Our medium blend of organic coffee scientifically formulated for liver vitality.

At Purity Coffee we make every decision based on health, and our vision is to improve the world’s health through coffee. We study the latest scientific research to improve continuously how we source, test, roast and deliver our coffees.

We begin with the following fundamental standards as a baseline 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, and we want consumers to have more choice 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 Protect is a balanced medium 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 liver protection:

Chlorogenic Acids

Coffee has a high concentration of chlorogenic acids (CGAs), which is why coffee is considered one of the most important contributors to antioxidant intake in many countries, since people drink it daily and often multiple times. There is an abundance of literature on coffee CGAs and their antioxidant activity. CGAs play one of the most important roles in coffee’s positive impact on liver health.

Impacts / Actions: Antioxidant activity, anti-inflammatory, antibacterial, anti-mutagenic, possible anti-opioid activity, hypoglycemic, and others.

Health Notes

  • Lighter roasted coffees are higher in chlorogenic acids (and organic acids like citric and malic), but also higher in acrylamide, which may affect the liver, so a balanced approach of a light-medium roast is needed for optimum health-roasted coffee. Chlorogenic acid adds bitterness in taste, not “sour” notes.


  • Plant phenolic compounds, chlorogenic acids specifically, and their metabolites have been studied both in epidemiologic research and animal models in vitro to gain more comprehensive understanding of the antimutagenic and antioxidant activity of polyphenols to prevent pathogenesis of a wide range of chronic disease states. Some of these studies have shown that the predominant CGA (5-CQA) can alleviate the oxidative stress induced by methamphetamine in rats by restoring liver superoxide dismutase (SOD) and glutathione peroxidase (GPx) [detoxifying enzymes] activities and preventing the accumulation of MDA (Koriem 2014).
  • Oral administration of 5-CQA also alleviated hepatic ischemia and reperfusion-induced liver injury by reducing inflammatory responses and increasing antioxidant defense systems (Koriem 2014).
  • Pharmacologic properties attributed to caffeoylquinic and dicaffeoylquinic acids include antiviral activity against adenovirus and herpes virus (Chiang 2002), as well as hepatoprotective activity in an experimental model of liver injury (Basnet 1996). CGA has shown anti-hepatitis B virus potency as well (Wang 2009).
  • Approximately 80%–100% of chlorogenic acids are extracted in coffee brewing yielding approximately 35–100 mg chlorogenic acids per 100-mL cup of Arabica coffee in free form and soluble fiber (Díaz-Rubio 2007). Although maintaining coffee brews at a high temperature (like on a hot plate) reduces chlorogenic acids and lactones concentrations, they are still present in relatively high amounts in medium-roasted coffees compared with most food sources (Clifford 2000). Non-coffee drinkers usually take in less than 100 milligrams of chlorogenic acids/day, whereas modest and heavy coffee drinkers ingest 0.1–2 grams (Farah 2012).
  • 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).
  • Part of the lactone is converted into caffeoylquinic acids after contact with the alkaline pH of human digestive fluids. Therefore, it is likely that a large proportion of lactones consumed in the brew return to their respective chlorogenic acid forms during digestion, indirectly increasing the total chlorogenic acids intake (Farah, 2013).
References: Koriem, 2014; Chiang, 2002; Basnet, 1996; Wang, 2009; Díaz-Rubio, 2007; Clifford, 2000; Farah, 2012 & 2013.

Diterpenes: Cafestol & Kahweol  (C&K)

Only found in the lipids of coffee, C&K are usually studied and discussed in tandem, since it is difficult to isolate them and kahweol is highly unstable when purified, as well as more sensitive to heat, oxygen, light and acids. These bioactive compounds and their derivatives, which are mainly salts or esters of saturated fatty acids (predominant) and unsaturated fatty acids, represent approximately 20% of the lipid fraction of coffee, with cafestol accounting for about 0.2%-0.6% of coffee weight.

Impacts / Actions: Antioxidant, hypoglycemic, hypolipidemic, antimicrobial, antiviral, and cafestol from high habitual coffee consumption is associated with reduced risk of developing type 2 diabetes (Mellbye 2015). Anticarcinogenic, hepatoprotective properties in vitro, agent for cancer chemopreventive blocking (Cavin 2002).

Health Notes

  • Coffee diterpenes have exhibited anticarcinogenic and hepatoprotective properties in vitro, they stimulate intracellular antioxidant defense mechanisms, as well as a common agent for cancer chemopreventive blocking.
  • C&K protect against several well-known carcinogens and exert anti-inflammatory actions when studied both in the lab or in the body.
  • In human liver epithelial cell lines, C&K was found to inhibit one of the human enzymes responsible for aflatoxin B1 activation, which helps explain some of the anticarcinogenic effects of C&K.


  • C&K protect against several well-known carcinogens and exert anti-inflammatory actions when studied both in the lab or in the body. Different mechanisms appear to be involved in these chemoprotective effects: an induction of conjugating enzymes in hepatic tissues, an increased expression of proteins involved in cellular antioxidant defense, and an inhibition of the expression and/or activity of cytochromes P450 involved in carcinogen activation (Cavin 2002).
  • C&K are bioactive compounds and their derivatives, which are mainly salts or esters of saturated fatty acids (predominant) and unsaturated fatty acids, represent approximately 20% of the lipid fraction of coffee, with cafestol accounting for about 0.2%-0.6% of coffee weight (Farah 2012).
  • The brewing method has a direct impact on the dosage of the compound: Paper filters trap most of the diterpenes, whereas French press, espresso, Turkish and Scandinavian coffee maximize diterpenes. You can see the oils floating on the surface of your coffee, if you reflect the light off of it the right way. C&K increase blood cholesterol level, which is something that some people may want to avoid, since they may indirectly increase the risk of cardiovascular diseases. If this is the case, choosing to brew the coffee with a paper filter using a pourover or drip method will virtually eliminate the diterpenes, while allowing the caffeine and chlorogenic acids to still be bioavailable.
  • In human liver epithelial cell lines, C&K treatment resulted in a reduction of aflatoxin B1-DNA binding correlated with the enzyme GST-mu, which is known to detoxify aflatoxin B1. C&K also was found to inhibit one of the human enzymes responsible for aflatoxin B1 activation, which helps explain some of the anticarcinogenic effects of C&K (Cavin 2002).
References: Mellbye, 2015; Cavin, 2002; Farah 2012; Guzzo, 2012


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

Health Notes

  • Melanoidins have been shown to have anticarcinogenic, antioxidant, antimicrobial and anti-inflammatory properties; antioxidant capacity of melanoidins is affected by gut microbiota fermentation.


  • Several studies carried out have shown that melanoidins extracted from coffee possess antioxidant activity. (Tagliazucchi, 2010).
  • 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 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 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 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).
References: Bekedamn, E.K., et. al., 2008; Tagliazucchi, 2010; Vitaglione, 2012; Moreira, 2015; Fogliano and Morales, 2011; Takenaka, 2005.


Uric acid is a normal component of urine, but high blood concentrations of uric acid can lead to gout and is associated with other medical conditions. Uric acid is synthesized mainly in the liver and intestines from the breakdown of purines by the enzyme Xanthine oxidase (XO). Inhibition of xanthine oxidase reduces the production of uric acid, and phenylindanes from coffee beverages have demonstrated potent XO inhibitory activities.

Health Notes

  • Studies have shown that men who drank 4-5 cups of coffee per day had a 40% decreased risk of gout, and with more than 6 cups had a 59% lower risk. In women, 1-3 cups showed a 22% lower risk of gout with more than 4 cups showing a 57% lower risk compared to those who drank no coffee. The researchers concluded 4+ cups of coffee per day lowers uric acid levels and decreases the incidence of gout.
  • The mean value of uric acid in coffee consumers was significantly lower in both normal and the diabetic population in a study of 200 healthy subjects (and 48 were coffee drinkers).
References: Fukuyama, 2018; Choi, 2007 & 2010; Towiwat, 2015; Bhaktha 2016.

Coffee Caffeine

Caffeine is an alkaloid found in leaves, seeds, and fruits of coffee, tea, cocoa, cola, and guarana plants. Within 10 minutes of drinking coffee, the stomach and first part of the intestine absorb the caffeine, and it reaches maximum concentration in the bloodstream within about an hour. The liver metabolizes the caffeine into paraxanthine, theobromine, and theophylline which contribute to enhancing its effects. Caffeine and theophylline act as an antagonists of adenosine receptors in humans—adenosine interacts with specific cell receptors, most noticeably inhibiting neural activity and causing drowsiness, but it performs numerous other actions in the body.

Impacts / Actions: Anti-inflammatory.

Health Notes

  • The beneficial effects of coffee and caffeine extract against liver fibrosis have been demonstrated by several studies using standard rodent models. In almost every study, coffee blocked toxin-induced liver fibrosis and cirrhosis. In one key study using rats, the scientists induced liver disease in the animals and then tested regular coffee, decaffeinated coffee and a water-caffeine solution. The regular coffee produced the most impactful positive results, showing that it was not just the caffeine that benefits the liver. “A reduction in hepatic TGF-β1 expression in the group receiving decaffeinated coffee indicates that caffeine may not be the solely hepatoprotective compound in coffee beverages.”
  • Caffeine seems to play an important role against liver injury, since fibrosis and inflammation were lower in the animals receiving regular coffee and caffeine.


  • In certain parts of the body caffeine modulates intracellular levels of cyclic adenosine monophosphate (cAMP), which regulates immune cell functions, plays an important role in metabolism and promotes the release of insulin from pancreatic beta cells. Upregulation of cAMP inhibits activation of inflammatory effector cells such as T cells. In T cells, cAMP downregulates various cellular functions, including cytokine production and cytotoxicity (Setkovsky 1988).
  • The anti-inflammatory properties of caffeine are also due to its function as a phosphodiesterase (PDE) inhibitor (Horrigan 2006). Phosphodiesterase inhibitors encourage blood vessel dilation and smooth muscle relaxation and are used to treat people with pulmonary hypertension or lung issues, sometimes even reversing some of the damage to the heart and lungs. More recently, Kreisel, et. al. suggested the use of PDE-5 to treat liver cirrhosis (2020).
  • The beneficial effects of coffee and caffeine extract against liver fibrosis have been demonstrated by several studies using standard rodent models. In almost every study, coffee blocked toxin-induced liver fibrosis and cirrhosis. In one key study using rats, the scientists induced liver disease in the animals and then tested regular coffee, decaffeinated coffee and a water-caffeine solution. The regular coffee produced the most impactful positive results, showing that it was not just the caffeine that benefits the liver. “A reduction in hepatic TGF-β1 expression in the group receiving decaffeinated coffee indicates that caffeine may not be the solely hepatoprotective compound in coffee beverages” (Furtado 2012).
  • 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).
  • Caffeine and Telomeres: Telomeres play a vital role in preserving the information in our genome. Telomeres are DNA–protein structures found at both ends of each chromosome that protect the genome from degradation, unnecessary recombination, repair, and interchromosomal fusion. Caffeine promotes the expression of telomerase reverse transcriptase (TERT), extending the telomere length and preventing cellular deterioration and loss of division/growth capacity (Tao2021).
    • Caffeine has also been shown to improve microscopic structural changes of the thymus, spleen and liver due to aging, which helps to clarify different ways coffee benefits health in regard to longevity (Tao 2021).
  • Caffeine and Adenosine: Research suggests that the protective effect of caffeine may be due to its blocking of adenosine, which is a potent internal regulator of inflammation and tissue repair (Chakraborti 2003). There are four subtypes of extracellular adenosine: A1, A2A, A2B, and A3 (Fredholm 2001). Activation of adenosine A2A receptors promotes tissue repair, wound healing, and matrix production (Montesinos 1997 & 2002), it reduces inflammation and prevents acute inflammatory injury in the liver [Ohta 2001]. In other cell types, adenosine A2A receptors stimulate collagen production via mitogen-activated protein (Revan 1996).
  • Because of the positive actions of adenosine, in 2001, Ohta et. al. tested the concern that caffeine might exacerbate tissue damage if consumed during an acute inflammation episode. They assessed the effect of acute and chronic caffeine treatment on acute liver inflammation. Their results showed that the dose of caffeine was critical to the body’s reaction: Caffeine at lower doses (10 and 20 mg/kg) strongly exacerbated acute liver damage and increased levels of proinflammatory cytokines. However, high doses of caffeine (100 mg/kg) completely blocked both liver damage and proinflammatory cytokine responses through an A2A receptor-independent mechanism (Ohta 2007).
  • Also, at high doses, caffeine inhibits cAMP, yet a low dose of caffeine regulates cAMP levels through antagonism of the A2A receptor. In short, the lower doses of caffeine were proinflammatory, which would be difficult to deduce from the observational/epidemiological studies. This is one reason that scientists believe it is the caffeine in conjunction with other compounds in coffee (chlorogenic acid, caffeic acid, ferulic acid, etc.), diterpenes (cafestol, kahweol), and trigonelline, which may exert liver protective effects (Farah et. al. 2019).

Cautionary notes on Caffeine:

  • Habitual caffeine consumption increases CYP1A2 activity, which has implications for the metabolism of various medications and synthesis of cholesterol, steroids and other lipids. Some drugs that inhibit CYP1A2 activity interfere with the metabolism and elimination of caffeine, increasing the risk of its toxic effects. Because several drug interactions may occur between caffeine and medications, patients taking caffeine-containing medicine or coffee drinkers taking drugs that interact with CYP1A2 may require dosage adjustments or need to avoid coffee, despite its potential benefits for the liver (Carrillo 2000). Drug interactions between caffeine and other psychoactive drugs may lead to caffeine-related or medication related side effects. For example, use of ketamine in combination with caffeine enhances its stimulant responses and lethal risk, suggesting a potentially toxic interaction, and the interaction between caffeine and antiepileptic drugs can increase seizure frequency (Hsu 2009, Jankiewicz 2007).
  • Drugs that should avoid caffeine include cimetidine (Tagamet), disulfiram (Antabuse), estrogens, fluconazole (Diflucan), fluvoxamine (Luvox), mexiletine (Mexitil), quinolone class antibiotics, and terbinafine (Lamisil). Use of ketamine in combination with caffeine may have a potentially toxic interaction, and the interaction between caffeine and antiepileptic drugs can increase seizure frequency (Carrillo 2000, Hsu 2009, Jankiewicz 2007).
  • Avoid caffeine at least 8 hours prior to going to bed, if it disturbs your sleep.
References: Setkovsky, 1988; Horrigan, 2006; Furtado, 2012; Pahlke, 2019; Schipp, 2018; Tao, 2021; Chakraborti, 2003; Fredholm, 2001; Montesinos, 1997 & 2002; Ohta, 2001 & 2007; Revan, 1996; Farah et. al., 2019; Carrillo, 2000; Hsu, 2009; Jnkiewicz, 2007.

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.

Liver Diseases and Coffee's Impact


There are an overwhelming number of studies that conclude that coffee drinking reduces liver fibrosis (please see bibliography). These studies avoid the mistakes of mid-century research into coffee: They adjust for confounding factors, like cigarette smoking and lifestyle issues.

Liver fibrosis results from chronic damage; eventually the ability of liver to regenerate fails, and hepatocytes are replaced by extracellular matrix (ECM). Fibrosis disorganizes the architecture of the liver anatomically and functionally, which is a characteristic of most types of chronic liver diseases. Under normal conditions of wound healing, tissues are replaced without cellular overgrowth, but injury to the liver from inflammation to physical disturbances or injury can lead to excessive connective tissue formation. Repair happens in a sequence that produces an inflammatory response with numerous actions involving neutrophils, macrophages, lymphocytes and leukocytes, the last one producing cytokines that trigger the proliferation of capillary production, fibroblasts and smooth muscle cells. If the liver is more severely damaged with longer inflammatory response, the tissue reconstruction (fibrotic process) can include an excessive amount of extracellular matrix (ECM), which ends up as scar tissue and fibrosis. The fibrotic cytokines and hepatic stellate cells (HSCs) are considered the key reason for this fibrous overgrowth, and coffee has been shown to block these effects by acting at various points of the pathological processes mentioned above (Farah 2019, V.1, p. 215). The main injuries to the liver that produce hepatic fibrosis include chronic hepatitis C or B infections, alcohol abuse, cholestasis, and nonalcoholic steatohepatitis.

Researchers have found that advanced liver fibrosis from chronic liver diseases (CLDs) of various etiologies is associated with low coffee and total caffeine consumption. Demonstrating the clinical significance of coffee consumption, Freedman et al. found that among patients with advanced fibrosis, those who consumed no coffee had a risk of hepatic decompensation or hepatocellular carcinoma (HCC) of 11.1 per 100 patient-years, compared to just 6.3 per 100 patient years in those consuming at least three cups of coffee per day, with no beneficial effect noted with tea or other sources of caffeine (Freedman 2009).

Coffee exerts protective effects against liver fibrosis through antioxidant action and the suppression of fibrogenic cytokines (that trigger ECM growth), TGF-β (a regulator of immune cells) and PDGF-β (an important regulator of cell growth, proliferation, and formation of blood vessels). Among many antioxidative and hepatoprotective components in coffee, the chlorogenic acids and other polyphenols have been suggested as relevant compounds due to their noteworthy levels in coffee (Farah 2019, Farah 2013, Farah 2006). These findings indicated that other components besides caffeine are involved in the hepatoprotective effects of coffee against liver fibrosis (Shin 2009).

Coffee has been shown to limit the progression of liver fibrosis in established liver disease (Shin 2010, Modi 2010, Shi 2009), and has been associated with reduced hepatic fibrosis in patients with liver diseases like hepatitis C (Molloy 2011). However, in 2017 a group of researchers in the Netherlands studied coffee’s effect on liver fibrosis that was not severe enough to present definite or readily observable symptoms yet. They evaluated whether coffee had an association with liver stiffness in over 2400 individuals from the general population, and found that frequent coffee consumption reduced liver stiffness, but not necessarily the steatosis (fatty liver). However, they concluded in the end that coffee consumption might still be useful to prevent progression to more advanced stages, such as inflammation and fibrosis (Alferink 2017).

The most impressive evidence came in 2015 with a meta-analysis that included 4 cross-sectional and 2 case-control studies with over 20,000 patients that showed that regular coffee consumption significantly reduces rates and severity of hepatic fibrosis in patients with liver disease. Caffeine itself was not significantly associated with the results, but regular coffee (naturally caffeinated) intake was significantly associated with reduced hepatic fibrosis. In some cases, depending on the degree, hepatic fibrosis could be reversed, and the liver could return to a normal structure. Coffee consumption can reduce the severity of fibrosis and may contribute to the repair of liver tissue. Coffee caffeine is associated with a significant reduction in risk of fibrosis among patients with nonalcoholic fatty liver disease (Shen 2015). The scientists recommended, “Given the potential benefits of regular coffee, patients with NAFLD should be encouraged to consume regular coffee daily.”

Progression of liver injury from fibrosis to cirrhosis is a slow and terminal process. Fatty liver disease and hepatitis-C have caused an increase in numbers of patients with fibrosis and cirrhosis over the past decade, and a simple, cost-effective mechanism to slow down the process seems to be readily available: Coffee. Even better: Good quality, organic, clean, mycotoxin-free coffee. Aflatoxins in particular are hepatocarcinogenic in humans, especially in conjunction with chronic hepatitis B virus infection (Wild 2010), so consuming coffee that is free of toxins is also critical to a healthy liver.

Metabolic Associated Fatty Liver Disease (MAFLD)

Nonalcoholic fatty liver disease (NAFLD) has been a term used for decades, but in 2019 an international consensus panel presented new terminology to better reflect its causes: Metabolic associated fatty liver disease [MAFLD]. We will use the two interchangeably for this review, because the vast body of literature refers to it as NAFLD.

MAFLD is a condition characterized by a buildup of fat in the liver, and is the most common liver disease globally with estimates at close to a billion people having a degree of the disease. “NAFLD is associated with many metabolic comorbidities, including obesity, type II diabetes, dyslipidemia, and metabolic syndrome. Its potential to develop into more severe liver conditions, such as nonalcoholic steatohepatitis, advanced fibrosis, cirrhosis and hepatocellular carcinoma, can lead to a state in which liver transplantation is the only treatment option available” (Chalasani 2012).

Because MAFLD is so pervasive, scientists turned their attention to the epidemiological and clinical evidence of the past 20 years that indicated coffee’s potential hepatoprotective effects, including antioxidative, anti-inflammatory, and antifibrotic activity. A 2013 study conducted a systematic review of the epidemiology, magnitude, and mechanisms of possible beneficial effects of coffee consumption in patients with NAFLD using 12 detailed prior studies:

  • Four continuous cycles of the National Health and Nutrition Examination Surveys (NHANES, USA 2001–2008) were used to investigate the effects of dietary behavior in NAFLD patients. Taking into account diet, nutrition, demographics, and other factors, findings showed a strong association between coffee consumption and protection against the development of NAFLD (Birerdinc 2012).
  • In an Italian study, 137 NAFLD cases and 108 controls were enrolled, and coffee intake determined by the absolute number of cups of coffee consumed. When compared with non-coffee drinkers, those who consumed coffee had less severe fatty liver evaluated by ultrasound “bright liver score”. Bright Liver Score (BLS) is the observation of bright liver echo pattern on ultrasound-- it is considered a sign of hepatic steatosis and provides accurate and reliable detection of moderate-severe fatty liver.
  • In a histological examination of liver biopsies using a questionnaire, researchers reported a strong inverse relationship between caffeine consumption and hepatic fibrosis, associating caffeine consumption with both the prevalence and severity of MAFLD (Molloy 2012).

More recently, coffee is associated with a significant reduction in risk of fibrosis among non-alcoholic steatohepatitis (NASH) patients (Kopzhassaruly 2020). NASH is the most severe form of metabolic associated fatty liver disease and is closely related to obesity, pre-diabetes, and diabetes. As with other studies, they showed dose-related results-- that those who drank 2-4 cups per day showed a significant difference to those who drank 1 cup per day.

In 2020, Alessio Calabrò et. al. conducted a literature review on coffee and MAFLD/NAFLD, and they summed up the beneficial effects of coffee consumption reported in dozens of papers, highlighting 7 key studies since 2014. These studies showed that coffee consumption in patients with NAFLD can be protective against liver steatosis, progression of fibrosis and liver damage, primarily through antioxidant activity and coffee caffeine intake, which improves insulin resistance and reduces the production of inflammatory and fibrogenic cytokines. Although the researchers found some controversy due to lack of information on types of coffee, dosages, etc., they concluded that 2-3 cups of coffee a day in patients with MAFLD should be encouraged.


Cirrhosis is a late-stage liver disease in which healthy liver tissue is replaced with scar tissue and the liver is permanently damaged. Scar tissue keeps your liver from working properly. Many types of liver diseases and conditions injure healthy liver cells, causing cell death and inflammation ( Cirrhosis always develops because of another liver problem or disease: alcohol abuse, nonalcoholic (or metabolic associated) fatty liver disease, hepatitis B, hepatitis C, certain autoimmune diseases, and other causes. Cirrhosis isn't curable, but it's treatable. Doctors have two main goals in treating this disease: Stop the damage to your liver, and prevent complications.

For several decades, researchers have been making connections between liver health and coffee consumption. Data collected from 1978-1985, supported the hypothesis that there were ingredients in coffee that protect the liver against cirrhosis, especially alcoholic cirrhosis. A 10-year study of 128,934 patients hospitalized with cirrhosis carried out by Klatsky et. al. (1992) showed coffee intake was associated with a lower prevalence of cirrhosis. In addition, coffee consumption seemed to help prevent death from cirrhosis.

Ten years later in a study of more than 700 individuals, a relationship was observed between how much coffee was consumed per day and risk of liver cirrhosis. The odds ratio[1] for liver cirrhosis decreased for each cup of coffee:

  • From 1.0 for those who did not drink coffee to 0.47 for those who consumed 1 cup of coffee daily,
  • 23 for consumers of 2 cups,
  • 21 for 3 cups, and
  • 16 for 4 cups

Was it just the caffeine in coffee that caused this? The team studied other beverages that had caffeine, and compared those with the risk of liver cirrhosis, and they found that caffeine alone was not significantly associated with lower cirrhosis risk. These findings support the hypothesis that coffee, but not other beverages containing caffeine, may inhibit the onset of alcoholic and nonalcoholic liver cirrhosis— and there must be something else in the coffee (Corrao 2001).

The following year, a study of 101 cirrhosis patients (with more than 1500 control subjects), risk among coffee drinkers showed a significant reduction in cirrhosis (the odds ratio was 0.54) compared with individuals who never drank coffee. Similar to the previous study, for those drinking more than 3 cups/day there was a significant trend for lower cirrhosis risk with an odds ratio of 0.29. Repeating assumptions from the previous study, the consumption of other caffeine-containing beverages did not reduce the occurrence of cirrhosis. The researchers followed up a few years later and continued to find evidence for a beneficial role of coffee consumption on reduced risk of death from liver cirrhosis. The mortality rate of people who drank 3 or more cups of coffee was lower than those who drank 2 cups of coffee or less (Tverdal 2003).

The correlation was also valid for alcoholic cirrhosis as well as cirrhosis from other causes, which was different than the study from the 1990s. There also seemed to be a threshold in how much coffee was effective: No further decline in mortality when the intake was more than three to four cups of coffee. The meta-analysis done by Kennedy et al. in 2016 concluded that an increase in daily coffee consumption of two cups is associated with a near halving of the risk of cirrhosis.

A number of research studies have examined the role of coffee in preventing liver cirrhosis with consistently positive and sometimes quite dramatic results. A 2002 study also published in the Annals of Epidemiology concluded that there is a 71% lower risk for those drinking more than three cups per day (Gallus 2002). Drinking three or more cups of coffee daily lowers the risk by up to 53% of liver disease progression for patients with chronic hepatitis C. Black tea or green tea, however, had no effect on liver disease (Freedman 2009).

[1] An odds ratio (OR) is a measure of association between an exposure and an outcome. The OR represents the odds that an outcome will occur given a particular exposure, compared to the odds of the outcome occurring in the absence of that exposure.

OR=1 Exposure does not affect odds of outcome.

OR>1 Exposure associated with higher odds of outcome.

OR<1 Exposure associated with lower odds of outcome.

Liver Cancer

Hepatocellular carcinoma (HCC) is a type of liver cancer that frequently stems from cirrhosis of the liver or hepatitis infection. It is becoming more common in developing countries and is often fatal. For decades scientists have studied the relationship between coffee consumption and preventive effect against liver cancer. In the 1990’s animal experiments showed chlorogenic acids in coffee had inhibitory effects against chemical carcinogenesis in liver tissue (Tanaka 1990).

Researchers found that the subjects with a history of liver disease had a significant inverse relationship between coffee consumption and liver cancer. They concluded that coffee may prevent liver cancer more effectively among subjects with liver disease than among those without liver disease, but at the same time their conclusion stated, “…coffee consumption is significantly associated with a decreased incidence of liver cancer.” (Shimazu 2005).

This followed with several epidemiologic studies:

A large scale study followed 90,000 Japanese subjects over ten years and in the Journal of the National Cancer Institute in 2005 concluded that coffee drinkers have half the risk of developing liver cancer as non-coffee drinkers. This effect was recorded for those who drank just one to two cups daily with increasing effect at three to four cups. Unfortunately, because decaffeinated coffee is rarely consumed in Japan, they could not make a distinction between caffeinated and decaffeinated coffee and could not determine if caffeine were partly responsible for the decreased risk of HCC (Inoue 2005). In a similar study in Italy, where coffee is widely consumed, men and women who drink coffee may be reducing their risk of liver cancer, but tea and decaf did not appear to share regular coffee's protective effects. Abstainers from coffee drinking resulted in a doubled risk for HCC with respect to moderate drinkers (<14 cups/week) (Montella 2007).

In another 2007 meta-analysis of published studies on HCC, quantitative information on coffee consumption from thousands of cases and controlled studies from Europe and Japan (approximately 240,000 thousand people, among them 2,260 diagnosed with HCC) had similar conclusions: They observed a 41% reduction in the risk of HCC among coffee drinkers compared with never-drinkers. Regardless of study design, geography and other bias, men and women who regularly drink coffee have a significantly reduced risk of developing liver cancer and other liver diseases, suggesting a continuum of favorable effect of coffee on liver function (Bravi 2007).

That same year another review of studies that represented hundreds of thousands of cases observed an inverse relation between coffee consumption and risk of liver cancer, and in 6 studies the association was statistically significant. Overall, an increase in consumption of 2 cups of coffee per day was associated with a 43% reduced risk of liver cancer, and the odds drop by 23% with each cup (Larsson 2007).

Additional large studies were done and showed similar results: High coffee consumption was significantly associated with a reduced risk of HCC in subjects, but was reduced in chronic hepatitis B patients by the dominant role of viral replication. They noted that further studies were needed to clarify the protective mechanism of specific ingredients in coffee and the possible interaction between coffee and underlying viral etiologies in the HCC development among chronic liver disease patients (Jang 2014).

The relationship between coffee intake and decreased risk of HCC appears to be consistent for several etiological types of chronic liver disease, including HCC. Lifetime coffee consumption is shown to be an independent protective factor against HCC.

In 2020 Bhurwal et. al. did a meta-analysis to evaluate the association of coffee with HCC or liver cancer development along with the amount of coffee needed to prevent HCC or liver cancer. They reviewed dozens of articles from 1996-2019 that associated coffee with liver cancer, narrowing them down to 20 studies for data. Their systematic review showed that drinking coffee provides benefits with a reduction in the risk of HCC or liver cancer and higher doses of coffee have higher benefits in terms of risk reduction.

Lab Testing: Min / Maxing the Compounds


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