What’s the Deal with Dairy?

In the past few months, I have presented research that suggests that following either a plant based vegan or a traditional paleo diet may be better for your health than following diet recommendations of the American Heart Association or American Diabetes Association.

To review, a plant based vegan diet consists of mainly vegetables, fruits, whole grains, legumes, nuts, and seeds. A traditional paleo diet includes mainly vegetables, some fruit, lean meats, eggs, nuts, and seeds. The vegan diet excludes meat and eggs while the paleo diet excludes grains. Both diets exclude dairy, processed foods, added sugar, and most saturated fat (some versions of the paleo diet include high amounts of saturated fat that are not typical of the more traditional paleo diet usually used in research studies). Meanwhile, the recommended diets of most mainstream nutrition groups include all of the foods in the vegan and paleo diets plus low-fat dairy, but still exclude processed foods, added sugar, and saturated fat.

The key food that is excluded from the paleo and vegan diets, but included in other recommended diets is DAIRY. This has prompted me to research whether or not dairy has a place in a healthy diet.

The Claim: Dairy is bad for you. You should avoid dairy if you want to have a healthy diet.

Google search: When I searched, “Is dairy bad for you?” I found the following arguments against dairy:

  • Milk is the perfect food, but only for calves
  • Milk doesn’t reduce fractures and may increase your risk of fractures
  • Countries that consume less dairy have the lowest rates of osteoporosis
  • Calcium and/or dairy may increase your risk of prostate cancer
  • 75% of the world’s population is lactose intolerant, especially people that are not of northern European descent
  • If you give up dairy, you should notice improvement with your sinuses, post-nasal drip, headaches, irritable bowel syndrome, energy, and weight
  • Dairy may cause acne

And the following arguments for dairy:

  • Dairy is a good source of nutrition. It includes high amounts of calcium, vitamin D, riboflavin, vitamin B12, potassium and phosphorus. It also contains vitamins A, B1, B6, selenium, zinc and magnesium. Grass-fed, full fat dairy also contains high amounts of omega-3 fatty acids, conjugated linoleic acid and vitamin K2.
  • Dairy improves bone density, reduces osteoporosis, and lowers the risk of fractures
  • Full-fat dairy is associated with a lower risk of obesity, type 2 diabetes, and heart disease
  • Dairy may be protective against colorectal cancer

Follow up questions

  • Are some types of dairy better or worse than others?
  • Is dairy good for some people and bad for others?

Peer-reviewed research

I searched “dairy consumption” on PubMed and included only reviews and meta-analyses. The 26 studies here are the most relevant reviews of how dairy consumption is associated with metabolic syndrome (heart disease, obesity, type 2 diabetes). Several of the studies included cancer and bone health outcomes. However, I did not include studies that only reviewed cancer or bone health outcomes without other components of metabolic syndrome. Of note, I did not come across any reviews that suggested dairy was associated with unfavorable cancer or bone health outcomes.

Complete abstracts are provided below with links to full studies. Many are free to access. Feel free to read them thoroughly, only read the sections in bold, or just skip to the “What We Know and Don’t Know Section”.

  1. Dairy products consumption and metabolic syndrome in adults: systematic review and meta-analysis of observational studies. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26416233
    • The association of dairy products consumption with risk of metabolic syndrome (MetS) has been inconsistently reported in observational studies. A systematic review and meta-analysis of published observational studies was conducted to quantitatively evaluate this association. Relevant studies were identified by searching PubMed and EMBASE databases and by carefully checking the bibliographies of retrieved full reports and related reviews. Eligible studies were observational studies that investigated the association between dairy products consumption and risk of MetS in adults, with risk estimates available. Random-effects model was assigned to calculate the summary risk estimates. The final analysis included 15 cross-sectional studies, one case-control study and seven prospective cohort studies. Higher dairy consumption significantly reduced MetS by 17% in the cross-sectional/case-control studies (odds ratio = 0.83, 95% confidence interval [CI], 0.73-0.94), and by 14% (relative risk [RR] = 0.86, 95% CI, 0.79-0.92) in cohort studies. The inverse dairy-MetS association was consistent in subgroup and sensitivity analyses. The dose-response analysis of the cohort studies conferred a significant 6% (RR = 0.94, 95% CI, 0.90-0.98) reduction in the risk of MetS for each increment in dairy consumption of one serving/d. No significant publication bias was observed. Our findings suggest an inverse dose-response relationship between dairy consumption and risk of MetS.
  2. Yogurt and dairy product consumption to prevent cardiometabolic diseases: epidemiologic and experimental studies. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24695891
    • Dairy products contribute important nutrients to our diet, including energy, calcium, protein, and other micro- and macronutrients. However, dairy products can be high in saturated fats, and dietary guidelines generally recommend reducing the intake of saturated fatty acids (SFAs) to reduce coronary artery disease (CAD). Recent studies question the role of SFAs in cardiovascular disease (CVD) and have found that substitution of SFAs in the diet with omega-6 (n-6) polyunsaturated fatty acids abundant in vegetable oils can, in fact, lead to an increased risk of death from CAD and CVD, unless they are balanced with n-3 polyunsaturated fat. Replacing SFAs with carbohydrates with a high glycemic index is also associated with a higher risk of CAD. Paradoxically, observational studies indicate that the consumption of milk or dairy products is inversely related to incidence of CVD. The consumption of dairy products has been suggested to ameliorate characteristics of the metabolic syndrome, which encompasses a cluster of risk factors including dyslipidemia, insulin resistance, increased blood pressure, and abdominal obesity, which together markedly increase the risk of diabetes and CVD. Dairy products, such as cheese, do not exert the negative effects on blood lipids as predicted solely by the content of saturated fat. Calcium and other bioactive components may modify the effects on LDL cholesterol and triglycerides. Apart from supplying valuable dairy nutrients, yogurt may also exert beneficial probiotic effects. The consumption of yogurt, and other dairy products, in observational studies is associated with a reduced risk of weight gain and obesity as well as of CVD, and these findings are, in part, supported by randomized trials.
  3. The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease. (2013) https://www.ncbi.nlm.nih.gov/pubmed/22810464
    • PURPOSE: To comprehensively review the data on the relationship between the consumption of dairy fat and high-fat dairy foods, obesity, and cardiometabolic disease.
    • METHODS: We have conducted a systematic literature review of observational studies on the relationship between dairy fat and high-fat dairy foods, obesity, and cardiometabolic disease. We have integrated these findings with data from controlled studies showing effects of several minor dairy fatty acids on adiposity and cardiometabolic risk factors, and data on how bovine feeding practices influence the composition of dairy fat.
    • RESULTS: In 11 of 16 studies, high-fat dairy intake was inversely associated with measures of adiposity. Studies examining the relationship between high-fat dairy consumption and metabolic health reported either an inverse or no association. Studies investigating the connection between high-fat dairy intake and diabetes or cardiovascular disease incidence were inconsistent. We discuss factors that may have contributed to the variability between studies, including differences in (1) the potential for residual confounding; (2) the types of high-fat dairy foods consumed; and (3) bovine feeding practices (pasture- vs. grain-based) known to influence the composition of dairy fat.
    • CONCLUSIONS: The observational evidence does not support the hypothesis that dairy fat or high-fat dairy foods contribute to obesity or cardiometabolic risk, and suggests that high-fat dairy consumption within typical dietary patterns is inversely associated with obesity risk. Although not conclusive, these findings may provide a rationale for future research into the bioactive properties of dairy fat and the impact of bovine feeding practices on the health effects of dairy fat.
  4. Dairy products, yogurt consumption, and cardiometabolic risk in children and adolescents. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26175484
    • The high prevalence of obesity in children is a global health issue. Obesity in children and adolescents can result in hypertension, dyslipidemia, chronic inflammation, and hyperinsulinemia, increasing the risk of death, as children grow into adulthood, and raising public health concerns. Type 2 diabetes in children and adolescents is a cardiovascular disease (CVD) risk factor. Dairy consumption may have a protective effect against the development of CVD, but there is scarce evidence of this in children and adolescents. Within the Healthy Lifestyle in Europe by Nutrition in Adolescence, the objective of this study was to investigate the relationship between dairy consumption and CVD risk factors in a sample of adolescents (aged 12.5-17.5 years) from 8 European cities. Overall, dairy products emerged as the food group that best identified adolescents at low CVD risk. Higher consumption of milk and yogurt and of milk- and yogurt-based beverages was associated with lower body fat, lower risk for CVD, and higher cardiorespiratory fitness.
  5. Dairy consumption and pre-school, school-age and adolescent obesity in developed countries: a systematic review and meta-analysis. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24655317
    • Childhood obesity, the primary health problem affecting children in developed countries, has been attributed in part to changes in dietary patterns. Secular trends suggest a decrease in childhood dairy consumption coinciding with the rise in obesity prevalence. The objective of the present systematic review and meta-analysis was to consider evidence of associations between dairy intake and adiposity in pre-schoolers, school-age children and adolescents in developed countries. Of 36 studies included in the systematic review, sufficient data for effect size estimation and inclusion in the meta-analysis were obtained from 22 studies. No significant association was found between dairy intake and adiposity in the aggregated data, although statistical heterogeneity was high (I(2) = 0.72). Among adolescents, however, dairy intake was inversely associated with adiposity (effect size -0.26, [-0.38, -0.14], P < 0.0001). Effect size was not predicted by exposure variable (milk vs. dairy), study design, statistical methods, outcome variables or sex. Interpretation of results was complicated by variability in study methods and insufficient adjustment for relevant confounders, particularly dietary reporting accuracy, sweetened beverage intake and pubertal development. Despite limitations, available data suggest a neutral effect of dairy intake on adiposity during early and middle childhood and a modestly protective effect in adolescence.
  6. Dairy product consumption and the metabolic syndrome. (2015) https://www.ncbi.nlm.nih.gov/pubmed/25605674
    • AIMS: To briefly summarize findings from epidemiological studies on the relationship between dairy product consumption and the metabolic syndrome(MetS).MATERIALS AND METHODS: A search for relevant literature was undertaken on Web of Science, Google scholar, Pubmed (2000 to July 2013), to identify observational studies which examined the association between dairy intake and MetS (prevalence or incidence), and for any randomized controlled trials investigating the effect of dairy intake on MetS.
    • RESULTS: Here we review the physiological effects and possible mechanisms involved of three main dairy constituents (calcium (Ca), protein, fat) on important components of the MetS. Effects of Ca may be related to intestinal binding to fatty acids or bile acids, or to changes in intracellular Ca metabolism by suppressing calciotropic hormones. Dietary proteins may increase satiety in both the short and longer term, which may result in a reduced energy intake. Dairy proteins are precursors of angiotensin-I converting enzyme-inhibitory peptides, which may lower blood pressure. To reduce the intake of saturated fatty acids (SFA), the consumption of low-fat instead of high-fat dairy products is recommended.
    • CONCLUSION: More research is warranted to better understand the physiological effects and the mechanisms involved of dairy products in the prevention and treatment of the MetS.
  7. Dairy products consumption and risk of type 2 diabetes: systematic review and dose-response meta-analysis. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24086304
    • BACKGROUND: The consumption of dairy products may influence the risk of type 2 diabetes mellitus (T2DM), but inconsistent findings have been reported. Moreover, large variation in the types of dairy intake has not yet been fully explored.
    • METHODS AND RESULTS: We conducted a systematic review and meta-analysis to clarify the dose-response association of dairy products intake and T2DM risk. We searched PubMed, EMBASE and Scopus for studies of dairy products intake and T2DM risk published up to the end of October 2012. Random-effects models were used to estimate summary relative risk (RR) statistics. Dose-response relations were evaluated using data from different dairy products in each study. We included 14 articles of cohort studies that reported RR estimates and 95% confidence intervals (95% CIs) of T2DM with dairy products intake. We found an inverse linear association of consumption of total dairy products (13 studies), low-fat dairy products (8 studies), cheese (7 studies) and yogurt (7 studies) and risk of T2DM. The pooled RRs were 0.94 (95% CI 0.91-0.97) and 0.88 (0.84-0.93) for 200 g/day total and low-fat dairy consumption, respectively. The pooled RRs were 0.80 (0.69-0.93) and 0.91 (0.82-1.00) for 30 g/d cheese and 50 g/d yogurt consumption, respectively. We also found a nonlinear association of total and low-fat dairy intake and T2DM risk, and the inverse association appeared to be strongest within 200 g/d intake.
    • CONCLUSION: A modest increase in daily intake of dairy products such as low fat dairy, cheese and yogurt may contribute to the prevention of T2DM, which needs confirmation in randomized controlled trials.
  8. Dairy consumption and CVD: a systematic review and meta-analysis. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26786887
    • Inverse associations between dairy consumption and CVD have been reported in several epidemiological studies. Our objective was to conduct a meta-analysis of prospective cohort studies of dairy intake and CVD. A comprehensive literature search was conducted to identify studies that reported risk estimates for total dairy intake, individual dairy products, low/full-fat dairy intake, Ca from dairy sources and CVD, CHD and stroke. Random-effects meta-analyses were used to generate summary relative risk estimates (SRRE) for high v. low intake and stratified intake dose-response analyses. Additional dose-response analyses were performed. Heterogeneity was examined in sub-group and sensitivity analyses. In total, thirty-one unique cohort studies were identified and included in the meta-analysis. Several statistically significant SRRE below 1.0 were observed, namely for total dairy intake and stroke (SRRE=0·91; 95% CI 0·83, 0·99), cheese intake and CHD (SRRE=0·82; 95% CI 0·72, 0·93) and stroke (SRRE=0·87; 95% CI 0·77, 0·99), and Ca from dairy sources and stroke (SRRE=0·69; 95% CI 0·60, 0·81). However, there was little evidence for inverse dose-response relationships between the dairy variables and CHD and stroke after adjusting for within-study covariance. The results of this meta-analysis of prospective cohort studies have shown that dairy consumption may be associated with reduced risks of CVD, although additional data are needed to more comprehensively examine potential dose-response patterns.
  9. Dairy consumption and risk of metabolic syndrome: a meta-analysis. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26433009
    • AIMS: To conduct a systematic review and meta-analysis of epidemiological studies in order to assess quantitatively the effect of dairy consumption on risk of metabolic syndrome.
    • METHODS: We searched for eligible studies published up to March 2015 through the PubMed and Embase databases and reviewed the references of relevant articles. Random-effects models were used to calculate the pooled relative risks with 95% CIs after adjusting for several confounders.
    • RESULTS: We identified nine prospective cohort studies including a total of 35,379 subjects and 7322 incident cases of metabolic syndrome, and 12 cross-sectional studies including 37 706 subjects. In the meta-analysis of prospective cohort studies, the pooled relative risk of incidence of metabolic syndrome for the highest vs. the lowest category of dairy consumption was 0.85 (95% CI 0.73-0.98), and for a 1-serving/day increment of dairy consumption, the pooled relative risk was 0.88 (95% CI 0.82-0.95). In the meta-analysis of cross-sectional studies, the pooled relative risk of prevalence of metabolic syndrome for the highest vs. the lowest category of dairy consumption was 0.73 (95% CI 0.63-0.86). The association was not significantly different by geographical region, follow-up time and adjustment factors.
    • CONCLUSION: Our findings indicate that dairy consumption is inversely associated with the incidence and prevalence of metabolic syndrome. Further well-designed cohort studies and randomized controlled trials are warranted to provide definitive evidence.
  10. Milk and dairy products: good or bad for human health? An assessment of the totality of scientific evidence. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27882862
    • BACKGROUND: There is scepticism about health effects of dairy products in the public, which is reflected in an increasing intake of plant-based drinks, for example, from soy, rice, almond, or oat.
    • OBJECTIVE: This review aimed to assess the scientific evidence mainly from meta-analyses of observational studies and randomised controlled trials, on dairy intake and risk of obesity, type 2 diabetes, cardiovascular disease, osteoporosis, cancer, and all-cause mortality.
    • RESULTS: The most recent evidence suggested that intake of milk and dairy products was associated with reduced risk of childhood obesity. In adults, intake of dairy products was shown to improve body composition and facilitate weight loss during energy restriction. In addition, intake of milk and dairy products was associated with a neutral or reduced risk of type 2 diabetes and a reduced risk of cardiovascular disease, particularly stroke. Furthermore, the evidence suggested a beneficial effect of milk and dairy intake on bone mineral density but no association with risk of bone fracture. Among cancers, milk and dairy intake was inversely associated with colorectal cancer, bladder cancer, gastric cancer, and breast cancer, and not associated with risk of pancreatic cancer, ovarian cancer, or lung cancer, while the evidence for prostate cancer risk was inconsistent. Finally, consumption of milk and dairy products was not associated with all-cause mortality. Calcium-fortified plant-based drinks have been included as an alternative to dairy products in the nutrition recommendations in several countries. However, nutritionally, cow’s milk and plant-based drinks are completely different foods, and an evidence-based conclusion on the health value of the plant-based drinks requires more studies in humans.
    • CONCLUSION: The totality of available scientific evidence supports that intake of milk and dairy products contribute to meet nutrient recommendations, and may protect against the most prevalent chronic diseases, whereas very few adverse effects have been reported.

  11. Long-term association between dairy consumption and risk of childhood obesity: a systematic review and meta-analysis of prospective cohort studies. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26862005
    • BACKGROUND/OBJECTIVES: Data from small-scale, short-term, clinical trials suggest a beneficial effect of dairy consumption on the risk of childhood obesity; however, the long-term association is unclear. Therefore, we aim to examine the longitudinal association between dairy consumption and the risk of overweight/obesity in children and adolescents by conducting a systematic review and meta-analysis of prospective cohort studies.
    • SUBJECTS/METHODS: Eligible studies were identified by searching PubMed and EMBASE through March 2015. Additional studies were retrieved via Google Scholar or a hand review of the reference lists from relevant articles. Pooled associations of interest were estimated by using a random-effects model. The heterogeneity for each pooled analysis was evaluated by I(2) statistic as well as by Cochran’s Q test. Publication bias was assessed by using both Egger’s and Begg’s tests.
    • RESULTS: Ten studies comprising 46,011 children and adolescents with an average 3-year follow-up were included. As compared with those who were in the lowest group of dairy consumption, children in the highest intake group were 38% less likely to have childhood overweight/obesity (pooled odds ratio (OR)=0.62; 95% confidence interval (CI): 0.49, 0.80). With each 1 serving/day increment in dairy consumption, the percentage of body fat was reduced by 0.65% (β=0.65; 95% CI: -1.35, 0.06; P=0.07), and the risk of overweight/obesity was 13% lower (OR=0.87; 95% CI: 0.74, 0.98).
    • CONCLUSIONS: Accumulated evidence from prospective cohort studies suggests that dairy consumption is inversely and longitudinally associated with the risk of childhood overweight/obesity. Further studies are warranted to examine the types of dairy products in relation to the risk of childhood overweight/obesity.
  12. Consumption of dairy foods and diabetes incidence: a dose-response meta-analysis of observational studies. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26912494
    • BACKGROUND: A growing number of cohort studies suggest a potential role of dairy consumption in type 2 diabetes (T2D) prevention. The strength of this association and the amount of dairy needed is not clear.
    • OBJECTIVE: We performed a meta-analysis to quantify the associations of incident T2D with dairy foods at different levels of intake.
    • DESIGN: A systematic literature search of the PubMed, Scopus, and Embase databases (from inception to 14 April 2015) was supplemented by hand searches of reference lists and correspondence with authors of prior studies. Included were prospective cohort studies that examined the association between dairy and incident T2D in healthy adults. Data were extracted with the use of a predefined protocol, with double data-entry and study quality assessments. Random-effects meta-analyses with summarized dose-response data were performed for total, low-fat, and high-fat dairy, (types of) milk, (types of) fermented dairy, cream, ice cream, and sherbet. Nonlinear associations were investigated, with data modeled with the use of spline knots and visualized via spaghetti plots.
    • RESULTS: The analysis included 22 cohort studies comprised of 579,832 individuals and 43,118 T2D cases. Total dairy was inversely associated with T2D risk (RR: 0.97 per 200-g/d increment; 95% CI: 0.95, 1.00;P= 0.04;I(2)= 66%), with a suggestive but similar linear inverse association noted for low-fat dairy (RR: 0.96 per 200 g/d; 95% CI: 0.92, 1.00;P= 0.072;I(2)= 68%). Nonlinear inverse associations were found for yogurt intake (at 80 g/d, RR: 0.86 compared with 0 g/d; 95% CI: 0.83, 0.90;P< 0.001;I(2)= 73%) and ice cream intake (at ∼10 g/d, RR: 0.81; 95% CI: 0.78, 0.85;P< 0.001;I(2)= 86%), but no added incremental benefits were found at a higher intake. Other dairy types were not associated with T2D risk.
    • CONCLUSION: This dose-response meta-analysis of observational studies suggests a possible role for dairy foods, particularly yogurt, in the prevention of T2D. Results should be considered in the context of the observed heterogeneity.
  13. Systematic Review of the Association between Dairy Product Consumption and Risk of Cardiovascular-Related Clinical Outcomes. (2016) https://www.ncbi.nlm.nih.gov/pubmed/28140321
    • The objective of this systematic review was to determine if dairy product consumption is detrimental, neutral, or beneficial to cardiovascular health and if the recommendation to consume reduced-fat as opposed to regular-fat dairy is evidence-based. A systematic review of meta-analyses of prospective population studies associating dairy consumption with cardiovascular disease (CVD), coronary artery disease (CAD), stroke, hypertension, metabolic syndrome (MetS), and type 2 diabetes (T2D) was conducted on the basis of the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement. Quality of evidence was rated by using the Grading of Recommendations Assessment, Development, and Evaluation scale. High-quality evidence supports favorable associations between total dairy intake and hypertension risk and between low-fat dairy and yogurt intake and the risk of T2D. Moderate-quality evidence suggests favorable associations between intakes of total dairy, low-fat dairy, cheese, and fermented dairy and the risk of stroke; intakes of low-fat dairy and milk and the risk of hypertension; total dairy and milk consumption and the risk of MetS; and total dairy and cheese and the risk of T2D. High- to moderate-quality evidence supports neutral associations between the consumption of total dairy, cheese, and yogurt and CVD risk; the consumption of any form of dairy, except for fermented, and CAD risk; the consumption of regular- and high-fat dairy, milk, and yogurt and stroke risk; the consumption of regular- and high-fat dairy, cheese, yogurt, and fermented dairy and hypertension risk; and the consumption of regular- and high-fat dairy, milk, and fermented dairy and T2D risk. Data from this systematic review indicate that the consumption of various forms of dairy products shows either favorable or neutral associations with cardiovascular-related clinical outcomes. The review also emphasizes that further research is urgently needed to compare the impact of low-fat with regular- and high-fat dairy on cardiovascular-related clinical outcomes in light of current recommendations to consume low-fat dairy.
  14. Dairy products consumption versus type 2 diabetes prevention and treatment; a review of recent findings from human studies. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24160191
    • INTRODUCTION: It has been claimed that the appropriate consumption of dairy products can be beneficial for the prevention and treatment of type 2 diabetes mellitus (T2DM).
    • OBJECTIVE: The objective of this review is to critically analyze the main scientific evidence about this topic.
    • METHODS: MEDLINE, PubMEd, Science Direct, SCIELO and LILACS were searched for studies published over the past 12 years exploring the effects of the consumption of dairy products or its components (calcium, vitamin D and magnesium) on T2DM.
    • RESULTS AND DISCUSSION: Epidemiological studies indicate that consumption of at least three servings of low-fat dairy products per day as a part of a healthy diet is crucial to reduce the risk of developing T2DM. The majority of the analyzed intervention studies reported beneficial effects of increased calcium and vitamin D ingestion on insulin sensitivity improvement and T2DM prevention.
    • CONCLUSIONS: Although the impact of dairy consumption to treat T2DM needs further investigation, the consumption of low-fat dairy products may be an important strategy to prevent and control T2DM.

  15. Meeting and exceeding dairy recommendations: effects of dairy consumption on nutrient intakes and risk of chronic disease. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23550782
    • The 2010 Dietary Guidelines for Americans indicate the US population is experiencing an epidemic of overweight and obesity while maintaining a nutrient-poor, energy-dense diet associated with an increased risk of osteoarthritis, cardiovascular disease, and type 2 diabetes. To build upon the review of published research in the Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010, this article aims to review the scientific literature pertaining to the consumption of dairy foods and the effects of dairy consumption on nutrient intakes and chronic disease risk published between June 2010, when the report was released, and September 2011. PubMed was searched for articles using the following key words: dairy, milk, nutrient intake, bone health, body composition, cardiovascular disease, type 2 diabetes, and blood pressure. Evidence indicates that increasing dairy consumption to the recommended amount, i.e., three servings daily for individuals ≥9 years of age, helps close gaps between current nutrient intakes and recommendations. Consuming more than three servings of dairy per day leads to better nutrient status and improved bone health and is associated with lower blood pressure and reduced risk of cardiovascular disease and type 2 diabetes.
  16. Consumption of Dairy Products in Relation to Changes in Anthropometric Variables in Adult Populations: A Systematic Review and Meta-Analysis of Cohort Studies. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27310919
    • BACKGROUND: The current state of knowledge regarding the association of dairy products and weight gain, overweight, and obesity is based on studies reporting contradicting and inconclusive results. The aim of the present study was thus to clarify the link between dairy consumption in relation to changes in anthropometric measures/adiposity by a meta-analytical approach.
    • METHODS: For the meta-analysis PubMed, EMBASE, Web of Sciences, and google scholar were searched by two independent authors up to May 2016 with no restriction to language or calendar date. Prospective cohort studies reporting about intake of dairy consumption (including milk, yogurt, cheese, butter) and changes in body weight or waist circumference, risk of overweight, obesity, or weight gain were eligible. Pooled effects were calculated using a random effects model, and also a fixed effect model for sensitivity analysis. Due to the heterogeneity of statistical analytical approaches of the studies the analysis were done separately for beta-coefficients of changes in body weight and/or waist circumference per serving of dairy, for differences in weight gain/gain in waist circumference when comparing extreme categories of dairy consumption, and for odds ratios in regard to weight gain, overweight/obesity, or abdominal obesity.
    • FINDINGS: 24 studies (27 reports) met the inclusion criteria for the systematic review, and 22 studies provided sufficient data for inclusion in the meta-analysis. The meta-analysis of the five studies on changes in body weight per serving of dairy no significant results could be found for whole fat dairy and low fat dairy. However, there was inverse association between changes in body weight for each serving’s increase of yogurt (beta: -40.99 gram/year, 95% CI, -48.09 to -33.88), whereas each serving’s increase of cheese was positively associated (beta: -10.97 gram/year, 95% CI, 2.86 to 19.07). Furthermore, the highest dairy intake category was associated with a reduced risk of abdominal obesity (OR: 0.85; 95% CI, 0.76 to 0.95), and risk of overweight (OR: 0.87; 95% CI, 0.76 to 1.00) compared to the lowest intake category. No significant association could be observed for risk of weight gain.
    • CONCLUSION: In summary the results of the meta-analysis still reflect that dairy consumption was not positively related to changes in body weight. Yogurt was the only dairy food that showed some evidence for a beneficial effect, where higher intakes were inversely associated a reduced risk of obesity, changes in body weight or waist circumference. Further research is needed, since the overall interpretation of the results is limited by heterogeneous risk estimates.
  17. Effect of dairy consumption on weight and body composition in adults: a systematic review and meta-analysis of randomized controlled clinical trials. (2012) https://www.ncbi.nlm.nih.gov/pubmed/22249225
    • BACKGROUND: Although several observational and experimental studies have investigated the effect of dairy consumption on weight and body composition, results are inconsistent.
    • OBJECTIVE: This systematic review and meta-analysis was conducted to summarize the published evidence from randomized controlled clinical trials (RCTs) regarding the effect of dairy consumption on weight, body fat mass, lean mass and waist circumference (WC) in adults.
    • DESIGN: PubMed, ISI Web of Science, SCOPUS, Science Direct and EMBASE were searched from January 1960 to October 2011 for relevant English and non-English publications. Sixteen studies were selected for the systematic review and fourteen studies were included in meta-analysis.
    • RESULTS: Our search led to 14, 12, 6 and 8 eligible RCTs that had data on weight, body fat mass, lean mass and WC, respectively. Overall, mean difference for the effect of dairy on body weight was -0.61 kg (95% confidence interval (CI): -1.29, 0.07, P=0.08). Increased dairy intake resulted in 0.72 kg (95% CI: -1.29, -0.14, P=0.01) greater reduction in fat mass, 0.58 kg (95% CI: 0.18, 0.99, P<0.01) gain in lean mass and 2.19 cm (95% CI: -3.42, -0.96, P-value <0.001) further reduction in WC than that in controls. Subgroup analysis revealed that increasing dairy intake without energy restriction in both intervention and control groups does not significantly affect weight, body fat mass, lean mass and WC; consumption of high-dairy weight loss diets led to 1.29 kg (95% CI: -1.98, -0.6, P<0.001) greater weight loss, 1.11 kg (95% CI: -1.75, -0.47, P=0.001) greater reduction in body fat mass, 0.72 kg (95% CI: 0.12, 1.32, P=0.02) gain in body lean mass and 2.43 cm (95% CI: -3.42, -1.44, P<0.001) additional reduction in WC compared with controls.
    • CONCLUSION: Increased dairy consumption without energy restriction might not lead to a significant change in weight or body composition; whereas inclusion of dairy products in energy-restricted weight loss diets significantly affects weight, body fat mass, lean mass and WC compared with that in the usual weight loss diets.

  18. How sound is the science behind the dietary recommendations for dairy? (2014) https://www.ncbi.nlm.nih.gov/pubmed/24646824
    • This review examined the evidence behind dietary guidelines for dairy. Most countries recommend consumption of dairy products; and when amounts are specified, recommendations are typically for 2 or 3 servings per day. Specific recommendations for dairy products are based partly on culture and availability but primarily on meeting nutrient requirements. Dairy products are a rich source of many minerals and vitamins as well as high-quality protein. Thus, dairy consumption is a marker for diet quality. A recent report found that yogurt specifically is a good marker of diet quality. The food patterns recommended by the 2010 Dietary Guidelines for Americans Advisory Committee (DGAC) include 3 cups of low-fat milk and milk products. Few people achieve their recommended intakes of several shortfall nutrients without meeting their recommendations for dairy. The evidence for a benefit of dairy consumption is moderate for bone health in children but limited in adults and moderate for cardiovascular disease, blood pressure, and diabetes and limited for metabolic syndrome. Newer data since the recommendations of the 2010 DGAC are presented. However, the strength of the evidence for dairy consumption and health is limited by the lack of appropriately powered randomized controlled trials.
  19. Association of dairy products consumption with risk of obesity in children and adults: a meta-analysis of mainly cross-sectional studies. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27756684
    • PURPOSE: The association of dairy products consumption with risk of obesity remains controversial. Therefore, we reviewed and quantitatively synthesized the evidence from observational studies with a meta-analysis.
    • METHODS: A literature search was performed in relevant databases. Random-effects model was used to pool odds ratios with 95% confidence intervals. Dose-response relationship was assessed by restricted cubic spline model.
    • RESULTS: Seventeen studies for total dairy products and 16 studies for milk with risk of obesity were eligible. The pooled odds ratios (95% confidence intervals) of obesity for the highest versus lowest category of total dairy products consumption were 0.54 (0.38-0.77) in children, 0.75 (0.69-0.81) in adults, and 0.74 (0.68-0.80) for both. Evidence of a nonlinear relationship was found (Pfor nonlinearity = .009). Milk consumption was also associated with risk of obesity [0.81 (0.75-0.88)] both in children [0.87 (0.80-0.95)] and in adults [0.77 (0.68-0.87)], and a linear relationship (Pfor nonlinearity = .598) suggested that risk of obesity decreased by 16% [0.84 (0.77-0.92)] for every 200 g/d increment of milk consumption.
    • CONCLUSIONS: This meta-analysis indicates that dairy products consumption may be associated with a decreased risk of obesity. This association may be of public health significance.
  20. Fermented dairy food and CVD risk. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26148916
    • Fermented dairy foods such as yoghurt and cheese are commonly found in the Mediterranean diet. Recent landmark research has confirmed the effect of the Mediterranean diet on reducing the CVD risk, but the relative contributions of fermented dairy foods have not been fully articulated. The present study provides a review of the relationship between fermented dairy foods consumption and CVD risk in the context of the whole diet. Studies show that people who eat healthier diets may be more likely to consume yoghurt, so there is a challenge in attributing separate effects to yoghurt. Analyses from large population studies list yoghurt as the food most negatively associated with the risk of weight gain (a problem that may lead to CVD). There is some suggestion that fermented dairy foods consumption (yoghurt or cheese) may be associated with reduced inflammatory biomarkers associated with the development of CVD. Dietary trials suggest that cheese may not have the same effect on raising LDL-cholesterol levels as butter with the same saturated fat content. The same might be stated for yoghurt. The use of different probiotic cultures and other aspects of study design remain a problem for research. Nevertheless, population studies from a range of countries have shown that a reduced risk of CVD occurs with the consumption of fermented dairy foods. A combination of evidence is necessary, and more research is always valuable, but indications remain that fermented dairy foods such as cheese and yoghurt are integral to diets that are protective against CVD.
  21. Effects of dairy intake on body weight and fat: a meta-analysis of randomized controlled trials. (2012) https://www.ncbi.nlm.nih.gov/pubmed/22932282
    • BACKGROUND: Some intervention studies have suggested that dairy products may influence body weight, but the results remain controversial.
    • OBJECTIVE: We identified and quantified the effects of dairy consumption on body weight and fat mass from randomized controlled trials (RCTs).
    • DESIGN: We conducted a comprehensive search of PubMed and EMBASE databases (to April 2012) of English reports of RCTs regarding dairy consumption on body weight, body fat, or body weight and body fat in adults. The results across studies were pooled by using a random-effects meta-analysis.
    • RESULTS: Twenty-nine RCTs were included with a total of 2101 participants. Overall, consumption of dairy products did not result in a significant reduction in weight (-0.14 kg; 95% CI: -0.66, 0.38 kg; I² = 86.3%). In subgroup analysis, consumption of dairy products reduced body weight in the context of energy restriction or short-term intervention (<1 y) trials but had the opposite effect in ad libitum dietary interventions or long-term trials (≥1 y). Twenty-two RCTs that reported results on body fat showed a modest reduction in the dairy group (-0.45 kg; 95% CI: -0.79, -0.11 kg; I² = 70.9%), and further stratified analysis indicated significant beneficial effects of dairy intervention on body fat in energy-restricted or short-term trials but not in long-term or ad libitum studies.
    • CONCLUSIONS: This meta-analysis does not support the beneficial effect of increasing dairy consumption on body weight and fat loss in long-term studies or studies without energy restriction. However, dairy products may have modest benefits in facilitating weight loss in short-term or energy-restricted RCTs.
  22. Effects of dairy protein and fat on the metabolic syndrome and type 2 diabetes. (2014) https://www.ncbi.nlm.nih.gov/pubmed/25396403
    • The incidence of the metabolic syndrome (MetS) and type 2 diabetes (T2D) is increasing worldwide. Evidence supports a negative relationship between the consumption of dairy products and risk of MetS and T2D. Dairy proteins are known to have a directly beneficial effect on hypertension, dyslipidemia, and hyperglycemia, but a detailed understanding of the underlying mechanisms is missing. It has been confirmed by observations that the insulinotropic effect of dairy proteins is associated with the amino acid composition; in particular branched-chain amino acids (BCAA) seem to be of vital importance. Dairy protein-derived peptides may also contribute to the insulinotropic effect via dipeptidyl peptidase-4 (DPP-4) inhibitory activity, and may lower the blood pressure (BP). The lipid metabolism may be improved by whey protein (WP), which acts to reduce the postprandial triglyceride (TG) response. The effect of dairy fat is much more controversial because of the potentially harmful effect exerted by saturated fatty acid (SFA) on metabolic health. Recent observations suggest less adverse effects of SFA on metabolic health than previous assumed. However, little is known about dairy lipid fractions belonging to the groups of monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), and phospholipids (PL). Dairy fat seems to act differently depending on the dairy product and the composition of macronutrients in the meal. Therefore, for a better understanding of the mechanisms behind the dairy protein and fat effect on MetS, we suggest that more human studies should be carried out to clarify the interactions of dairy protein and fat with macronutrients in the meal and other dairy components, such as micronutrients and microorganisms from fermented products.
  23. Dairy product intake in children and adolescents in developed countries: trends, nutritional contribution, and a review of association with health outcomes. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24330063
    • Despite its contribution to nutrient intake and status, consumption of milk and dairy products by children and adolescents in many countries has waned in recent decades, with a substantial proportion of youth failing to meet intake recommendations. Dairy products remain an important dietary source of multiple micronutrients, including calcium, phosphorus, magnesium, zinc, iodine, potassium, vitamin A, vitamin D, vitamin B12 , and riboflavin (vitamin B2 ). In addition, dairy products provide children with energy, high-quality protein, and essential and nonessential fatty acids. A review of evidence was conducted to evaluate associations between milk or dairy product intake and health outcomes in children and adolescents. Results suggest a neutral or inverse association between consumption of milk and dairy products in children and adolescents and indicators of adiposity, incidence of dental caries, and hypertension. Available data indicate that dairy products are important for linear growth and bone health during childhood. Additional research–in particular, controlled intervention trials and long-term prospective cohort studies–is warranted to better understand how dairy intake affects health outcomes in children and adolescents.
  24. Dairy products on metabolic health: current research and clinical implications. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24445013
    • Dairy products have been thought to have a beneficial role in the metabolic syndrome (MetS). MetS constitutes a cluster of risk factors for an increased mortality, including obesity, impaired glucose homeostasis, hypertension and atherogenic dyslipidemia. Individuals with MetS are also often in a chronic, low-grade inflammatory state. The objective of this review is to examine recent meta-analyses and clinical studies on the association between dairy products consumption and these MetS risk factors. Findings from studies demonstrate that weight loss related to dairy product intake is due to the combination of an energy-restricted diet with consumption of dairy products. Further, a limited number of studies have shown beneficial effects of dairy consumption on plasma lipids, blood pressure, glucose homeostasis or inflammatory and oxidative stress profiles. Overall, this review article suggests that adults should consume at least 2-3 servings of dairy products per day within a well-balanced diet and a healthy lifestyle for metabolic health. Yet, higher dairy product consumption may have additional beneficial effects, but more well-designed intervention studies are needed to ascertain these effects.
  25. Comprehensive Review of the Impact of Dairy Foods and Dairy Fat on Cardiometabolic Risk. (2016) https://www.ncbi.nlm.nih.gov/pubmed/28140322
    • Because regular-fat dairy products are a major source of cholesterol-raising saturated fatty acids (SFAs), current US and Canadian dietary guidelines for cardiovascular health recommend the consumption of low-fat dairy products. Yet, numerous randomized controlled trials (RCTs) have reported rather mixed effects of reduced- and regular-fat dairy consumption on blood lipid concentrations and on many other cardiometabolic disease risk factors, such as blood pressure and inflammation markers. Thus, the focus on low-fat dairy in current dietary guidelines is being challenged, creating confusion within health professional circles and the public. This narrative review provides perspective on the research pertaining to the impact of dairy consumption and dairy fat on traditional and emerging cardiometabolic disease risk factors. This comprehensive assessment of evidence from RCTs suggests that there is no apparent risk of potential harmful effects of dairy consumption, irrespective of the content of dairy fat, on a large array of cardiometabolic variables, including lipid-related risk factors, blood pressure, inflammation, insulin resistance, and vascular function. This suggests that the purported detrimental effects of SFAs on cardiometabolic health may in fact be nullified when they are consumed as part of complex food matrices such as those in cheese and other dairy foods. Thus, the focus on low-fat dairy products in current guidelines apparently is not entirely supported by the existing literature and may need to be revisited on the basis of this evidence. Future studies addressing key research gaps in this area will be extremely informative to better appreciate the impact of dairy food matrices, as well as dairy fat specifically, on cardiometabolic health.
  26. Impact of dairy products on biomarkers of inflammation: a systematic review of randomized controlled nutritional intervention studies in overweight and obese adults. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23446894
    • BACKGROUND: Recent data from cross-sectional studies suggest that consumption of dairy products is inversely associated with low-grade systemic inflammation, but a cause-and-effect relation can be confirmed only with results from randomized controlled trials.
    • OBJECTIVE: We reviewed the results of randomized controlled nutritional intervention studies that have assessed the impact of dairy product consumption (ie, milk, yogurt, and/or cheese) on biomarkers of inflammation in adults (aged ≥18 y).
    • DESIGN: We performed a systematic literature search in PubMed in April 2012, which was limited to randomized controlled trials in humans published in English. Studies that included pregnant or lactating women or that did not include a low-dairy control intervention were excluded.
    • RESULTS: Eight trials that were conducted in overweight or obese adults were included in the review. The only study that had identified change in the inflammatory profile as its primary outcome measure showed that dairy food consumption improved pro- and antiinflammatory biomarker concentrations compared with the low-dairy control diet. Three of the 7 studies in which inflammation was a secondary or undefined outcome showed improvement in key inflammatory biomarkers, ie, C-reactive protein, IL-6, or TNF-α after dairy product consumption, whereas the other 4 studies showed no effect.
    • CONCLUSIONS: Dairy product consumption does not exert adverse effects on biomarkers of inflammation in overweight or obese adults. Several methodologic factors and limitations among existing studies do not allow differentiation between a beneficial or neutral impact of dairy products on inflammation. Further studies specifically designed to assess inflammation-related outcomes are warranted.

What We Know and Don’t Know

  • This topic has been studied extensively. I was able to find more than 20 literature reviews or meta-analyses on how dairy impacts metabolic syndrome. Each of these reviews detailed many other studies of moderate or high quality. In all, tens of thousands of participants of all ages have been studied.

24 of the 26 reviews reported an inverse relationship between dairy consumption and markers of metabolic syndrome. Each study varied in terms of which types of dairy and which markers of metabolic syndrome were studied as well as which findings were the most significant. The two remaining reviews found that increasing dairy in calorie restricted diets helped reduce weight in the short term, but did not help reduce weight in long term non-restricted diets. None of the studies found dairy to be harmful to health in any way. All analyses showed dairy to be either neutral or beneficial to health with a majority claiming benefits for at least one symptom of metabolic syndrome.

Of the studies that separated low-fat from regular-fat dairy, the regular-fat dairy fared either equal to or better than the low-fat. Saturated fat in dairy (including cheese) did not adversely affect participants’ health or blood lipids as expected and several of the reviews called for reconsideration of the recommendation to consume low-fat dairy. A few of the studies continued to recommend low-fat dairy, but this seemed to be due to staying consistent with previous recommendations rather than presenting results showing adverse effects of regular fat dairy.

Of the studies that separated different dairy products, yogurt consistently had the most favorable outcomes. Yogurt seemed especially protective against cardiovascular disease, obesity, and type 2 diabetes. One study found that people who consumed more cheese were more likely to be obese, but this finding was not consistent across the research.

A few of the studies focused on children and adolescents. They found that the children who consumed the most dairy had the fewest problems with obesity.

Most of the studies found an inverse relationship between dairy consumption and markers of metabolic syndrome. That suggests that the more dairy a person consumes, the healthier they are. Some studies recommended 2-3 servings per day while other recommended more than 3.

The research I found did not address the topic of lactose intolerance. The majority of the research I found was done on participants from “developed” countries that recommended dairy in their health guidelines. These included the U.S., Canada, and Europe. Therefore, it’s hard to say whether the outcomes would apply to Africa and Asia. Common sense would suggest that people who are lactose intolerant should avoid dairy or use medication to assist digestion.

Conclusions and Applications

If you’re not lactose intolerant, you can and should include dairy in your healthy diet. Regular-fat is just as good, or, maybe even better for you than low-fat. Consuming about 3 servings of dairy per day, especially yogurt and milk, is likely to be beneficial to your health. The benefits include helping you maintain a healthy weight, decreasing your likelihood of developing heart disease and type 2 diabetes, and providing tons of necessary nutrients. Although I did not specifically research the association between dairy and cancer or bone health, the evidence I came across all suggests dairy is beneficial in these areas as well.

Dairy is not as it seems, likely to be the reason people who follow a paleo or vegan diet tend to be healthier. Perhaps simply cutting large groups of food out of your diet tends to make you eat less overall. Or maybe it makes you more likely to cook healthy foods at home rather than go out and risk being unsure of which ingredients are being used.

Based on a TON of research, we can confidently keep dairy in the “healthy” category. Evidence supports all the traditional paleo foods, all the plant-based vegan foods, and all the dairy as good for health. The general consensus across all nutrition camps still discourages consumption of highly processed foods, refined grains, and added sugar. The jury is still out on saturated fat, so that will be my next topic to tackle!

Is Advil Preventing You From Getting Pregnant?

This month, I’m taking a break from diet to explore another important area in health and wellness: fertility. Any girl who’s ever turned to Google or Pinterest in search of increasing fertility has no doubt encountered hundreds of tips and tricks. As usual, some are reliable and others are based on myth and anecdote.

Eat vegan. Eat Paleo. Eat whole-30. No smoking. No alcohol. Some alcohol. No caffeine. Some caffeine. Prenatal vitamins. Ovulation predictors. Work out more. Work out less. Yoga. Acupuncture. Hypnosis. Basal body temperature. Do it every day. Don’t do it every day. Test for STDs. Get a semen analysis. Test your tubes. Test for endometriosis.

One recommendation in particular caught my attention. I came across a headline saying that NSAIDs (non-steroidal anti-inflammatory drugs) can prevent ovulation. I had never heard about this before and decided to take a deeper look.

NSAIDs are over-the-counter pain medications that work by blocking enzymes that make prostaglandins (which cause swelling and are interpreted as pain). Many people take these medications fairly often for headaches, backaches, joint pain, menstrual cramps, toothaches, other injuries, and even heart disease.

Some common OTC NSAIDs are: Aspirin (Bayer, Excedrin), Ibuprofen (Advil, Motrin, Nuprin), Ketoprofen (Actron, Orudis), and Naproxen (Aleve). Others are available with a prescription.

The Claim: Taking NSAIDs can reduce fertility by preventing ovulation.

Initial Search: A quick Google search came up with the following results:

WebMD: NSAIDs may hinder ovulation and lower levels of the female hormone progesterone. They cite a study by Sami Salman, MD, from the University of Baghdad. This study is available below in the peer-reviewed research section. Essentially, he studied 39 women taking either an NSAID or a placebo for 10 consecutive days, beginning on day 10 of the menstrual cycle. Ovulation was reduced by 75-93% depending on which drug the patients were taking compared to the control group. He stated that progesterone levels also dropped for the experimental groups. After discontinuing treatment, all of the women ovulated normally during their next cycle. Dr. Salman even proposed that these findings could help them develop a new contraceptive.

Medscape: Pharmacist Darrell Hullsz describes how some side effects of NSAIDs are well known including gastrointestinal, cardiovascular, and renal problems as well as problems toward the end of pregnancy. He says that problems with ovulation have been reported for several decades, but that these problems are still not widely known. An enzyme, COX-2, that is active in the ovaries during follicular development, is blocked by NSAIDs. This prevents the follicule from rupturing (egg from being released). Women see all the other signs of ovulation including elevated body temperature and progesterone levels, but the egg is never released. He goes a step further stating that COX-2 inhibitors may also disrupt fertilization, implantation, and establishment of the placenta. He references the study mentioned above by WebMD as well as two other studies listed below in the peer-reviewed section that oppose the claim by suggesting that delayed follicular rupture is unlikely to cause infertility.

Many other popular health news websites also cite Dr. Salman’s study including: ScienceDaily, Daily Mail, Pharmaceutical Journal, Holistic Primary Care, TheraSpecs, and many fertility blogs and centers.

Follow-up Questions:

If NSAIDs really do affect fertility, does timing and dosage matter? Would it be ok to take NSAIDs during your period, but avoid it during the middle and end of your cycle? Is a lower dose safer?

Are there other painkillers that are safer to take when trying to conceive?

Peer reviewed Research:

These are all of the relevant studies I found. Most did not have full text available. I have provided abstracts with the most important findings from each study in bold.



Background: NSAIDs are popular and used as analgesics, antipyretics and anti-inflammatory agents for more than a century. They are sold without a prescription and taken by millions of patients every day all over the world. There has been recent concerns as to their use in females at child bearing age, as many animal studies showed unfavourable effects on ovulation.

Objectives: To study the effects of short term use of NSADs at their conventional dosages on ovulation.

Methods: Thirty nine women at fertile age were chosen as volunteers to take part in this study, they visited the Rheumatology consultation clinic in Baghdad Hospital, suffering from minor backpain and received one of the three test drugs (diclofenac 100mg once daily, naproxen 500mg twice daily & etoricoxib 90mg once daily). Treatment with the above drugs was given for ten days starting at day ten of the onset of the menstrual cycle. A blood sample was taken from each patients for hormonal analysis (progesterone level) together with an ultra sonsography to assess the mean diameter of the dominant follicle. At day twenty the patient came back for another ultra sonography & to give a blood sample for another check for progesterone level. A fourth group served as controls, who received no treatment (control volunteers).

Results: There was significant inhibition of ovulation in patients treated with diclofenac, naproxen & etoricoxib. Diclofenac was the highest inhibitor of ovulation compared to the other two drugs (naproxen & etoricoxib). A significant decrease in progesterone level in all three groups in compared to the control group was found. Functional cysts have been observed in one third of patients by the end of the treatment period with diclofenac, naproxen & etoricoxib due to unruptured follicles these disappeared at the next cycle.

Conclusions: The findings may serve as an alarm of the harmful effects of these drugs on female fertility and be taken into consideration in females planning to have a child. The above results may open the door for looking for an emergency contraceptive safer than those at use.



Ovulation constitutes the central event in ovarian physiology, and ovulatory disfunction is a relevant cause of female infertility. Non-steroidal anti-inflammatory drugs (NSAIDs), widely used due to their analgesic and anti-inflammatory properties, consistently inhibit ovulation in all mammalian species investigated so far, likely due to the inhibition of cyclooxygenase 2 (COX-2), the inducible isoform of COX, that is the rate-limiting enzyme in prostaglandin (PG) synthesis. COX-2 inhibition has major effects on ovulation, fertilization and implantation, and NSAID therapy is likely implicated in human infertility and could be an important, frequently overlooked, cause of ovulatory disfunction in women. Although there is compelling evidence for a role of PGs in ovulation, the molecular targets and the precise role of these compounds in the ovulatory process are not fully understood. Morphological studies from rats treated with indomethacin (INDO), a potent inhibitor of PG synthesis, provide evidence on the actions of NSAIDs in ovulation, as well as on the possible roles of PGs in the ovulatory process. Cycling rats treated with INDO during the preovulatory period show abnormal ovulation, due to disruption of the spatial targeting of follicle rupture at the apex. Noticeably, gonadotropin-primed immature rats (widely used as a model for the study of ovulation) show age-dependent ovulatory defects similar to those of cycling rats treated with INDO. These data suggest that NSAID treatment disrupts physiological mechanisms underlying spatial targeting of follicle rupture at the apex, which are not fully established in very young rats. We summarize herein the ovulatory defects after pharmacologic COX-2 inhibition, and discuss the possible mechanisms underlying the anti-ovulatory actions of NSAIDs.



Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently prescribed to women of child-bearing age. Three case series highlight the possibility of a link between NSAIDs and reversible infertility. The pharmacological target of NSAIDs is cyclo-oxygenase (COX), which catalyses the first rate-limiting step in the production of prostaglandins. COX-2, one of two isoenzymes, is active in the ovaries during follicular development. Its inhibition is thought to cause luteinised unruptured follicle (LUF) syndrome, an anovulatory condition characterised by clinical signs of ovulation but in the absence of follicular rupture and ovum release. The evidence linking regular NSAID use to reversible LUF syndrome comes from animal studies and three clinical studies. COX-2-deficient mice have severely compromised ovulation in the presence of apparently normal follicular development. Experimental administration of prostaglandins induced ovulation in rabbits and this was blocked by the administration of indomethacin. The three clinical studies demonstrated the induction of delayed follicular rupture or LUF in previously ovulating women by the administration of NSAIDs. A link can therefore be identified between NSAID use and reversible female infertility and NSAID withdrawal should be considered prior to or concurrent with fertility investigations.



BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective cyclooxygenase-2 inhibitors may interfere with ovulation and the rupture of the follicle, causing reversible infertility.

METHOD: Literature review.

RESULTS: Reversible infertility is shown both in animal and human studies of these drugs. As determined by ultrasound, the drugs may delay or inhibit ovulation. These findings are also confirmed by a few randomized controlled studies showing an increase in time from the luteinizing hormone surge to rupture of the follicle and an increased size of the unruptured follicle. Most of the hormone analyses show values in accordance with the ovulation/menstrual cycle. Also, two epidemiological studies have shown an association between NSAID use and spontaneous abortion. These studies have methodological weaknesses and their findings have to be elucidated in future studies.

INTERPRETATION: Women with fertility problems should avoid not only the selective cyclooxygenase-2 inhibitors, but also the traditional NSAIDs. However, women with rheumatic disease responding well to therapy should consult their physicians before stopping treatment. Reduced dose of a NSAID and temporary stop of drug treatment early in the menstrual cycle, or alternative drug treatment, may be a solution. NSAIDs should not be used in the last eight weeks of pregnancy.

  • 5. Reversible ovulatory failure associated with the development of luteinized unruptured follicles in women with inflammatory arthritis taking non-steroidal anti-inflammatory drugs. (1996) https://www.ncbi.nlm.nih.gov/pubmed/8646437



The case histories of three young women with ankylosing spondylitis, rheumatoid arthritis and a seronegative inflammatory polyarthritis undergoing investigations for infertility are presented. In each, non-steroidal anti-inflammatory drug (NSAID) therapy was associated with the recurrent development of luteinized unruptured ovarian follicles and normal ovulation following drug withdrawal. It is suggested that NSAID therapy may be an important and frequently overlooked cause of anovulation and infertility.


Abstract (1) There have been isolated reports of reversible female infertility linked to NSAIDs. The likely mechanism is ovulatory failure due to non rupture of mature follicles. (2) If a woman who presents with infertility is found to be taking a NSAID, the role of the drug should be considered before launching costly, invasive investigations or starting medically assisted reproduction.



OBJECTIVE: To highlight the possible association between infertility and treatment with long-term non-steroidal anti-inflammatory drug (NSAIDs). NSAIDs act mainly through the inhibition of cyclooxygenase, the enzyme that catalyses the synthesis of prostaglandins, which are essential mediators of ovulation, implantation and placentation of the conceptus.

METHODS: Case reports of four women suffering from severe arthritis, on long-term NSAIDs and undergoing extensive investigation and treatment for infertility.

RESULTS: During the last 2 yr, four out of five women with severe arthritis and difficulty conceiving were counselled to stop NSAIDs, and they successfully conceived shortly after the withdrawal of NSAIDs.

CONCLUSION: NSAIDs, used largely for the treatment of rheumatological conditions, may be responsible for some cases of infertility.


Abstract: Non-steroidal anti-inflammatory drugs are widely used in the treatment of inflammatory joint diseases. Many patients suffering from these disorders are young women during their childbearing years. We report three cases of infertility where the cause may have been NSAID-induced ‘luteinized unruptured follicle’ syndrome. This phenomenon is well recognized in obstetric circles, and we would like to bring it to the attention of rheumatologists since it is not documented in the rheumatological literature.



STUDY QUESTION: Does use of commonly used over-the-counter (OTC) pain medication affect reproductive hormones and ovulatory function in premenopausal women?

SUMMARY ANSWER: Few associations were found between analgesic medication use and reproductive hormones, but use during the follicular phase was associated with decreased odds of sporadic anovulation after adjusting for potential confounders.

WHAT IS KNOWN ALREADY: Analgesic medications are the most commonly used OTC drugs among women, but their potential effects on reproductive function are unclear.

STUDY DESIGN, SIZE, DURATION: The BioCycle Study was a prospective, observational cohort study (2005-2007) which followed 259 women for one (n = 9) or two (n = 250) menstrual cycles.

PARTICIPANTS, SETTING, METHODS: Two hundred and fifty-nine healthy, premenopausal women not using hormonal contraception and living in western New York state. Study visits took place at the University at Buffalo.

MAIN RESULTS AND THE ROLE OF CHANCE: During study participation, 68% (n = 175) of women indicated OTC analgesic use. Among users, 45% used ibuprofen, 33% acetaminophen, 10% aspirin and 10% naproxen. Analgesic use during the follicular phase was associated with decreased odds of sporadic anovulation after adjusting for age, race, body mass index, perceived stress level and alcohol consumption (OR 0.36 [0.17, 0.75]). Results remained unchanged after controlling for potential confounding by indication by adjusting for ‘healthy’ cycle indicators such as amount of blood loss and menstrual pain during the preceding menstruation. Moreover, luteal progesterone was higher (% difference = 14.0, -1.6-32.1, P = 0.08 adjusted) in cycles with follicular phase analgesic use, but no associations were observed with estradiol, LH or FSH.

LIMITATIONS, REASONS FOR CAUTION: Self-report daily diaries are not validated measures of medication usage, which could lead to some classification error of medication use. We were also limited in our evaluation of aspirin and naproxen which were used by few women.

WIDER IMPLICATIONS OF THE FINDINGS: The observed associations between follicular phase analgesic use and higher progesterone and a lower probability of sporadic anovulation indicate that OTC pain medication use is likely not harmful to reproduction function, and certain medications possibly improve ovulatory function.



OBJECTIVE: To assess the effect of ibuprofen, a nonspecific inhibitor of prostaglandin synthesis, on ovulation.

DESIGN: Prospective, randomized, double-blind, placebo-controlled cross-over study.

SETTING: University Medical Center.

PATIENT(S): Twelve normally cycling women between ages 20 and 40.

INTERVENTION(S): Subjects were randomized to either oral ibuprofen (800 mg) or placebo three times per day, beginning when the maximum diameter of the leading follicle reached 16 mm by ultrasound, and continuing for 10 days total. The second cycle was a washout period, and in the third cycle, the subjects were crossed over to the alternate regimen from the first cycle. The probability of delayed follicular collapse was determined using the binomial distribution, and changes in P levels were compared using the paired t test.

MAIN OUTCOME MEASURE(S): Urinary LH surge, follicular collapse by serial transvaginal ultrasonography, and serum midluteal P levels.

RESULT(S): Eleven of 12 subjects detected an LH surge with both ibuprofen and placebo. Five of 11 women demonstrated a >or=2-day increase in time interval from detection of the LH surge to follicular collapse, and 3 of those 5 had been randomized to ibuprofen. This represents a 27% (3 of 11; 95% confidence limits: 1%, 53%) rate of delay for follicular collapse for ibuprofen. There was no difference in average midluteal P levels for ibuprofen or placebo.

CONCLUSION(S): If ibuprofen inhibits follicular collapse, this effect is seen in a small group of study subjects, and this information should be clinically reassuring to patients who take nonsteroidal anti-inflammatory drugs. Serum midluteal P levels were unaffected by administration of ibuprofen.

What we know and don’t know

The research I found doesn’t give us a very definitive answer. 8 out of the 10 studies or reviews point to a strong association between NSAIDs and ovulation problems. However, in most of these studies, subjects took high doses for an extended period of time (at least 10 consecutive days). Some of them used NSAIDs that are unpopular or unavailable in the US. 1 out of the 10 studies suggests a weak association between NSAIDs and ovulation problems and 1 out of the 10 studies actually suggests that NSAIDs can improve ovulation.

Here is a table to help make the findings more clear

Study number Number/description of subjects Type of study Outcome with NSAIDs
1 39 women Control trial (non-random) poor
2 rats Unsure, review? poor
3 3 women Case studies poor
4 unsure Review poor
5 3 women Case studies poor
6 “isolated reports” Review poor
7 4 women Case studies poor
8 3 women Case studies poor
9 259 women Control trial (non-random) good
10 12 women Randomized control trial Poor in a small group


The majority of studies reporting poor outcomes are case studies involving 3 or 4 women. They may even be citing the same 3 or 4 women in multiple articles. It is difficult to know details (such as exactly which medications the women were taking and for how long) from the abstracts. However, we do know that in study 1 most of the women were taking medications not available in the US. In study 9 however, the women were mostly using Advil. This might make findings from study 9 more relevant. Study 10 is the highest quality in terms of research design, but with only 12 subjects, the results may not be reliable.

The possible mechanism responsible for ovulation problems while using NSAIDs is well described and seems plausible. According to this research, it has been observed in all mammals. However, studies involving mice and rats may still not be relevant to humans.


Overall, it seems like there is some good evidence to suggest that taking NSAIDs regularly can cause problems with ovulation. Unfortunately, there is still some controversy. I wasn’t able to find any good information on lower doses or the importance of timing, but subjects in these studies all took the medications around the time of ovulation.

I was also unable to find any information on good alternatives. Study 9, which claimed painkillers do not cause ovulation problems, didn’t separate out NSAIDs and acetaminophen. A quick Google search suggests that acetaminophen (like Tylenol) is safe during pregnancy, but may reduce estrogen and luteinizing hormones in the body. This could affect fertility.  I have yet to look deeper into this claim.


My recommendation would be for anyone who has had unexplained infertility for more than 3 months to stop taking NSAIDs and use Tylenol for mild/occasional pain relief (unless your doctor doesn’t think this would be safe). Fertility treatments are often very expensive and might be avoided by simply switching pain medication.

Is Paleo Best for Avoiding Metabolic Syndrome?

The Paleolithic (Paleo) diet has become incredibly popular over the past decade. I even tried it myself for about a year. The enthusiastic supporters and wild claims surrounding this diet are similar to what we see in the vegan diet. Just in case you’ve been living under a rock (or have never entered a CrossFit gym), here is a brief description of the Paleo diet.

The idea is to eat things that would have been available to cave men, before agriculture. This would include meat, seafood, vegetables, fruits, eggs, nuts and seeds. It would exclude grains, legumes, dairy, refined sugars and oils, and all processed foods. Some versions of the diet include potatoes, whole unpasteurized dairy, saturated fats, organ meats, salt, red wine, and very dark chocolate, while others do not.

The Claim

The best way to achieve optimal nutrition and prevent/reverse markers of metabolic syndrome is to eat a Paleo diet consisting of meat, seafood, vegetables, fruits, eggs, nuts, and seeds.

Initial Google Search

Dr. Loren Cordain is considered to be the founder of the “Paleo movement”. He has authored many peer reviewed articles and written several popular books over the past few decades promoting the diet. Other popular Paleo experts include: Robb Wolf (author of The Paleo Solution and credited for popularizing the Paleo diet through the CrossFit community), Mark Sission (author of The Primal Blueprint and website Mark’s Daily Apple), Gary Taubes (author of Good Calories, Bad Calories and Why We Get Fat), Dave Asprey (of Bulletproof Coffee), David Perlmutter (author of Wheat Belly), Melissa Hartwig (of Whole30), and Diane Sanfilippo (author of Practical Paleo).

These and other supporters of the diet say you can eat Paleo foods until you’re full without counting calories and you’ll lose weight, build muscle, and reduce or eliminate markers of metabolic syndrome. They also postulate that many humans are gluten and lactose intolerant. They think eating gluten/grains causes leaky gut and inflammation while dairy products cause allergies, digestive problems, inflammation and autoimmune diseases. They say that with the Paleo diet, the body learns to fuel itself with fat more efficiently and that fat is a better source of energy because it keeps you feeling full longer and prevents energy crashes. Some make even more extreme claims such as that variations of the diet cure autism, autoimmune conditions, and mental illness.

For the purpose of this blog, I will focus on the more traditional Paleo diet which focuses on lean meats, fish, vegetables, fruits, eggs, nuts and seeds; and the claim that eating this way will reduce or prevent metabolic syndrome.

Follow-up Questions

Does the Paleo diet work better than the Vegan diet for weight loss, diabetes, and heart disease?

Are there some variations of the diet that are better than others?

Peer Reviewed Research

Inclusion criteria: clinical trial or review of multiple clinical trials that compare the Paleo diet to another “healthy” control diet. Outcomes must measure markers of metabolic syndrome.

1. Metabolic and physiologic effects from consuming a hunter-gatherer (Paleolithic)-type diet in type 2 diabetes. (2015) https://www.ncbi.nlm.nih.gov/pubmed/25828624

Interpretation: Researchers studied 24 patients with type 2 diabetes. 14 ate a Paleo diet and 10 ate the American Diabetes Association (ADA) diet for 14 days. Both groups had improved metabolic profiles. The Paleo group did better in terms of glucose control and cholesterol.

2.  Favourable effects of consuming a Palaeolithic-type diet on characteristics of the metabolic syndrome: a randomized controlled pilot-study. (2014) https://www.ncbi.nlm.nih.gov/pubmed/25304296

Interpretation: Researchers studied 34 people with at least two characteristics of metabolic syndrome. 18 were assigned to the Paleo group and 14 to the healthy reference diet. 32 people completed the study for 2 weeks. The Paleo group had lower blood pressure, lower total cholesterol, lower triglycerides, and higher HDL than the reference group. No changes were observed for intestinal permeability, inflammation, and salivary cortisol.

3. Paleolithic nutrition for metabolic syndrome: systematic review and meta-analysis. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26269362

Interpretation: 4 randomized control trials with a total of 159 participants were reviewed to determine whether a Paleo diet improved metabolic syndrome better than a typical healthy diet. The diets were tested for between 1 week and 3 months. Overall, the Paleo diet improved waist circumference, blood pressure, triglycerides, HDL cholesterol and fasting blood pressure (all measures) better than the typical healthy diet.

4. Cardiovascular, Metabolic Effects and Dietary Composition of Ad-Libitum Paleolithic vs. Australian Guide to Healthy Eating Diets: A 4-Week Randomised Trial. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27223304

Interpretation: 39 healthy women were studied. 22 ate a Paleo diet and 17 ate the recommended Australian healthy diet for 4 weeks. There were no differences in cardiovascular or metabolic markers between the groups at the end of the study.

5. Paleolithic nutrition improves plasma lipid concentrations of hypercholesterolemic adults to a greater extent than traditional heart-healthy dietary recommendations. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26003334

Interpretation: 20 adults with poor cholesterol profiles were studied. They ate an ADA heart healthy diet for 4 months and then a Paleo diet for 4 months. The Paleo diet resulted in lowered total cholesterol, LDL and triglycerides and raised HDL better than the traditional heart healthy diet.

6. Beneficial effects of a Paleolithic diet on cardiovascular risk factors in type 2 diabetes: a randomized cross-over pilot study. (2009) https://www.ncbi.nlm.nih.gov/pubmed/19604407

Interpretation: 13 patients with type 2 diabetes were studied. They ate a Paleo diet for 3 months and then the standard recommended diabetes diet for 3 months. The Paleo diet showed better outcomes than the diabetes diet in: blood glucose, triacylglycerol, diastolic blood pressure, weight, BMI, waist circumference, and HDL (all measures).

What We Know and Don’t Know

These studies certainly have their limitations. They have few participants and they study changes over short durations. However, the findings are very consistent. For people with markers of metabolic syndrome, the Paleo diet works better than the recommended healthy diet to improve their condition.

Interestingly, we found the same results with the Vegan diet. It seems that both the Paleo diet AND the Vegan diet are better choices than the ADA diet (commonly recommended healthy diet) to control metabolic syndrome. This finding led me to wonder what exactly the ADA diet consists of.

Their website recommends meals that consist of non-starchy vegetables on half your plate and lean meats and whole grains on the other half. They encourage consumption of beans, dark leafy greens, citrus fruits, berries, sweet potatoes, nuts, fish, low fat milk, and yogurt. They discourage consumption of saturated fats, foods high in cholesterol, alcohol, refined grains, and sugar. In short, the ADA diet is the perfect combination of everything included in the Vegan and Paleo diets with the addition of low fat dairy.

This leaves us with another whole list of questions. Is dairy the culprit for metabolic disease? Are there studies directly comparing Paleo and Vegan diets? Is the success of these diets simply reflecting that people lose more weight and improve their health by cutting out more things from their diets? Should some people cut everything from their diets except for the foods represented by both the Vegan AND Paleo diets?

There was one study from the group above that had different results from the rest. Study number 4 was the only one that found no significant differences between participants who ate a Paleo diet and participants who ate the standard healthy diet. This study was also the only one to use healthy participants rather than people with metabolic syndrome. Additionally, the study only used women while the other studies included both men and women (although a few were primarily women). This study may suggest that different populations benefit differently from the diets.

Conclusions and Applications

After completing this research, I am more curious than ever to start investigating dairy. I’d like to see whether the ADA diet without dairy works better than the ADA diet with dairy. I’d also like to see how the ADA diet without dairy would compare to the Vegan and Paleo diets. I’m not sure what I’ll find in the research since these questions are pretty specific.

Also, I’d like more information on which diets might be best for specific populations. I’m a young healthy woman who likes to lift weights. I may not need to be eating the same way as an older overweight, sedentary man. Or, maybe I do.

For now, I won’t be making any changes. Eat food. Mostly plants. Not too much.

Please share your comments and insights!

Can Common Foods Stop Cancer?

Hippocrates said it first, “Let food be thy medicine”. People have been trying to heal disease with food for thousands of years. Several prominent doctors have claimed that food can even heal cancer. Today I am going to explore one of these claims.

Internal medicine doctor, William Li, gave a viral TED Talk in 2012 describing how he believes food can prevent and even help cure many kinds of cancer. A reader provided me with the link to the talk below and asked for my thoughts.


In order to understand his hypothesis, a little bit of background info on a process called angiogenesis is needed. Here is the description from the National Cancer Institute:

“What is angiogenesis?

Angiogenesis is the formation of new blood vessels. This process involves the migration, growth, and differentiation of endothelial cells, which line the inside wall of blood vessels.

The process of angiogenesis is controlled by chemical signals in the body. These signals can stimulate both the repair of damaged blood vessels and the formation of new blood vessels. Other chemical signals, called angiogenesis inhibitors, interfere with blood vessel formation. Normally, the stimulating and inhibiting effects of these chemical signals are balanced so that blood vessels form only when and where they are needed.

Why is angiogenesis important in cancer?

Angiogenesis plays a critical role in the growth and spread of cancer. A blood supply is necessary for tumors to grow beyond a few millimeters in size. Tumors can cause this blood supply to form by giving off chemical signals that stimulate angiogenesis. Tumors can also stimulate nearby normal cells to produce angiogenesis signaling molecules. The resulting new blood vessels “feed” growing tumors with oxygen and nutrients, allowing the cancer cells to invade nearby tissue, to move throughout the body, and to form new colonies of cancer cells, called metastases.

Because tumors cannot grow beyond a certain size or spread without a blood supply, scientists are trying to find ways to block tumor angiogenesis. They are studying natural and synthetic angiogenesis inhibitors, also called antiangiogenic agents, with the idea that these molecules will prevent or slow the growth of cancer.”

There are many FDA approved drugs that treat cancer by preventing or slowing angiogenesis. Dr. Li promotes these drugs. However, he also makes the claim that many foods work just as well or even better than these drugs at inhibiting angiogenesis.

The Claim

Certain foods can inhibit angiogenesis just as well as or better than drugs to treat cancer patients.

Initial Search

After spending several hours googling things like “cancer diet” and “angiogenesis food”, I kept coming up with results leading me back to Dr. Li’s TED Talk. I also came across several websites and foundations represented by Dr. Li including: Eat to Beat, The Angiogenesis Foundation, Alternative Daily, Forks Over Knives, Food Revolution, Collective Evolution, and everyone’s favorite doctor, Dr. Oz.

Interestingly, not one mainstream reputable source mentioned his hypothesis and I was unable to find other doctors in his line of work. Could it be a conspiracy? Big Pharma? Or…….MONSANTO??? Kidding. But really, he seems to be the only one out there peddling this stuff.

Some of his associations provide links to articles by other professionals. However, you have to register to get access to them and many of the authors don’t have doctorates or even any credentials at all.

Several more reputable sources including: MD Anderson, the American Institute of Cancer Research, the World Cancer Research Fund, and WebMD do list foods that can help lower your risk of cancer. However, they do not discuss angiogenesis. I can’t tell whether it’s because the topic is too scientific or because they help prevent cancer through another mechanism or because they just don’t know how the foods help. None of these sources claim that foods can cure cancer or that foods work as well as or better than drugs for prevention and/or treatment. It’s worth noting that many of the foods are similar to those Dr. Li recommends. All of the food lists are heavy on fruits, veggies, legumes and spices. Some include coffees, teas, nuts and even yogurt and sea foods.

Follow-up Questions

What is the quality of the research to support this claim? Are we going to find a bunch of retrospective observational studies that rely on people to remember what they ate over long periods of time?

Do any animal foods also have anti-angiogenic properties?

Do any studies compare outcomes of cancer patients who treated with diet to those who treated with anti-angiogenic drugs?

Reader Comments (see link above to Dr. Li’s TED Talk via Forks Over Knives)

Peer Reviewed Research

1.Tumor Angiogenesis as a Target for Dietary Cancer Prevention (2012) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3184418/

This is the only peer reviewed article I found directly linking diet to angiogenesis and cancer treatment. Dr. Li from the TED Talk is the first author. It is not a clinical trial, but a review of how specific micronutrients in specific plant foods promote anti-angiogenesis or otherwise inhibit cancer.

First he presents a list of “angiogenic factors” that have been discovered. He then lists “endogenous inhibitors of angiogenesis” that suppress cancer growth. He then describes how genes work to control when new blood vessels are formed. He states that small cancers are common once people reach about 40-50 years of age and that the inhibitors of angiogenesis prevent these cancers from growing too much and becoming dangerous.

Li goes on to describe how some cancers progress to hyperplasia, dysplasia, and then invasive carcinoma by recruiting surrounding blood vessels and enabling new vessels to form. New blood vessels are able to form “by the production and release of one or more angiogenic growth factors…”. He describes how cancers grow and metastasize from there.

Dr. Li discusses current angiogenic therapies that have been proposed and that are in use today. He stresses early treatment before new blood vessels are able to start forming.

Finally, he lists antiangiogenic factors in common foods. For each food, he cites research that supports how they might be preventing cancer in mice, in vitro (test tube), or in human observational epidemiologic or prospective cohort studies. He provides links to all of the studies cited. The factors he describes include:

Green tea catechins, genistein (found in soy beans), resveratrol (found in mulberries, peanuts, grapes, and grape products), lycopene (found in tomatoes, watermelon, and papaya), omega-3 polyunsaturated fatty acids (found in salmon, herring, mackerel, anchovies, sardines and trout), glucosinolates, isothiocynates and indole-3-carbinol (found in cruciferous vegetables such as cabbage, broccoli, cauliflower, collard greens, mustard greens, radishes, brussel sprouts, bok choy, and kale), flavonoids and quercetin (found in many fruits and vegetables), anthocyanins (pigments in berries and grapes), proanthocyanidins (found in cacao and some fruits and vegetables), ellagitannins (found in fruits, vegetables and nuts), manaquinone (vitamin K2 found in dark leafy vegetables and cheese), curcumin (turmeric), beta-cryptoxanthin (found in brightly colored foods).

In the discussion section, Dr. Li does state some of the flaws in the types of studies he reviewed. No human controlled experimental trials have been done. However, he still trusts overall that foods with antiangiogenic factors will help prevent cancer. Interestingly, his paper does not make the claim that these foods work as good as or better than cancer treatments that are already on the market. Instead, he suggests that these foods should be used to help prevent cancer rather than to treat. The paper also never makes bold claims that eating these foods will prevent cancer; only that they may lower one’s chances. Most of the studies he cited showed modest reductions in specific forms of cancer paired with study designs that are known to have high rates of error.

Many other studies address how certain diets can impact cancer. However, I did not find anything other than Dr. Li’s article that claims that the diets are working by inhibiting the growth of new blood vessels. Here are a few reviews, meta-analyses, and one randomized trial I found related to the general question of how diets may cause or help prevent cancer.

2. Influence of a diet very high in vegetables, fruit, and fiber and low in fat on prognosis following treatment for breast cancer: the Women’s Healthy Eating and Living (WHEL) randomized trial. (2007) https://www.ncbi.nlm.nih.gov/pubmed/17635889

CONCLUSION: Among survivors of early stage breast cancer, adoption of a diet that was very high in vegetables, fruit, and fiber and low in fat did not reduce additional breast cancer events or mortality during a 7.3-year follow-up period.

3. Roles of caloric restriction, ketogenic diet and intermittent fasting during initiation, progression and metastasis of cancer in animal models: a systematic review and meta-analysis. (2014) https://www.ncbi.nlm.nih.gov/pubmed/25502434

CONCLUSIONS: Caloric restriction and ketogenic diet are effective against cancer in animal experiments while the role of intermittent fasting is doubtful and still needs exploration. More clinical experiments are needed and more suitable patterns for humans should be investigated.

4. Vegetarian diets, low-meat diets and health: a review. (2012) https://www.ncbi.nlm.nih.gov/pubmed/22717188

RESULTS: Both vegetarian diets and prudent diets allowing small amounts of red meat are associated with reduced risk of diseases, particularly CHD and type 2 diabetes. There is limited evidence of an association between vegetarian diets and cancer prevention. Evidence linking red meat intake, particularly processed meat, and increased risk of CHD, cancer and type 2 diabetes is convincing and provides indirect support for consumption of a plant-based diet.

5. Diet and cancer: risk factors and epidemiological evidence. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24374225

CONCLUSIONS: There is a direct relationship between unhealthy diet and lifestyle with the increase of tumor development and cancer risk. For this reason, a good nutritional status based on a balanced diet constitutes one of the main preventive factors from tumors. However the mixed results from epidemiologic studies hinder to get unequivocal and consistent evidence about the interaction between diet and cancer risk. More epidemiological studies will be needed in the future to clarify this issue.

6. Diet and Colorectal Cancer Risk in Asia–a Systematic Review. https://www.ncbi.nlm.nih.gov/pubmed/26225683

ABSTRACT SELECTION: We found that red meats, processed meats, preserved foods, saturated/animal fats, cholesterol, high sugar foods, spicy foods, tubers or refined carbohydrates have been found by most studies to have a positive association with colorectal cancer risk. Inversely, calcium/dairy foods, vitamin D, general vegetable/fruit/fiber consumption, cruciferous vegetables, soy bean/soy products, selenium, vitamins C,E and B12, lycophene, alpha-carotene, beta-carotene, folic acid and many other vitamins and minerals play a protective role against colorectal cancer risk. Associations of fish and seafood consumption with colorectal cancer risk are still inconclusive due to many varying findings, and require further more detailed studies to pinpoint the actual correlation. There is either a positive or no association for total meat consumption or white meats, however their influence is not as strong as with red and processed meats.

7. Nutrition and cancer. (2015) translated from Spanish https://www.ncbi.nlm.nih.gov/pubmed/26267778

RESULTS: Fruits and vegetables are the foods that can prevent from cancer disease, soya and fishes also have demonstrated as preventive from some types of malignancies. Clear factors causing cancer are red meat and processed meat, dairy products and alcohol. The protective roles of vitamins, antioxidants and micronutrients still have to be deeply investigated. Obesity is a clear risk factor for cancer, calorie reduction has been proposed as a factor that has protective properties in laboratory studies, but this has to be demonstrated in a clinical scenario.

8. Meat, dairy, and cancer. (2014)  https://www.ncbi.nlm.nih.gov/pubmed/24847855

ABSTRACT: In 2007 the World Cancer Research Fund and American Institute for Cancer Research (WCRF/AICR) report judged that the evidence for an association between red and processed meat consumption and colorectal cancer was convincing. In addition, the effect of other animal products on cancer risk has been studied, and the WCRF/AICR report concluded that milk probably decreases the risk of colorectal cancer but diets high in calcium probably increase the risk of prostate cancer, whereas there was limited evidence for an association between milk and bladder cancer and insufficient evidence for other cancers. There are several potential mechanisms relating meat to cancer, including heterocyclic amines, polycyclic aromatic hydrocarbons, N-nitroso compounds, and heme iron. Although the evidence in favor of a link between red and processed meat and colorectal cancer is convincing, the relations with other cancers are unclear. In this review, we summarize cohort studies conducted by the National Cancer Institute on meat and dairy intake in relation to cancer since the 2007 WCRF/AICR report. We also report the findings of meta-analyses published since 2007.

9. Dairy products and cancer. (2011) https://www.ncbi.nlm.nih.gov/pubmed/22081693

ABSTRACT SELECTION: Based on a systematic review of the epidemiologic literature, the World Cancer Research Fund and American Institute for Cancer Research report concluded there was a probable association between milk intake and lower risk of colorectal cancer, a probable association between diets high in calcium and increased risk of prostate cancer, and limited evidence of an association between milk intake and lower risk of bladder cancer. For other cancers, the evidence was mixed or lacking.

10. Adherence to Mediterranean diet and risk of cancer: an updated systematic review and meta-analysis of observational studies. (2015)https://www.ncbi.nlm.nih.gov/pubmed/26471010

ABSTRACT SELECTION: The aim of the present systematic review and meta-analysis of observational studies was to gain further insight into the effects of adherence to Mediterranean Diet (MD) on overall cancer mortality, incidence of different types of cancer, and cancer mortality risk in cancer survivors. An overall population of 1,784,404 subjects was included in the present update. The highest adherence score to an MD was significantly associated with a lower risk of all-cause cancer mortality, colorectal cancer, breast cancer, gastric cancer, prostate cancer, liver cancer, head and neck cancer, pancreatic cancer, and respiratory cancer. No significant association could be observed for esophageal/ovarian/endometrial/and bladder cancer, respectively. Among cancer survivors, the association between the adherence to the highest MD category and risk of cancer mortality, and cancer recurrence was not statistically significant. The updated meta-analyses confirm a prominent and consistent inverse association provided by adherence to an MD in relation to cancer mortality and risk of several cancer types.

11. Mediterranean diet and cancer: epidemiological evidence and mechanism of selected aspects. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24267672

DISCUSSION: The most recent pooled analyses of epidemiological studies supported strongly the hypothesis that the Mediterranean diet may play a role in preventing several types of cancers, especially those of digestive tract, whereas contrasting results were reported for hormone-dependent cancers. Specific aspects of the Mediterranean diet such as high fruit and vegetables and low red processed meat intake may explain such protective effects. Moreover, evidence regarding olive oil and whole grains increase the beneficial effects of such dietary pattern against cancer.

12. Nutrition and prostate cancer: an overview. (2014)https://www.ncbi.nlm.nih.gov/pubmed/25367323

ABSTRACT SELECTION: Obesity and metabolic syndrome are important risk factors for prostate cancer and their management is key. The amount and type of fats consumed are also clearly related to prostate cancer risk. Saturated fats and trans fats are identified as having a negative impact. Nutraceuticals and supplements, particularly antioxidants, polyphenols and soy have evidence for benefit for prevention of prostate cancer and progression of the disease.

13. Ketogenic Diet and Cancer-a Perspective. (2016)https://www.ncbi.nlm.nih.gov/pubmed/25503112

ABSTRACT SELECTION: Exercise or severe restriction of caloric intake is not always advisable for patients, in particular those suffering from cancer. The ketogenic diet (KD), characterized by high fat, moderate protein and very low carbohydrate composition can evoke a physiological state similar to that triggered by exercise or fasting. These attributes of KD prompted its possible use in treatment of a number of metabolic diseases, including several types of malignancies. Although results from clinical studies employing KD in the treatment of cancer are still limited, the results obtained from animal models are encouraging and show that KD presents a viable option as an adjunct therapy for cancer.

14. The role of dietary factors in prevention and progression of breast cancer. (2014)https://www.ncbi.nlm.nih.gov/pubmed/25503112

RESULTS: Consumption of well-done red meat appears to be associated with increased risk of BC, whereas fish may be protective. Total cholesterol, triglyceride levels and glycaemic load should be monitored and controlled in at risk populations because they may be associated with increased risk of BC, although the exact mechanisms involved are not clear. Alcohol intake should be minimized since it is a risk factor for BC. High intake of polyphenol/phyto-oestrogen -rich food (i.e. flavonoids, soya products), as well as fibres, fruits and vegetables, may have potential protective effects against BC occurrence but the results might vary according to hormonal status. Vitamin D supplements appear protective against BC development and similarly other vitamins and oligo-elements might decrease BC risk, although further large prospective studies are required.

15. Dietary intake and ovarian cancer risk: a systematic review. (2014)https://www.ncbi.nlm.nih.gov/pubmed/24142805

ABSTRACT SELECTION: Higher risk for ovarian cancer was shown for total, animal, and dairy fat (five of nine studies), as well as total nitrate and possibly total vitamin C. No associations were demonstrated for red meat, fiber, vitamin A, vitamin E, β-carotene, or folate. Vegetables were associated with lower risk in one of three studies; fruit showed no association, although risk estimates were all greater than 1.0. Isoflavones and flavonoids were associated with modestly lower risk in two studies and tea intake was associated with lower risk in one of two studies. This review suggests that no specific dietary factors are consistently associated with ovarian cancer risk.

What we know and don’t know:

After the research, we can see that angiogenesis is a necessary process for cancers to grow and become dangerous. We know there are FDA approved drugs to help slow this process. We also know that people who eat a lot of fruits, vegetables, fish, soy, and tea tend to have lower chances of developing most types of cancer than people who drink a lot of alcohol, eat a lot of red and processed meat, eat a lot of trans and saturated fat, and eat foods cooked at high temperatures. There is quite a bit of data to support these general ideas, but few randomized control trials. That means it may be hard to assign cause and effect and the studies may have other various flaws making them less reliable.

Research does not directly support that eating certain properties of plant foods can prevent cancer from establishing a blood supply. However, the research does not directly deny that this is happening. I wasn’t able to find any studies to directly test this hypothesis. No studies were found that compare treating patients with medication to treating patients with diet.

Even if plants are helping to protect people from cancer by way of antiangiogenic properties, it is highly unlikely that plant foods could replace medications. Dr. Li himself doesn’t even suggest this in his own paper. Additionally, Dr. Li’s research supports consumption of certain animal products such as fish, which is conveniently overlooked when presented by vegan groups.

Another common theme throughout the research in the relationship between cancer and diet is simply that eating less can help. Several studies show that reducing calories lowers the chance of developing cancer and that being overweight is a huge cancer risk factor. Some studies also show that a ketogenic diet can prevent and even help treat cancer. In fact, I was able to find more support for ketogenic diets as a cancer treatment than for vegan or nearly vegan diets.

Conclusions and applications:

What should we do with this information? Here’s my list of ideas based on my research:


  • Eat lots of fruits and vegetables every day
  • Eat fish several times a week
  • Soy products are probably good for you, although this is another hot topic
  • Avoid processed meat
  • Eat less red meat and opt for cuts that don’t need to be well done
  • Avoid processed foods, trans fats and sugar
  • Avoid alcohol
  • Maintain a healthy weight
  • If you already have cancer, traditional treatments work better than a plant-based diet, although a ketogenic diet may be helpful.

Should I go Vegan?

Every few years, Netflix stirs the pot with another vegan “documentary”. First it was Food Inc. and Forks Over Knives, then Cowspiracy, and, most recently, What the Health. I’m sure there have been others. These films can be pretty convincing and surely do tempt some people to try veganism for themselves. They do a great job of presenting peer reviewed studies to support their claims. They also show remarkable recoveries from chronic disease.

However, as I’m sure you suspect, they use some pretty sneaky tactics to overstate their claims. They usually cherry pick their studies while ignoring everything that might conflict with their agenda. They report relative rather than absolute risks. They interview doctors who have personal biases. They malign research and medical agencies that refuse to change their policies based on cherry-picked evidence. They try to convince people that correlation is causation. And sometimes, they even lie outright.

Many bloggers and YouTubers have already “debunked” a lot of the points in these films. My purpose in this blog, therefore, is not to repeat what many have already said. My purpose is to determine what the research really says about vegan diets.

The Claim:

If you eat a whole-foods, plant-based vegan diet, you will not get heart disease, diabetes, or other symptoms of metabolic syndrome. If you already have these diseases, a vegan diet will cure them.

Results from initial search:

There are many reasons why people might choose a vegan diet. Some believe it’s healthier than eating meat while others are more concerned about the environment and animal welfare. It’s widely accepted a vegan diet can be a very healthy option as long as you are sure to get a variety of proteins from different grain and legume combinations, supplement with vitamin B12, and possibly add other supplements to get essential fatty acids.

Most experts also agree that farmed animals are causing plenty of environmental harm, not to mention harm caused to the animals themselves. These concerns are certainly valid. Some people argue that if you purchase animal products from local farmers markets, you can avoid supporting factory farming and have less impact on the environment. Others disagree, stating that all animals fear death and should not be slaughtered for food.

The environmental and animal welfare aspects of a vegan diet, while important, are not within the scope of this blog. I will say that personally, I believe it’s important to support local farms and farms that allow animals to live as naturally as possible. The “Certified Humane” stamp on some animal products is the best indicator of humane animal treatment that can be found at typical grocery stores. Other markers such as “pasture-raised” or “free range” are misleading and practically meaningless when issued by the USDA.

 When it comes to the health benefits of a vegan diet, there is quite a bit more controversy. Some pro-vegan arguments include:

  • Vegan diets help mitigate some of the world’s biggest health issues such as obesity, diabetes, heart disease and cancer because plants are high in fiber, vitamins, minerals, and antioxidants while being low in saturated fat.
  • Processed meat causes cancer.
  • Animal products contain saturated fat which caused heart disease.
  • You can get more than enough protein by eating and combining high protein grains and legumes.
  • Groups of people who live the longest usually eat vegetarian or vegan diets.
  • Vegan diets are better for you gut health.

Some pro-omnivore arguments include:

  • Iron, zinc, calcium, vitamin B12, DHA and EPA are lacking in vegan diets. Over time, these cause bone loss, heart disease, and other health problems.
  • People have been eating meat and animal products for thousands of years. Refined grains and sugar are really what’s causing increased rates of metabolic syndrome and cancer.
  • It can be difficult to get enough complete protein through plant sources alone.

Follow-up questions

  • If you supplement and make sure you’re eating foods high in protein, is it really that hard to get all your nutrition from a vegan diet?
  • It seems the jury is still out on saturated fat. Could it affect different people differently?
  • Have studies compared vegan diets to other whole food diets that include meat or just to the standard American diet?
  • If vegans really do have better metabolic profiles, how much better are they?
  • Many studies may claim to demonstrate health benefits of vegan diets. Are there other studies that claim equivalent or even better health benefits of other diets?

Reader comments and questions (send me some!)

Peer-reviewed research

Inclusion criteria: search terms “vegan diet” on PubMed. Published in last 10 years. Reviewed first 5 pages of results. Vegan diet compared to another diet considered to be healthy. Outcomes related to disease markers for diabetes and heart disease in humans. Italics are my interpretation.

1.Veganism Is a Viable Alternative to Conventional Diet Therapy for Improving Blood Lipids and Glycemic Control. https://www.ncbi.nlm.nih.gov/pubmed/24922183 (2015)

No access to full text. Conclusion suggests vegan diets are somewhat better than healthy omnivorous diets to help people with type 2 diabetes and/or high cholesterol. The authors seem to have reviewed several studies to come to this conclusion. We can’t tell how much better vegan diets are or whether or not the results were clinically significant.

2. Beyond meatless, the health effects of vegan diets: findings from the Adventist cohorts. https://www.ncbi.nlm.nih.gov/pubmed/24871675 (2014)

Full text available. This study compares large groups of vegan/vegetarian, and omnivorous Adventists from several different studies. Vegetarians had a 55% lower chance of developing hypertension and a 25-49% lower chance of developing type-2 diabetes than omnivores. Vegetarians had a 23% lower chance of developing GI cancers, a 50% lower chance of developing colon cancer, and a 35% lower chance of developing prostate cancer. When vegans and vegetarians were separated out, the vegans had even lower chances of developing these diseases. This study only reported relative percentages, not absolute percentages. This study makes a good argument that a vegetarian diet is at least slightly healthier than a diet that includes meat in terms of chronic disease.

3. Vegan diet and blood lipid profiles: a cross-sectional study of pre and postmenopausal women. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24712525

Full text available. This study measured different types of cholesterol in vegetarians, vegans, and omnivores. We now know that HDL cholesterol is good and LDL cholesterol is bad. Many doctors look at the ratio of LDL to HDL and consider it to be a much better measure of health than looking at total cholesterol or LDL or HDL alone. This study says that in premenopausal women, a vegan diet decreases HDL, but does not decrease LDL. The vegetarian diet decreases HDL, but decreases LDL even more. Therefore, the vegetarians would have a better ratio than the vegans. The omnivore ratio was comparable to the vegetarians. The findings only applied to the premenopausal group.

4. Effect of a 6-month vegan low-carbohydrate (‘Eco-Atkins’) diet on cardiovascular risk factors and body weight in hyperlipidaemic adults: a randomised controlled trial. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24500611

Full text available. 50 people were divided into 2 groups of 25 (one group ate a low carb vegan diet while the other group ate a high carb vegan diet). After 6 months, only 13 people were left in the high carb group and 10 in the low carb group. It seems that the main finding in this study is that the diets aren’t easy to stick to. In the end, most people in the low carb group had better cholesterol than those in the high carb group. However, people in both groups made significant progress in terms of weight loss and cholesterol.

5. Effect of a Brown Rice Based Vegan Diet and Conventional Diabetic Diet on Glycemic Control of Patients with Type 2 Diabetes: A 12-Week Randomized Clinical Trial. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27253526

Full text available. A strict vegan diet controls blood sugar better than a healthy omnivorous diet, but for most people, it’s very hard to stick to. The difference between how much each diet decreased blood sugar was relatively small. However, the sample size was small and compliance with the diets varied.

6. Comparison of a Restricted and Unrestricted Vegan Diet Plan with a Restricted Omnivorous Diet Plan on Health-Specific Measures. (2015) https://www.ncbi.nlm.nih.gov/pubmed/27417779

Full text available. 12 people ate a plant based vegan diet with no refined grains, sugar, or sweeteners. 12 people ate a similar diet, but were allowed lean protein and skim milk. 11 people ate a vegan diet, but were allowed refined grains, sugar, and sweeteners. Participants ate these diets for 21 days. All 3 diets showed improvements in health. Cholesterol was improved in the vegan and non-vegan groups who avoided refined grains and sugar. Cholesterol did not improve in the vegan group that continued eating refined grains and sugar. Blood pressure was reduced in all groups, but most in the vegan group that avoided refined grains and sugar.

7. Effect of diet on type 2 diabetes mellitus: a review. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24352832

No access to full text. Vegan, vegetarian, low carb, and Mediterranean diets have all helped people with type 2 diabetes to control their blood sugar. Different people respond differently.

8. A low-fat vegan diet and a conventional diabetes diet in the treatment of type 2 diabetes: a randomized, controlled, 74-wk clinical trial. (2009) https://www.ncbi.nlm.nih.gov/pubmed/19339401

Full text available. 49 people were assigned to the low-glycemic vegan group and 50 to the conventional healthy diet group. The study lasted 74 weeks. Both groups improved in terms of weight, blood sugar, and cholesterol. Blood sugar and cholesterol improved significantly more in the vegan group than the conventional group.

9. Vegetarian diets and incidence of diabetes in the Adventist Health Study-2. (2013) https://www.ncbi.nlm.nih.gov/pubmed/21983060

More than 40,000 healthy people were studied. They were categorized as either: vegan, lacto ovo vegetarian, pesco vegetarian, semi-vegetarian or non-vegetarian (reference group). The researchers wanted to see how many developed diabetes over the next 2 years. Diabetes developed in 0.54% of vegans, 1.08% of lacto ovo vegetarians, 1.29% of pesco vegetarians, 0.92% of semi-vegetarians and 2.12% of non-vegetarians. After other lifestyle factors were controlled for, vegan and vegetarian diets (but not ones including fish) still offered protection against diabetes. Black people were more likely to develop diabetes than white people, but all people benefited from a vegetarian diet.

10. A two-year randomized weight loss trial comparing a vegan diet to a more moderate low-fat diet. https://www.ncbi.nlm.nih.gov/pubmed/17890496 (2007)

This is a randomized trial which can provide more reliable evidence than retrospective or observational studies. The researchers compared a low fat mostly vegan diet to a more traditional low fat/low cholesterol diet. However, the vegan diet did allow for a very small amount of meat and dairy. They also studied whether group support meetings were helpful. All participants were postmenopausal women. After 2 years, the vegan group had kept off about 3 kilograms whereas the control group had kept off about 1. This study only measured weight loss, but we know that being overweight is strongly associated with metabolic syndrome.

11. Comparative effectiveness of plant-based diets for weight loss: a randomized controlled trial of five different diets. https://www.ncbi.nlm.nih.gov/pubmed/25592014(2015)

Full text not available. This study assigned 63 overweight people to vegan, vegetarian, pesco-vegetarian, semi-vegetarian or omnivorous diets. The vegan group lost an average of 7.5% of their body weight after 6 months. The other groups lost about 3%. Calories were not purposefully restricted.

What we know and don’t know

Looking at these studies, we can see that a vegan diet may be a good idea for some people. But, as expected, the results were not as incredible as our favorite Netflix documentaries would suggest.

All of the research I found supports a vegan diet in people who are at risk for metabolic syndrome. However, the effects of the diet were modest and some studies show the diet can be hard to stick to. When people are allowed to eat freely without counting calories, they tend to lose only 5-10% of their body weight by switching to a vegan diet. This moderate amount of weight loss does seem to help reduce other markers of disease, so a vegan diet is likely to help people at risk. However, it is an overstatement to say that a vegan diet cures metabolic diseases.

The studies here did present a few flaws/risks that should be mentioned. First, vegan diets tend to lower good cholesterol (HDL) more than bad cholesterol (LDL) in some people. This may actually give some people a worse overall cholesterol profile. Additionally, most of these studies didn’t parse out different populations of people. For example, we know the diet can help middle aged people who are overweight, but is it also good for children, athletes, or expectant mothers? There are studies available to address these questions, but they were not reviewed here. It does seem that for the populations studied, it is reasonable to get all your nutrition from a vegan diet plus a vitamin B12 supplement.

Several of these studies found that reducing or eliminating refined grains and sugars had equal or even better results than avoiding animal products on health outcomes. Many did not allow the vegan group or the control group to eat refined carbohydrates because they purpose was to compare a vegan diet with another “healthy” diet. This suggests that a diet low in processed foods is healthier than a diet low in animal products, but, that a diet low in both categories of foods may be best.

In these studies, saturated fat was assumed to be “unhealthy” from the beginning. Therefore, it is difficult to determine what effects would be seen if saturated fat levels were increased. Other studies do address this question, but not within the context of a vegan diet.

It is important to remember that in all studies that are not double-blind, randomized, controlled, and include placebo, there is some room for bias. These studies generally found somewhat better health outcomes for vegans than for other groups. There are other studies that show better outcomes for other diets such as Mediterranean or paleo. These diets could each deserve their own blogs.

Conclusions and Applications

This research confirms one of my favorite quotes by author Michael Pollan.

Eat food, mostly plants, not too much.

Over and over we see that these are words of wisdom to live by if you want to be as healthy as possible. I might add slightly alter the quote to include the words “ethically sourced” if it were me.

Please share your comments and thoughts!


Does Sensory Integration Therapy Work?

Fidget toys are all the rage these days. You probably know someone who swears they help kids focus. You may even use them yourself. Fidget toys are just one of the many compensatory items that may be recommended for children with sensory processing disorder. If you’ve never heard of sensory processing disorder, here’s what you need to know. In the 1970s, Dr. A. Jean Ayres, occupational therapist, first described sensory processing difficulties. She explained that people make sense of the world through 7 senses: vision, hearing, taste, smell, touch, proprioception (sense of body awareness) and vestibular sense (sense of movement).  A person may be overly (hyper) or under (hypo) sensitive to one or more of the 7 senses.

The Claim:

Sensory integration therapy (SIT) teaches the brain to respond in a more organized (appropriate) way to sensations and movement.

Let’s dig in!

Results from initial search:

A sensory processing disorder (also called sensory integration disorder/dysfunction) diagnosis is usually made by an occupational therapist through a series of checklists by observing the child and interviewing the caregivers. The sensory problems generally affect the child’s ability to learn, interact with others, and participate in daily activities. Most children on the autism spectrum are reported to have sensory processing disorder as well as many children with ADHD and even some children with no other conditions. Here are some examples of what sensory processing disorder might look like:

Hypersensitivity to sound: extreme responses to or fear of common sounds like flushing toilets, coughing, or clanking silverware; inability to tune out background noises

Hypersensitivity to touch: Avoidance of touching or hugging people; refusal to wear many types of clothing or extreme discomfort when tags are not cut from clothing; fear of touching messy things like food, glue or play-doh

Hyposensitive vestibular sense and/or proprioceptive sense: desire to run and crash into furniture or other objects constantly; Constant need to jump or swing; no fear of getting hurt

Sensory processing disorder is not recognized as a mental disorder in the ICD-10 and many doctors do not believe it really exists as a disorder on its own. Most psychologists do recognize that children have sensory challenges, but see them as part of another developmental disorder or delay, such as autism.

Occupational therapists, as well as some other educators and professionals believe sensory processing disorder is at the root of many behavioral and learning challenges and that it can be treated, to some extent, with sensory integration therapy. Sensory integration therapy looks at how a child processes each type of sensory input and recommends things that can be done to help the child normalize the way he or she interprets the input.

They believe they are helping to literally reorganize the sensory system in the brain rather than simply provide coping mechanisms and compensatory strategies.

This is thought to be achieved through a prescribed “sensory diet” individualized for each child. When the sensory diet is followed, the child is expected to become more tolerant of sensory input and more calm, alert and focused. Different activities are assigned depending on whether the sense needs to be heightened or attenuated. Here is an example of a sensory diet:

To help calm and organize the proprioceptive and vestibular senses: rock on a chair or horse, climb stairs, push a grocery cart or something heavy, wear weighted vests or blankets

To help arouse hyposensitive proprioceptive and vestibular senses: use more erratic motion such as running, playing catch, and spinning around

To help organize touch, use textures and deep pressures such as: swaddles, bear hugs, joint compressions, finger paint, glitter glue, putty, rice bins

To organize the auditory sense, use: calming our arousing music, white noise, noise canceling head phones

To organize vision, use: sunglasses, lava lamps, mobiles, drawing, minimal patterns and clutter, non-fluorescent lighting

To organize smell and taste, use: essential oils, candles, warm and cold foods, blow bubbles, suck through straws

Follow-up questions:

    • How are brains of people with sensory problems different?
    • Does SIT really make changes to the brains of these people? Can we see the changes or measure them indirectly?
    • Even if the brain isn’t actually changing, can sensory diets help children learn, focus, and be more successful in relationships with others?

Reader comments

    • Most of my readers claim to either: work with or know people with sensory challenges, or have sensory challenges of their own. I would love to hear what’s worked for you! If you are an occupational therapist, your expertise is welcome!

Peer reviewed research:

  • https://www.ncbi.nlm.nih.gov/pubmed/22641765 Sensory integration therapies for children with developmental and behavioral disorders. (2012)
    • Summary of report: It is unclear whether children who present with sensory-based problems have an actual “disorder” of the sensory pathways of the brain or whether these deficits are characteristics associated with other developmental and behavioral disorders. Because there is no universally accepted framework for diagnosis, sensory processing disorder generally should not be diagnosed. Other developmental and behavioral disorders must always be considered, and a thorough evaluation should be completed. Difficulty tolerating or processing sensory information is a characteristic that may be seen in many developmental behavioral disorders, including autism spectrum disorders, attention-deficit/hyperactivity disorder, developmental coordination disorders, and childhood anxiety disorders. Occupational therapy with the use of sensory-based therapies may be acceptable as one of the components of a comprehensive treatment plan.
  • https://www.ncbi.nlm.nih.gov/pubmed/22318118 Occupational therapy and sensory integration for children with autism: a feasibility, safety, acceptability and fidelity study. (2012)
    • Ten children diagnosed with autism spectrum disorder ages 4-8 years received intensive occupational therapy intervention using sensory integration principles following a manualized protocol. Measures of feasibility, acceptability and safety were collected from parents and interveners, and fidelity was measured using a valid and reliable fidelity instrument.
    • The intervention is safe and feasible to implement, acceptable to parents and therapist, and therapists were able to implement protocol with adequate fidelity.
    • This study did not measure whether the therapy actual worked as purported.
  • https://www.ncbi.nlm.nih.gov/pubmed/23893373 Pilot study: efficacy of sensory integration therapy for Japanese children with high-functioning autism spectrum disorder. (2014)
    • 20 children with high functioning autism (IQ of 70 or above) who had previously received therapy were studied. 8 children had received individualized sensory integration therapy and 12 children had received traditional group therapy.
    • The Miller Assessment for Preschoolers (Japanese version) was given to each child before and after 8-10 months of treatment. The results showed that Total score and all Index scores except for Verbal Index increased significantly in the SIT group, while only Total score increased in the GT group. Furthermore, the SIT group showed more improvement compared with the GT group in Total score and on Coordination, Non-verbal, and Complex Index scores.
    • The study had several limitations including testing group vs. individual therapy and being an analysis of previously collected data. Evidence for the efficacy of sensory integration therapy based on this study is present, but weak.
  • https://www.ncbi.nlm.nih.gov/pubmed/25005509 Parents’ explanatory models and hopes for outcomes of occupational therapy using a sensory integration approach. (2014)
    • Summary: 275 Parents hoped occupational therapy would help their children develop self-understanding and frustration tolerance to self-regulate their behavior in socially acceptable ways. They specifically wished for improvements in: self-regulation, interaction with peers, improvement in skilled motor activities, and self-confidence.
    • This study did not test whether sensory integration therapy worked; only what outcomes parents hoped for.
  • https://www.ncbi.nlm.nih.gov/pubmed/25184475 State of measurement in occupational therapy using sensory integration. (2014)
    • This article discussed how sensory integration therapy is being measured. The authors stated the need for additional measurement tools that take into account: descriptions of the child, how well the therapist or patient adhered to the treatment, dosage of treatment, outcome measurements with qualitative and quantitative data.
    • This article basically stated that sensory integration therapy needs to be measured more accurately.
  • https://www.ncbi.nlm.nih.gov/pubmed/24214165 An intervention for sensory difficulties in children with autism: a randomized trial. (2014)
    • 32 children ages 4-8 with autism and IQ greater than 65 were divided into treatment and control groups. The treatment group received sensory integration therapy and the control group did not. Some members of both groups received other types of therapy too, such as ABA.
    • The sensory integration group scored significantly better than the control group on several measures of the Goal Attainment Scale including self-care, social activities, and decreased caregiver assistance.
    • This study used more rigorous methods than most others, but still had flaws. The number of participants was small and all patients had a relatively high IQ.
  • https://www.ncbi.nlm.nih.gov/pubmed/25460221 A systematic review of sensory-based treatments for children with disabilities. (2015)
    • Thirty studies involving 856 participants met our inclusion criteria and were included in this review. Considerable heterogeneity was noted across studies in implementation, measurement, and study rigor. This means the studies were very different in quality and how the therapy was carried out.
    • The research on sensory-based treatments is limited due to insubstantial treatment outcomes, weak experimental designs, or high risk of bias.
    • The systematic review concluded that there is insufficient evidence to support the use of sensory integration therapy.
  • https://www.ncbi.nlm.nih.gov/pubmed/24477447 A systematic review of sensory processing interventions for children with autism spectrum disorders. (2015)
    • This systematic review examined the research evidence (2000-2012) of two forms of sensory interventions, sensory integration therapy and sensory-based intervention, for children with autism spectrum disorders and concurrent sensory processing problems.
    • “Sensory integration therapy” was defined as clinic-based interventions that use sensory-rich, child-directed activities to improve a child’s adaptive responses to sensory experiences. “Sensory-based interventions were characterized as classroom-based interventions that use single-sensory strategies, for example, weighted vests or therapy balls, to influence a child’s state of arousal.
    • 5 studies used sensory integration therapy and 14 studies used sensory-based intervention. Two randomized control trials using sensory integration therapy found positive effects using Goal Attainment Scaling (a popular and reliable way test to measure progress). The other 3 studies found positive effects for reducing behaviors linked to sensory problems. Few positive effects were found in sensory-based intervention studies.
    • This study also emphasized the need for more rigorous trials and better measurements.

What we know and don’t know:

  • These 8 articles were the only relevant studies I could find when searching PubMed. I would imagine there may be more research out there in journals specific to occupational therapy. I’m not sure why my search didn’t yield more results, especially since some of the studies I found were reviews of several others.
  • From what I found, it seems like the way SIT is implemented varies greatly and is hard to measure. Many measurements are subjective (looking at results such as whether the parents think the intervention is working). It may also be hard to tease out whether the SIT was what helped the child make progress or whether it might have been something else like behavior modification or maturity.
  • None of the research I found attempted to prove that children with sensory processing disorder had real neurological differences. They also did not attempt to show that after treatment, the children’s brains looked more like those of children without sensory processing disorder.
  • A few studies had promising results. Here’s what they had in common:
    • They measured pre and post treatment via the goal attainment scales which breaks down precisely how proficient a child is at a task/skill and how much help they need.
    • Therapy was provided to each child individually and not in a group setting.
    • Progress was reported in terms of the child getting better at functional skills, not having a more “normal” sensory processing system.

Conclusions and applications:

  • So, does sensory integration therapy change the brain? I wasn’t able to find any evidence that this is true. Does sensory integration therapy work? Maybe. From what I’ve learned, it seems that some children get better at things like self-care skills, social skills, and compliant behavior when they have SIT. My inclination is that the sensory diet can help get a child’s body and mind in a state more ready to learn. For example, some people are able to focus on school work better when Mozart is playing in the background while other people need complete silence. Many children are able to sit at their desks and focus much better after an hour of recess than without. I may be wrong, but right now, the theory that sensory integration therapy changes the sensory system neurologically is more of a hypothesis. There is not any evidence to support that notion.
  • Should occupational therapists continue using SIT? There definitely needs to be more high quality research in this area. For now, though, I think SIT should be used as a strategy or technique to help children improve other skills. This is the way I see SIT used most commonly today. Therapists often use sensory organizing strategies like brushing or weighted vests to help a child calm down and focus on a task. So, indirectly, it’s probably making a difference, at least for some kids. However, if the therapist, for example, said they were having a child swing in order to organize the child’s vestibular system, there may be a problem. There isn’t any evidence to support that swinging (or any other activity) can change the vestibular system.

That’s my 2 cents based on what I found in the research so far. I’m always open to learn more. What do my OT friends think about SIT and how it should be used?






Are Diet Sodas Really That Bad?

Today I’m reviewing one of the topics that interest me the most: Diet Coke. I’m one of the weirdos who actually likes the taste of Diet Coke better than regular Coke. I think it’s because Diet was usually what we had in my house growing up. And also because it doesn’t leave my teeth feeling all grimy like regular Coke. I gave up Diet Coke all together from about 2012-2015 after hearing about how terrible it was, even compared to sugary drinks. However, lately I’ve been skeptical of most health claims and decided it probably wasn’t a big deal. Out of my own curiosity and because of requests from other readers, today I’m giving artificial sweeteners the full review.

  1. The Claim

Regular soda is bad for you, but diet soda is even worse. It makes you gain even more weight and causes cancer. It’s a neurotoxin and is basically the same as drinking formaldehyde.

  1. Results from Initial Search

I trolled the internet for hours just to see what I would find. The internet was pretty split, just as it is for most controversial health claims. A few of the sites making diet drinks out to be the devil were: Health.com, Clark.com, Dr. Axe, Breastcancer.org, and MD Anderson.org.

These sites made claims that diet drinks trick your taste buds into craving sweeter foods and overcompensating for the calories not provided in the drink. Some state diet drinks trigger insulin and glucose intolerance leading to type 2 diabetes, weight gain, heart disease, and other symptoms of metabolic syndrome.

Other health problems they considered to be associated with diet drinks included: kidney damage, tooth erosion, compromised lungs, migraines, depression, anxiety, short term memory loss, multiple sclerosis, fibromyalgia, hearing loss, fatigue, brain tumors, epilepsy, chronic fatigue syndrome, birth defects, Alzheimer’s, ADHD, Parkinson’s, gut dysbiosis, DNA damage causing breast cancer, liver cancer, lymphoma, and leukemia, urinary and bladder cancer, depression, and lower bone density.

Some sites, such as WebMD, Authoritynutrition.com, and Nerdfitness.com were more cautious with their claims. They generally agreed that drinking diet soda didn’t help people lose weight and that it only caused cancer when given to lab animals in amounts that greatly exceed the acceptable daily intake (ADI). However, they supported the notion that people probably give themselves permission to eat other unhealthy foods to compensate for the diet soda. They also agreed that diet soda increases a person’s risk for diabetes. These sites were careful to say that just because conditions like diabetes and weight gain were associated with drinking diet soda, diet soda was not necessarily the cause. Perhaps people who know they are at risk for metabolic syndrome choose to drink diet soda more often than the general population.

Finally, several sites claim diet soda probably doesn’t cause any health problems if limited to 1-2 cans per day, with the exception of tooth decay. However, tooth decay is caused by the acidity of the drink, not the artificial sweetener.  These sites include: Mayo Clinic, Examine.com, and Cancer.org (American Cancer Society).  They say there is no evidence to suggest diet soda causes weight gain, spikes insulin levels, or inhibits fat loss. Evidence for overcompensation is mixed and metabolic syndrome associations are confounded by other dietary behaviors. The American Cancer Society fights the formaldehyde claim by explaining that the amounts are not harmful. Methanol from fruit juice breaks down into 10 times more formaldehyde than aspartame. They also state that the FDA sets a max daily safe amount of each artificial sweetener (acceptable daily intake) which is set to many times less than the smallest amount that could cause concerns in lab animals. An average size person would need to drink 19 cans of diet soda per day to reach levels that might be dangerous. The exception to this is people with Phenylketonuria (PKU). This is a rare genetic disorder where people can’t break down phenylalanine found in many foods. These people should avoid diet soda.

  1. Follow-Up Questions

Once again, I’ve found that I need to narrow my focus. How should I do this? I decided to focus on the middle group from the list above. This is the group that regards diet soda with caution. They don’t claim it causes every health problem known to man, but they are concerned that it may paradoxically contribute more to weight gain than weight loss. They also believe diet soda may contribute to metabolic syndrome, especially type 2 diabetes. This seems like the area with the most debate and valid health concerns.

There may be evidence to link artificial sweeteners to other health risks, but these will have to be explored more in depth at another time. My peer reviewed research below was narrowed to focus mainly on artificial sweeteners and weight gain/metabolic syndrome. You will notice that some of the experimental designs I reviewed looked at other health effects along with weight gain and metabolic syndrome markers.

  1. Reader Comments

None yet. Please leave me questions and/or articles you’ve found on topics you’d like me to explore!

  1. Primary Source Review

The first group of studies is in chronological order and generally concludes that artificial sweeteners are safe and may help with weight loss. The second group is also in chronological order and generally concludes that artificial sweeteners may be harmful and do not help with weight loss.

Group 1

  • Effect of drinking soda sweetened with aspartame or high-fructose corn syrup on food intake and body weight. https://www.ncbi.nlm.nih.gov/pubmed/2349932 (1990)
    • Healthy, normal-weight people were divided into groups that were given either aspartame sweetened soda or soda with high fructose corn syrup. They were allowed to eat their regular diets. A control group that was not given soda was also included.
    • Results: The group that got diet soda ate fewer calories than the control group during the 3-week study. The males that drank diet soda lost weight, but not the females. All members of the group that drank regular soda gained weight. Both the diet and regular soda groups ate less sugar in other forms than the control group without affecting intake of other nutrients. Researchers concluded that diet soda reduces sugar intake and may help control calorie intake and body weight.
  • Effects of consumption of caloric vs noncaloric sweet drinks on indices of hunger and food consumption in normal adults. https://www.ncbi.nlm.nih.gov/pubmed/2021127 (1991)
    • 20 healthy subjects consumed water, aspartame, saccharin or sucrose (sugar) sweetened drinks 3 hours after breakfast.  The subjects recorded how hungry they felt 15 and 45 minutes after their drink. Researchers also measured how much they ate at lunch.
    • Hunger reports were highest for the people who drank water and lowest for the people that drank sugar. There were no differences in how much people ate at lunch.
    • Results: artificial sweeteners do not increase hunger or food intake.
  • The effect of aspartame as part of a multidisciplinary weight-control program on short- and long-term control of body weight.  https://www.ncbi.nlm.nih.gov/pubmed/9022524 (1997)
    • 163 obese women were divided into an aspartame group and a non-aspartame group during a 19 week weight loss program, a 1 year maintenance program, and a 2 year follow up period.
    • During the weight loss program, both groups lost about 10% of initial body weight.
    • After the 1 year maintenance, the aspartame group regained 2.6% of the weight and the non-aspartame group regained 5.4% of the weight.
    • After the 2 year follow up, the aspartame group regained 4.6% of the weight and the non-aspartame group regained 9.4% of the weight.
    • Researchers suggest including aspartame in a long term weight loss program may help with maintenance.
  • Nonnutritive sweetener consumption in humans: effects on appetite and food intake and their putative mechanisms. https://www.ncbi.nlm.nih.gov/pubmed/19056571 (2009)
    • Literature review conclusions: People who consume artificial sweeteners generally do not compensate by eating more. The addition of artificial sugar poses no benefit for weight loss or reduced weight gain without purposeful calorie restriction. Consuming artificial sweeteners probably does not contribute to weight gain or obesity.
  • Low-calorie sweeteners and body weight and composition: a meta-analysis of randomized controlled trials and prospective cohort studies. https://www.ncbi.nlm.nih.gov/pubmed/24944060 (2014)
    • 15 randomized control trials (RCT) and 9 prospective cohort studies (PCS) that looked at the relationship between low-calorie sweeteners and body weight were reviewed.
    • The randomized control trials associated low calorie sweeteners with reduced body weight, BMI, fat mass, and waist circumference.
    • The prospective cohort studies found that low calorie sweeteners were not associated with body weight or fat mass, but were associated with higher BMI.
    • RCTs provide more reliable evidence than PCSs. Therefore, researchers suggest substituting artificially sweetened beverages for regular calorie versions may result in moderate weight loss and be useful on a maintenance plan.
  • Substitution of sugar-sweetened beverages with other beverage alternatives: a review of long-term health outcomes.  https://www.ncbi.nlm.nih.gov/pubmed/25746935 (2015)
    • 6 cohort studies and 4 RCTs with acceptable to high quality ratings through 2013 were analyzed.
    • All studies associated substituting sugar sweetened beverages with other types of beverages (did not specify) with lower weight gain.

Group 2

  • Effects of artificial sweeteners on body weight, food and drink intake. https://www.ncbi.nlm.nih.gov/pubmed/21138816 (2010)
    • Mice were divided into 2 groups: control and artificial sweetener. The mice who were fed artificial sweeteners were given the acceptable daily intake which can be compared to reasonable human consumption. All mice were allowed to eat as much regular chow as they wanted.
    • Results: consumption of artificial sweeteners resulted in significantly increased body weight even though food intake was the same for all groups.
  • Cytotoxic effect of aspartame (diet sweet) on the histological and genetic structures of female albino rats and their offspring. https://www.ncbi.nlm.nih.gov/pubmed/24159687 (2012)
    • Rats were divided into control groups and experimental groups. Experimental groups were fed the acceptable daily intake of aspartame.
    • Every 2 weeks, measurements were taken. Researchers found that the experimental groups had decreased body weight, high histological lesions, increases in chromosomal aberration and DNA fragmentation compared to controls.
  • Saccharin and aspartame, compared with sucrose, induce greater weight gain in adult Wistar rats, at similar total caloric intake levels. https://www.ncbi.nlm.nih.gov/pubmed/23088901 (2013)
    • Rats were divided into 3 groups and fed either: yogurt with sucrose (sugar), yogurt with saccharin, or yogurt with aspartame. Amounts of sweetener were a reasonable amount that could compare to levels of human consumption. Physical activity was restrained
    • Conclusion: After 12 weeks, there was no difference in caloric intake among groups. The groups fed artificial sweeteners gained more weight than the group fed sugar. Researchers think this is due to either retention in fluid or decreased physical activity.
  • Effects of a nonnutritive sweetener on body adiposity and energy metabolism in mice with diet-induced obesity. https://www.ncbi.nlm.nih.gov/pubmed/24140095 (2014)
    • Obese mice were divided into 3 groups: sugar, artificial sweetener, and water. Amounts were consistent with what might be consumed by a human. After 4 weeks, measurements were taken.
    • Results: The mice that drank sugar had increased weight, body fat and hyperglycemia compared to the others. The group that drank artificial sugar had increased body fat, hyperinsulinemia, leptin levels and triglycerides compared to controls.
  • Impact of aspartame and saccharin on the rat liver: Biochemical, molecular, and histological approach. https://www.ncbi.nlm.nih.gov/pubmed/26015492 (2015)
    • Rats were divided into 5 groups: control, acceptable daily dose aspartame, acceptable daily dose saccharin, 4 times daily dose aspartame and 4 times daily dose saccharin
    • After 8 weeks, rats given artificial sweeteners had significantly reduced weight. However, they also had increased risk of liver cancer due to decreased suppression of a tumor gene, lower antioxidant levels, and “histological changes reflecting the hepatoxic effect of aspartame and saccharin”.
  • Metabolic and feeding behavior alterations provoked by prenatal exposure to aspartame.  https://www.ncbi.nlm.nih.gov/pubmed/25543075 (2015)
    • I did not have access to the full article
    • Results: When female animals consume artificial sweetener during pregnancy, their offspring are more likely to have negative outcomes in adulthood including: higher consumption of sweet foods, increased blood glucose, LDL and triglycerides. The effects were more pronounced in males than females.
  • Artificial sweeteners are not the answer to childhood obesity http://www.sciencedirect.com/science/article/pii/S0195666315001294 (2015)
    • I did not have access to the full article
    • Artificial sweeteners are associated with increased risk of the same chronic diseases as sugar consumption. Researchers are not sure exactly why, but make several suggestions:
      • Diminished release of hormones involved in blood glucose regulation
      • Altered gut microbiota which also may impair glucose regulation
      • Exposure to hyper-sweet foods may increase preference for sweetness
  • Low-calorie sweetener use and energy balance: Results from experimental studies in animals, and large-scale prospective studies in humans. https://www.ncbi.nlm.nih.gov/pubmed/27129676 (2016)
    • This is a review of animal and human studies.
    • Researchers state that both animal and human studies find that low calorie sweeteners are associated with weight and fat gain, obesity, cardiometabolic risk, and even total mortality even when other lifestyle factors are controlled for.
  • Aspartame intake is associated with greater glucose intolerance in individuals with obesity. https://www.ncbi.nlm.nih.gov/pubmed/27216413 (2016)
    • Cross-sectional survey, nationally representative sample. 2856 adults tested. Results are based on what people in the study reported that they ate or drank within the last 24 hours.
    • Discussion: aspartame is associated with obesity-related deteriorations in glucose tolerance and fasting glucose. Consumption of aspartame may be associated with greater diabetes risk in people who are obese. Aspartame was related to impairments in glucose tolerance for overweight people, but not lean people. However, very few lean people reported consuming aspartame.
    • Conclusion: aspartame may be associated with greater glucose intolerance, particularly for those with obesity.
    • The authors don’t think people with diabetes purposefully chose diet sodas because they only included people who were not already diagnosed with diabetes.
  • Effects of long-term administration of aspartame on biochemical indices, lipid profile and redox status of cellular system of male rats. https://www.ncbi.nlm.nih.gov/pubmed/26247507 (2016)
    • Rats were divided into 4 groups and given either: water, 15 mg/kg aspartame, 35 mg/kg or 70 mg/kg daily for 9 weeks.
    • Results: the groups receiving 15, 35 and 70 mg/kg aspartame had “increased lipid peroxidation products in the kidney, liver and brain”. The 35 and 70 mg/kg groups had increased levels of total cholesterol, triglycerides, and LDL as well as other health problems.
  1. What We Know and Don’t Know

Looking at these studies, we can see a few trends. First of all, diet soda seems to be pretty bad for rodents. Not a single study using mice or rats found the artificial sweetener to be harmless. The studies I reviewed all gave the rodents small amounts of sweetener that could reasonably be consumed in an equivalent ratio by humans. So, if mice and rats have fat gain, higher LDL and triglycerides, glucose intolerance, liver cancer, and chromosomal problems at low levels of consumption, are humans at risk too? Maybe. All of these rodent studies have been done fairly recently (many published in 2015 and 2016) and have not been repeated on humans. I’d be willing to bet this is because humans are harder to control and have much longer life spans. 3 weeks in mouse time is probably something like 3 decades in human.

The studies involving humans were mostly done in the 90’s. They looked at large groups of people and collectively determined mild weight benefits for people drinking diet sodas compared to regular sodas. They didn’t usually measure the same other kinds of health outcomes as the rodent studies. We don’t really know how artificial sweeteners affect us at a metabolic level over long periods of time because there are so many confounding variables.  There is some consistency when it comes to people who are already overweight or diabetic. These people seem to experience more glucose intolerance related to artificial sweeteners than healthy people at lower body weights.

During my research I didn’t come across any overt conflicts of interest. However, some may exist on either side of the fence.

  1. Conclusions and Applications

I was actually quite surprised at the end of this one. I had initially thought the research would show artificial sweeteners to be harmless at reasonable doses. I figured the rodent studies would reflect very high levels of sweetener being force fed until poor health outcomes were reached. I was wrong about this. Mice and rats had some pretty alarming health outcomes at fairly low doses after just a few weeks. As the dose increased, health decreased. The human studies, even the RCTs, were broad and outdated. They relied on measurements such as BMI which have little to do with actual health. Their outcomes showed very modest weight reductions and didn’t delve deeply into other components of metabolic syndrome.

In my review, I mainly focused on weight, diabetes, and metabolic markers. I didn’t get into the other issues such as cancer and neurotoxicity. Admittedly, I think arguments claiming diet soda causes these problems are fairly weak, but I might be surprised to see what I find here as well.

My personal conclusion is that diet sodas are probably just as bad for a person’s health as regular sodas, possibly in different ways. However, neither diet nor regular soda is going to kill you if consumed occasionally. Both diet and regular soda can be treated like dessert. Eat sparingly. I’d rather have ice cream for dessert anyway. As for beverages, Topo Chico for the win!

I would love to hear some opinions on this!