I can't say whether my Lipoprotein(a) levels have ever been measured before my first acknowledgement of it in 2019.
But first things first: what is Lipoprotein(a)?
In short, Lipoprotein(a) is a substance built in the liver to transport fat within the blood.
Or, in other and more complicated words: Lipoprotein(a) [Lp(a)] is an apoB-containing lipoprotein bound to a hydrophilic, highly glycosylated protein called apolipoprotein(a) [apo(a)] (More info).
At first sight, Lipoprotein(a) is nothing too fancy, somewhat close to cholesterol and actually a bit off the radar as it is not part of any regular analysis by most doctors. A possible reason for this might be that
it is said that Lipoprotein(a) is determined by your genes and
can't be influenced by medicine or lifestyle
So yes, the question of why it should be measured in the first place when the result can't be influenced makes sense, right?
However, even though it is said it can't be influenced, there is a recommendation that you should have levels below 30 mg/dl. Levels above that are classified as dangerous with a higher likelihood of facing a stroke or heart attack 👀
Let's quickly recall: The levels of one's Lipoprotein(a) are given by birth and can't be influenced.
So, whether or not you have higher or lower levels of this substance is fate, luck or bad luck.
In short: You are doomed.
And it looks like I am, too, because my measurement in 2019 was a whopping 113 mg/dl - close to 4-fold higher than the upper tolerance of something called The heart's quiet killer.
Is there anymore to say?
I think yes, there is: Challenge accepted.
Scepticism at work
In disbelief and a state of having-nothing-to-lose, I started digging.
And guess what: there seems to be room to tackle one's Lipoprotein(a) levels despite what appears to be common knowledge 🙌
While they haven't succeeded in finding medicine that can influence Lp(a) levels, it looks like vitamins can. And here is the crux - firstly, it is vital to understand the role of Lipoprotein(a) better than what has been said in the definition I gave above. Lp(a) is more than just a transporter carrying around fat in the vessels.
One theory I looked at from Prof. Linus Pauling and Dr. Matthias Rath says Lipoprotein (a) is a surrogate for ascorbate. See the abstract below 👇
Abstract: The concept that lipoprotein(a) [Lp(a)] is a surrogate for ascorbate is suggested by the fact that this lipoprotein is found generally in the blood of primates and the guinea pig, which have lost the ability to synthesize ascorbate, but only rarely in the blood of other animals. Properties of Lp(a) that are shared with ascorbate, in accordance with this hypothesis, are the acceleration of wound healing and other cell-repair mechanisms, the strengthening of the extracellular matrix (e.g., in blood vessels), and the prevention of lipid peroxidation. High plasma Lp(a) is associated with coronary heart disease and other forms of atherosclerosis in humans, and the incidence of cardiovascular disease is decreased by elevated ascorbate. Similar observations have been made in cancer and diabetes. We have formulated the hypothesis that Lp(a) is a surrogate for ascorbate in humans and other species and have marshaled the evidence bearing on this hypothesis.
Understanding Paulings/Rath Theory
Pauling/Rath "observed that Lp(a) is found primarily in the plasma of those species that are unable to synthesize ascorbate".
Humans belong to those species, as our ancestors lost their ability to synthesise Vitamin C 40 million years ago. In case of Vitamin C deficiency, the human body boosts the production of Lp(a) to compensate and step in to fix, e.g. damaged blood vessels or act as an antioxidant. So, high levels of Lp(a) result from low levels of Vitamin C in the body.
However, as Paracelsus stated, dosis sola venenum facit - and "Lp(a) in the material wall would strengthen the arteries, but atherosclerosis would occur [...], if this function were to operate to too great extent".
And here, we come to the point of understanding why there is a recommendation for Lp(a) levels. It is not a recommendation but the information that Lp(a) levels above 30mg/dl double the risk of facing cardiovascular disease - high levels of Lp(a) at a too great extent can lead to atherosclerosis, can lead to thrombosis, can lead to heart attack or stroke - even without hyperlipidemia.
With that knowledge, it makes sense to lower Lp(a) below that threshold, but it doesn´t explain why people differ significantly in their Lp(a) levels. Some people do not seem to have high levels.
Do they all have optimal Vitamin C levels?
I doubt that, and the answer I found to the question is time. It looks like 40 million years are simply not enough for the body to have developed "the control mechanisms for apo(a) synthesis at the optimum level."
And thus, it is genetics (or coincidence); some have higher levels, some have lower levels, and it is on us to ensure we get our Lp(a) levels in check - below 30mg/dl.
Paulig/Rath "postulate that ascorbate can reduce or prevent the development of atherosclerosis by lowering plasma Lp(a), decreasing lipoprotein infiltration into the arterial wall, and preventing lipid peroxidation." and further: "We suggest that Lp(a) levels may be decreased by ascorbate."
As I said: Challenge accepted.
In the following months, after getting my initial Lp(a) levels, I tried to influence them and yes: It worked. While I significantly reduced my Lp(a) from 2019 to 2021, my last measure came back with an increase:
Difference to previous
July 9, 2019
January 24, 2020
-31 mg/dl ⬇️
May 14, 2021
-23,3 mg/dl ⬇️
December 9, 2022
The levels are not back to where they were in 2019, but the increase worries me. Admittingly, I didn´t pay too much attention to a proper Vitamin C intake last year.
However, while it is possible that the measure, as done by a different laboratory, has no significant meaning, I will not sit idly.
With 2023 approaching, my new years' resolution is clear: I am now going on a quest to lower my Lp(a) levels - below 30mg/dl.
I give myself six months before I recheck my levels in June 2023 - in the same laboratory as this December measure. This, however, will only be my first recheck. Depending on the outcome, I will adjust my strategy and do another check in December 2023.
The desired outcome is that the levels eventually go down below 30mg/dl to normalise my risk of developing cardiovascular disease.
As you can imagine, I will once again rely on the hypothesis of Pauling/Rath that Lp(a) is a surrogate for ascorbate - and ramp up my Vitamin C intake to approx. 10g/day. I will want to avoid having a lower intake of less than 3g/day. Bodily reactions naturally determine the upper limit.
Besides Vitamin C, I will use other Vitamins and minerals to support my efforts - mainly Vitamin A, B, D, E, K, and Lysin. However, the focus is on Vitamin C.