Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly. In fact, “high LDL-C may be protective is in accordance with the finding that LDL-C is lower than normal in patients with acute myocardial infarction”.



Cardiovascular medicine
Research
Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review
http://bmjopen.bmj.com/content/6/6/e010401.full?sid=cfb00014-f0a8-407d-ae71-a3278160ca49

Uffe Ravnskov1, David M Diamond2, Rokura Hama3, Tomohito Hamazaki4, Björn Hammarskjöld5, Niamh Hynes6, Malcolm Kendrick7, Peter H Langsjoen8, Aseem Malhotra9, Luca Mascitelli10, Kilmer S McCully11, Yoichi Ogushi12, Harumi Okuyama13, Paul J Rosch14, Tore Schersten15, Sherif Sultan6, Ralf Sundberg16
Author affiliations
Abstract

Objective It is well known that total cholesterol becomes less of a risk factor or not at all for all-cause and cardiovascular (CV) mortality with increasing age, but as little is known as to whether low-density lipoprotein cholesterol (LDL-C), one component of total cholesterol, is associated with mortality in the elderly, we decided to investigate this issue.

Setting, participants and outcome measures We sought PubMed for cohort studies, where LDL-C had been investigated as a risk factor for all-cause and/or CV mortality in individuals ≥60 years from the general population.

Results We identified 19 cohort studies including 30 cohorts with a total of 68 094 elderly people, where all-cause mortality was recorded in 28 cohorts and CV mortality in 9 cohorts. Inverse association between all-cause mortality and LDL-C was seen in 16 cohorts (in 14 with statistical significance) representing 92% of the number of participants, where this association was recorded. In the rest, no association was found. In two cohorts, CV mortality was highest in the lowest LDL-C quartile and with statistical significance; in seven cohorts, no association was found.

Conclusions High LDL-C is inversely associated with mortality in most people over 60 years. This finding is inconsistent with the cholesterol hypothesis (ie, that cholesterol, particularly LDL-C, is inherently atherogenic). Since elderly people with high LDL-C live as long or longer than those with low LDL-C, our analysis provides reason to question the validity of the cholesterol hypothesis. Moreover, our study provides the rationale for a re-evaluation of guidelines recommending pharmacological reduction of LDL-C in the elderly as a component of cardiovascular disease prevention strategies.

This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

http://dx.doi.org/10.1136/bmjopen-2015-010401
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Strengths and limitations of this study

This is the first systematic review of cohort studies where low-density lipoprotein cholesterol (LDL-C) has been analysed as a risk factor for all-cause and/or cardiovascular mortality in elderly people.

Lack of an association or an inverse association between LDL-C and mortality was present in all studies.

We may not have included studies where an evaluation of LDL-C as a risk factor for mortality was performed but where it was not mentioned in the title or in the abstract.

We may have overlooked relevant studies because we have only searched PubMed.

Minor errors may be present because some of the authors may not have adjusted LDL-C by appropriate risk factors.

Some of the participants with high LDL-C may have started statin treatment during the observation period and, in this way, may have added a longer life to the group with high LDL-C and some of them may have started with a diet able to influence the risk of mortality.

We may have overlooked a small number of relevant studies because we only searched papers in English.

Introduction
Rationale

For decades, the mainstream view has been that an elevated level of total cholesterol (TC) is a primary cause of atherosclerosis and cardiovascular disease (CVD). There are several contradictions to this view, however. No study of unselected people has found an association between TC and degree of atherosclerosis.1 Moreover, in most of the Japanese epidemiological studies, high TC is not a risk factor for stroke, and further, there is an inverse association between TC and all-cause mortality, irrespective of age and sex.2

In a recent meta-analysis performed by the Prospective Studies Collaboration, there was an association between TC and CV mortality in all ages and in both sexes.3 However, even in this analysis, the risk decreased with increasing age and became minimal after the age of 80 years. Since atherosclerosis and CVD are mainly diseases of the elderly, the cholesterol hypothesis predicts that the association between CV mortality and TC should be at least as strong in the elderly as in young people. There may be a confounding influence in these studies, however, because TC includes high-density lipoprotein cholestrol (HDL-C), and multiple studies have shown that a high level of HDL-C is associated with a lower risk of CVD.
Objectives

We examined the literature assessing low-density lipoprotein cholesterol (LDL-C) as a risk factor for mortality in elderly people. Since the definition of CVD varies considerably in the scientific literature, we have chosen to focus on the association between LDL-C and all-cause and CVD mortality, because mortality has the least risk of bias among all outcome measures. If Goldstein and Brown’s recent statement that LDL-C is ‘the essential causative agent’ of CVD4 is correct, then we should find that LDL-C is a strong risk factor for mortality in elderly people.


Methods
Search strategy

UR and RS searched PubMed independently from initial to 17 December 2015. The following keywords were used: ‘lipoprotein AND (old OR elderly) AND mortality NOT animal NOT trial’. We also retrieved the references in the publications so as not to miss any relevant studies. The search was limited to studies in English.
Inclusion and exclusion criteria

All included studies should meet the following criteria: the study should be a cohort study of people aged 60 years or older selected randomly from the general population, or a study where the authors had found no significant differences between the participants and the source population’s demographic characteristics. The studies should include an initial assessment of LDL-C levels, the length of the observation time and information about all-cause and/or cardiovascular mortality at the end of follow-up. The studies should also include information about the association between LDL-C and all-cause and/or CVD mortality. We excluded studies that did not represent the general population (eg, case–control studies; case reports; studies that included patients only); studies where data about elderly people were not given separately, and studies without multivariate correction for the association between LDL-C and all-cause and/or CV mortality. We accepted studies where the authors had excluded patients with serious diseases or individuals who had died during the first year.
Study selection, data items and extraction

Studies where the title or abstract indicated that they might include LDL-C data of elderly people, were read in full, and the relevant data were extracted by at least three of the authors, for example, year of publication, total number of participants, sex, length of observation time, exclusion criteria, LDL-C measured at the start and the association between initial LDL-C and risk of all-cause and/or at follow-up. When more than one adjusted HR was reported, the HR with the most fully adjusted model was selected.

Quality assessment

The design of the study satisfies almost all points of reliability and validity according to the Newcastle Ottawa Scale as regards selection, comparability and exposure.5 Thus, all studies represented elderly people only; ascertainness of exposure (eg, measurement of LDL-C) was present in all studies, and outcome was unknown at the start. It can be questioned if all of the studies represented the general population because, as shown below, in some of them various types of disease groups were excluded.

Results
Study selection

Our search gave 2894 hits. We excluded 160 studies, which were not in English, and 2452 studies because, judged from the abstract, it was obvious that they were irrelevant.

The rest of the papers were read in full; 263 of these studies were excluded for the following reasons: (1) the participants did not represent the general population; (2) LDL-C was not measured at the start; (3) follow-up information was not given for the elderly separately; or (4) no information was present about mortality during the observation period (figure 1). One of the studies6 was excluded because it included the same individuals as in a previous study.7
Figure 1

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Figure 1

Flow Chart. CV, cardiovascular; LDL-C, low-density lipoprotein cholesterol.
Study characteristics

The remaining 19 studies including 30 cohorts with a total of 68 094 participants met the inclusion criteria (figure 1). All-cause mortality was recorded in 28 cohorts. In 16 of these cohorts (representing 92% of the individuals), the association was inverse and with statistical significance in 14; in 1 of the cohorts, the association was mirror-J-formed with the lowest risk in the highest quartile; in the rest of the papers, no association was found. CV mortality was recorded in nine cohorts; in one of them, the association was almost U-shaped with the lowest risk in the highest quartile (curvilinear fit: p=0.001); in one of them, the association was mirror-J-formed and also with the lowest risk in the highest quartile (curvilinear fit: p=0.03); in the other seven cohorts, no association was found (table 1).

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Table 1

Association between LDL-C and all-cause mortality and CVD mortality, respectively, in 19 studies including 30 cohorts with 68 094 individuals from the general population above the age of 60 years
Risk of bias across studies

One explanation for the increased risk of mortality among people with low cholesterol is that serious diseases may lower cholesterol soon before death occurs. Evidence to support this hypothesis may be obtained from 10 of the studies in which no exclusions were made for individuals with terminal illnesses. However, in four of the studies, participants with a terminal illness or who had died during the first observation year were excluded. In one of those studies,8 LDL-C was not associated with all-cause mortality; in the three others,16 ,20 ,24 which included more than 70% of the total number of participants in our review, LDL-C was inversely associated with all-cause mortality and with statistical significance. Thus, there is little support for the hypothesis that our analysis is biased by end of life changes in LDL-C levels.

It is also potentially relevant that all studies did not correct for the same risk factors, and some of them did not inform the reader about which risk factors they corrected for. However, taking all studies together, 50 different risk factors were corrected for in the Cox analyses (table 2).

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Table 2

Factors corrected for in the multifactorial analyses of each study

It is worth considering that some of the participants with high LDL-C may have started statin treatment during the observation period. Such treatment may have increased the lifespan for the group with high LDL-C. However, any beneficial effects of statins on mortality would have been minimal because most statin trials have had little effect on CVD and all-cause mortality, with a maximum reduction of mortality of two percentage points. It is therefore relevant that the 4-year mortality among those with the highest LDL-C in the included cohorts was up to 36% lower than among those with the lowest LDL-C. Furthermore, in the largest study20 that included about two-thirds of the total number of participants in our study, the risk was lower among those with the highest LDL-C than among those on statin treatment.

It is also possible that those with the highest LDL-C were put on a different diet than those with low LDL-C. However, this potential bias in mortality outcomes could have gone in both directions. Some of the individuals with high LDL-C may have followed the official dietary guidelines and exchanged saturated fat with vegetable oils rich in linoleic acid. In a recent study, the authors reported that among participants who were older than 65 at baseline, a 30 mg/dL decrease in serum cholesterol was associated with a higher risk of death (HR 1.35, 95% CI 1.18 to 1.54).26 If applied to the general population, this finding suggests that the conventional dietary treatment for high cholesterol with vegetable oil replacing saturated fat may actually increase mortality in those individuals with high LDL-C. Thus, the lack of an association between LDL-C and mortality may have been even stronger than reported since the dietary intervention may have been counterproductive.

Finally, it is potentially relevant that we limited our literature search to PubMed. In preliminary searches with PubMed, OVID and EMBASE, we identified 17 relevant studies in PubMed, but only 2 in OVID and EMBASE, and these 2 studies were found in PubMed as well. Therefore, it is highly unlikely that there are studies with findings with divergent results from those we have reported here, as all of them reported either no association or an inverse association between LDL-C and mortality.
Discussion

Assessments of the association between serum cholesterol and mortality have been studied for decades, and extensive research has shown a weak association between total cholesterol and mortality in the elderly; several studies have even shown an inverse association. It is therefore surprising that there is an absence of a review of the literature on mortality and levels of LDL-C, which is routinely referred to as a causal agent in producing CVD4 and is a target of pharmacological treatment of CVD.

Our literature review has revealed either a lack of an association or an inverse association between LDL-C and mortality among people older than 60 years. In almost 80% of the total number of individuals, LDL-C was inversely associated with all-cause mortality and with statistical significance.

These findings provide a paradoxical contradiction to the cholesterol hypothesis. As atherosclerosis starts mainly in middle-aged people and becomes more pronounced with increasing age, the cholesterol hypothesis would predict that there should be a cumulative atherosclerotic burden, which would be expressed as greater CVD and all-cause mortality, in elderly people with high LDL-C levels.

Our results raise several relevant questions for future research. Why is high TC a risk factor for CVD in the young and middle-aged, but not in elderly people? Why does a subset of elderly people with high LDL-C live longer than people with low LDL-C? If high LDL-C is potentially beneficial for the elderly, then why does cholesterol-lowering treatment lower the risk of cardiovascular mortality? In the following we have tried to address some of these questions.
Inverse causation

A common argument to explain why low lipid values are associated with an increased mortality is inverse causation, meaning that serious diseases cause low cholesterol. However, this is not a likely explanation, because in five of the studies in table 1 terminal disease and mortality during the first years of observation were excluded. In spite of that, three of them showed that the highest mortality was seen among those with the lowest initial LDL-C with statistical significance.18 ,20 ,24
Is high LDL-C beneficial?

One hypothesis to address the inverse association between LDL-C and mortality is that low LDL-C increases susceptibility to fatal diseases. Support for this hypothesis is provided by animal and laboratory experiments from more than a dozen research groups which have shown that LDL binds to and inactivates a broad range of microorganisms and their toxic products.27 Diseases caused or aggravated by microorganisms may therefore occur more often in people with low cholesterol, as observed in many studies.28 In a meta-analysis of 19 cohort studies, for instance, performed by the National Heart, Lung and Blood Institute and including 68 406 deaths, TC was inversely associated with mortality from respiratory and gastrointestinal diseases, most of which are of an infectious origin.29 It is unlikely that these diseases caused the low TC, because the associations remained after the exclusion of deaths occurring during the first 5 years. In a study by Iribarren et al, more than 100 000 healthy individuals were followed for 15 years. At follow-up, those whose initial cholesterol level was lowest at the start had been hospitalised significantly more often because of an infectious disease that occurred later during the 15-year follow-up period.30 This study provides strong evidence that low cholesterol, recorded at a time when these people were healthy, could not have been caused by a disease they had not yet encountered.

Another explanation for an inverse association between LDL-C and mortality is that high cholesterol, and therefore high LDL-C, may protect against cancer. The reason may be that many cancer types are caused by viruses.31 Nine cohort studies including more than 140 000 individuals followed for 10–30 years have found an inverse association between cancer and TC measured at the start of the study, even after excluding deaths that occurred during the first 4 years.32 Furthermore, cholesterol-lowering experiments on rodents have resulted in cancer,33 and in several case–control studies of patients with cancer and controls matched for age and sex, significantly more patients with cancer have been on cholesterol-lowering treatment.32 In agreement with these findings, cancer mortality is significantly lower in individuals with familial hypercholesterolaemia.34

That high LDL-C may be protective is in accordance with the finding that LDL-C is lower than normal in patients with acute myocardial infarction. This has been documented repeatedly without a reasonable explanation.35–37 In one of the studies,37 the authors concluded that LDL-C evidently should be lowered even more, but at a follow-up 3 years later mortality was twice as high among those whose LDL-C had been lowered the most compared with those whose cholesterol was unchanged or lowered only a little. If high LDL-C were the cause, the effect should have been the opposite.
Conclusions

Our review provides the first comprehensive analysis of the literature about the association between LDL-C and mortality in the elderly. Since the main goal of prevention of disease is prolongation of life, all-cause mortality is the most important outcome, and is also the most easily defined outcome and least subject to bias. The cholesterol hypothesis predicts that LDL-C will be associated with increased all-cause and CV mortality. Our review has shown either a lack of an association or an inverse association between LDL-C and both all-cause and CV mortality. The cholesterol hypothesis seems to be in conflict with most of Bradford Hill’s criteria for causation, because of its lack of consistency, biological gradient and coherence. Our review provides the basis for more research about the cause of atherosclerosis and CVD and also for a re-evaluation of the guidelines for cardiovascular prevention, in particular because the benefits from statin treatment have been exaggerated.38–40
Acknowledgments

The study has been supported by a grant from Western Vascular Institute.
References


Ravnskov U. Is atherosclerosis caused by high cholesterol? QJM 2002;95:397–403. doi:10.1093/qjmed/95.6.397
FREE Full TextGoogle Scholar

Hamazaki T, Okuyama H, Ogushi Y, et al. Towards a paradigm shift in cholesterol treatment—a re-examination of the cholesterol issue in Japan. Ann Nutr Metab 2015;66(Suppl 4):1–116. doi:10.1159/000381654
Google Scholar

Lewington S, Whitlock G, Clarke R, et alProspective Studies CollaborationLewington S, Whitlock G, Clarke R, et al. Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths. Lancet 2007;370:1829–39. doi:10.1016/S0140-6736(07)61778-4
CrossRefPubMedWeb of ScienceGoogle Scholar

Goldstein JL, Brown MS. A century of cholesterol and coronaries: from plaques to genes to statins. Cell 2015;161:161–72. doi:10.1016/j.cell.2015.01.036
CrossRefPubMedGoogle Scholar

Stang A. Critical evaluation of the Newcastle-Ottawa scale for the assessment of the quality of nonrandomized studies in meta-analyses. Eur J Epidemiol 2010;25:603–5. doi:10.1007/s10654-010-9491-z
CrossRefPubMedWeb of ScienceGoogle Scholar

Psaty BM, Anderson M, Kronmal RA, et al. The association between lipid levels and the risks of incident myocardial infarction, stroke, and total mortality: the Cardiovascular Health Study. J Am Geriatr Soc 2004;52:1639–47. doi:10.1111/j.1532-5415.2004.52455.x
CrossRefPubMedWeb of ScienceGoogle Scholar

Fried LP, Kronmal RA, Newman AB, et al. Risk factors for 5-year mortality in older adults: the Cardiovascular Health Study. JAMA 1998;279:585–92. doi:10.1001/jama.279.8.585
CrossRefPubMedWeb of ScienceGoogle Scholar

Zimetbaum P, Frishman WH, Ooi WL, et al. Plasma lipids and lipoproteins and the incidence of cardiovascular disease in the very elderly: the Bronx Aging Study. Arterioscler Thromb 1992;12:416–23. doi:10.1161/01.ATV.12.4.416
Abstract/FREE Full TextGoogle Scholar
Kronmal RA, Cain KC, Ye Z, et al. Total serum cholesterol levels and mortality risk as a function of age. A report based on the Framingham data. Arch Intern Med 1993;153:1065–73. doi:10.1001/archinte.1993.00410090025004
CrossRefPubMedWeb of ScienceGoogle Scholar
Räihä I, Marniemi J, Puukka P, et al. Effect of serum lipids, lipoproteins, and apolipoproteins on vascular and nonvascular mortality in the elderly. Arterioscler Thromb Vasc Biol 1997;17:1224–32. doi:10.1161/01.ATV.17.7.1224
Abstract/FREE Full TextGoogle Scholar
Chyou PH, Eaker ED. Serum cholesterol concentrations and all-cause mortality in older people. Age Ageing 2000;29:69–74. doi:10.1093/ageing/29.1.69
Abstract/FREE Full TextGoogle Scholar
Weverling-Rijnsburger AW, Jonkers IJ, van Exel E, et al. High-density vs low-density lipoprotein cholesterol as the risk factor for coronary artery disease and stroke in old age. Arch Intern Med 2003;163:1549–54. doi:10.1001/archinte.163.13.1549
CrossRefPubMedWeb of ScienceGoogle Scholar
Schupf N, Costa R, Luchsinger J, et al. Relationship between plasma lipids and all-cause mortality in nondemented elderly. J Am Geriatr Soc 2005;53:219–26. doi:10.1111/j.1532-5415.2005.53106.x
CrossRefPubMedWeb of ScienceGoogle Scholar
Tikhonoff V, Casiglia E, Mazza A, et al. Low-density lipoprotein cholesterol and mortality in older people. J Amer Geriatr Soc 2005;53:2159–64. doi:10.1111/j.1532-5415.2005.00492.x
CrossRefPubMedWeb of ScienceGoogle Scholar
Störk S, Feelders RA, van den Beld AW, et al. Prediction of mortality risk in the elderly. Am J Med 2006;119:519–25. doi:10.1016/j.amjmed.2005.10.062
CrossRefPubMedWeb of ScienceGoogle Scholar

Akerblom JL, Costa R, Luchsinger JA, et al. Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders. Age Ageing 2008;37:207–13. doi:10.1093/ageing/afn017
Abstract/FREE Full TextGoogle Scholar
Upmeier E, Lavonius S, Lehtonen A, et al. Serum lipids and their association with mortality in the elderly: a prospective cohort study. Aging Clin Exp Res 2009;21:424–30. doi:10.1007/BF03327441
CrossRefPubMedWeb of ScienceGoogle Scholar

Nilsson G, Ohrvik J, Lönnberg I, et al. Ten-year survival in 75-year-old men and women: predictive ability of total cholesterol, HDL-C, and LDL-C. Curr Gerontol Geriatr Res 2009:158425. doi:10.1155/2009/158425doi:10.1155/2009/158425
Google Scholar
Werle MH, Moriguchi E, Fuchs SC, et al. Risk factors for cardiovascular disease in the very elderly: results of a cohort study in a city in southern Brazil. Eur J Cardiovasc Prev Rehabil 2011;18:369–77. doi:10.1177/1741826710389405
CrossRefPubMedWeb of ScienceGoogle Scholar

Bathum L, Depont Christensen R, Engers Pedersen L, et al. Association of lipoprotein levels with mortality in subjects aged 50+without previous diabetes or cardiovascular disease: a population-based register study. Scand J Prim Health Care 2013;31:172–80. doi:10.3109/02813432.2013.824157
Google Scholar
Linna M, Ahotupa M, Löppönen MK, et al. Circulating oxidised LDL lipids, when proportioned to HDL-C emerged as a risk factor of all-cause mortality in a population-based survival study. Age Ageing 2013;42:110–13. doi:10.1093/ageing/afs074
Abstract/FREE Full TextGoogle Scholar
Jacobs JM, Cohen A, Ein-Mor E, et al. Cholesterol, statins, and longevity from age 70 to 90 years. J Am Med Dir Assoc 2013;14:883–8. doi:10.1016/j.jamda.2013.08.012
CrossRefPubMedGoogle Scholar
Takata Y, Ansai T, Soh I, et al. Serum total cholesterol concentration and 10-year mortality in an 85-year-old population. Clin Interv Aging 2014;9:293–300. doi:10.2147/CIA.S53754
Google Scholar

Lv YB, Yin ZX, Chei CL, et al. Low-density lipoprotein cholesterol was inversely associated with 3-year all-cause mortality among Chinese oldest old: data from the Chinese Longitudinal Healthy Longevity Survey. Atherosclerosis 2015;239: 137–42. doi:10.1016/j.atherosclerosis.2015.01.002
Google Scholar
Blekkenhorst LC, Prince RL, Hodgson JM, et al. Dietary saturated fat intake and atherosclerotic vascular disease mortality in elderly women: a prospective cohort study. Am J Clin Nutr 2015;101:1263–8. doi:10.3945/ajcn.114.102392
Abstract/FREE Full TextGoogle Scholar

Ramsden CE, Zamora D, Majchrzak-Hong S, et al. Re-evaluation of the traditional diet-heart hypothesis: analysis of recovered data from Minnesota Coronary Experiment (1968–73). BMJ 2016;353:i1246. doi:10.1136/bmj.i1246
Abstract/FREE Full TextGoogle Scholar

Ravnskov U, McCully KS. Vulnerable plaque formation from obstruction of vasa vasorum by homocysteinylated and oxidized lipoprotein aggregates complexed with microbial remnants and LDL autoantibodies. Ann Clin Lab Sci 2009;39:3–16.
Abstract/FREE Full TextGoogle Scholar

Ravnskov U. High cholesterol may protect against infections and atherosclerosis. QJM 2003;96:927–34. doi:10.1093/qjmed/hcg150
FREE Full TextGoogle Scholar

Jacobs D, Blackburn H, Higgins M, et al. Report of the conference on low blood cholesterol: mortality associations. Circulation 1992;86:1046–60. doi:10.1161/01.CIR.86.3.1046
Abstract/FREE Full TextGoogle Scholar

Iribarren C, Jacobs DR Jr., Sidney S, et al. Cohort study of serum total cholesterol and in-hospital incidence of infectious diseases. Epidemiol Infect 1998;121:335–47. doi:10.1017/S0950268898001435
CrossRefPubMedGoogle Scholar

Read SA, Douglas MW. Virus induced inflammation and cancer development. Cancer Lett 2014;345:174–81. doi:10.1016/j.canlet.2013.07.030
CrossRefPubMedGoogle Scholar

Ravnskov U, McCully KS, Rosch PJ. The statin-low cholesterol-cancer conundrum. QJM 2012;105:383–8. doi:10.1093/qjmed/hcr243
FREE Full TextGoogle Scholar

Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA 1996;275:55–60. doi:10.1001/jama.1996.03530250059028
CrossRefPubMedWeb of ScienceGoogle Scholar

Neil HA, Hawkins MM, Durrington PN, et al. Non-coronary heart disease mortality and risk of fatal cancer in patients with treated heterozygous familial hypercholesterolaemia: a prospective registry study. Atherosclerosis 2005;179:293–7. doi:10.1016/j.atherosclerosis.2004.10.011
CrossRefPubMedWeb of ScienceGoogle Scholar

Reddy VS, Bui QT, Jacobs JR, et al. Relationship between serum low-density lipoprotein cholesterol and In-hospital mortality following acute myocardial infarction (The lipid paradox). Am J Cardiol 2015;115:557–62. doi:10.1016/j.amjcard.2014.12.006
CrossRefPubMedGoogle Scholar

Sachdeva A, Cannon CP, Deedwania PC, et al. Lipid levels in patients hospitalized with coronary artery disease: an analysis of 136,905 hospitalizations in get with the guidelines. Am Heart J 2009;157:111–17. doi:10.1016/j.ahj.2008.08.010
CrossRefPubMedWeb of ScienceGoogle Scholar

Al-Mallah MH, Hatahet H, Cavalcante JL, et al. Low admission LDL-cholesterol is associated with increased 3-year all-cause mortality in patients with non ST segment elevation myocardial infarction. Cardiol J 2009;16:227–33.
PubMedGoogle Scholar

Diamond DM, Ravnskov U. How statistical deception created the appearance that statins are safe and effective in primary and secondary prevention of cardiovascular disease. Expert Rev Clin Pharmacol 2015;8:201–10. doi:10.1586/17512433.2015.1012494
Google Scholar

Kristensen ML, Christensen PM, Hallas J. The effect of statins on average survival in randomised trials, an analysis of end point postponement. BMJ Open 2015;5:e007118. doi:10.1136/bmjopen-2014-007118
Abstract/FREE Full TextGoogle Scholar

de Lorgeril M, Rabaeus M. Beyond confusion and controversy, Can we evaluate the real efficacy and safety of cholesterol-lowering with statins? J Controversies Biomed Res 2015;1:67–92. doi:10.15586/jcbmr.2015.11
Google Scholar

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Lisa Haven: If You Thought Fukushima Was Over With You’re Dead Wrong! Guess What’s Happening Now?



If You Thought Fukushima Was Over With You’re Dead Wrong! Guess What’s Happening Now?
Thursday, April 12, 2018 8:56
By Lisa Haven
http://beforeitsnews.com/politics/2018/04/were-being-nuked-you-wont-believe-what-fukushima-is-doing-now-outrage-2994495.html

Fukushima, that’s the name of the nuclear power plant that will go down in history as one of the worst events of it’s time and it will leave millions of cancer patients in its path.

Emigrate While You Still Can! Learn More…

For years this nuclear plant has been wreaking havoc on our oceans and on our bodies, ever since it’s destruction on March 11, 2011 when an earthquake and tsunami stroked the area. Sadly, the mainstream media have kept this disaster “on the down-low” in order to not panic the public, just as they did when Chernobyl took out millions with cancer.

With sieverts now reaching 530 and talks that they could go as high as 5,000, the mainstream media is forced to report on this devastation, however they fail to mention the repercussions it will have on humanity.

In the video below I prove just how bad this event really is and the effects it is still having on those here in America…
<a href="http://” target=”_blank”>The Video

Here’s what the globalists have to say about decreasing the worlds population, and I believe, they allow things like Fukushima specifically for that:

At the United Nations Biodiversity Assessment on Sustainable Human Population; US Senate September 9, 1994:

“A reasonable estimate for an industrialized world society at the present North American material standard of living would be one billion people. This must be implemented within 30-50 years, 2/3’s of the population must be cut.”

“The UN says property rights are not absolute and unchanging, but are there for the convenience of whatever government wants to do.” – Michael Coffman

Price Phillip, Duke of Edinburg:

“If I were reincarnated, I would wish to be returned to Earth as a killer virus to lower human population levels.”

Henry Kissinger:

“Depopulation should be the highest priority of U.S. foreign policy towards the Third World.”

Theodore Roosevelt:

“Society has no business to permit degenerates to reproduce their kind”

Ted Turner, in an interview with Audubon Magazine:

“A total world population of 250-300 million people, a 95% decline from present levels, would be ideal.”

Thomas Ferguson, State Department Office of Population Affairs:

“There is a single theme behind all our work–we must reduce population levels. Either governments do it our way, through nice clean methods, or they will get the kinds of mess that we have in El Salvador, or in Iran or in Beirut. Population is a political problem. Once population is out of control, it requires authoritarian government, even fascism, to reduce it….”“Our program in El Salvador didn’t work. The infrastructure was not there to support it. There were just too goddamned many people…. To really reduce population, quickly, you have to pull all the males into the fighting and you have to kill significant numbers of fertile age females….” “The quickest way to reduce population is through famine, like in Africa, or through disease like the Black Death….”

Alexander King, Bertrand Schneider – Founder and Secretary, respectively, The Club of Rome, The First Global Revolution, pgs 104-105, 199:

“In searching for a new enemy to unite us, we came up with the idea that pollution, the threat of global warming, water shortages, famine and the like would fit the bill…. But in designating them as the enemy, we fall into the trap of mistaking symptoms for causes. All these dangers are caused by human intervention and it is only through changed attitudes and behavior that they can be overcome. The real enemy, then, is humanity itself.”

Paul Ehrlich in The Population Bomb:

“A cancer is an uncontrolled multiplication of cells; the population explosion is an uncontrolled multiplication of people…. We must shift our efforts from the treatment of the symptoms to the cutting out of the cancer. The operation will demand many apparently brutal and heartless decisions.” Stanford Professor ”

Jacques Cousteau UNESCO Courier 1991:

“In order to save the planet it would be necessary to kill 350,000 people per day.”

Robert Walker, former chair of PepsiCo and Proctor & Gamble on water:

“Water is a gift of nature. Its delivery is not. It must be priced to insure it is used sustainably….Ted Turner makes the radical statement that, “A total population of 250-300 million people, a 95% decline from present levels, would be ideal,””

Club of Rome, The First Global Revolution, 1991:

“In searching for a new enemy to unite us, we came up with the idea that pollution, the threat of global warming, water shortages, famine and the like would fit the bill (this is absolute proof that man made global warming is a fabrication)…. But in designating them as the enemy, we fall into the trap of mistaking symptoms for causes. All these dangers are caused by human intervention and it is only through changed attitudes and behavior that they can be overcome. The real enemy, then, is humanity itself.”

Bill Gates TED Talk

“First, we’ve got population. The world today has 6.8 billion people. That’s headed up to about nine billion. Now, if we do a really great job on new vaccines, health care, reproductive health services, we could lower that by, perhaps, 10 or 15 percent, but there we see an increase of about 1.3.”

They Are Killing Us From the Skies: Death by Respiratory Disease Has Skyrocketed



“Chemtrail Cough” is Sweeping the Nation — Death by Respiratory Disease Has Skyrocketed
February 11, 2018
http://www.unseen-pedia.com/chemtrail-cough-sweeping-nation-death-respiratory-disease-skyrocketed/

Have you noticed that everyone around you is congested and coughing? I am calling this new syndrome “chemtrail cough.”

My wife is coughing, I am coughing and now even our dogs are coughing. In just four years death by respiratory disease has skyrocketed from 8th in the world to 3rd and possibly even 2nd.

If someone in congress receives a letter with a little bit of white powder in it the capitol is evacuated and the media freaks out and starts screaming “terrorists.”

However, right over their heads, hundreds of tons of nano aluminum and barium are being sprayed on them daily and yet nobody seems to care.

Yesterday I heard Alex Jones start his broadcast by saying his throat hurt and his voice was messed up because of something in the air but he didn’t know what it was.

Just one hour before his show started I heard the world’s leading expert on the subject of chemtrailsand geoengineering (Dane Wiginton) conduct an interview and he sounded terrible too.

Alex often talks about what people will put up with. One of his ideas is to go door to door in Austin and ask homeowners if it would be OK to put cameras in their bedrooms and then record their responses.

Of course, no sane person would allow that yet they do allow the NSA and countless other agencies and private corporations to do exactly the same thing via their smart TVs and smart phones.

Here’s my idea. How would anyone from Infowars or any other patriot radio show like it if I cornered your kid somewhere, opened a can of bug spray and emptied the entire can on their face?

You probably wouldn’t like it too much and yet you tolerate the EXACT same thing to be done to your kids on a daily basis by Bill Gates and the rest of the geo-engineering fanatics.

How is this not the number one story in the world all day and every day? Has everyone in the alternative media lost their minds too? We know that nano sized particulate of aluminum is very harmful to the brain and is responsible for killing everything that lives and yet it is rarely discussed and very little effort is directed to exposing it and stopping it.

Don’t people understand that if we don’t stop this right now there will be nothing left to live and fight for?

They are turning the sky over the entire country white daily. I have saved these recent satellite images to illustrate just how much material they are dumping on us. The sprayers repeat the same pattern day after day with very few exceptions.

Satellite Images

Sunday morning (5/25/14)

Sunday afternoon (5/25/14)

Monday morning (5/26/14)

Monday afternoon

Tuesday morning (5/27/14)

Tuesday afternoon (5/27/14)

They typically spray heavily first thing in the morning and greet the sun as it rises. They then spray all day long following the sun as it crosses the sky. They then spray heavily in the west as the sun sets.

The aluminum and barium (blanketing us all day) dissipates and falls to the ground in the early evening. The planes then return to their bases to refuel, rearm and get ready for the next attack the next morning.

Unless all radio talk show hosts come together and put an end to this craziness called geo-engineering it is my opinion that all life on earth will die and the battle for the future of humanity will be lost.

Dane Wigington should be on every radio show at least once a week to cover the latest developments in the collapse of our ecosystem. It’s accelerating and nothing is being done to curtail these insane programs.

Source humansarefree

Lying Little Shit Hogg: SHOCK: David Hogg Changes Story, Wasn’t At School When Cruz Opened Fire By Peter D’Abrosca – Mar 26, 2018


SHOCK: David Hogg Changes Story, Wasn’t At School When Cruz Opened Fire
By Peter D’Abrosca – Mar 26, 2018

https://bigleaguepolitics.com/breaking-david-hogg-changes-story-wasnt-school-cruz-opened-fire/

In a not-yet-released CBS Documentary, David Hogg, Marjory Stoneman Douglas High School student who has become the face of the gun control movement, changes his entire story and admits that he was not at the school during the event.

In a Time interview done within hours of the shooting Hogg recounted, “Our first response was ‘that sounded a lot like a gun shot’ and we closed the door.” Hogg claimed that he was in his AP enviromental science class during the shooting. He also made videos of himself and other students, regarding gun control, purportedly while the shooting was going on.

But CBS News has released some transcripts from its “39 Days” documentary, in which student David Hogg is quoted.

“On the day of the shooting, I got my camera and got on my bike and rode as fast as I could three miles from my house to the school to get as much video and to get as many interviews as I could because I knew that this could not be another mass shooting,” Hogg said in his CBS News interview.

The shooting occurred in the afternoon, after alleged shooter Nikolas Cruz was dropped off after 2 PM.

“While I was in there, I thought, ‘What impact have I had? What will my story be if I die here? And the only thing I could think of was, pull out my camera and try telling others. As a student journalist, as an aspiring journalist, that’s all I could think: Get other people’s stories on tape. If we all die, the camera survives, and that’s how we get the message out there, about how we want change to be brought about,” Hogg recalled.


Watch David Hogg tell two different stories below:

Interesting. However, Hogg made some videos purportedly DURING the shooting from inside the school.

Here is Hogg’s interview with TIME magazine following the shooting in which he claimed that he was in his AP environmental science class at the time the shooting occured:

When Hogg heard a “pop” while sitting in an AP environmental science class around 2:30 p.m. Wednesday, he told his teacher it sounded strangely like a gunshot. But there had been a fire drill that very morning and talk of a “Code Red” exercise to prepare for an active shooter. This must just be a surprise drill, he reasoned.

And then the fire alarm sounded. Dutifully acting on it, Hogg and other students tried to exit the building. A janitor—Hogg doesn’t know his name but calls him an angel—knew where the shots were coming from and sent the students back. Then a culinary arts teacher, Ashley Kurth, pulled Hogg and others inside, locked the door, and made them hide in a closet. Checking Twitter and Instagram, Hogg—who’s an editor at the school’s TV station—found the news that the shooting was real and ongoing.

The shots continued for what felt like an eternity. Hogg considered the possibility that he would not live to see the end of the day.

“While I was in there, I thought, ‘What impact have I had? What will my story be if I die here?’” Hogg told TIME in the hours following the ordeal. “And the only thing I could think of was, pull out my camera and try telling others. As a student journalist, as an aspiring journalist, that’s all I could think: Get other people’s stories on tape. If we all die, the camera survives, and that’s how we get the message out there, about how we want change to be brought about.”

Pretty big contradiction there.

Here is some of “student reporter” David Hogg’s interviews with his classmates, purportedly during the shooting. By the way, there is no way Hogg could have gotten into the school during the shooting, because the Broward County Sheriff’s Office set up a perimeter around the school during the shooting, all the while refusing to enter the school to stop the bloodshed.

Here is Hogg claiming to be inside the school during the shooting.

Here are Hogg’s interviews with his classmates, purportedly during the shooting:

Sheriff Scott Israel’s Broward County Sheriff’s Office made a concerted effort to not enter the Parkland high school during February’s mass shooting, instead allowing the shooting to happen.

The mainstream media is finally reporting on police and emergency scanner audio tapes that show the full extent of the Sheriff’s Office’s complicity in the horror at Marjory Stoneman Douglas High School.

“Do not approach the 12 or 1300 building, stay at least 500 feet away,” Sheriff’s Office deputy Scot Peterson said over radio dispatch, disproving his claim that he didn’t go inside the school because he was ordered not to do so if he didn’t have body cameras on. School surveillance footage has still not been released, and is unlikely to ever be released.

Big League Politics first reported on audiotapes showing that the Sheriff’s Office set up a perimeter around the high school during the shooting, after learning that multiple people were shot dead inside the high school. The police dispatcher ordered police to “hold all perimeters” while the shooter was still at large. Thirty minutes after learning of the active shooter situation, the Sheriff’s Office was still holding its perimeter and dispatchers were reporting “The shooter is not down. The shooter is not down.”

Our reporting proved that Israel’s office lied by claiming that they only set up a perimeter around the school AFTER the shooting, not during the shooting. In fact, they set up a perimeter four minutes after learning that people were shot dead inside.

Don’t You Take Anything That Big Pharma Isn’t Making Money On. Next they will be putting people into jail for using homeopathic medications.



(Chamille White/Shutterstock.com)

FDA Is Taking a More Aggressive Stance Toward Homeopathic Drugs
https://www.sciencealert.com/fda-takes-more-aggressive-stance-toward-homeopathic-drugs?perpetual=yes&limitstart=1

“Just silly from a scientific point of view.”
LAURIE MCGINLEY, THE WASHINGTON POST
19 DEC 2017

The US Food and Drug Administration (FDA) on Monday proposed a tougher enforcement policy toward homeopathic drugs, saying it would target products posing the greatest safety risks, including those containing potentially harmful ingredients or being marketed for cancer, heart disease and opioid and alcohol addictions.

Homeopathy is based on an 18th-century idea that substances that cause disease symptoms can, in very small doses, cure the same symptoms.

Modern medicine, backed up by numerous studies, has disproved the central tenets of homeopathy and shown that the products are worthless at best and harmful at worst.

Under US law, homeopathic drugs are required to meet the same approval rules as other drugs. But under a policy adopted in 1988, the agency has used “enforcement discretion” to allow the items to be manufactured and distributed without FDA approval.

Agency officials don’t plan to begin requiring that homeopathic products get approval – officials say that would be impractical – but they are signalling stepped-up scrutiny for items deemed a possible health threat.

Examples of high-risk products include ones that are administered by injection, are intended for vulnerable populations like children or the elderly, or are marketed for serious diseases, the agency said.

The FDA’s proposed approach, outlined in a draft guidance that will be open for public for 90 days, comes more than a year after homeopathic teething tablets and gels containing belladonna were linked to 400 injuries and the deaths of 10 children.

An FDA lab analysis later confirmed that some of the products “contained elevated and inconsistent levels of belladonna”, a toxic substance, the agency said.

Once a niche field, homeopathy has grown into to a US$3 billion industry that peddles treatments for everything from cancer to colds, FDA Commissioner Scott Gottlieb noted in a statement.

“In many cases, people may be placing their trust and money in therapies that may bring little or no benefit in combating serious ailments, or worse – that may cause significant and even irreparable harm” because of poor manufacturing quality or unsafe ingredients, he said.

Still, he said, the agency wants to balance its safety concerns with the desires of consumers who want to continue using the products.

Under its planned approach, many products won’t be considered high risk and will remain available to consumers, Janet Woodcock, director of the FDA’s Center for Drug Evaluation and Research, told reporters during a teleconference.

But she said, the agency would “go after” products that cause – or might cause – “overt harm”.

The National Center for Homeopathy, which advocates for homeopathy and is based in Mount Laurel, NJ, says on its website that “homeopathy is a safe, gentle, and natural system of healing that works with your body to relieve symptoms, restore itself, and improve your overall health.”

Steven Salzberg, a biomedical engineer at Johns Hopkins University who in the past has criticised the FDA for not taking action against homeopathy, said it was “terrific” that the agency now plans to try to rein in the industry.

He cautioned that product makers are likely to “hit back hard with lots of spurious claims in an effort to confuse consumers and to protect their profits.”

Salzberg added that homeopathic products’ packaging suggests that the items “cure all sorts of conditions – pain, colds, asthma, indigestion, arthritis, you name it – and yet there’s not a whit of evidence” that they cure anything.

The homeopathy field, he said, is “just silly from a scientific point of view, more like a religious belief than a scientific belief.”

In July, Britain’s National Health System announced plans to stop doctors from prescribing homeopathic drugs. Simon Stevens, the system’s chief executive, described homeopathy as “at best a placebo and a misuse of scarce NHS funds”.

The move came years after the House of Commons called on the government health service to stop paying for homeopathic prescriptions, saying, “To maintain patient trust, choice and safety, the Government should not endorse the use of placebo treatments, including homeopathy.”

In April 2015, the FDA held public hearings on the way it regulates homeopathic products as part of an effort to get public input on its enforcement polices.

The agency said Monday that as a result of the hearing and 9,000 comments submitted by the public, the FDA had decided to propose a new “comprehensive, risk-based enforcement approach to drug products labelled as homeopathic and marketed without FDA approval.”

Over the past several years, the FDA has issued warnings about other homeopathic drug products, including zinc-containing intranasal products that may cause a loss of sense of smell; certain homeopathic asthma products that have not been effective in treating asthma and other products that contain strychnine, a poison used to kill rodents.

2017 © The Washington Post

This article was originally published by The Washington Post.

Nuclear waste “piling up at bottom” — Lava-like material has spread all over… “hanging like icicles” — Mystery orange substance seen


Expert: Melted fuel found at Fukushima — Corium up to 6 feet thick below reactor — Nuclear waste “piling up at bottom” — Lava-like material has spread all over… “hanging like icicles” — Mystery orange substance seen (VIDEO)

 
Published: July 24th, 2017 at 3:52 pm ET
By

1,263 comments

Kyodo, Jul 22, 2017 (emphasis added): In big step forward, Tepco finds melted fuel at bottom of reactor 3 in Fukushima… The debris was clearly identifiable to at least one nuclear expert. “The images that appear to be melted fuel debris match those found in the (1986) Chernobyl crisis,” said Tadashi Narabayashi, a specially appointed professor of nuclear engineering working at Hokkaido University. “It’s definitely fuel debris… It’s an epoch-making event.”

New York Daily News, Jul 22, 2017: Underwater robot captures images of melted fuel at wrecked Fukushima nuclear plant — An underwater robot captured photos of 3-foot thick lumps of melted nuclear fuel covering the floor

Sky News, Jul 24, 2017: Melted nuclear fuel spotted in Fukushima reactor — The radioactive material has been spotted and pictured by a submersible robot…

CNN, Jul 24, 2017: [The robot] has revealed appears to be stalactites of melted nuclear fuel, [Tepco] said… the robot sent back 16 hours worth of images of massive, lava-like fuel deposits

AP, Jul 23, 2017: [Images] showed massive deposits believed to be melted nuclear fuel covering the floor

Asahi Shimbun, Jul 23, 2017: Melted nuke fuel images show struggle facing Fukushima plant — Images captured on July 22 of solidified nuclear fuel debris at the bottom of a containment vessel of the crippled Fukushima No. 1 nuclear power plant show the enormity of decommissioning of the facility… [TEPCO] also discovered that the nuclear fuel debris has spread throughout the containment vessel.

AP, Jul 22, 2017: [TEPCO] said the robot found large amounts of lava-like debris apparently containing fuel that had flowed out of the core… TEPCO spokesman Takahiro Kimoto said it was the first time a robot camera has captured what is believed to be the melted fuel. “That debris has apparently fallen from somewhere higher above. We believe it is highly likely to be melted fuel or something mixed with it,” Kimoto said…

Kyodo, Jul 23, 2017: The robot was sent closer to the bottom of the reactor on Saturday and found possible fuel debris scattered in a wide area.

Japan Times, Jul 21, 2017: Fukushima robot finds potential fuel debris hanging like icicles in reactor 3… The objects spotted this time look like icicles… Tepco is pinning its efforts on technology not yet invented to get the melted fuel out of the reactors.

Reuters, Jul 21, 2017: Tepco detected black-colored material that dangled like icicles that could be nuclear debris near the bottom of the reactor’s pressure vessel that contained the fuel rods, the report said, citing unnamed sources.

Bloomberg, Jul 21, 2017: New images show what is likely to be melted nuclear fuel hanging from inside one of Japan’s wrecked Fukushima reactors… [Tepco] released images on Friday showing a hardened black, grey and orange substance

Financial Times, Jul 24, 2017: [Kimoto] was reluctant to speculate on the nature of seemingly corroded orange patches in the images.

NHK, Jul 23, 2017: [TEPCO] says Saturday’s probe found lumps that are highly likely to be fuel debris piling up at the bottom of the containment vessel… The deposits are estimated to be one to two meters thick. Images released on Saturday show black, rock-like lumps and what appear to be pebbles and sand accumulating at the bottom.

ENENews: “Nuclear Engineer: My biggest concern is Fukushima plant will collapse”



Nuclear Engineer: My biggest concern is Fukushima plant will collapse… Concrete under reactors is being “eaten away”… “There’s ongoing chemical attacks” — Containment structures are tilting, in jeopardy of falling over (AUDIO)
Published: March 17th, 2017 at 6:19 am ET
By ENENews
http://enenews.com/nuclear-engineer-my-biggest-concern-is-fukushima-plant-will-collapse-concrete-under-reactors-is-being-eaten-away-theres-ongoing-chemical-attacks-containment-structures-are-t?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+ENENews+%28Energy+News%29

KGO 810 AM, Feb 9, 2017 (at 9:15 in):
Pat Thurston, host (emphasis added): “There’s a story that’s going around the internet, Snopes says there’s nothing to verify that this is true — I guess Tepco is denying it — but there’s a story going around that the containment structure is in jeopardy — its tilting — it’s in jeopardy of falling over, so we’ll talk about that too — if that is even a possibility. Were that to happen, what would that mean?… First, to the issue of the potential for a collapse of the building — for the building to topple over — for it to somehow to collapse. Is that a thing? Can that happen?”

Arnie Gundersen, nuclear engineer: “Yeah, it can happen — and that’s my biggest concern. Tepco is building a wall along the ocean… it’s trapping all this groundwater onsite, and essentially making the ground mushy… There’s already significant damage [to the reactor buildings] — the entire coast of Japan dropped three feet during that earthquake and never rebounded… But the Fukushima site didn’t fall straight, it fell at an angle, it’s about a two inch incline across the site now. So the buildings are in mushy ground and they’re not quite straight. The other part is that there’s a toxic brew of radioactive chemicals inside there, but there’s also just chemicals – they’re eating away at the concrete and they’re eating away at the steel. It’s a nasty chemical broth inside these plants. My fear is that if there’s a Richter 7 quake, not the Richter 9 that happened 6 years ago, if there’s a Richter 7 quake on that site it could breach those containments… The horse is out of the barn at that point… (discussion continues at 32:00 in) On toppling over… probably half the concrete inside the containment that was originally there has been eaten away by the hot radioactive fuel — and there’s ongoing chemical attacks — so I really think the concrete under the containment is pretty darn punky [“resembling punk in being soft or rotted”] right now, and is getting punkier as time goes on.”