I had to go in for minor surgery recently. The surgeon asked what medications I was taking and asked me to stop taking aspirin for a short period before the surgery, to which I agreed. I take aspirin for headaches and so needed to find another solution in the meantime. Acetaminophen/paracetamol and ibuprofen are the two practical options. Both of these have clear negative effects. I’ll discuss those effects and ways I found to limit their damage in another article. I thought I should mention some of the reasons why someone would take aspirin even if it wasn’t required to treat pain. There are some risks with aspirin. It can cause stomach problems for some people. It can cause bruising and it can cause damage to the inner ear. The stomach damage can be mitigated by mixing it with some other substances (sodium bicarbonate and glycine). Bruising ameliorated by vitamin K2 MK4. I need about 1mg of K2 for every 300mg of aspirin. Aspirin has a lot of benefits but you should consider the risks too if you take it. Toxinless has a good rundown of a lot of those substances.
“Aspirin protects cells in many ways, interrupting excitotoxic processes by blocking nitric oxide and prostaglandins, and consequently it inhibits cell proliferation, and in some cases inhibits glycolysis, but the fact that it can inhibit FAS/fatty acid synthase (Beynen, et al., 1982) is very important in understanding its role in cancer.
There are several specific signals produced by lactate that can promote growth and other features of cancer, and it happens that aspirin antagonizes those: HIF, NF-kappaB, the kinase cascades, cyclin D1, and heme oxygenase.”
Benefits Of Aspirin
“Aspirin’s use fighting cancer has the potential to increase pension liabilities by as much as $100 billion by extending lifespans, a risk modeler says in a report. The pension costs for men in the U.K. could rise by 0.7% within 20 years if more people begin taking aspirin daily, according to a statement by Risk Management Solutions Inc. this week. An increase of that magnitude across the more than $13 trillion in pension liabilities in North America and Europe would be about the same as everyone giving up smoking within a generation, the modeling firm says.”
Aspirin & Dementia
Significantly, treatment with low-dose anti-inflammatory drugs (aspirin vs placebo in drinking water, equivalent to 100 mg/day in humans) completely blocked tumor- induced episodic memory impairment without affecting tumor-induced sickness or tumor growth. These data suggest that safe, available anti-inflammatories may be repurposed to prevent and treat cognitive impairment in cancer patients and survivors.
Researchers at the Boyce Thompson Institute and John Hopkins University discovered that salicylic acid, the primary breakdown product of aspirin, binds to GAPDH, thereby stopping it from moving into a cell’s nucleus, where it can trigger the cell’s death. The study, which appears in the journal PLOS ONE, also suggests that derivatives of salicylic acid may hold promise for treating multiple neurodegenerative diseases.
A breakdown product of aspirin blocks cell death associated with Alzheimer’s, Parkinson’s and Huntington’s diseases
In addition to its central role in glycolysis, HsGAPDH participates in several pathological processes, including viral replication and neuronal cell death. The anti-Parkinson’s drug deprenyl has been shown to suppress nuclear translocation of HsGAPDH, an early step in cell death and the resulting cell death induced by the DNA alkylating agent N-methyl-N’-nitro-N-nitrosoguanidine. Here, we demonstrate that SA, which is the primary metabolite of aspirin (acetyl SA) and is likely responsible for many of its pharmacological effects, also suppresses nuclear translocation of HsGAPDH and cell death.
In the PS19 transgenic mouse model of FTD, administration of salsalate after disease onset inhibited p300 activity, lowered levels of total tau and tau acetylated at K174, rescued tau-induced memory deficits and prevented hippocampal atrophy. The tau-lowering and protective effects of salsalate were diminished in neurons expressing K174Q tau. Targeting tau acetylation could be a new therapeutic strategy against human tauopathies.
In this study, we investigated whether aspirin is neuroprotective in inflammation-mediated neurodegenerative diseases….These results suggest that aspirin protects dopaminergic neurodegeneration by inhibiting the microglial-mediated oxidative stress/inflammatory response and by regulating the production of anti-inflammatory cytokines.
Aspirin protects dopaminergic endotoxin neurons against lipopolysaccharide-induced neurotoxicity in primary midbrain cultures.
Findings show that administration of single ECS daily for consecutive 8 days results in enhancement of 5-HT-mediated behavior (lithium-induced head twitches) and in disruption of the retention of CAR. Aspirin and ondansetron administration significantly increased the retention of conditioned avoidance response compared to control. Ondansetron and aspirin significantly prevented ECS-induced attenuation of the retention of conditioned avoidance response also. On the other hand, ondansetron and aspirin significantly retarded the ECS-induced enhancement of 5-HT-mediated behavior.Inhibition of the serotonergic transmission by aspirin is responsible for its nootropic and neuroprotective actions.
Aspirin & Cancer
A new study presented this week to the American Association for the Study of Liver Diseases — found that daily aspirin therapy was significantly associated with a reduced risk in hepatitis B virus‐related liver cancer.
Researchers from Oregon Health and Science University have found that aspirin may slow the spread of some types of colon and pancreatic cancer cells.
Aspirin frequency, dose, and duration were self-reported in the 2004 IWHS questionnaire. Women were followed-up to 2011. Cancer cases were ascertained by linkage to the Iowa State Health Registry. These findings suggest that aspirin use may prevent incident breast, colon, pancreatic, and ovarian cancer in elderly women.
Epidemiological studies and other experimental studies suggest that ASA use reduces the risk of different cancers including breast cancer (BC) and may be used as a chemopreventive agent against BC and other cancers. These studies have raised the tempting possibility that ASA could serve as a preventive medicine for BC.
We find that ASA not only prevents breast tumor cell growth in vitro and tumor growth in nude mice xenograft model through the induction of apoptosis, but also significantly reduces the self-renewal capacity and growth of breast tumor-initiating cells (BTICs)/breast cancer stem cells (BCSCs) and delays the formation of a palpable tumor.
Moreover, ASA regulates other pathophysiological events in breast carcinogenesis, such as reprogramming the mesenchymal to epithelial transition (MET) and delaying in vitro migration in BC cells. Collectively, ASA has a therapeutic or preventive potential by attacking possible target such as TGF-β in breast carcinogenesis.
The increasingly available evidences, however, arises more than one question on whether or not aspirin should be already given as an adjuvant agent in colorectal cancer. If on one side, in fact, evidences come from observational studies, it is also true that the magnitude of available data is impressive, and almost all point to just one, evident, direction.
The prospected benefits of this “old/innovative” anticancerdrug in terms of morbidity and mortality seem already to outweigh concerns about GI bleeding, which is rarely life threatening, and cerebral bleeding, which is extremely rare.
Acquired chemoresistance has curtailed cancer survival since the dawn of chemotherapy. Accumulating evidence suggests a major role for cancer stem cells (CSC) in chemoresistance, although their involvement in acquired resistance is still unknown. The use of aspirin has been associated with reduced cancer risk and recurrence, suggesting that the anti-inflammatory drug may exert effects on CSCs.
Treatment with aspirin prior to chemotherapy suppressed the acquisition of chemoresistance by perturbing the nuclear translocation of NFκB in preexisting CSCs. Therefore, disruptions to the NFκB–IL6 feedback loop prevented CSC induction and sensitized preexisting CSCs to chemotherapy. Collectively, our findings suggest that combining aspirin and conventional chemotherapy may offer a new treatment strategy to improve recurrence-free survival of breast cancer patients.
When people with cancer ask for my recommendations, they usually think I’m joking when I tell them to use aspirin, and very often they don’t take it, on the basis of what seems to be a very strong cultural prejudice. Several years ago, a woman whose doctors said it would be impossible to operate on her extremely painful “inflammatory breast cancer,” had overnight complete relief of the pain and swelling from taking a few aspirins. The recognized anti-metastatic effect of aspirin, and its ability to inhibit the development of new blood vessels that would support the tumor’s growth, make it an appropriate drug to use for pain control, even if it doesn’t shrink the tumor. In studies of many kinds of tumor, though, it does cause regression, or at least slows tumor growth. And it protects against many of the systemic consequences of cancer, including wasting (cachexia), immunosuppression, and strokes.
Opiates are the standard medical prescription for pain control in cancer, but they are usually prescribed in inadequate quantities, “to prevent addiction.” Biologically, they are the most inappropriate means of pain control, since they increase the release of histamine, which synergizes with the tumor-derived factors to suppress immunity and stimulate tumor growth.
It has recently become standard practice in most places to advise a person who is having a heart attack to immediately chew and swallow an aspirin tablet.
Aspirin & Diabetes
Disappearance of glycosuria and the return of fasting sugar to normal in a young diabetic during aspirin treatment for acute rheumatism led to reinvestigation of the effect of salicylate in diabetes mellitus.
An intensive two-weeks course of aspirin abolished glycosuria and lowered the fasting blood sugar to normal or near normal in seven mild to moderately severe diabetics. No decisive effect on glucose tolerance was obtained, though the blood-sugar curves were always lower during aspirin administration than they were either before or after. Moderate ketonuria in two patients was reduced to normal with aspirin.
Clinical improvement accompanied the biochemical changes induced by aspirin, and, while serious toxic manifestations were not conspicuous, tinnitus and deafness were annoying. The possible place of aspirin in the treatment of diabetes mellitus is discussed. The action of aspirin in diabetes mellitus has been located in the tissues, and this is of interest in the light of the proper establishment of the drug as a peripheral-acting metabolic stimulant.
In summary, high-dose salicylate and inactivation of IKK-β prevent fat-induced insulin resistance in skeletal muscle by blocking fat-induced defects in insulin signaling and action and represent a potentially novel class of therapeutic agents for type 2 diabetes.
High-dose aspirin treatment resulted in a ∼25% reduction in fasting plasma glucose, associated with a ∼15% reduction in total cholesterol and C-reactive protein, a ∼50% reduction in triglycerides, and a ∼30% reduction in insulin clearance, despite no change in body weight. During a mixed-meal tolerance test, the areas under the curve for plasma glucose and fatty acid levels decreased by ∼20% and ∼50%, respectively. Aspirin treatment also resulted in a ∼20% reduction in basal rates of hepatic glucose production and a ∼20% improvement in insulin-stimulated peripheral glucose uptake under matched plasma insulin concentrations during the clamp. In conclusion, these data support the hypothesis that IKKβ represents a new target for treating type 2 diabetes mellitus.
Our data demonstrate that aspirin treatment not only reduces iNOS protein levels, but also S-nitrosylation of IRbeta, IRS-1 and Akt. These changes are associated with improved insulin resistance and signalling, suggesting a novel mechanism of insulin sensitisation evoked by aspirin treatment.
Differences between NES-B and NES-G cells in NF-κB activation by acid and bile salts can account for their differences in CDX2 expression, and their CDX2 expression can be blocked by aspirin. These findings might explain why some patients with GORD develop Barrett’s oesophagus while others do not, and why aspirin might protect against development of Barrett’s oesophagus.
Aspirin could reverse the effects of tooth decay and could lead to fewer fillings being needed in the future, researchers in Belfast have said.
Initial research at Queen’s University has found aspirin stimulates stem cells in teeth, enhancing tooth regeneration.
“The next step is to work with our pharmacy colleagues to try to develop a vehicle to put it in to the teeth, after that clinical trials.”
“We are not really talking about 10 or 20 years time, it will probably be in the near future that it could be tried in a clinical trial with patients,” she said. “There is huge potential to change our approach to one of the biggest dental challenges we face.”
However, aspirin reduced pulmonary neutrophilia and tissue damaging neutrophil proteases (Matrix Metalloproteinase (MMP)-8/-9), reduced BAL concentrations of tumour necrosis factor α and reduced systemic and pulmonary TXB2. There was no difference between high-dose and low-dose aspirin. In the EVLP model, aspirin reduced BAL neutrophilia and alveolar injury as measured by histological damage.
These are the first prospective human data indicating that aspirin inhibits pulmonary neutrophilic inflammation, at both low and high doses. Further clinical studies are indicated to assess the role of aspirin in the prevention and treatment of acute respiratory distress syndrome (ARDS).
Platelet activation reduces pulmonary microvascular blood flow and contributes to inflammation; these factors have been implicated in the pathogenesis of COPD and emphysema. We hypothesized that regular use of aspirin, a platelet inhibitor, would be associated with a slower progression of emphysema-like lung characteristics on CT imaging and a slower decline in lung function.
Regular aspirin use was associated with a more than 50% reduction in the rate of emphysema progression over 10 years. Further study of aspirin and platelets in emphysema may be warranted.
The results show that acetaminophen alone increases brain serotonin as well as norepinephrine levels with a concomitant inhibition of liver TDO activity. In contrast, aspirin did not alter the levels of these monoamines but increased serotonin turnover in the brain while acetaminophen decreased the turnover. When combined with acetaminophen, aspirin overrides the reduced serotonin turnover induced by acetaminophen. This report demonstrates the potential of these agents to alter neurotransmitter levels in the brain.
Aspirin & Hypertension
Pulmonary arterial hypertension (PAH) is characterized by increasing pulmonary pressure, right ventricular failure, and death. The typical pathological changes include medial hypertrophy, intimal fibrosis and in situ thrombosis. Serotonin (5-HT) and other factors contribute to the development of pathologic lesions. Aspirin (ASA), a platelet aggregation inhibitor, inhibits 5-HT release from platelets.
These results showed that Aspirin ASA treatment effectively attenuated MCT-induced pulmonary hypertension, right ventricular hypertrophy, and occlusion of the pulmonary arteries. The effects of ASA was associated with a reduction of 5-HT.
Notably, prostaglandin E2 (PGE2) can promote the formation of a Candida biofilm. Recently, the inhibition of PGE2 has received much attention. Studies have shown that cyclooxygenase (COX) inhibitors, such as aspirin, ibuprofen, and indomethacin, combined with fluconazole can significantly reduce Candida adhesion and biofilm development and increase fluconazole susceptibility; the MIC of fluconazole can be decrease from 64 to 2 μg/ml when used in combination with ibuprofen.
Research suggests that: (1) 3-OH oxylipins in some yeasts are probably also produced by mitochondria through incomplete β-oxidation; (2) aspirin inhibits mitochondrial β-oxidation and 3-OH oxylipin production; (3) yeast sexual stages, which are probably more dependent on mitochondrial activity, are also characterized by higher 3-OH oxylipin levels as compared to asexual stages; (4) yeast sexual developmental stages as well as cell adherence/flocculation are more sensitive to aspirin than corresponding asexual growth stages; and (5) mitochondrion-dependent asexual yeast cells with a strict aerobic metabolism are more sensitive to aspirin than those that can also produce energy through an alternative anaerobic glycolytic fermentative pathway in which mitochondria are not involved.
In the present study, a catheter disk model system was used to investigate the effects of nonsteroidal anti-inflammatory drugs (all cyclooxygenase inhibitors) on biofilm formation by three strains of C. albicans. Seven of nine drugs tested at a concentration of 1 mM inhibited biofilm formation. Aspirin, etodolac, and diclofenac produced the greatest effects, with aspirin causing up to 95% inhibition.
Preventing GI Damage From Aspirin
These findings indicate that sodium bicarbonate in amounts equivalent to one-third of a teaspoonful of baking soda protects the gastric mucosa against aspirin-induced damage and prevents the usual fall in potential difference after aspirin.
When taken with ascorbic acid, the patient-reported tolerability of aspirin has been shown to be comparable to paracetamol and placebo. The existing body of evidence is relevant to short-term therapy with analgesic aspirin doses, and extrapolation to long-term therapy with low-dose aspirin is not appropriate. The purported benefit of an aspirin and ascorbic acid combination is a local observance and is not suspected to influence the adverse GI effects experienced as a result of systemic prostaglandin inhibition. Nevertheless, ascorbic acid may be a viable addition to the strategies employed to improve the gastrointestinal tolerability of aspirin.
To determine the tolerability of a glycine (Gly)-containing Aspirin acetylsalicylic acid (ASA) preparation (Gly-ASA), investigators selected 1135 patients for a noninterventional trial of Gly-ASA 50 to 300 mg daily. After an average treatment period of 42.6 days, tolerability rating scores and the frequency of 5 gastrointestinal (GI) complaints were compared with those reported for any previous treatment, including plain ASA. After treatment with Gly-ASA, the mean percentage of patients without GI complaints increased more than 2-fold, from 28.2% to 60.6%. Furthermore, the mean percentage of patients reporting any GI symptoms as “always” present decreased from 8.5% to 0.5%. Gly-ASA tolerability was rated “excellent” or “good” by 98% of the patients. In 10 patients (0.9%), Gly-ASA treatment was terminated prematurely due to GI intolerance (n=4) and nonmedication-related causes (n=6). With respect to long-term treatment compliance, the improved tolerability profile observed with this Gly-ASA preparation indicates an important advantage over nonglycine-containing ASA alternatives.
Both aspirin ASA-preparations induced comparable gastroduodenal damages during the whole test period: The lesions score of both groups on day 7, 14 and day 28 was almost identical. In contrast to plain ASA, where 9 of 10 volunteers reported gastrointestinal side effects, all subjects receiving ASA in combination with glycine did not complain from any dyspeptic symptoms, i.e. epigastric pain etc. The reasons for the apparent better tolerability of Aspirin in combination with glycine are discussed.