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

We continue to look for the best coffees and we’re always researching ways to make our coffee even healthier. 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 EASE 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 Dark Roast still has antioxidant capacity, but total CGA is about half the original. 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. Acrylamide levels decrease the darker the coffee is roasted. Purity EASE Dark Roast has even lower acrylamide than Purity FLOW.
  3. Purity EASE 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:

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.

The key beneficial compounds for a healthy dark roast coffee:


Melanoidins are what make coffee (and foods) brown when roasted, baked or toasted. Coffee melanoidins may enhance immune-stimulating properties, serve as dietary fiber, and may contribute to reducing the risk of colon cancer.

They are formed during the Maillard reaction, when sugars and amino acids combine at high temperatures and low water activity. They may be considered bioactive compounds (Bekedam, E.K., 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.

Impacts / Actions: Antioxidant activity, metal-chelating, antibacterial, prebiotic functionality

Effect of Roast

  • High molecular weight melanoidins are formed as roasting gets darker. Melanoidins have metal chelating properties (antioxidant activity).
  • Melanoidins may decrease colon inflammation through improved microbiota balance (prebiotic effect). Dark roasted coffee shows promotion of Bifidobacterium [BB12], a well-known probiotic, via melanoidins as the main substrates.


  • Coffee melanoidins may act as soluble fiber enhancing immune-stimulating properties and contributing significantly to reducing the risk of colon cancer (Vitaglione, 2012; Moreira, 2015; Fogliano, 2011). 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).
  • 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 (Garsetti, 2000; Folmer, 2017). This improves the reduced/oxidized glutathione balance in the colon. Glutathione is an antioxidant produced in our cells.
  • Coffee melanoidins seem to have a protective effect on liver steatosis in obese rats (Vitaglione, 2012), which suggests that the melanoidins in coffee may have an influence on liver fat and functionality. Glutathione may be involved.
  • Coffee melanoidins inhibit lipid peroxidation. 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 disease and even atherosclerosis (Tagliazucchi, 2010).
  • Coffee melanoidins are able to chelate transition metal ions, that is they are able to bind Zn2+, Cu2+, and Fe2+ (Takenaka, 2005; Morales, 2005). Metal-chelating ability is key to inhibiting lipid peroxidation, among other benefits.
  • Coffee melanoidins may act to promote the growth of a beneficial colon microbiota, affecting inflammatory pathways in the colon and consequently in the liver (Folmer, 2017). Oddly, antioxidative structures formed in coffee melanoidins are similar to vitamin E. These appear to activate their scavenging properties gradually (Bekedam, 2008).
  • Several studies carried out have shown that melanoidins extracted from coffee possess antioxidant activity. 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, 2010).
References: Vitaglione, 2012; Moreira, 2015; Fogliano and Morales, 2011; Sales, 2019.

Trigonelline & Niacin

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, and it breaks down to niacin and nicotinic acid and N-methylpyridinium at higher temperatures, as well as volatiles such as pyridine and pyrazines. Trigonelline plus nicotinic acid helps regulation of liver enzymes, which is closely related to the suppression of triglyceride accumulation as well as progression of diabetes.

Impacts / Actions: Antioxidant activity, anti-tumorigenic, anticarcinogenic,anticariogenic, antimicrobial, hypoglycemic, hypocholesterolemic.

Effect of Roast

  • As coffee is roasted, the content of trigonelline decreases and niacin increases. In the coffee beverage, this niacin is highly bioavailable.
  • Niacin (nicotinic acid) is essential for specific oxidation–reduction reactions in the body. It has been shown to reduce some neurological disorders, such as dementia.


  • Trigonelline at the dark roast level converts to higher niacin levels. In the coffee beverage, this niacin is highly bioavailable (Trugo, 2003). Niacin (nicotinic acid) is essential for specific oxidation–reduction reactions in the body. Trigonelline plus chlorogenic acids reduced early glucose and insulin response, which helps 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 progression of diabetes.
  • Trigonelline acts on up-regulating antioxidant enzyme activities and decreasing lipid peroxidation in the pancreas (Verzelloni, 2010).

NOTE: Volumes have been written about trigonelline, but for this paper the research purpose was the relationship between dark roasting and trigonelline. Trigonelline is an effective compound in prevention of diabetes and related kidney diseases (Virtanen, 2019). The content of trigonelline decreases continuously throughout roasting, while nicotinic acid and N-methylpyridinium increases, with N-methylpyridinium being the major thermal product up to the dark-medium roast, similar to the Purity Dark Roast.

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


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).

Impacts / Actions: Antioxidant activity, lower stimulatory effect on gastric acid secretions, possibly assists in weight control, anticarcinogenic (possibly with colon cancer), DNA protective effects.

Effect of Roast

  • Dark roast has higher N-methylpyridinium.
  • Gastric acid secretion lower after consuming dark roast blend coffee compared to the medium roast blend.
  • N-methylpyridinium-rich, dark roasted coffee reduced the bodyweight in pre-obese subjects
  • CGA and N-methylpyridinium were identified as inducers of Nrf2, considered the master regulator of cell survival.
  • Potential DNA protective effect.


  • Gastric acid secretion was less effectively stimulated after administration of a dark roast blend coffee compared to the medium roast blend. The dark roast measured higher concentration of N-methylpyridinium 87 mg/l compared to the medium roast (29 mg/l), but lower trigonelline and CGA (Rubach, 2014).
  • A N-methylpyridinium-rich, dark roasted coffee reduced the bodyweight in pre-obese subjects, indicating a significant potential for body weight control by dark roast coffee brews containing high amounts of NMP (Kotyczka, 2011).
  • 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).
  • Numerous studies indicate that damage of the genetic material plays a crucial role in a variety of human diseases, in particular in the etiology of cancer. Chronical consumption (8 weeks) of a pure arabica dark-roast coffee blend significantly reduced spontaneous DNA strand breaks in blood cells of healthy volunteers, pointing to a DNA protective effect (Pahlke, 2019) and (Schipp 2018).
  • A strong increase of the activity of N-methylpyridinium, which catalyzes the detoxification of numerous genotoxic carcinogens, was observed in the liver. In addition, a pronounced increase of the antioxidant activity of plasma was detected in experiments, indicating that N-methylpyridinium may contribute substantially to the ROS protective properties of coffee (Al-Serori, 2019).
References: Rubach, 2014; Kotyczka, 2011; Boettler, 2011; Pahlke, 2019 and Schipp 2018.

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 represents approximately 30% of the available original CGA amount (Farah, 2005).

Impacts / Actions: Antioxidant activity, possible anti-opioid activity, hypoglycemic, and potential effects on brain function independent of the pharmacological effects of caffeine.

Effect of Roast

  • Chlorogenic acid lactones (CGL) are created during the coffee roasting process from chlorogenic acids (CGA).
  • As with CGA, a fraction of CGL is absorbed in the digestive tract. The remaining amount is metabolized by the gut microbiota and the metabolites (phenolic acids) with antioxidant and anti-inflammatory activities can still be absorbed or protect the colon from free radicals.


  • 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 and DePaula, 2019).
  • Part of the lactone was converted into caffeoylquinic acids after contact with the alkaline pH of human digestive fluids. 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).
  • Chlorogenic acid lactones were shown to exert blood glucose-normalizing effects in rats, and these effects were later observed for the chlorogenic acids themselves (Farah, 2013).
  • It has been found in a mouse model that chlorogenic acid affects spontaneous locomotor activity, suggesting that chlorogenic acid or its metabolite 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. 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, 2009).
References: Farah, 2005 & 2013; Díaz-Rubio, 2007. (Note: A dark roast mixture was used in this study); Sales, 2019.


Roasted coffee is the major known food source of norharman and harman β-carbolines. Considered mostly as neuroactive substances with a wide spectrum of reported pharmacological and neuroactive actions, binding to many receptors in the brain, including opiate, and frequently act as inhibitors to regulate neurotransmitters. They are MAO inhibitors, being increasingly associated with a beneficial effect in Parkinson disease. Their health effects are being extensively studied.

Impacts / Actions: Antioxidant activity, possible anti-opioid activity, hypoglycemic, antidepressant. Reduced rate of development of Parkinson’s disease (Ascherio, 2004).

Effect of Roast

  • Amounts of harman and norharman levels are very low in green coffee and increase significantly during roasting, but are highly variable. It is indicated that a darker roasted coffee will be higher in harman and norharman β-carbolines.


  • Norharman and harman are potent competitive and reversible monoamine oxidase (MAO) inhibitors, in both rat and humans. The high amounts of these β-carbolines in roasted coffee place them in the top of the suspected list for compounds with probable influence on Parkinson’s disease course (Casal, 2015)
  • Robusta coffee has higher values of norharman and harman compounds. Purity dark roast will be exclusively arabica coffee, which did demonstrate high levels of β-carbolines, although not the amount of robusta. Purity continues to search for a robusta green coffee that meets its standards.
  • Amounts of harman and norharman levels are very low in green coffee and increase significantly during roasting, but are highly variable. It is indicated that a darker roasted coffee will be higher in harman and norharman β-carbolines (Gomes, 2006).
  • Norharman and harman extracted from coffee brews exhibited inhibitory properties on recombinant human MAO-A and -B isozymes, catalyzing the oxidative deamination of kynuramines (Herraiz, 2006).
  • The amounts produced during roasting are variable, but generally speaking, norharman increases during roasting and harman decreases after 240°C (464°F) (Casal, 2015).
References: Casal, 2015; Rodrigues, 2019.

More to come…

The literature clearly states more research needs to be done in humans on these issues. There are so many studies, that we have the potential either to refine the dark roast to match future literature, or come up with an additional roast based on findings by the researchers. In particular, because norharman and harman β-carbolines and N-methylpyridinium are unique in coffee, these may yield more information in the areas of mental health and gastro-intestinal benefits, respectively.

Depression, Cognitive Decline, Alzheimer's and Parkinson's Diseases

A vast number of papers have been written on coffee’s impact on the brain and mental health. Coffee can influence cognitive functioning, improve memory and protect the brain’s oxidative system. Some of this is roast-level dependent. Purity Coffee will continue to explore how:

  • Dark roast coffee extracts are more potent inhibitors of amyloid-beta oligomerization (the main component of the amyloid plaques found in the brains of people with Alzheimer's disease) than light roast coffee extract. Phenylindane, found in dark roast, is a potent inhibitor of both amyloid-beta and tau fibrillization. (Mancini, 2018)
  • Parkinson's disease is the second most common neurodegenerative disorder, affecting 1% of the world population age 65 and older. Regular coffee consumption has been epidemiologically associated with a reduced risk for Parkinson disease, particularly in regard to the caffeine. (Chen, 2019). However, the compounds in dark roast that are shown to be beneficial for Alzheimer’s disease are also being investigated for Parkinson’s. That said, the concern with Parkinson’s points to extremely dark roasted coffee.
  • The results indicated that the intake of coffee, similar to caffeine, improved long-term memory when tested with object recognition. In addition, chronic coffee and caffeine ingestion reduced the lipid peroxidation of brain membranes and increased the concentration of reduced-glutathione. Chronic coffee ingestion, through the protection of the antioxidant system, may play an important role in preventing age-associated decline in cognitive function. (Abreu, 2011).
  • The sensory characteristics of dark roast coffee (roast–aroma and flavor, burnt–aroma and flavor, bitter, and body) might elicit positive-high energy feelings for some. Tobacco (flavor) and cocoa (aroma) may also be responsible for positive emotions (content, good, and pleasant). Citrus and acidity seemed to be negative sensory drivers as they induced the feeling of being off-balance (Bhumiratana, et. al 2019).
  • Intermediate and high molecular weight melanoidins do not appear to be digested or taken up in the blood stream at all. There is not much information available on the bioavailability of coffee melanoidin antioxidants, and melanoidins have low digestibility. It is likely that coffee melanoidins will pass the GI-tract, and if the antioxidants are not destroyed by gastric conditions, the roasting-induced antioxidants should show antioxidant activity. This could provide protection against a wide range of radicals throughout the GI-tract, but more research needs to be done (Bekedam, 2008).
  • The roasts used in the Boettler study were very different than what Purity would ever consider using. Their dark roast was done extremely quickly and to too high a temperature. In addition, the conclusion admitted that although there appears to be an impact on the Nrf2 pathway, there actually was no significance statistically. Also, all studies were supported by the same company, so may have had a financial interest stake in its results, i.e. conflict of interest.
  • Scientists approach the study of β-carbolines in coffee cautiously, due to their strong biological actions on the nervous system and coffee being a rich dietary source. Some propose that these compounds are involved in the pathogenesis of Parkinson’s and further studies are needed. Older studies (Ostergren, 2004) indicate that it is possible norharman may cross the cerebral barrier and accumulate in the cortex. The lowest roast level indicated in the study by Gomes (2006) was about 8°C (46°F) higher (that’s A LOT in coffee roasting) than Purity’s dark roast level. The Gomes study approached PAH-levels too high above what Purity has set as its safe standard to avoid PAHs. The Purity Dark Roast β-carboline level should be “in moderation” to have the beneficial effects indicated by the literature without going too far.
  • Chlorogenic acid should be seen in light of their relative percentage in comparison with CGA. As coffee is roasted darker, CGA decline, but the lag time and temperature of CGL must be considered in terms of overall percent, when considering levels.
  • Studies of β-carbolines in coffees are confounded significantly due to the common issues of studying coffee (cultivar, soil and inputs, growing conditions, processing methods, drying methods, storage time, roast level, etc.), but seem to have even wider swings of results than other compounds. The coffee brew method and water-to-coffee ratio is a major confounder, too (Rodrigues, 2019).
  • There is still so much research to be done on roast level and coffee compounds, which is confounded by the vastness of coffee cultivars, farming practices, processing techniques, roasting machines and brew methods, that anything written here will need to be revised annually. Overwhelmingly, though, the literature points to coffee being good for health, and dark roast being helpful to (or easier on) the digestive tract.
  • Everyone has a unique biome within, and people will have different responses to a given coffee.

What we are excited about...

As more people choose to buy coffee for health, we are eager to learn more about coffee’s possibilities. Outside of the decisions we’ve made, there are so many things at play that we still don’t know, and scientists continue to provide insights. Here are our top take-aways:

  • None of the research stated that they had used specialty grade (higher quality), certified organic coffee. We assume, then, that the coffee was likely commercial grade and conventionally grown. We can only imagine what results might be with a healthier coffee.
  • The literature shows how there are dozens of choices Purity can make in roasting that positively impacts health. These findings support our vision to further develop coffees for different conditions. This gives more choice for consumers based on their health concerns.

Lab Testing: Min-Maxing the Compounds


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.