This study was recently published, pushing the hypothesis that L-Carnitine in meats could be a connection between meats and cardiovascular disease risk, via TMAO (Trimethylamine oxide). It has received a lot of media coverage today. But there is a lot of speculation in this study.
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Carnitine and Heart Disease- Positive Results
8.1. Blood Pressure
ALCAR in conjunction with ALA can potentially reduce hypertension in via their combined anti-oxidant and pro-energetic effects[165] as well as insulin resistance and glucose tolerance in those with compromised cardiac health[166] with minimal to no side-effects at the dosage of 2g a day. At this dose of 2g daily, it has been implicating in reducing blood pressure in persons with poor glucose tolerance by almost 10 points systolic, with some decrease in diastolic as well.[49]
A dose of 4.5g GPLC has been shown to increase nitric oxide levels after 28 days of supplementation in some persons,[1] and does so at a dose of 3g as well.[33]
May benefit blood pressure in unhealthy persons (metabolic syndrome, high blood pressure). Has the mechanisms to improve blood pressure independent of a disease state via nitric oxide, but it is unclear how it affects blood pressure in those with normal blood pressure.
8.2. Disorders of Blood Flow
Carnitine, in the form of Propionyl-L-Carnitine (PLC, or GPLC if bound to Glycine), has been shown to improve symptoms of intermittent claudication. PLC supplementation at a dose of 1-3g a day seems to reliably increase maximum walking time in persons suffering from intermittent claudication[14][167][15] and improve quality of life.[13] The benefit does not appear to be dose dependent, and seems to benefit persons with more severe symptoms to a greater degree than persons with lesser symptoms.
PLC aids peripheral arterial diseases in general as it increases peripheral microcirculation.[168][169] In persons with peripheral arterial diseases, PLC supplementation can increase strength and exercise performance[170] although exercise itself can also be seen as therapeutic.[171]
Quite promising for periphery artery disease and intermittent claudication
8.3. Aging
During aging, defects in oxidative phosphorylation occur exclusively in Interfibrillar mitochondria, located between myofibrils.[172][173] Due to substrate poorly oxidized when introduced into complexes I, III, and IV and not alleviated by uncoupling it appears the aging 'defect' associated with cardiac mitochondria is located in the Electron Transport Chain.[113]Enzymatic activity of complexes III (through cytochrome C binding) and IV also appear to be decreased during cardiac aging.[172][174][175]
It appears these damages may be secondary to cardiac Ischemia.[113] Ischemia causes damage to the Electron Transport Chain after 10-20 minutes via reducing activity of complex I[176] and reducing phosphorylation at complex V and adenine dinucleotide translocase.[177][178] Complex III[176] and IV[179] are hindered at longer periods of Ischemia. It appears that the general process of Ischemia hits elderly persons harder than youth[180] despite some level of damage at both ages.[181]
Acetyl-L-Carnitine is proposed to target these defects its various mitochondrial benefits, discussed elsewhere. One such benefit is seen when aged rats were given a bolus of Acetyl-L-Carnitine 3 hours before cardiac Ischemia, and suffered less damage.[182] The same benefits were not seen with adult hearts subject to Ischemia, and the damage induced to aged hearts defaulted to similar levels as adult hearts.[182][113]
Another possible mechanism is increasing levels of CPT1 in the myocardium, without affecting overall carnitine levels.[183] A decline of this rate-limiting step is seen during aging, thus upregulating it may attenuate changes seen with aging. It has been noted in human hearts that less fatty acid oxidation occurs with aging, causing a shift towards cardiac glucose metabolism[184]which are thought to be due to less CPT1 activity.[185][186]
