Global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013: a systematic analysis for the Global Burden of Disease Study 2013.

BACKGROUND: In 2010, overweight and obesity were estimated to cause 3·4 million deaths, 3·9% of years of life lost, and 3·8% of disability-adjusted life-years (DALYs) worldwide. The rise in obesity has led to widespread calls for regular monitoring of changes in overweight and obesity prevalence in all populations. Comparable, up-to-date information about levels and trends is essential to quantify population health effects and to prompt decision makers to prioritise action. We estimate the global, regional, and national prevalence of overweight and obesity in children and adults during 1980-2013. METHODS: We systematically identified surveys, reports, and published studies (n=1769) that included data for height and weight, both through physical measurements and self-reports. We used mixed effects linear regression to correct for bias in self-reports. We obtained data for prevalence of obesity and overweight by age, sex, country, and year (n=19,244) with a spatiotemporal Gaussian process regression model to estimate prevalence with 95% uncertainty intervals (UIs). FINDINGS: Worldwide, the proportion of adults with a body-mass index (BMI) of 25 kg/m(2) or greater increased between 1980 and 2013 from 28·8% (95% UI 28·4-29·3) to 36·9% (36·3-37·4) in men, and from 29·8% (29·3-30·2) to 38·0% (37·5-38·5) in women. Prevalence has increased substantially in children and adolescents in developed countries; 23·8% (22·9-24·7) of boys and 22·6% (21·7-23·6) of girls were overweight or obese in 2013. The prevalence of overweight and obesity has also increased in children and adolescents in developing countries, from 8·1% (7·7-8·6) to 12·9% (12·3-13·5) in 2013 for boys and from 8·4% (8·1-8·8) to 13·4% (13·0-13·9) in girls. In adults, estimated prevalence of obesity exceeded 50% in men in Tonga and in women in Kuwait, Kiribati, Federated States of Micronesia, Libya, Qatar, Tonga, and Samoa. Since 2006, the increase in adult obesity in developed countries has slowed down. INTERPRETATION: Because of the established health risks and substantial increases in prevalence, obesity has become a major global health challenge. Not only is obesity increasing, but no national success stories have been reported in the past 33 years. Urgent global action and leadership is needed to help countries to more effectively intervene. FUNDING: Bill & Melinda Gates Foundation.

Connecting Climate Change Mitigation to Global Land Regeneration, Doubling Worldwide Livestock, and Reduction of Early Deaths from Noncommunicable Diseases.

Aim and background This article aims to link early deaths due to diet-related noncommunicable diseases at the global level, low animal food intake, primarily in developing countries, regenerative/organic agriculture, worldwide food security, and global warming mitigation. On statistically modeling Global Burden of Disease (GBD) risk factor and health outcome data, the unexpected finding was that early deaths (death before age 70) per year per 100k population due to noncommunicable diseases (NCDs, such as coronary artery disease, emphysema, liver failure, kidney failure, and cancers) were much higher in cohorts with low consumption of animal-sourced foods (processed meat, red meat, dairy, fish, poultry, eggs, and saturated fats). Relatively low NCD rates are associated with high animal food consumption. This unexpected finding led to exploring the implications of climate change. Methods I critiqued the Intergovernmental Panel on Climate Change's (IPCC's) definitions of "sustainability in land management, sustainable intensification (of agriculture), climate-smart agriculture," and "sustainability-focused socioeconomic pathway 1 (SSP1)"-the most climate-favorable scenario that the IPCC modeled. I modeled doubling the global livestock together with global regenerative/organic agriculture compared with the IPCC's SSP1, using the IPCC's mean 2010-2019 global anthropogenic greenhouse gas emissions (GHGs) as the baseline for comparison. Results This study found that all the IPCC's agricultural land-related definitions of interest were aspirational without detailing the farming methods used and those not allowed. The IPCC's land management-related definitions differed from the same or similar terms in the literature. The status quo net global agriculture and other land use GHGs (2010-2019) totaled 11.9 ± 4.4 gigatonnes (GT) carbon dioxide equivalent per year (11.9 ± 4.4 GTCO2-eq yr-1). The IPCC's modeling of the SSP1 scenario reduced GHGs to 3 GTCO2-eq yr-1 by 2050. Transitioning to global regenerative/organic agriculture (5 billion hectares) and doubling the global livestock for human consumption and agricultural land fertilization corresponded to net global GHGs = -24.1 GTCO2-eq yr-1 for 2-3 decades, totaling -482 to -723 GTCO2-eq of CO2 sequestration. Conclusions Doubling global livestock combined with worldwide regenerative/organic agriculture has the potential to mitigate climate change significantly more than SSP1 while providing global food security by reversing land degradation. Worldwide transitioning from intensive industrial agriculture that degrades land to regenerative/organic agriculture that sequesters CO2 in soil ​​​​​and doubling global livestock would require initial support with finances, resources, and additional workers for farms in both developing and developed countries. Subsequently, farms and farmers would be sustainably self-supporting with food sales. Retaining the existing farm workers and attracting hundreds of millions more workers would likely require transitioning most agricultural lands into worker-owned cooperatives.

The EAT-Lancet Commission's Planetary Health Diet Compared With the Institute for Health Metrics and Evaluation Global Burden of Disease Ecological Data Analysis.

Background This article aimed to compare the EAT-Lancet Commission's "Planetary Health Diet" (PHD) with the Institute for Health Metrics and Evaluation (IHME) Global Burden of Disease Study 1990-2017 (GBD2017) dietary and other risk factor data. In the PHD/GBD comparison, we also intended to show the relevance of a new multiple regression analysis methodology with dietary and non-dietary risk factors (independent variables) for noncommunicable disease (NCD) deaths/100000/year in males and females 15-69 years old from 1990 to 2017 (NCDs, dependent variable). Methods We formatted worldwide GBD2017 dietary risk factors and NCD data on 1120 worldwide cohorts to obtain 7846 population-weighted cohorts. Each cohort represented about one million people, totaling about 7.8 billion people from 195 countries. With an empirically derived methodology, we compared the PHD animal- and plant-sourced food recommended ranges (kilocalories/day=KC/d) with optimal dietary ranges (KC/d) from GBD cohort data. Using GBD data subsets with low and high animal food consumption cohorts, our new GBD multiple regression formula derivation methodology equated risk factor formula coefficients to their population-attributable risk percents (PAR%s). Results We contrasted PHD recommendations for the available 14 dietary risk factors (KC/d means and ranges) with our GBD analysis methodology's optimal ranges for each dietary variable (KC/d mean and range): PHD beef, lamb, and pork mean: 30 KC/d (range: 0-60 KC/d)/GBD processed meat: 8.86 (1.69-16.03)+GBD red meat: 44.52 (20.37-68.68), PHD fish: 40 (0-143)/GBD: 19.68 (3.45-35.90), PHD whole milk or equivalents: 153 (0-306)/GBD: 40.00 (18.89-61.11), PHD poultry: 62 (0-124)/GBD: 56.10 (24.13-88.07), PHD eggs: 19 (0-37)/GBD: 19.42 (9.99-28.86), PHD: saturated oils 96 (0-96)/GBD added saturated fatty acids (SFA): 116.55 (104.04-129.07), PHD all added sugars: 120 (0-120)/GBD sugary beverages: 286.37 (256.99-315.76), PHD tubers or starchy vegetables: 39 (0-78)/GBD potatoes: 84.16 (75.75-92.58)+GBD sweet potatoes: 9.21 (4.05-14.37), PHD fruits: 126 (63-189)/GBD: 63.03 (21.61-113.71), PHD vegetables: 78.32 (9.48-196.14)/GBD: 85.05 (66.75-103.36), PHD nuts: 291 (0-437)/GBD nuts and seeds: 10.97 (5.95-15.98), PHD whole grains: 811 (811/811)/GBD: 56.14 (50.53-61.76), PHD legumes: 284 (0-379)/GBD: 59.93 (45.43-74.43), and total animal food PHD: (0/400)/GBD: 329.84 (212.49-447.19). Multiple regression low and high animal food subsets' (animal foods mean=147.09 KC/d versus animal foods mean=482.00 KC/d) formulas each with 28 dietary and non-dietary risk factors (independent variables) accounted for 52.53% and 28.83% of their respective total formula PAR%s with NCDs (dependent variable). Conclusions GBD data modeling supported many but not all the PHD dietary recommendations. GBD data suggested that the amount of consumption of animal foods was the dominant determinate of NCDs of countries globally. Adding to the univariate associations, multiple regression risk factor formulas with risk factor coefficients equated to their PAR%s further elucidated dietary influences on NCDs. This paper and the soon-to-be-released IHME GBD2021 (1990-2021) data should help inform the EAT-Lancet 2.0 Commission's work.

Future body mass index modelling based on macronutrient profiles and physical activity.

BACKGROUND: An accurate system of determining the relationship of macronutrient profiles of foods and beverages to the long-term weight impacts of foods is necessary for evidence-based, unbiased front-of-the-package food labels. METHODS: Data sets on diet, physical activity, and BMI came from the Food and Agriculture Organization (FAO), the World Health Organization (WHO), the Diabetes Control and Complications Trial (DCCT), and Epidemiology Diabetes Intervention and Complications (EDIC). To predict future BMI of individuals, multiple regression derived FAO/WHO and DCCT/EDIC formulas related macronutrient profiles and physical activity (independent variables) to BMI change/year (dependent variable). Similar formulas without physical activity related macronutrient profiles of individual foods and beverages to four-year weight impacts of those items and compared those forecasts to published food group profiling estimates from three large prospective studies by Harvard nutritional epidemiologists. RESULTS: FAO/WHO food and beverage formula: four-year weight impact (pounds)=(0.07710 alcohol g+11.95 (381.7+carbohydrates g per serving)*4/(2,613+kilocalories per serving)-304.9 (30.38+dietary fiber g per serving)/(2,613+kilocalories per serving)+19.73 (84.44+total fat g)*9/(2,613+kilocalories per serving)-68.57 (20.45+PUFA g per serving)*9/(2,613+kilocalories per serving))*2.941-12.78 (n=334, R(2)=0.29, P < 0.0001). DCCT/EDIC formula for four-year weight impact (pounds)=(0.898 (102.2+protein g per serving)*4/(2,297+kilocalories per serving)+1.063 (264.2+carbohydrates g per serving)*4/(2,297+ kilocalories per serving)-13.19 (24.29+dietary fiber g per serving)/ (2,297+kilocalories per serving)+ 0.973 (74.59+(total fat g per serving-PUFA g per serving)*9/(2,297+kilocalories per serving))*85.82-68.11 (n=1,055, R(2)=0.03, P < 0.0001). (FAO/WHO+ DCCT/EDIC formula forecasts averaged correlated strongly with published food group profiling findings except for potatoes and dairy foods (n=12, r=0.85, P = 0.0004). Formula predictions did not correlate with food group profiling findings for potatoes and dairy products (n=10, r= -0.33 P=0.36). A formula based diet and exercise analysis tool is available to researchers and individuals: http://thehealtheconomy.com/healthTool/. CONCLUSIONS: Two multiple regression derived formulas from dissimilar databases produced markedly similar estimates of future BMI for 1,055 individuals with type 1 diabetes and female and male cohorts from 167 countries. These formulas predicted the long-term weight impacts of foods and beverages, closely corresponding with most food group profiling estimates from three other databases. If discrepancies with potatoes and dairy products can be resolved, these formulas present a potential basis for a front-of-the-package weight impact rating system.

Pharmacotherapy for mild hypertension.

BACKGROUND: People with no previous cardiovascular events or cardiovascular disease represent a primary prevention population. The benefits and harms of treating mild hypertension in primary prevention patients are not known at present. This review examines the existing randomised controlled trial (RCT) evidence. PRIMARY OBJECTIVE: To quantify the effects of antihypertensive drug therapy on mortality and morbidity in adults with mild hypertension (systolic blood pressure (BP) 140-159 mmHg and/or diastolic BP 90-99 mmHg) and without cardiovascular disease. SEARCH METHODS: We searched CENTRAL (2011, Issue 1), MEDLINE (1948 to May 2011), EMBASE (1980 to May 2011) and reference lists of articles. The Cochrane Database of Systematic Reviews and the Database of Abstracts of Reviews of Effectiveness (DARE) were searched for previous reviews and meta-analyses of anti-hypertensive drug treatment compared to placebo or no treatment trials up until the end of 2011. SELECTION CRITERIA: RCTs of at least 1 year duration. DATA COLLECTION AND ANALYSIS: The outcomes assessed were mortality, stroke, coronary heart disease (CHD), total cardiovascular events (CVS), and withdrawals due to adverse effects. MAIN RESULTS: Of 11 RCTs identified 4 were included in this review, with 8,912 participants. Treatment for 4 to 5 years with antihypertensive drugs as compared to placebo did not reduce total mortality (RR 0.85, 95% CI 0.63, 1.15). In 7,080 participants treatment with antihypertensive drugs as compared to placebo did not reduce coronary heart disease (RR 1.12, 95% CI 0.80, 1.57), stroke (RR 0.51, 95% CI 0.24, 1.08), or total cardiovascular events (RR 0.97, 95% CI 0.72, 1.32). Withdrawals due to adverse effects were increased by drug therapy (RR 4.80, 95%CI 4.14, 5.57), ARR 9%. AUTHORS' CONCLUSIONS: Antihypertensive drugs used in the treatment of adults (primary prevention) with mild hypertension (systolic BP 140-159 mmHg and/or diastolic BP 90-99 mmHg) have not been shown to reduce mortality or morbidity in RCTs. Treatment caused 9% of patients to discontinue treatment due to adverse effects. More RCTs are needed in this prevalent population to know whether the benefits of treatment exceed the harms.

Diet as prophylaxis and treatment for venous thromboembolism?

BACKGROUND: Both prophylaxis and treatment of venous thromboembolism (VTE: deep venous thrombosis (DVT) and pulmonary emboli (PE)) with anticoagulants are associated with significant risks of major and fatal hemorrhage. Anticoagulation treatment of VTE has been the standard of care in the USA since before 1962 when the U.S. Food and Drug Administration began requiring randomized controlled clinical trials (RCTs) showing efficacy, so efficacy trials were never required for FDA approval. In clinical trials of 'high VTE risk' surgical patients before the 1980s, anticoagulant prophylaxis was clearly beneficial (fatal pulmonary emboli (FPE) without anticoagulants = 0.99%, FPE with anticoagulants = 0.31%). However, observational studies and RCTs of 'high VTE risk' surgical patients from the 1980s until 2010 show that FPE deaths without anticoagulants are about one-fourth the rate that occurs during prophylaxis with anticoagulants (FPE without anticoagulants = 0.023%, FPE while receiving anticoagulant prophylaxis = 0.10%). Additionally, an FPE rate of about 0.012% (35/28,400) in patients receiving prophylactic anticoagulants can be attributed to 'rebound hypercoagulation' in the two months after stopping anticoagulants. Alternatives to anticoagulant prophylaxis should be explored. METHODS AND FINDINGS: The literature concerning dietary influences on VTE incidence was reviewed. Hypotheses concerning the etiology of VTE were critiqued in relationship to the rationale for dietary versus anticoagulant approaches to prophylaxis and treatment.Epidemiological evidence suggests that a diet with ample fruits and vegetables and little meat may substantially reduce the risk of VTE; vegetarian, vegan, or Mediterranean diets favorably affect serum markers of hemostasis and inflammation. The valve cusp hypoxia hypothesis of DVT/VTE etiology is consistent with the development of VTE being affected directly or indirectly by diet. However, it is less consistent with the rationale of using anticoagulants as VTE prophylaxis. For both prophylaxis and treatment of VTE, we propose RCTs comparing standard anticoagulation with low VTE risk diets, and we discuss the statistical considerations for an example of such a trial. CONCLUSIONS: Because of (a) the risks of biochemical anticoagulation as anti-VTE prophylaxis or treatment, (b) the lack of placebo-controlled efficacy data supporting anticoagulant treatment of VTE, (c) dramatically reduced hospital-acquired FPE incidence in surgical patients without anticoagulant prophylaxis from 1980 - 2010 relative to the 1960s and 1970s, and (d) evidence that VTE incidence and outcomes may be influenced by diet, randomized controlled non-inferiority clinical trials are proposed to compare standard anticoagulant treatment with potentially low VTE risk diets. We call upon the U. S. National Institutes of Health and the U.K. National Institute for Health and Clinical Excellence to design and fund those trials.

Case report of 5 siblings: malnutrition? Rickets? DiGeorge syndrome? Developmental delay?

BACKGROUND: Parents of six children are facing a trial on charges of aggravated manslaughter in the care a 5 1/2 month old infant who died suddenly and neglect of their four older children for causing them to be malnourished by feeding them all an exclusively raw foods vegan diet. Both parents declined plea bargains and plan to defend themselves in court. CASE PRESENTATION: The fifth child born to a married couple was breast-fed until 2 1/2 months. Subsequently, the parents fed the baby an exclusively raw foods diet prepared in a blender at home. The four older children, ages 18 months-6 1/2 years also ate an exclusively raw foods vegan diet. None of the four older children had significant previous injuries or serious illnesses. At autopsy, the infant weighed 3180 mg (6.99 pounds) and appeared emaciated. The thymus gland was absent and parathyroid glands were not located. The lungs were "congested." DiGeorge anomaly cannot be ruled out from these findings. Although, the coroner ruled that "malnutrition" was the sole cause of death, malnutrition, according to the World Health Organization definition, cannot be diagnosed in this infant. Compared with standard growth charts, the older children fell 2.1-4.1 standard deviations below the mean for North American children in height and weight. Labs were normal except for a low cholesterol level in all and a low prealbumin in one of three children tested. Therefore, malnutrition cannot be diagnosed in these children. The pediatrician diagnosed rickets in the four-year-old. However, chest x-rays were normal in all and long bone x-rays showed minimal changes in one child--no sign of rickets. The clinical diagnosis of rickets was not confirmed by the Center for Disease Control's criteria. A psychologist diagnosed the 18-month-old as developmentally delayed to the level of a 15-month-old, but this diagnosis is questionable. CONCLUSION: The raw foods vegan diet and possibly inherited small stature from the father's side account for their relatively low heights and weights. Catch-up growth will probably occur on the standard American diet but would have also been expected if they had remained on a vegan diet.

Cardiovascular Disease Death Before Age 65 in 168 Countries Correlated Statistically with Biometrics, Socioeconomic Status, Tobacco, Gender, Exercise, Macronutrients, and Vitamin K.

BACKGROUND: Nutrition researchers recently recognized that deficiency of vitamin K2 (menaquinone: MK-4-MK-13) is widespread and contributes to cardiovascular disease (CVD). The deficiency of vitamin K2 or vitamin K inhibition with warfarin leads to calcium deposition in the arterial blood vessels. METHODS: Using publicly available sources, we collected food commodity availability data and derived nutrient profiles including vitamin K2 for people from 168 countries. We also collected female and male cohort data on early death from CVD (ages 15-64 years), insufficient physical activity, tobacco, biometric CVD risk markers, socioeconomic risk factors for CVD, and gender. The outcome measures included (1) univariate correlations of early death from CVD with each risk factor, (2) a multiple regression-derived formula relating early death from CVD (dependent variable) to macronutrient profile, vitamin K1 and K2 and other risk factors (independent variables), (3) for each risk factor appearing in the multiple regression formula, the portion of CVD risk attributable to that factor, and (4) similar univariate and multivariate analyses of body mass index (BMI), fasting blood sugar (FBS) (simulated from diabetes prevalence), systolic blood pressure (SBP), and cholesterol/ HDL-C ratio (simulated from serum cholesterol) (dependent variables) and dietary and other risk factors (independent variables). RESULTS: Female and male cohorts in countries that have vitamin K2 < 5µg per 2000 kcal/day per capita (n = 70) had about 2.2 times the rate of early CVD deaths as people in countries with > 24 µg/day of vitamin K2 per 2000 kcal/day (n = 72). A multiple regression-derived formula relating early death from CVD to dietary nutrients and other risk factors accounted for about 50% of the variance between cohorts in early CVD death. The attributable risks of the variables in the CVD early death formula were: too much alcohol (0.38%), too little vitamin K2 (6.95%), tobacco (6.87%), high blood pressure (9.01%), air pollution (9.15%), early childhood death (3.64%), poverty (7.66%), and male gender (6.13%). CONCLUSIONS: Worldwide dietary vitamin K2 data derived from food commodities add much understanding to the analysis of CVD risk factors and the etiology of CVD. Vitamin K2 in food products should be systematically quantified. Public health programs should be considered to increase the intake of vitamin K2-containing fermented plant foods such as sauerkraut, miso, and natto.

Diet and diabetic retinopathy: insights from the Diabetes Control and Complications Trial (DCCT).

OBJECTIVE: We explore the influence of lifestyle on the progression of retinopathy. DESIGN: Post hoc statistical analysis. SUBJECTS/SETTING: One thousand forty-one patients with type 1 diabetes from 29 specialty clinics. INTERVENTION: The Diabetes Control and Complications Trial (DCCT) lifestyle data (diet, exercise, and tobacco use) and retinopathy-related risk factors (mean arterial pressure, the low-density lipoprotein/high-density lipoprotein cholesterol ratio [LDL-C/HDL-C], serum triglycerides, glycosolated hemoglobin [HbA1c] levels, body mass index [BMI], and insulin utilization) were related to the rate of progression of retinopathy. MAIN OUTCOME MEASURES: Correlation between lifestyle data with progression of retinopathy and retinopathy-related risk factors. RESULTS: The percentage of calories as total fatty acids at baseline and overall positively correlated with prestudy and overall progression of retinopathy (r = .15, P < .0001 and r = .14, P < .0001, respectively). Average overall percentage of calories as dietary fiber inversely correlated with prestudy and overall progression of retinopathy (r = -.07, P = .0102 and r = -.10, P < .0002, respectively). The progression of retinopathy correlated with mean arterial pressure (prestudy r = .09, P = .0004 and overall r = .20, P < .0001), LDL-C/HDL-C (prestudy r = .13, P < .0001 and overall r = .15, P < .0001), serum triglycerides (prestudy r = .18, P < .0001 and overall r = .26, P < .0001), HbA1c (prestudy r = .10, P < .0001 and overall r = .45, P < .0001), BMI (prestudy r = .08, P <.0034 and overall r = .05, P = .08), insulin utilization (prestudy r = .19, P < .0001 and overall r = .14, P < .0001), tobacco use (prestudy r = .08, P < .0231 and overall r = .09, P < .0011), and the intensive vs conventional therapy study group (on-study r = -.27, P < .0001). CONCLUSION: Tobacco use and diet, particularly the consumption of fatty acids and dietary fiber, are significantly associated with the rate of progression of diabetic retinopathy and retinopathy-related risk factors.

Anticoagulants for nonvalvular atrial fibrillation (NVAF)--drug review.

Vitamin K-inhibiting anticoagulants, especially warfarin, have become standard treatment for reducing the incidence of strokes and systemic emboli in patients with nonvalvular atrial fibrillation (NVAF). The randomized controlled trials that form the scientific basis for the efficacy of anticoagulants in prophylaxis of embolic events show small but statistically significant benefit with warfarin and other vitamin K inhibitors. The generalizability of these randomized trials to clinical practice is highly questionable because of the low percentage of NVAF patients from the participating institutions that entered the trials, the relatively young age of the patients, and the superior anticoagulation monitoring compared with that in general practice. Indirect comparisons of warfarin with aspirin by looking at separate meta-analyses of placebo-controlled randomized trials give potentially biased results. The meta-analyses of trials directly comparing warfarin with aspirin have diametrically opposing conclusions. In contrast to observational studies of general medical practice, randomized trials significantly underestimate the bleeding risks of warfarin. Anticoagulants for stroke prophylaxis for NVAF cause about 17,000 major bleeds in the United States per year, of which about 4000 are fatal. In 5 randomized trials with follow-up periods of 1.3-2.3 years, 10% to 38% of patients permanently discontinued anticoagulants. The 2-year average follow up of patients in the randomized trials is too short to predict the long-term impact of anticoagulation on the natural history of NVAF. Aspirin should be preferred over anticoagulants in prophylaxis against cardiogenic embolism in NVAF patients.

Anticoagulation therapy for venous thromboembolism.

CONTEXT: On the basis of theoretical rationale, heparoids and vitamin K antagonists are prescribed to prevent complications of venous thromboembolism (VTE, including pulmonary emboli [PE] and deep vein thrombosis [DVT]). They have been employed as the standard of care for treatment of VTE for over 40 years. OBJECTIVE: Critique the evidence supporting the efficacy of anticoagulants for the treatment of VTE in reducing morbidity and/or mortality. DATA SOURCES: This includes a search of reference lists and Medline. STUDY SELECTION: This includes studies concerning the diagnosis and incidence of PE and DVT, efficacy of anticoagulants in preventing complications, risks of anticoagulant therapy, and the costs of diagnosis and the treatment of VTE. DATA EXTRACTION: I analyzed references cited in reviews and meta-analyses of VTE, and from Medline searches concerning diagnosis and treatment. The data quality and validity of studies depended on the consistency of findings and statistical significance of the data. DATA SYNTHESIS: No placebo-controlled trials of anticoagulants as treatment of PE with objective criteria for diagnosis have been published. Three randomized trials of anticoagulants vs no anticoagulants in DVT showed no benefit with heparin and vitamin K antagonists (combined all-cause mortality: anticoagulants = 6/66, un-anticoagulated controls = 1/60, P = .07). No placebo-controlled trials of low-molecular-weight heparins or thrombolytic drugs have been done; therefore, their efficacy in VTE depends entirely on randomized comparisons with unfractionated heparin. They have not been proven safer or more efficacious than unfractionated heparin. Thrombolysis causes more major and fatal bleeds than heparin and is no more effective in preventing PE. Diagnosing and treating VTE patients in the United States with anticoagulants costs 3.2 dollars to 15.5 billion dollars per year (1992 dollars). Bleeding and complications of angiography cause 1017-3525 deaths annually. CONCLUSION: Anticoagulants have not been proven efficacious or safe in VTE. The bleeding risks and other complications of anticoagulation are unacceptably high. The use of anticoagulants for patients with VTE should be reconsidered.

Diet and tobacco use: analysis of data from the diabetic control and complications trial, a randomized study.

CONTEXT: The Diabetic Control and Complications Trial (DCCT) researchers kept careful records of the food consumption and tobacco using habits of type 1 diabetic subjects. However, they did not report the relationship of tobacco using habits with dietary intake. OBJECTIVE: Analyze the relationship between tobacco smoking and intake of macro and micronutrients. DESIGN: Randomized controlled trial. SETTING: Referral clinics in 27 academic centers. PATIENTS: Type 1 diabetics. INTERVENTION: Using the data sets of the DCCT, this study analyzed the strengths of the associations between smoking and macronutrient consumption, hemoglobin A1c (HbA1c), body mass index (BMI), and serum lipid levels at the study baseline, 2 years, and 4 years. MAIN OUTCOME MEASURES: Statistically significant correlations between smoking and nutrient intake, HbA1c, and serum lipid levels. RESULTS: Cigarette, cigar, or pipe use at each time interval correlated with significantly increased caloric intake in males but not in females. In both males and females, tobacco users consumed more fat, cholesterol, and alcohol. Female smokers had higher serum low-density lipoprotein (LDL)/high-density lipoprotein (HDL) ratios and triglycerides. Serum cholesterols, LDL/HDL ratios, LDL cholesterols, and triglyceride determinations in male tobacco users significantly exceeded those in nonsmoking males. HDL cholesterols were lower in both female and male tobacco users. Nutrient intake of former tobacco users resembled that of nonusers rather than current users. CONCLUSIONS: A significant association exists between smoking and a diet with higher risks of atherosclerosis, cancer, and other degenerative diseases. The strong association of tobacco with heart disease, stroke, vasculopathies, and various malignancies may be in part due to its association with a higher fat diet. The higher fat diet of tobacco users probably accounts in part for their higher risk of developing type 2 diabetes and hyperlipidemia. Tobacco users should be informed about the diet and tobacco use association.