Coffee Intake and obesity

C H A P T E R

24 Coffee Intake and obesity Gustavo D. Pimentel*, Thayana O. Micheletti*, Renata C. Fernandes*, Astrid Nehlig† *

Clinical and Sports Nutrition Research Laboratory (LABINCE), Faculty of Nutrition, Federal University of Goia´s (UFG), Goia´s, Brazil †French Medical Research Institute, INSERM U 663, Faculty of Medicine, Strasbourg, France

O U T L I N E Obesity, Coffee Consumption, and Its Compounds

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Coffee and Reduction of Obesity Risk: A Vision From Epidemiological Studies

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Coffee and Its Components

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Coffee and the Mechanisms That Underlie the Protective Effects Against Obesity Appetite Regulation, Satiety, and Hormone Sensitivity

335 335

Thermogenesis, Lipid Metabolism, and Lipolysis Antiinflammatory Actions Cardiovascular Protections Microbiota and Other Possible Mechanisms

337 339 343 344

Potential Adverse Effects of Coffee Effects of Coffee on BP Effects of Coffee on Cholesterol

344 344 345

Conclusion

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References

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OBESITY, COFFEE CONSUMPTION, AND ITS COMPOUNDS Obesity is classified as an excess of body fat and defined when the body mass index (BMI) achieves 30 mg/kg. Estimation of prevalence and secular trend for obesity from 1960 to 2025 is increasing in several countries; for example, it is estimated that by 2025, 45% of the population of the United States will be obese, and this figure will reach 28% in England, and 25% in Brazil.1

Nutrition in the Prevention and Treatment of Abdominal Obesity https://doi.org/10.1016/B978-0-12-816093-0.00024-0

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# 2019 Elsevier Inc. All rights reserved.

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In the midst of the obesity consequences are insulin resistance, inflammation, dyslipidemia, high blood pressure (BP), liver injury among others. In addition, these disturbances can be aggravated by the consumption of excess calories, saturated and trans fatty acids2–6 leading to cardiovascular diseases (CVDs).7 Even though genetic factors may play a role in the etiology of obesity,8–10 there is now convincing evidence that obesity is strongly associated with modifiable factors, such as diet and exercise. Likewise, in the 1950s Linus Pauling established an opposite association between obesity and longevity.11 At same time, the first evidence of a link between coffee and body weight was published. However, these findings were contradictory; indeed, it was observed that the intake of coffee decreased liquid intake and led to body weight reduction12; however, it has been clearly shown that low coffee intake does not reduce water consumption or body weight. In the 1960s, two other studies13,14 also showed contradictory effects, but there were methodological errors, namely in the first study a lean group was treated with 400 mg/kg caffeine and the obese/hyperglycemic group only with 80 mg/kg13 and in the second study, diabetic humans treated with caffeine had increased serum glucose levels, but some individuals consumed frequently a hypoglycemiant drink.14 In the mid-1960s and 1970s, beneficial actions of coffee and caffeine intake on glucose homeostasis and atherosclerotic disease were first reported.15–17 After 1970, several epidemiological, physiological, and molecular studies tried to understand how coffee and its compounds improve the metabolic consequences of obesity. Likewise, coffee has been very consumed by the population of many countries.18–21 According to International Coffee Organization,22 the current annual coffee consumption is highest in Europe (2.4–12.0 kg/person/year), followed by South America (0.8–6.8 kg/person/year), North America and Oceania (2.4–4.5 kg/person/year), Central America (0.8–4.5), and Asia (
0.8–4.5 kg/person/year) and Africa (
0.8–2.4 kg/person/year) (Fig. 1). When considering caffeine, the main component of coffee, the mean caffeine intake per capita in the Western society reaches 300 mg per day, coming mainly from dietary sources such as coffee, tea, cola drinks, and chocolate.23 Data from the National Health and Nutrition Examination Surveys (NHANES III) showed that the American population consumes roughly 236 mg caffeine per day from coffee and tea.18 However, in Brazil the data are scarce.24 Thus, the coffee and caffeine consumption is largely appreciated as dietetic compounds potentially able to reduce chronic diseases risk, for instance obesity and its complications.25–28 The beneficial effects of the several kinds of coffee are probably a composite action of various coffee compounds such as caffeine, antioxidant phenolic compounds, minerals, vitamins, and fibers. Consequently, the coffee constituents might have the potential to improve the deleterious factors of obesity, such as dyslipidemia, inflammation, hypertension, insulin and leptin resistance, and modified gut microbiota.

COFFEE AND REDUCTION OF OBESITY RISK: A VISION FROM EPIDEMIOLOGICAL STUDIES The association between coffee and the risk of developing obesity has been repeatedly studied. Data from prospective and cohort studies indicate an inverse association between coffee consumption and the obesity consequences independently of race, age, or gender. IV. FOODS AND MACRONUTRIENTS IN OBESITY

2.4 – 4.5 kg

2.4 – 12.0 kg

≤ 0.8 – 4.5 kg

0.8 – 4.5 kg 2.4 – 4.5 kg

≤ 0.8 – 6.8 kg

FIG. 1

Current annual coffee consumption per capita per year in the world.

≤ 0.8 – 2.4 kg

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Central obesity along with hyperglycemia, hypertension, increased serum triacylglycerol (TAG) and decreased high-density lipoprotein (HDL) cholesterol characterize risk factors components of the metabolic syndrome (MS). MS is characterized by the coexistence of these risk factors and may contribute to a fivefold increase in the risk of type 2 diabetes mellitus (DM2) and double the risk of developing CVD over 5–10 years.29 MS a condition that affects 20%–25% of adult global population and a lower risk of developing MS and T2DM in coffee consumers has been reported in epidemiological studies. A meta-analysis of eight studies, published up to 2016, reported that individuals with the highest coffee consumption were 13% less likely to develop MS.30 Chlorogenic acids (CGAs) are the main phenolic compounds in coffee. Studies in humans demonstrate that CGA is able to reduce BP and postprandial glucose uptake. In another study we compared the consumption of 40 g/day of green or black coffee in 18 healthy subjects for 2 weeks. There was a significant decrease in systolic blood pressure (SBP), body weight and BMI, diastolic blood pressure (BDP), waist circumference, and abdominal fat after the two interventions.31 When considering coffee intake and DM2, since 2002 several epidemiological studies19,26,27,32–41 have been showing that regular coffee consumption reduces the risk of developing DM2. Indeed, as outlined in Table 1 subjects who drank between two and three cups of coffee daily had an approximately 25% lower risk to develop diabetes than those who did not drink more than one cup per day. Those who drank than 4–6 cups per day has a risk reduction of 35% which increased with the number of cups up to 55% in those who drank more than 10 cups per day. A set of meta-analyzes have established a relationship between coffee consumption and the incidence of diabetes based on six investigations including a total of 225,516 individuals. The results showed that total coffee consumption was inversely correlated with the incidence of diabetes (RR D 0.93, 95% CI 0.91–0.95).42 An additional meta-analysis of 12,586 Brazilians observed a correlation between coffee intake of at least two cups per day and a 23% reduction in the diagnosis of diabetes.43 Additionally, the majority of studies showed that the protective effects of coffee can be found either with caffeinated, decaffeinated, or filtered coffee. The risk reduction of DM2 by coffee is rather observed after long-term consumption, i.e., over 12 consecutive months.44–46 TABLE 1 Summary of all Prospective and Cohort Studies That Showed Reduction of Type 2 Diabetes Mellitus Risk With Coffee Intake Dose (Cupsa per day)

% Reduction DM Riskb

0–1

No protection

2–3

25

4–6

35

6

42

10

55

a b

Cup of 150 mL, with average of 60 mL of caffeine, besides of other compounds from coffee. Approximate values.

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Although some studies prove the benefits of coffee consumption in glucose metabolism, this is a controversial topic. New evidence suggests that the effects on body and the amount of coffee and caffeine ingested can also be influenced by genetic factors.47,48 Genome-wide association studies (GWAS) have demonstrated that genetic variations in the cytochrome P450 1A1 and 1A2 and aryl-hydrocarbon receptor (AHR) gene affect caffeine metabolism and modulate the coffee and caffeine outcomes. The enzyme CYP1A2 is responsible for approximately 95% of hepatic caffeine clearance in the liver and AHR is responsible for inducing CYP1A1 and CYP1A2 transcription. Thus, the single-nucleotide polymorphism (SNP) can modify the enzymatic activity and accelerate (homozygous for the CYP1A2*1A/*1A genotype) or slow down (carriers of the * 1F allele) caffeine’s metabolism. Studies have shown an association between coffee intake and increased risk of glucose intolerance49 and metabolic complications50, 51 in individuals who have the polymorphism (carriers of the * 1F allele) and are slow caffeine metabolizers. Regarding coffee consumption and reduction of MS indicators, several studies reported that the main pillars of this improvement are both weight and adiposity loss52–56 while caloric intake has less or no significance.57 Besides, it is likely that the reduction of body weight by coffee consumption might be one of the main factors responsible for the reduction of DM2 risk. In this respect, we have carried out in adults and adolescents a lifestyle program leading to weight loss and consequently diminishing the serum levels of cholesterol, endotoxin, insulin, TAGs and leptin, and increasing adiponectin, hence reducing the MS indicators.4,58–60 Some epidemiological studies also support the hypothesis that habitual coffee consumption is associated with reduction of a variety of obesity indicators, in particular the improvement of glucose tolerance, lipid profile, and resistance to insulin, leptin and adiponectin hormones.

COFFEE AND ITS COMPONENTS Among coffee components, caffeine has received most attention due to its physiological and pharmacological properties, mainly regarding its effect on DM2, obesity and CVDs,26,27,35,40,43,44,46 as well as others obesity-unlike diseases.61–65 Physiologically, caffeine can be entirely absorbed by the stomach and small intestine within 45 min after consumption and it reaches maximal concentration in the bloodstream in 15–120 min.66 Recently, it was shown that the caffeine and it metabolites are found in the blood after moderate coffee intake.67 Once absorbed, caffeine is distributed throughout the whole body.68 A linear correlation between the concentrations of caffeine in blood and brain (r ¼ 0.86) and between concentrations in plasma and kidney (r ¼ 0.91) was observed.69 Furthermore, caffeine can cross the placenta and be available in the mother’s milk.70 Caffeine metabolism takes place in the liver, starting by the removal of the methyl 1 and 7 groups in a reaction catalyzed by cytochrome P450, enabling the formation of three methylxanthines: paraxanthine (84%), theobromine (12%), and theophylline (4%). Each component has a different role in human physiology; in particular, paraxanthine increases lipolysis; theobromine stimulates blood vessel dilatation and increases urine volume; and theophylline controls glucose metabolism.71

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TABLE 2 Caffeine Levels of Select Foods and Drinks Food or Drink

Caffeine (mg)

Regular coffee, brewed from grounds, caffeinated

a

95 a

Regular coffee, brewed from grounds, decaffeinated a

509

Coffee, brewed, espresso a

62

Regular instant coffee

a

Decaffeinated instant coffee b

2 29

Carbonated beverage, cola b

108

Energy drink

c

9

Milk chocolate bar Yerba mate tea

2

a

78

a

55

Black tea

a

35

Green tea a

Cup of 237 mL or 8 fl oz. Can of 355 mL or 12 fl oz. c Bar of 44 g or 1.55 oz. USDA. Agricultural Research Service, 200776and others.74,75 b

Blood levels of caffeine or its metabolites reflect coffee intake in the preceding hours.67,72 Nevertheless, caffeine intake may not correlate strongly with coffee intake, as it also depends on the intake of other sources of caffeine, such chocolate, energy drink, cola soft drinks, and others. Caffeine concentrations from coffee are highest when compared to tea, soft drinks, and energy drinks.73 After of coffee, yerba mate tea (Ilex paraguarienses) is considered the tea that contains more caffeine, e.g., 237 mL of yerba mate tea contain 78 mg and 237 mL of black or green tea 55 and 35 mg of caffeine, respectively.74,75 The approximative caffeine content of some foods and drinks is summarized in Table 2. The Canadian Clinical Practice Guidelines77 reported that for the average adult, a daily caffeine intake of 400–450 mg is not associated with any adverse effects. The recommendation for pregnant women and those who are breastfeeding is reduced to 300 mg/day; and for children, it depends on age (Table 3). TABLE 3

Recommendation for Daily Caffeine Intake According to Age

Individuals

Caffeine (mg)

Children

–

4–6 year old

45.0

7–9 year old

62.5

10–12 year old

85.0

Adults

400

Pregnant/breastfeeding women

300

77

Canadian Clinical Practice Guidelines.

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COFFEE AND THE MECHANISMS THAT UNDERLIE THE PROTECTIVE EFFECTS AGAINST OBESITY At the moment, several mechanisms of action that underlie coffee intake and the potential role of its components have been proposed for the improvement of obesity metabolic consequences. Mechanistic studies are discussed below.

Appetite Regulation, Satiety, and Hormone Sensitivity The hypothesis that habitual coffee consumption improves peripheral metabolism consequences is related to numerous mechanisms as its likely effects on hormones, adiposity, and appetite regulation, which are important modulators of obesity. Lopez-Garcia et al.,78 in a study of 12-year follow-up assessing both men and women showed that individuals who consumed coffee lost more weight than those who did not. A randomized, placebo-controlled, and double-blind study with overweight men and women showed that a high-caffeine diet (524 mg per day) reduces body weight, fat mass, and waist circumference, and increases satiety compared with a low-caffeine diet (151 mg per day).79 Increased caffeine consumption (511 mg per day) leads to higher satiety than low caffeine intake (149 mg per day).80 Recently, an American study demonstrated that consuming a beverage containing caffeine and catechins from green tea in combination with soluble fiber reduced the caloric consumption in the next meal.81 Furthermore, other studies suggest that yerba mate, a tea type with large content of caffeine reduces food intake and increases serum glucagon-like peptide 1 (GLP-1) levels.5,82 Additionally, coffee influences the secretion of gastrointestinal peptides, gastric inhibitory polypeptide (GIP) and GLP-1, lowering glucose absorption in the small intestine,83–85 and activating central anorexigenic neurons (POMC/CART). Moreover, the secretion of these gut hormones seems to reach the hypothalamus and inhibit the orexigenic neurons (AgRP/NPY).86–88 Likewise, McCarty89 reports higher GLP-1 release after consumption of drinks containing CGA, such as coffee. Another suggested mechanism is the direct stimulation of pancreatic beta cells by caffeine and theophylline.90 Recently, the van Dam’s group observed an increase in GLP-1 concentrations 30 min after consumption of 12 g decaffeinated coffee, 1 g CGA and 500 mg trigonelline compared to the placebo group.91 The same was observed in healthy volunteers, i.e., increased postprandial secretion of GLP-1 after decaffeinated coffee compared with control group (without coffee).85 In Fig. 2, we schematically resumed the effects of coffee and its compounds on appetite regulation, adiposity, β-cell damage, and hormones sensitivity. The beneficial effects of coffee’s compound other than caffeine on obesity should be highlighted. Coffee is a major source of the polyphenol CGA in the human diet and may modulate glucose metabolism by various mechanisms: increasing insulin sensitivity92; attenuating intestinal glucose absorption85; blunting protein tyrosine phosphatase 1B, a negative modulator of the insulin pathway93; inhibiting or retarding the action of α-glucosidase94; inhibiting glucose transporters at the intestinal stage95; reducing or inhibiting glucose-6phosphatase hydrolysis at the hepatic stage, which may reduce plasma glucose output, leading to reduced plasma glucose concentration96–98; stimulating glucose transport in the soleus

IV. FOODS AND MACRONUTRIENTS IN OBESITY

FIG. 2 Schematic diagram showing the effects of coffee and its compounds on the reduction of food intake and insulin resistance. The consumption of coffee, theophylline, or chlorogenic acid leads to several beneficial actions. It (1) increases serum GPL-1 and GIP levels, (2) blunts β-cell damage, (3) increases C-peptide levels, (4) inhibits glucose absorption, (5) reduces blood insulin and glucose concentrations, (6) possibly these effects activate the neuropeptides POMC/CART and reduce NPY/AgRP hence decreasing food intake and insulin resistance.

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muscle and increasing the phosphorylation of the 5’ AMP-activated protein kinase (AMPK) and acetyl-coA carboxylase (ACC) as well as the activation of Akt and translocation of glucose transport protein 4 (GLUT 4) to the plasma membrane99; increasing GLP-1 and GIP levels in blood and improving the oral glucose tolerance test.82,85,89,91,100 Moreover, CGA neutralizes the deleterious effects of free fatty acids on the function of beta cells in insulin resistant overweight subjects.89 These metabolic effects of coffee and its compounds on glucose metabolism are summarized in Fig. 3. Nevertheless, it is important to take into account potential confounding by other foods sources of CGA, such as apples and other fruits.92 Thus, it is suggested that the beneficial effects of coffee on appetite regulation and hormones sensitivity is reached by ingestion of caffeine or the phenolic compound, CGA.

Thermogenesis, Lipid Metabolism, and Lipolysis Among the possible therapeutic targets of coffee are the increase of metabolic rate and energy expenditure.101,102 A study showed that the intake of 300 mg per day of caffeine induced the energy expenditure by 79 kcal per day, maintaining the body weight stable.103 Moreover, other evidence suggests that coffee intake can increase the energy expenditure as well as lipid and carbohydrate oxidation.104 However, a study of the 1980s showed that caffeine stimulates the metabolic rate in both lean and obese subjects, but with greater fat oxidation in lean than obese subjects.101 Another study of the end of the 1980s observed that a single dose of 100 mg caffeine was able to raise the resting metabolic rate mainly in lean, but not in obese individuals.105 Although the thermogenic effects are larger in lean than in obese humans, it is clear that the stimulation of energy expenditure in the treatment of obesity is appropriate as a strategy of nutritional education in clinical practice. Considering that an individual may become overweight with a daily over-intake of approximately 50–100 kcal, the increase of energy expenditure of 80–150 kcal per day could counterbalance such as weight gain.103,104 In addition, the increase of 5% of energy expenditure in obese and 7% in lean subjects is able to control body weight. Additionally the changes of metabolic rate with caffeine consumption also occur through increased skin and internal temperature.102,106 The potential relationship between coffee and energy expenditure has emerged in the 1980s, but has been attributed more recently to the potential mechanisms that could explain the thermogenic effects of coffee. Among the mechanisms are: (1) the inhibition of phosphodiesterase-induced degradation of intracellular cyclic AMP (cAMP), in which cAMP activates proteins of the lipolytic pathway such as protein kinase A (PKA), that phosphorylates the hormone sensitive lipase (HSL), perilipin releasing the free fatty acids available and glycerol to stimulate the adrenoceptor leading to thermogenesis107–111; (2) stimulation of norepinephrine secretion and activation of thermogenesis112,113; and (3) upregulation of the expression of uncoupling proteins (UCP-1, 2, and 3) in brown adipose tissue. The latter effect has been shown both at the level of UCP-2 and 3 in the skeletal muscle of mouse113 and UCP-2 in cell culture114 after consumption of either caffeine or coffee. These UCPs are located inside the mitochondrial membrane and are responsible for dissipating the electrochemical gradient generated by respiratory activity. Thus, the UCPs uncouple the mitochondrial respiration from oxidative phosphorylation producing energy to disperse as heat instead of being used for adenosine tri-phosphate synthesis.107

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FIG. 3 Diagram of metabolic effects of coffee and its compounds on glucose metabolism and insulin signaling. In healthy subjects, insulin binds to it receptors, which phosphorylates at the tyrosine level its substrates (insulin receptor substrates 1 and 2) that activates the phosphatidylinositol 3-kinase (PI3K) leading to serine phosphorylation of Akt that increases glucose transporter (GLUT) to the plasmatic membrane which in turn favors the uptake of glucose by liver cells, muscle, and adipose tissue which is used as energy source. Glucose uptake can also be enhanced via the 50 -AMP-activated protein kinase (AMPK). However, insulin signaling is blocked/impaired and AMPK activity inactivated in obese individuals. Thus, coffee consumption (3 cups of 150 mL per day) or chlorogenic acid is able to activate GLUT proteins and to induce AMPK phosphorylation mainly in adipose tissue, liver, and skeletal muscle.

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Likewise, a study in differentiated 3 T3-L1 adipocytes115 and in humans found a higher lipolytic rate after treatment with caffeine, independently from physical activity level, active lifestyle,116 or not.117,118 Moreover, a recent in vitro study observed that HepG2 cell depleted the TAG content and cholesterol levels through blunting of lipogenesis, mainly of the sterol regulatory element-binding protein genes (SREBP1c and 2), fatty acid synthase (FAS) and stearoyl-CoA desaturase (SCD1), and stimulation of lipolysis via expression of AMPK and ACC.119 However, no changes in lipolysis indicators are found with consumption of decaffeinated coffee.116,120 Therefore, caffeine represents the potential target to induce lipolysis and prevents diet-induced MS in obese rats.121 Taken together, it is possible that both caffeine and coffee increase thermogenesis and lipolysis acting as key modulators on obesity disturbances. In Fig. 4, the main mechanisms of action of coffee and caffeine in the regulation of these mechanisms are illustrated.

Antiinflammatory Actions Recently, the use of coffee as a source of polyphenols and antiinflammatory activity has been recognized worldwide.122,123 These phenolic compounds are derived from plant metabolites that have beneficial advantages against oxidative stress and inflammation-related diseases. The European Prospective Investigation into Cancer and Nutrition (EPIC) study on 36,037 individuals evaluated the consumption of different sources of phenolic acids and found that coffee was the main food source of phenolic acids compared to fruits, vegetables, and nuts.124 A cross-sectional study looking at 2554 male and 763 female Japanese workers showed that coffee intake was negatively associated with blood leptin, TAGs, and C-reactive protein levels.123 Another recent cohort study performed with 4455 Japanese men and 5942 Japanese women reported lower serum C-reactive protein concentrations in individuals that coffee intake.125 In humans, it was also reported that habitual coffee intake may ameliorate alcohol-induced hepatic inflammation, mainly via reduction of C-reactive protein.126 Furthermore, in rodents the treatment with coffee prevents liver fibrosis by means of inhibition of gene expression of the inducible nitric oxide synthase (iNOS), transforming growth factor (TGF)-beta, TNF-α, interleukin-1β, and platelet-derived growth factor (PDGF)-beta in liver tissues, and iNOS in macrophages.127 In addition, Kempf et al.67 demonstrated in 2010 that habitual coffee consumption of eight cups (150 mL per cup) of filtered coffee per day reduced interleukin-18 and 8-isoprostane and increased adiponectin levels compared with individuals who did not consume coffee. A study on women in the Nurses’ Health Study found that the usual consumption of four cups or more per day of caffeine-containing coffee was associated with serum adiponectin concentrations 20% higher than habitual consumption of less than four cups of coffee per day.128 Therefore, it is possible to suggest that a moderate-to-high coffee consumption reduces subclinical inflammation and increases adiponectin, a CVD-linked adipokine. Once activated, adiponectin binding to its receptors (AdipoR1 and AdipoR2) phosphorylates AMPK at 172 threonine which activates peroxisome proliferator-activated receptor gamma (PPARγ) blocking the translocation of nuclear factor kappa B (NFκB) in the nucleus reducing inflammatory cytokines (Figs. 5 and 6). Likewise, it is known in humans that the NFκB action is suppressed through PPARγ activation.129

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FIG. 4 Main mechanisms of action of coffee and caffeine in increased thermogenesis. Coffee and caffeine consumption may increase thermogenesis by: (1) activation in the brown adipose tissue (BAT), liver or skeletal muscle of uncoupling proteins (UCP1, 2, and 3), (2) release of noradrenaline and adrenaline and increase of lipolysis, and (3) inhibition of phosphodiesterase-induced degradation of intracellular cyclic AMP (cAMP), by which cAMP activates proteins of the lipolysis pathway such as protein kinase A (PKA), that phosphorylates the hormone sensitive lipase (HSL) and perilipin releasing free fatty acids available and glycerol to stimulate the adrenoceptors leading to thermogenesis.

FIG. 5 Schematic diagram showing the effects of coffee on the reduction of proinflammatory molecules. In obese patients the inflammatory signaling is activated as demonstrated hereafter. High intake of trans or saturated fatty acids as well lipopolysaccharide (LPS) content in the blood has been demonstrated to induce proinflammatory cytokines production through the nuclear factor kappa B (NFκB) pathway after activation of the toll-like receptor 4 (TLR4). Activation of TLR4 initiates the myeloid differentiation primary-response gene 88 (MyD88)-dependent signaling pathway. Binding of MyD88 to the cytoplasmic domain of TLR4 which activates TNF receptor-associated factor 6 (TRAF6) which is recruited and the IRAK-1 phosphorylation/TRAF6 complex dissociates from TLRs and TRAF6 interacts with various proteins, forming a large complex that leads to activation of transforming growth factoractivated kinase 1 (TAK1). TAK1 phosphorylates the IκB kinase kinase (IKK) complex and phosphorylated IκB is targeted for proteasomal degradation. Thus, NFκB is activated in the p65 subunit and then translocates to the nucleus where it binds to its target genes to produce proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), interleukin 1-beta (IL-1β), interleukin 13 (IL-13), inducible nitric oxide synthase (iNOS), and C-reactive protein. On the other hand, coffee and chlorogenic acid consumption can reduce proinflammatory cytokines in the blood, brain, and peripheral tissues and blunt the TLR4 expression reducing inflammation and obesity consequences.

FIG. 6 Schematic diagram showing the effects of coffee on the reduction of cardiovascular disease indicators, and inflammatory parameters in the bloodstream, liver, and white adipose tissue. Obese patients have frequently high adipose tissue and hepatic steatosis accompanied by higher proinflammatory protein expression. Thus, coffee intake reduces adiposity and steatosis as well as inflammation by inhibiting tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), interleukin 1-beta (IL-1β), total cholesterol, triacylglycerols, glycemia and insulin, and increasing blood adiponectin levels. Adiponectin binding to its receptors (AdipoR1 and AdipoR2) which phosphorylates the 50 AMP-activated protein kinase (AMPK) at threonine 172 that activates the peroxisome proliferator-activated receptor gamma (PPARγ) blocking the translocation of nuclear factor kappa B (NFκB) into the nucleus reducing the inflammatory cytokines.

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Aiming to understand the effects of CGA on inflammation, Shi et al.130 found that this acid diminished the toll-like receptor 4 (TLR-4), myeloid differentiation factor 88 (MyD88), iNOS, cyclooxygenase-2 (COX-2), NFκB activation, various proinflammatory cytokines in rats with carbon tetrachloride (CCl(4))-induced liver fibrosis. Additionally, in women with DM2, higher caffeinated coffee intake was associated with lower plasma C-reactive protein levels and in healthy women, only decaffeinated coffee led to reduction of C-reactive protein. Thus, it seems that both caffeinated and decaffeinated as well as the compounds from coffee are responsible for modulating the inflammatory process and blocking its signaling cascade hence preventing or treating obesity-associated metabolic disturbances. The inflammatory pathways and the role of coffee on the modulation of proinflammatory proteins are summarized in Figs. 5 and 6.

Cardiovascular Protections More than 20 years ago, two meta-analyses have reported that the consumption of five or more cups of coffee per day may increases the risk of myocardial infarction and coronary death in approximately 40%–60% of the population.131, 132 It is known that caffeine intake stimulates the release of adrenaline, producing multiple effects on the cardiovascular system such as increase BP, heart rate, endothelial dysfunction. On the other hand, other coffee components, such as phenolic compounds (especially CGA), magnesium, trigonelline, and others, are capable of improving glucose and lipid metabolism and exert an antioxidant activity that reduces chronic inflammation and stress Thus, it is plausible that the acute effects of caffeine can be offset by the beneficial effects of these other components.133 On the contrary, studies in humans and animal models published in the last years reported that the habitual coffee intake reduces CVD risk.78,134,135 Likewise, the acute intake of caffeine (200 mg) was able to improve the endothelial function and to reduce proinflammatory cytokines.135 In a Netherland cohort study on 37,514 individuals it was observed that those who drank 2.1–3 cups of coffee per day decreased by 21% the risk of developing coronary heart disease.136 Furthermore, a study performed with 93,676 postmenopausal women from the Women’s Health Initiative Observational Study reported that total caffeine, regular coffee, decaffeinated coffee, and regular tea intake were not associated with the risk of sudden cardiac death.134 A dose-response meta-analysis of seven cohorts, including 205,349 individuals and 44,120 cases of hypertension, found a 1% decreased risk of hypertension for each additional cup of coffee per day.137 Thus, it can be considered that both there are evidence that caffeinated and decaffeinated coffee and their constituents reduce or at least do not affect the CVD risk factors. In rodents, the administration of caffeine (25 mg/kg/day) before myocardial ischemia/reperfusion was able to reduce myocardial injury by inhibiting inflammation and apoptosis markers, such as poly(ADP-ribose) polymerase (PARP), iNOS, IL-6, and TNF-α.138 Besides, a recent study suggested that the CGAs may be an attractive opportunity for decreasing inflammation, BP, DM2 markers, and platelet aggregation. In addition, caffeine was reported to increase flow-induced arterial dilation.52

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Microbiota and Other Possible Mechanisms Microbiota is known by modulate energy homeostasis, digestion, and metabolism of nutrients. Thus low-grade inflammation-related diseases, such as obesity have emerged as an attractive opportunity for researchers that are trying to understand how nutrients may modify the gut microbiota and improve health.87,139–141 Some authors suggested that coffee may have prebiotic- and probiotic-like properties leading to modification in gut microbiota composition.142,143 Recently, Nakayama et al.143 demonstrated in A/J mice, specific pathogen-free rodents, that were treated with coffee (500 μL per day) some antibiotic actions that were attributed to the inhibition of bacterial growth, such as Escherichia coli and Clostridium spp., an increase of Bifidobacterium spp. and no significant change of Bacteroidetes sp. and Lactobacillus sp. in proximal colon. Furthermore, these authors found higher aquaporin-8 expression in both proximal colon and distal small intestine. These findings are extremely fascinating since coffee consumption can modulate gut microbiota and improve intestinal balance in individuals with impaired gut microbiota, such as individuals with MS, inflammatory bowel disease and cancer. Another factor that may be attributed to healthy gut is the higher aquaporin-8 expression in the intestine. It is a transmembrane water channel protein expressed in hepatocytes and intestine144,145 that facilitates water transport. Lower aquaporin-8 expression is related to impaired healthy gut in mouse with food allergy and diarrhea145 and in patients with ulcerative colitis.76 In addition to beneficial effects of coffee, iron absorption is blocked by polyphenol compounds of coffee, such as CGA which might be one of the mechanisms that underlie the protective effects of coffee intake on glucose metabolism.146–148 Indeed, iron accumulates and DM2 risk increases with higher body weight.149 A review study has shown that the induction of iron deficiency in impaired glucose tolerant subjects improves insulin sensitivity.150 Moreover, phenolic acids are also found in other nutrients, teas, such as chamomile (Matricaria recutita L.), vervain (Verbena officinalis L.), lime flower (Tilia cordata Mill.), pennyroyal (Mentha pulegium L.), peppermint (Mentha piperita L.), black tea, and products rich in cocoa.147 It appears that these compounds may decrease iron content by 47%–94% depending whether they are absorbed together or closely to each other. In summary, gut microbiota and reduction of iron are possible mechanisms by which the habitual coffee intake might improve the metabolic consequences of obesity.

POTENTIAL ADVERSE EFFECTS OF COFFEE Effects of Coffee on BP Ingestion of coffee and hypertension has been controversial in the literature. In a metaanalysis published in 2005,139 16 studies published between January 1966 and January 2003 concerning coffee, caffeine and hypertension were isolated, comprising a total number of 1010 subjects. For all studies, a mean significant increase of 2.04 mmHg (CI95%: 1.10–2.99)

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of systolic blood pressure (SBP) and of 0.73 mmHg (CI95%: 0.14–1.31) of diastolic BP was found. When data on coffee (n ¼ 18, mean quantity ingested: 725 mL/day) and on caffeine (n ¼ 7, mean quantity of caffeine ingested: 410 mg/day) were analyzed separately, increases in BP were larger for caffeine alone (systolic BP: +4.16 mmHg; 2.13–6.20; diastolic BP: +2.41 mmHg; 0.98–3.84) than for coffee alone (systolic BP: +1.22 mmHg; 0.52–1.92; diastolic BP: +0.49 mmHg; 0.06–1.04). The difference between data from coffee and caffeine seems to indicate that other components in coffee could compensate for the increase of BP linked to caffeine. A recent systematic review151 on the general population shows that moderate ingestion of coffee (one or two cups per day) was not associated with risk of hypertension, when compared with not drinkers. Furthermore, the consumption of three or more cups of coffee per day was associated with a decreased hypertension risk. This effect has been attributed to caffeine’s diuretic and natriuretic activity. Other components also can act on reducing BP, such as potassium, magnesium and the major polyphenol in coffee, CGA. The potential hypotensive role of the CGAs in coffee was recently reviewed.140 CGAs supplementation, both acute and chronic, decreased BP in rat model of hypertension.141,142 In two human studies performed vs placebo CGAs also significantly decrease both systolic and diastolic BP.143,144 This effect could be attributed to CGAs and their metabolites that would attenuate oxidative stress and hence act by improving endothelial function and NO bioavailability at the arterial level. The authors hypothesized that a diet rich in CGAs could constitute a nonpharmacological approach in the prevention or treatment of arterial hypertension. The presence of a large amount of CGAs in coffee could explain the difference between the effects of coffee and caffeine on BP. Thus, for people at risk of hypertension, such as subjects obese or with MS, it appears preferable to consume caffeine in the form of coffee to avoid/limit the increases in BP generated by the consumption of caffeine alone.

Effects of Coffee on Cholesterol Cholesterol linked to low-density lipoproteins (LDL-cholesterol) and triglycerides have a high atherogenic potential and their increase is potentially harmful; obese people are particularly at risk in this respect. Coffee is a bean and as such, rich in lipids. In older studies, the acute ingestion of coffee was reported to increase total cholesterol, and especially total cholesterol and triglycerides. This effect is generally observed only after the ingestion of over three cups boiled unfiltered coffee per day. It is due to the action of the diterpenes (kahweol and mainly cafestol). Classically, filtered, instant, and espresso coffee do not significantly affect lipid metabolism. The consumption of relatively high quantities of coffee was also associated with the increase in the plasma level of homocysteine that is possibly also associated to increased cardiovascular risk. However, the consumption or adequate supplementation of folic acid prevents the increase in plasma homocystein.145 The cardiovascular risk of coffee is not supported by recent studies. In populations at risk it is advised to act primarily on lifestyle, i.e., stop smoking, increase physical activity, and quality of diet.

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CONCLUSION Altogether, since the 1950s the habitual coffee intake and its compounds have been attractive for scientific investigators and clinical health professionals. Several epidemiological studies demonstrated that coffee consumption of 3 cups per day or its phenolic compounds may reduce the risk factors for obesity. Furthermore, the numerous mechanisms that underlie coffee actions have shown their adequacy for improving the insulin resistance, inflammation, body weight, and protecting from CVDs. However, it is necessary to consider the individual genetic backgrounds.

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IV. FOODS AND MACRONUTRIENTS IN OBESITY