Heavy Caffeine Consumption Research Articles

Effect of caffeine on mitochondrial biogenesis in the skeletal muscle - A narrative review.

Caffeine is one of the most widely used substances as recreational drug for performance-enhancement in sport, underpinned by a strong evidence base. Although the effects of caffeine are widely investigated within the scope of performance physiology, the molecular effects of caffeine within skeletal muscle remain unclear. Evidence from invitro and invivo models suggest that caffeine regulates the glucose metabolism in the skeletal muscle. Moreover, caffeine seems to stimulate CaMKII, PPARδ/β, AMPK and PGC1α, classical markers of exercise-adaptations, including mitochondrial biogenesis and mitochondrial content. This review summarizes evidence to suggest caffeine-effects within skeletal muscle fibers, focusing on the putative role of caffeine on mitochondrial biogenesis to explore whether caffeine supplementation might be a strategy to enhance mitochondrial biogenesis.

The influence of CYP1A2 genotype in the blood pressure response to caffeine ingestion is affected by physical activity status and caffeine consumption level

This study aimed to investigate whether the influence of CYP1A2 genotype in the blood pressure (BP) response to caffeine ingestion was affected by physical activity status and habitual caffeine consumption. Thirty-seven participants (19–50 years old) took place in the study and were categorized according to i) genotype: CYP1A2 (AA) “fast metabolizer”, and CYP1A2 (AC) “slow metabolizer”; ii) physical activity level: sedentary (S) and physically active (A); and iii) caffeine consumption level: non-habitual caffeine consumer (NC) and habitual heavy caffeine consumer (C). All groups had BP assessed before (basal) and 1 hourh after (post) caffeine ingestion (6 mg·kg−1). It was observed that AC genotype individuals had increased basal-DBP and post-caffeine SBP when compared to AA individuals. Additionally, acute caffeine ingestion increased SBP only in the AC group. It was also found that physical activity only modulated the BP responses to acute caffeine ingestion in AC individuals. Furthermore, the results indicated that the habitual heavy caffeine consumers AC individuals had increased basal-DBP when compared to the AA ones. Our results suggest that the influence of CYP1A2 genotype in the basal and post-caffeine BP response to caffeine ingestion is modified by physical activity status and caffeine consumption level.

Regular Physical Activity Increases the Systolic Blood Pressure Response to Acute Caffeine Ingestion in Nonhabitual Caffeine Consumers

Background: Physical activity and caffeine consumption induce adaptations to the cardiovascular system, which can change basal and postcaffeine blood pressure (BP) and heart rate (HR) parameters. We hypothesized that physical activity would attenuate the pressor effects of acute caffeine ingestion regardless of caffeine consumption level. Methods: We evaluated the influence of regular physical activity and chronic caffeine consumption on basal and post-caffeine ingestion BP and HR. Sixty subjects (19–50 years old) participated in an interventional study. To evaluate the influence of regular physical activity and caffeine consumption, the participants were divided into four groups: sedentary nonhabitual caffeine consumers (S), sedentary habitual heavy caffeine consumers (SC), physically active nonhabitual caffeine consumers (A), and physically active habitual heavy caffeine consumers (AC). All groups had BP and HR assessed before (basal) and one hour after (post) caffeine ingestion (6 mg.kg−1 of body mass). Results: We found that group A had an increased systolic blood pressure (SBP) from 119.2 ± 11.3 to 124.2 ± 14.3 mmHg after acute caffeine ingestion. Lack of regular physical activity was associated with a significant increase in diastolic BP after caffeine ingestion (group S; 69.1 ± 7.7 vs. 73.8 ± 8.3 and group SC; 71.6 ± 9.5 vs. 75.3 ± 8.4). Group AC showed lower basal DBP than group SC (64.61 ± 8.1 and 71.5 ± 7.8 mmHg, respectively). Conclusion: Acute caffeine ingestion increases the SBP in physically active nonhabitual caffeine consumers.

Smoking and caffeine consumption: a genetic analysis of their association.

Smoking and caffeine consumption show a strong positive correlation, but the mechanism underlying this association is unclear. Explanations include shared genetic/environmental factors or causal effects. This study employed three methods to investigate the association between smoking and caffeine. First, bivariate genetic models were applied to data of 10 368 twins from the Netherlands Twin Register in order to estimate genetic and environmental correlations between smoking and caffeine use. Second, from the summary statistics of meta‐analyses of genome‐wide association studies on smoking and caffeine, the genetic correlation was calculated by LD‐score regression. Third, causal effects were tested using Mendelian randomization analysis in 6605 Netherlands Twin Register participants and 5714 women from the Avon Longitudinal Study of Parents and Children. Through twin modelling, a genetic correlation of r0.47 and an environmental correlation of r0.30 were estimated between current smoking (yes/no) and coffee use (high/low). Between current smoking and total caffeine use, this was r0.44 and r0.00, respectively. LD‐score regression also indicated sizeable genetic correlations between smoking and coffee use (r0.44 between smoking heaviness and cups of coffee per day, r0.28 between smoking initiation and coffee use and r0.25 between smoking persistence and coffee use). Consistent with the relatively high genetic correlations and lower environmental correlations, Mendelian randomization provided no evidence for causal effects of smoking on caffeine or vice versa. Genetic factors thus explain most of the association between smoking and caffeine consumption. These findings suggest that quitting smoking may be more difficult for heavy caffeine consumers, given their genetic susceptibility.

Dietary factors and the risk of glaucoma: a review.

Glaucoma is an optic neuropathy characterized by a progressive typical pattern of optic neurodegeneration and visual field loss. A relatively high proportion of glauctomatous individuals admit to interest in dietary modification in an attempt to manage their disease. Heavy caffeine consumption appears to have a transient effect on increasing intraocular pressure (IOP). This effect may be clinically insignificant for nonglaucomatous individuals, but the association warrants clinical consideration in those with the disease. Studies investigating the relationship between self-reported antioxidant intake and risk of glaucomatous disease have reported conflicting results. Preliminary studies investigating the relationship between self-reported glaucoma diagnosis and consumption of the oxidants calcium and iron suggest a possible relationship indicating increased risk of the disease with increased consumption of these dietary factors. Initial reports in the literature suggest a potential role for dietary modification in the treatment of glaucomatous optic neuropathy. Further study, with randomized controlled trials, may be necessary to further characterize these relationships.

Adolescents and caffeine containing beverages: To take or not to take energy drinks?

Energy drinks (EDs) are beverages marketed to improve energy, weight loss, attention, athletic performance, and concentration. Caffeine is the main active ingredient in EDs; many of them contain 70–80 mg of caffeine for a 33 cl serving. Heavy caffeine consumption, such as drinking EDs, has been associated with serious consequences such as seizures, mania, stroke, and sudden death. Adolescent's and child's caffeine consumption should not exceed 100 mg/day and 2.5 mg/kg/day, respectively. The daily caffeine's intake should take account of all sources of this substance (coffee, tea, soft and energy drinks). Objective: (1) To investigate the extent of energy drink consumption in adolescents; (2) to understand the reasons why teens’ consumption is widespread; (3) to estimate the amount of daily caffeine taken from coffee and beverages containing caffeine (including EDs). Methods: A self-report questionnaire related to EDs’ consumption has been developed and then proposed to 1232 students aged 12–19 years old (mean age 14.8 ± 3.8). The data have been collected and then analyzed. Results: According to our surveys, EDs are consumed by 378/1232 (30.7%) of subjects; among them 27/378 (7.1%) drink these beverages 1 time/day at least, 122/378 (32.3%) 1–2 times/week and 179/378 (47.3%) 1–2 times/month. Most of them, 341/378 (90.2%) admit to consume EDs for the flavour, 147/378 (38.9%) find them refreshing, 68/378 (18%) and 39/378 (10.3%) declare to achieve an improvement in sports performance and intellectual activity, respectively. 270/378 (71.4%) of participants declare to consume these beverages when outside, 106/378 (28%) at meals, 74/378 (19.6%) in front of TV/PC, only 39/378 (10.3%) at school and 38/378 (10%) during or after physical exercise. We have also evaluated the amount (in mg) of caffeine (from coffee and caffeinated beverages) taken daily. Among consumers of caffeine (891/1232 – 72.3%), 495/891 (55.5%) consume less than the daily maximum level allowed, 265/891 (29.7%) consume between 100 and 200 mg/day of caffeine and 131/891 (14.7%) exceed the maximum dose, consuming daily more than 200 mg and up to 300 mg/day. Conclusions: Our data show that, among a pediatric population consuming caffeine, 396/891 of subjects (44.4%) exceeded the maximum recommended dose. Pediatricians should be aware of the possible effects of EDs and screen for their consumption to educate children and their families to decrease or eliminate the inappropriate use of these beverages.

Enhanced visualization of acute macular neuroretinopathy by infrared imaging and spectral optical coherence tomography

Dear Editor, Acute macular neuroretinopathy (AMNR) is a rare condition of unknown etiology, first described in 1975 by Bos and Deutman.[1] It is characterized by subacute visual impairment that can either be transient or permanent, generally seen in young women, unilaterally or bilaterally.[1,2] Ophthalmoscopically round or oval parafoveal, brown-reddish lesions are typical. Red-free photography, scanning laser ophthalmoscopy (SLO), and optic coherence tomography (OCT) have been introduced for better evaluation of AMNR lesions.[3,4,5] A 22-year-old female patient complained of visual impairment in her right eye for 2 days. She was diagnosed with familial mediterranean fever 14 years ago. Best corrected visual acuity was 2/10 OD and 10/10 OS. Anterior segment examination and intraocular pressure were unremarkable. The pupillary reflex was normal and afferent pupillary defect was not detected. Results of color vision testing with Ishihara plates were 3/15 in the right eye and 15/15 in the left eye. Fundoscopy revealed no obvious changes [Fig. 1a]. However, there was a dark macular lesion in 1 disc diameter on the infrared reflectance (IR) image [Fig. 1b]. Fundus autofluorescence findings were unremarkable for both eyes [Fig. 1c]. Fundus fluorescein angiography (FFA) with Heidelberg retinal angiography-2 showed subtle retinal pigment epithelium defect [Fig. 1d]. Visual field analysis with Goldmann perimetry showed paracentral scotoma. Macular evaluation with spectral OCT revealed disruption of IS/OS junction and thinning of outer nuclear layer with increased reflectivity [Fig. 1e]. Figure 1 (a) Fundus examination showed normal macular appearance. (b) The infrared imaging demonstrated sharply demarcated dark macular lesion. (c) Fundus autofluorescence imaging was normal. (d) Fundus fluorescein angiography was almost normal except a subtle ... On the first month of presentation, best corrected visual acuity (BCVA) was 3/10, color vision testing was 15/15 with Ishihara plates in the affected eye; there was neither pupillary reflex abnormality nor afferent pupillary defect. OCT showed thinning of the outer nuclear layer with subfoveal IS/OS disruption. After 3 months, BCVA was 3/10 in the right eye. IR imaging showed attenuation of the lesion [Fig. 2a]. Spectral OCT demonstrated realignment of the outer photoreceptor layer and the IS/OS junction besides focal thinning of the outer nuclear layer [Fig. 2b]. Figure 2 (a) The infrared imaging demonstrated attenuation of the dark lesion 3 months after onset. (b) Spectral OCT showed realignment of IS/OS junction but a focal thinning of outer nuclear layer AMNR is a rare condition that had been reported primarily among young women in their child-bearing ages.[1] Several risk factors were defined like hypertension, acute inflammatory processes, oral contraceptive use, eclampsia, heavy caffeine consumption, trauma, postpartum hypotension, and hypotensive shock.[1,2] The diagnosis was complicated in our patient because the typical lesion was not evident biomicroscopically. Fluorescein angiography was almost normal. However, with the IR imaging mode of high resolution angiography (HRA) 2, the lesion became evident. While AMNR was first believed to involve the inner retina, later studies using OCT demonstrated that the outer retina is primarily affected.[4,5] High-speed ultrahigh resolution OCT images showed focal depression of the external limiting membrane, IS/OS junction, photoreceptors, and retinal pigment epithelium. The inner retina appeared normal.[4] In our case, spectral OCT demonstrated disruption of IS/OS junction and thinning of the outer nuclear layer with increased reflectivity at initial examination. During follow-up, hyper-reflectivity disappeared, but the visual acuity remained unchanged and a focal thinning of the outer nuclear layer persisted. In conclusion, the diagnosis of AMNR remains a challenge due to subtlety in retinal changes and rarity of the disease.

More on ADORA

Letter to the editors of Psychopharmacology: We recently published a review on genetic factors influencing responses to caffeine and consumption of caffeine (Yang et al. 2010). Unfortunately, our review went to press just before an important additional paper was published on this topic (Rogers et al. 2010). Here, we attempt to integrate the new findings from Rogers et al. with the conclusions of our review. The recently published study by Rogers et al. (2010) investigated whether single nucleotide polymorphisms (SNPs) associated with caffeine-induced anxiety might also affect habitual caffeine intake and whether habitual intake moderates the anxiogenic effect of caffeine. The experiment examined associations between SNPs in two adenosine receptors (ADORA2A and ADORA1) and caffeine-induced anxiety in non-consumers/light consumers and medium/ heavy consumers of caffeine. Consistent with previous reports (Alsene et al. 2003; Childs et al. 2008), the researchers found an association between the T/T genotype of rs5751876 (p=0.002) and caffeine-induced anxiety. Similar results were found for rs3761422 (p=0.004), which is in strong linkage disequilibrium with rs5751876. There were no associations with other SNPs in the eight ADORA2A loci (α= 0.00625, adjusted for multiple testing) or the seven ADORA1 loci (α=0.00714) tested. However, this effect was moderated by habitual consumption. All non-consumers/light consumers exhibited significant increases in anxiety after caffeine while medium/heavy consumers did not, regardless of genotype. Contrary to their hypothesis, total caffeine consumption did not differ among different genotypes. Thus, it appears that while rs5751876 is associated with anxiety after caffeine, this effect may be moderated by habitual consumption such that regular consumers develop tolerance to the anxiogenic effects of caffeine. The authors conclude that susceptibility to caffeine-induced anxiety does not appear to influence levels of habitual caffeine intake. These findings corroborate some previous findings (Childs et al. 2008, Alsene et al. 2003), but are inconsistent with another study (Cornelis et al. 2007). The association between rs5751876 T/T genotype and caffeine-induced anxiety is consistent with reports by Childs et al. (2008) and Alsene et al. (2003); however, the lack of association between this genotype and caffeine consumption is not consistent with findings reported by Cornelis et al. (2007), who found that rs5751876 T/T individuals, particularly smokers, consumed less caffeine. The two studies were conducted in very different populations: the Rogers study recruited healthy Caucasian Europeans with mean age of 30–35 years, whereas the Cornelis study tested Costa Rican survivors of myocardial infarction with mean age of 56– 57 years. Therefore, other factors such as age and survival differences may have contributed to the observed effects of ADORA2A genotype on caffeine consumption. The finding that frequent consumers of caffeine report less anxiety than lighter consumer, regardless of genotype, can be explained by several factors. First, in heavy caffeine consumers, the potential anxiogenic effects of acute doses of the drug may be masked by presence of, and relief from, caffeine A. Yang : E. Childs :A. A. Palmer :H. de Wit (*) Department of Psychiatry and Behavioral Neuroscience, University of Chicago, 5841 S. Maryland Ave, MC 3077, Chicago, IL 60637, USA e-mail: hdew@uchicago.edu

Nocturnal awakenings and difficulty resuming sleep: Their burden in the European general population

Objectives To (1) define the prevalence and importance of nocturnal awakenings (NA) in the general population, and (2) investigate its associations with daytime impairment, physical diseases, and psychiatric disorders. Methods This is a cross-sectional telephone study conducted in the general population of France, United Kingdom, Germany, Italy, and Spain. A representative sample consisting of 22,740 non-institutionalized individuals aged 15 or over was interviewed regarding sleeping habits, health, sleep and mental disorders. Nocturnal awakenings were evaluated according to their frequency per week and per night and their duration. Results At the time of the interview, 31.2% (95% confidence interval: 30.6–31.8%) of the sample reported waking up at least 3 nights per week and 7.7% (7.4% to 8.0%) of the sample had difficulty resuming sleep (DRS) after they woke up. Duration of the symptom was longer than one year in 78.8% of the cases. DRS had greater impacts on daytime functioning than any other kind of NA or other insomnia symptoms with odds ratios five to seven times higher than individuals waking up once or twice within the same night. Individuals with painful physical condition or with a psychiatric disorder were more than four times more likely to have DRS. Other significant factors associated with NA were hypertension, cardio-vascular disease, upper airway disease, diabetes, and heavy caffeine consumption. Conclusions Nocturnal awakenings are highly prevalent in the general population and strongly associated with various physical diseases and psychiatric disorders. There is also a dose response effect in the associations: odds ratios increased with the number of awakenings during the same night and the difficulty resuming sleep once awakened. The study shows that nocturnal awakenings are complex and should be assessed systematically.

Personality traits associated with caffeine intake and smoking

Objectives Some studies find a relationship between certain personality traits, as impulsivity or sensation seeking, and caffeine consumption, but these studies do not consider the potential confounding effect of smoking on caffeine intake, a co-occurrence that has been well demonstrated in epidemiological and clinical studies. The main objective of this cross-sectional study was to analyze the association of personality with caffeine intake controlling for the effects of smoking; a secondary objective was to explore the effect of caffeine intake on the previously known relationship between personality and smoking. Methods A sample of 498 adults answered a self-questionnaire including socio-demographic variables, and items regarding consumption of tobacco and caffeine. Personality was measured by the Temperament and Character Inventory (TCI-125). We analyzed the association of personality traits with both caffeine intake and smoking, controlling the possible confounding effects of sex, age and each substance with the other one. Results Logistic regression analyses showed that the temperamental dimension of novelty seeking was associated with heavy caffeine consumption (> 200 mg/day) (adjusted OR = 2.0; 95% CI: 1.1–3.9), controlling for the effect of smoking. Moreover, novelty seeking was associated with both smoking (adjusted OR = 1.8; 95% CI: 1.1–2.9) and heavy smoking (> 20 cigarettes/day) (adjusted OR = 1.8; 95% CI: 1.0–3.7), after controlling for the effect of caffeine intake. Conclusion Our study offers an epidemiological evidence of the relationship of novelty seeking, considered to be associated with low basal dopaminergic activity, with both nicotine consumption and heavy caffeine intake, two substances that enhance dopaminergic neurotransmission.

Fewer but heavier caffeine consumers in schizophrenia: A case-control study

According to the literature, there is an association between schizophrenia and caffeine consumption, but it is not clear whether schizophrenia is associated with either higher prevalence of daily caffeine intake or the amount consumed. In this study we compared our previously published schizophrenia patients ( n = 250) with a control sample ( n = 290) after controlling for demographic variables and tobacco and alcohol consumption. Current caffeine intake was less frequent in schizophrenia patients (59%, 147/250) than in controls (70%, 204/290). In the multivariate analyses, caffeine intake was less frequent at an older age and in schizophrenia patients, and more frequent in smokers and alcohol users. Among caffeine consumers, heavy caffeine intake (≥ 200 mg/day) was significantly associated with schizophrenia (64%, 94/147 in schizophrenia versus 36%, 73/204 in controls), as well as older age and smoking. Daily amount of caffeine intake and smoked cigarettes correlated significantly in the schizophrenia group but not in the control group; the correlation of caffeine intake with nicotine dependence was low and non-significant in both groups. The association between current smoking and heavy caffeine intake may be partly explained by a pharmacokinetic effect: tobacco smoke compounds induce caffeine metabolism by the cytochrome P450 1A2. Although schizophrenia by itself may be associated with heavy caffeine intake in caffeine users, part of this association was explained by the association between schizophrenia and smoking. The relationship between caffeine and alcohol intake appeared to be more complex; alcohol and caffeine use were significantly associated, but within caffeine users alcohol was associated with less frequent heavy caffeine consumption among smokers. In future studies, the measurement of plasma caffeine levels will help both to better define heavy caffeine intake and to control for smoking pharmacokinetic effects.

Effects of caffeine on cognitive and autonomic measures in heavy and light caffeine consumers

Caffeine effects on arousal and cognition were assessed in relation to habitual caffeine intake. After drinking either decaffeinated coffee or decaffeinated coffee plus 300 mg caffeine, 22 heavy caffeine consumers (HCCs) and 26 light caffeine consumers (LCCs) were examined on various cognitive, autonomic, and anxiety measures. In LCCs only, caffeine significantly improved performance of the Wisconsin Card Sorting Test, and significantly increased state anxiety scores. Caffeine significantly increased spontaneous skin conductance responses in HCCs and LCCs alike. The HCCs and LCCs did not differ on measures of trait anxiety or neuroticism. Results are discussed in terms of the cognitive enhancing and nonspecific arousing effects of caffeine in relation to caffeine tolerance.

Coffee and doughnut maculopathy: a cause of acute central ring scotomas

AIMSTo report the clinical features of five patients with non-progressive central ring scotomas of acute onset associated with excellent retained visual acuity.METHODSComplete neuro-ophthalmological examinations were performed. Visual fields were performed...

Moderate to heavy caffeine consumption during pregnancy and relationship to spontaneous abortion and abnormal fetal growth: a meta-analysis

The objective was to determine the association of moderate to heavy caffeine consumption during pregnancy on spontaneous abortion and birth weight in humans. Data sources used included a computerized literature search of MEDLINE (1966–July 1996); EMBASE (1988–November 1996); Psychlit I (1974–1986); Psychlit II (1987–1996); CINAHL (1982–May 1996) and manual search of bibliographies of pertinent articles. Inclusion criteria were: English language research articles; pregnant human females; case control or cohort design; documented quantity of caffeine consumption during pregnancy; control group with minimal or no caffeine consumption (0 to 150 mg caffeine/d); documented data regarding spontaneous abortion and/or fetal growth. The exclusion criteria were: case reports; editorials; review papers. The methods section of each study was examined independently by two blinded investigators with a third investigator adjudicating disagreements. Two independent investigators extracted data onto a standardized form. A third investigator adjudicated discrepancies. We compared a caffeine-exposed group (>150 mg/d) and controls (0 to 150 mg/d), using Mantel–Haenszel pooling. Of the 32 studies meeting inclusion criteria, 12 had extractable data (6 for spontaneous abortion, 7 for low birth weight, 1 common study). Mantel–Haenszel odds ratio (CI 95%) was 1.36 (1.29–1.45) for spontaneous abortion in 42,988 pregnancies. The overall risk ratio was 1.51 (1.39–1.63) for low birthweight (<2500 g) in 64,268 pregnancies. Control for confounders such as maternal age, smoking, and ethanol use was not possible. We concluded that there is a small but statistically significant increase in the risks for spontaneous abortion and low birthweight babies in pregnant women consuming >150 mg caffeine per d. A possible contribution to these results of maternal age, smoking, ethanol use, or other confounders could not be excluded.

Heavy caffeine intake in pregnancy and sudden infant death syndrome

AIMSTo examine the association between maternal caffeine consumption during pregnancy and the risk of sudden infant death syndrome (SIDS).METHODSA nationwide case-control study surveying parents of 393 SIDS victims and parents...

Caffeine-induced disturbances of early neurogenesis in whole mouse embryo cultures

In toto mouse embryos were cultivated at embryonic day 8.5 for 26 h with 105, 310 or 620 μM caffeine; 105–310 μM correspond to concentrations transferred by the placenta of heavy caffeine consumers. Failure of neural tube closure, excessive proliferation of neuroepithelial cells and premature evagination of telencephalic vesicles were present in 50% of treated embryos. When reaching the embryonic neural tube before neuronal migration, caffeine regionally modifies the schedule and/or rate of neural cell proliferation.

Three prospective registries to monitor prenatal maternal exposures: the acyclovir in pregnancy, the antiretroviral pregnancy and the lamotrigine in pregnancy registries

The objective was to determine the association of moderate to heavy caffeine consumption during pregnancy on spontaneous abortion and birth weight in humans. Data sources used included a computerized literature search of MEDLINE (1966–July 1996); EMBASE (1988–November 1996); Psychlit I (1974–1986); Psychlit II (1987–1996); CINAHL (1982–May 1996) and manual search of bibliographies of pertinent articles. Inclusion criteria were: English language research articles; pregnant human females; case control or cohort design; documented quantity of caffeine consumption during pregnancy; control group with minimal or no caffeine consumption (0 to 150 mg caffeine/d); documented data regarding spontaneous abortion and/or fetal growth. The exclusion criteria were: case reports; editorials; review papers. The methods section of each study was examined independently by two blinded investigators with a third investigator adjudicating disagreements. Two independent investigators extracted data onto a standardized form. A third investigator adjudicated discrepancies. We compared a caffeine-exposed group (>150 mg/d) and controls (0 to 150 mg/d), using Mantel–Haenszel pooling. Of the 32 studies meeting inclusion criteria, 12 had extractable data (6 for spontaneous abortion, 7 for low birth weight, 1 common study). Mantel–Haenszel odds ratio (CI95%) was 1.36 (1.29–1.45) for spontaneous abortion in 42,988 pregnancies. The overall risk ratio was 1.51 (1.39–1.63) for low birthweight (<2500 g) in 64,268 pregnancies. Control for confounders such as maternal age, smoking, and ethanol use was not possible. We concluded that there is a small but statistically significant increase in the risks for spontaneous abortion and low birthweight babies in pregnant women consuming >150 mg caffeine per d. A possible contribution to these results of maternal age, smoking, ethanol use, or other confounders could not be excluded.

Caffeine Consumption during Pregnancy and Spontaneous Abortion

We conducted a case-control study of spontaneous abortion in Santa Clara County, California between 1986 and 1987. We analyzed data on 607 cases and 1,284 controls to evaluate the potential association between caffeine consumption during the first trimester of pregnancy and spontaneous abortion. About 70% of the women consumed caffeinated coffee, tea, and/or soda; 7% of the women consumed more than an average of 300 mg of caffeine daily. The crude odds ratio (OR) for heavy caffeine consumption (greater than 300 mg/day) was 1.55 (95% CI: 1.04-2.31), which decreased to 1.22 (95% CI: 0.80-1.87) after controlling for confounding factors. For these heavy users, nausea modified the association of spontaneous abortion and caffeine; heavy caffeine consumers reporting nausea had a doubled risk for spontaneous abortion (adjusted OR = 2.10, 95% CI: 1.20-3.70), in contrast to those who did not report nausea (adjusted OR = 0.53, 95% CI: 0.27-1.04). Heavy caffeine consumers who decreased their caffeine intake early in pregnancy had a risk of spontaneous abortion similar to that of nonconsumers.

Caffeine consumption during pregnancy and fetal growth.

The purpose of this study was to examine the association between maternal caffeine consumption and low birthweight, intrauterine growth retardation, and prematurity, adjusting for multiple confounders. Data obtained from birth certificates and interviews on 1,230 women with singleton live births were analyzed to evaluate the potential influence of caffeine consumption during the first trimester on fetal growth. The crude odds ratio for intrauterine growth retardation in infants of women reporting heavy caffeine consumption (greater than 300 mg/day) was 3.86 (95% CI = 1.80, 8.40) which decreased to 2.90 (95% CI = 1.23, 6.87) after controlling for confounding factors. The adjusted odds ratio for low birthweight and heavy maternal caffeine consumption was also elevated (OR = 2.05; 95% CI = 0.86, 4.88). Women who reduced their caffeine intake from greater than 300 mg/day to less than that early in pregnancy had lower risks of delivering infants with either intrauterine growth retardation or low birthweight than women who continued to consume that amount. Preterm delivery appeared to be unrelated to caffeine consumption. Taken together with studies reporting similar findings, these results suggest that heavy caffeine consumption increases the risk for fetal growth retardation.