We Spent a Million Bucks and Then We Had To Do Something

2011 ◽  
Vol 31 (6) ◽  
pp. 460-471 ◽  
Author(s):  
David Schleifer

Many scholars assume that industry meddles in scientific research in order to defend their products. But this article shows that industry meddling in science can have a variety of consequences. American food manufacturers long denied that trans fats were associated with disease. Academic scientists, government scientists, and activists in fact endorsed trans fats as a healthier alternative to saturated fats. But in 1990, a high-profile study showed that trans fats increased risk factors for heart disease more than saturated fats did. Industry funded a U.S. Department of Agriculture study that they hoped would exonerate trans fats. But the industry-funded U.S. Department of Agriculture study also indicated that trans fats increased risk factors for heart disease more than saturated fats. Industry quickly began developing trans fat alternatives. This confirms that corporations get involved in science in order to defend their products. But involvement in science can be the very means by which corporations persuade themselves to change their products.

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Piotr Bandosz ◽  
Maria Guzman-Castillo ◽  
Simon Capewell ◽  
Tomasz Zdrojewski ◽  
Julia Critchley ◽  
...  

Background: Poland has experienced one of the most dramatic declines in coronary heart disease (CHD) mortality rates in recent decades. This decline reflects the use of evidence based treatments and, crucially, population wide changes in diet. Our aim is to explore the potential for further gains in Poland by achieving population wide reductions in smoking, dietary salt and saturated fat intake and physical inactivity levels. Methods: A validated and updated policy model was used to forecast potential decreases in CHD deaths by 2020 as consequence of lifestyle and dietary changes in the population. Data from the most recent Polish risk factor survey was used for the baseline (2011). We modeled two different policy scenarios regarding possible future changes in risk factors: A) conservative scenario: reduction of smoking prevalence and physically inactivity rates by 5% between 2011 and 2020, and reduction of dietary consumption of energy from saturated fats by 1% and of salt by 10%. B) ideal scenario: reduction of smoking and physically inactivity prevalence by 15%, and dietary reduction of energy from saturated fats by 3% and of salt by 30%. We also conducted extensive sensitivity analysis using different counterfactual scenarios of future mortality trends. Results: Baseline scenarios. By assuming continuing declines in mortality and no future improvements in risk factors the predicted number of CHD deaths in 2020 would be approximately 13,600 (9,838-18,184) while if mortality rates remain stable, the predicted number of deaths would approximate 22,200 (17,792-26,688). Conservative scenario. Assuming continuing declines in mortality, small changes in risk factors could result in approximately 1,500 (688-2,940) fewer deaths. This corresponds to a 11% mortality reduction. Under the ideal scenario, our model predicted some 4,600 (2,048-8,701) fewer deaths (a 34% mortality reduction). Reduction in smoking prevalence by 5% (conservative scenario) or 15% (ideal scenario) could result in mortality reductions of 4.5% and 13.8% respectively. Decreases in salt intake by 10% or 30% might reduce CHD deaths by 3.0% and 8.6% respectively. Replacing 1% or 3% of dietary saturated fats by poly-unsaturates could reduce CHD deaths by 2.6% or 7.7% Lowering the prevalence of physically inactive people by 5%-15% could decrease CHD deaths by 1.2%-3.7%. Conclusion: Small and eminently feasible population reductions in lifestyle related risk factors could substantially decrease future number of CHD deaths in Poland, thus consolidating the earlier gains.


Hematology ◽  
2016 ◽  
Vol 2016 (1) ◽  
pp. 323-330 ◽  
Author(s):  
Flora E. van Leeuwen ◽  
Andrea K. Ng

Abstract Long-term survivors of Hodgkin lymphoma (HL) experience several late adverse effects of treatment, with second malignant neoplasms (SMNs) and cardiovascular diseases (CVDs) being the leading causes of death in these patients. Other late effects have also been identified, such as pulmonary dysfunction, endocrinopathies (thyroid dysfunction, infertility), neck muscle atrophy, and persistent fatigue. HL survivors have two- to fourfold increased risks to develop SMNs and CVD compared with the general population. With respect to SMNs, radiotherapy is associated with 1.5- to 15-fold increased risk of solid malignancies. The relative risk (RR) of solid tumors increases steadily with increasing follow-up time from 5 to 15 years since radiotherapy, and remains elevated for at least 40 years. The RR of solid SMNs increases strongly with younger age at first treatment. Risks of lung, breast, and gastrointestinal (GI) cancers increase with higher radiation dose. Alkylating agent chemotherapy, especially procarbazine, does not only increase risk of leukemia but also of solid malignancies, in particular, cancers of the lung and GI tract. In contrast, gonadotoxic chemotherapy decreases the risk of radiation-associated breast cancer, through induction of premature menopause. Smoking appears to multiply the radiation- and chemotherapy-associated risks of lung cancer. Both radiotherapy and chemotherapy for HL may cause cardiovascular toxicity. Radiotherapy increases the risk of coronary heart disease, valvular heart disease, congestive heart failure (HF), and pericarditis, whereas anthracycline-containing chemotherapy increases the risks of HF and valvular heart disease. Cardiovascular toxicity following radiotherapy is usually observed from 5 to at least 35 years after therapy, whereas anthracycline-related toxicity is already observed during treatment, up to at least 25 years. The joint effects of anthracyclines, radiotherapy, and conventional cardiovascular risk factors (eg, hypertension, smoking, and physical inactivity) appear to be additive rather than multiplicative. HL survivors need lifelong risk-based screening for selected SMNs and CVDs. Furthermore, preventive strategies should include lifestyle and drug-based interventions to minimize exposure to conventional risk factors for cancer and CVD.


1995 ◽  
Vol 41 (10) ◽  
pp. 1504-1508 ◽  
Author(s):  
L H Breimer ◽  
G Wannamethee ◽  
S Ebrahim ◽  
A G Shaper

Abstract The possibility that low concentrations of serum bilirubin may be associated with increased risk of ischemic heart disease has been examined in a prospective study of 7685 middle-aged British men. During 11.5 years there were 737 major ischemic heart disease (IHD) events. A U-shaped relationship was observed between serum bilirubin and risk of IHD. Low bilirubin was associated with several cardiovascular risk factors, in particular smoking, low concentrations of high-density lipoprotein cholesterol, low forced expiratory volume in 1 s, and low serum albumin. The U-shaped relationship persisted even after adjusting for several risk factors. Compared with men in the lowest fifth of the distribution (bilirubin < 7 mumol/L), those in the middle range (8-9 mumol/L) showed a 30% reduction in relative risk [RR = 0.68 (95% confidence intervals 0.51-0.89)] in IHD, whereas men in the top fifth (> 12 mumol/L) showed similar risk to the lowest fifth [RR = 0.99 (95% confidence intervals 0.73-1.34)], which persisted after exclusion of men with bilirubin > 17 mumol/L. The significance of this U-shaped relationship is unclear, but it could be interpreted as support for the role of endogenous antioxidants in the etiology of IHD.


Author(s):  
Daein Choi ◽  
Sungjun Choi ◽  
Seulggie Choi ◽  
Sang Min Park ◽  
Hyun‐Sun Yoon

Background There is emerging evidence that rosacea, a chronic cutaneous inflammatory disease, is associated with various systemic diseases. However, its association with cardiovascular disease (CVD) remains controversial. We aimed to investigate whether patients with rosacea are at increased risk of developing CVD. Methods and Results This retrospective cohort study from the Korean National Health Insurance Service‐Health Screening Cohort included patients with newly diagnosed rosacea (n=2681) and age‐, sex‐, and index year–matched reference populations without rosacea (n=26 810) between 2003 and 2014. The primary outcome was subsequent CVD including coronary heart disease and stroke. Multivariable Cox regression analyses were used to evaluate adjusted hazard ratios for subsequent CVD adjusted for major risk factors of CVD. Compared with the reference population (13 410 women; mean [SD] age, 57.7 [9.2] years), patients with rosacea (1341 women; mean [SD] age, 57.7 [9.2] years) displayed an increased risk for CVD (adjusted hazard ratios, 1.20; 95% CI, 1.03–1.40) and coronary heart disease (adjusted hazard ratios, 1.29; 95% CI, 1.05–1.60). The risk for stroke was not significantly elevated (adjusted hazard ratios, 1.12; 95% CI, 0.91–1.37). Conclusions This study suggests that patients with rosacea are more likely to develop subsequent CVD. Proper education for patients with rosacea to manage other modifiable risk factors of CVD along with rosacea is needed.


1997 ◽  
Vol 77 (04) ◽  
pp. 697-700 ◽  
Author(s):  
Jacek Musiał ◽  
Andrzej Pająk ◽  
Anetta undas ◽  
Ewa Kawalec ◽  
Roman Topór-Mądry ◽  
...  

SummaryThrombosis plays a major role in the development of atherosclerosis and its acute vascular complications. Epidemiological studies have shown that elevated levels of plasma fibrinogen are associated with an increased risk of coronary heart disease (CHD). It is not clear whether this association is linked to hemostatic functions of fibrinogen which serves as a substrate for thrombin. Generation of thrombin in vivo can be evaluated by measurement of its specific markers in plasma, i.e. thrombin-antithrombin III complex (TAT) and prothrombin fragment 1+2 (F1+2). We determined plasma levels of TAT and F1+2 in a population sample of southeastern Poland and evaluated relations of these markers with plasma fibrinogen, factor VII coagulant activity (FVIIc), and other known CHD risk factors. The population studied consisted of 215 men and 251 women, aged 43-75 years. Final analysis was performed on 195 men and 222 women.The distribution of plasma TAT and F1+2 concentrations were highly skewed with the higher median values for women than for men. Log values of TAT correlated with log values of F1+2 in men (r = 0.27, p <0.01) and in women (r = 0.15, p <0.05). In the regression analysis both markers were positively related to age in women but not in men. After adjustment to age there was a positive relation between TAT and fibrinogen in both sexes. In women, but not in men, F1+2 showed a positive association with FVIIc. Total plasma cholesterol was negatively related to TAT in women only. There was no association between thrombin generation markers and plasma triglycerides, HDL-choles- terol, LDL-cholesterol, blood pressure, cigarette smoking and body mass index (BMI).The association of plasma fibrinogen and FVIIc with thrombin generation markers points to an important role of the hemostatic system in the pathogenesis of atherosclerosis and coronary heart disease in humans.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
G Gill ◽  
S Fernandez ◽  
M Soud ◽  
M Mete ◽  
N Malhotra ◽  
...  

Abstract Introduction Traditional risk factors for coronary heart disease have been reported in around 85% patients who present with myocardial infarction. More recently, inflammation and immune mediated diseases have been associated with ischemic heart disease. Inflammatory Bowel Disease (IBD) is an immune mediated disorder which comprises of ulcerative colitis and Crohn's disease. Estimated prevalence of IBD in the United States in 2004 was 1.4 million people. These patients have an overall increased risk of thrombotic complications with microvascular thrombosis hypothesized to contribute in disease pathogenesis. Results from a recent meta-analysis were consistent with increased risk of ischemic heart disease among IBD patients, with risk greater in females and younger patients, although heterogeneity was considerable in overall data. Also, in a recent study, IBD was found to be associated with an increased risk of acute myocardial infarction and heart failure despite lower prevalence of coronary risk factors in IBD patients. IBD pathogenesis involves sustained activation of immune responses with upregulation of cytokines including but not limited to IL-1 beta, IL-6 and TNF-alpha. Upregulation of these cytokines has also been reported in coronary atherosclerosis. Based on above information, we explored incidence of MACE (Major Adverse Cardiac Event) in this patient population from our health system data-base. Methods Propensity scores were estimated for all 15,292 (0.4%) patients with inflammatory bowel disease from a total patient pool of 3,917,894 patients in our health system to assemble a 1:1 matched cohort balanced for age, gender, race and known cardiovascular risk factors including hypertension, hyperlipidemia, diabetes mellitus and smoking (current and former). ICD-9 and ICD-10 codes were used to identify cardiovascular risk factors and outcomes. Results Matched patients (n=30,584) had a mean age of 51 years, with 58% of all being women, and 63% Caucasian. During the median follow up of 4.4 years all-cause mortality was observed in 1.7% and 1.2% of patients from IBD and non-IBD groups respectively (hazard ratio {HR}, 1.31; 95% confidence interval {CI}, 1.08–1.58; p=0.005). Combined outcome for myocardial infarction or all-cause mortality was noted in 4.1% and 3.4% from IBD and non-IBD groups respectively (HR, 1.16; 95% CI, 1.03–1.30; p=0.014) while HRs for cardiovascular mortality, myocardial infarction and unstable angina independently were 1.04 (0.74–1.47; p=0.833), 1.05 (0.89–1.23; p=0.591) and 1.10 (0.83–1.46; p=0.524) respectively. Conclusion Inflammatory bowel disease did not show association with myocardial infarction, cardiovascular mortality or unstable angina when matched for known cardiovascular risk factors, but was associated with increased all-cause mortality and combined end-point of all-cause mortality or myocardial infarction.


2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 10082-10082
Author(s):  
Talya Salz ◽  
Emily Craig Zabor ◽  
Peter de Nully Brown ◽  
Susanne Oksbjerg Dalton ◽  
Nirupa Jaya Raghunathan ◽  
...  

10082 Background: Increased risk of myocardial infarction (MI) and cerebrovascular accident (CVA) among NHL survivors is commonly attributed to NHL treatment. The extent to which pre-existing CV risk factors also contribute to increased risk is unknown. We investigated this association among an entire national population of NHL survivors who have a full range of important CV risk factors. Methods: Using Danish population-based registries, we identified all adults diagnosed with primary aggressive NHL from 2000-2010 and followed them for MI and CVA from 9 months after diagnosis through 2012. MI and CVA diagnoses were ascertained from the nationwide Hospital Discharge Register and Cause of Death Register. CV risk factors (hypertension, dyslipidemia, and diabetes), vascular disease, and intrinsic heart disease prevalent at NHL diagnosis were ascertained algorithmically using the National Prescription Register and the Hospital Discharge Register. Cumulative anthracycline dose was coded continuously. Receipt of radiation was coded dichotomously for both chest and neck. Controlling for age, sex, treatment, and CV diseases, we used Cox multivariate regression to test the association between pre-existing CV risk factors and subsequent CVA or MI. Results: Among 2604 patients with NHL, median age was 62, and median follow-up time was 2.4 years. Overall, 131 patients were diagnosed with MI or CVA. Before NHL diagnosis, 40% of patients had at ≥1 CV risk factor, 13% had vascular disease, and 6% had intrinsic heart disease. 90% of the patients were treated with anthracyclines, 9% had received chest radiation, and 15% had received neck radiation. Patients with ≥1 CV risk factor had an increased risk of MI or CVA compared to patients with none (HR = 1.5 [95% CI = 1.1-2.2). Prevalent vascular disease, prevalent intrinsic heart disease, and NHL treatment were not associated with MI or CVA (p’s > 0.05). Conclusions: In a large, well-characterized, and nationally representative cohort of NHL survivors, prevalent CV risk factors were associated with later CVA and MI. To prevent MI and CVA among survivors, decisions about post-treatment monitoring should take into account prevalent CV risk.


Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Eric L Ding ◽  
Katerina M De Vito ◽  
Hongyu Wu ◽  
Qi Sun ◽  
An Pan ◽  
...  

Introduction: Studies indicate dietary types of fats are associated with risk of coronary heart disease (CHD). Traditional broad classifications may incompletely capture the diversity of fatty acids on CHD. The novel lipid index Dietary Lipophilic Load (DLL) reflects a unique combination of fatty acid fluidity, intermolecular attraction, plus relative fat quantity, while Dietary Lipophilic Index (DLI) is a measure of average fat fluidity, regardless of fat quantity. Thus, we evaluated the association, DLL and DLI, with risk of incident CHD. METHODS: Participants included 30,932 women in the Women’s Health Study (WHS), who were free of major chronic diseases at baseline. DLL was calculated by weighted summation of the multiplicative product of each fatty acid’s intakes (g/day) and its melting points (Celcius); DLI was calculated by dividing DLL by total fat intake (g/day). Hazard ratios (HRs) were adjusted for established risk factors, with updated dietary data, and potential mediators. We also investigated hypothesized interactions with C-Reactive Protein (CRP). RESULTS: There were 1137 cases of incident CHD in 525,828 person-years over 19 years follow-up. At baseline in over 27,000 women with blood samples, DLL and DLI were not correlated with serum cholesterol, triglyceride, HbA1c, ICAM-1, or CRP biomarkers (r<0.02 for all). In overall multivariate analysis, DLL was associated with higher risk of CHD (extreme quintile HR=1.40, 95%CI: 1.11-1.76, P trend=0.0002), while DLI was not (HR=0.83, 95%CI: 0.67-1.03, P trend=0.75). DLL results were independent beyond adjustment for dietary trans, saturated, monounsaturated, and polyunsaturated fats, nor their aggregate adjustment or the P:S ratio. DLL effects persisted even adjusting for CRP (HR=1.29, P-trend=1 mg/dL for DLL (extreme quintile HR=1.38, 1.02-1.88), than among individuals with low CRP <1 mg/dl for DLL (HR=1.08, 0.68-1.72), with P-interaction<0.0001. Furthermore, CRP also modified DLI, where effects again diverged among higher CRP (HR=0.98, 0.73-1.31) versus low CRP (HR=0.45, 0.27-0.74), with P-interaction<0.0001. Moreover, adjustment of triglycerides, HbA1c, ICAM-1, LDL or HDL cholesterol also did not materially affect overall results. CONCLUSION: Results indicate that DLL is associated with increased risk of incident CHD, independent of traditional risk factors, conventional dietary fat classifications, and major CHD biomarkers. Effects of DLL and DLI appear to be modified by levels of CRP. DLL appears to be an important novel dietary fat index that captures additional CHD risk information beyond biomarkers and traditional dietary fat categories. Further studies are warranted.


1970 ◽  
Vol 19 (1-2) ◽  
pp. 243-247 ◽  
Author(s):  
M. Feinleib ◽  
R. J. Havlik ◽  
P. O. Kwiterovich ◽  
J. Tillotson ◽  
R. J. Garrison

During the past two decades prospective epidemiologic studies have established the association between several risk factors and coronary heart disease. Elevations of serum cholesterol and blood pressure, obesity, lack of physical activity and cigarette smoking are among the factors which have been related to an increased risk of heart disease. We are now entering a period in which vigorous efforts will be made to modify these factors in order to prevent the occurrence of heart disease. An important part of this effort will be to determine to what extent these factors are genetically controlled and to what extent they can be modified by manipulation of the individual environment. Recognizing this need, the Field Epidemiological Research Section, National Heart Institute, NIH, has recently embarked on a study of cardiovascular disease risk factors in a large sample of adult male twins. The purpose of the present report is to describe the protocol and methods to be used and the importance of this study to current research in cardiovascular disease.


Author(s):  
Martin Stagmo ◽  
Steen Juul-Möller ◽  
Bo Israelsson

Background Ambulatory electrocardiogram monitoring (Holter) with ST-analysis as a measure of myocardial ichemia has in populations with coronary heart disease been shown to predict major coronary events: death, myocardial infarction or coronary revascularization. There has, however, been conflicting evidence regarding the usefulness of this technique in identification of healthy subjects with increased risk for coronary heart disease. The aim of this study was to assess if Holter monitoring with ST-analysis could be used to predict future major coronary events in asymptomatic middle-aged men with a defined aggregation of traditional risk factors for coronary heart disease. Methods One hundred and fifty-five asymptomatic participants from the city of Malmö, Sweden, with known levels of conventional cardiovascular risk factors underwent Holter monitoring for analysis of transient ST-segment depression at the age of 55 years. Fifteen years after the Holter monitoring, hospital records, diagnosis and death registries were revisited for major coronary events. Results An ST-segment depression of 1 mm or greater (0.1 mV) was considered significant for myocardial ischemia and was found in 54 of the 155 men. There were no significant differences in risk factors in the two groups at baseline. The 15-year incidence of a first major coronary event was significantly higher in men with ST-segment depression (39%) than in men without ST-segment depression (20%) ( P < 0.015). A Holter electrocardiogram could predict future major coronary events with a positive and negative predictive value of 35 and 80%, respectively. Conclusions Holter monitoring can be used as a complement to conventional risk factor evaluation in deciding whether or not to treat risk factors for CHD in asymptomatic subjects.


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