EASE

Our dark roast organic coffee specifically formulated for easy digestion.

At Purity Coffee® we make every decision based on health first. We use the latest scientific research to optimize how we source, test, roast and deliver our coffees.

We begin with these fundamental baseline standards from which we develop additional standards as the science presents new information.

  • Certified organic and tested free of pesticides and other contaminants
  • Mold-free
  • Mycotoxin-free
  • Rainforest Alliance Certified for environmental and social standards
  • Specialty grade for exceptional taste and highest quality beans
  • Regeneratively and/or biodynamically farmed for sustainability

At Purity Coffee, we continue looking for the best coffees and researching ways to make our coffee healthier. We want consumers to have more choices in coffee to meet their health goals. The deeper we go, the more we understand that coffee is extremely complex, and various beneficial compounds can be created and destroyed at different roast levels.

Purity EASE is our “dark roast”.

It is not roasted so dark as to produce unhealthy levels of PAH, because we take the coffee out before it reaches the temperature cited in the scientific literature where PAH begins to form rapidly. Our dark roast follows a profile laid out in the scientific literature and hits several points that have been proven to be critical. Generally, throughout the literature, dark roast appears to be an appropriate choice for individuals with digestive issues and seems to have positive effects on the brain.

 When comparing Purity Dark Roast to Purity Original, here are a few points to consider:

  1. Because of the high content of chlorogenic acids, coffee is considered the most important contributor to antioxidant intake in many populations. Purity EASE still has antioxidant capacity, but the total CGA is about half the original (FLOW). On the other hand, high chlorogenic acids may stimulate gastric fluid secretions in some people, and for these people a darker roast may be a better choice.
  2. After being formed, acrylamide tends to decrease as roasting progresses. Purity EASE has even lower acrylamide than Purity FLOW.
  3. Purity Dark Roast coffee does not come close to PAH temperatures. We do not get close to either an Italian Roast or French Roast like in the color chart below. So our dark roast is actually a dark-medium roast.

Purity EASE Roast Profile

There are many ways roasters describe a coffee's color, and most terms are not precise, but rather suggestive.

Purity FLOW is a medium roast, which is a bit darker than the industry's sample roast level to evaluate (or "cup") specialty coffee. Purity EASE is darker than medium, and what some might say is a "Full City" roast. It is not as dark as what many consider Italian or French roast.

Purity EASE is formulated for:

Digestive system support
Microbiota balance
Lower pH than our original roast

The key beneficial compounds for a healthy dark roast coffee:

Melanoidins

Melanoidins are what make coffee (and other foods) brown when roasted, baked or toasted. They are formed during the Maillard reaction, when certain sugars and amino acids combine at high temperatures and low water activity. They may be considered bioactive compounds (Bekedam et. al. 2008). The extent of roasting-induced antioxidant formation is directly linked to the extent of melanoidin formation, and the longer we roast, the more intermediate and high-molecular-weight melanoidins are produced. The following impacts/actions are associated with melanoidins: Antioxidant activity, metal-chelating, antibacterial, and prebiotic functionality.

Coffee melanoidins may act as soluble fiber, enhancing immune-stimulating properties and contributing to reducing the risk of colon cancer. This likely happens by decreasing colon inflammation through improved microbiota balance (prebiotic effect) and by increasing the elimination rate of carcinogens through higher colon motility (urge to use the bathroom) (Vitaglione et al. 2012; Moreira et al. 2015; Fogliano & Morales 2011).

Coffee melanoidins do not seem to be absorbed in humans, but they can function as an antioxidant dietary fiber with an overall antioxidant capacity via embedded low molecular compounds. Melanoidins can act like a ‘sponge’ for free radicals in the gut. This improves the reduced/oxidized glutathione balance in the colon. Glutathione is an antioxidant produced in our cells (Garsetti 2000).

There are additional benefits of coffee melanoidins in the gut: They may promote the growth of a beneficial colon microbiota, affecting inflammatory pathways in the colon and the liver (Sales et al. 2019). Oddly, antioxidative structures formed in coffee melanoidins are similar to vitamin E. These appear to activate their scavenging properties gradually (Bekedam et al. 2008).

The antioxidant activity of melanoidins isolated from different brews was studied, and some showed that the radical scavenging ability of coffee melanoidins was higher in the dark-roasted coffee, others exhibited higher radical scavenging activity, and still others showed radical scavenging ability of coffee melanoidins was not affected by the degree of roasting (Tagliazucchi et al. 2010).  

In addition to radical scavenging, coffee melanoidins are able to chelate transition metal ions, that is they can bind Zn2+, Cu2+, and Fe2+. Metal-chelating ability is key to inhibiting lipid peroxidation, among other benefits (Takenaka et al. 2005; Morales et al. 2005). Increasing evidence shows that oxidized lipids, advanced lipid oxidation end products, and lipid peroxidation play a major role in developing most oxidative stress-related diseases. Lipid peroxidation occurs in all human neurodegenerative diseases, such as Alzheimer’s disease, Parkinson's disease and even atherosclerosis (Tagliazucchi et al. 2010).

Finally, coffee melanoidins seem to have a protective effect on liver steatosis in obese rats, which suggests that the melanoidins in coffee may influence liver fat and functionality. Glutathione may be involved (Vitaglione et al. 2012).

References: Vitaglione, 2012; Moreira, 2015; Fogliano and Morales, 2011; Sales, 2019.

Chlorogenic Acid Lactones

Chlorogenic acid lactones (CGL) are bitter compounds with antioxidant capacity created during the coffee roasting process from dehydration of chlorogenic acids (CGA). The maximum amount of CGL in roasted coffee represents approximately 30% of the available original CGA amount (Farah et al. 2005). CGA are shown to have the following impacts/actions: Antioxidant activity, possible anti-opioid activity, hypoglycemic, and potential effects on brain function independently of the pharmacological effects of caffeine.

CGL exhibit opiate receptor binding activity with characteristics like those of opiate antagonists and can reverse morphine-induced analgesia in mice. However, acute pharmacologic effects are unlikely with normal coffee consumption. Like chlorogenic acids, these compounds are partly absorbed (Farah & de Paula 2018).

After contact with the alkaline pH of human digestive fluids, part of the lactone was converted into caffeoylquinic acids part. Therefore, it is likely that a large proportion of these lactones consumed in the brew return to their respective chlorogenic acid forms during digestion, indirectly increasing the total chlorogenic acids intake (Farah 2013).

It has been found in a mouse model that the major chlorogenic acid affects spontaneous locomotor activity, suggesting that it or a derivative could pass the blood-brain barrier. The chlorogenic acid lactones are less polar than their parent compounds and should be more permeable to the blood-brain barrier (De Paulis et al. 2004). One study showed a significant correlation between the levels of chlorogenic acid lactones in coffee and neuron cell survival. This suggests that chlorogenic lactones might contribute to the increased protective effects against H2O2-induced death of neuron cells (Chu et al. 2009).

References: Farah, 2005 & 2013; Díaz-Rubio, 2007. (Note: A dark roast mixture was used in this study); Sales, 2019.

Norharman and Harman B-carbolines

Roasted coffee is the major known food source of norharman and harman β-carbolines. Considered mostly neuroactive substances, β-carbolines show a wide spectrum of reported pharmacological and neuroactive actions. They can bind to receptors in the brain, including opiate receptors, and they frequently act as inhibitors to regulate neurotransmitters. So far only norharman and harman β-carbolines have been reported in coffee (any reference in this review to β-carbolines refers to only these two). Their health effects are being extensively studied. The following impacts/actions are associated with β-carbolines: Antioxidant activity, possible anti-opioid activity, hypoglycemic, and antidepressant. Reduced rate of development of Parkinson’s disease (Ascherio 2004).

Norharman and harman are potent competitive and reversible monoamine oxidase (MAO) inhibitors, in both rats and humans. The high amounts of these β-carbolines in roasted coffee place them among those at the top of the list for compounds with probable influence on Parkinson’s disease course (Casal 2015)

Amounts of harman and norharman are very low in green coffee and increase significantly during roasting, but in a variable way. It is indicated that a darker roasted coffee will be higher in harman and norharman and generally speaking, norharman increases during roasting and decreases after 240°C (464°F) (Casal 2015; Gomes 2006).

References: Casal, 2015; Rodrigues, 2019.

Trigonelline

Trigonelline is a plant hormone, one of the more abundant sources of nitrogen in green coffee, and a product of niacin metabolism. Green coffees contain about 1% trigonelline, of which 50-80% is degraded upon roasting; it breaks down to niacin or nicotinic acid and N-methylpyridinium at higher temperatures, and also into volatiles such as pyridine and pyrazines. The following impacts/actions are associated with trigonelline: Antioxidant activity, anti-tumorigenic, anticarcinogenic, anti-cariogenic, antimicrobial, hypoglycemic, and hypocholesterolemic.

Niacin (nicotinic acid) is essential for specific oxidation–reduction reactions in the body. At dark roast levels trigonelline converts to higher niacin levels. This niacin is highly bioavailable in the coffee beverage (Trugo 2003).

The content of trigonelline decreases continuously throughout roasting, while nicotinic acid and N-methylpyridinium increase, with N-methylpyridinium being the major thermal product up to the dark-medium roast, similar to the Purity Dark Roast.

Trigonelline plus chlorogenic acids reduced early glucose and insulin response, which was shown to help prevent type 2 diabetes (Viera 2019). Trigonelline plus nicotinic acid helps regulation of liver enzymes, which is closely related to the suppression of triglyceride accumulation, as well as the progression of diabetes.

Trigonelline acts on up-regulating antioxidant enzyme activities and decreasing lipid peroxidation in the pancreas (Verzelloni 2010). Lipid peroxidation is generally described as a process under which oxidants such as free radicals attack lipids, especially polyunsaturated fatty acids.

References: Trugo, 2003.; Farah, 2005 & 2009.

N-methylpyridinium

N-methylpyridinium is formed during roasting from trigonelline as a non-volatile degradation product. While small amounts of trigonelline and nicotinic acid are present in many foods other than coffee, the occurrence of N-methylpyridinium in our daily diet seems to be restricted to roasted coffee (Viera 2019).

Although it is in lower concentrations than CGA, N-methylpyridinium the following impacts/actions are associated with N-methylpyridinium: Antioxidant activity, lower stimulatory effect on gastric acid secretions, possibly assists in weight control, anticarcinogenic (possibly with colon cancer), and DNA protective effects.

CGA and N-methylpyridinium were identified as inducers of Nrf2, considered the master regulator of oxidative stress. Nrf2 represents one of the main cell defense mechanisms and major regulators of cell survival. N-methylpyridinium represented an even more potent extract in vitro and in vivo than CGA (Boettler 2011).

N-methylpyridinium demonstrated an increase in activity in the liver, catalyzing the detoxification of numerous genotoxic carcinogens. In addition, a notable increase in the antioxidant activity of plasma was detected in experiments, indicating that N-methylpyridinium may contribute substantially to the properties of coffee against reactive oxygen species (ROS) (Al-Serori 2019). ROS are free radicals, or unstable molecules that contain oxygen and easily react with other molecules in a cell. A buildup of reactive oxygen species in cells may cause damage to DNA, RNA, and proteins, and may cause cell death (Ref: https://www.cancer.gov/).

References: Rubach, 2014; Kotyczka, 2011; Boettler, 2011; Pahlke, 2019 and Schipp 2018.

Purity Coffee® EASE Certificates of Analysis

Click the links below to view the lab results for EASE. Results are based upon 15g of roasted & ground coffee, which is equal to the recommended amount used for brewing one 8 oz cup of coffee.

Citations and Studies Which Support Our Views

  1. Abreu R.V., Silva-Oliveira E.M., Moraes M.F.D., Pereira G.S., Moraes-Santos T. (2011). Chronic coffee and caffeine ingestion effects on the cognitive function and antioxidant system of rat brains. Pharmacology Biochemistry and Behavior, V. 99, I. 4, 659-664. https://doi.org/10.1016/j.pbb.2011.06.010
  2. Al-Serori H., Setayesh T., Ferk F., Mišík M., Waldherr M., Nersesyan A. and Knasmüller S. (2019)DNA Protective Properties of Coffee: From Cells to Humans. Coffee: Consumption and Health Implications. A. Farah Ed., Ch.4, Royal Society of Chemistry
  3. Ascherio A., Weisskopf M.G., O’Reilly E.J., McCullough M.L., Calle E.E., Rodriguez C., et al. (2004). Coffee consumption, gender, and Parkinson’s disease mortality in the cancer prevention study II cohort: the modifying effects of estrogen. Am J Epidemiol, 160(10):977–84.
  4. Bakuradze T, Boehm N, Janzowski C, Lang R, Hofmann T, Stockis J-P, Albert FW, Stiebitz H, Bytof G, Lantz I, Baum M, Eisenbrand G (2011) Antioxidant-rich coffee reduces DNA damage, elevates glutathione status and contributes to weight control: results from an intervention study. Mol Nutr Food Res 55(5):793–797. https ://doi.org/10.1002/mnfr.20110 0093
  5. Bekedam E, Loots M, Schols H, Van Boekel M, Smit G 2008. Roasting Effects on Formation Mechanisms of Coffee Brew Melanoidins. J. Agric. Food Chem. 2008, 56, 16, 7138–7145
  6. Bhumiratana N., Wolf M., Chambers E., and Adhikari K. (2019) Coffee Drinking and Emotions: Are There Key Sensory Drivers for Emotions? Beverages, 5(2), 27, https://doi.org/10.3390/beverages5020027
  7. Boettler U., Volz N., Pahlke G., Teller N., Kotyczka C., Somoza V., Marko D. (2011b). Coffees rich in chlorogenic acid or N-methylpyridinium induce chemopreventive phase II-enzymes via the Nrf2/ARE pathway in vitro and in vivo. Molecular Nutrition & Food Research, 55(5), 798–802. https://doi.org/10.1002/mnfr.201100115.
  8. Borrelli R. C., Visconti A., Mennella C., Anese M., and Fogliano V. (2002). Chemical characterization and antioxidant properties of coffee melanoidins. J Agric Food Chem 50, 6527–6533.
  9. Butterfield D. A., Bader Lange M. L., and Sultana R. (2010). Involvements of the lipid peroxidation product, HNE, in the pathogenesis and progression of Alzheimer’s disease. Biochim Biophys Acta 1801, 924–929.
  10. Cardona, F., Andrés-Lacueva C., Tulipani S., Tinahones F. J., & Queipo-Ortuño M. I. (2013). Benefits of polyphenols on gut microbiota and implications in human health. The Journal of Nutritional Biochemistry, 24(8), 1415–1422. doi:10.1016/j.jnutbio.2013.05.001.
  11. Casal S. (2015). Chapter 82 - Neuroactive β-Carbolines Norharman and Harman in Coffee. Coffee in Health and Disease Prevention, Pages 737-743.
  12. Chen J.F., (2019). Caffeine and Parkinson’s Disease: From Molecular Targets to Epidemiology Clinical Trials. Coffee: Consumption and Health Implications. A. Farah Ed., Ch. 7, Royal Society of Chemistry.
  13. Chu Y.-F., Brown P. H., Lyle B. J., Chen Y., Black R. M., Williams C. E., … Cheng I. H. (2009). Roasted Coffees High in Lipophilic Antioxidants and Chlorogenic Acid Lactones Are More Neuroprotective than Green Coffees. Journal of Agricultural and Food Chemistry, 57(20), 9801–9808. doi:10.1021/jf902095z
  14. Circu ML, Aw TY. (2011). Redox biology of the intestine. Free Radic Res. 45(11-12):1245–1266. doi:10.3109/10715762.2011.611509
  15. Daglia M., Papetti A., Aceti C., Sordelli B., Gregotti C., and Gazzani G. (2008). Isolation of high molecular weight components and contribution to the protective activity of coffee against lipid peroxidation in a rat liver microsome system. J Agric Food Chem 56, 11653–11660. 24
  16. de Marco L. M., Fischer S., and Henle T. (2011). High molecular weight coffee melanoidins are inhibitors for matrix metalloproteases. J Agric Food Chem 59, 11417– 11423.
  17. de Paulis, Commers, Farah .Zhao , McDonald . Galici,. Martin (2004). 4-Caffeoyl-1,5-quinide in roasted coffee inhibits [3H]naloxone binding and reverses anti-nociceptive effects of morphine in mice. Psychopharmacology 176: 146-153.
  18. Del Pino-García R., González-SanJosé M. L., Rivero-Pérez M. D., and Muñiz P. (2012). Influence of degree of roasting on the antioxidant capacity and genoprotective effect of 23 instant coffee: contribution of the melanoidin fraction. J Agric Food Chem 60, 10530–10539.
  19. Delgado-Andrade C., and Morales F. J. (2005). Unravelling the contribution of melanoidins to the antioxidant activity of coffee brew. J Agric Food Chem 53, 1403–1407.
  20. Delgado-Andrade C., Rufian-Henares J. A., and Morales F. J. (2005). Assessing the antioxidant activity of melanoidins from coffee brews by different antioxidant methods. J Agric Food Chem 53, 7832–7836.
  21. Díaz-Rubio M. E., & Saura-Calixto F. (2007). Dietary Fiber in Brewed Coffee. Journal of Agricultural and Food Chemistry, 55(5), 1999–2003. doi:10.1021/jf062839p.
  22. Dittrich R., Dragonas C., Kannenkeril D., Hoffmann I., Mueller A., Beckmann M. W., and Piscetsrieder M. (2009). A diet rich in Maillard reaction products protects LDL against copper induced oxidation ex vivo, a human intervention trial. Food Res Int 42, 1315–1322.
  23. Etserbauer, H, Wag G., and Puhl H. (1993). Lipid peroxidation and its role in atherosclerosis. Br Med Bull 49, 566–576.
  24. Farah A. editor (2019). Coffee: Production, Quality and Chemistry. Royal Society of Chemistry.
  25. Farah A. editor (2019). Coffee: Consumption and Health Implications. Royal Society of Chemistry.
  26. Farah A. (2018) Nutritional and health effects of coffee. Lashermes P. (ed.), Achieving sustainable cultivation of coffee, Burleigh Dodds Science Publishing,Cambridge, UK., 1-31.
  27. Farah A. (2013). Coffee: Emerging Health Effects and Disease Prevention. IFTPress, Ch. 2, 22-58.
  28. Farah A., de Paulis T., Moreira D.P., Trugo C., Martin P. (2006). Chlorogenic Acids and Lactones in Regular and Water-Decaffeinated Arabica Coffees. Agricultural and Food Chemistry, 54, 374-381.
  29. Farah A., de Paulis T., Trugo C., Martin P. (2005). Effect of Roasting on the Formation of Chlorogenic Acid Lactones in Coffee. Agricultural and Food Chemistry, 53, 1505-1513.
  30. Faist V., and Erbersdobler H. F. (2001). Metabolic transit and in vivo effects of melanoidins and precursor compounds deriving from the Maillard reaction. Ann Nutr Met 45, 1–12
  31. Fogliano ,V., and Morales F. J. (2011). Estimation of dietary intake of melanoidins from coffee and bread. Food Funct 2, 117–123.
  32. Gniechwitz D., Reichardt N., Ralph J., Blaut M., Steinhart H., and Bunzel M., (2008). Isolation and characterisation of coffee melanoidin fraction. J Food Sci Agric 88, 2153– 2160.
  33. Gomes A.F.R. (2006). Caracterização do teor de norarmana e harmana em cafésverdes e torrados [M.S. thesis]. Portugal: Oporto University.
  34. Gorelik S., Kanner J. Schurr D., and Kohen R. (2013). A rational approach to prevent postprandial modification of LDL by dietary polyphenols. J Funct Food 5, 163–169.
  35. Gorelik S., Lapidot T., Shaham I., Granit R., Ligumsky M., Kohen, R, and Kanner J. (2005). Lipid peroxidation and coupled vitamin oxidation in simulated and human gastric fluid inhibited by dietary polyphenols: health implications. J Agric Food Chem 53, 3397–3402.
  36. Gorelik S., Ligumsky M., Kohen R., and Kanner J. (2008). A novel function of red wine polyphenols in humans: prevention of absorption of cytotoxic lipid peroxidation products. FASEB J 22, 41–46. 21
  37. Goya L., Delgado-Andrade C., Rufián-Henares J. A., Bravo L., and Morales F. J. (2007). Effect of coffee melanoidins on human heparoma hepG2 cells. Protection against oxidative stress induced by tert-butylhydroperoxide. Mol Nutr Food Res 51, 536–545.
  38. GudrunP, Attakpaha E, Aichingera G, Ahlberga K, Hochkogler CM, Schwiger K, Schipp D, Somoza V, Marko D. (2019). Dark coffee consumption protects human blood cells from spontaneous DNA damage. Journal of Functional Foods. Volume 55, April 2019, Pages 285-295
  39. Hall S., Yuen J.W., Grant G.D. (2018). Bioactive Constituents in Caffeinated and Decaffeinated Coffee and Their Effect on the Risk of Depression—A Comparative Constituent Analysis Study. Beverages, 4, 79; doi:10.3390/beverages4040079.
  40. Herraiz T., Chaparro C. (2006). Human monoamine oxidase enzyme inhibition by coffee and β-carbolines norharman and harman isolated from coffee. Life Sciences 78, 795-802.
  41. Hu G.L., Wang X, Zhang L., Qiu M.H. (2019). The sources and mechanisms of bioactive ingredients in coffee. Food & Function, 10, 3113. DOI: 10.1039/c9fo00288j
  42. Kanner J. (2007). Dietary advanced lipid oxidation endproducts are a risk factor to human health. Mol Nutr Food Res 51, 1094–1101.
  43. Kanner J., and Lapidot T. (2001). The stomach as a bioreactor: dietary lipid peroxidation in the gastric fluid and the effects of plant-derived antioxidants. Free Rad Biol Med 31, 1388–1395.
  44. Kreuzer J., White A. L., Knott T. J., Jien M. L., Mehrabian M., Scott J., Young S. G., and Haberland M. E. (1997). Amino terminus of apolipoprotein B suffices to produce recognition of malondialdehyde-modified low density lipoprotein by the scavenger receptor of human monocyte-macrophages. J Lipid Res 38, 324–342. 20.
  45. Leitinger N. (2005). Oxidized phospholipids as triggers of inflammation in atherosclerosis. Mol Nutr Food Res 49, 1063–1071.
  46. Leonarduzzi G., Sevanian A., Sottero B., Arkan M. C., Biasi F., Chiarpotto E., Basaga H., Poli G. (2001). Up-regulation of the fibrogenic cytokine TGF-beta1 by oxysterols: a mechanistic link between cholesterol and atherosclerosis. FASEB J 15, 1619–1621.
  47. Mancini R.S., Wang Y., Weaver D.F. (2018). Phenylindanes in Brewed Coffee Inhibit Amyloid-Beta and Tau Aggregation. Frontiers in Neuroscience. doi: 10.3389/fnins.2018.00735.
  48. Marques V., Farah A. (2009). Chlorogenic acids and related compounds in medicinal plants and infusions. Food Chemistry 113, 1370-1376.
  49. Min B., and Ahn D. U. (2005). Mechanism of lipid peroxidation in meat and meat products-A review. Food Sci Biotechnol 14, 152–163.
  50. Morales F. J. (2005). Assessing the non-specific hydroxyl radical scavenging properties of melanoidins in a Fenton-type reaction system. Anal Chim Acta 534, 171–176.
  51. Morales F. J., Fernández-Fraguas C., Jiménez-Pérez S. (2005). Iron-binding ability of melanoidins from food and model systems. Food Chem 90, 821–827.
  52. Morales F. J., Jiménez-Pérez S. (2004). Peroxyl radical scavenging activity of melanoidins in aqueous systems. Eur Food Res Technol 218, 515–520.
  53. Moreira A. S. P., Nunes F. M., Domingues M. R., and Coimbra M. A., (2012). Coffee melanoidins: structure, mechanisms of formation and potential health impacts. Food Funct 3, 903–915.
  54. Negre-Salvayre A., Auge N., Ayala V., Basaga H., Boada J., Brenke R., Chapple S., Cohen G., Feher J., Grune T., Lengyel G., Mann G. E., Pamplona R., Poli G., PorteroOtin M., Riahi Y., Salvayre R., Sasson S., Serrano J., Shamni O., Siems W., Siow R. C. M., Wiswedel I., Zarkovic K., and Zarkovic N. (2010). Pathological aspects of lipid peroxidation. Free Rad Res 44, 1125–1171.
  55. Nunes F.M., Cruz A.C.S., Coimbra M.A. (2012). Insight into the Mechanism of Coffee Melanoidin Formation Using Modified “in Bean” Models. J. Agric. Food Chem 60, 8710-8719.
  56. Östergren A., Annas A., Skog K., Lindquist N.G., Brittebo E.B. (2004) Longterm retention of neurotoxic β-carbolines in brain neuromelanin.J Neural Transm;111:141–57.
  57. Palinski W., Rosenfeld M. E., Ylä-Herttuala S., Gurtner G. C., Socher S. S., Butler S. W., Parthasarathy S., Carew T. E., Steinberg D., and Witztum J. L. (1989). Low density lipoprotein undergoes oxidative modification in vivo. PNAS 86, 1372–1376.
  58. Perrone D., Farah A., and Donangelo C. M. (2012). Influence of coffee roasting on the incorporation of phenolic compounds into melanoidins and their relationship with antioxidant activity of the brew. J Agric Food Chem 60, 4265–4275.
  59. Reichardt N., Gniechwitz D., Steinhart H., Bunzel M., and Blaut M. (2009). Characterization of high molecular weight coffee fractions and their fermentation by human intestinal microbiota. Mol Nutr Food Res 53, 287–299.
  60. Rodrigues D.A., Casal S., β-Carbolines, Coffee: Production, Quality and Chemistry, A. Farah Ed., Ch. 31, Royal Society of Chemistry.
  61. Rubach M, Lang R, Bytof G, Stiebitz H, Lantz I, Hofmann T, Somoza V. (2014) A dark brown roast coffee blend is less effective at stimulating gastric acid secretion in healthy volunteers compared to a medium roast market blend. Molecular Nutrition Food Research, 58, 1370-1373. Doi: 10.1002/mnfr.201300890.
  62. Rufian-Henares J. A., and Morales F. J. (2007). Effect of in vitro enzymatic digestion on antioxidant activity of coffee melanoidins and fractions. J Agric Food Chem 55, 10016– 10021.
  63. Rufian-Henares J.A. and Morales F. (2007). Functional Properties of Melanoidins: In vitro antioxidant, antimicrobial and antihypertensive activities. Food Research International, 40(8), 995-1002.
  64. Sales A., DePaula J., Mellinger C., Gomes da Cruz A., Miguel M.A., Farah A. (2019). Effect of regular and decaffeinated roasted coffee (Coffea arabica and Coffea canephora) extracts and bioactive compounds on in vitro probiotic bacteria growth. Submitted for publication. Laboratório de Química e Bioatividade de Alimentos & Núcleo de Pesquisa em Café -NUPECAFÉ Instituto de Nutrição Universidade Federal do Rio de Janeiro.
  65. Schipp D., Tulinska J., Sustrova M. et al.(2019) Consumption of a dark roast coffee blend reduces DNA damage in humans: results from a 4-week randomised controlled study. Eur J Nutr., 58: 3199. https://doi.org/10.1007/s00394-018-1863-2.
  66. Shearer J., Sellars E.A., Farah A., Graham T.E., Wasserman D.H. (2007). Can. J. Physiol. Pharmacol. 85: 823-830.
  67. Siegel S. J., Bieschke J., Powers E. T., and Kelly J. W. (2007). The oxidative stress metabolite 4-hydroxynonenal promotes Alzheimer protofibril formation. Biochemistry 46, 1503–1510.
  68. Silván J. M.; Morales F. J.; Saura-Calixto F. (2010). Conceptual Study on Maillardized Dietary Fiber in Coffee. J. Agric. Food Chem., 58, 12244–12249, doi:10.1021/jf102489u.
  69. Staprans I., Pan X. M., Rapp J. H., and Feingold K. R. (2003). Oxidized cholesterol in the diet is a source of oxidized lipoproteins in human serum. J Lipid Res 44, 705–715.
  70. Staprans I., Pan X. M., Rapp J. H., and Feingold K. R. (2005). The role of dietary oxidized cholesterol and oxidized fatty acids in the development of atherosclerosis. MolNutr Food Res 49, 1075–1082.
  71. Staprans I., Rapp J. H., Pan X. M., Kim. K. Y., and Feingold K. R. (1994). Oxidized lipids in the diet are a source of oxidized lipid in chylomicrons of human serum. Arterioscler Thromb 14, 1900–1905.
  72. T. Bakuradze T, Lang R, Hofmann T, Eisenbrand G, Schipp D, Galan J, Richling E. (2015). Consumption of a dark roast coffee decreases the level of spontaneous DNA strand breaks: a randomized controlled trial. Eur J Nutr., 54: 149. https://doi.org/10.1007/s00394-014-0696-x.
  73. Tagliazucchi D., Verzelloni E., and Conte A. (2010). Effect of dietary melanoidins on lipid peroxidation during simulated gastro-intestinal digestion: their possible role in the prevention of oxidative damage. J Agric Food Chem 58, 2513–2519.
  74. Takenaka M., Sato N., Asakawa H., Wen X., Murata M., and Homma S. (2005). Characterization of a metal-chelating substance in coffee. Biosci Biotechnol Biochem 69, 26–30.
  75. Trugo L. C. (2003). Analysis of coffee products. In Encyclopedia of Food Science and Nutrition; Caballero B., Trugo L., Finglas P., Eds.; Academic Press: London; pp 1498-1506.
  76. Vegas O., Pinho O., Ferreira I.M. (2019). Polycyclic Aromatic Hydrocarbons. Coffee: Production, Quality and Chemistry. A. Farah Ed. Ch. 32. Royal Chemistry Society.
  77. Verzelloni E., Tagliazucchi D., and Conte A. (2010). From balsamic to healthy: traditional balsamic vinegar melanoidins inhibit lipid peroxidation during simulated gastro-intestinal digestion of meat. Food Chem Toxicol 48, 2097–2102.
  78. Viera Porto A.C., Farah A. (2019) Potential Effects of Trigonelline and Derivatives on Health. Coffee: Consumption and Health Implications, A. Farah Ed., Ch. 18, Royal Society of Chemistry.
  79. Virtanen H., Soares R.N., Shearer J. (2019). Coffee in the Development, Progression and management of Type 2 Diabetes. Coffee: Consumption and Health Implications, A. Farah Ed., Ch. 6, Royal Society of Chemistry.
  80. Vitaglione P., Morisco F., Mazzone G., Amoruso D. C., Ribecco M. T., Romano A., Fogliano V., Caporaso N., and D’Argenio G. (2010). Coffee reduces liver damage in a rat model of steatohepatitis: the underlying mechanisms and the role of polyphenols and melanoidins. Hepatology, 52, 1652–1661.