From the present data it emerges that the major dietary precursor of trimethylamine and its N-oxide in man is trimethylamine N-oxide itself, with little additional contribution from choline or carnitine. It appears, therefore, that the only foods which should present problems to ‘fish-odour syndrome’ patients would be seafoods. Clearly, in clinical practice, the issue is more complicated than this ( Ayesh et al., 1993; Mitchell, 1996). It is appreciated that the number of subjects examined in this present study was small, and that differences in gut microflora between individuals, and even within the same individual over time, may vastly influence enterobacterial liberation of these amines from their precursors ( Hill, 1995). The large inter-individual differences found within the significant increases of trimethylamine and N-oxide output following fish ingestion (mean coefficient of variation=0.17, range=0.03 to 0.42) are presumably testimony to this. It is possible that certain individuals with overt ‘fish-odour syndrome’ may possess gut microflora which are able to readily liberate trimethylamine from these other potential precursors (choline and carnitine), thereby widening the list of potentially problematic foods. Indeed, modulation of the gut microflora, with the selective ablation of such culpable microbes, may lend itself as a means of maintenance therapy within these patients.
A comprehensive literature search yielded 153 studies, 13, published from 1989-2007, were deemed eligible. All the trials were comparison trials of L-carnitine compared with placebo or control in the setting of acute myocardial infarction.
This systematic review of the 13 controlled trials in 3,629 patients, involving 250 deaths, 220 cases of new heart failure, and 38 recurrent heart attacks, found that L-carnitine was associated with:
-Significant 27% reduction in all-cause mortality (number needed to treat 38)
-Highly significant 65% reduction in ventricular arrhythmias (number needed to treat 4)
-Significant 40% reduction in the development of angina (number needed to treat 3)
-Reduction in infarct size
Although, this is an interesting article on carnitine that points to another metabolite (gamma-butyrobetaine) that could be atherogenic: http://www.cell.com/cell-metabolism/abstract/S1550-4131(14)00453-7A significant increase in the plasma concentrations of trimethylamine-N-oxide from baseline was evident only for the 2-g dose of L-carnitine (from 34.5 +/- 2.0 to 149 +/- 145 microM)
apod wrote:Is there an ideal form of choline / carnitine that doesn't carry as much of a risk of TMAO / atherosclerosis?
The oldest, on which most currently available drug therapies are based, is the cholinergic hypothesis, which proposes that Alzheimer's disease is caused by reduced synthesis of the neurotransmitter acetylcholine. ApoE4 plays a crucial role in the cholinergic dysfunction associated with Alzheimer's disease. An isoform-dependent impaired regulation of the transport of phospholipids in the brain of apoE4 carriers could explain the reduced levels of phosphatidylcholine, phosphatidylethanolamine and choline reported in Alzheimer's disease. This, in turn, may lead to decreased acetylcholine synthetic capacities. http://www.ncbi.nlm.nih.gov/pubmed/8618881
Studies on a number of different populations have found that the average intake of choline was below the adequate intake. Looking at cronometer, my intake averages out around 350-400mg. The recommended adequate intake (AI) for choline is 550mg for men.
With choline, I'm seeing different forms like citicholine, alpha-gpc, phosphatidlcholine, choline citrate, and choline bitartrate, and carnitine in forms like L-carnitine, L-carnitine Fumarate, ALCAR, GPLC, and LCLT. Are these cardioprotective or proatherogenic? Are any of these forms better for APOE4? Is it best to get it from diet? (It seems like I've read that vegetarians don't have as much of an issue with TMAO?)
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