‘I took a trip to Nurofen Near Aspirin-by-sea, And all along my journey There were many sights to see. Like Anadin, and Panadol, Two lovely seaside towns, And a place called Alka Seltzer Nestling in the downs….now I’m safely home again, I’m tired for goodness sake, I’ve got a splitting headache, But I don’t know what to take!’Darryl Ashton

When you live in a world where serotonin is the ‘happy hormone’, and where an ‘estrogen deficiency’ is plausible, a whole range of things that wouldn’t otherwise be imaginable, become possible, and many things are more confusing than might otherwise be the case.

One of the biggest problems with a drug like aspirin, is that it has a tendency to work a little bit too well, and when it comes to making money, that’s not necessarily a good thing.

“Multiple clinical studies have demonstrated a link between long-term aspirin use and a reduction in the incidence and mortality of several cancer types, including colorectal, stomach, esophageal, breast, lung, prostate and liver cancers.”

“Patients who present with NVUGIB [nonvariceal upper gastrointestinal bleeding] on aspirin had reduced in-hospital mortality and fewer adverse outcomes, while those on anticoagulants had increased in-hospital complications.”

“…accumulating evidence points to cardioprotective doses of aspirin and other NSAIDs being chemopreventive against colorectal cancer and possibly other cancers of the stomach, esophagus, breast, ovary, and lung…”

Because aspirin can be seen, in some ways, as a basic promoter of healthy metabolic function, it isn’t surprising that it can also help to reduce levels of things like serotonin and estrogen.

“SALICYLATE is a powerful metabolic stimulant…in man…In hypothyroid patients it is possible to restore the basal metabolic rate to normal levels with…aspirin daily in divided doses.”

“…aspirin treatment significantly decreased the serum TSH response to TRH…”

“Aspirin elevated ATP levels not only in intact cortical neurons but also in isolated brain mitochondria…”

“The most striking finding in the Sertoli cells of 3-week-old hypothyroid rats was the dramatic enhancement of oestradiol formation…”

From a biological perspective, this information can explain some of the beneficial effects that aspirin has been shown to have in relation to protection from stress and disease.

Good quality biological experimentation does little, however, to provide justification for the sale of the newer more profitable drugs that are less effective, and often have a negative or harmful impact.

“…results show that acetaminophen alone increases brain serotonin as well as norepinephrine levels…In contrast, aspirin did not alter the levels of these monoamines but increased serotonin turnover in the brain while acetaminophen decreased the turnover.”

“NE [norepinephrine] added to pineal organ cultures increased by 72% the conversion of testosterone into estradiol…”

That’s partly why it’s so important for business, that the waters remain murky.

“Acetaminophen/paracetamol [Tylenol/Panadol] is the most widely used drug of the world. At the same time, it is probably one of the most dangerous compounds in medical use, causing hundreds of deaths in all industrialized countries due to acute liver failure…”

The polyunsaturated fats are part of this confusing story, and a great deal of time, effort and money has gone into ensuring that their harmful effects are downplayed and their reputation as a health food remains intact.

The polyunsaturated fats (PUFA) powerfully suppress metabolism. They have been shown to increase both serotonin and estrogen levels. Aspirin very effectively reduces the release of stored unsaturated fats into circulation and protects against serotonin and estrogen.

“Mean estradiol levels were 10.5% lower among women who used NSAIDs at least 15 days per month, compared to women with no NSAID use…Women in the highest versus lowest category of total analgesic use had significantly lower levels of estradiol…”

“Inhibition of the serotonergic transmission by aspirin is responsible for its nootropic and neuroprotective actions.”

“The arachidonate inhibition was dose-dependent in the tissue steroid hormone receptors, except for dose-dependent potentiation of the brain cortical estrogen receptors…results suggest the generalized modulatory effect of arachidonate on the steroid hormone receptors in the central and peripheral tissues.”

Estrogen, the polyunsaturated fats, and the substances of stress in general are known to promote cancer. Aspirin protects against the development and advancement of numerous disease states including many different forms of cancer.

“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/breast cancer stem cells and delays the formation of a palpable tumor.”

“Aspirin-only users had a 49% reduced risk of HCC [hepatocellular carcinoma] and a 50% reduced risk of death from CLD [chronic liver disease], whereas non-aspirin NSAIDs-only users experienced a 34% reduced risk of CLD mortality but no reduced risk of HCC…”

“Use of aspirin…has been associated with a decrease in the risk of several cancers, including breast cancer…NSAIDs…reduce prostaglandin synthesis; prostaglandins stimulate aromatase gene expression and thereby stimulate estrogen biosynthesis…The results for ibuprofen…were generally weaker…acetaminophen…was not associated with a reduction in the incidence of breast cancer…evidence…supports…aspirin…(which may operate through inhibition of estrogen biosynthesis) as effective chemopreventive agents for breast cancer.”

Acetaminophen/paracetamol use leads to an increase in serotonin and there is evidence that it causes more harm in association with breakdown products of the polyunsaturated fats. Acetaminophen has also been shown to have cancer promoting effects. Serotonin promotes estrogen and there are experiments which suggest that Panadol/Tylenol can be estrogenic.

“…diets high in SFA (beef tallow) or MUFA (olive oil) decreased…susceptibility to hepatotoxicity compared to diets high in linoleic acid (corn oil)…after acetaminophen intoxication…”

“These novel findings demonstrate that therapeutic acetaminophen concentrations specifically stimulate estrogen-responsive breast cancer cell DNA synthesis, suggesting that this drug may exert estrogenic effects.”

A suppressed metabolism promotes inflammation as well as rising levels of the stress substances, estrogen, serotonin and nitric oxide. PUFA causes inflammation and inflammation creates more stress. Aspirin protects against stress and inflammation.

The stress substances – cortisol, estrogen, serotonin, nitric oxide [NO] and others – interfere with oxidative metabolism and promote the release of free fatty acids into circulation. The more unsaturated these fats are, the more inflammatory, metabolism interfering and disease promoting they are.

“Acute stress exposure…caused brain expression of iNOS, an increase in plasma glutamate and brain TNF-alpha, induction of oxidative indicators in brain and a fall in brain ATP levels. Prior administration of aspirin…inhibited all these effects caused by stress…”

The stress substances interact with PUFA in such a way as to increase their damaging potential.

“To characterize the potential role of lipid peroxidation products in atherogenesis, we assessed the effect of 4-hydroxy-2-nonenal (HNE)…When added together, low concentrations of HNE and 5-HT synergistically induced…an increase in cell number…antiplatelet and antioxidant therapies may be useful for the prevention of…proliferative disorders associated with atherosclerosis…”

“NO activates cyclooxygenase and lipoxygenase, leading to the production of physiologically relevant quantities of prostaglandin E2 (PGE2) and leukotrienes. In the case of iNOS, the massive release of NO, PGE2, and leukotrienes produces toxic effects…”

Knowing this adds to an understanding of the synergistic nature of aspirin’s disease protective capabilities. Aspirin also protects against the harm caused by other more dangerous drugs that have been shown to worsen the inflammatory stress state.

“Aspirin significantly inhibits the IL-1 beta-stimulated expression of iNOS, NO, and PGE(2) in ovarian dispersates cultured in vitro.”

“Aspirin ameliorated oxidative stress by downregulating Nox4 and inducible nitric oxide synthase…”

“Administration of an overdose of paracetamol to control rats resulted in an appreciable decrease of GSH [glutathione] concentration…Simultaneous administration of…ASA [aspirin] resulted in a reduction of the paracetamol-induced depletion of GSH in all instances…”

If evidence relating to this were to be accepted in the mainstream, it would make it much harder to rationalize the sale of products – like the highly unsaturated fish and seed oils, as heart-protective, anti-inflammatory health food – and tougher for corporations to avoid responsibility for harm caused by new drugs.

It’s no wonder that it has become so difficult for consumers to decide what to trust will help with their issues, and what is best to be avoided.

“Prescribers need to be aware of patients’ individual responses to paracetamol and the observed increased toxicity with regular and higher dosing within standard analgesic dose ranges.”

“Use of diclofenac…and ibuprofen…was associated with a significantly increased risk of OHCA [out-of-hospital cardiac arrest]…”

Even well intentioned health professionals are being influenced by heavily biased information which undermines their ability to provide the most useful, best possible advice.

Many of the arguments used in the case against sugar – harming it’s reputation, and scaring the public – are underpinned by the same false and misleading doctrines used against aspirin (in favor of alternative ‘anti-inflammatory’ products), creating the shaky foundations upon which this fragile house of cards is resting.

It would be financially counter-productive to encourage notions which explain how both aspirin and sugar, for instance, might, in similar ways, protect against the promoters of inflammation and disease (such as cortisol, estrogen, serotonin, nitric oxide and PUFA), via an impact upon fundamental biological processes.

“…sugar may provide the fuel needed to meet the energetic demands of stress, which may reduce the need for glucocorticoid-driven energy catabolism and mobilization of the body’s energy stores.”

“…findings strongly suggest an increase in intracellular ATP levels as the most probable explanation for the protective effect of fructose, and point to fructose as a potentially useful therapeutic tool for protection of the liver late in paracetamol intoxication.”

“…alterations of metabolism enhance the development of hepatocellular carcinoma (HCC). Aspirin is able to inhibit the growth of cancers…through controlling abnormal lipid metabolism.”

The inflammatory relationship between stress and the polyunsaturated free fatty acids is rarely acknowledged in the mainstream, not to mention how it is worsened in combination with many popular pharmaceutical products.

“Acetaminophen is a commonly used drug that induces serious hepatotoxicity…Both linoleic acid and arachidonic acid–substrates in eicosanoid biosynthesis–were significantly influenced by overdose…results hence attest to the hazard of acetaminophen overdose on the temporal homeostasis of hepatic concentrations of free fatty acids…”

“…studies postulated that an APAP [acetaminophen] metabolism triggering lipid peroxidation was responsible for liver injury…PUFA oxidation markers were expressed immunohistochemically in almost all degenerative hepatocytes 3–24 hr after APAP injection…”

To put it another way, you could say that the polyunsaturated fats and paracetamol are two things that cause inflammatory disease, whereas aspirin and sugar are two things that protect against such states. Both function synergistically, although ironically it is aspirin and sugar which can combine to powerfully benefit metabolic performance.

From this perspective, anti-sugar as well as anti-aspirin propaganda, can be seen to be coming off branches of the same agenda tree.

When a supplement or medicine – or even a particular food – works to improve the function of metabolism via amelioration of basic biological processes, it tends to promote overall recuperation. This is not good for business.

Many tried and true products behaving in such a way (regardless of their long and successful history) have suffered the fate of exposure to ongoing, relentless negative publicity campaigns.

One effective way to achieve this, is to gradually muddy the waters of physiology, letting the increasing confusion enable the justification of almost any reasoning.

It’s then possible to maintain the illusion that pharmaceutical and medical science and research is tirelessly moving towards better understanding and more effective methods of prevention and treatment.

Of course even the best things can be misused, every possible angle is not always seen, and things don’t always go according to plan.

You don’t have to take my word for it. Do some reading. Enquire. Find out for yourself.

See more here

Aspirin curtails the acetaminophen-induced rise in brain norepinephrine levels.

Aspirin attenuates pulmonary arterial hypertension in rats by reducing plasma 5-hydroxytryptamine levels.

The epigenetic effects of aspirin: the modification of histone H3 lysine 27 acetylation in the prevention of colon carcinogenesis in azoxymethane- and dextran sulfate sodium-treated CF-1 mice

Aspirin suppresses the abnormal lipid metabolism in liver cancer cells via disrupting an NFκB-ACSL1 signaling.

Excessive Sugar Consumption May Be a Difficult Habit to Break: A View From the Brain and Body

Aspirin and salicylate protect against MPTP-induced dopamine depletion in mice.

Salicylate or aspirin inhibits the induction of the inducible nitric oxide synthase in rat cardiac fibroblasts.

Acetaminophen inhibits liver trytophan-2,3-dioxygenase activity with a concomitant rise in brain serotonin levels and a reduction in urinary 5-hydroxyindole acetic acid.

Effect of ibuprofen on cardioprotective effect of aspirin.

Influence of thyroid hormone on androgen metabolism in peripuberal rat Sertoli cells.

Lipid peroxidation product 4-hydroxy-2-nonenal acts synergistically with serotonin in inducing vascular smooth muscle cell proliferation.

Acetaminophen alters estrogenic responses in vitro: stimulation of DNA synthesis in estrogen-responsive human breast cancer cells.

Analgesic use and sex steroid hormone concentrations in postmenopausal women

The role of aspirin in carcinogenesis

Gastric adaptation to injury by repeated doses of aspirin strengthens mucosal defence against subsequent exposure to various strong irritants in rats.

Prenatal exposure to paracetamol/acetaminophen and precursor aniline impairs masculinisation of male brain and behaviour.

Aspirin and salicylate protect against MPTP-induced dopamine depletion in mice.

Non-steroidal anti-inflammatory drug use is associated with increased risk of out-of-hospital cardiac arrest: a nationwide case–time–control study

Aspirin, Nonaspirin Nonsteroidal Anti-inflammatory Drug, and Acetaminophen Use and Risk of Invasive Epithelial Ovarian Cancer: A Pooled Analysis in the Ovarian Cancer Association Consortium

High dose of aspirin moderates diabetes-induced changes of heart glycogen/glucose metabolism in rats.

Emergence of aspirin as a promising chemopreventive and chemotherapeutic agent for liver cancer

Acetylsalicylic acid inhibits the pituitary response to exercise-related stress in humans.

Rapeseed oil-rich diet alters hepatic mitochondrial membrane lipid composition and disrupts bioenergetics.

Reduction by acetylsalicylic acid of paracetamol-induced hepatic glutathione depletion in rats treated with 4,4′-dichlorobiphenyl, phenobarbitone and pregnenolone-16-alpha-carbonitrile.

Aspirin, NSAID, and Acetaminophen Use and the Risk of Endometrial Cancer

Analgesic use and the risk of kidney cancer: a meta-analysis of epidemiologic studies

Aspirin potentiates the effect of ephedrine on the thermogenic response to a meal in obese but not lean women.

Protective effect of aspirin against dexamethasone-induced cataract in cultured rat lens.

Analgesic use in relation to sex hormone and prolactin concentrations in premenopausal women.

Aspirin intake and the use of serum ferritin as a measure of iron status.

Beneficial effect of aspirin against interferon-α-2b-induced depressive behavior in Sprague Dawley rats.

The nitric oxide hypothesis of aging.

Changes in thyroid hormones by treatment with aspirin and prednisolone in subacute thyroiditis with hyperthyroidism.

Aspirin dose dependently inhibits the interleukin-1 beta-stimulated increase in inducible nitric oxide synthase, nitric oxide, and prostaglandin E(2) production in rat ovarian dispersates cultured in vitro.

Acetaminophen-induced liver injury: Implications for temporal homeostasis of lipid metabolism and eicosanoid signaling pathway.

Evaluation of nootropic and neuroprotective effects of low dose aspirin in rats

Non-steroidal anti-inflammatory drug use is associated with increased risk of out-of-hospital cardiac arrest: a nationwide case–time–control study

Comparison of the Metabolic Stimulating Action of Aspirin and Thyroid

Acetaminophen/paracetamol: A history of errors, failures and false decisions.

Dietary saturated and monounsaturated fats protect against acute acetaminophen hepatotoxicity by altering fatty acid composition of liver microsomal membrane in rats

Aspirin inhibits the production of reactive oxygen species by downregulating Nox4 and inducible nitric oxide synthase in human endothelial cells exposed to oxidized low-density lipoprotein.

Association of frequency and duration of aspirin use and hormone receptor status with breast cancer risk.

Immunohistochemical Detection of Polyunsaturated Fatty Acid Oxidation Markers in Acetaminophen-Induced Liver Injury in Rats

Reduction by acetylsalicylic acid of paracetamol-induced hepatic glutathione depletion in rats treated with 4,4′-dichlorobiphenyl, phenobarbitone and pregnenolone-16-alpha-carbonitrile.

Time-dependent effects of low-dose aspirin on plasma renin activity, aldosterone, cortisol, and catecholamines.

Norepinephrine stimulates testosterone aromatization and inhibits 5 alpha reduction via beta-adrenoceptors in rat pineal gland.

Acetaminophen use in pregnancy and neurodevelopment: attention function and autism spectrum symptoms

Nonsteroidal Anti-inflammatory Drug Use, Chronic Liver Disease, and Hepatocellular Carcinoma

Aspirin blocks growth of breast tumor cells and tumor-initiating cells and induces reprogramming factors of mesenchymal to epithelial transition.

Cardiolipin Fatty Acid Remodeling Regulates Mitochondrial Function by Modifying the Electron Entry Point in the Respiratory Chain

Paracetamol: not as safe as we thought? A systematic literature review of observational studies

Aspirin inhibits stress-induced increase in plasma glutamate, brain oxidative damage and ATP fall in rats.

Inhibition of cardiac mitochondrial respiration by salicylic acid and acetylsalicylate.

The effect of aspirin and indomethacin on the TRH response in man.

Estimates of benefits and harms of prophylactic use of aspirin in the general population

Arachidonic acid as a possible modulator of estrogen, progestin, androgen, and glucocorticoid receptors in the central and peripheral tissues.

An oxidized metabolite of linoleic acid stimulates corticosterone production by rat adrenal cells.

Aspirin Has a Protective Effect Against Adverse Outcomes in Patients with Nonvariceal Upper Gastrointestinal Bleeding.

Prevention of paracetamol-induced liver injury by fructose.

Inhibition of glutamate release via recovery of ATP levels accounts for a neuroprotective effect of aspirin in rat cortical neurons exposed to oxygen-glucose deprivation.

Topically applied aspirin rapidly decreases histamine-induced itch.

Effects of Low-Dose Aspirin on Acute Inflammatory Responses in Humans


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