DiseasesHeart Attack—What Really Causes It, and How Can It Be Prevented?
Sources: 12 · Article: 15 547 characters
Jerzy Jaśkowski and Andrzej Frydrychowski present conflicting explanations: Jerzy Jaśkowski points to chemical changes, while Andrzej Frydrychowski says a coronary artery becomes blocked.
- Jerzy Jaśkowski links heart attacks to a local increase in CO2 and a change in pH; Andrzej Frydrychowski describes tissue death after a vessel is blocked by a clot or grows shut.
- Andrzej Frydrychowski recommends controlling high blood pressure and diabetes, quitting smoking, changing one's diet, and exercising; he also mentions supplements.
- Jerzy Zięba warns that calcium supplements may be associated with a higher risk of heart attack, while Andrzej Frydrychowski also emphasizes iodine and regulating emotions.
What the authors write
Jerzy Jaśkowski
A heart attack is said to result from a local increase in CO2, increased acidity, and phosphate crystallization, which stiffens cells and prevents them from contracting.
„If, for some reason, a small group of cells begins to produce an increased amount of carbon dioxide, it causes carbonic acid to form, meaning a change in pH. Even a change of 0.1 causes phosphate crystallization, which means stiffening and a lack of contraction—and that is precisely a heart attack.”Jeżeli z jakiegoś powodu mała grupa komórek zaczyna produkować zwiększoną ilość dwutlenku węgla, to on powoduje powstanie kwasu węglowego, czyli zmianę pH, a zmiana nawet o 0,1 powoduje krystalizację fosforanów, czyli usztywnienie i brak skurczu – a to właśnie zawał.
Jerzy Jaśkowski
According to Jerzy Jaśkowski, an atherosclerotic plaque usually does not cause a heart attack, and changes in pH lead to local phosphate crystallization.
„If there is a local increase in CO2, CO2 combines with water to form an acid. The acid causes local changes in pH, even by 0.1. This change causes local phosphate crystallization. And this changes the charge on the vessel wall to positive.”Jeżeli miejscowo dojdzie do lokalnego wzrostu CO2, to CO2 w połączeniu z wodą tworzy kwas. Kwas powoduje lokalnie zmiany ph, nawet o 0.1 stopnia. Ta zmiana powoduje miejscową krystalizację fosforanów. A to zmienia ładunek ściany naczynia na elektrododatni.
Jerzy Jaśkowski
Jerzy Jaśkowski claims that a blood clot forms after circulation stops, rather than stopping it.
„Research conducted more than 35 years ago by Manfred von Ardenne proved that a blood clot forms after circulation stops and is not the cause of circulation stopping. Strangely, this research was quickly erased from textbooks.
Dr. Duanne Graveline, a doctor and astronaut, published research results showing that the use of statins, so widely pushed on Polish patients, inhibits the enzyme HMG-CoA reductase.”Przeprowadzone już przed ponad 35 laty badania Manfreda von Ardena udowodniły, że skrzeplina powstaje po ustaniu krążenia, a nie jest przyczyną ustania krążenia. Dziwnym trafem to badanie szybko wymazano z podręczników.
Dr Duanne Graveline, lekarz i astronauta, opublikował wyniki badań, w których udowadnia, że stosowanie statyn, tak szeroko wciskanych polskim pacjentom, powoduje zahamowanie enzymu reduktazy HMG – CoA.
Andrzej Frydrychowski
Andrzej Frydrychowski describes a heart attack as partial death of heart muscle after a coronary artery is blocked because it grows shut or is obstructed by a clot.
„If a coronary artery becomes blocked because it has grown shut or is obstructed by a clot, partial tissue death occurs in the area supplied by the blocked vessel—that is, a heart attack occurs. Academic medicine performs miracles here—it restores blood flow by inserting what is called a”Jeżeli naczynie wieńcowe ulegnie zamknięciu, na skutek zarośnięcia czy zatkania skrzepem, dochodzi do jego częściowej martwicy w obrębie zakresu unaczynienia zatkanego naczynia, czyli dochodzi do zawału mięśnia sercowego. Medycyna akademicka robi tutaj cuda – przywraca ukrwienie poprzez wstawienie tzw.
Andrzej Frydrychowski
Andrzej Frydrychowski identifies high blood pressure and diabetes as conditions that damage blood vessels and recommends treating them and addressing their causes.
„The most important thing is to treat two conditions that have a harmful effect on blood vessels. These are high blood pressure and diabetes. If we have them, treatment is essential, not only with medication. The cause of these conditions should be removed. In the case of diabetes, stop eating carbohydrates; in the case of high blood pressure, control your weight and take potassium supplements.”Najważniejsze jest leczenie dwóch jednostek chorobowych, mających zgubny wpływ na naczynia. Są to nadciśnienie tętnicze i cukrzyca. Jeżeli na nie chorujemy, to niezbędne jest leczenie, nie tylko lekami. Należy usunąć przyczynę tych chorób. W przypadku cukrzycy – odstawić węglowodany, a w chorobie nadciśnieniowej – kontrolować wagę i suplementować potas.
Andrzej Frydrychowski
Andrzej Frydrychowski recommends quitting smoking, limiting carbohydrates in diabetes, and controlling weight and taking potassium supplements for high blood pressure.
„In the case of diabetes, stop eating carbohydrates; in the case of high blood pressure, control your weight and take potassium supplements. Quitting smoking is extremely important. Of course, you should take suitable supplements. The foundation is vitamin D3 supplementation (10,000 IU/day plus 200 mcg of vitamin K2MK7).”W przypadku cukrzycy – odstawić węglowodany, a w chorobie nadciśnieniowej – kontrolować wagę i suplementować potas. Niezwykle ważne jest rzucenie palenia papierosów. Oczywiście należy zażywać odpowiednie suplementy. Podstawą jest suplementacja witaminą D3 (10 000 IU/dobę plus 200 mcg witaminy K2MK7).
Andrzej Frydrychowski
Andrzej Frydrychowski recommends testing homocysteine and CRP and claims that elevated homocysteine, not cholesterol, is responsible for plaque formation.
„Cholesterol is not responsible for the formation of atherosclerotic plaque; an elevated homocysteine level is. Conventional medicine recommends lowering it below the physiological level, which is 200 mg/dl (below 5 mmol/l). We are given a prescription for statins, and that is when complications begin.”Za powstawanie blaszki miażdżycowej nie odpowiada cholesterol, a podwyższony poziom homocysteiny. Medycyna klasyczna zaleca nam obniżać jego wartość poniżej wartości fizjologicznych, to jest 200 mg/dl (poniżej 5 mmol/l). Dostajemy receptę na statyny i dopiero wtedy zaczynają się powikłania.
Andrzej Frydrychowski
Andrzej Frydrychowski recommends coenzyme Q10 after a heart attack and after age 50, omega-3s, changing one's diet in favor of fats, and exercise.
„After a heart attack, and also after age 50, we should start taking coenzyme Q10 regularly. This will improve the energy production of heart muscle cells. We should also reduce inflammation by including omega-3s in our daily diet (oily fish, plant oils). Changing our diet is very important. Let’s cut out all carbohydrates in favor of fat. And let’s not forget to exercise.”Po zawale, a także po 50. roku życia powinniśmy na stałe rozpocząć suplementację koenzymem Q10. Poprawi nam to energetykę komórek mięśnia sercowego. Zadbajmy również o zmniejszenie stanu zapalnego, włączając na co dzień omegi 3 (tłuste ryby, oleje roślinne). Bardzo ważna jest modyfikacja naszej diety. Wyrzućmy wszystkie węglowodany na korzyść tłuszczu. Nie zapominajmy o ruchu.
Andrzej Frydrychowski
Andrzej Frydrychowski recommends exercise as an important part of looking after one's health.
„It is also worth being active—nature made us so that we cannot be healthy without movement. It is built into our health. But we move far too little and do everything we can to limit it. Does any doctor recommend exercise? After all, the patient is ill, has circulatory failure and other conditions that limit physical exertion.”Warto się także ruszać – natura tak nas stworzyła, że bez ruchu nie możemy być zdrowi. Jest on wbudowany w nasze zdrowie. Tego ruchu jednak mamy zdecydowanie za mało i robimy wszystko, żeby go ograniczyć. Czy któryś z lekarzy zaleca ruch? Przecież pacjent jest chory, ma niewydolność krążenia i inne schorzenia, które ograniczają wysiłek.
Andrzej Frydrychowski
Andrzej Frydrychowski links iodine deficiency to harmful effects on the cardiovascular system and recommends adding kelp algae to the diet as a source of iodine.
„Iodine deficiency, which is very common in our population, has a negative effect on our cardiovascular system. Iodine stabilizes heart rhythm, lowers blood pressure, and makes the blood thinner. If we do not want to use Lugol’s solution, we should at least add kelp (brown seaweed, which contains a lot of iodine) to our diet.”Niedobór jodu, tak częsty w naszej populacji, wpływa negatywnie na nasz układ sercowo-naczyniowy. Jod stabilizuje rytm serca, obniża ciśnienie tętnicze i sprawia, że krew jest bardziej rozrzedzona. Jeśli nie chcemy stosować płynu Lugola, to chociaż wprowadźmy do naszej diety Kelp (brunatne algi morskie, które zawierają dużo jodu).
Andrzej Frydrychowski
Andrzej Frydrychowski says that negative emotions harm the heart and recommends regulating them.
„What has a destructive effect on our heart? Negative emotions, frustration, fear, anxiety and disappointment, anger, hatred. What should we do, then? Regulate our emotions. What benefits will we gain? A cascade of more than 1,400 biochemical changes will be triggered, helping the body rebuild and regenerate.”Co wpływa destrukcyjnie na nasze serce? Negatywne emocje, frustracja, lęk, niepokój i rozczarowanie, złość, nienawiść. Co zatem robić? Tonować nasze emocje. Jakie odniesiemy z tego korzyści? Nastąpi wyzwolenie kaskady ponad 1400 zmian biochemicznych, sprzyjających odbudowie i regeneracji organizmu.
Jerzy Zięba
Jerzy Zięba claims that women who took calcium supplements were more likely to develop artery calcification, have a heart attack, or have a stroke than women who did not take them.
„Many readers may find it surprising that recently published research (2011) indicates that women who took calcium supplements to prevent osteoporosis were more likely to develop artery calcification, have a heart attack, or have a stroke than women who did not take calcium supplements.”Dla wielu czytelników dziwnym wyda się fakt, że niedawno opublikowane badania (2011) wskazują, że kobiety, które brały suplementy wapnia, po to, żeby zapobiec osteoporozie były bardziej narażone na wytworzenie zwapnień w tętnicach, zawał serca czy udar mózgu, niż kobiety, które suplementów wapnia nie brały.
Andrzej Frydrychowski
Andrzej Frydrychowski claims that mortality is higher at the lowest cholesterol level than at an elevated level.
„Third, mortality is much higher in the group with the lowest cholesterol level compared with the group whose level is elevated. I don’t think this needs comment [2].
Fourth, many studies have shown that high doses of statins increase the incidence of diabetes by reducing the cells’ sensitivity to insulin [3].”Po trzecie, śmiertelność jest dużo wyższa w grupie o najniższym poziomie cholesterolu w porównaniu do grupy, który ma podwyższony poziom. Chyba tego nie trzeba komentować [2].
Po czwarte, w wielu pracach wykazano, że wysokie dawki statyn, powodują wzrost zachorowań na cukrzycę, poprzez zmniejszenie wrażliwości komórek na insulinę [3].
Andrzej Frydrychowski
Andrzej Frydrychowski claims that statins may cause calcification of the coronary arteries, ischemia in cells, and weakened heart muscle function.
„Fifth, statins may cause calcification of the coronary arteries, resulting in ischemia in cells. This then damages the mitochondria in heart cells. The mechanism for producing coenzyme Q10 is blocked (the result is weakened heart muscle function).”Po piąte, statyny mogą być przyczyną zwapnienia tętnic wieńcowych, powodując niedokrwienie komórek. Wówczas następuje uszkodzenie mitochondriów komórek serca. Blokowany jest mechanizm powstawania koenzymu Q10 (efektem jest osłabienie pracy mięśnia sercowego).
Research from PubMed · Europe PMC
We selected 3 studies with the best, positive results. This is a selection, not a full review of all research.
Total number of studies on this topic in PubMed: 48 146.
A meta-analysis found that LDL-lowering treatment reduces the risk of a first and a subsequent heart attack.
Aim of the study: Reducing elevated low-density lipoprotein cholesterol (LDL-C) is central to global efforts to prevent myocardial infarction (MI). While many studies have evaluated LDL-C-lowering therapies in first-time and recurrent MI prevention, direct comparisons of their relative efficacy are lacking. Therefore, we conducted a systematic review and meta-analysis to compare the efficacy of LDL-C-lowering therapies in first-time vs. recurrent MI prevention.
Results: We searched three databases until 30 November 2024, for randomized controlled trials (RCTs) with at least 1000 patient-years of follow-up. Efficacy was quantified as relative risk (RR) with 95% confidence intervals (CIs). Differences in benefit magnitude were assessed using Cochran's Q test. Data were pooled with a random-effects model, and heterogeneity was measured using the I2 statistic. Additionally, we applied the Cochrane Risk of Bias Tool to evaluate study quality and utilized the GRADE method to assess the certainty of the evidence. This study included 22 large-scale RCTs involving 180 304 participants. In first-time MI prevention, LDL-C-lowering therapies achieved a remarkable 38% reduction in MI risk [12 RCTs; 79 604 participants; RR, 0.62 (95% CI, 0.55-0.69); P < 0.001]. In recurrent MI prevention, these therapies were associated with a more modest but significant 16% risk reduction [11 RCTs; 100 700 participants; RR, 0.84 (95% CI, 0.80-0.88); P < 0.001].
Money for the studyuniversity or foundation · Scientific Research Fund of Xinxiang Medical University
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studycombined analysis of many studies (meta-analysis)
“Not stated” does not mean nobody paid — the database does not always record it.
A meta-analysis found that the polypill was associated with fewer heart attacks and major cardiovascular events than usual care.
Aim of the study: Myocardial infarction (MI) is one of the leading causes of death from cardiovascular diseases (CVDs). Despite various drugs and treatments, the outcomes have often been unsatisfactory. The purpose of this meta-analysis aimed to analyze the effects of polypill intervention on the incidence of MI and the related risk factors, blood pressure, and blood lipids.
Results: A total of 14 trials (N = 59,346) were included, with a mean age of 63.2 ± 10.0 years. The results showed that compared to the usual care group, polypill group was associated with a significant reduction of the incidence of MI (OR = 0.76; 95% CI: 0.59 to 0.99; p = 0.04) and MACE (OR = 0.79; 95% CI: 0.65 to 0.97; p = 0.03). The risk reduction for CVD mortality (OR = 0.85; 95% CI: 0.65 to 1.11; p = 0.20) and all-cause mortality (OR = 0.99; 95% CI: 0.95 to 1.03; p = 0.59) did not reach statistical significance contrast with the usual care group. Participants who were in polypill group was observed that the change of SBP level (SMD = -0.13; 95% CI: -0.25 to 0.00; p = 0.04), DBP level (SMD = -0.13; 95% CI: -0.19 to -0.06; p = 0.00), and LDL level (SMD = -0.21; 95% CI: -0.36 to -0.06; p = 0.01) reached statistical significance.
Money for the studynot stated
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studycombined analysis of many studies (meta-analysis)
“Not stated” does not mean nobody paid — the database does not always record it.
A meta-analysis found that antiplatelet drugs reduced heart attack risk in people at increased risk of vascular events.
Aim of the study: To determine the effects of antiplatelet therapy among patients at high risk of occlusive vascular events.
Results: Overall, among these high risk patients, allocation to antiplatelet therapy reduced the combined outcome of any serious vascular event by about one quarter; non-fatal myocardial infarction was reduced by one third, non-fatal stroke by one quarter, and vascular mortality by one sixth (with no apparent adverse effect on other deaths). Absolute reductions in the risk of having a serious vascular event were 36 (SE 5) per 1000 treated for two years among patients with previous myocardial infarction; 38 (5) per 1000 patients treated for one month among patients with acute myocardial infarction; 36 (6) per 1000 treated for two years among those with previous stroke or transient ischaemic attack; 9 (3) per 1000 treated for three weeks among those with acute stroke; and 22 (3) per 1000 treated for two years among other high risk patients (with separately significant results for those with stable angina (P=0.0005), peripheral arterial disease (P=0.004), and atrial fibrillation (P=0.01)).
Money for the studyuniversity or foundation · Wellcome Trust
Do the authors have ties to companies?not stated
Did a manufacturer help with the study?unknown
Type of studycombined analysis of many studies (meta-analysis)
“Not stated” does not mean nobody paid — the database does not always record it.
Perspectives and opinion materials
The content below presents the authors’ opinions, interpretations and hypotheses. It is not treated as equal to scientific studies and systematic reviews.
Orthomolecular Medicine News Service Opinion material
„It was detected that the odds of acute myocardial infarction increased by 10 times. Those who had suffered a myocardial infarction (MI) were 5.7 times more likely to suffer an MI after immunization.”It was detected that the odds of acute myocardial infarction increased by 10 times. Those who had suffered a myocardial infarction (MI) were 5.7 times more likely to suffer an MI after immunization.
Orthomolecular Medicine News Service Opinion material
„Woods KL, Fletcher S (1994) Long-term outcome after intravenous magnesium sulphate in suspected acute myocardial infarction: the second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2). Lancet 343:816-819. Shechter M, Hod H, Rabinowitz B, Boyko V, Chouraqui P (2003) Long-term outcome of intravenous magnesium therapy in thrombolysis-ineligible acute myocardial infarction patients. Cardiology 99:205-210. Theuwissen E, Smit E, Vermeer C (2012) The role of vitamin K in soft-tissue calcification. Adv Nutr. 3:166-173. Schurgers LJ, Spronk HMH, Soute BAM, et al.”Woods KL, Fletcher S (1994) Long-term outcome after intravenous magnesium sulphate in suspected acute myocardial infarction: the second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2). Lancet 343:816-819. Shechter M, Hod H, Rabinowitz B, Boyko V, Chouraqui P (2003) Long-term outcome of intravenous magnesium therapy in thrombolysis-ineligible acute myocardial infarction patients. Cardiology 99:205-210. Theuwissen E, Smit E, Vermeer C (2012) The role of vitamin K in soft-tissue calcification. Adv Nutr. 3:166-173. Schurgers LJ, Spronk HMH, Soute BAM, et al.
Orthomolecular Medicine News Service Opinion material
„(1990) Myocardial infarction is inversely associated with plasma 25-hydroxyvitamin D3 levels: a community-based study. Int J Epidemiol. 19:559-63. Manson JE, Cook NH, Lee IM, et al. (2019) Marine n-3 Fatty Acids and Prevention of Cardiovascular Disease and Cancer. N Engl J Med. 380:23-32. Manson JE, Cook NR, Lee IM, et al. (2019) Vitamin D supplements and prevention of cancer and cardiovascular disease.”(1990) Myocardial infarction is inversely associated with plasma 25-hydroxyvitamin D3 levels: a community-based study. Int J Epidemiol. 19:559-63. Manson JE, Cook NH, Lee IM, et al. (2019) Marine n-3 Fatty Acids and Prevention of Cardiovascular Disease and Cancer. N Engl J Med. 380:23-32. Manson JE, Cook NR, Lee IM, et al. (2019) Vitamin D supplements and prevention of cancer and cardiovascular disease.
Pisaczek does not judge who is right. It shows what was written and where to read it. Every sentence above has its source.