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Dean Pomerleau

Hot Beverages/Foods & Risk of Esophageal Cancer

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Dean, thanks for the recent posts!


About the mocha method: note that most mocha brewers are made out of aluminum! Aluminum is not benign. PubMed will show this, as long as industry-financed papers are excluded.


About the second paper: this is extremely useful! I don't drink much tea because I'm still not non-worried about manganese (and am getting tons from my new hemp seed consumption), but from a basic chemistry standpoint, it's good to know that there's something about the caffeine molecule that makes it harder to dislodge at lower temperatures than other molecules in tea -- something that could well be relevant to the question of the ratio of non-caffeine bennies to caffeine bennies (1) in different methods of preparing coffee.




(1) Some aren't sure whether caffeine is beneficial, but it seems to be, against Parkinson's, and possibly against Alzheimer's.

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It uses paper filters to get rid of the harmful junk in coffee that Michael talks about.plunger instead.



It's not at all clear to me that cafestol and kahweol are best characterized as "harmful junk."  While there is evidence that they are associated with increased LDL levels,  the exact type of LDL involved is not clear,   nor, afaik, have any direct harmful effects  been established.


On the other hand, there appears to be abundant evidence of positive benefits from cafestol and kahweol (see below.)


Elsewhere Dean made the argument:



...my point is that if your blood pressure is fine, as is the case with most CR practitioners, thankfully including you, it would seem the health benefits of caffeine (e.g. reduced dementia risk, reduced parkinson's risk, reduced heart disease risk, reduced all-cause mortality etc.) would be equivalently enjoyed whether you are a fast or slow metabolizer.


I'm wondering why a similar argument wouldn't be valid in relation to cafestol and kahweol:  if your blood lipids are fine, as in the case of most CR practitioners, it would seem that the health benefits of cafestol and kahweol need not be tossed aside out of fear of a possible increase in LDL levels.  (I'm not giving up my polyphenol-rich, lusciously foamy, lipidly-alive Greek coffee!)



Coffee provides a natural multitarget pharmacopeia against the hallmarks of cancer

Excerpts (emphasis added):


A cup of coffee also contains lipids, which are mainly found in the form of two diterpene alcohols: cafestol and kahweol (Fig. 1). These molecules are sensitive to the roasting process and also largely removed from coffee

when it is brewed using a paper filter (Fig. 2) (Silva et al.2012).



By analyzing the effects of the consumption of coffee by rats, Ferk et al. (2014) noticed that coffee consumption

prevents DNA damage and that this protective effect is stronger when the coffee is prepared using a metal filter, which releases more caffeine, cafestol and kahweol (Fig. 1). The two coffee lipids, cafestol and kahweol, are anti-genotoxic compounds that prevent the deleterious effects of reference carcinogens N-nitrosodimethylamine, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, ferric ion-nitrilotriacetic acid and H2O2 in human hepatoma HepG2 cells (Majer et al. 2005), NIH/3T3 mouse embryo fibroblast cell line (Lee and Jeong 2007) and healthy human lymphocytes (Bichler et al. 2007). They act directly as ROS scavengers, and they increase the level of UDP- glucuronosyltransferase and glutathione S-transferase (GST), two enzymes involved in the detoxification of DNA-reactive metabolites. In addition, they act also on the DNA-repair machinery by activating the induction of O-6-methylguanine-DNA methyltransferase, a DNA-repair enzyme (Huber et al. 2003). In a more recent study, both cafestol and kahweol were also described as inhibitors of cytochrome P450, an enzyme responsible, among other things, for the activation of carcinogens and thus DNA damage (Silva et al. 2012).




Cafestol (Fig. 1), a diterpene homologous to kahweol,  also inhibits HUVEC proliferation and migration in a dose dependent manner at concentrations as low as 20 lM. At the same concentration, the mechanistic analysis shows that it partially or completely inhibits the phosphorylation of VEGFR2, Akt and focal adhesion kinase (FAK), but does not affect Erk 1/2, although a concentration of 5 lM was sufficient to significantly decrease the tube formation in a Matrigel assay (Wang et al. 2012).




In agreement with its anti-angiogenic properties, kahweol (Fig. 1) (25 lM) reduces the expression of MMP-2

and completely inhibits this enzyme and the protease urokinase (50 lM) (Cardenas et al. 2011). At a lower

concentration (5 lM), it inhibits the migration and invasion of several human cancer cells lines, such as MDA-MB-231 (breast), A549 (lung) and PC3 (prostate). Under the same conditions, kahweol decreases the expression levels and activities of MMP-2 and MMP-9 in MDA-MB-231 cells via STAT-3 inactivation (Kim et al. 2012).




Cafestol (Fig. 1), one of the main diterpene alcohols, induces apoptosis in renal carcinoma Caki-1 cells by promoting the up-regulation of the pro-apoptotic proteins Bim and Bax and the down-regulation of the anti-apoptotic proteins cellular FLICE (FADD-like IL-1b-converting enzyme) inhibitory protein (cFLIP), Bcl-2, Mcl-1, and BclxL via the inhibition of the Akt pathway (Choi et al. 2011). With kahweol (Fig. 1), these proteins can both trigger the apoptosis of human malignant pleural mesothelioma cells by decreasing protein and mRNA levels of the transcription factor Sp1. Although structurally similar, cafestol most effectively cleaved Bid, caspase-3 and PARP, whereas kahweol induced apoptosis by up-regulating Bax and down-regulating Bcl-xL (Lee et al. 2012).






Cafestol, a Coffee-Specific Diterpene, Is a Novel Extracellular Signal-Regulated Kinase Inhibitor with AP-1-Targeted Inhibition of Prostaglandin E2 Production in Lipopolysaccharide-Activated Macrophages




Coffee is a popular beverage worldwide with various nutritional benefits. Diterpene cafestol, one of the major components of coffee, contributes to its beneficial effects through various biological activities such as chemopreventive, antitumorigenic, hepatoprotective, antioxidative and antiinflammatory effects. In this study, we examined the precise molecular mechanism of the antiinflammatory activity of cafestol in terms of prostaglandin E2 (PGE2) production, a critical factor involved in inflammatory responses. Cafestol inhibited both PGE2 production and the mRNA expression of cyclooxygenase (COX)-2 from lipopolysaccharide (LPS)-treated RAW264.7 cells. Interestingly, this compound strongly decreased the translocation of c-Jun into the nucleus and AP-1 mediated luciferase activity. In kinase assays using purified extracellular signal-regulated kinase 2 (ERK2) or immunoprecipitated ERK prepared from LPS-treated cells in the presence or absence of cafestol, it was found that this compound can act as an inhibitor of ERK2 but not of ERK1 and mitogen-activated protein kinase kinase 1 (MEK 1). Therefore our data suggest that cafestol may be a novel ERK inhibitor with AP-1-targeted inhibitory activity against PGE2 production in LPS-activated RAW264.7 cells.





Suppressive effects of the kahweol and cafestol on cyclooxygenase-2 expression in macrophages.




Inducible cyclooxygenase-2 (COX-2) has been suggested to play a role in the processes of inflammation and carcinogenesis. Recent studies have shown the chemoprotective effects of kahweol and cafestol, which are coffee-specific diterpenes. This study investigated the effects of kahweol and cafestol on the expression of COX-2 in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages. Kahweol and cafestol significantly suppressed the LPS-induced production of prostaglandin E2, COX-2 protein and mRNA expression, and COX-2 promoter activity in a dose-dependent manner. Furthermore, kahweol blocked the LPS-induced activation of NF-κB by preventing IκB degradation and inhibiting IκB kinase activity. These results will provide new insights into the anti-inflammatory and anti-carcinogenic properties of kahweol and cafestol.


PMID: 15225655






Natural diterpenes from coffee, cafestol and kahweol induce apoptosis through regulation of specificity protein 1 expression in human malignant pleural mesothelioma






Malignant pleural mesothelioma (MPM) is a highly aggressive cancer with a very poor prognosis. Several clinical studies such as immunotherapy, gene therapy and molecular targeting agents have been tried for treatment of malignant mesothelioma, however, there is no application for effective clinical treatment. Coffee has various biological functions such as anti-oxidant, anti-inflammatory, anti-mutagenic and anti-carcinogenic activities. The therapeutic activities of the bioactive compounds in coffee was sugested to influence intracellular signaling of MPM. Regarding to the cancer-related functions, In this study, suppression of Sp1 protein level followed by induction of MSTO-211H cell apoptosis by cafestol and kahweol were investigated in order to determine Sp1's potential as a significant target for human MPM therapy as well.





Anti-Angiogenic and Anti-Inflammatory Properties of Kahweol, a Coffee Diterpene






Epidemiological studies have shown that unfiltered coffee consumption is associated with a low incidence of cancer. This study aims to identify the effects of kahweol, an antioxidant diterpene contained in unfiltered coffee, on angiogenesis and key inflammatory molecules.


Methodology/Principal Findings


The experimental procedures included in vivo angiogenesis assays (both the chicken and quail choriallantoic membrane assay and the angiogenesis assay with fluorescent zebrafish), the ex vivo mouse aortic ring assay and the in vitro analysis of the effects of treatment of human endothelial cells with kahweol in cell growth, cell viability, cell migration and zymographic assays, as well as the tube formation assay on Matrigel. Additionally, two inflammation markers were determined, namely, the expression levels of cyclooxygenase 2 and the levels of secreted monocyte chemoattractant protein-1. We show for the first time that kahweol is an anti-angiogenic compound with inhibitory effects in two in vivo and one ex vivo angiogenesis models, with effects on specific steps of the angiogenic process: endothelial cell proliferation, migration, invasion and tube formation on Matrigel. We also demonstrate the inhibitory effect of kahweol on the endothelial cell potential to remodel extracellular matrix by targeting two key molecules involved in the process, MMP-2 and uPA. Finally, the anti-inflammatory potential of this compound is demonstrated by its inhibition of both COX-2 expression and MCP-1 secretion in endothelial cells.




Taken together, our data indicate that, indeed, kahweol behaves as an anti-inflammatory and anti-angiogenic compound with potential use in antitumoral therapies. These data may contribute to the explanation of the reported antitumoral effects of kahweol, including the recent epidemiological meta-analysis showing that drinking coffee could decrease the risk of certain cancers.




Edited by Sibiriak

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