Are There Studies That Show Grass Fed Beef Causes Heart Disease
Curr Atheroscler Rep. Author manuscript; available in PMC 2013 Dec 1.
Published in final edited form equally:
PMCID: PMC3483430
NIHMSID: NIHMS409637
Unprocessed Crimson and Processed Meats and Risk of Coronary Avenue Disease and Blazon 2 Diabetes – An Updated Review of the Evidence
Renata Micha
Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. Department of Food Science and Engineering science, Unit of Human being Diet, Agricultural Academy of Athens, Athens, Greece
Georgios Michas
Department of Internal Medicine, Full general Hospital of Kalamata, Kalamata, Greece
Dariush Mozaffarian
Departments of Epidemiology and Nutrition, Harvard School of Public Health, 665 Huntington Ave Bldg 2-319, Boston, MA 02115, USA. Division of Cardiovascular Medicine and Channing Sectionalisation of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 665 Huntington Ave Bldg 2-319, Boston, MA 02115, USA
Abstract
Growing bear witness suggests that effects of ruby-red meat consumption on coronary heart disease (CHD) and type 2 diabetes could vary depending on processing. We reviewed the prove for effects of unprocessed (fresh/frozen) cherry and processed (using sodium/other preservatives) meat consumption on CHD and diabetes. In meta-analyses of prospective cohorts, higher gamble of CHD is seen with candy meat consumption (RR per 50 k: i.42, 95 %CI = one.07–1.89), but a smaller increase or no risk is seen with unprocessed meat consumption. Differences in sodium content (~400 % higher in processed meat) appear to account for about two-thirds of this take chances divergence. In similar analyses, both unprocessed red and processed meat consumption are associated with incident diabetes, with higher take a chance per g of processed (RR per 50 g: 1.51, 95 %CI = 1.25–ane.83) versus unprocessed (RR per 100 one thousand: 1.nineteen, 95 % CI = 1.04–1.37) meats. Contents of heme iron and dietary cholesterol may partly account for these associations. The overall findings advise that neither unprocessed ruby-red nor processed meat consumption is beneficial for cardiometabolic health, and that clinical and public health guidance should especially prioritize reducing candy meat consumption.
Keywords: Review, Meat, Ruby-red meat, Processed meat, Cardiovascular affliction, Diabetes
Introduction
Red meat consumption is considered a major dietary take chances cistron for cardiometabolic diseases, including coronary centre disease (CHD) and type ii diabetes mellitus (DM). In a 2010 meta-assay, we provided show that relationships of meat consumption with development of these conditions might vary depending on the extent of processing [1••], i.e., whether or non the meat is unprocessed (eastward.g., fresh or frozen) or has been processed and preserved for long-term storage, due east.g., by adding high amounts of salt and/or other preservatives such equally nitrates. Since the publication of our findings, several additional studies have evaluated how eating unprocessed cerise meats or processed meats relates to evolution of CHD and DM. Understanding potential differences in the associations of these different types of meats with disease outcomes, as well as the magnitude and dose-response of such furnishings, is relevant for elucidating the potentially relevant harmful constituents and for informing priorities for clinical and public health dietary guidance.
In this written report, we review the current evidence for furnishings of unprocessed reddish and processed meat consumption on CHD and DM. Relevant issues considered herein include: (1) the characterizations and definitions of the blazon of meat consumed, (2) the evidence for effects on clinical endpoints, including the magnitudes and dose-responses of effect, (three) the potential mechanisms for like or differing associations of different meat types with diverse cardiometabolic diseases, (4) the potential for bias in the evidence, and (v) the implications of the testify for clinical and public health priorities.
Categorizations of Meat Consumption
For understanding relations with disease endpoints, foods are oftentimes investigated in broad groupings, such as total meats, vegetables, fruits, fish, nuts, and and then on. Such categories are helpful to grouping together like foods when they have like potential wellness effects, simply can provide incomplete or misleading information when foods with differing wellness effects are combined into a single group. For example, whereas fish consumption is typically considered every bit a single category, we and others have shown that consumption of fatty or oily fish, which are highest in omega 3 s, is nigh strongly associated with lower CHD mortality, whereas consumption of fried fish or fish sandwiches, which are typically low in omega-three south and can be commercially fried in unhealthy oils, are non [ii]. Similarly, at that place are potentially of import nutritional differences in different types of meat, including the contents of calories, specific fats, iron, or preservatives such as sodium or nitrites. Different cooking methods (e.thou., broiling, baking, grilling, frying) could besides likely modify health effects—for example, charring and blackening of meats introduces products such equally heterocyclic amines and polycyclic aromatic hydrocarbons that likely increase cancer risk [iii]—but the effects of cooking methods on cardiometabolic run a risk take thus far been studied much less and will non be considered farther in the present review.
Based on fatty, cholesterol, and fe contents, meats are oft broadly categorized into red (east.m., beef, pork, lamb) or white (due east.thou., craven, turkey, rabbit) meats. Each of these types of meat tin can also be either preserved, typically past the addition of loftier levels of common salt and/or chemical preservatives (referred to future as "candy meat"), or consumed without such preservatives (referred to future as "unprocessed meat"). Boosted potential categories could include offal meat (i.e., organ meat) or non-domesticated meat (i.due east., game).
Considering these dissimilar major groupings and possible sub-groupings, it becomes evident that many differing definitions and categorizations of meats could be considered. Considering long-term studies of CHD and DM must be very large and follow participants for many years, the dietary assessment methods in such studies generally do not allow reliable quantification of every possible subtype of meat. Rather, the nearly reliable groupings of types of meat that accept been considered in such studies, which we will review herein, are of total unprocessed red meat consumption, including beef, pork, and lamb; and total processed meat consumption, including salary, hot dogs, sausage, salami, and processed deli or luncheon meats.
Evaluating Effects of Meat Consumption on Cardiometabolic Health
Dietary habits can impact a broad range of intermediate biologic pathways, including blood cholesterol concentrations, lipoprotein levels, blood force per unit area, insulin resistance, endothelial function, inflammation, adiposity, arrhythmic risk, and myocardial part and efficiency [4]. Consequently, effects of dietary habits on any 1 or fifty-fifty several of these surrogate outcomes are often insufficient for making strong inference well-nigh effects on clinical endpoints. An Plant of Medicine report on the use of biomarkers and similar surrogate markers concluded that the evidence does non back up using such markers, including LDL cholesterol levels, as a surrogate endpoint for the effects of dietary habits on clinical events [5].
Several authors and organizations have proposed comprehensive methods for evaluating effects of dietary habits on chronic disease endpoints [6–ix]. These methods each highlight the primacy of bear witness derived from studies of clinical endpoints rather than surrogate markers. Dietary habits and chronic disease endpoints can be studied in well-conducted randomized controlled trials (RCTs) or well-conducted, large prospective cohort studies, with further careful pooling of such findings in systematic reviews and meta-analyses to derive the all-time bachelor prove from all studies worldwide. Similar to almost other lifestyle risk factors (e.g., smoking, concrete activity, obesity, consumption of salt, dietary cholesterol, fruits, vegetables, nuts, whole grains), the effects of meat consumption on cardiometabolic endpoints take not, to our knowledge, been investigated in whatever RCTs. This is unsurprising given practical, ethical, and price considerations, as well equally inherent methodological limitations, such every bit the disability to perform blinding and inevitable noncompliance and crossover during the long periods of fourth dimension required to detect effects on chronic disease. Thus, prospective cohort studies provide the best bachelor prove to estimate causal effects of meat consumption on cardiometabolic events, with consideration of evidence for temporality, consistency, magnitude, and dose-response, as well as support from studies of biomarkers and surrogate markers to provide plausible biologic mechanisms [6–nine]. We review this evidence below.
Coronary Heart Disease
In a 2010 systematic review and meta-analysis [one••], nosotros separately evaluated the associations of unprocessed red and processed meats with the evolution of cardiometabolic events. For comparability across studies, all reported RR's were standardized to 100 g serving sizes for unprocessed ruby-red meats and 50 chiliad serving sizes for processed meats. To minimize potential bias, particular efforts were made to extract or directly obtain from the authors the risk estimates with the greatest control for potential confounders, and rough take a chance estimates were excluded a priori. Whenever possible, the multivariable model was selected that did non include variables that could be potential intermediates in the causal pathway (e.one thousand., blood cholesterol concentrations).
We identified a total of three prospective cohort studies and ane instance-control study that evaluated the relationship between unprocessed red meat consumption and incident CHD [x–13]. The pooled dose-response, including 56,311 participants and 769 events, found no significant clan between unprocessed red meat consumption and CHD chance (RR = 1.00 per 100 thousand serving/solar day, 95 % CI = 0.81–1.23) (Fig. ane). Pooled findings restricted to prospective cohorts [x–12] were like to the overall pooled guess (RR = 0.92, 95 % CI = 0.74–1.15).
Take chances of incident coronary heart disease (CHD) associated with each 100 g serving per day of unprocessed cerise meats (height; three accomplice studies and one case-control written report, 56,311 participants, and 769 events); and each 50 g serving per day of processed meats (lesser; four cohort studies and one example-command study, 614, 062 participants, and 21,308 events). The study by Sinha et al. (2009) assessed total cardiovascular (CHD plus stroke) bloodshed merely. Solid diamonds and lines stand for the study-specific relative risk (RR) and 95 % CI, respectively, derived from generalized least squares models for tendency (GLST). The dashed line and open diamond represent the overall pooled RR and 95 % CI, respectively, equally derived from both two-stage and one-phase GLST to the lowest degree squares for trend estimation. Reproduced with permission from Micha et al. (2010) [1••]
We identified six observational studies including 614,062 participants and 21,308 events [one••] that evaluated candy meat consumption and incident CHD [10, 12–15]. In pooled analyses, each 50 g serving/day of processed meats was associated with 42 % college chance (RR = 1.42, 95 % CI = ane.07–one.89) (Fig. 1). This stonger clan was seen despite the smaller serving size (50 g) compared with unprocessed red meats (100 thousand). Matching the serving sizes, each 100 chiliad serving/twenty-four hour period of processed meats was associated with 2-fold higher risk of CHD (RR = 2.02, 95 % CI = 1.14–3.57). When the assay was restricted to prospective cohorts [10, 12, 14, 15], similar findings were observed, with 44 % higher CHD risk per 50 g serving/day (RR = i.44, 95 % CI = ane.07–1.95). Of note, in many of these studies, processed hot dogs and deli meats, which would include processed poultry meats (craven, turkey), were included in total processed meats merely were not separately assessed.
Following publication of these findings, ii large studies have evaluated the associations between eating unprocessed red meat and risk of incident CHD [16•] and CVD mortality [17•]. In the prospective Nurse'due south Health Study (NHS), Bernstein and colleagues evaluated the association betwixt unprocessed red and processed meat consumption and CHD gamble [xvi•]. The assay included 84,136 women with three,162 CHD events. After adjusting for various lifestyle and dietary factors, each 100 g serving/day of unprocessed cherry meats was associated with 19 % higher adventure of CHD (RR = 1.19, 95 % CI = i.07–1.32), and each fifty g serving/day of processed meats was associated with xx % higher risk (RR = one.20, 95 % CI = 1.03–1.twoscore). Matching the serving sizes, each daily 100 g serving of processed meats was associated with 44 % higher risk (RR = ane.44, 95 % CI = ane.06–1.96), or nigh 2-fold higher than the take a chance for 100 m of unprocessed meats. Pan and colleagues [17•] re-evaluated the NHS and added the Health Professionals Follow-up Study (HPFS) cohort to assess the relationships between unprocessed red and processed meat consumption and risk of CVD death [17•]. Pooling the results of the two cohorts, each serving/24-hour interval of unprocessed red meats was associated with 18 % higher risk of CVD bloodshed (RR = 1.xviii, 95 % CI = 1.thirteen–ane.23), and each serving/day of processed meats was associated with 21 % higher chance of CVD mortality (RR = 1.21, 95 % CI = 1.13–1.31). Matching for serving sizes, each daily 100 chiliad serving of processed meats was associated with 46 % higher risk (RR = 1.46, 95 % CI = 1.28–i.72), about 2-fold college compared to unprocessed red meats.
The findings from both our 2010 meta-analysis [1••] and these ii updated publications propose that for every 100 thou serving/day, processed meat consumption has substantial associations with cardiovascular events (RR's of 2.02, 1.44, and 1.46 in our meta-analysis, the updated NHS analysis, and the updated NHS/HPFS assay, respectively). In comparison, unprocessed ruby-red meat consumption has lesser or no associations with cardiovascular events (respective RR's of i.00, 1.19, and ane.eighteen, respectively). Notably, these RR's correspond to daily consumption of 100 thou of these meats, i.e., one serving/day or vii servings/week. The corresponding RR'southward for weekly consumption of 100 1000 (i.e., one serving/calendar week) are 1.eleven, i.05, and 1.06 for processed meat consumption, and 1.00, ane.03, and 1.02 for unprocessed red meat consumption.
The magnitudes of these RR'southward for daily vs. weekly consumption are informative for considering risk across populations. For example, based on our analysis of 2003–2006 NHANES dietary recall information, the median free energy-adjusted intakes of unprocessed red meats and processed meats among American adults are one.nine and 1.half-dozen 100 one thousand servings/week (0.3 and 0.2 servings/day), respectively, and the 90th percentile intakes are 9.2 and 6.half dozen servings/week (1.3 and 0.9 servings/day), respectively. Thus, the risk observed per weekly serving is relevant to much of the US population, and the risk seen per daily serving is relevant to the highest consumers of meats.
What about subcategories of unprocessed ruby or processed meats, east.g., hamburger, hot dogs, or cafeteria meats alone? Unfortunately, relatively few studies have reported on such subcategories, raising concern for both publication bias and less generalizability. In our meta-analysis [1••], we identified just two prospective cohorts that reported associations of subtypes of unprocessed red meats with CHD [eleven], and no prospective studies that reported associations of subtypes of processed meats with CHD. The 2 newer reports described above [16•, 17•] updated the findings from two earlier reports on subtypes of unprocessed reddish and processed meats and CVD. Overall, associations appeared relatively similar for subtypes of unprocessed red meats, as well as for nigh subtypes of processed meats (including deli meats that would often be candy craven or turkey), except that bacon and hot dogs appeared associated with relatively college CHD adventure compared with other processed meat subtypes.
Type 2 Diabetes Mellitus
Using the methods reported in our meta-analysis [1••], an updated meta-analysis past Pan and colleagues [18•] evaluated the relationship between unprocessed blood-red and processed meat consumption and incident DM, including our previously identified studies plus updated findings from iii Harvard cohorts [19–21]. Consistent with our meta-analysis, serving sizes were standardized to 100 thousand for unprocessed reddish and 50 g for processed meats. Ix prospective accomplice studies, including 447,333 individuals and 28,206 events, assessed the human relationship between unprocessed blood-red meat consumption and incident DM (Fig. ii). Six of nine studies observed a meaning independent positive human relationship. In a pooled analysis, each daily 100 g serving of unprocessed red meats was associated with 19 % college risk (RR = 1.nineteen, 95 % CI = ane.04–1.37). Per weekly 100 g serving, the corresponding RR was i.03 (95 % CI = 1.01–1.05).
Risk of incident type 2 diabetes associated with each 100 g serving per solar day of unprocessed blood-red meats (top; nine cohort studies, 447,333 participants, and 28,206 events) and fifty g serving per day of candy meats (bottom; eight cohorts, 372,391 participants, and 26,234 events). Reproduced with permission from Pan et al. (2010) [18•]. Squares and lines are study-specific RRs and 95 % CI, respectively. Dashed line and open diamond are pooled gauge and 95 % CI, respectively
Eight prospective cohort studies, including 372,391 individuals and 26,234 events, assessed the relationship between candy meat consumption and incident DM (Fig. 2). Eight of nine studies observed a pregnant independent positive relationship. In a pooled analysis, each 50 thousand daily serving of processed meats was associated with 51 % higher adventure (RR = one.51, 95 % CI = i.25–1.83). Matching the serving sizes for comparability, each daily 100 g serving of processed meats was associated with a more than ii-fold college risk of diabetes (RR = 2.28, 95 % CI = 1.56–3.35). Per weekly 100 thou serving, the corresponding RR was ane.06 (95 % CI = ane.03–i.09).
Similar to our meta-analysis [1••], in these updated reports candy meats were predominantly red meats merely also included some processed poultry meats (e.g., chicken or turkey deli meats and hot dogs) that were not separately evaluated. Much less is known near these or other subtypes of candy meats. In our systematic review and meta-analysis [i••], nosotros identified five prospective cohort studies [xix–23] that reported RR's for subtypes of processed meat consumption and incident DM. The pooled dose-response demonstrated that each daily serving of bacon (2 slices) was associated with 2-fold higher risk of incident DM (RR = 2.07, 95 % CI = 1.40–3.04); of hot dogs, with similarly 2-fold higher run a risk (RR = 1.92, 95 % CI = 1.33–2.78); and of other processed meats, with relatively like 66 % higher take chances (RR = 1.66, 95 % CI = 1.thirteen–2.42). Thus, although overall data are nevertheless somewhat limited, the bachelor prove suggests that different types of processed meats, including cafeteria meats that would be often be processed white meats, have relatively similar associations with DM.
Following the publication of these findings, Fretts and colleagues evaluated relationships between unprocessed red and processed meat consumption and incident diabetes in the Strong Center Family Study [24•], a population of American Indians with loftier rates of obesity and diabetes. In multivariable adapted assay including 2,001 participants and 243 incident DM cases, high vs. low candy meat consumption was associated with 35 % higher risk (RR = ane.35, 95 % CI = 0.81–2.25), while high vs. depression unprocessed ruby meat consumption was not associated with risk (RR = 0.88, 95 % CI = 0.57, 1.35). In this [24•] and other prospective cohorts [xx–22], relatively similar relationships were observed for various subtypes of unprocessed red meats.
Potential Underlying Mechanisms
Similarities and differences in constituents of unprocessed red and processed meats can inform potential mechanisms for their varying relationships with CHD and DM. For example, the average saturated fatty content of unprocessed red and candy meats is like (Tabular array ane), making it unlikely that saturated fat content accounts for the different observed relationships with disease hazard. This is supported past evidence for no overall association of saturated fat consumption with incident CHD or DM [4, 25–30], peradventure because such effects vary depending on both the food source of saturated fat [31] and the macronutrient replacing saturated fat [27]. Average total fat content is higher in processed meats, but largely due to higher contents of monounsaturated and polyunsaturated fats, which are not linked to higher CHD or DM risk. Together these findings suggest that other components of meats may be relevant to cardiometabolic effects.
Table 1
Average nutritional and preservative contents in unprocessed ruby and candy meats per 50 grand servings, as consumed in the U.s.a.
| Per 50 g of meat | Red meats mean ± SE (median) | Processed meats hateful ± SE (median) |
|---|---|---|
| Energy (kcal) | 123.three ± 0.seven (124.1) | 138.one ± 2.0 (150.6) |
| Full fat (% energy) | 49.6 ± 0.iii (54.ane) | 57.5 ± 0.6 (69.4) |
| Total fat (k) | 7.i ± 0.i (7.7) | ten.2 ± 0.two (12.3) |
| Saturated fat (% energy) | 18.7 ± 0.1 (20.iv) | nineteen.four ± 0.3 (22.8) |
| Saturated fat (g) | 2.vii ± 0.0 (2.9) | 3.5 ± 0.1 (4.four) |
| Monounsaturated fat (% energy) | 21.4 ± 0.1 (23.nine) | 25.3 ± 0.3 (thirty.7) |
| Monounsaturated fat (g) | three.1 ± 0.0 (three.3) | 4.5 ± 0.one (5.three) |
| Polyunsaturated fat (% energy) | 2.vii ± 0.0 (1.7) | 6.4 ± 0.one (half-dozen.1) |
| Polyunsaturated fat (thou) | 0.4 ± 0.0 (0.2) | 1.1 ± 0.0 (0.6) |
| Protein (% free energy) | 46.2 ± 0.3 (41.5) | 35.4 ± 0.5 (27.4) |
| Protein (1000) | 13.6 ± 0.0 (13.v) | 9.8 ± 0.ane (viii.8) |
| Sodium (mg) | 154.8 ± 3.4 (127.i) | 621.vii ± 7.half-dozen (575.8) |
| Potassium (mg) | 161.0 ± 0.8 (152.8) | 170.2 ± 1.9 (153.6) |
| Cholesterol (mg) | 41.nine ± 0.2 (43.8) | 34.1 ± 0.3 (28.iii) |
| Iron (mg) | ane.1 ± 0.0 (i.ii) | 0.6 ± 0.0 (0.half dozen) |
| Nitrates (mg) | three.three ± 0.0 (two.9) | 4.6 ± 0.1 (3.0) |
| Nitrites (mg) | 0.5 ± 0.0 (0.seven) | 0.eight ± 0.0 (0.half-dozen) |
| Nitrosamines (3g) | 0.1 ± 0.0 (0.2) | 0.3 ± 0.0 (0.two) |
Boilerplate contents of dietary cholesterol are similar in unprocessed red and candy meats, or even a fleck lower in the latter, probable due to low-cholesterol white cafeteria meats (Table one). Whereas few prospective studies have evaluated dietary cholesterol and incident CHD or DM, the available evidence suggests little association with incident CHD in the general population, but a positive association with incident DM [26, 32–35]. Thus, dietary cholesterol content could partly account for the associations of unprocessed ruby and processed meat consumption with DM, although the similar contents of dietary cholesterol would non explicate the substantially higher DM gamble seen with processed meats.
Dietary heme iron may increase oxidative stress and insulin resistance, and has been associated with college risk of DM [36–38]. Thus, heme iron in both unprocessed scarlet and processed meats could partly explicate their relations with incident DM. Nonetheless, average heme atomic number 26 content is lower in processed meats (consistent with higher fatty and lower protein; Table 1), then this also would non explicate the stronger association of candy meats with DM risk.
Among major constituents, the largest difference between candy and unprocessed meats is in the content of preservatives, especially sodium (Table 1). On boilerplate, processed meats incorporate nearly 400 % more sodium and 50 % more nitrates per gram. Dietary sodium increases blood pressure level (BP), and may too increase peripheral vascular resistance and impair arterial compliance [39]. Based on the established effects of sodium on BP [40] and the human relationship between BP and clinical CHD events [41], the average sodium consumed from one daily 50 g serving of candy meats would predict about 27 % college risk of CHD, or more than two-third (on the log RR scale) of the observed 42 % college run a risk seen in cohort studies. Thus, sodium content alone is likely to account for a substantial portion of the observed CHD hazard with processed meat consumption. In add-on, the much lower average sodium content in unprocessed meats likely explains its smaller association with CHD. Other preservatives used in candy meats, such as nitrates and their byproducts (e.g., peroxynitrite), experimentally promote endothelial dysfunction, atherosclerosis, and insulin resistance [42–44]; and streptozotocin, a nitrosamine-related chemical compound, is a known diabetogenic compound [45]. Nitrites and nitrous compounds take as well been associated with type 1 diabetes in children [46, 47]; while in adults, nitrate concentrations have been used every bit a biomarker of endothelial dysfunction [48] and impaired insulin response [49]. Thus, higher nitrates/nitrates in processed meats could further explain their stronger relationships with both CHD and DM.
Different meat training methods could too influence wellness furnishings. High temperature commercial cooking or frying, normally used in preparing candy meats, tin can introduce heterocyclic amines and polycyclic aromatic hydrocarbons, which could increase risk of both CHD and DM [fifty–52]. Relatively little homo enquiry has been done on meat training methods and these disease outcomes, and farther study is urgently needed.
Meat Consumption and Cardiometabolic Diseases—Potential for Bias
Because the major criteria for evaluating causality [6–ix], at that place appears to exist consistency, temporality, dose-response, and plausible mechanisms for each of the associations described above. In observational studies, residual confounding due to imprecisely measured or unmeasured confounders can never be fully excluded. Thus, a key additional benchmark is the magnitude of the clan, which (if large) tin can provide reassurance that residuum confounding is less likely to fully explicate the human relationship; or (if small) tin raise concern that much or all of the observed associations may be due to bias or rest misreckoning. For candy meats and risk of CHD and DM, the magnitudes of the associations suggest that residual misreckoning is unlikely to fully account for the observed college risk. For unprocessed meats and take chances of CHD and DM, even so, the more pocket-size associations practice raise concern for potential bias.
It is relevant to consider the plausible directions of furnishings of such bias. In each of the cohorts that have evaluated meat consumption and chronic diseases, greater meat consumption is associated with less favorable lifestyle and dietary behaviors, including for case less physical activity, increased smoking, increased full free energy (consistent with higher BMI), and lower fruit, vegetable, dietary fiber, whole grains and fish intake, and college alcohol and trans fatty intake [15, 16•, 17•, eighteen•, 22, 23]. Rest confounding by these factors, or their correlates, would crusade overestimation of harmful furnishings of meat consumption. Consequently, the magnitude of the observed harmful associations betwixt unprocessed red or processed meat consumption and CHD and DM could exist overestimated, particularly in studies that do non comprehensively adjust for a range of lifestyle and dietary habits.
The possible magnitude of such overestimation can be challenging to quantify. In such circumstances, use of a "negative control" is informative: i.e., the evaluation of a separate health outcome for which the exposure of interest has trivial plausible biologic mechanism or expectation for a meaningful causal issue. One recent report provides useful data in this regard [15]. This large prospective cohort study reported positive associations for both total (candy and unprocessed) red meat and candy meat consumption and take a chance of cancer and CVD mortality (separate associations for unprocessed red meats were not published and could not be obtained by direct contact with the authors). Notably, this report too evaluated other causes of mortality, including a category of "all other deaths" that would predominantly exist from chronic pulmonary diseases, pneumonia, diabetes, and chronic liver illness [53, 54]. Except for diabetes, at that place is fiddling plausible biologic mechanism for a large issue of meat intake on these other types of deaths, and certainly none expected to be as great as effects on cancer or cardiovascular decease. All the same, in this analysis, the observed associations of full scarlet meat and processed meat consumption with these "other deaths" was actually considerably stronger than for cancer or cardiovascular deaths. One could hypothesize that meat consumption did have some very powerful, heretofore unrecognized causal effects on deaths from chronic pulmonary illness, pneumonia, and chronic liver disease. More than plausibly, participants consuming more than meats had other important lifestyle behaviors affecting mortality that were not fully accounted for in the assay. Plausible confounders included major risk factors that were assessed but measured with imprecision, such as education, physical activity, smoking, alcohol use, adiposity, and fruit and vegetable consumption; and other potential confounders not included in the model at all, such as income, second-mitt smoke, air pollution, alcohol patterns (e.g., rampage drinking), and consumption of starches, refined carbohydrates, sugars, trans fat, dietary fiber, whole grains, basics, seeds, and legumes [54]. Overall, the findings in this study for "all other deaths" suggest that meaningful balance misreckoning and bias are present, causing overestimation of harms of meat consumption in this cohort.
Bias can also reduce observed associations. In large observational studies, random errors in measurement of self-reported diet can cause bias toward the null, causing underestimation of true associations. Similarly, aligning for factors which could be potential intermediates in the causal pathway between meat consumption and CHD or DM would also cause bias toward the naught. Several of the studies in our meta-analysis did adjust for factors that could exist either confounders or intermediates, mainly blood lipids and/or blood pressure concentrations [12, thirteen, xix, 21, 55–57]. Thus, the net furnishings of residual confounding (which hither would overestimate furnishings) versus random errors in dietary assessment and overadjustment for intermediates (which here would underestimate effects) should always be considered. Large observed effects in the setting of comprehensive covariate adjustment are reassuring; small observed furnishings in the setting of incomplete adjustment are apropos, particularly when relations with "negative control" outcomes are similar or fifty-fifty more robust.
Conclusions
The available evidence indicates strong associations of processed meat consumption with incident CHD and DM, more modest associations of unprocessed red meat consumption with incident DM, and smaller or no associations of unprocessed red meat consumption with incident CHD. Our review of this evidence also highlights the importance of appropriate categorization of meat types and careful consideration of magnitudes and directions of bias (e.g., due to confounding, overadjustment, or misclassification) when evaluating associations of meat intake with clinical endpoints. The most relevant constituents for cardiometabolic furnishings may include dietary cholesterol, heme iron, and nitrates/nitrites for risk of DM; and sodium and nitrates/nitrites for risk of CHD. These findings suggest that clinical and public health guidance should prioritize reduction of candy meat consumption to reduce CHD and DM take a chance, besides as reduction of sodium and other preservative contents of processed meats. The 2010 US Dietary Guidelines for Americans recommend selecting lean meats, increasing the amount of seafood consumed in place of some meat and poultry, and specifically limiting processed meats [58]. The recommendation to select lean meats was partly based on saturated fat and dietary cholesterol content and consistent effects on blood LDL-cholesterol. Interestingly, our assay suggests that other constituents may be more relevant.
Our findings have additional implications. Starting time, it may be misguided to promote consumption of candy deli meats, such as processed chicken, turkey, or bologna, as "healthy" alternatives on the basis of their lower total fatty or saturated fat contents. The electric current bear witness suggests that processed meats are particularly harmful for CHD and DM, and that the content of sodium and other preservatives, rather than total fat or saturated fat, may be about relevant. While further investigation is needed to determine if unlike subcategories of candy meats have unlike effects on cardiometabolic chance, based on the electric current evidence information technology would exist prudent to minimize consumption of all candy meats. 2d, because sodium and peradventure other preservatives appear specially relevant, particularly for CHD run a risk, new industry focus on reducing these additives would exist particularly of import for reducing the harms of processed meat consumption.
Whereas the prove indicates that reducing processed meat consumption should exist a priority for clinical and public health guidance, and that unprocessed red meat consumption has smaller furnishings on DM and little or no outcome on CHD, no evidence from these studies suggested any cardiometabolic benefits of unprocessed red meat consumption. Additionally, cattle farming has tremendous agin environmental impacts, including on deforestation, water use, and carbon and methyl hydride emissions [59]. Thus, healthier alternatives with strong evidence for cardiometabolic benefits, such as fish, basics, fruits, whole grains, and vegetables, are vastly preferable dietary choices to consuming unprocessed red meats. Still, for individual and public health focus, prioritizing reduction in processed meats as well every bit other harmful dietary factors, such every bit partially hydrogenated vegetable oils, high-sodium foods, and refined grains, starches, and sugars, is likely to produce the largest net benefits for both private and population wellness.
Footnotes
Disclosure R. Micha: none; Thou. Michas: none; D. Mozaffarian: Received ad hoc honoraria from Nutrition Impact, Unilever, and SPRIM.
Contributor Information
Renata Micha, Section of Epidemiology, Harvard Schoolhouse of Public Health, Boston, MA, USA. Department of Food Science and Technology, Unit of Human Nutrition, Agronomical University of Athens, Athens, Greece.
Georgios Michas, Department of Internal Medicine, Full general Hospital of Kalamata, Kalamata, Greece.
Dariush Mozaffarian, Departments of Epidemiology and Nutrition, Harvard School of Public Health, 665 Huntington Ave Bldg two-319, Boston, MA 02115, U.s.. Segmentation of Cardiovascular Medicine and Channing Partitioning of Network Medicine, Department of Medicine, Brigham and Women'due south Hospital and Harvard Medical School, 665 Huntington Ave Bldg 2-319, Boston, MA 02115, USA.
References
Papers of particular interest, published recently, take been highlighted as:
• Of importance
•• Of major importance
••1. Micha R, Wallace SK, Mozaffarian D. Red and processed meat consumption and chance of incident coronary heart disease, stroke, and diabetes mellitus: a systematic review and meta-analysis. Circulation. 2010;121(21):2271–83. The outset systematic review and meta-analysis that assessed relationships betwixt unprocessed crimson and processed meat consumption and chance of incident coronary heart disease, stroke, and type 2 diabetes. This meta-analysis provided evidence that the effects of meat consumption on cardiometabolic outcomes might vary depending on the extent of processing i.e., whether or not the meat is fresh (unprocessed) or has been processed and preserved for long-term storage, typically by adding high amounts of salt, besides as other preservatives such every bit nitrates. [PMC free article] [PubMed] [Google Scholar]
two. Mozaffarian D, Wu JH. Omega-3 fatty acids and cardiovascular disease: furnishings on risk factors, molecular pathways, and clinical events. J Am Coll Cardiol. 2011;58(20):2047–67. [PubMed] [Google Scholar]
3. Turesky RJ, Le Marchand Fifty. Metabolism and biomarkers of heterocyclic aromatic amines in molecular epidemiology studies: lessons learned from aromatic amines. Chem Res Toxicol. 2011;24 (eight):1169–214. [PMC free article] [PubMed] [Google Scholar]
4. Mozaffarian D. Braunwald's Heart Disease: a Textbook of Cardiovascular Medicine. Philadelphia: 2012. Chapter 48: Diet and Cardiovascular Diseases. [Google Scholar]
five. Found of Medicine of the National Academies. Evaluation of Biomarkers and Surrogate Endpoints in Chronic Affliction. 2010. [Google Scholar]
half-dozen. Micha R, Kalantarian S, Wirojratana P, et al. Estimating the global and regional burden of suboptimal diet on chronic disease: methods and inputs to the assay. Eur J Clin Nutr. 2012;66 (one):119–29. [PubMed] [Google Scholar]
7. World Wellness Organisation. World Wellness Organ Tech Rep Ser. Vol. 916. Geneva: 2003. Nutrition, nutrition and the prevention of chronic diseases: report of a joint WHO/FAO adept consultation; pp. i–viii.pp. i–149. [PubMed] [Google Scholar]
9. World Cancer Inquiry Fund/American Institute for Cancer Inquiry. Food, Nutrition, Physical Action, and the Prevention of Cancer: a Global Perspective. Washington DC: AICR; 2007. [Google Scholar]
10. Whiteman D, Muir J, Jones Fifty, et al. Dietary questions as determinants of mortality: the OXCHECK experience. Public Health Nutr. 1999;2(4):477–87. [PubMed] [Google Scholar]
11. Ascherio A, Willett WC, Rimm EB, et al. Dietary iron intake and risk of coronary disease among men. Circulation. 1994;89(iii):969–74. [PubMed] [Google Scholar]
12. Shush Five, Zhao Y, Lee AH, et al. Health-related behaviours equally predictors of mortality and morbidity in Australian Aborigines. Prev Med. 2007;44(2):135–42. [PubMed] [Google Scholar]
13. Martinez-Gonzalez MA, Fernandez-Jarne Eastward, Serrano-Martinez M, et al. Mediterranean diet and reduction in the adventure of a get-go acute myocardial infarction: an operational good for you dietary score. Eur J Nutr. 2002;41(iv):153–60. [PubMed] [Google Scholar]
fourteen. Liu J, Stampfer MJ, Hu FB, et al. Dietary fe and cerise meat intake and run a risk of coronary heart illness in postmenopausal women. Am J Epidemiol. 2003;157:S100. [Google Scholar]
15. Sinha R, Cantankerous AJ, Graubard BI, et al. Meat intake and mortality: a prospective report of over half a million people. Arch Intern Med. 2009;169(half-dozen):562–71. [PMC free article] [PubMed] [Google Scholar]
•16. Bernstein AM, Lord's day Q, Hu FB, et al. Major dietary protein sources and run a risk of coronary centre illness in women. Apportionment. 2010;122(ix):876–83. Bernstein and colleagues evaluated the association between unprocessed cherry and processed meat consumption and incidence of coronary center disease in the Nurse's Health Study cohort. [PMC free article] [PubMed] [Google Scholar]
•17. Pan A, Sun Q, Bernstein AM, et al. Red meat consumption and mortality: results from two prospective cohort studies. Arch Intern Med. 2012;172(7):555–63. Pan and colleagues evaluated the Nurse'south Health Study and the Health Professionals Follow-upwardly Study cohort to assess the associations betwixt unprocessed scarlet and candy meat consumption and risk of CVD death. [PMC free article] [PubMed] [Google Scholar]
•eighteen. Pan A, Sun Q, Bernstein AM, et al. Ruddy meat consumption and risk of type 2 diabetes: 3 cohorts of US adults and an updated meta-analysis. Am J Clin Nutr. 2011;94(four):1088–96. An updated meta-analysis, using the methods reported in our meta-analysis [1], which evaluated the relationship betwixt unprocessed red and processed meat consumption and incident blazon 2 diabetes, including our previously identified studies plus updated findings from iii Harvard cohorts [19–21] [PMC free commodity] [PubMed] [Google Scholar]
xix. Fung TT, Schulze M, Manson JE, et al. Dietary patterns, meat intake, and the risk of type 2 diabetes in women. Arch Intern Med. 2004;164(20):2235–40. [PubMed] [Google Scholar]
20. Schulze MB, Manson JE, Willett WC, et al. Processed meat intake and incidence of Type 2 diabetes in younger and middle-anile women. Diabetologia. 2003;46(11):1465–73. [PubMed] [Google Scholar]
21. van Dam RM, Willett WC, Rimm EB, et al. Dietary fatty and meat intake in relation to risk of type 2 diabetes in men. Diabetes Care. 2002;25(3):417–24. [PubMed] [Google Scholar]
22. Song Y, Manson JE, Buring JE, et al. A prospective study of red meat consumption and type 2 diabetes in middle-aged and elderly women: the women's health study. Diabetes Care. 2004;27 (ix):2108–15. [PubMed] [Google Scholar]
23. Villegas R, Shu XO, Gao YT, et al. The association of meat intake and the run a risk of type two diabetes may be modified past body weight. Int J Med Sci. 2006;3(4):152–9. [PMC free article] [PubMed] [Google Scholar]
•24. Fretts AM, Howard BV, McKnight B, et al. Associations of candy meat and unprocessed ruddy meat intake with incident diabetes: the Strong Centre Family unit Study. Am J Clin Nutr. 2012;95(iii):752–8. Fretts and colleagues evaluated relationships between unprocessed ruddy and processed meat consumption and incident diabetes in the Strong Heart Family Study cohort, in a population of American Indians characterized by relative high rates of obesity and diabetes. [PMC free article] [PubMed] [Google Scholar]
25. Jakobsen MU, O'Reilly EJ, Heitmann BL, et al. Major types of dietary fatty and risk of coronary heart affliction: a pooled analysis of xi cohort studies. Am J Clin Nutr. 2009;89(v):1425–32. [PMC gratuitous article] [PubMed] [Google Scholar]
26. Meyer KA, Kushi LH, Jacobs DR, Jr, et al. Dietary fat and incidence of type 2 diabetes in older Iowa women. Diabetes Intendance. 2001;24(9):1528–35. [PubMed] [Google Scholar]
27. Micha R, Mozaffarian D. Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the bear witness. Lipids. 2010;45(ten):893–905. [PMC complimentary article] [PubMed] [Google Scholar]
28. Feskens EJ, Virtanen SM, Rasanen L, et al. Dietary factors determining diabetes and dumb glucose tolerance. A 20-year follow-up of the Finnish and Dutch cohorts of the Vii Countries Study. Diabetes Care. 1995;xviii(8):1104–12. [PubMed] [Google Scholar]
29. Galgani JE, Uauy RD, Aguirre CA, et al. Effect of the dietary fat quality on insulin sensitivity. Br J Nutr. 2008;100(three):471–9. [PubMed] [Google Scholar]
30. Riserus U, Willett WC, Hu FB. Dietary fats and prevention of type 2 diabetes. Prog Lipid Res. 2009;48(i):44–51. [PMC free article] [PubMed] [Google Scholar]
31. de Oliveira Otto MC, Mozaffarian D, Kromhout D, et al. Dietary intake of saturated fatty by nutrient source and incident cardiovascular disease: the Multi-Ethnic Study of Atherosclerosis. Am J Clin Nutr. 2012;96(2):397–404. [PMC free article] [PubMed] [Google Scholar]
32. Djousse L, Gaziano JM. Dietary cholesterol and coronary avenue disease: a systematic review. Curr Atheroscler Rep. 2009;11 (half-dozen):418–22. [PubMed] [Google Scholar]
33. Salmeron J, Hu FB, Manson JE, et al. Dietary fat intake and adventure of type 2 diabetes in women. Am J Clin Nutr. 2001;73 (6):1019–26. [PubMed] [Google Scholar]
34. Siri-Tarino PW, Sun Q, Hu FB, et al. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010;91(3):535–46. [PMC free article] [PubMed] [Google Scholar]
35. Djousse L, Gaziano JM, Buring JE, et al. Egg consumption and run a risk of type 2 diabetes in men and women. Diabetes Intendance. 2009;32 (ii):295–300. [PMC complimentary article] [PubMed] [Google Scholar]
36. Rajpathak South, Ma J, Manson J, et al. Fe intake and the risk of blazon 2 diabetes in women: a prospective cohort report. Diabetes Care. 2006;29(vi):1370–6. [PubMed] [Google Scholar]
37. Lee DH, Folsom AR, Jacobs DR., Jr Dietary iron intake and Blazon 2 diabetes incidence in postmenopausal women: the Iowa Women'south Wellness Study. Diabetologia. 2004;47(2):185–94. [PubMed] [Google Scholar]
38. Zhao Z, Li S, Liu Grand, et al. Body iron stores and heme-iron intake in relation to risk of blazon ii diabetes: a systematic review and meta-analysis. PLoS Ane. 2012;7(7):e41641. [PMC free commodity] [PubMed] [Google Scholar]
39. Sacks FM, Campos H. Dietary therapy in hypertension. N Engl J Med. 2010;362(22):2102–12. [PubMed] [Google Scholar]
40. He FJ, MacGregor GA. Issue of modest salt reduction on claret pressure: a meta-analysis of randomized trials. Implications for public health. J Hum Hypertens. 2002;16(xi):761–lxx. [PubMed] [Google Scholar]
41. Singh GM, Danaei One thousand, Farzadfar F, et al. Consequence sizes for cardiovascular disease and diabetes outcomes of metabolic risk factors for population-based comparative risk cess (CRA) Int J Cardiol. 2012 Nether Review. [Google Scholar]
42. Forstermann U. Oxidative stress in vascular affliction: causes, defense force mechanisms and potential therapies. Nat Clin Pract Cardiovasc Med. 2008;5(vi):338–49. [PubMed] [Google Scholar]
43. McGrowder D, Ragoobirsingh D, Dasgupta T. Furnishings of Southward-nitroso-N-acetyl-penicillamine administration on glucose tolerance and plasma levels of insulin and glucagon in the dog. Nitric Oxide. 2001;5(4):402–12. [PubMed] [Google Scholar]
44. Portha B, Giroix MH, Cros JC, et al. Diabetogenic effect of N-nitrosomethylurea and Due north-nitrosomethylurethane in the adult rat. Ann Nutr Aliment. 1980;34(5–6):1143–51. [PubMed] [Google Scholar]
45. Gajdosik A, Gajdosikova A, Stefek Grand, et al. Streptozotocin-induced experimental diabetes in male Wistar rats. Gen Physiol Biophys. 1999;18(Spec No):54–62. [PubMed] [Google Scholar]
46. Virtanen SM, Jaakkola L, Rasanen 50, et al. Nitrate and nitrite intake and the risk for blazon 1 diabetes in Finnish children. Babyhood Diabetes in Finland Study Grouping. Diabet Med. 1994;eleven(7):656–62. [PubMed] [Google Scholar]
47. Parslow RC, McKinney PA, Law GR, et al. Incidence of childhood diabetes mellitus in Yorkshire, northern England, is associated with nitrate in drinking water: an ecological analysis. Diabetologia. 1997;xl(v):550–six. [PubMed] [Google Scholar]
48. Kleinbongard P, Dejam A, Lauer T, et al. Plasma nitrite concentrations reflect the degree of endothelial dysfunction in humans. Gratuitous Radic Biol Med. 2006;twoscore(ii):295–302. [PubMed] [Google Scholar]
49. Pereira EC, Ferderbar S, Bertolami MC, et al. Biomarkers of oxidative stress and endothelial dysfunction in glucose intolerance and diabetes mellitus. Clin Biochem. 2008;41(xviii):1454–60. [PubMed] [Google Scholar]
50. Binkova B, Smerhovsky Z, Strejc P, et al. Deoxyribonucleic acid-adducts and atherosclerosis: a written report of accidental and sudden death males in the Czechia. Mutat Res. 2002;501(1–two):115–28. [PubMed] [Google Scholar]
51. Lakshmi VM, Schut HA, Zenser Television. 2-Nitrosoamino-3-methylimi-dazo[4,5-f]quinoline activated past the inflammatory response forms nucleotide adducts. Food Chem Toxicol. 2005;43(11):1607–17. [PubMed] [Google Scholar]
52. Bogen KT, Keating GA. U.Southward. dietary exposures to heterocyclic amines. J Expo Anal Environ Epidemiol. 2001;11(3):155–68. [PubMed] [Google Scholar]
53. Anderson RN, Rosenberg HM. Disease classification: measuring the effect of the Tenth Revision of the International Classification of Diseases on cause-of-decease data in the United states. Stat Med. 2003;22(9):1551–70. [PubMed] [Google Scholar]
54. Mozaffarian D. Meat intake and mortality: evidence for harm, no effect, or do good? Curvation Intern Med. 2009;169(xvi):1537–eight. writer reply 1539. [PubMed] [Google Scholar]
55. Salonen JT, Nyyssonen Chiliad, Korpela H, et al. Loftier stored iron levels are associated with backlog take chances of myocardial infarction in eastern Finnish men. Apportionment. 1992;86(3):803–11. [PubMed] [Google Scholar]
56. Kontogianni MD, Panagiotakos DB, Pitsavos C, et al. Human relationship between meat intake and the development of acute coronary syndromes: the CARDIO2000 case-control report. Eur J Clin Nutr. 2008;62(2):171–7. [PubMed] [Google Scholar]
57. Tavani A, Bertuzzi K, Gallus S, et al. Run a risk factors for non-fatal acute myocardial infarction in Italian women. Prev Med. 2004;39 (1):128–34. [PubMed] [Google Scholar]
59. Steinfeld H, Gerber P, Wassenaar T, et al. FAO. Livestock's Long Shadow: Environmental Problems and Options. Rome: 2006. [Google Scholar]
60. Centers for Disease Control and Prevention. National Wellness and Nutrition Examination Survey. [cited; Available from: http://www.cdc.gov.nchs/nhanes.htm.
61. Griesenbeck JS, Steck MD, Huber JC, Jr, et al. Development of estimates of dietary nitrates, nitrites, and nitrosamines for use with the Curt Willet Food Frequency Questionnaire. Nutr J. 2009;8:16. [PMC costless article] [PubMed] [Google Scholar]
Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3483430/
0 Response to "Are There Studies That Show Grass Fed Beef Causes Heart Disease"
Post a Comment