The study found no link between consuming butter and an increased risk of heart disease or stroke, instead finding that butter might actually be slightly protective against type 2 diabetes. And although consuming butter was linked with an increased risk of early death, the increase in risk was extremely small, the researchers said. 
 
 "Overall, our results suggest that butter should neither be demonized nor considered 'back' as a route to good health," study co-author Dr. Dariush Mozaffarian, dean of the Friedman School of Nutrition Science and Policy at Tufts University in Massachusetts, said in a statement. The findings "do not support a need for major emphasis in dietary guidelines on either increasing or decreasing butter consumption," the researchers wrote in their study. [7 Foods Your Heart Will Hate] 
 
 Butter is relatively high in saturated fat, which is generally considered a "bad" fat. But, increasingly, researchers are looking at the overall effects of eating certain foods, rather than focusing on specific nutrients by themselves, the researchers said. That's because the combination of nutrients in a food, like butter, may have a different effect on people's health than any single nutrient alone. 
 
 In the new study, the researchers analyzed information from nine earlier studies that together included more than 636,000 people in 15 countries who were followed for 10 to 23 years, on average. During that time, 28,271 people died; 9,783 were diagnosed with heart disease; and 23,954 were diagnosed with type 2 diabetes. The average amount of butter that the people in the studies consumed ranged from one-third of a tablespoon daily to 3 tablespoons daily. 
 
 A daily serving of butter (14 grams or about 1 tablespoon) was linked with a 1 percent higher risk of death during the study period. On the other hand, a daily serving of butter was linked with a 4 percent reduced risk of type 2 diabetes. 
 
 There was no relationship found between eating butter and being diagnosed with heart disease, the researchers said. 
 
 The findings suggested butter may be a "middle-of-the-road" food, said study co-author Laura Pimpin, also of Tufts University. For example, butter may be healthier for you than foods high in sugar or starch, which have been linked with an increased risk of heart disease and diabetes, Pimpin said. 
 
 However, butter may be a worse for you than other spreads and cooking oils that are richer in "healthy fats," she said. These alternatives include soybean, canola, flaxseed and extra-virgin olive oil, along with some types of margarine. Such spreads and oils contain more unsaturated fats, which are generally considered healthier than saturated fats. 
 
 More research is needed to understand why consuming butter is linked with a slightly lower risk of type 2 diabetes, Mozaffarian said. Some previous studies have also found a link between consuming dairy fat from yogurt and cheese and a lower risk of type 2 diabetes. 
 
 The new study looked only at the association between people's butter consumption and their risk of heart disease, early death and types 2 diabetes, so it cannot prove for certain that butter does or does not cause these conditions. There may be factors that the study did not take into account, such as people's physical activity levels or their genetic risk factors, which could affect the results, the researchers said. 
 
 The study is published today (June 29) in the journal PLOS ONE. 
 
 Original article on Live Science. ||||| This systematic review and meta-analysis suggests relatively small or neutral overall associations of butter with mortality, CVD, and diabetes. These findings do not support a need for major emphasis in dietary guidelines on either increasing or decreasing butter consumption, in comparison to other better established dietary priorities; while also highlighting the need for additional investigation of health and metabolic effects of butter and dairy fat. 
 
 We searched 9 databases from inception to May 2015 without restriction on setting, or language, using keywords related to butter consumption and cardiometabolic outcomes. Prospective cohorts or randomized clinical trials providing estimates of effects of butter intake on mortality, cardiovascular disease including coronary heart disease and stroke, or diabetes in adult populations were included. One investigator screened titles and abstracts; and two reviewed full-text articles independently in duplicate, and extracted study and participant characteristics, exposure and outcome definitions and assessment methods, analysis methods, and adjusted effects and associated uncertainty, all independently in duplicate. Study quality was evaluated by a modified Newcastle-Ottawa score. Random and fixed effects meta-analysis pooled findings, with heterogeneity assessed using the I 2 statistic and publication bias by Egger’s test and visual inspection of funnel plots. We identified 9 publications including 15 country-specific cohorts, together reporting on 636,151 unique participants with 6.5 million person-years of follow-up and including 28,271 total deaths, 9,783 cases of incident cardiovascular disease, and 23,954 cases of incident diabetes. No RCTs were identified. Butter consumption was weakly associated with all-cause mortality (N = 9 country-specific cohorts; per 14g(1 tablespoon)/day: RR = 1.01, 95%CI = 1.00, 1.03, P = 0.045); was not significantly associated with any cardiovascular disease (N = 4; RR = 1.00, 95%CI = 0.98, 1.02; P = 0.704), coronary heart disease (N = 3; RR = 0.99, 95%CI = 0.96, 1.03; P = 0.537), or stroke (N = 3; RR = 1.01, 95%CI = 0.98, 1.03; P = 0.737), and was inversely associated with incidence of diabetes (N = 11; RR = 0.96, 95%CI = 0.93, 0.99; P = 0.021). We did not identify evidence for heterogeneity nor publication bias. 
 
 Competing interests: The authors have completed and submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest and Dr. Mozaffarian reports ad hoc honoraria or consulting from Boston Heart Diagnostics, Haas Avocado Board, Astra Zeneca, GOED, and Life Sciences Research Organization; chapter royalties from UpToDate; and scientific advisory board Elysium Health. Harvard University has been assigned patent US8889739 B2, listing Dr. Mozaffarian as one of three co-inventors, for “Use of transpalmitoleic acid in identifying and treating metabolic disease”. This does not alter our adherence to PLOS ONE policies on sharing data and materials. 
 
 A systematic review of the evidence for of the relationship between butter consumption and long-term health is of considerable importance, both for understanding food-based health as well as informing dietary recommendations for clinicians and policy makers. The US Department of Agriculture has documented a 40-year record high in US butter consumption in 2014 [ 13 ], making a synthesis of the evidence on butter and major chronic diseases highly relevant and timely. 
 
 For example, growing evidence supports potential metabolic benefits of certain dairy products, such as yogurt and possibly cheese, on risk of type 2 diabetes [ 5 , 6 ], which may even relate to benefits of dairy fat. [ 7 – 9 ] However, the relationship of butter, which is highest in dairy fat, with diabetes remains unclear. The long-term effects of butter consumption on other major endpoints, such as all-cause mortality and CVD, are also not well-established. Previous reviews have evaluated only some of these outcomes, included butter as part of a wider investigation into dairy foods or types of fats [ 10 – 12 ], and utilized methods that provided imprecise estimates of effect, precluded dose-response evaluation, or may have introduced unintended bias (e.g., due to inclusion of crude, unadjusted effect estimates). 
 
 Growing uncertainty and changing views on the role of butter in cardiovascular disease (CVD) have been prominently discussed, including in the New York Times and Time Magazine. [ 1 , 2 ] This has partly arisen from increasing controversy on the utility of focusing on isolated macronutrients, such as saturated fat, for determining risk of chronic diseases. Mounting evidence indicates a need to shift away from isolated macronutrients toward food-based paradigms for investigating dietary priorities for chronic diseases. [ 3 , 4 ] The 2015 Dietary Guidelines Advisory Committee (DGAC) recommended replacing animal fats, including butter, with non-hydrogenated vegetable oils high in unsaturated fats and relatively low in saturated fatty acids. [ 4 ] Yet, the DGAC also concluded that further research was needed on the effects of saturated fat from different food sources, including animal products, on cardiovascular risk, because different food sources contain varying specific fatty acid profiles as well as other constituents that may result in distinct lipid and metabolic effects. [ 4 ] 
 
 Heterogeneity between studies was quantified using the I 2 statistic, with statistical significance (P<0.05) evaluated by the Q statistic. [ 21 ] We considered I2 values between 25% and 50%, between 50% and 75% and above75% as upper thresholds for low, moderate, and high heterogeneity, respectively. We planned pre-specified subgroup analyses to further explore potential heterogeneity in results by gender, population mean age and body mass index, duration of follow-up, and study quality score. Restricted cubic spline models [ 22 ] with knots at the 25th, 50th, and 75th percentiles were used to examine potential nonlinear relations. 
 
 Reported hazard ratios were assumed to approximate relative risks (RRs). We used the two-stage generalized least-squares trend estimation method described by Greenland and Longnecker [ 17 , 18 ] to perform dose-response analysis and compute study-specific linear estimates and 95% CIs across categories of butter intake. Butter intakes across studies were standardized at the study level to 14 g/d, corresponding to one United Stated Department of Agriculture-defined serving. [ 19 ] Study-specific dose-response estimates were then pooled to derive an overall estimate using inverse-variance weighted DerSimonian and Laird meta-analysis with random effects. [ 20 ] Because random effects can result in larger weights for small outlier studies, we also conducted fixed effects meta-analysis for comparison. For reports presenting results only by study subgroups (e.g., men, women), we first pooled the study-specific subgroups using fixed-effect meta-analysis to obtain a single estimate per study. 
 
 We adapted the Newcastle-Ottawa quality scale(NOS) [ 16 ] to assess study quality, based on five criteria evaluating the reporting and appropriateness/representativeness of participant inclusion and exclusion criteria (combining the first two items of the NOS Selection scale), participant attrition (NOS adequacy of follow-up item), control for confounding (NOS Comparability scale), assessment of exposure (NOS ascertainment of exposure item), and assessment of outcome (combining the first two items of the NOS Outcome scale). One point was allocated per criterion met, the sum of which provided an overall quality score. A score between 0 and 3 was considered low-quality; and 4 to 5, high-quality. Quality scores were assessed independently and in duplicate by two investigators, with any differences resolved by consensus. 
 
 When more than one multivariable model was reported, we used the risk estimate including the greatest number of potential confounders but not potential mediators (e.g., blood cholesterol). If the main multivariable model included covariates which could either be confounders or intermediates, this was utilized rather than a model with crude or minimal covariate adjustment. When energy intake was included as a covariate, body mass index was not considered to be an intermediate variable, so models adjusting for body mass index were extracted (this only arose in one study, by Buijsse et al. [ 14 ]). The effect results from the Guasch-Ferre et al. [ 15 ] study were estimated using the models of risk of diabetes associated with substitution of olive oil for equivalent amounts of butter, and our results were confirmed and validated by contact with the authors. 
 
 Data from the included studies were independently extracted in duplicate by two investigators using a standardized and piloted electronic form (Microsoft Excel). Any differences in extraction were resolved by consensus. Information was extracted on the publication (first author name, contact information, publication year), study details (name, location, design), population (age, gender, race, socioeconomic status, body mass index), sample size, dates of recruitment, duration of follow-up, dietary assessment (dates, method, definition, categories), outcome(s) (assessment method, definition), covariates and analysis methods, and multivariate-adjusted effect estimates and associated uncertainty. To evaluate dose-response, we extracted continuous effect estimates when available; and for categorical analyses, collected additional information on median exposure, number of participants or person-years, and number of events in each category. Missing information in any category was obtained by direct author contact or, if necessary, estimated using a standard approach (see S5 File ). 
 
 Studies were also excluded if evaluating only children or populations with major end-stage diseases such as cancer; if duration of intervention or follow-up was less than 3 months; if consumption of butter was not separately distinguishable from other dairy product or fats; if evaluating only soft endpoints (e.g. angina pectoris, coronary insufficiency); or, for observational studies, if providing only unadjusted (crude) effect estimates. When duplicate publications were identified, the report including the largest number of cases for each endpoint of interest was selected. If references were only available in abstract form (e.g. from meeting proceedings or conference presentations), data were extracted if sufficient detail was available; if not, a relevant publication was searched for in PubMed. 
 
 In addition, among studies excluded by title and abstract screening, several were identified evaluating overall dietary patterns (e.g., Mediterranean, Western, etc.) To ensure that we were not missing effect estimates for butter contained within these reports (e.g., in supplementary tables on the individual components of these dietary patterns), we also reviewed the full texts of the first 15 identified studies of dietary patterns. None of these studies reported individual effect estimates for butter, so further diet pattern studies lacking any information on butter in the title or abstract were excluded 
 
 We performed a systematic search for all prospective cohort studies and randomized clinical trials examining butter consumption and all-cause mortality, CVD including CHD and stroke, or type 2 diabetes. Electronic searches were performed using PubMed ( www.ncbi.nlm.nih.gov/pubmed ), EMBASE ( www.scopus.com ), The Cochrane Library ( www.cochranelibrary.com ), Web of Knowledge ( www.webofscience.com ), CAB Abstracts and Global Health ( www.ovid.com ), CINAHL ( www.ebscohost.com ) and grey literature searches of SIGLE ( www.opengrey.eu ) and ZETOC ( www.zetoc.mimas.ac.uk/ ) from the earliest indexing year of each database through May 2015, without language or other restrictions. Search terms included butter, margarine, dairy, dairy products, yogurt, cheese, ghee, animal fat, solid fat, cardiovascular diseases, heart disease, stroke, myocardial infarction, heart attack, cerebrovascular disease, cerebrovascular accident, sudden death, diabetes, mortality and deaths; see S3 File for a full listing. For all final included articles, we further performed hand-searches of citation lists and a review of the first 20 related references on PubMed for additional eligible reports. 
 
 Visual inspection of funnel plots and Egger’s test suggested little evidence for asymmetry or presence of small-study effects for any CVD (p = 0.866), stroke (p = 0.913), CHD (p = 0.769), or diabetes (p = 0.369), although the relatively small number of studies limited statistical power of Egger’s test ( S1 Fig ). Egger’s test could not estimate small-study effects for all-cause mortality (N = 2 studies). No trimming was identified for all-cause mortality or CVD using Duval and Tweedie’s “Trim and Fill” method ( S2 Fig ). For diabetes, this approach did estimate one missing study, the addition of which resulted in a theoretical corrected pooled estimate of RR = 0.95 (95%CI = 0.93, 0.98; P = 0.001). 
 
 While total numbers of subjects and cases were large, the relatively low number of separate studies precluded meaningful subgroup analyses by study or participant characteristics, which were therefore not performed. Similarly, potential nonlinearity in dose-response could not be meaningfully evaluated for total mortality. Evidence for nonlinearity was not identified for butter intake and CVD or diabetes (by cubic spline regression, P for nonlinearity = 0.364 and 0.160, respectively). 
 
 Diet was generally assessed by detailed, semi-quantitative food frequency questionnaires; one cohort utilized a structured diet history interview ( Table 1 ). The median butter consumption across studies ranged from 4.5g/d (0.3 servings/d) in the European Prospective Investigation into Cancer and Nutrition (EPIC) studies to 46 g/d (3.2 servings/d) in Finland. Mean participant age ranged from 44 to 71 years. All studies were published between 2005 and 2015, and included 1 in the Netherlands, 2 in the US, 2 in Finland, 2 in Sweden, and 2 from the multi-country, multi-cohort EPIC study which included 8 country-specific cohorts from Denmark, France, Italy, Germany, the Netherlands, Spain, Sweden and the UK. Five of the studies presented results from models with optimal covariate adjustment including demographics, clinical risk factors, and other dietary habits; the remainder provided results with moderate covariate adjustment. 
 
 Discussion 
 
 In this systematic review and meta-analysis of prospective studies, we found a small positive association between butter consumption and all-cause mortality, no significant association with incident CVD or CVD subtypes, and a modest inverse association with type 2 diabetesNo RCTs of butter intake were identified in our literature search. Because several of the identified reports included multiple country-specific cohorts, the total numbers of nation-specific cohorts, participants, and clinical events appear reasonably robust. Indeed, together these studies included more than 28,000 total deaths, nearly 10,000 cases of incident CVD, and nearly 24,000 cases of incident diabetes. We found limited formal evidence for between-study heterogeneity or publication bias, and all reports had high quality scores. Together, these findings suggest relatively small or neutral associations of butter consumption with long-term health. 
 
 Current dietary recommendations on butter and dairy fat are largely based upon predicted effects of specific individual nutrients (e.g., total saturated fat, calcium), rather than actual observed health effects. Our findings add to a growing body of evidence on long-term health effects of specific foods and types of fats. [12, 32, 33] Conventional guidelines on dietary fats have not accounted for their diverse food sources nor the specific individual fatty acid profiles in such foods. [4] Different foods represent complex matrices of nutrients, processing, and food structure, which together influence net health effects. [3, 34] Thus, studying intakes of foods, as in the present investigation, is crucial to elucidate health impact. Our novel results, together with other prior research described below, indicate a need for further funding, evaluation, and reporting on health effects of butter and dairy fat on mechanistic pathways and long-term health outcomes. 
 
 While prior meta-analyses have evaluated total dairy or some dairy subtypes and incident diabetes, to our knowledge none have evaluated butter and type 2 diabetes. [6, 12] A meta-analysis of butter and all-cause mortality identified no significant association (highest category vs. lowest: RR = 0.96; 95%CI = 0.95, 1.08) [10], but did not include the more recent large report from Sluik et al. [30](258,911 participants, 12,135 deaths) and also included two smaller studies not meeting our inclusion criteria: one having only crude (unadjusted) estimates, [35] and another evaluating polyunsaturated fats or margarine in comparison to butter, rather than butter separately. [36] A meta-analysis evaluating dairy consumption and CVD found no association between butter consumption and stroke (2 cohorts: RR = 0.94; 95%CI = 0.84, 1.06) or CHD (3 cohorts: RR = 1.02, 95%CI = 0.88, 1.20), but only evaluated high vs. low categories of intake rather than conducting dose-response analyses utilizing all available data. [5] Another meta-analysis included dose-response findings on butter consumption and stroke, but not CHD, CVD, diabetes, or all-cause mortality, and arrived at similar findings for stroke as seen in the present study. [11] In comparison to these prior reports, we evaluated up-to-date reports and full dose-response analyses for all-cause mortality, CVD including CHD and stroke, and type 2 diabetes; providing the most comprehensive investigation to-date of butter consumption and risk of long-term major health endpoints. 
 
 Our investigation also adds to and expands upon prior studies evaluating other dairy foods and dairy fat biomarkers in relation to cardiometabolic outcomes. In a multi-ethnic US population, serum levels of pentadecanoic acid (15:0), the odd-chain saturated fat most strongly associated with self-reported butter intakes (r = 0.13), were associated with lower CVD and CHD risk. [37] This is consistent with a meta-analysis of odd-chain saturated fat biomarkers demonstrating inverse associations with CHD [33]. A prior meta-analysis of dairy consumption and CVD suggested protective associations with total CVD (for highest vs lowest category of intake: 12% lower risk) and stroke (13% lower risk), with conflicting results for major subtypes of dairy. [5] Dairy fat has also been linked to lower risk of diabetes, based on studies of circulating fatty acid biomarkers [8, 9] and studies of self-reported consumption of dairy products, which have seen protective associations for yogurt and perhaps cheese, and null associations for both low-fat and whole-fat milk. [12, 27] 
 
 Given adverse effects of certain dairy fats (e.g. 16:0) on cardiometabolic risk factors such as LDL-cholesterol and fasting glucose [38, 39], our findings suggest potential presence of other mechanistic benefits of butter that might at least partly offset these harms. For instance, saturated fats also increase HDL-C, lower VLDL-C and chylomicron remnants, and lower lipoprotein(a) [40, 41]; while potential cardiometabolic benefits have been identified for calcium, fat-soluble vitamin D, medium-chain saturated fats, branched-chain fats, trace ruminant trans fats, or other processes related to fermentation (e.g. cheese) or active bacterial cultures (e.g. in yogurt). For example, dietary calcium may decrease fatty acid synthase and increase lipolytic activity in adipocytes, [42] reduce blood pressure by modulation of smooth muscle reactivity, [43, 44] and reduce weight gain. [45] Vitamin D may reduce dyslipidemia and improve blood pressure through maintenance of calcium homeostasis, stimulation of insulin production and release, and regulation of the renin-angiotensin-aldosterone system. Higher dairy fat consumption has been linked to lower liver fat and greater hepatic and systemic insulin sensitivity [46] which could relate to inhibition of hepatic de novo lipogenesis by specific dairy fatty acids. [8] Branched-chain fatty acids in dairy fat may promote healthier bacterial microbiome composition and function. Dairy fat also contains monounsaturated fats which might improve glycemic responses and insulin sensitivity. [47, 48] Other dairy-related factors, such as probiotic bacteria in yogurt and menaquinones in fermented milk and cheeses, may improve insulin sensitivity, reduce weight gain, and reduce inflammation through microbiome and vitamin-K related pathways; [49, 50] such pathways would be less relevant for butter, which has been linked to greater weight gain. [51, 52] Clearly, additional mechanistic studies on health effects of butter, dairy fat, and dairy foods are warranted. 
 
 Our results suggest relatively small or neutral overall associations of butter with mortality, CVD, and diabetes. These findings should be considered against clear harmful effects of refined grains, starches, and sugars on CVD and diabetes; [53–55] and corresponding benefits of fruits, nuts, legumes, n-6 rich vegetable oils, and possibly other foods such as fish on these endpoints. In sum, these results suggest that health effects of butter should be considered against the alternative choice. For instance, butter may be a more healthful choice than the white bread or potato on which it is commonly spread. In contrast, margarines, spreads, and cooking oils rich in healthful oils, such as soybean, canola, flaxseed, and extra-virgin olive oil, appear to be healthier choices than either butter or refined grains, starches, and sugars. [15, 56, 57] In Guasch-Ferre’s analysis of the Nurses Health Study, substitution of 8 g olive oil for an equivalent amount of butter was associated with an 8% reduction in the risk of type 2 diabetes (RR = 0.92 (95%CI = 0.87, 0.97). [15] Thus, even with an absence of major health associations in the present investigation, healthier (and less healthy) alternatives may be available. Our findings suggest a major focus on eating more or less butter, by itself, may not be linked to large differences in mortality, cardiovascular disease, or diabetes. In sum, our findings do not support a need for major emphasis in dietary guidelines on butter consumption, in comparison to other better established dietary priorities. In any meta-analysis, the effects of potential publication bias should be considered. Such bias increases the probability that large, positive associations, rather than small or null findings, will be published. In this case, the identified studies each reported generally modest or null findings. Considering the number of large prospective studies globally having data on dietary habits (including butter consumption) and these outcomes, it is evident that many additional cohort studies have collected such data but not analyzed or reported their findings. Such “missing,” unpublished studies may be more likely to have null effects. This may be particularly relevant for total mortality, with only 2 identified publications: additional publications might plausibly move findings toward the null. For diabetes, where a larger count of publications allowed better assessment for bias, the “trim and fill” method identified one theoretical missing study, with a protective point estimate. 
 
 Our investigation has several strengths. We followed stringent eligibility criteria that maximized inclusion of high quality, comparable studies. Our comprehensive literature search of multiple databases together with author contacts for clarification and missing data maximized statistical power and minimized the possibility of missed reports. While relatively few publications reported on certain outcomes, the identified studies were large, included multiple nation-specific cohorts and thousands of cases, and were of high quality; and as described above, it would be unlikely that publication bias would explain small or null (as opposed to large) associations. The inclusion of generally healthy participants followed since the 1980s and 1990s to the present provided populations generally free of lipid-lowering medications, which might otherwise mask full effects of butter on CVD. The identified cohorts provided a wide range of butter intakes, increasing power to detect an effect, if present. The dose-response analyses maximized use of all reported data, increasing precision. 
 
 Potential limitations should be considered. The health effect of any food could be modified by a person’s background diet, genetics, or risk factor profile. This is true for any lifestyle, pharmacologic, or other health intervention—effects may be modified by other treatments or underlying characteristics—but this does not lessen the relevance of evaluating the average population effect. We did not observe any obvious differences in associations based on country or region, where background dietary patterns might differ; but the number of identified studies precluded robust investigation of potential sources of heterogeneity. While the majority of studies adjusted for major demographic, clinical, and dietary covariates, residual confounding may be present. Because butter consumption is associated with generally worse diet patterns and lifestyle habits [58, 59], such residual confounding may overestimate potential harms of butter for mortality, and underestimate potential benefits of butter for CVD or diabetes. Error or bias in measurement of dietary intake from self-reports, as well as the long periods between dietary assessment and follow-up in several studies (10 years or more), may attenuate findings. On the other hand, even with such limitations, many other dietary factors in these and other cohorts have identified significant associations with mortality, CVD, and diabetes, so this is unlikely to be the sole explanation for the null findings. We did not identify any randomized clinical trials of our hard endpoints, although such a long-term trial focused on butter alone might be prohibitively expensive and impractical. Our results are based on best available observational findings, and long-term interventional studies were not found, limiting inference on causality. 
 
 In conclusion, the available evidence indicates small or neutral associations of butter consumption with all-cause mortality, CVD, and type 2 diabetes. ||||| An analysis by Tufts University researchers has failed to find a link between butter consumption and cardiovascular disease. And hallelujah to that—the ongoing hysteria against butter can now finally come to an end. 
 
 For years we’ve been told to reduce the amount of butter in our diets. Health guidelines, many of which have been around since the 1970s, have warned us about the dangers of eating food high in saturated fats, claiming—and often without merit—that they contribute to heart problems and other health issues. Increasingly, however, scientists are learning that saturated fats aren’t the demons they’ve been made out to be. 
 
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 A new study published in PLOS ONE is now bolstering this changing tide of opinion, showing there’s no link between butter and chronic disease. This gigantic analysis—a meta-study that included a total of 636,151 individuals across 15 countries, and involving 6.5 million person-years of follow-up—showed no association between the consumption of butter and cardiovascular disease. 
 
 What the researchers did find, however, was that butter could be linked to a decrease—yes, a decrease—in a person’s chance of developing diabetes. Each daily tablespoon of butter was linked to a four percent lower risk of diabetes. 
 
 The downside is that researchers did connect butter with all-cause mortality, however. For each tablespoon of butter consumed each day, the researchers observed a one percent increase in all-cause mortality risk, that is, death from any cause. The researchers suspect this connection is due to other factors; people who eat butter, for example, tend to have generally worse diets and lifestyles. 
 
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 So does this mean we can start slathering butter on our toast and waffles with reckless abandon, and douse our popcorn in this golden syrup of deliciousness? Well, not quite. This study shows that butter on its own isn’t a pure evil. But it shouldn’t be considered a health food, either. As the researchers put it, butter is a kind of “middle-of-the-road” food. And as is often the case, it’s the foods we put the butter on that’s the problem. 
 
 Indeed, butter is healthier than sugar or starches like bread, which have been linked to an increased risk of cardiovascular disease and diabetes. On the other hand, butter is worse than many margarines and cooking oils, such as those rich in healthy fats, like soybean, canola, flaxseed, and extra virgin olive oils. Importantly, margarine made from trans fats should be avoided like the plague. 
 
 As study co-author Dariush Mozaffarian succinctly put it: “Overall, our results suggest that butter should neither be demonized nor considered ‘back’ as a route to good health.” 
 
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 Mozaffarian and his colleagues said further research is still required to understand why butter is connected to a lower risk of diabetes, but similar things have been observed in studies of dairy fat. This could imply that other factors are at play. As the researchers concede, ‘[Our] study does not prove cause-and-effect.” 
 
 [PLOS ONE] ||||| BOSTON (Embargoed until 2 PM EDT, June 29, 2016)--Butter consumption was only weakly associated with total mortality, not associated with cardiovascular disease, and slightly inversely associated (protective) with diabetes, according to a new epidemiological study which analyzed the association of butter consumption with chronic disease and all-cause mortality. This systematic review and meta-analysis, published in PLOS ONE, was led by Tufts scientists including Laura Pimpin, Ph.D., former postdoctoral fellow at the Friedman School of Nutrition Science and Policy at Tufts in Boston, and senior author Dariush Mozaffarian, M.D., Dr.P.H., dean of the School. 
 
 Based on a systematic review and search of multiple online academic and medical databases, the researchers identified nine eligible research studies including 15 country-specific cohorts representing 636,151 unique individuals with a total of 6.5 million person-years of follow-up. Over the total follow-up period, the combined group of studies included 28,271 deaths, 9,783 cases of cardiovascular disease, and 23,954 cases of new-onset type 2 diabetes. The researchers combined the nine studies into a meta-analysis of relative risk. 
 
 Butter consumption was standardized across all nine studies to 14 grams/day, which corresponds to one U.S. Department of Agriculture estimated serving of butter (or roughly one tablespoon). Overall, the average butter consumption across the nine studies ranged from roughly one-third of a serving per day to 3.2 servings per day. The study found mostly small or insignificant associations of each daily serving of butter with total mortality, cardiovascular disease, and diabetes. 
 
 "Even though people who eat more butter generally have worse diets and lifestyles, it seemed to be pretty neutral overall," said Pimpin, now a data analyst in public health modelling for the UK Health Forum. "This suggests that butter may be a "middle-of-the-road" food: a more healthful choice than sugar or starch, such as the white bread or potato on which butter is commonly spread and which have been linked to higher risk of diabetes and cardiovascular disease; and a worse choice than many margarines and cooking oils - those rich in healthy fats such as soybean, canola, flaxseed, and extra virgin olive oils - which would likely lower risk compared with either butter or refined grains, starches, and sugars." 
 
 "Overall, our results suggest that butter should neither be demonized nor considered "back" as a route to good health," said Mozaffarian. "More research is needed to better understand the observed potential lower risk of diabetes, which has also been suggested in some other studies of dairy fat. This could be real, or due to other factors linked to eating butter - our study does not prove cause-and-effect." 
 
 ### 
 
 Additional authors of this study are Jason HY Wu, M.Sc., Ph.D., and Hila Haskelberg, Ph.D., both of The George Institute for Global Health, University of Sydney, Australia; and Liana Del Gobbo, Ph.D., formerly a postdoctoral fellow at the Friedman School and currently a research fellow in cardiovascular medicine at Stanford School of Medicine. 
 
 This work was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health, under award number 5R01HL085710. For conflicts of interest disclosure, please see the study. 
 
 Pimpin L, Wu JHY, Haskelberg H, Del Gobbo L, Mozaffarian D (2016) Is Butter Back? A Systematic Review and Meta-Analysis of Butter Consumption and Risk of Cardiovascular Disease, Diabetes, and Total Mortality. PLoS ONE 11(6): e0158118. doi:10.1371/journal.pone.0158118 
 
 About the Friedman School of Nutrition Science and Policy at Tufts University 
 
 The Gerald J. and Dorothy R. Friedman School of Nutrition Science and Policy at Tufts University is the only independent school of nutrition in the United States. The school's eight degree programs - which focus on questions relating to nutrition and chronic diseases, molecular nutrition, agriculture and sustainability, food security, humanitarian assistance, public health nutrition, and food policy and economics - are renowned for the application of scientific research to national and international policy.
– We might all owe Paula Deen an apology. A study published this week in PLOS ONE finds no connection between eating butter and an increased risk of cardiovascular disease. On the contrary, researchers found eating butter might actually make people slightly healthier by reducing the risk of diabetes. Researchers from Tufts University looked at nine previous studies of more than 636,000 people who ate between one-third a tablespoon of butter and three tablespoons of butter per day, Live Science reports. For the purposes of the study, they called one tablespoon of butter a daily serving. Researchers found that eating butter was in no way associated with a risk of stroke or heart disease and reduced the risk of type 2 diabetes by 4%. "Hallelujah," Gizmodo responds to the study, pointing out that warnings about the dangers of butter have been around since the 1970s. But that doesn't mean it's time to eat an entire butter sculpture. Researchers say that while butter may actually be healthier than sugars and starches, it's probably still worse for you than olive oil or some margarines. "Overall, our results suggest that butter should neither be demonized nor considered 'back' as a route to good health," researcher Dariush Mozaffarian says in a press release. Researchers did find that eating butter led to a 1% higher risk of death, though they chalk that up to the fact that "people who eat more butter generally have worse diets and lifestyles." (This guy found edible butter dating back to Jesus.)