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Orthomolecular Medicine News Service, October 6, 2022
Lipoprotein(a): The biggest risk factor for heart attack and stroke?
My self-experiment with the Pauling therapy and vitamin C
by Hans W. Diel
OMNS (Oct. 6, 2022) Lipoprotein(a) belongs to the group of so-called lipoproteins, which are small particles that help transport water-insoluble lipids, cholesterol and cholesterol esters in the blood. In order to enable the transport of these substances in the aqueous phase of the blood, they are bound to proteins. The core of lipoprotein(a) consists of an LDL particle. The main difference from LDL is that lipoprotein(a) is equipped with an additional protein, the “sticky” apolipoprotein(a), which “envelopes” the LDL particle. A test specific for lipoprotein(a) is required to measure its blood level, because a standard LDL test cannot determine how much of LDL is lipoprotein(a).
Lipoprotein(a) is considered the greatest risk factor for heart attack and stroke. One in five people is affected by this risk factor – usually without knowing it – and has too much lipoprotein(a) in their blood. This is a hidden danger to health.
A link between high lipoprotein(a) and premature myocardial infarction was suspected as early as the 1970s. Today the link has been proved by numerous epidemiological and genetic studies. The studies concluded that those with the highest lipoprotein(a) values had a 3-4 times higher risk of myocardial infarction than those with the lowest values. [1,2]
I only found out that I belong to the group of people who carry this risk factor, high lipoprotein(a), after my first heart attack eleven years ago. At that time my blood level was 79 mg/dl. I don’t know how high it was before the heart attack, because the level had never been checked in any previous examinations, neither by my family doctors nor by cardiologists or in university hospitals. Until then, I was completely unaware of this “lipoprotein(a)”, which is referred to as “lp(a)” for short.
I don’t know whether my parents or grandparents had elevated lp(a) concentrations and whether I might be hereditarily predisposed. And I also don’t know how long my coronary heart disease existed before the myocardial infarction, because it had never been diagnosed until then.
The doctors in the heart clinic measured lp(a) after the heart attack, but didn’t say a word about it, so I didn’t pay any further attention to the increased value in the laboratory report. The German doctor Ulrich Strunz was the first person to make me aware of the importance of high lp(a) for my heart disease. As he said, it is the most dangerous risk factor for the blood vessels and the actual cause of my coronary heart disease.
Conventional medicine does not yet have any drugs for a therapy to lower high lp(a) levels, although this substance has been studied for almost 60 years.
Since then this “scary” lp(a) has given me no peace. I have read, systematically researched and compiled as much as I could about lp(a) and heart disease. Among the first texts I looked into were the publications by Linus Pauling, which he wrote together with the physician Matthias Rath. [3-7] I wanted to know why Linus Pauling, one of the most important biochemists of the 20th century, recommended such simple natural substances as vitamin C and lysine to prevent lp(a) from sticking to the blood vessels. The reference to this recommendation by Linus Pauling had been given to me by Dr. Strunz.
In these publications, answers to the question of the cause of atherosclerosis, myocardial infarction and heart disease were given that completely deviate from conventional theories. [3-7] They develop the hypothesis that:
- A primary cause of atherosclerosis and heart attack is a chronic deficiency of vitamin C and other micronutrients
- Due to the vitamin C deficiency which leads to decreased collagen production, the arterial walls become weakened and unstable
- In this threatening situation, the body tries to repair the artery walls in a “makeshift” way by depositing repair molecules
- For this purpose, the body increasingly produces such repair molecules, of which the aforementioned lp(a) plays the decisive role
- If vitamin C deficiency continues, the accumulation of lp(a) leads to the development of atherosclerotic plaques and to myocardial infarction and stroke.
- Lp(a) only becomes a risk factor when the arterial walls are injured, caused by chronic vitamin deficiency. Then it is deposited on the arterial walls.
This hypothesis convinced me more than the conventional theory, which for decades has denounced high cholesterol as a danger to heart health. I did not have high cholesterol levels or any of the other so-called risk factors. I didn’t smoke, didn’t drink alcohol, wasn’t overweight, had no high blood pressure, no stress, did not lack exercise, and did not suffer from diabetes. All those risk factors considered dangerous and even causative for heart disease did not apply to me. Everything was always in order during my medical examinations.
Nevertheless I got two heart attacks. The first one happened during training. The second heart attack, five years later, during a 10 km run. I only survived thanks to immediate resuscitation. I must have puzzled the doctors with this.
It was clear to me that I would not have a third chance to survive such an event. I had to prevent this in any case. The doctors’ prognoses were poor: high-risk patient, heart failure therapy, low life expectancy.
I began to fight for my life.
The Pauling therapy
I decided to try out Linus Pauling’s recommendations for lp(a) therapy and the treatment of cardiovascular diseases in a self-experiment – despite dire warnings from the doctors. Pauling’s basic approach is to provide the body with the essential vitamins – first and foremost vitamin C – and other micronutrients in the therapeutic amounts it needs to heal. He recommended vitamin C in a dosage of 6-18 g (6,000-18,000 mg) per day, or until the bowel tolerance limit is reached, and lysine in a dosage of 5-6 g per day. 
This treatment method, supplemented by the intake of the amino acid proline (up to 2,000 mg per day) recommended by Matthias Rath, became known as “Pauling therapy”. In my self-experiment, I took these substances in a dosage tailored to my individual needs – supplemented by other vitamins and vital substances (especially: Niacin and other B vitamins, vitamins E, D, and A, and amino acids arginine, citrulline) My self-experiment spanned five years.
The results of my self-experiment in brief
- In the period from 2011 (after my first heart attack) to 2021, a total of 30 lp(a) measurements were performed.
- The lp(a) value at the beginning of my self-test in June 2016 was 110 mg/dl = about 260 nmol/l. This was two weeks after my second heart attack and the highest value measured up to that point.
- The lp(a) value at the last measurement in April 2021 was 50 mg/dl = about 120 nmol/l
- With the Pauling therapy, the drop in lp(a) level was therefore more than half. It was lowered by almost 55 percent to 120 nmol/l, which corresponds closely to the threshold value recommended by the international professional societies (50 mg/dl or 120 nmol/l)
- This self-experiment revealed that the lp(a) value is not – as is generally claimed – unchangeable. The value is subject to considerable fluctuations, and with the application of natural remedies a significant influence and reduction can be achieved
- In the course of the self-experiment, there have been significant improvements in my state of health and my heart disease
- My discontinuing the medicines prescribed by the doctors had no adverse effect.
The decisive role of the Pauling therapy for this success is obvious, documented by my records. More important than the lp(a)-lowering in my self-experiment were the effects on my health and on the healing of my heart disease. And these were extremely positive, confirmed by the report on my cardiological control examinations. It says: cardio pulmonary complete stable condition, asymptomatic patient, no angina pectoris symptoms, no relevant stenosis, ECG unremarkable, good systolic pump function.
More than that, I was able to put my body under full load. Even the cardiac arrhythmias that I had for a long time no longer occurred. Only the Pauling therapy could have caused this success, because I did not use any medication.
After the findings of my self-experiment I trust even more in the Pauling therapy and will continue with it. And I hope to do so for many years to come.
I am not a doctor, and I believe you should work with yours if you want to implement any of the recommendations and experiences from my self-experiment. Do not discontinue any medication without the approval of your doctor.
(Hans W. Diel is the author of Lipoprotein(a) – The biggest risk factor for heart attack and stroke? Everything you should know about it and how you can protect yourself with natural remedies [German]. ?Druckpunkt Ruhr UG, 2022)
1. Kamstrup PR, Benn M, Tybjaerg-Hansen A,Nordestgaard BG (2008) Extreme lipoprotein(a) levels and risk of myocardial infarction in the general population: the Copenhagen City Heart Study. Circulation. 117:176-184. https://pubmed.ncbi.nlm.nih.gov/18086931
2. Kamstrup PR Tybjaerg-Hansen A, Steffensen R, Nordestgaard BG (2009) Genetically elevated lipoprotein(a) and increased risk of myocardia infarction. JAMA. 301:2331-2339. https://pubmed.ncbi.nlm.nih.gov/19509380
3. Rath M, Pauling L. (1990a) Hypothesis: Lipoprotein(a) is a surrogate for ascorbate. PNAS USA 87:6204-6207. https://pubmed.ncbi.nlm.nih.gov/2143582
4. Rath M, Pauling L. (1991) Solution to the Puzzle of Human Cardiovascular Disease: Its primary cause is ascorbate deficiency, leading to the deposition of lipoprotein(a) and fibrinogen/fibrin in the vascular wall. J Orthomolecular Med. 6(3-4):125-134. https://www.dr-rath-foundation.org/wp-content/uploads/2018/03/Solution-to-the-Puzzle-of-Human-Cardiovascular-Disease.pdf
5. Rath M. (1992c) Lipoprotein-a reduction by ascorbate. J Orthomolecular Med. 7:81-82. https://isom.ca/wp-content/uploads/2020/01/JOM_1992_07_2_04_LipoproteinA_Reduction_by_Ascorbate.pdf
6. Rath M, Pauling L. (1992) Unified Theory of Human Cardiovascular Disease Leading the Way to the Abolition of This Disease as a Cause for Human Mortality. J. Orthomolecular Med. 7:5-15. https://isom.ca/wp-content/uploads/2020/01/JOM_1992_07_1_02_A_Unified_theory_of_Human_Cardiovascular_Disease_Leading-.pdf
7. Rath M, Pauling L. (1991b) Apoprotein(a) is an adhesive protein. Journal of Orthomolecular Medicine 6:139-143. https://isom.ca/wp-content/uploads/2020/01/JOM_1991_06_3-4_05_Apoproteina_Is_An_Adhesive_Protein.pdf
8. Pauling L. (1986) How to Live Longer and Feel Better. (2006 Revised Ed) OSU Press. ISBN-13: 978-0870710964
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