestinal²⁶ and neurological symptoms,^{432, 442} psychiatric symptoms,^443-446 sleep problems,^{444, 447} glucose elevations,¹⁸² and a range of other symptoms reported on statins also arise in mitochondrial dysfunction.^{379, 448-457
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Thus, in an analysis of data, presented in the Australian Adverse Drug Reaction Bulletin, it was noted that “Statin-associated peripheral neuropathy may persist for months or years after withdrawal of the statin… In two ADRAC (Adverse Drug Reactions Advisory Committee) cases of persistent peripheral neuropathy, motor and sensory conduction tests showed minimal recovery 4 and 12 months, respectively, after discontinuation of simvastatin, despite clinical improvement.”561


As reviewed here, AEs on statins may signal a mitochondrial vulnerability, which may alter or perhaps even reverse an otherwise favorable impact of statins on cell energetics. And AEs may signal occurrence of a net prooxidant rather than antioxidant effect of statins53 with possible unfavorable implications for a range of statins' proposed pleiotropic effects.892


Full report here: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2849981/?tool=pmcentrez

Dr. Klinghardt's Treatment of Lyme Disease

http://articles.mercola.com/sites/articles/archive/2009/08/04/Dr-Klinghardts-Treatment-of-Lyme-Disease.aspx

Extract:

Regular lab parameters affected by Lyme:


•Abnormal lipid profile (moderate cholesterol elevation with significant LDL elevation)

•Insulin resistance

•Borderline low white blood cells, normal SED rate and CRP

•Normal thyroid hormone tests but positive Barnes test and excellent response to giving T3

•Type 2 (high cortisol, low DHEA) or type 3 adrenal failure (low cortisol and DHEA)

•Low testosterone and DHEA

•Decreased urine concentration (low specific gravity)

•Complex changes in cytokines, interferones, NK cells, white blood cell indicators, etc.
 
...

Symptomen van een dopaminestoornis

Symptomen van een dopaminestoornis

• besluiteloosheid
• arm aan initiatieven
• depressie
• angst
• uitputting
• chronisch vermoeid, de hele dag kunnen slapen
• tremor

Supplement: Tyrosine: 1 à 2 x 500 mg per dag (nooit 's avonds)

zit in pompoenzaden, amandelen, avocado's, bananen, haring, kaas, sesamzaad

Niet geschikt bij migraine, hoge bloeddruk of tegelijkertijd met antidepressiva


Extra:
Vit B = nodig voor aanmaak neurotransmitters
Vit C minimaal 2g
magnesium
Visolie EPA DHA 1 g


Goed supplement bij depressie algemeen:
Nutramin Emotio Balans, 1 x ochtend en 1 x avond
Niet bij zwangerschap of borstvoeding