Scientific literature cites a wide range of values for caffeine content in food products. The authors suggest the following standard values for the United States: coffee (5 oz) 85 mg for ground roasted coffee, 60 mg for instant and 3 mg for decaffeinated; tea (5 oz): 30 mg for leaf/bag and 20 mg for instant; colas: 18 mg/6 oz serving; cocoa/hot chocolate: 4 mg/5 oz; chocolate milk: 4 mg/6 oz; chocolate candy: 1.5–6.0 mg/oz. Some products from the United Kingdom and Denmark have higher caffeine content. Caffeine consumption survey data are limited. Based on product usage and available consumption data, the authors suggest a mean daily caffeine intake for US consumers of 4 mg/kg. Among children;’younger than 18 years of age who are consumers of caffeine-containing foods, the mean daily caffeine intake is about 1 mg/kg. Both adults and children in Denmark and UK have higher levels of caffeine intake. 
This chapter provides details about the production, trade, and consumption of caffeine, which is probably the world’s most widely used drug. The focus is on caffeine derived from coffee, which accounts for about 54% of all caffeine use, because other chapters in the volume give details of tea and cocoa consumption. Tea accounts for about 43% of all caffeine consumption. Total world caffeine consumption in 1981 was estimated to be approximately 120,000 tonnes, equivalent to 70 mg a day for each inhabitant. The per capita rate of caffeine use in Canada and the United States is approximately three times that for the world as a whole, but only half that of a heavy coffee-consuming country such as Sweden or a heavy tea-consuming country such as the United Kingdom. 
Genetics of caffeine consumption and responses to caffeine
Caffeine is widely consumed in foods and beverages and is also used for a variety of medical purposes. Despite its widespread use, relatively little is understood regarding how genetics affects consumption, acute response, or the long-term effects of caffeine.
This paper reviews the literature on the genetics of caffeine from the following: (1) twin studies comparing heritability of consumption and of caffeine-related traits, including withdrawal symptoms, caffeine-induced insomnia, and anxiety, (2) association studies linking genetic polymorphisms of metabolic enzymes and target receptors to variations in caffeine response, and (3) case-control and prospective studies examining relationship between polymorphisms associated with variations in caffeine response to risks of Parkinson’s and cardiovascular diseases in habitual caffeine consumers.
Twin studies find the heritability of caffeine-related traits to range between 0.36 and 0.58. Analysis of polysubstance use shows that predisposition to caffeine use is highly specific to caffeine itself and shares little common disposition to use of other substances. Genome association studies link variations in adenosine and dopamine receptors to caffeine-induced anxiety and sleep disturbances. Polymorphism in the metabolic enzyme cytochrome P-450 is associated with risk of myocardial infarction in caffeine users.
Modeling based on twin studies reveals that genetics plays a role in individual variability in caffeine consumption and in the direct effects of caffeine. Both pharmacodynamic and pharmacokinetic polymorphisms have been linked to variation in response to caffeine. These studies may help guide future research in the role of genetics in modulating the acute and chronic effects of caffeine.
High-dose Caffeine Intrauterine Exposure Altered Neuronal Morphology and Spatial Distribution in Murine Models Cerebral Cortex
Caffeine is a neurostimulant that is globally consumed with little or no restrictions by various groups of people. Though concerns have been raised over the possible effects of caffeine exposure during intrauterine life or pregnancy; there are not enough empirical evidences to establish the specific potential effects of caffeine exposure on the devolvement and the functions of the brain. The current investigation examined the possible effects of caffeine exposure at various dosages modelled after human consumption quantities in murine models. The experimental animals- pregnant mice, were grouped into four and labelled A, B, C and D respectively. Anhydrous caffeine was dissolved in distilled water and administered to animals daily using oral gavages. The Control Group was labelled A and the pregnant mice were fed ad libitum throughout the experiment to serve as the reference and normal in the context of results interpretation; the Group B animals were administered the moderate caffeine dosage [10 mg/kg body weight]; Group C received moderately high dosage [50 mg/kg body weight] and the Group D received the excessively high caffeine dosage [120 mg/kg body weight] throughout pregnancy- from the day 1 of pregnancy to parturition. The mice litters were allowed to develop until Day 12 Postnatal life, and then sacrificed. The brain tissues were excised and processed using the Haematoxylin and Eosin histological technique. Histomorphological results showed that caffeine exposure at the excessively high dosage altered neuronal morphology and spatial distribution with evidence of limitations in dendritic and axonal development and elaboration. Caffeine at the lower dosages showed potentials to mildly influence neuronal spatial distribution; with glias not showing extensive morphological or spatial alterations. 
In vivo Evidence of Mice Hippocampal Alterations Resulting from High Dose Caffeine Exposure during Intrauterine Life
Caffeine ingestion during pregnancy requires attention and investigation towards assessing the level of safety and possible effects on the brain and mental health. Caffeine ingestion during pregnancy has been discouraged despite concerns about lack of adequate facts to support this presumption and that such position is being taken based on speculations or inadequate facts. To this end, this research investigated the effects of caffeine exposure on hippocampus at various dosages during intrauterine life. Eighteen pregnant mice were divided into three groups A-C. Group A were fed ad libitum on mice feed pellets throughout the experimental duration to serve as control. Group B were administered the lower dosage [50 mg/kg body weight] of caffeine while Group C were administered high dosage [120 mg/kg body weights] of caffeine during intrauterine life by oral gavage. Brain tissues of the animals were excised after being sacrificed by cervical dislocation at Day 12 of postnatal life. The tissues were processed using the Haematoxylin and Eosin staining technique and the results were subject to histomorphological analysis. Caffeine at the high dosage substantially compromised hippocampal formation and dentate gyrus structural integrity; particularly by limiting cellular differentiation and elaboration of the cells. The differentiation of neurons into the typical pyramidal cells of the hippocampus was largely limited. 
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 Yang, A., Palmer, A.A. and de Wit, H., 2010. Genetics of caffeine consumption and responses to caffeine. Psychopharmacology, 211(3), pp.245-257.
 Owolabi, J.O., Olatunji, S.Y. and Olanrewaju, A.J., 2016. High-dose Caffeine Intrauterine Exposure Altered Neuronal Morphology and Spatial Distribution in Murine Models Cerebral Cortex. Journal of Applied Life Sciences International, pp.1-10.
 Owolabi, J.O., Olanrewaju, A.J. and Olatunji, S.Y., 2016. In vivo Evidence of Mice Hippocampal Alterations Resulting from High Dose Caffeine Exposure during Intrauterine Life. Journal of Advances in Biology & Biotechnology, pp.1-7.