Pancreatic ductal adenocarcinomas are distinguished by their robust desmoplasia, or fibroinflammatory response. Dominated by non-malignant cells, the mutated epithelium must therefore combat, cooperate with or co-opt the surrounding cells and signalling processes in its microenvironment. It is proposed that an invasive pancreatic ductal adenocarcinoma represents the coordinated evolution of malignant and non-malignant cells and mechanisms that subvert and repurpose normal tissue composition, architecture and physiology to foster tumorigenesis. The complex kinetics and stepwise development of pancreatic cancer suggests that it is governed by a discrete set of organizing rules and principles, and repeated attempts to target specific components within the microenvironment reveal self-regulating mechanisms of resistance. The histopathological and genetic progression models of the transforming ductal epithelium must therefore be considered together with a programme of stromal progression to create a comprehensive picture of pancreatic cancer evolution. Understanding the underlying organizational logic of the tumour to anticipate and pre-empt the almost inevitable compensatory mechanisms will be essential to eradicate the disease.
An ED screening program identified patients with undiagnosed prediabetes and type 2 diabetes or undermanaged disease, particularly among racial and ethnic minorities and patients with low income, researchers reported in JAMA Network Open.
“Regarding type 2 diabetes, a few studies have conducted short-term screening of all ED patients,” Kirstie K. Danielson, PhD, associate professor of endocrinology, diabetes and metabolism in the department of medicine at the University of Illinois, Chicago, and colleagues wrote. “To our knowledge, ED screening for type 2 diabetes in underserved populations that built into daily clinical care and uses clinical recommendations has not been developed.”
ED screening can help identify people with undiagnosed prediabetes or type 2 diabetes.
Researchers conducted this pilot program in an ED in Chicago from February to April 2021. Using a best practice alert built into the electronic medical record, researchers identified patients for diabetes screening based on American Diabetes Association criteria: all adults aged 45 years or older, and those aged 18 to 44 years who had a BMI of 25 kg/m2 and no prior diabetes diagnosis and no HbA1c record for the past 3 years. Of 8,441 total patients who visited the ED, 1,085 were flagged as at risk for type 2 diabetes. Of these patients, 758 had prediabetes, 265 had diabetes and 62 had severe diabetes.
Researchers were able to follow-up with 352 of these patients for HbA1c information: 264 with prediabetes (mean age, 51.7 years; 56.8% women) and 88 with type 2 diabetes (mean age, 53.8 years; 47.7% women). Overall, 19.6% of patients were Hispanic, 64.8% were non-Hispanic Black, 9.7% were non-Hispanic white and 6% were non-Hispanic of other race.
Median income of all patients’ ZIP codes was at the 44th percentile of U.S. income. In addition, 50% of patients had public insurance and 4% were uninsured. Of note, 25% of patients self-reported that they were diagnosed with prediabetes or type 2 diabetes before the study, but only 58% reported receiving treatment for their disease, according to the researchers.
“The pilot sample reached by telephone was likely biased toward higher socioeconomic status, indicating those not reached are more likely underserved,” the researchers wrote. “Next steps involve testing implementation strategies to link these new patients to diabetes education and care.”
Caffeine (CAF) is a well-documented performance aid ingested by athletes either before or during exercise. The acute performance benefits have been reviewed previously across a range of activities including muscular strength/power (Warren et al., 2010), anaerobic power (Grgic, 2018), and endurance (Conger et al., 2011; Doherty & Smith, 2004; Graham, 2001). In general, the mechanism by which CAF appears to reduce fatigue has been ascribed to influence metabolism of substrate (e.g., fat) and/or the central nervous system via adenosine antagonism. Other purported potential neuromuscular effects include direct effects on muscle via intracellular calcium (Herrmann-Frank et al., 1999), increased motor unit recruitment (Warren et al., 2010), and/or central nervous system activation (Kalmar & Cafarelli, 2004; Warren et al., 2010). However, from the historical perspective, the metabolic theory was initially advanced with classic studies (Costill et al., 1978; Ivy et al., 1979), indicating endurance performance improvements appeared linked to greater fat oxidation and/or increased lipolysis which, in turn, might delay fatigue by sparing endogenous stores of carbohydrate. The latter assumption has been disassociated as the basis of ergogenic benefits during exercise (Jeukendrup & Randell, 2011).
The metabolic theory of increased fat oxidation with CAF during exercise persisted for decades (Graham, 2001; LeBlanc et al., 1985) until more recent studies suggested that, in fact, the opposite might occur (i.e., increased carbohydrate metabolism; Graham et al., 2008; Yeo et al., 2005) following CAF administration. Furthermore, it was suggested (Graham et al., 2008) the ergogenic benefits of CAF may not be the result of shifts in either carbohydrate or fat metabolism; although, this does not rule out the possibility that fat metabolism is augmented with CAF. A recent meta-analysis on 19 studies (Collado-Mateo et al., 2020) indicated CAF increased fat metabolism during exercise based on whole-body gas exchange variables (e.g., respiratory exchange ratio [RER] and calculated fat oxidation rates) but that fitness level modulated this effect (i.e., CAF had less effect in trained individuals who may have higher fat oxidative capacity during exercise). However, these findings contrast an earlier meta-analysis that found no effect of CAF on RER during exercise while increasing blood glucose and lactate (Glaister & Gissane, 2018). Thus, despite two meta-analyses on the topic, the fat metabolic theory as a physiological effect of CAF during exercise remains debatable. Several studies have also reported enhanced fat metabolism after consuming CAF under resting conditions (Acheson et al., 2004; Bellet et al., 1965, 1968; Jo et al., 2016), suggesting the metabolic equivalent of tasks level (from rest to low-intensity exercise) may be an important mediating factor. Moreover, the methods used to assess fat metabolism vary, with some studies reporting blood biomarkers of lipolysis and others relying exclusively on whole-body gas exchange data. Other factors related to the research design may also impact the degree of CAF’s effect on fat metabolism. These include the CAF dose administered and individual variability in the response to CAF, specifically when comparing men to women who may rely on fat metabolism to a greater degree (Cano et al., 2022).
Although previous reviews (Guest et al., 2021) and meta-analyses (Grgic et al., 2020; Pickering & Kiely, 2019) have reported effects of CAF on exercise performance, few (Collado-Mateo et al., 2020; Glaister & Gissane, 2018) have quantified the effect of CAF on fat metabolism during exercise. Inexplicably, those two aforementioned studies do not agree, despite basing conclusions solely on gas exchange data. No meta-analysis to our knowledge has determined CAF’s impact based upon the metabolic equivalent of tasks level (inclusive of rest upwards to higher exercise intensity) or utilized additional biomarkers of fat metabolism (i.e., blood parameters). Therefore, our purpose was to determine effects of CAF ingestion on fat metabolism using a comprehensive systematic review of the published literature and meta-analysis. We also sought to quantify the influence of factors moderating this effect such as the biomarkers assessed, rest compared with exercise, CAF dosage, and participant characteristics.
Methods
Systematic Literature Review
For this study, the preferred reporting items for systematic reviews and meta-analyses guidelines were followed (Moher et al., 2015). The electronic databases PubMed, SPORTDiscus, and Web of Science were searched through December 31, 2021 using the search terms: CAF AND (fat OR lipid) AND (metabolism OR oxidation). In addition, reference lists from each relevant study and review articles were examined for inclusion of additional studies in the analysis.
Inclusion/Exclusion Criteria
Studies meeting the following criteria were included in the analysis: (a) published in a peer-reviewed journal, (b) human participants free from any medical condition known to alter metabolic rate, (c) crossover study design that included both a CAF and placebo condition, and (d) reported some method of fat metabolism providing means and variances. Studies that included additional substances during CAF conditions were included if the investigational and placebo conditions were identical with the exception of CAF. Studies reporting either resting, exercise conditions, or both in the same study were included in the systematic review. Data were excluded if: (a) exercise was not primarily aerobic, (b) CAF/placebo were consumed < 30 min prior to data collection, or (c) CAF/placebo were not ingested/swallowed (i.e., mouth rinse or chewing gum). We defined aerobic exercise as ≥ 5 consecutive min of activity since > 80% of energy is supplied by the aerobic energy system (Gastin, 2001).
A total of 149 articles were identified for potential analysis. The review and selection process for identification of the included articles are summarized in Figure 1. After full-text review, 94 studies were retained and 55 studies excluded based on: did not report fat metabolism data, not a within-subjects study design, and missing placebo condition. Preferred reporting items for systematic reviews and meta-analyses guidelines, study quality assessment, and study methods are available in the Supplementary Material S1 (available online) and the Supplementary Table S1 (available online).
Figure 1
Selection of articles for meta-analysis of fat metabolism when consuming CAF. CAF = caffeine.
Citation: International Journal of Sport Nutrition and Exercise Metabolism 2023; 10.1123/ijsnem.2022-0131
Study data were extracted from text or relevant tables. If data were not reported elsewhere, figures were used for data extraction. Figures were enlarged, and the mean and variance data presented were measured to the nearest millimeters using the appropriate scale of the figure. Data from each study were converted into the same format by calculating the effect size (ES) as the standardized difference in means. The standardized difference in means was calculated as:
(MCAF−MPla)SDPooled,
where M is the mean, and SDPooled is the pooled SD (Borenstein et al., 2009) and calculated as:
where rCAF,Pla was the intertrial correlation between CAF and placebo conditions (Borenstein et al., 2009). In three study populations, we calculated rCAF,Pla from the reported data (Bellet et al., 1965; Wiles et al., 1992). For studies in which the correlations were not available, the mean of the reported correlations was used (r = .474 for exercise and r = .580 for resting studies). Hedges correction (Hedges’ g) was used to account for potential bias resulting from small sample sizes. Standardized difference in means and SE were multiplied by the correction factor (Borenstein et al., 2009):
1−{3[4×(nCAF,Pla−1)]}.
Other data extracted from each study included: authors; publication year; participant demographic information (sex, age, height, body mass); maximal oxygen uptake (VO2max); fasting state; CAF dose; fat metabolism biomarker; timing of data measurements; exercise intensity; exercise testing protocol; habitual CAF use; timing of CAF administration; and dietary control methods.
In studies that reported more than one fat metabolism outcome from the same population of participants, the mean study ES and their associated variances were used to calculate the meta-analyses’ overall ESs for each study. When a study reported data for more than one independent group, an ES was calculated for each group. Each independent group was then treated as an independent study (Borenstein et al., 2009). In the meta-analysis by fat assessment method, multiple methods were often utilized within the same study. In these cases, each method was analyzed independently. For steady state, submaximal exercise protocols, mean data were used in the calculation of the ES. In studies that reported data during different intensities, the ES was calculated for each intensity. In both cases, the average ES across all data points was used to calculate the overall ES for a given study.
Overall ESs were calculated using a random-effects model that accounts for true variation in effects occurring from study to study as well as random error within a given study. Heterogeneity was assessed using Q and I2 statistics. To assess whether moderator variables could explain variation in ES among studies, subgroup meta-analyses and meta-regressions (method of moments model) were conducted. Subgroup meta-analyses examined effects of categorical data: rest versus exercise, fat metabolism assessment method (blood vs. gas exchange based upon RER; Zuntz, 1901), CAF dosage (small, moderate, and large; Pickering & Kiely, 2019), exercise intensity, participants’ sex, habitual CAF use (yes or no without threshold levels), or fasted state (≥3 hr; Jeukendrup et al., 1998). Gas exchange data were reported as RER (ratio of carbon dioxide production to oxygen consumption) or by calculating fat oxidation in grams per minute based on oxygen consumption from standardized formulas (Zuntz, 1901). Meta-regressions also assessed the association between CAF ES for fat metabolism relative to continuous data (CAF dosage, body mass index [BMI], fitness level based on VO2max, age, and exercise intensity).
Most studies reported approximate values for exercise intensity, typically using percentage of VO2max (%VO2max). For studies that did not report exercise intensity, we based our estimate from the exercise description provided by the authors (see Supplementary Table S1 [available online]). To determine the intensity during resting conditions, if oxygen consumption data were not available, one metabolic equivalent of tasks (i.e., 3.5 ml·kg−1·min−1) was used as the estimated metabolic rate. If VO2max data were available, the intensity was then calculated (e.g., resting value of 3.5 ml·kg−1·min−1 ÷ maximal value of 45 ml·kg−1·min−1 = 8%).
The effect of publication bias was addressed by combining a funnel plot assessment with the Duval and Tweedie (2000) trim and fill correction. Orwin’s Fail-Safe N test determined the number of missing studies that would have been needed to bring the overall ES down to a level favoring the placebo condition for fat metabolism (Borenstein et al., 2009).
All data were presented as mean ± 95% confidence interval (CI). ES thresholds of |0.2|, |0.5|, and |0.8| were considered small, medium, and large, respectively (Cohen, 1988). An α level of .05 was used to indicate statistical significance. All calculations were completed using comprehensive meta-analysis (version 2.2.064, Biostat).
Results
Study Characteristics
Ninety-four studies published between 1965 and 2021 were included. In 11 studies, data from two independent populations were presented, for a total of 105 independent study populations and 435 separate ESs. Data from five different measures assessing fat metabolism were presented: plasma free fatty acids (FFAs), plasma glycerol, triglycerides, RER, and fat oxidation calculated from RER (gas exchange data). Fifty-five percent of studies presented data using more than one method to assess fat metabolism. Most studies (63%) reported participants in a fasted state ≥ 3 hr from last meal (mean duration: 7.1 hr, median: 8 hr). CAF dosage used in the studies varied considerably, averaging 5.7 mg/kg (median: 5.0 mg/kg, range: 1.0–15.0 mg/kg).
Participant Characteristics
Data from 984 participants were included (828 males/146 females). Most studies utilized relatively small sample sizes (mean n = 9.4, median: 9, range: 5–24). In 72% of studies, all participants were males, 9% of studies consisted of only females, and 18% of studies included both males and females presented combined. In studies that combined males and females, ∼70% of participants were males. One study did not identify sex (Wiles et al., 1992). In general, the average participant was young adult (mean age: 26.1 years), lean (mean BMI: 23.7 kg/m2), and fit (mean VO2max: 54.1 ml·kg−1·min−1). However, there was variation across a range (age: 15.6–71 years, BMI: 18.3 to 29.6 kg/m2, VO2max: 27.6 to 75.5 ml·kg−1·min−1).
Fat Metabolism With CAF Consumption
Of the 105 study populations that reported fat metabolism after ingesting CAF, overall ESs ranged from −2.36 (greater fat metabolism with placebo) to 3.87 (greater fat metabolism with CAF; see Supplementary Figure S1 (a–c) [available online]). Overall, the ES was 0.39 (95% CI [0.30, 0.47], p < .001), reflecting a small effect of CAF on fat metabolism (Figure 2A). There was significant heterogeneity across studies, Q(104) = 315.22, p < .001. The within-study heterogeneity was moderate (I2 = 67.0%), while the between-study heterogeneity was low (τ2 = .12).
Figure 2
Summary ES of the subgroup meta-analyses examining the effects of CAF on fat metabolism during rest and exercise. The center of each diamond reflects the mean ES, while the width of the diamond represents the 95% CI. CAF = caffeine; ES = effect size; CI = confidence interval. *Significant difference between methods (p = .02).
Citation: International Journal of Sport Nutrition and Exercise Metabolism 2023; 10.1123/ijsnem.2022-0131
Subgroup meta-analyses were used to assess effects of moderator variables as potential underlying explanation for the heterogeneity.
Resting Versus Exercise Conditions
Of the 105 independent study populations, data during resting conditions were reported in 13 studies, data during exercise conditions in 34 studies, and during both resting and exercise conditions in 58 studies. A total of 71 and 92 independent ESs were reported for rest and exercise, respectively. Across all studies, ES for fat metabolism during both rest (ES = 0.51, 95% CI [0.41, 0.62], p < .001) and exercise (ES = 0.35, 95% CI [0.26, 0.44], p < .001) conditions were significantly increased with CAF; however, the ES for rest was greater versus exercise, Q(1) = 5.33, p = .02, (Figure 2B). ES for fat metabolism reporting both rest (ES = 0.49, 95% CI [0.37, 0.60], p < .001) and exercise (ES = 0.44, 95% CI [0.33, 0.56], p < .001) in the same study were increased with CAF, but not different between rest and exercise, Q(1) = 0.26, p = .61.
Meta-regression was also completed for CAF ES on fat metabolism relative to exercise intensity (%VO2max) for combined rest and exercise data. This inverse relationship was significant with a slope of −0.003 (95% CI [−0.004, −0.001], p < .001), indicating a slight decrease in fat metabolism as exercise-intensity increases above rest. Meta-regression completed on only the exercise studies found an inverse relationship but it was not statistically significant (slope = −0.002, 95% CI [−0.006, 0.002], p = .32).
Fat Metabolism Assessment Method
Five different fat metabolism biomarkers were reported across studies. The most common method reported was RER (n = 77), and least common was triglycerides (n = 9). CAF significantly increased fat metabolism based upon FFA, glycerol, RER, and calculated fat oxidation with ESs ranging from 0.19 (RER) to 0.56 (glycerol, FFA; p < .001) but not based on triglycerides (ES = 0.30, 95% CI [−0.02, 0.62], p = .07; Figure 3A). The ESs based on RER were small and significantly lower compared with the ES using FFA and glycerol, Q(4) = 23.54, p < .05. There were no other significant differences between fat metabolism assessment methods.
Figure 3
Summary ES of the subgroup meta-analyses examining the effects of CAF on fat metabolism by (A) fat assessment method and (B) blood lipolysis metrics versus gas analysis metrics. The center of each diamond reflects the mean ES, while the width of the diamond represents the 95% CI. CAF = caffeine; ES = effect size; CI = confidence interval; FFA = free fatty acid; RER = respiratory exchange ratio. *Significant difference between methods (p < .05).
Citation: International Journal of Sport Nutrition and Exercise Metabolism 2023; 10.1123/ijsnem.2022-0131
Biomarkers used to assess fat metabolism were then categorized by lipolytic blood measures (at least one of either FFA, glycerol, or triglycerides across 64 studies) versus gas analysis (RER and/or fat oxidation in 84 studies). ESs using blood biomarkers (ES = 0.55, 95% CI [0.43, 0.67], p < .001) and gas analysis (ES = 0.26, 95% CI [0.16, 0.37], p < .001) were significantly greater than zero (Figure 3B), although blood biomarkers ESs were greater, Q(1) = 12.61, p < .001. In 43 studies including both blood and gas analysis measures, ES for blood measures (ES = 0.58) remained significantly larger than gas exchange (ES = 0.28), Q(1) = 7.07, p = .01.
Other Potential Modifier Variables
Figure 4 summarizes the impact of other factors on CAF ES on fat metabolism. When assessed by sex, CAF naive or regular user, CAF dosage, or fasted status prior to testing, all subgroup ESs were significantly different from zero (favoring increased fat metabolism with CAF). Studies with men (ES = 0.40, 95% CI [0.30, 0.50]), men and women combined (ES = 0.37, 95% CI [0.17, 0.56]), and only women (ES = 0.34, 95% CI [0.03, 0.65]) had significant ES with CAF (p < .05; Figure 4A) with no differences between subgroups (p = .90). There were also no differences within moderator variables: habitual CAF use (Figure 4B), CAF dosage (Figure 4C), or fasting condition (Figure 4D). Meta-regression evaluated these variables as continuous data relative to ES: BMI (slope = 0.020, 95% CI [−0.021, 0.061], p = .33), age (slope = 0.000, 95% CI [−0.009, 0.009], p = .95), VO2max (slope = −0.005, 95% CI [−0.012, 0.001], p = .11), and CAF dosage (slope = 0.002, 95% CI [−0.024, 0.027], p = .90), which were also not statistically significant.
Figure 4
Summary ES of the subgroup meta-analyses examining the effects of CAF on fat metabolism by (A) sex, (B) habitual CAF use, (C) CAF dose, and (D) fasting state. The center of each diamond reflects the mean ES, while the width of the diamond represents the 95% CI. CAF = caffeine; CI = confidence interval; ES = effect size.
Citation: International Journal of Sport Nutrition and Exercise Metabolism 2023; 10.1123/ijsnem.2022-0131
Publication bias was assessed by examining a funnel plot of SE versus ES. Minor asymmetry was noted in the plot; thus, a Duval and Tweedie’s (2000) trim and fill correction to the overall ES was calculated. This correction shifted the overall ES from 0.39 (95% CI [0.30, 0.47], p < .001) to 0.25 (95% CI [0.16, 0.35], p < .001; Figure 5), which did not change interpretation of results (small ES with CAF). Using the Orwin’s Fail-Safe N test to reduce the overall ES down to a trivial negative overall ES (i.e., ES = −0.10), we assumed that the missing studies had a mean ES of −0.20. Given these criteria, the ES of 474 independent groups (compared with 105 retrieved) would have theoretically been needed to be omitted from our search to conclude fat metabolism is not increased with CAF versus placebo.
Figure 5
Funnel plot of the ES of CAF on fat metabolism versus the SE. The observed studies are shown as open circles and the observed ES is presented as the open diamond. The Trim and Fill adjustment is presented with the imputed studies as filled circles and the mean imputed ES as a filled diamond. The vertical line on the graph represents the mean imputed ES, and the angled outer lines represent the 95% confidence intervals. CAF = caffeine; ES = effect size.
Citation: International Journal of Sport Nutrition and Exercise Metabolism 2023; 10.1123/ijsnem.2022-0131
Our aim was to determine whether CAF increases fat oxidation. In our analysis of 94 studies with 105 independent groups (984 participants), CAF ingestion significantly increased fat metabolism with a small effect (ES = 0.39) based upon gas exchange and blood parameters. The increase in fat metabolism tended to be greater when consumed during rest compared with exercise, although both conditions significantly elevated fat metabolism. Unlike a previous meta-analysis (Collado-Mateo et al., 2020) which only included 19 exercise studies, we found this effect to be independent of various individual factors including fitness level, sex, and CAF dosage.
In the present study, our subgroup analysis comparing rest to exercise conditions (Figure 2B) suggests that the impact of CAF on fat metabolism may be more definitive under resting conditions. It is well known that fat oxidation decreases as exercise intensity increases, consistent with a greater reliance on carbohydrate (Glaister & Gissane, 2018). For the studies under resting conditions included in our analysis, most (63%) were reported under fasting conditions. These conditions might optimize fat metabolism regardless of participants’ fitness level or sex as these factors may contribute to greater variability among individuals’ metabolic response during exercise (particularly as intensity increases). Because of energy requirements at rest and low-intensity exercise, >90% of the energy are supplied from fat sources as compared with the shift to carbohydrate oxidation (>90% of energy) during high-intensity exercise (Romijn et al., 1993). Maximal fat oxidation rates are considered to be between 59% and 64% of VO2max in trained individuals but lower (47%–52% of VO2max) in the general population (Achten & Jeukendrup, 2004). Our results suggest the original metabolic theory with CAF ingestion is valid while under both rest and exercise, but prescribing an “optimal” intensity for enhancing fat metabolism may be less definitive across the exercise spectrum with different populations.
Fat metabolism has historically been measured using biomarkers related to lipolysis in the blood (i.e., FFA, glycerol) or indicators of whole-body substrate oxidation using gas exchange at steady state conditions (RER and calculations of fat oxidation). Breakdown of triglyceride occurs in many tissues of the body providing FFA which can be utilized endogenously for energy production except in adipose tissue which releases FFA and glycerol to supply nonadipose tissues (Schweiger et al., 2014). Since fat may be oxidized within skeletal muscle during exercise, the most optimal and sensitive methods to assess blood markers of lipid oxidation continue to evolve (Schweiger et al., 2014). In the present study, all methods reportedly linked to fat oxidation (with the exception of blood triglycerides) increased after consuming CAF. Blood triglycerides were also the least commonly reported measure (9% of studies) and may be less physiologically relevant. However, expressing fat metabolism using blood biomarkers (including triglycerides) yielded a significantly higher ES than gas exchange measures (RER and calculated fat oxidation) (Figure 3B). The ES based on blood biomarkers across all studies was moderate (ES = 0.55). In studies reporting gas exchange data, a majority of the studies demonstrated a positive ES. In those studies reporting both measures, this difference between lipolytic blood markers and gas exchange was further confirmed (Figure 3C). Therefore, while fat metabolism increased after consuming CAF based upon either blood biomarkers or gas exchange data, blood lipolytic biomarkers elicited more consistent changes. We can only speculate a reason for this discrepancy but perhaps is linked to concomitant increases in glycogenolysis (simultaneously influencing carbohydrate oxidation) with CAF.
Numerous studies have reached the opposite conclusion regarding metabolic effects of CAF when assessed based upon gas exchange variables: either no change or significant decreases in fat metabolism after ingesting CAF. While CAF likely mobilizes fatty acids from adipose tissue, RER measures do not consistently indicate increased fat oxidation during exercise (Glaister & Gissane, 2018). Furthermore, there is little evidence to support the hypothesis that CAF exerts its ergogenic effect due to enhanced fat oxidation (Graham et al., 2008). In contrast, a recent meta-analysis (Collado-Mateo et al., 2020) found a significant but small ES for RER during exercise (ES = −0.33), a magnitude remarkably similar to our gas exchange data in the present meta-analysis (ES = 0.26). Our values were expressed in the positive direction as increased fat oxidation unlike the former (Collado-Mateo et al., 2020), which report ES for RER as negative values (indicative of decreased RER). Both meta-analyses contradict a previous one (Glaister & Gissane, 2018) indicating RER during exercise was not significantly impacted by CAF. Exercise studies in that meta-analysis (Glaister & Gissane, 2018) were delimited to 5–30 min bouts of 60%–85%VO2max and also reported higher blood glucose and lactate with CAF dosages between 3 and 6 mg/kg. Inclusion criteria for the previous two meta-analyses of RER data resulted in two very different sets of studies, which may account for the differential findings between them. Of the combined 33 studies included between the two meta-analyses, only three studies were common to both (Collado-Mateo et al., 2020; Glaister & Gissane, 2018). In the present meta-analysis, 77 of 94 studies reported RER data. All but two of the studies included in these earlier meta-analyses were included in our analysis.
The metric used to assess fat metabolism after consuming CAF could be critical in the interpretation of results, particularly when measures do not align within studies. One study (Yeo et al., 2005) found CHO metabolism significantly increased (and fat oxidation decreased) during exercise at 64%VO2max after CAF. Increased CHO metabolism was based on RER data; however, FFA and glycerol suggested a nonsignificant increase in fat metabolism. These seemingly contradictory findings of decreased fat metabolism reported by gas analysis data while blood biomarkers suggest increased lipolysis were reported by others (Casal & Leon, 1985; Lee et al., 2012; Spriet et al., 1992; Wells et al., 1985) with authors’ interpretation varying. While not mechanistic, our findings suggest the method used can yield differential results regarding fat metabolism after ingesting CAF and should be considered when interpreting CAF’s effect.
Unlike the recent meta-analysis (Collado-Mateo et al., 2020), we did not find a CAF dose–response effect on fat metabolism. Those authors reported the ES for fat metabolism was significantly higher for “threshold” CAF doses above 3 mg/kg, although not a true dose–response since > 6.0 mg/kg did not exhibit a greater ES. However, a high degree of variability (I2 = 92%) was reported specifically in their subgroups comparing the high CAF dose (6 mg/kg). The number of studies in their low dose (< 3 mg/kg) was also more limited (n = 5) than in our present meta-analysis (n = 18). In contrast, we found no dose–response effect of CAF on fat metabolism or a minimum 3 mg/kg “threshold level effect.” All CAF doses demonstrated increased fat metabolism over placebo (p < .05) with no apparent benefit from consuming larger CAF doses (Figure 4c). When two or more CAF doses were investigated in the same study (see Supplementary Table S1 [available online]), there was no clear dose–response effect with CAF dosage ranging from 1.0 to 15.0 mg/kg. Dose–response studies did not appear in the literature until 1995 (Spriet, 2014), and doses of ∼3 mg/kg were commonly considered “low” dose. Seven of the 12 studies included doses of 3.0 mg/kg or less, and six studies included doses of 6.0 mg/kg or greater. We speculate that by including resting studies, the impact of CAF on fat metabolism may be less influenced by other potential factors at play during exercise (intensity, participant fitness level) and enhance the possibility to elicit more consistent metabolic effects at “lower” CAF dosages (∼3 mg/kg). To that end, a CAF dosage of only 100 mg has been shown to increase resting energy expenditure by 3%–4% although fat oxidation was not measured (Dulloo et al., 1989). The lack of a clear CAF dose–response effect has also been previously demonstrated related to endurance performance (Conger et al., 2011) and ratings of perceived exertion (Doherty & Smith, 2005), although (Spriet, 2014) suggests higher CAF doses, while not needed for central nervous system antagonism of adenosine (i.e., influencing performance and perceived exertion), might be necessary for metabolic actions (e.g., lipolysis). Additional investigations with multiple CAF dosages (particularly at the low end) may prove beneficial in our understanding and alter the present findings.
Strengths and Limitations
With 105 different participant populations and nearly 1,000 participants included in the analysis, this large sample size allowed for a number of important subgroup analyses to address several key moderator variables considered important for assessing the impact of CAF. However, there are inherent limitations related to risk of bias. Our search did not include unpublished or non-English studies, thus making it likely we did not capture every relevant study on fat metabolism after CAF ingestion within the gray literature. While omission of relevant studies may have altered the individual ESs, we do not believe that it would have significantly impacted our overall conclusions based on the Orwin’s Fail-Safe N and Duval–Tweedie tests (Figure 5).
Another limitation of our approach is that the ergogenicity of CAF for exercise performance cannot be tied to fat oxidation as the underlying mechanism. Of interest, however, is emerging evidence that low doses (< 3 mg/kg) may be ergogenic and our results found that fat oxidation occurs similarly with low versus moderate doses. The exercise protocols used in each study also varied considerably. Since mean values were utilized to compute ES, this approach may limit the ability to interpret results during specific exercise conditions. Increases in lipolytic biomarkers do not always align with increased fat oxidation as referenced earlier. A strength of our analysis was for studies that measured both gas exchange and lipolytic markers (Figure 3C), results suggest lipolysis occurs to a moderate degree while RER decrease may be tempered. Whether this differential effect is potentially due to concomitant increases glycogenolysis with CAF (and reports of increased carbohydrate metabolism) which offset the relative contribution of fat substrate being oxidized is unclear since we did not systematically extract measures of carbohydrate oxidation.
Practical Applications
Understanding factors that increase fat oxidation are important not only for optimizing exercise performance but also for clinically relevant conditions such as reducing obesity and metabolic syndrome (Achten & Jeukendrup, 2004). That CAF increased fat oxidation in women (similar to men) and was not dependent on fitness level would suggest metabolic advantages in weight control for sedentary populations, especially since the rest effect was equal to or greater than exercise of varying intensities. Exercise intensity and duration both impact fat oxidation, but the optimal intensity remains obscure (Achten & Jeukendrup, 2004). Our results suggest exercise coupled with CAF (even at low dosages) may enhance fat oxidation, potentially providing metabolic advantages. This statement concurs with significant ES observed with CAF on weight control variables (lowered body mass, fat mass, and BMI) with CAF (Tabrizi et al., 2019). However, we acknowledge generalizations are challenging due to the large interindividual variability in substrate utilization (Achten & Jeukendrup, 2004). Despite the backdrop of individual variability related to several factors, our meta-analysis finds CAF increases fat oxidation across a range of CAF dosages and individual characteristics.
Conclusions
Based upon 94 studies with variable findings regarding fat metabolism after ingesting CAF under both resting and exercise conditions, we report a highly significant but small effect (ES = 0.39) of CAF to increase fat metabolism. The ES of CAF was at least equal to or greater during rest compared with exercise and robust regardless of participants’ sex, fitness level, habitual CAF use, fasted state, or CAF dosage. However, the ES was lower when studies utilized methods based upon whole-body gas exchange analysis compared with lipolytic blood parameters (e.g., glycerol, FFA). Therefore, the fat metabolic theory for CAF for exercise (and rest) remains viable based on this systematic review of the literature and meta-analysis.
About one in 10 Americans are living with diabetes, and between 90 and 95 percent of them have Type 2 diabetes. Compelling evidence suggests that increasing your coffee intake could lower your risk for this condition.
Researchers found that people who increased their coffee intake by one cup more per day experienced an 11 percent lower risk of eventually getting Type 2 diabetes.
People who reduced their coffee intake by one cup per day, on the other hand, saw their risk of developing diabetes increase by 17 percent.
“These changes in risk were observed for caffeinated, but not decaffeinated coffee, and were independent of initial coffee consumption and four-year changes [during the study period] in other dietary and lifestyle factors,” the study authors specified.
These findings build on research from 2009 that found an association between increased coffee drinking and reduced risk of Type 2 diabetes.
A systematic review and meta-analysis of studies find that drinking coffee can help our bodies to burn more fat, which addresses a big risk factor for Type 2 diabetes: being overweight.
“In our analysis of 94 studies with 105 independent groups (984 participants), CAF [caffeine] ingestion significantly increased fat metabolism,” the study authors concluded.
“This is likely due to the presence of antioxidants and other beneficial compounds in coffee,” Dr. Michael Green, an OB/GYN at Winona, a female-founded antiaging wellness center, and OB hospitalist and site director for OBHG at Northridge Medical Center in Northridge, California, told The Epoch Times.
Coffee Slashes Type 2 Risk for Women with Gestational Diabetes
Compared with the general, healthy female population, women who have experienced gestational diabetes may have a 10-fold increased risk of developing Type 2 diabetes. Drinking coffee may lower this risk, according to scientists at the Global Centre for Asian Women’s Health at the National University of Singapore.
For 24 years, the scientists’ recent study looked at over 4,500 women, mostly white, with a history of gestational diabetes, to compare long-time coffee consumption with risk.
Women who drank two to three cups of coffee decreased their risk by 17 percent, and those who drank one cup or less experienced a 10 percent reduced risk, the study found.
Decaffeinated coffee didn’t have similar benefits, but the study noted that relatively few women preferred it, which could be why no link was detected.
Taking any drug, even caffeine, during pregnancy or while breastfeeding could present risks. The U.S. Food and Drug Administration (FDA) recommends talking to your doctor about whether you should limit your caffeine intake.
Reduces Risk of Common Diabetes Complications
Type 2 diabetes can increase our risk of eye problems, and cardiovascular and kidney disease.
A meta-analysis found that the more coffee that participants with Type 2 diabetes reported drinking, the lower their risk of experiencing mortality associated with cardiovascular disease. Researchers did emphasize, however, that more research is needed regarding the type of coffee, whether sugar and cream were added, and participants’ history of cardiovascular disease, to present more confident results.
Researchers investigated the relationship between coffee consumption and the decline in kidney function in patients with Type 2 diabetes.
They looked at 3,805 patients with an average age of 64 years (2,112 men, 1,693 women) with Type 2 diabetes and found higher coffee consumption reduced the risk of declining kidney function. Compared with no coffee consumption, those drinking two or more cups per day saw greater risk reduction.
Diabetic retinopathy is a condition affecting blood vessels in the back of the eye. It can cause vision loss and blindness in people living with diabetes. A recently published scientific report evaluated the association between diabetic retinopathy prevalence and coffee consumption within a Korean population.
Researchers analyzed data from 1,350 participants with Type 2 diabetes who underwent diabetic retinopathy examination to find that those who drank two or more cups of coffee per day had lower odds of developing the condition, compared to those who didn’t drink any coffee.
“Coffee has [also] been shown to improve cognitive function and boost alertness, which can benefit people with type 2 diabetes who may experience fatigue and lack energy,” said Green.
Coffee Reduces Risk of Liver Disease in People with Type 2 Diabetes
Often, NAFLD is a “silent” condition, with few or no symptoms. Composed of different disorders of the liver caused by the accumulation of fat, it can cause liver scarring and cancer.
A new study finds coffee could reduce the severity of NAFLD in people who have Type 2 diabetes and are overweight.
Researchers surveyed 156 overweight, middle-aged participants, of which 98 had Type 2 diabetes, about how much coffee they drank. They also collected daily urine samples that were used to measure caffeine and noncaffeine metabolites, which are natural products resulting from the digestion of coffee.
Findings show that those with higher coffee caffeine consumption, as indicated by urine samples, were much less likely to experience liver disease.
The researchers concluded that caffeine and plant-based micronutrients called polyphenols, found in coffee, may contribute to reducing the severity of NAFLD.
Drink Moderately
Of course, too much of anything, even something otherwise healthy, can cause problems. Coffee is no different. The FDA cautions that for healthy adults, about 400 milligrams a day—or four or five cups of coffee, is an amount not “generally associated” with dangerous, negative effects.
“For the most part, as long as you consume coffee moderately, there are no major health concerns,” said Dr. Sreenivas Gudimetla, a cardiologist at Texas Health Fort Worth and Texas Health Physicians Group, told The Epoch Times.
Herbs and spices were used by ancient cultures to heal the body, mind, and spirit. While the western world has largely replaced these natural remedies with pharmaceuticals, roughly 80 percent of people worldwide still use traditional or ancient medicine. This is not surprising considering that more than 80 percent of pharmaceuticals are derived or developed from natural products, including plants. In this series, we will explore the healing power of herbs and spices while learning how to incorporate these ancient remedies into our daily diet.
Mint (Mentha) is widely used for its culinary, medicinal, and aromatherapeutic properties. It represents a group of perennial herbs that includes 18 species and 11 hybrids. The most commonly known are peppermint, spearmint, and wild mint.
Today, mint is primarily known for its refreshing taste and aroma. However, in ancient times, it was recognized for its numerous health benefits.
In the Middle Ages, peppermint was used to polish teeth and to keep rats and mice out of stores. By the 18th century, in Western Europe, peppermint was used for nausea, morning sickness, vomiting, menstrual disorders, and respiratory infections. Mint was listed in the London Pharmacopoeia in 1721 as a remedy for colds, headaches, sores, and venereal disease.
Mint was also acknowledged for its ability to interact with the central nervous system in traditional medicine. For example, in South Africa, the dried leaves were burned and the smoke inhaled as a treatment for mental illness. In Mediterranean countries, mint was used to treat neuralgia (nerve pain), as well as an anticonvulsant and sedative.
Recently, scientists have confirmed the many healing properties of mint through numerous studies demonstrating its effectiveness in regulating the nervous system.
Modern Science Catches up to Ancient Wisdom
While the healing power of mint has been harnessed among ancient cultures for thousands of years, modern medicine has been slow to recognize its benefits. However, the perception of mint is changing as scientists have begun validating the wisdom of the ancients through studies that demonstrate numerous healing abilities, such as:
Fights cancer: Peppermint inhibited the growth of colon cancer cells, according to a study published in the Journal of the Science of Food and Agriculture. Peppermint may also inhibit prostate cancer growth. According to preclinical research, peppermint contains menthol, which was reported to induce prostate cancer cell death.
Reverses diabetes: Mint is a “promising treatment” for diabetes, according to a study published in 2017. Mint was found to decrease fasting blood sugar, total cholesterol, triglycerides, and low-density lipoprotein-cholesterol. “These effects were comparable with the effects of [the] standard antidiabetic drug (glibenclamide),” according to the researchers.
Alleviates pain from osteoarthritis: Combining peppermint with rosemary essential oil reduced pain from osteoarthritis by increasing antioxidant capacity and improving the integrity of the structure of the knee joint in rats, according to a study published in 2021.
Improves memory and cognitive ability: Peppermint aroma can enhance memory and increase alertness, according to a study published in the International Journal of Neuroscience. A second study confirmed that peppermint, whether exposed orally or through aroma, positively affected cognition and mood.
“Treats” Alzheimer’s disease: Mint extracts protect nerve cells and can be used as “possible sources of treatments in managing AD,” according to a review article published in the journal Antioxidants in 2020. For example, mint extract reportedly protects against age-induced stress and neurodegeneration and improves memory and cognitive ability.
Diminishes skin aging: Peppermint peel skin treatment was effective in treating signs of skin aging, including discoloration, wrinkles, and skin inelasticity, according to a study published in the Journal of Biological Regulators and Homeostatic Agents.
Relieves allergies: Peppermint may relieve symptoms of allergic rhinitis, according to a 2001 study. Peppermint inhibited histamine release from rat mast cells. Nasal symptoms, including sneezing and nasal rubbing, were also inhibited. Consequently, peppermint extract “may be clinically effective in alleviating the nasal symptoms of allergic rhinitis,” according to the researchers.
Diminishes shingles-associated pain: A 2002 case study reported that applying peppermint oil directly to the skin resulted in an “almost immediate improvement” in pain caused by shingles. Pain relief persisted 4-6 hours after application. Furthermore, peppermint continued to exert a “strong analgesic effect on neuropathic pain” during the two months of follow-up monitoring.
Improves sleep: Aromatherapy with peppermint essential oil reportedly improved sleep quality in cardiac and cancer patients.
Promotes alertness: The smell of peppermint led to increased alertness among drivers, as well as decreased frustration, fatigue, and anxiety, according to a study published in the North American Journal of Psychology.
Antifungal: The most common human fungal pathogen is Candida albicans. It is normally present in small amounts in the mouth, skin, and gastrointestinal tract. When out of balance, it can result in painful mucosal infections such as vaginal yeast infections and oral thrush. Peppermint showed strong antifungal action against Candida albicans, according to a 2021 article in Mini-Reviews in Medicinal Chemistry.
Soothes irritable bowel syndrome (IBS): Enteric-coated peppermint oil capsules were reported as safe and effective in the treatment of irritable bowel syndrome, according to a study in the Journal of Gastroenterology. 79 percent of adult patients who consumed the capsules three to four times daily, 15-30 minutes before meals for one month reported an alleviation of the severity of abdominal pain, 56 percent were entirely pain-free and 83 percent reported less abdominal distension.
The healing effect of enteric-coated peppermint oil extends to children, as well as adults. Seventy-five percent of children receiving peppermint oil for two weeks reported reduced severity of pain associated with IBS, according to a study in the Journal of Pediatrics. The researchers concluded, “Peppermint oil may be used as a therapeutic agent during the symptomatic phase of IBS.”
Mint may be effective, in part, in relieving symptoms of IBS by relaxing the muscles of the gastrointestinal tract. According to a study in Gastroenterology, researchers concluded that peppermint oil had a relaxing effect on the smooth muscles of the gastrointestinal tract of rabbits and guinea pigs due to reducing calcium influx.
Relieves tension headache: Local topical application with peppermint oil is effective in treating tension-type headaches, the most common form of headache. Peppermint oil is as effective at relieving tension headache as acetylsalicylic acid (aspirin) or paracetamol (acetaminophen).
Relieves nausea: A 2016 study concluded that “peppermint oil inhalation is a viable first-line treatment for nausea in postoperative cardiac surgery patients.” Post-surgery, 34 patients experienced nausea with an average nausea rating of 3.29 on a scale of 0 to five, with 5 being the greatest nausea. Two minutes after inhaling peppermint oil, the average nausea rating significantly dropped to 1.44.
Likewise, a 2021 study concurred that peppermint essential oil is “an effective independent or complementary modality for relief” of nausea and vomiting in hospitalized patients when inhaled using aromatherapy.
Reduces anxiety: Peppermint has been shown to reduce anxiety. For instance, a 2022 study concluded that peppermint essential oil inhalation significantly reduced anxiety in patients with acute coronary syndrome.
Relieves coughing: A 2013 study, reported that patients with chronic cough benefited from inhaling menthol, an active component of mint. Compared to the placebo, patient’s cough thresholds were significantly higher following inhalation of nebulized menthol.
How to Add Mint to Your Diet
The whole mint plant is edible, including the stems, leaves, and flowers, and can be used in culinary and medicinal applications. Mint can also be consumed as an essential oil.
How to procure mint
Mint can be grown in your yard or indoors. The plant needs a good amount of sun, plenty of water, and space to grow. Alternatively, fresh mint can often be purchased at a local farmers market or grocery store. Dried mint can also be purchased online. Only consume mint that is organically or regeneratively grown.
Simple ways to incorporate mint into your diet
Herbal tea: Boil water, reduce heat to simmer, add 5-10 mint leaves and stems, cover, and steep for 10 minutes.
Smoothies: Add a few fresh mint leaves or a drop of essential peppermint oil to your favorite smoothie or drink—pairs nicely with lemonade (see recipe below).
Soups: Add a few mint leaves to soup while cooking. Cream-based soups, such as pea soup, are ideal.
Salads: Toss a few mint leaves on your salad to enhance the flavor. Mint pairs well with cucumber and pomegranate.
Dressing: Grind fresh or dried mint with a pinch of salt in a mortar and pestle and add to an olive oil and vinegar dressing.
Desserts: Mint pairs well with chocolate, such as peppermint bark, peppermint fudge brownies, or chocolate peppermint ice cream.
For a refreshing drink on a hot summer day, try mint lemonade!
Mint lemonade
Yields 8 glasses
Ingredients:
1-1/2 cups freshly squeezed lemon juice (~10 large organic lemons)
½ teaspoon lemon zest
5 cups cold filtered water
1 cup lukewarm filtered water
½ cup raw, unfiltered local organic honey
1 cup organic mint leaves, loosely packed
2 ice cubes
Instructions:
Juice lemons and add to a glass pitcher along with 5 cups cold water.
In a high-powered blender, combine 1 cup lukewarm water, lemon zest, honey, and mint leaves. Blend until thoroughly combined. Add to glass pitcher and stir until combined.
Add ice to the pitcher. Garnish each glass with a sprig of fresh mint. Serve immediately or store covered in the refrigerator for up to 3 days.
Please do not try this recipe if you are allergic or sensitive to any of the ingredients.
Precautions and Possible Interactions
Pregnant or breastfeeding women should consult their healthcare provider before consuming mint. Peppermint may interact with some prescription drugs, such as cyclosporine, acid-reducing medications, ulcer medications, calcium channel blockers, and other drugs used for hypertension or high blood pressure. People with a hiatal hernia, gastroesophageal reflux disease, diarrhea, or a condition where the stomach does not produce enough acid should consult with a healthcare provider before consuming mint. Peppermint oil is contraindicated in children under two years of age.
Research into the oral microbiome and e-cigarettes is starting to reveal the consequences of vaping
The minty flavors of vape juice might temporarily cover up bad breath but the root cause of halitosis is a bacterial imbalance, which is made worse by the habit of smoking electronic cigarettes.
As long as vaping continues, helpful oral bacteria are killed off, weakening the body’s defenses against bacteria that cause tooth decay and bad breath. In fact, there’s a systemic cascade of disease associated with the destruction of certain tiny organisms that live in the mouth. Decaying teeth and offensive breath are signs of bigger problems, and even top-notch oral hygiene habits cannot overcome damage created by dysbiosis, an imbalance of bacteria.
“Somewhere along the line, somebody convinced them that vaping is safer than smoking. But safer is not safe,” said Dr. Elle Campbell, a family integrative physician. “There are really negative side effects to vaping.”
She may not be a dentist, but Campbell and other doctors that make up the American Academy for Oral & Systemic Health are educating themselves about the connection between oral health and disease for their patients’ sake. And they are raising alarm about vaping, which became popularized after Chinese pharmacist Hon Lik patented the first e-cigarette, in 2003.
While Lik’s intentions were benign—his dad was a heavy smoker and died of lung cancer, motivating him to develop a less-harmful alternative—long-term research was lacking. On top of that, two decades of evolving science includes revelations on the vital role of the microbiome in oral and overall health.
Meanwhile, the e-cigarette industry exploded on the premise of “safer,” which has never been proven. Proliferation of a wide variety of products has gone largely unmonitored, creating unknown complications for users and layers of complexity for scientists who are trying to contextualize harm.
E-cigarettes fit in the palm of the hand, sometimes so small they’re easily hidden, and use a battery to heat up a liquid solution (vape juice) in order to produce an aerosol. They can be activated by a button or by inhaling. Nicotine, tetrahydrocannabinol (THC), and cannabinoid (CBD) oils can all be used in vapes. These solutions can contain any number of carcinogens and toxicants.
Despite many unknowns, there are plenty of facts including studies about the impact on the microbiome—the colony of microorganisms including bacteria that live in and on the body—that tell a compelling story.
How Vaping Kills Microbes
Vaping assaults the oral microbiome with chemicals, additives, and sweeteners that stick to the teeth. It can damage the enamel and kill off the healthy bacteria that stem the tide of plaque.
Mouths are full of flora that keep the environment balanced by killing off pathogenic invaders. It’s a system that works relatively well unless it’s thrown off balance by toxins—chemicals, medications, and sugary, processed foods that are associated with low levels of healthy bacteria.
“We have to have bacteria in our mouth. They’re the good guys,” Campbell said. “They keep our gums and our tissues strong and healthy. If there was no bacteria in our mouth, we’d lose all our teeth.”
Too much bad bacteria also causes bad breath. That same imbalance associated with halitosis causes periodontal disease as well as mouth and digestive cancers, according to a 2020 study published in the Journal of Clinical Medicine. Periodontal or gum disease damages the soft tissues of the mouth and can lead to tooth loss.
Smoking cigarettes already increases one’s chances of gum disease fourfold, and research has established that periodontitis is associated with a pathogen-rich oral biome. But as one 2020 study published in Science Advances pointed out, it can take more than a decade for visual signs of periodontal disease to manifest.
The article stated there’s reason to believe oral microbiome changes happen earlier in vaping than in smoking and there are other mechanisms that vary from smoking, warranting more extensive studies. “…e-cigarettes have the potential to shift the host-microbiome equilibrium, posing a significant risk for future disease,” according to the article.
Among the estimated 5.66 million adults who currently vape, 23 percent didn’t smoke previously, and most were younger than 35 according to the Journal of the American Medical Association.
A study published in early 2022 in Molecular and Oral Microbiology showed a six-month shift in the oral microbiome of 101 e-cigarette patients. Their bacterial composition more closely resembled that of smokers, including high numbers of periodontal-disease-associated pathogens and proinflammatory cytokines all indicative of microbiome dysbiosis and advanced disease. A study that came out in November in the Journal of the American Dental Association validated the relationship between vaping and tooth decay.
How it happens isn’t explicitly clear but could be linked to several factors that are unique to vaping, including the temperature of the aerosols that penetrate the protective biofilm on the teeth. Vaping also has a more alkaline pH, as well as unique properties such as heated metals that sometimes turn up in the aerosol and propylene glycol, which is generally considered safe in food but is known to damage enamel and lower saliva levels.
E-juice typically contains four ingredients: nicotine, water, flavoring, and propylene glycol or vegetable glycerin (or both). The solution itself can contain toxins, and the heating process can also create a unique thermal decomposition of toxic compounds. A January 2022 review in Toxins found various studies showing toxicants such as carbonyls, formaldehyde, acetaldehyde, acrolein and more. Other studies have found additional contaminants, like dangerous chemicals used in pesticides, metabolites commonly found in blood and feces, and endotoxins.
The aerosol toxins can also alter the immune system in harmful ways. Oral pathogens can then sneak in under lowered defenses and cause inflammation of the gums, bleeding, and gum pockets that allow pathogens to seep in further and cause decay in the teeth and gums. Redness, swelling, and bleeding are signs of periodontal disease.
Damaging the Whole System
Not only is the structure, health, and appearance of the mouth under attack from dysbiosis, but the imbalance opens the door for pathogens to invade the entire body.
“What happens in the mouth doesn’t stay in the mouth. It goes everywhere,” Campbell said. “As a family doctor, the reason I’m concerned more is that those very same bacteria increase our risk for heart attack, stroke, cancer, diabetes, and Alzheimer’s disease. These bacteria get in our bloodstream and once they’re in our bloodstream, all bets are off.”
Even though the gut and mouth have separately unique microbiomes, individual microorganisms can travel both ways as demonstrated in a September, 2022 Clinical Science study.
A periodontist and certified functional medicine practitioner, Dr. Alvin Danenburg said pathogens can compromise the body in numerous ways, but the damage can also be reversed when smoking ceases.
“You can’t stop the mouth infection without addressing the gut, and you can’t stop the gut infection without addressing the mouth because they communicate back and forth,” he said. “The beautiful part of this is both are very treatable.”
In addition to quitting vaping, Danenberg said getting adequate sleep, improving diet, being mindful of chemical exposure, exercising without overdoing it, and addressing stress can all help balance the microbiome.
More Evidence to Warn Kids of Vaping
Teenagers and young adults, who tend to eat more sugar-laden diets, are particularly at risk from a collision of unhealthy habits impacting the microbiome. One in four students vapes, according to 2019 data from JAMA. They’re also the target of a lot of misleading messaging.
“It’s not their fault,” Danenberg said. “When the industry tells us this is a great alternative to cigarette smoking and it tastes good and it’s harmless, you know why not. The sad thing is the research is just starting now.”
Many e-cigarette liquids were found to contain aldehydes, toxins related to sugar, and high sucrose levels, according to a 2018 study in Nicotine and Tobacco Research.
“Because sugar added to tobacco alters the smoke in cigarettes by modifying sensory impact of nicotine and other tobacco alkaloids, it is possible that sugar in e-cigarettes may make the product more appealing,” researchers wrote. “Furthermore, most product labels did not list sugars or provide warnings about aldehydes on the labels.”
Campbell said young people should tell healthcare providers about their lifestyle choices and risk factors and ask for oral cancer screenings. She advocates for parents to have their children use oral hygiene products, gum, and mints containing xylitol. While not a substitute for quitting vaping, good oral care, or a healthy lifestyle, there’s evidence that xylitol can help protect against cavities.
Overcoming addiction isn’t easy, and nicotine is highly addictive because of how fast it enters the bloodstream and the euphoria users get when dopamine levels rise. Only about 6 percent of smokers are able to quit each year, according to the U.S. National Institutes of Health.
“There’s lots of reasons people might want to pick nicotine,” Campbell said. “But there’s other stuff in that vaped chemical. They’re exposing their body to a toxic burden that they may not have appreciated.”
Vaping is clouded with mixed messages, not unlike cigarette marketing from 80 years ago. An advertising campaign in 1946 featured the slogan, “More doctors smoke Camels than any other cigarette.”
Danenberg is concerned there may be even greater harm associated with vaping compared to cigarette smoking.
“Eventually science caught up with them and figured that smoking was unhealthy. Look how many years it took for that to happen,” he said. “It’s going to take a long time to get the research that’s published and being actually investigated today to the clinicians like dentists and physicians to let them know to get their patients information.”
Did you know that gut health may be an important tool in fighting depression? Researchers are learning more about the gut-brain connection and how we might harness this relationship for better mental health.
The Gut-Brain Connection
There’s a name for this connection: the gut-brain axis.
According to a chapter in “Translational Bioinformatics and Systems Biology for Understanding Inflammation,” the gut-brain axis is a bidirectional communication system between the central nervous system (CNS) and the gastrointestinal (GI) tract, also known as the enteric nervous system or “second brain.” It is also the largest part of the autonomic nervous system. Its circuitry allows it to coordinate gastrointestinal functions and plays an essential role in maintaining equilibrium within the body, including the brain.
Jeremy Appleton, a naturopathic physician who has researched the gut-brain axis, says our gut microbiome and its connection with our brain have a significant effect on every part of the body.
“Every system in the body seems to be influenced by the quality of our microbiome and also the quality of that interface where those bacteria reside in us,” he explains. “It’s definitely a symbiotic relationship that we have with them.”
The gut microbiome can alter the function of the enteric nervous system by activating stress pathways in the brain (“bottom-up”). The process can also happen in reverse (“top-down”).
Stress and depression can disrupt the gut’s microbiome through stress hormones, inflammation, and changes within the autonomic nervous system—which regulates involuntary processes in the body such as heart rate, blood pressure, respiration, and digestion (top-down). These changes can cause gut bacteria to release substances that can affect our eating behavior and mood.
Alternately, gut bacteria can increase stress responsiveness and increase the risk of depression (bottom-up).
According to the chapter mentioned above, animal studies have found that the gut microbiome is an important factor behind mood, pain, cognition, and obesity. It’s an interesting relationship that may provide important clues into various neuropsychiatric diseases including schizophrenia, autism, and affective disorders (such as depression and bipolar disorder).
Our gut microbiome also makes a group of chemicals called short-chain fatty acids when they break down fermentable, resistant starches (prebiotics), and some dairy products.
Short-chain fatty acids are believed to play a major role in gut health and in regulating neuro-immunoendocrine functions. The neuro-immunoendocrine network is comprised of the nervous system, endocrine system, and immune system. These systems work together and use neurotransmitters, hormones, and cytokines (proteins that can stimulate the immune system or slow it down) to keep the body in balance.
These acids are also thought to play an important role in microbiota-gut-brain communication. Changes in short-chain fatty acids have been linked to depressive symptoms and GI symptoms. They may additionally affect the way our brain works and may be used to help treat brain disorders in the future.
Short-chain fatty acids can also cross and reinforce the integrity of the blood-brain barrier to protect the brain from inflammation, increase the production of new neurons, contribute to the synthesis of serotonin, and improve neuron function.
All of this has an impact on our behavior, says Appleton.
“There are all kinds of implications. Not just for mood, but also for neurologic conditions like autism and serotonin metabolism, and how that is all affected with major depression,” he explains.
Depression and Dysbiosis
Dysbiosis occurs when there is an imbalance in the body’s normal gut microbiome. This happens for a variety of reasons, including infection, diet, exposure to antibiotics, exercise level, and sleep patterns. It is believed to trigger inflammation and dysregulation of the immune system.
Leaky gut can also disrupt the gut microbiome. It occurs when the tight barrier within our intestines develops cracks or holes and allows partially digested food and toxins to penetrate other tissues.
Numerous studies have shown a connection between the disruption of the gut microbiome and depression. Research has demonstrated that the gut microbiome is linked with the production of serotonin and its precursor, tryptophan. Serotonin is a chemical that transmits messages between nerve cells in the brain and the body. It is involved in mood, sleep, cognition, digestion, and other processes. Low levels of serotonin are associated with depression.
It’s also been suspected that the neurotransmitter GABA may be affected by our microbiome. GABA blocks signals between nerve cells in the brain and the spinal cord. Decreased levels of GABA may contribute to the development of depression and mood disorders.
One study involved the transfer of fecal matter from depressed humans into microbe-deficient rats, causing depressive-like behavior in the rats.
Another study published in December 2022 in Nature Communications compared the fecal matter of 1,054 participants with depression against a cohort of 1,539 subjects. The study made an association between 13 types of bacteria and depressive symptoms. Each bacterium is known to be involved with the synthesis of key neurotransmitters, suggesting that the gut microbiome is an important causal factor in depression.
Heal Your Gut, Heal Your Mind
Healing your gut and your mind require interventions that address both sides of the complicated gut-brain connection.
According to Appleton, research into the gut-brain axis has exploded in the last 15–20 years; unfortunately, the “lessons learned” are rarely applied by most practitioners.
“In terms of depression, it’s something that we still in mainstream medicine, we just really aren’t looking at when we’re talking about moods,” says Appleton. “We’re not looking at the health of their gut—it still hasn’t become intuitive for us.”
Appleton says that instead of just prescribing drugs or supplements to address depression, clinicians should look at dysbiosis and/or evaluate for leaky gut syndrome “as part of the standard operating procedure.”
A holistic approach to treating depression is the best approach, according to Appleton. He says he wouldn’t tell a patient not to take an antidepressant; however, if medication is the only treatment, “you’re going to touch part of the problem, but you’re not going to treat the whole problem,” explains Appleton.
Angelo Pezzote holds a doctorate in pharmacy and is a board-certified psychiatric pharmacist and clinical mental health counselor. He marries the two professions with mind and body and works almost as a psychiatrist would.
Although Pezzote assists prescribers with medication recommendations, his focus is less on medications and more on “nutritional psychiatry”—he works with clients to replenish and enhance the gut microbiome through methods such as lifestyle changes, stress reduction, exercise, and healthy eating.
Pezzote says that while some people do need medication, many may be overmedicated or rely on medication as their “one and only answer” for depression.
“I think for a lot of patients, they’re just used to ‘here, take this pill and you’re going to feel happy’ and that’s just not the way reality is. A lot of people on their antidepressants still feel sad and they need more than just a pill.”
Appleton agrees.
Managing stress is a major component of healing the gut. Pezzote says that stress “throws off” the immune system, causing inflammation, which is linked to depression and other mood disorders. Through managing stress, you can manage stress hormones that influence the gut microbiome.
“It’s really stress that gets people off balance,” says Pezzote.
Movement, meditation, yoga, tai chi, quality sleep, meaningful social interaction, having fun, and finding joy also can help manage stress and consequently help the gut.
Eating a plant-rich diet is very important in maintaining a healthy gut microbiome, given that the gut microbiome loves fiber and prebiotics—things we can’t digest.
Prebiotic foods include chicory root, garlic, onions, and leeks.
Pezzote recommends a plant-rich diet, incorporating low-fat dairy, limiting processed meat and red meat, as well as refined sugar and flour, and increasing whole grains, healthy fats, and complex carbohydrates.
Probiotics can also help improve the gut microbiome. They can be found in foods including kefir, yogurt, kimchi, tempeh, and other fermented foods and probiotic supplements. Since probiotic supplements are not regulated by the U.S. Food and Drug Administration, it is important to choose probiotics that have a quality seal from a third-party inspector.
Pezzote recommends choosing a multi-strain probiotic that includes Lactobacillus for best results. As always, speak with your physician before starting a probiotic supplement.
Clinical evidence indicates that probiotics can improve symptoms in those suffering from Major Depressive Disorder. A clinical trial conducted in the Netherlands showed “significantly reduced overall cognitive reactivity to sad mood” after four weeks of probiotics. Other studies have replicated these results, indicating that probiotics may be an important tool in the fight against depression.
“If I had MDD or major anxiety disorder, I would be going top down and bottom up. It makes a lot of sense given the bidirectional nature of the gut-brain axis,” Appleton said.
Pezzote says healing the gut and treating depression cannot be solved with one intervention only.
“It’s like the spokes on a wheel: One spoke doesn’t balance the wheel. It’s all the spokes,” he says. “And we need not just medication, we need a bunch of things to go along with that as necessary in order to have good, healthy, balanced microbiomes.”
These study findings were so controversial, they had to undergo additional peer-review and scrutiny before being published. Their publication even warranted a special editor’s note justifying the journal’s decision to publish the story. Will the findings be taken seriously?
STORY AT-A-GLANCE
A U.S. and Canadian government-funded observational study found that drinking fluoridated water during pregnancy lowers children’s IQ; a 2022 study by the same team will assess the neurotoxicity of early-life exposure to fluoride
In the earlier study, a 1 milligram per liter increase in concentration of fluoride in mothers’ urine was associated with a 4.49-point decrease in IQ among boys only, while a 1-mg higher daily intake of fluoride was associated with a 3.66 lower IQ score in both genders between ages 3 and 4
The findings were hotly criticized by pro-fluoride agents, including the American Council on Science and Health (ACSH) and the Science Media Centre (SMC), two well-known front groups for the chemical industry
As of January 2022, there are at least 74 studies showing fluoride exposure damages children’s brains and lowers IQ; there are at least 60 that found that fluoride exposure impairs the learning and/or memory capacity of animals
There are also more than 2,000 other studies detailing other health effects
Research published in 2017 found that, compared to a mother who drinks fluoride-free water, a child of a mother who drinks water with 1 part per million of fluoride can be predicted to have an IQ that is 5 to 6 points lower. They also found there was no threshold below which fluoride did not affect IQ
The August 19, 2019, issue of JAMA Pediatrics[1] delivered an unexpected bombshell: A U.S. and Canadian government-funded observational study found that drinking fluoridated water during pregnancy lowers children’s IQ.
The research, led by a Canadian team of researchers at York University in Ontario, looked at 512 mother-child pairs living in six Canadian cities. Fluoride levels were measured through urine samples collected during pregnancy.
They also estimated the women’s fluoride consumption based on the level of fluoride in the local water supply and how much water and tea each woman drank. The children’s IQ scores were then assessed between the ages of 3 and 4. As reported by the Fluoride Action Network (FAN):[2]
“They found that a 1 mg per liter increase in concentration of fluoride in mothers’ urine was associated with a 4.5-point decrease in IQ among boys, though not girls.
When the researchers measured fluoride exposure by examining the women’s fluid intake, they found lower IQ’s in both boys and girls: A 1 mg increase per day was associated with a 3.7 point IQ deficit in both genders.”
Support for the Importance of This Study
The findings were deemed so controversial, the study had to undergo additional peer-review and scrutiny before publication, making it one of the more important fluoride studies to date.
Its import is also demonstrated by the fact that it was accompanied by an editor’s note[3] explaining the journal’s decision to publish the study, and a podcast[4] featuring the chief editors of JAMA Pediatrics and JAMA Network Open, in which they discuss the study.
An additional editorial[5] by David Bellinger, Ph.D., a world-renowned neurotoxicity expert, also pointed out that “The hypothesis that fluoride is a neurodevelopmental toxicant must now be given serious consideration.” Few studies ever receive all of this added treatment. According to the editor’s note:[6]
“Publishing it serves as a testament to the fact that JAMA Pediatrics is committed to disseminating the best science based entirely on the rigor of the methods and the soundness of the hypotheses tested, regardless of how contentious the results may be.”
Chemical Industry Front Groups Defend Fluoride
Surprisingly, the findings were widely reported by most major media outlets, including Reuters,[7] The Washington Post,[8] CNN, NPR, Daily Beast and others, effectively reigniting the scientific debate about whether water fluoridation is a good idea.
Not surprisingly, the findings were hotly criticized by pro-fluoride agents, including the American Dental Association (ADA),[9] the American Council on Science and Health[10] (ACSH) and the Science Media Centre[11] (SMC).
It’s well worth noting that the ACSH and SMC are well-known front groups for the chemical industry, and they will defend all chemicals, regardless of what’s under discussion, so seeing dismissive articles from these groups is more or less par for the course. You can learn more about these groups in the articles hyperlinked above.
It’s also worth noting that Fox, which in 2014 made a similar study headline news,[12] wasn’t satisfied with just presenting the latest study as news and, instead, invited its resident doctor, Marc Siegel, to comment[13] — and that comment began by blaming tooth decay, not fluoride, on lower IQs. Siegel ended with a rambling diatribe against the study and a scathing criticism of JAMA Pediatrics for even having published it:
“I’m far more worried about tooth decay than I am about fluoride … There’s no way that fluoride would lower your IQ more than having tooth decay … It’s a ridiculous study … complete poppycock … The Journal of the American Medical Association Pediatrics should not have put this in.”
As for the ADA, it’s been promoting water fluoridation as a health benefit for over a century and a half. To change its stance would clearly result in a loss of face, and might even expose the association to liability. The loss of scientific credibility alone is likely enough to encourage the ADA to hold on to the status quo.
The same goes for the U.S. Centers for Disease Control and Prevention which, despite the more than 2,700 studies[14] against it, maintains water fluoridation is one of the top 10 great public health achievements of the 20th century.[15]
AAP Support of Water Fluoridation Is Hypocritical
A bit tougher to explain is the American Academy of Pediatrics’ continued support of water fluoridation, despite a study linking fluoride intake among pregnant women with a “small dip” in their children’s IQ.[16]
Of any group, the AAP really should reconsider its stance on this issue, seeing how it has officially recognized the hazardous influence of hormone-disrupting chemicals on child development. Of course, the American Dental Association and American College of Obstetricians and Gynecologists went right along with the AAP, are apparently unconcerned about that “small” dip in IQ.
What’s hypocritical is that in 2018, the AAP issued a policy statement[17] warning parents to avoid endocrine-disrupting chemicals — commonly found in processed food, fast food wrappers and plastics, for example — and while fluoride was not specified as an example of a chemical to be avoided, research shows fluoride has hormone disrupting potential placing it in the exact same category. As noted by FAN:[18]
“Fluoride was definitively identified as an endocrine disruptor in a 2006 report[19] [20] by the U.S. National Research Council of the National Academies (NRC). This report states:
‘In summary, evidence of several types indicates that fluoride affects normal endocrine function or response … Fluoride is therefore an endocrine disruptor in the broad sense of altering normal endocrine function or response … The mechanisms of action … appear to include both direct and indirect mechanisms …”
Fluoride Action Network Addresses Study Critique
In the featured video, Paul Connett, Ph.D., founder and current director of the FAN, addresses some of the criticism and why this particular study is such an important wake-up call for health care practitioners and pregnant women.
“[Fluoride exposure] during pregnancy will lower the IQ of their children. Only if you think a child’s tooth is more important than a child’s brain would you not be disturbed by that,” Connett says. “You can repair a child’s tooth. You cannot repair a child’s brain once it’s been impacted during fetal development.”
One pro-fluoride critique against the JAMA Pediatric study is that it doesn’t show cause and effect. “Well, no epidemiological study proves cause and effect,” Connett says. “That’s a given! To say it doesn’t show cause and effect is a redundant statement.” Other pro-fluoride voices argue the effect size is small — only 4.49 IQ points[21] for boys, on average. However, as Connett points out:
“If you shift the entire population over by 3 or 4 IQ points, you would almost halve the number of geniuses in your society … and you would increase by about 50% the number of mentally handicapped children. So, on a population [basis] such shifts are highly, highly significant.”
A third manufactured controversy revolves around the fact that only boys were impacted by maternal urine levels of fluoride. Some hitch their critique of the study on this simple gender difference.
However, it should come as no surprise that boys and girls can be affected in different ways by the same toxic compound, as their development is affected by various hormones, including sex hormones, and toxins affect various hormones in different ways. We’ve seen this type of gender difference in many other instances as well.
“However you cut it, you have to be so wedded to fluoridation not to take this incredibly seriously,” Connett says. “Remember, there is absolutely no evidence whatsoever — no scientific evidence — that a fetus exposed to fluoride has lowered dental decay.
There’s no evidence you’re protecting the baby from future decay during pregnancy. So, ANY evidence suggesting it may be damaging the brain has to be taken seriously …
We have potential harm [on the one side] … and on the other side you have something that is totally unnecessary. Why on earth would any doctor hesitate to advise pregnant women: ‘Don’t drink fluoridated water during pregnancy’?”
Other Studies Support Link Between Fluoride and IQ Loss
What’s more, as Connett so strongly points out, while this particular study has received a great deal of media attention, it’s not the only one raising a red flag. There are at least 74 studies listed in FAN’s scientific database showing that fluoride exposure damages children’s brains and lowers IQ.[22] There are at least 60 that found that fluoride exposure impairs the learning and/or memory capacity of animals.[23]
There are also a couple of thousand other studies detailing other adverse health effects. When you add in animal research, there are more than 300 studies demonstrating fluoride can cause:[24]
Brain damage, especially when coupled with iodine deficiency
Reduced IQ
Impaired ability to learn and remember
Neurobehavioral deficits such as impaired visual-spatial organization
Impaired fetal brain development
In his video commentary, Connett briefly mentions the importance of the 2017 “Bashash study.” This was an international study effort led by professor Howard Hu, who at the time of the study’s publication was at the University of Toronto. The study is known as the “Bashash study” after the lead author, Morteza Bashash, Ph.D. The team also includes researchers from McGill, Harvard, Mount Sinai, Michigan, Indiana and the National Institute of Public Health of Mexico.
Funding for this research came from the U.S. National Institutes of Health, National Institute of Environmental Health Sciences and the U.S. Environmental Protection Agency. The finalized study[25][26] was published in the September 2017 issue of Environmental Health Perspectives.
This study was remarkable for the fact that it followed participants for 12 years, involved several well-respected researchers, employed rigorous methodology and controlled for virtually all conceivable factors.
Here too, they found a strong relationship between the urinary level of fluoride in pregnant women and the subsequent IQ in their children. They also found a dose-dependent relationship, so the higher the mother’s urine level of fluoride, the lower the IQ in the offspring.
According to the Bashash study, compared to a mother who drinks fluoride-free water, a child of a mother who drinks water with 1 part per million of fluoride can be predicted to have an IQ that is 5 to 6 points lower. What’s more, they found there was no threshold below which fluoride did not affect IQ.
A New Study Will Assess Neurotoxicity on the Brain
In January 2022, York University announced that the same research team that found the connection between fluoride and children’s IQs has obtained close to $2 million from the National Institutes of Health to assess both the neurotoxicity of early-life exposure to fluoride and the thyroid-disrupting effects of fluoride in pregnancy.[27]
The researchers will use baby tooth dentin — tissue beneath the enamel — to measure fluoride “ring” markers on the dentin.
“Sampling tooth layers that correspond to specific life stages will provide critical information for when exposure occurred and how much reached the developing brain,” lead researcher Christine Till said in a press release.
“Our earlier research measured urinary fluoride levels in pregnant women, which does not tell us how much fluoride reached the fetus and when … The tooth dentin is an optimal biomarker because it will provide evidence that fluoride crosses the placenta. This will give a better understanding of the critical window of when exposure becomes harmful to the developing brain.”
Your Contributions Are Making a Difference
FAN is part of the Mercola Health Liberty Coalition, founded in 2011 — the mission of which is to inform and educate about the fraud and deceptions created by the junk food, chemical and pharmaceutical industries. Other Health Liberty partners include the National Vaccine Information Center, the Organic Consumers Association and Consumers for Dental Choice.
Not only has your support been helpful to catalyze the removal of fluoride but you have been able to help us make massive changes with two other health issues as well:
GMOs — When we first started, the average person in the U.S. did not know what GMOS were. Now, not only do they know but they are also aware how dangerous they are. Your support has allowed FOIA requests to be filed that produced critical evidence resulting in juries awarding plaintiffs billions of dollars from Bayer/Monsanto, with another 13,000 cases pending and a possibility of bankrupting this evil giant.
Dental mercury — Charlie Brown has coordinated worldwide bans on the use of mercury in dentistry that has already resulted in banning mercury in dentistry in many countries, with the likely complete elimination of amalgam within the next few years.
Again and again, we see “controversial” and “contentious” stances proven prudent and correct given enough time for sufficient science to accumulate. It’s important for you to recognize that your donations to these organizations through the years have allowed these successes to manifest. The latest JAMA Pediatrics study brings us another major step forward in the process to eliminate water fluoridation.
Editors Compare Anti-Fluoridation to Anti-Vaccine Sentiments
As noted by JAMA Pediatrics editor-in-chief, Dr. Dimitri Christakis, in the JAMA podcast (embedded above):
“Before there were anti-vaxxers there were anti-fluoriders, and the traditional teaching when I was going through residency in my early professional career was, ‘fluoride is completely safe and all of these people trying to take it out of the water are nuts. It’s the best thing that’s ever happened for children’s dental health and we need to push back and get it into every water system’ …
So, when I first saw this title [‘Association Between Maternal Fluoride Exposure During Fetal Development and IQ Scores in Offspring in Canada’], my initial inclination was, ‘What the hell?’”
Christakis goes on to express shock at the discovery that only 3% of European residents, while 66% of Americans and 38% of Canadians drink fluoridated water (statistics noted in the JAMA Pediatrics paper[28]), as he was under the assumption that all developed countries fluoridated all their water supplies. This just goes to show the general ignorance that still exists even among well-educated health professionals.
Christakis and JAMA Network Open editor-in-chief Dr. Frederick Rivara also express mutual surprise that the effect of water fluoridation on IQ was so great. They point out that a 5-point reduction is significant indeed, as it’s “on par with lead.”
Christakis goes on to discuss the fact that there have been other studies suggesting fluoride may be a neurotoxin. “Which, again, was totally news to me. I thought it was junk science,” he says. Rivara agrees, saying such studies have in the past been likened to “junk” anti-vaccine science.
Christakis admits he struggled with the findings — basically because of his preconceptions of the science. He certainly did not want to be the one putting out “junk science” that might lead to a deterioration of children’s dental health. This is precisely why the study was put through additional reviews to make sure the methodology and findings were sound. In the end, the research was solid enough to pass the tests.
It’s interesting to hear Christakis and Rivara talk about their struggle to accept the idea that water fluoridation may be harmful — at the very least until the child starts developing teeth. But even toddlers may be harmed, the pair admit, as toddlers and young children’s brains are still developing.
It’s even more interesting to hear them equate their struggles to that of the vaccine safety question for, indeed, the very same struggle to accept the idea that vaccines can cause harm is identical to the struggle to accept that water fluoridation may be damaging our children.
Both are considered unassailable public health victories, and no one wants to entertain the idea that we may inadvertently be causing grave harm on a populationwide basis. Yet that’s a very real probability, as this study shows (and many others as well).
Fluoride Is an Environmental Pollutant as Well
Overall, it makes absolutely no sense to fluoridate municipal water supplies. First of all, it’s forced medication without oversight — there’s no way to ascertain the dosage any given person is getting, or what effect it’s having on their health.
When it comes to fetuses and infants, water fluoridation is useless, as there’s no scientific evidence to even remotely suggest it has a beneficial impact on future dental health, and it certainly does not make sense to “prevent cavities” in those without teeth.
Furthermore, the vast majority of the fluoride in the water never ever touches a tooth. It’s simply flushed down the drain, becoming an environmental pollutant. As noted by Edward Groth III, a staff officer on the Environmental Studies Board, Commission on Natural Resources, with the National Research Council back in 1975:[29]
“Environmental contamination by fluorides exposes many organisms to potentially toxic effects and may exert some stress on the ecological interrelationships among plant and animal populations … [T]he available evidence does support the view that fluorides are pollutants with considerable potential for producing ecological damage.”
Groth’s article, “Fluoride Pollution,”[30] which appeared in the journal Environment: Science and Policy for Sustainable Development, summarizes the ecological impacts of low-level fluoride pollution, pointing out fluoride has been found to accumulate in the bodies of insects, birds and mammals, in some cases to potentially toxic levels, thus increasing fluoride levels in the food chain as a whole.
There are also reports of toxic effects in algae and freshwater vertebrates, and “indications that aquatic vegetation may also concentrate the element.” Substantial amounts of fluoride are also entering farmland, where it’s taken up by soil organisms.
“Possible conversion of fluoride into fluoracetate (more toxic than fluoride itself and related organic forms), and the likelihood that fluoride may enter into synergistic actions with other contaminants, greatly expand the potential for ecological damage by low-level fluoride contamination,” Groth writes.[31]
Water Fluoridation Is a Clear Form of Water Contamination
It’s also important to realize that the fluoride added to our water is an untreated industrial waste product from the fertilizer industry — not a pharmaceutical grade product — that is suddenly deemed a health product once it’s purposely added to water.
As long as the chemical is on the premises of a fertilizer company, it’s actually classified as hazardous waste, requiring costly disposal measures to comply with hazardous waste regulations.
This fluorosilicic acid is frequently contaminated with lead, arsenic, uranium, radium, aluminum and other industrial contaminants. In other words, water fluoridation can be likened to a legal water contamination scheme.
For a review of the oft-neglected history of water fluoridation, read through “Toxic Treatment: Fluoride’s Transformation from Industrial Waste to Public Health Miracle” in the March 2018 issue of Origins,[32] a joint publication by the history departments at The Ohio State University and Miami University. As noted in “Toxic Treatment:”
“Without the phosphate industry’s effluent, water fluoridation would be prohibitively expensive. And without fluoridation, the phosphate industry would be stuck with an expensive waste disposal problem.”
There’s also very little evidence to suggest water fluoridation actually has a beneficial impact on tooth decay, while there’s unequivocal evidence of harm, as it causes dental fluorosis. Origins writes:[33]
“Only a handful of countries fluoridate their water — such as Australia, Ireland, Singapore, and Brazil, in addition to the United States. Western European nations have largely rejected the practice. Nonetheless, dental decay in Western Europe has declined at the same rate as in the United States over the past half century …
This is not to vilify the early fluoridationists, who had legitimate reason to believe that they had found an easy and affordable way to counter a significant public health problem.
However, the arguments and data used to justify fluoridation in the mid-20th century — as well as the fierce commitment to the practice — remain largely unchanged, failing to take into account a shifting environmental context that may well have rendered it unnecessary or worse.”
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