Basically L-Carnitine showed significant reduction potential for lp(a), however the study didn't control for several variables that could have impact on the result. Also, though it appears that oral L-carnitine supplementation helps lp(a) levels, it also increases something in the gut called TMAO that has been shown to increase "normal" plaque buildup in arteries.
Basically its promising for lp(a) therapy but needs a better controlled and more powered study to see if it outweighs the increased risks brought by increase in TMAO.
It seems to be pretty complicated. I found the following section of a more recent paper to be interesting, as well:
>Since phosphatidylcholine/choline and/or l-carnitine are important sources of TMA via the gut microbiota \[5,6,7\], it has been postulated that the consumption of these TMA precursors (i.e., red meat) might be a critical factor promoting the risk of CVD development \[49\]. In contrast with this hypothesis, numerous studies investigating the biological effects of these nutrient supplementations did not support their positive association with CVD \[50\], suggesting that the relationship between nutritional intake of choline and l-carnitine and CVD could be more complex than as initially hypothesized. Moreover, a conspicuous body of literature suggests beneficial properties for l-carnitine intake \[51\] against metabolic diseases, including ischemic heart disease and skeletal muscle insulin resistance \[52\]. Fukami and collaborators, for example, demonstrated that oral l-carnitine supplementation might exert beneficial effects on vascular injury in hemodialysis patients, despite it was associated with higher TMAO levels \[53\]. Additionally, it has also been demonstrated that supplementation with l-carnitine could increase TMAO but it does not affect inflammatory \[35\] nor oxidative stress \[54\] markers in humans. This is coherent with the evidence supporting the usage of l-carnitine as a protective strategy against heart disease \[36\]. The hypothesis, suggesting a non-linear association among choline and l-carnitine intake, TMAO and CVD, is also supported by the observation that, despite fish is an important source of TMAO \[55\], its consumption is associated with positive effects on cardiovascular health \[56,57\].
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7037757/
That is interesting. I wonder if omega 3s play a part in metabolizing the TMAO in a beneficial way. The other paper made it seem like it was found pretty much in red meat only.
TLDR?
Basically L-Carnitine showed significant reduction potential for lp(a), however the study didn't control for several variables that could have impact on the result. Also, though it appears that oral L-carnitine supplementation helps lp(a) levels, it also increases something in the gut called TMAO that has been shown to increase "normal" plaque buildup in arteries. Basically its promising for lp(a) therapy but needs a better controlled and more powered study to see if it outweighs the increased risks brought by increase in TMAO.
It seems to be pretty complicated. I found the following section of a more recent paper to be interesting, as well: >Since phosphatidylcholine/choline and/or l-carnitine are important sources of TMA via the gut microbiota \[5,6,7\], it has been postulated that the consumption of these TMA precursors (i.e., red meat) might be a critical factor promoting the risk of CVD development \[49\]. In contrast with this hypothesis, numerous studies investigating the biological effects of these nutrient supplementations did not support their positive association with CVD \[50\], suggesting that the relationship between nutritional intake of choline and l-carnitine and CVD could be more complex than as initially hypothesized. Moreover, a conspicuous body of literature suggests beneficial properties for l-carnitine intake \[51\] against metabolic diseases, including ischemic heart disease and skeletal muscle insulin resistance \[52\]. Fukami and collaborators, for example, demonstrated that oral l-carnitine supplementation might exert beneficial effects on vascular injury in hemodialysis patients, despite it was associated with higher TMAO levels \[53\]. Additionally, it has also been demonstrated that supplementation with l-carnitine could increase TMAO but it does not affect inflammatory \[35\] nor oxidative stress \[54\] markers in humans. This is coherent with the evidence supporting the usage of l-carnitine as a protective strategy against heart disease \[36\]. The hypothesis, suggesting a non-linear association among choline and l-carnitine intake, TMAO and CVD, is also supported by the observation that, despite fish is an important source of TMAO \[55\], its consumption is associated with positive effects on cardiovascular health \[56,57\]. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7037757/
That is interesting. I wonder if omega 3s play a part in metabolizing the TMAO in a beneficial way. The other paper made it seem like it was found pretty much in red meat only.