Paul J. Rosch

Lack of an association or an inverse association between low-density-lipoprotein cholesterol and mortality in the elderly: a systematic review

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.

Bioelectromagnetic and subtle energy medicine: the interface between mind and matter.

The concept of a “life energy” can be found in many cultures in the present time, as well as in past eras reaching back to the ancients. Variously called qi (chi), ki, the “four humors,”prana, “archaeus,”“cosmic aether,”“universal fluid,”“animal magnetism,” and “odic force,” among other names, this purported biofield is beginning to yield its properties and interactions to the scientific method. Subtle energy is the term used in this chapter, which traces the recent history of subtle energy studies from Harold Saxton Burr and Björn Nordenström to Jim Oschman and Jacques Benveniste. This work takes signaling in living systems from the chemical/molecular to the physical/atomic level of communication. Effects on heart rate variability, stress response, inflammation, and the vagus nerve have been demonstrated and raise the question ‐ Can the power of subtle energies be harnessed for health enhancement? It is fully accepted that good health depends on good communication both within the organism and between the organism and its environment. Sophisticated imaging procedures brought to bear on telomere, stem cell, and genetic research are confirming the ability of meditation and some other traditional practices to promote optimal health through stress reduction.

Statins Do Not Protect Against Cancer: Quite the Opposite

TO THE EDITOR: In their cohort study of statin-treated patients and nontreated controls, Cardwell et al concluded that statin treatment may prevent colorectal cancer. However, there are significant flaws in their study. At least nine studies have shown that cancer is associated with low cholesterol, measured 10 to 30 years before diagnosis. Because most patients receiving statin treatment have lived most of their lives with high cholesterol, risk for cancer mortality might have been lower even without statin treatment compared with the untreated cohort with normal or low cholesterol. A similar study by Nielsen et al supports this interpretation, because mortality was lowest among those who were treated with the lowest statin dose. Furthermore, adherence to statins is low, particularly when prescribed for primary prevention. In a Canadian study including 85,000 patients, 75% had stopped the treatment at 2-year follow-up. To claim that statin treatment protects against cancer is therefore impossible with the method used by Caldwell et al. Instead, cancer mortality should be related to the achieved lipid values, as reported by Matsuzaki et al, who administered simvastatin 5 to 10 mg per day to 47,000 patients. After 6 years, cancer mortality was 3 higher in patients whose total cholesterol was 160 mg/dL compared with those whose cholesterol was normal or high (P .001). In fact, evidence that statin treatment may cause cancer is much stronger. Several cholesterol-lowering drugs, including statins, have been found to be carcinogenic in rodents in doses that produce blood concentrations of the drugs similar to those attained in treating patients. In accordance, breast cancer occurred in 12 of 286 women in the treatment group of the CARE (Cholesterol and Recurrent Events) trial, but only in one of 290 in the placebo group (P .002). In the PROSPER (Prospective Study of Pravastatin in the Elderly at Risk) trial, cancer occurred in 245 of 2,891 patients in the treatment group, but only in 199 of 2,913 in the placebo group (P .02). In the SEAS (Simvastatin and Ezetimibe in Aortic Stenosis) trial, cancer occurred in 39 of 944 patients in the treatment group, but only in 23 of 929 in the placebo group (P .05). In the two first simvastatin trials, nonmelanoma skin cancer was seen more often as well, and with statistical significance if the results are calculated together (256 of 12,454 v 208 of 12,459; P .028). The latter finding may explain the current so-called epidemic of nonmelanoma skin cancer. Several case-control studies have also shown that patients with cancer have been treated with statins significantly more frequently than controls without cancer matched for age and sex. Furthermore, a recent study showed that 10 years of statin therapy increased women’s risk of invasive ductal carcinoma by 83% and their risk of invasive lobular carcinoma of the breast by 97%. An apparent contradiction is that meta-analyses of the statin trials have found no increase of cancer. However, since the publication of the HPS (Heart Protection Study) trial, the number of nonmelanoma skin cancers—the easiest malignancies to detect early—has not been reported in any trial. Furthermore, it may take 10 to 20 years before exposure to carcinogenic chemicals results in cancer. Bronchial cancer, for instance, does not appear until after 10 years of smoking, and the length of almost all the statin trials has only been 5 years at most. As noted, it may be that statins per se are not carcinogenic but rather that this adverse effect results from their ability to lower blood lipids. More than a dozen research groups have documented that lipoproteins, particularly LDL, partake in the immune system by binding and inactivating all kinds of microorganisms and their toxic products. Because certain microorganisms have been incriminated as a possible cause of different malignancies, including colorectal cancer, it is difficult to understand how lowering LDL cholesterol could prevent cancer. Association never proves causation. Although it may be difficult to prove that statins can cause or prevent cancer, the preponderance of evidence favors the former.

Cholesterol does not cause coronary heart disease in contrast to stress

The belief that coronary atherosclerosis is due to high cholesterol from increased saturated fat intake originated from experiments in herbivorous animals. It was reinforced by reports allegedly demonstrating this sequence of events in various populations but ignoring contradictory data. The idea has been perpetuated by powerful forces using similar tactics to preserve the profit and the reputations of those who promote this doctrine. Opponents find it difficult to publish their scientifically supported opinions. The advent of statins has further fuelled this fallacious lipid hypothesis, despite compelling evidence that their effect is not due to cholesterol lowering and that serious side effects have been suppressed and alleged benefits have been hyped. The adverse effects of the cholesterol campaign on health, quality of life, the economy and medical research are inestimable. It is imperative that public health officials, physicians and patients are apprised of proof that it is misguided, malicious and malignant.

Genes and stress cause coronary atherosclerosis not saturated fat

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Could proton pump inhibitors cause cancer

Response to: Wilhelm SM, Rjater RG, Kale-Pradhan PB. Perils and pitfalls of long-term effects of proton pump inhibitors. Expert Rev. Clin. Pharmacol. 6(4), 443–451 (2013).

The cholesterol hypothesis: time for the obituary?

Abstract The cholesterol hypothesis links cholesterol intake and blood levels to cardiovascular disease. It has had enormous impact on health care and society during decades, but has little or no scientific backing that is relevant for the human species. Apparently, the hypothesis is false and should be buried.

LDL-C Does Not Cause Cardiovascular Disease: a comprehensive review of current literature

ABSTRACT Introduction: For half a century, a high level of total cholesterol (TC) or low-density lipoprotein cholesterol (LDL-C) has been considered to be the major cause of atherosclerosis and cardiovascular disease (CVD), and statin treatment has been widely promoted for cardiovascular prevention. However, there is an increasing understanding that the mechanisms are more complicated and that statin treatment, in particular when used as primary prevention, is of doubtful benefit. Areas covered: The authors of three large reviews recently published by statin advocates have attempted to validate the current dogma. This article delineates the serious errors in these three reviews as well as other obvious falsifications of the cholesterol hypothesis. Expert commentary: Our search for falsifications of the cholesterol hypothesis confirms that it is unable to satisfy any of the Bradford Hill criteria for causality and that the conclusions of the authors of the three reviews are based on misleading statistics, exclusion of unsuccessful trials and by ignoring numerous contradictory observations.