Bitter Chocolate Book Pdf 73 [VERIFIED]
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Copper is a cofactor for a number of enzymes and is required for processes, including iron transport, glucose metabolism, infant growth, and brain development (190, 259). Copper deficiency can lead to anemia and pancytopenia, causing hypertension, inflammation, and myocardial hypertrophy (214). Copper deficiency has been linked to glucose intolerance, cardiac arrhythmia, and hypercholesterolemia in animals and humans (134); however, elevated copper status may also be harmful. High serum copper concentration is associated with an increased risk of cardiovascular death (206), all-cause, cancer, and cardiovascular mortality (142). Chocolate is a significant source of copper for Americans; milk chocolate provides 10% of the U.S. RDA for copper per 100-kcal serving, whereas dark chocolate provides 31%, and cocoa powder 23% per tablespoon (1, 184). Despite the potential detrimental effects of excess copper, the prevention of copper deficiency is, nevertheless, important for the maintenance of cardiovascular health. Because a 1000-kcal serving of chocolate would need to be consumed to reach the RDA for copper, it is unlikely that chocolate consumption would elevate serum copper concentrations to harmful levels.
In 2009, a study in Stockholm, Sweden assessed cardiac mortality in a particularly high-risk group: nondiabetic patients hospitalized with a first myocardial infarction (116). After a mean 8.6 years of follow-up, patients who reported eating chocolate twice or more per week were 66% less likely to suffer a cardiac death compared to those who reported never eating chocolate. After adjustment for demographic and socioeconomic variables, coffee consumption, and intake of sweets, there was a significant, linear, inverse relationship between frequency of chocolate consumption and cardiac mortality (p=0.01). Total mortality, however, was not associated with chocolate consumption.
A cross-sectional analysis of data from 2217 participants in the NHLBI Family Heart Study identified an inverse relationship between chocolate consumption and calcified atherosclerotic plaque in the coronary arteries (61). Individuals who reported consuming (any type of) chocolate two or more times per week were 32% less likely to have prevalent coronary artery calcification compared with those who never ate chocolate. The odds ratios decreased with increasing frequency of chocolate consumption and were adjusted for age, sex, energy intake, waist-to-hip ratio, education, smoking, alcohol consumption, total cholesterol:HDL ratio, nonchocolate candy intake, and diabetes mellitus.
Because of their high flavonoid content, the cocoa solids present in chocolate are typically hypothesized to affect measures of cardiovascular health, whereas other components of chocolate products (e.g., cocoa butter) are thought to have little or no effect. Given this reasonable assumption, the results of a study by Kris-Etherton et al. are surprising (135). In their study, consumption of milk chocolate as a substitute for a high-carbohydrate snack bar improved levels of serum HDL and triglycerides. This improvement occurred despite the fact that the milk chocolate bar increased the total fat and saturated fat in the diet. Because milk chocolate contains a relatively small proportion of cocoa solids, this finding might suggest that a component in chocolate other than flavonoids (possibly stearic acid) was responsible. However, in another trial, HDL increased by 11.4% and 13.7% when subjects consumed dark chocolate and polyphenol-enriched dark chocolate, respectively, but not when they consumed white chocolate (181). One possible explanation for the results of Kris-Etherton et al. is that the chocolate bar's displacement of a high-carbohydrate snack, rather than some active compound in the chocolate bar itself, led to the change in lipid levels.
A 2010 meta-analysis of eight trials summarized the short-term impact of cocoa consumption on blood lipids (119). The data from these trials indicate that cocoa may significantly reduce LDL cholesterol, and may also reduce total cholesterol when consumed in low doses by individuals with cardiovascular risk factors. This meta-analysis supports a lipid-lowering effect of cocoa, but it is limited by the small total sample (n=215), the paucity of well-designed trials, and the heterogeneity of the studies included. Whether cocoa products substantially improve lipid levels in the blood remains unclear. There is, however, convincing evidence that consumption of chocolate in most forms has at worst, a neutral effect on the lipid profile. This evidence should allay fears that the high saturated fat content of chocolate would negate the effects of its other health-promoting compounds. Further, although cocoa may not appreciably change the quantity of lipids in the blood, it may change their quality, that is, their ability to cause blood vessel damage.
Levels of oxidized LDL in the blood have been shown to predict CAD better than total cholesterol, triglycerides, HDL, and LDL (63, 110). In general, intervention studies suggest that cocoa can inhibit LDL oxidation. Decreased levels of plasma-oxidized LDL have been observed in subjects after long-term daily consumption of cocoa powder (14, 15) and dark chocolate (267). These effects might be attributed to epicatechin, which attenuates LDL oxidation and protects the endothelium from the actions of oxidized LDL (246). However, some studies suggest that consumption of chocolate low in flavonoids may also be beneficial. In two studies, milk chocolate (135) and white chocolate (181) inhibited LDL oxidation. In the latter study, a marker of lipid peroxidation decreased 11.9% after consumption of white chocolate, dark chocolate, or dark chocolate enriched with polyphenols (181). These results indicate that the fatty acids in chocolate may play an important role in LDL oxidation.
Massolt and colleagues (156) demonstrated that the smell of chocolate could suppress appetite in humans. In their study, 12 females were given chocolate to eat and then randomized to either smell chocolate or to serve as a control (no eating or smelling). At the start of these sessions, insulin, glucagon-like peptide-1 (GLP-1), and cholecystokinin (CCK), but not glucose, were found to correlate with appetite levels. They also found that ghrelin levels correlated inversely with appetite. Chocolate eating and smelling both resulted in appetite suppression with no relationship seen between appetite levels and insulin, GLP-1, or CCK levels. Of note, the smell of dark chocolate (85% cocoa) resulted in a satiation response that was inversely correlated with ghrelin levels. As higher levels of ghrelin increase food intake and increase fat mass (257), these provocative findings suggest that regular cocoa and chocolate consumption may reduce appetite and possibly weight gain.
Parker et al. reviewed the psychoactive properties and mood effects of cocoa in 2006, with some noteworthy conclusions (195). They contend that a psychoactive component of cocoa is not likely to be the cause of chocolate cravings because milk chocolate, which contains a lower proportion of cocoa solids than dark chocolate or cocoa powder, is typically preferred. Rather, the unique orosensory properties of chocolate, which are responsible for its pleasurable taste, are the most likely explanation (195).
Some population-based studies suggest that dairy intake may be positively associated with acne, and clinical trials indicate that a high glycemic index or glycemic load diet may also play a role in acne severity and duration (25, 70). Currently, evidence does not support a link between chocolate or any other specific food and acne, though few well-designed studies have been undertaken (47).
The American College of Gastroenterology names chocolate as one of the foods that may contribute to GERD symptoms, though it acknowledges a lack of rigorous testing of this hypothesis (58). Chocolate has been found to reduce lower esophageal sphincter pressure (179, 282). Yet, no studies have investigated whether eliminating chocolate from the diet can improve symptoms. There is currently not sufficient evidence to suggest that dietary modifications of any kind can improve GERD symptoms or pathological measures (123). Interestingly, one study found that chocolate was the most often cited constipation-causing food among patients with constipation-predominant irritable bowel syndrome (177), but no other studies have investigated this reported effect.
It has been hypothesized that phenylethylamine, present in chocolate, could provoke a migraine (160, 161). The perceived association between chocolate and migraines appears to be a widely held misconception. In one study investigating trigger factors of migraines, the proportion of patients who reported having heard that chocolate could be a migraine trigger (61.7%) was significantly and substantially greater than the proportion who identified chocolate as a trigger based on their own experience (14.3%, p
The tendency in Western science when a food appears to have specific health effects is to seek the active ingredient. Indeed, specific effects of chocolate may be attributable to specific constituents, such as flavonoids. However, just as the active ingredient making a food such as spinach or broccoli highly nutritious may be nothing less than spinach or broccoli, the same may be true of chocolate. The active ingredient in chocolate may be chocolate, or at least cacao, with overall health effects representing at least the sum of diverse parts.
There is, however, much interest in, and potential gain from, elucidating those parts and their mechanisms of action. Table 6 begins to suggest an array of mechanistic pathways, enumerating various constituents of chocolate, and their actions at diverse sites. Numerous cytokines and enzyme systems are influenced by various polyphenols in chocolate. Some of these pathways clearly involve direct antioxidant effects, whereas others likely do not. Among the unknowns is which of the many polyphenolic compounds in chocolate exert specific effects, and this area invites further investigation. 153554b96e
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