Towards a Paradigm Shift in Cholesterol Treatment. A Re-examination of the Cholesterol Issue in Japan: Abstracts

Hamazaki, Tomohito; Okuyama, Harumi; Ogushi, Yoichi; Hama, Rokuro

doi:10.1159/000381654

Cited by 30 publications

(23 citation statements)

References 16 publications

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“…Consistently, decreasing the intake of these dietary components has been shown to lead to increased incidence of MI, as explained above and elsewhere [6, 17]. …”

Section: Critical Review Of the Eas Consensus Statement 2017 Based Onsupporting

confidence: 73%

“…Moreover, the process of ASCVD development is affected by lifestyle-related factors even though the genetic factors (SNPs) themselves are not altered. In fact, in the past when infection was the major cause of death, people with familial hypercholesterolemia (FH)-related genes lived longer than average because LDL-C competitively inhibits the infection process (Chapter 1 in [17]). Thus, Mendelian randomization studies essentially involve multiple confounders.…”

Section: Eas Consensus Statement 2017 Based On Mendelian Randomizatiomentioning

confidence: 99%

“…Thus, the subgroup with the highest TC levels, which is likely to include the majority of individuals with FH, exhibited a strikingly high hazards ratio for CHD compared with the majority of participants, while no significant positive associations were detected among the other TC subgroups. It has been suggested that the NIPPON DATA80 study population included a higher than average proportion of FH cases, with a prevalence ranging from 1.5-fold higher (for women) to 3-fold higher (for men) than in the general population (0.2%) [17]. Thus, we need to clarify the relationship between plasma cholesterol level and CHD mortality.…”

Section: Critical Review Of the Eas Consensus Statement 2017 Based Onmentioning

confidence: 99%

“…Earlier, we noted that all-cause mortality was inversely associated with plasma TC or LDL-C among the general population over 40 years of age [6, 48]. One exception is NIPPON DATA80 where the highest TC group exhibited higher all-cause mortality, with the TC-mortality curve exhibiting a mirror J-shape [17]. We propose that the mirror J-shape is observed only when the proportion of FH is high [6, 48].…”

Section: Critical Review Of the Eas Consensus Statement 2017 Based Onmentioning

confidence: 99%

“…26). Moreover, high LDL-C levels are beneficial for suppressing viral infection; for example, hepatitis C virus competes with LDL at the LDL receptor for entry into hepatocytes, and distinct inverse associations of hepatic cancer mortality with TC or LDL-C have been noted (reviewed by Hamazaki et al [17]). Statins also suppress thioredoxin disulfide reductase [102] and glutathione reductase, resulting in elevated peroxide tone (reactive oxygen species and lipid peroxides), which is a major risk factor for carcinogenesis.…”

Section: Critical Review Of the Consensus Statement 2017 Based On Stamentioning

confidence: 99%

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A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017

Okuyama

Hamazaki²,

Hama³

et al. 2018

Pharmacology

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Background: The Consensus Statement from the European Atherosclerosis Society (EAS) Consensus Panel 2017 concludes on the basis of 3 different types of clinical studies that low-density lipoprotein (LDL) causes atherosclerotic cardiovascular disease (ASCVD). In Mendelian randomization studies, rare genetic mutations affecting LDL receptor function were found to cause higher or lower LDL-C levels, which are associated with correspondingly altered ASCVD risk. In prospective cohort studies and randomized controlled trials (RCTs) of statins, a remarkably consistent log-linear association was demonstrated between the absolute magnitude of LDL-C exposure and ASCVD risk. The EAS Statement proposes that any mechanism of lowering plasma LDL concentration should reduce the risk of ASCVD events proportional to the absolute reduction in LDL-C and the cumulative duration of exposure to lower LDL-C. However, as we explain, we do not find this conclusion acceptable. Summary: Our review points out that different interpretations are possible for the results of Mendelian randomization studies. As for prospective cohort studies, many inconsistent reports on the association of LDL-C and ASCVD were disregarded when drafting the Statement, reports with and without genetic factors related to LDL receptor function should be analyzed separately, and the term ASCVD in the Statement is used inappropriately because myocardial infarction and cerebral infarction differ in their association with LDL-C. As for RCTs, clinical reports on statins published before and after the implementation of new regulations affecting clinical trials (2004/2005) should not both be included in meta-analyses because the evaluated efficacy of statins changed markedly, and the irreversible adverse effects of statins need to be evaluated more rigorously now that their mechanisms have been elucidated. Key Messages: Apart from the EAS hypothesis that LDL causes ASCVD, recent pharmacological/biochemical studies, as summarized in this review and elsewhere, have revealed that atherosclerosis is caused by statins taken to lower LDL-C, as well as by warfarin and some types of vegetable fats and oils, in the absence of significantly elevated LDL-C levels. Thus, the promotion of statin treatment by the Statement is rather risky and we do not feel that the conclusions are justified for the prevention of ASCVD.

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“…Consistently, decreasing the intake of these dietary components has been shown to lead to increased incidence of MI, as explained above and elsewhere [6, 17]. …”

Section: Critical Review Of the Eas Consensus Statement 2017 Based Onsupporting

confidence: 73%

Section: Eas Consensus Statement 2017 Based On Mendelian Randomizatiomentioning

confidence: 99%

Section: Critical Review Of the Eas Consensus Statement 2017 Based Onmentioning

confidence: 99%

Section: Critical Review Of the Eas Consensus Statement 2017 Based Onmentioning

confidence: 99%

Section: Critical Review Of the Consensus Statement 2017 Based On Stamentioning

confidence: 99%

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A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017

Okuyama

Hamazaki²,

Hama³

et al. 2018

Pharmacology

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How can we deliver on the promise of precision medicine in oncology and beyond? A practical roadmap for action

Baird,

Westphalen,

Blum

et al. 2023

Health Science Reports

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Background Precision medicine (PM) is a form of personalized medicine that recognizes that individuals with the same condition may have different underlying factors and uses molecular information to provide tailored treatments. This approach can improve treatment outcomes and transform lives through favorable risk/benefit ratios, avoidance of ineffective interventions, and possible cost savings, as evidenced in the field of lung cancer and other oncology/therapeutic settings, including cardiac disease, diabetes, and rare diseases. However, the potential benefits of PM have yet to be fully realized. Discussion There are many barriers to the implementation of PM in clinical practice, including fragmentation of the PM landscape, siloed approaches to address shared challenges, unwarranted variation in availability and access to PM, lack of standardization, and limited understanding of patients' experience and needs throughout the PM pathway. We believe that a diverse, intersectoral multistakeholder collaboration, with three main pillars of activity: generation of data to demonstrate the benefit of PM, education to support informed decision‐making, and addressing barriers across the patient pathway, is necessary to reach the shared goal of making PM an accessible and sustainable reality. Besides healthcare providers, researchers, policymakers/regulators/payers, and industry representatives, patients in particular must be equal partners and should be central to the PM approach―from early research through to clinical trials and approval of new treatments―to ensure it represents their entire experience and identifies barriers, solutions, and opportunities at the point of delivery. Conclusion We propose a practical and iterative roadmap to advance PM and call for all stakeholders across the healthcare system to employ a collaborative, cocreated, patient‐centered methodology to close gaps and fully realize the potential of PM.

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Statins: Rationale, Mode of Action, and Side Effects

Sultan

D'Souza

Zabetakis

et al. 2019

The Impact of Nutrition and Statins on Cardiovascular Diseases

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Towards a Paradigm Shift in Cholesterol Treatment. A Re-examination of the Cholesterol Issue in Japan: Abstracts

Cited by 30 publications

References 16 publications

A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017

A Critical Review of the Consensus Statement from the European Atherosclerosis Society Consensus Panel 2017

How can we deliver on the promise of precision medicine in oncology and beyond? A practical roadmap for action

Statins: Rationale, Mode of Action, and Side Effects

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