I've recently discovered that I can handle filtered coffee much better than unfiltered coffee.
There are some substances in coffee that are filtered out by a simple paper filter.
One example is cafestol [1], but there may be others.
Quote from Wikipedia:
In filtered coffee drinks such as drip brewed coffee, it is present in only negligible amounts, as the paper filter in drip filtered coffee retains the diterpenes.
[1] https://en.wikipedia.org/wiki/Cafestol
Filtering your coffee is such a splendid idea! It is hard to see why not anyone else promotes this simple method. In the past month I have been drinking my coffee solely filtered and I hardly anymore get the bad reactions from coffee. I only wish I had done so in the past 20 years. My suffering surely would have been less excruciating at critical times. If anyone suffers from coffee, but simply can’t abandon it like me then this is an absolutely must try. Actually I have known about the filtering method for some time, but I was rather skeptic about the whole thing, so I can only blame my own pessimism.
Nevertheless as for the precise method I make my coffee drinks with an espresso machine using grounded coffee half-loaded in the holder just as I have always done. Then I pour the hot coffee through two washable cloth coffee filters put together and a regular filter with a handle. I wash the filters with some clean flowing water after each use, which is a bit of a hassle, but it certainly worth the time. Alternatively one may buy throwaway paper filters, but I haven’t tried those yet, so I can’t make a comparison.
Most people in America and Japan drink their coffee filtered unlike us in Europe, so they may not even realize that this could be a problem. Coffee contains a great number of bioactive compounds, so it is really hard to say why it has this or that effect. Certainly though cafestol could be the main culprit as pointed out before.
I also tested some other supplements to figure this out. Guarana as a caffeine source actually proved somewhat beneficial for POIS, but it takes almost a days time for the effects to be noticeable which makes me question the modus operandi of caffeine. Green coffee extract as a source of chlorogenic acid was less beneficial than guarana, but I couldn’t note a detrimental reaction, though of course the cursory test might not reveal every detail. The white kidney bean pod tea as another source of trigonelline was actually beneficial, but this may have been due to other compounds as well. Nevertheless these compounds can be mostly ruled out as the causative for the coffee related problems. Thus it is very likely that cafestol as a compound that increases cholesterol could be the main reason for the adverse effects.
Some research that may help in understanding the underlying mechanism:
Unfiltered coffees contain higher amounts of cafestol and kahweol. These are chemicals found in oil droplets floating in the coffee and also in the sediment. Studies have shown that these substances can raise triglyceride levels and LDL cholesterol levels.https://bartalks.net/study-links-unfiltered-coffee-to-be-health-problems/Coffee consumption is associated with reduced risk of metabolic syndrome, obesity and diabetes, which may be related to the effects of coffee and its bioactive components on lipid metabolism. Coffee contains caffeine, a known neuromodulator that acts as an adenosine receptor antagonist, as well as other components, such as chlorogenic acids, trigonelline, cafestol and kahweol.
Roasting coffee beans degrades heat unstable compounds (e.g. phenolic acids and trigonelline) and changes their sensory profile. For instance, light or medium roast coffee beans are used to make coffee drinks with more chlorogenic acids (CGA) than dark roast coffee beans. Brewing methods influence the coffee drink composition as well; Turkish-style coffee drink had higher concentrations of diterpenes (cafestol and kahweol) than filtered coffee drink.
Although kahweol and cafestol are structurally similar, their effects on lipid metabolism have been shown to be different; cafestol was more effective as cholesterol-raising factor, while kahweol was more effective as an adipogenesis inhibitor.
Coffee can regulate the fatty acid translocase (FAT/CD36/SR-B2), a key transmembrane protein for lipid uptake and transport. Caffeine, CGA and trigonelline have shown to decrease the diet-induced hepatic CD36 overexpression. CD36 is not only important for the uptake of dietary fatty acids, but also its ability to bind lipoproteins in the liver. Thus, the decreased expression of CD36 by coffee compounds is probably related to changes in blood lipid profile, including reduced triglycerides, cholesterol and LDL levels. It was further suggested that caffeine, CGA and trigonelline regulated CD36 via AMPK- and PPARG -dependent pathways.
It is suggested that the decreased lipid uptake and transport is related to lipogenesis inhibition; FABP4 (also called aP2), a target for PPARG, was downregulated by caffeine and kahweol in adipocytes.
The lipolytic effects of coffee compounds are regulated by an additional pathway, the mammalian target of rapamycin (mTOR). mTOR was inhibited by coffee, caffeine, trigonelline and kahweol in vivo or in vitro. Consistently, the lipolytic effects of caffeine were related to autophagy-lysosomal pathway dependent on AMPK and CaMK, known to crosstalk with mTOR.https://sci-hub.st/https://link.springer.com/article/10.1007/s10068-019-00662-0In addition, filtering can change coffee composition, for example, paper-filtering can lead to a drastic decrease in lipid and vitamin content. Lastly, the way of consumption can affect bioavailability of coffee compounds. For example, the addition of milk or non-dairy creamers have been shown to either impair or delay the bioavailability of polyphenols.
A group of less well-known substances of coffee are the melanoidins, defined as high-molecular-weight nitrogenous and brown-colored compounds. They have been proposed to exert beneficial effects on human health in terms of antioxidant and antiinflammatory function, but as the exact structure of these components are largely unknown, exact health mechanisms remain to be elucidated.
Caffeine is a methylxanthine, which contains three main metabolites: theobromine, paraxanthine, and theophylline. Caffeine is almost exclusively metabolized in the liver, which has led to the question of reverse causality—perhaps patients with cirrhosis drink less coffee because of more pronounced side-effects.
Moreover, CGA completely inhibited fatty acid synthesis (FAS), conceivably by phosphorylation of AMPK and subsequent downregulation of acetyl-CoA carboxylase (ACC), as AMPK knockout cells did not show CGA-mediated inhibition of glucose production. The authors found that CGA lowered the mRNA expression of genes involved in (I) hepatic fat accumulation, mediated by PPARG1 and G2, cluster of differentiation (CD) 36, fatty acid binding protein 4, and monoacylglycerol O-acyltransferase 1.
It was suggested that the preventive effect of polyphenols worked via downregulation of mRNA lipogenic genes (i.e., FAS, ACC1, and stearoyl-CoA desaturase1), and SREBP1c, the main regulator of FAS. Vitaglione et al found that not only polyphenols but also decaffeinated coffee (DC) and melanoidins affected steatosis via (I) modulation of inflammatory genes, that is, interleukin (IL) 4, 6, and 10 increment, and interferon (IFN) g and TNFa decrement; (II) increased fatty acid beta oxidation; and (III) reduced liver oxidative stress mediated by glutathione.
Takahashi et al did not examine lipid content of the liver but found lower lipid metabolism-related genes regulated by PPARG (i.e., complement factor D, fatty acid binding protein 2, ACC, and CD36), in both CC and DC, albeit more pronounced in CC, implying an additive effect of caffeine. Five in vivo studies on caffeine and steatosis identified caffeine as antisteatogenic.
Caffeic acid, a specific 5-lipoxygenase inhibitor, was used therapeutically in carbon tetrachloride (CCl4) poisoned rats and led to lower liver enzymes, liver collagen content, and lipid peroxidation as measured by malondialdehyde (MDA; a marker for oxidative stress).
Paradoxically there was one study that showed a deleterious effect of Turkish (unfiltered, diterpenoid-rich) coffee on fibrosis, inflammation, and lipid peroxidation even without exposure to an exogenous toxin, suggesting a potential toxic effect of this type of coffee. This study is in contrast to all other studies on whole CC or DC and fibrosis that did not find a direct toxic effect.
Diterpenoids are well-studied coffee compounds in carcinogenesis. Schilter et al studied the effect of diterpenoids in rats without administration of an exogenous toxin. The authors found a dose-dependent increase of glutathione S-transferases (GST)-placental form. GSTs are glutathione catalyzing enzymes and induction of GST has been associated with reduced carcinogenesis. The GST-inducing capacity of kahweol and cafestol, with or without presence of an exogenous toxin, was confirmed by later studies. In addition, Cavin et al found a 50% decrease in DNA adduct formation after diterpenoid administration, potentially leading to fewer mutations in proto-oncogenes and tumor-suppressor genes. Lastly, mRNA expression of carcinogen-detoxifying phase II mechanisms (CYP450 and sulfotransferase 1A1) was decreased upon diterpenoid treatment but not after unfiltered coffee administration. Moreover, CYP2B2 and CYP1A1 activities were increased upon both filtered and unfiltered CC in this study.
Boekschoten et al conducted two trials in which healthy volunteers were given unfiltered coffee or coffee oils, high in cafestol. Both trials showed an increase in serum transaminases (with a large interindividual variance) and a slight decrease in GGT and alkaline phosphatase.https://sci-hub.st/https://www.thieme-connect.com/products/ejournals/abstract/10.1055/s-0038-1666869We conclude that cafestol suppresses bile acid synthesis by downregulation of cholesterol 7alpha-hydroxylase and of, to a lesser extent, sterol 27-hydroxylase in cultured rat hepatocytes, whereas kahweol and isokahweol are less active. We suggest that suppression of bile acid synthesis may provide an explanation for the cholesterol-raising effect of cafestol in humans.
Cafestol suppressed bile acid synthesis more potently (2- to 4-fold) than the mixture at the same concentration. In fact, the mixture appeared to counteract the effects of cafestol on bile acid synthesis and cholesterol 7alpha-hydroxylase mRNA level. We conclude therefore that cafestol is the active compound and suggest that kahweol and isokahweol are less active or not active.https://www.ahajournals.org/doi/full/10.1161/01.ATV.17.11.3064They show that filtered coffee is associated with a lower mortality than no coffee or unfiltered coffee and that the increased risk of ischaemic heart disease mortality for unfiltered coffee is partly through its association with total cholesterol. They conclude that the lowest mortality was among consumers of 1–4 cups of filtered coffee per day. One possible mechanism in the prevention of cardiovascular disease might be caffeine, which is a xanthine with various vascular effects and mechanisms of action. Caffeine increases intracellular calcium in endothelial cells and stimulates the production of nitric oxide through the expression of endothelial nitric oxide synthase enzyme. Caffeine in coffee also has favourable effects on metabolic syndrome and insulin resistance, with no significant association with the risk of new-onset atrial fibrillation or, rather, a reduced risk of atrial fibrillation with the consumption of intermediate amounts of caffeinated coffee (1–7 cups/week). The inverse association between caffeine consumption and all-cause mortality was also observed in chronic kidney disease. However, caffeine may not be associated with filtered or unfiltered coffee.https://journals.sagepub.com/doi/full/10.1177/2047487320920415Molecular docking analysis revealed a strong affinity binding between all active compound of tea or coffee with CD36, but not with PPARG. Except EGCG, the active compound of tea and coffee fulfil the criteria of drug-likeness.https://www.phcogj.com/article/1735Decaffeinated coffee and green tea extract inhibit foam cell atherosclerosis by lowering inflammation and improving cholesterol influx/efflux balance through upregulation of PPARG and miR-155.
Upregulation of CD36 expression causes oxLDL endocytosis. Thus, lipid accumulation inside macrophages leads to endoplasmic reticulum (ER) stress, and stimulates the production of inflammatory cytokines through the activation of NFkB signalling and the reduction of anti-inflammatory cytokines.
Although many studies have revealed the health benefits of coffee, several reports showed opposite, detrimental results. Coffee contains several active compounds, mainly chlorogenic acid (CGA), followed by diterpenes (kahweol, cafestol), and trigonelline. Light-roasted coffee yields the highest antioxidant concentration compared with green coffee or full roasted coffee.
The decaffeinated coffee and green tea extract reduced CD36 and increased ABCA1 expression in ox-LDL stimulated macrophages. The endocytosis of ox-LDL is mainly regulated by CD36 whereas ABCA1 plays a significant role in cholesterol efflux.
PPARG is an antiatherogenic transcription factor that contributes to the suppression of foam cell formation. Moreover, experiments with primary macrophages indicated that IL-10 directly stimulated the efflux of cholesterol by activating the PPARG-LXR-ABCA1/ABCG1 pathway. PPARG-deficient macrophages showed impaired phagocytosis. In macrophage lipid metabolism processes, PPARG directly increases the expression of ABCA1, which was confirmed by our report.
Interestingly, PPARG also directly increased CD36 expression. Based on other studies, we suggest that CD36 expression is not determined solely by PPARG expression. However, there are other factors that affect CD36 expression, such as the presence of IL-34, and ER stress. In addition to a direct effect, PPARG may indirectly work on influx and efflux mechanisms by modulating the inflammatory process.https://f1000research.com/articles/10-1175While trigonelline may be not filtered out, it is yet another suspicious compound in coffee.
Yeransian et al. showed that arabica green coffee contained ca 1%, robusta 0.7% and liberica 0.25% of trigonelline. Part of the trigonelline found in coffee seeds is transformed into nicotinic acid (niacin) during roasting.https://www.researchgate.net/profile/Paulo-Mazzafera/publication/223122085_Trigonelline_in_coffee/links/5fa86c9692851cc286a05a07/Trigonelline-in-coffee.pdfDrinking coffee has been associated with the development of several endocrine-related cancers. The interpretation of these data has often been limited to the role that caffeine plays. Trigonelline (Trig), a niacin-related compound, is a natural constituent of coffee accounting for ~1% dry matter in roasted beans.
When cells were cotreated with suboptimal doses of E2 (10 pmol/L) and Trig (100 pmol/L), an additive enhancement of MCF-7 growth was observed. In the absence of E2, Trig stimulated MCF-7 cell proliferation in a dose-responsive manner and significantly enhanced cell growth at concentrations as low as 100 pmol/L.
After caffeine, Trig is the second most abundant alkaloid compound in raw coffee beans and makes up ~1% of the dry matter of roasted coffee beans. Trig has been demonstrated to have several biological activities, including an antimicrobial agent inhibiting the growth of Streptococcus mutans, a bacterium closely associated with the development of dental caries in humans. In vitro Trig (30–100 umol/L) was associated with regeneration of dendrites and axons in cortical neurons and this effect was correlated to improved spatial memory in rats. In addition, treatment with Trig (2.5–40 umol/L) has been shown to inhibit the invasion of liver cancer cells in vitro.
Trig induced the reporter, suggesting that not only can it activate the receptor, but it also induces the molecular action of ERalpha, the predominant form of the receptor in MCF-7 cells.
Coffea arabica contains the highest concentrations of Trig compared with other varieties and is the species most commonly used when preparing the beverage. In addition to bean type, degree of roasting also decreases Trig content.https://academic.oup.com/jn/article/139/10/1833/4670305
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