Fish Oil Fables

CountFishula Even though people like to blame sugar for blood sugar issues, and many recommend fish oil as a miracle cure for diabetes (and a variety of other inflammatory conditions), lots of good science has demonstrated reasons why the opposite is true in both cases.

“The PUFA [polyunsaturated fatty acid] diet contained a high proportion of n-3 fatty acids…Average blood glucose concentrations during the third week were significantly higher…on PUFA than on the saturated fat diet…”

“…effects of…fish-oil supplementation (6 g/d) on…plasma glucose disappearance (Rd glucose)…Fish oil…reduced glucose metabolic clearance rate…Carbohydrate oxidation tended to be less stimulated…Lipid oxidation tended to be more stimulated…fish oil reduced the rate of plasma glucose disappearance by 26% by reducing glucose metabolic clearance rate…”

“…dietary fish oil supplementation adversely affected glycemic control in NIDDM [non-insulin-dependent diabetes mellitus] subjects…The effect of safflower oil supplementation was not significantly different from fish oil…fish oil supplementation should be used with caution…”

It is a popularly held belief (based on scant biological evidence) that fish oil and some other polyunsaturated fats (PUFAs), make up an important part of a healthy diet, that they can be safely used for protection against inflammatory illness, and that not getting enough can eventually lead to what is often referred to as an ‘essential fatty acid deficiency.’

Rather than being harmful however, avoiding exposure to the omega-3 (and omega-6) PUFAs, has been shown to promote increased glucose uptake and help improve overall metabolic function.

“After omega-3 fatty acid withdrawal, fasting glucose returned to baseline. Omega-3 fatty acid treatment in type II diabetes leads to rapid but reversible metabolic deterioration, with elevated basal hepatic glucose output and impaired insulin secretion…Caution should be used when recommending omega-3 fatty acids in type II diabetic persons.”

Evidence suggests that under these kinds of conditions, where PUFA circulation is reduced and metabolism is allowed to work more effectively, a reasonably high sucrose diet (combined with protein and other important nutrients), can help protect against stress and inflammation, and can improve blood sugar regulation issues and other symptoms related to diabetes. Sucrose and fructose have been used as a treatment for diabetes.

“Dietary intakes of total carbohydrates, starch, sucrose, lactose or maltose were not significantly related to diabetes risk after adjustment for confounders…in the residual method for energy adjustment, intakes of fructose and glucose were inversely related to diabetes risk.”

“Strong evidence exists that substituting fructose for glucose or sucrose in food or beverages lowers peak postprandial blood glucose and insulin concentrations…”

Polyunsaturated fats (PUFAs) coming from fish oils, quickly and easily break down (due to lipid peroxidation), into a variety of highly reactive chemicals which have very harmful and inflammatory effects, interfering with metabolism as well as preventing cells from being able to effectively use glucose for fuel.

The breakdown products of fish oil (and other PUFAs) include substances like acrolein, malondialdehyde, 4-hydroxy-2-hexenal, 4-hydroxy-2-nonenal, and crotonaldehyde.

“Marine lipids contain a high proportion of polyunsaturated fatty acids (PUFA), including the characteristic long chain (LC) n-3 PUFA. Upon peroxidation these lipids generate reactive products, such as malondialdehyde (MDA), 4-hydroxy-2-hexenal (HHE) and 4-hydroxy-2-nonenal (HNE), which can form covalent adducts with biomolecules and thus are regarded as genotoxic and cytotoxic. PUFA peroxidation can occur both before and after ingestion.”

The fish oils have been shown to speedily suppress immune function, often resulting in a temporary reduction in existing processes of inflammation. This can give the illusory appearance of improvement, as a consequence of some short term symptom reduction.

In the longer term, however, the immunomodulatory stress promoting impact of these so called ‘anti-inflammatory’ fats, have many anti-metabolic effects, such as worsening blood sugar dysregulation issues (and other diabetes related symptoms), as well as increasing the likelihood of degenerative and inflammatory conditions, including cancer and Alzheimer’s disease.

“…consistent evidence for immunomodulatory effects of dietary ω-3 PUFA (EPA + DHA) intakes. High LCω-3PUFA consumption may alter the immune response to microbes in the gut, alter the community structure of the microbiota and enhance susceptibility to IBD and infection-induced inflammation and cancer.”

“…long-term intake of limited amounts of oxidized n-3 PUFA…enhances markers of oxidative stress and inflammation…partly due to intestinal absorption of 4-HHE…high DHA supplementation…causes a significant increase in plasma levels of 4-HHE…the oxidized n-3 PUFA diet induced higher IL-6, MCP-1 in plasma, and activation of transcription factor NF-κB…implicated in…inflammation…altogether our results suggest a link between oxidized n-3 PUFA and metabolic inflammation…”

Fish oil consumption has been shown to promote the release of the inflammatory stress substance nitric oxide, and there are studies which attempt to frame this as something which is beneficial for metabolic health.

But it’s almost always possible to interpret the physiological responses to stress as being something good, often because of short term suppression of symptoms. This is common with regards to nitric oxide, due in part to its protective role in relation to local and acute issues.

“Dietary supplementation with fish oils has been shown to augment endothelium-dependent relaxations, principally by improving the release of nitric oxide from injured endothelium…”

“We investigated the effects of EPA [eicosapentaenoic acid…omega 3] and elevated glucose on NO production by human endothelial cells…EPA…significantly enhanced [NO2] production…EPA-E decreased the glucose-mediated inhibition of NO production…”

“…we investigated the effects of two different types of natural fish oils containing different amounts of the n-3 PUFAs eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)…the stabilized DHA-rich oil increased the brain NOS activity (+33%, P < 0.01).”

In the longer term however, there are a great many studies which show that systemic increases in nitric oxide promote disease, including diabetes, Alzheimer’s and cancer and numerous other inflammatory conditions. Just because we have mechanisms available to us which protect against stress, does not mean that using a substance like fish oil (that can trigger a stress response and cause what looks like immediate improvements), is doing good things for long term function of metabolism.

Acrolein, a major breakdown product of fish oil and other omega-3 fats, has been shown to promote nitric oxide, and rising levels of acrolein are associated with the progression of the diseases of inflammation, contradicting studies which try to imply that fish oil is protective.

“ACR [acrolein] could stimulate iNOS [inducible nitric oxide synthase] and COX-1/COX-2, producing lymphocyte migration and increases of NO [nitric oxide] and PGs [prostaglandins].”

“Inducible nitric oxide (NO) synthase (iNOS) protein expressions were markedly induced in bladders 24 h after acrolein treatment…”

“Lipid peroxidation leads to the formation of a number of aldehydes by-products, including malondialdehyde (MDA), 4-hydroxy-2-nonenal (HNE), and acrolein…acrolein is the most reactive…In brain from patients with AD [Alzheimer’s disease], acrolein has been found to be elevated in hippocampus and temporal cortex where oxidative stress is high. Due to its high reactivity, acrolein is not only a marker of lipid peroxidation but also an initiator of oxidative stress…”

“…results showed that α-linolenic acid, an omega-3 fatty acid, generated more acrolein and crotonaldehyde than did linoleic acid, an omega-6 fatty acid…Omega-3 fatty acids might be easily degraded to smaller monoaldehydes or dicarbonyls…Omega-3 fatty acids have been considered as health improvement components for a long time. However, on the basis of the results presented here, use of omega-3 fatty acids should be re-evaluated in vivo for safety purposes.”

Acrolein has also been shown to promote the release of serotonin, and serotonin (much like nitric oxide), is an inflammatory stress substance that directly interferes with the function of energy metabolism. In fact nitric oxide can promote serotonin release, another good reason to be wary of claims that fish oil is beneficial. Serotonin has been shown to be another potential driver of insulin resistance and diabetes progression.

“Recent reports showed that acrolein, a metabolite of chemotherapeutic agents, is a TRPA1 agonist, and we have observed that acrolein increased the release of 5-HT [serotonin]…”

“…suppressing 5-HT [serotonin] signaling might represent a new target for anti-obesity treatment by increasing energy expenditure and improving insulin resistance…”

Acrolein, nitric oxide and serotonin aside, there are numerous other reasons to be concerned about what happens when you consume omega-3 PUFA.

4-hydroxy-2-hexenal [4-HHE] is another thing that increases throughout the system when fish oil breaks down. 4-HHE promotes oxidative stress, and oxidative stress is not disputed as a significant promoter of inflammation and disease. It’s hard not to be concerned about claims that fish oil protects against inflammation.

“Trans-4-hydroxy-2-hexenal (HHE) is a major…product of n-3 PUFA oxidation and, like HNE, is an active biochemical mediator resulting from lipid peroxidation. HHE adducts are elevated in disease states…”

“Oxidative stress is involved in the pathophysiology of insulin resistance and its progression towards type 2 diabetes. The peroxidation of n-3 polyunsaturated fatty acids produces 4-hydroxy-2-hexenal (4-HHE), a lipid aldehyde with potent electrophilic properties able to interfere with many pathophysiological processes…4-HHE is produced in type 2 diabetic humans…and blunts insulin action in skeletal muscle. 4-HHE…plays a causal role in the pathophysiology of type 2 diabetes and might constitute a potential therapeutic target to taper oxidative stress-induced insulin resistance.”

Malondialdehyde (MDA) is another well known product of the breakdown of fish oil (and PUFA in general) and there is a great deal of science which shows a direct connection between rising levels of MDA and many inflammatory disease states, including diabetes, sepsis, stroke, heart disease, traumatic brain injury and breast, lung and other cancers.

“Marine long-chain polyunsaturated fatty acids…are rapidly oxidized, generating highly reactive malondialdehyde (MDA), 4-hydroxy-2-hexenal (HHE) and 4-hydroxy-2-nonenal (HNE)…These oxidation products may interact with DNA and proteins, thus possibly leading to impaired cell functions…higher aldehyde levels were reached in the intestinal lumen than in the initial meal, demonstrating that GI digestion promotes oxidation. Hence, epithelial cells may be exposed to elevated amounts of reactive aldehydes for several hours after a meal containing fish oil.”

“Herring developed higher concentrations of MDA and HHE during gastric digestion compared to salmon, which initially contained lower levels of oxidation products. Cooked salmon generated higher MDA concentrations during digestion than raw salmon.”

“Lipid peroxidation by reactive oxygen species leads to the formation of highly reactive malondialdehyde (MDA), and extensive MDA is found in diabetes…A significant 2-fold increase in serum MDA also correlated the increased IL-25 and IL-8 mRNA in PBLCs of diabetic patients…These new results suggest that MDA can promote lymphocyte activation via induction of inflammatory pathways and networks.”

“Oxidative stress has been implicated in the pathogenesis of sepsis-induced organ dysfunction…The presence of high serum MDA levels supports the hypothesis that increased oxidative stress, particularly lipid peroxidation, contributes to sepsis pathophysiology.”

“MDA levels increased in type 2 diabetes, especially in patients on insulin therapy. Chronic hyperglycemia and other biomarkers, such as urinary albumin, were correlated with MDA levels, suggesting the involvement of lipid peroxidation in the pathogenesis of diabetes complications.”

“Plasma MDA levels in cancer patients were significantly higher than those in controls…Average MDA levels were 6.33 micromol/L in breast cancer patients and 5.87 micromol/L in lung cancer patients…further evidence of the relationship between lipid peroxidation and cancer…”

Crotonaldehyde, like acrolein, is another by-product of the break down of fish oil which has been connected to the progression of inflammation and disease, including cancer and Alzheimer’s.

Yes, there are other ways (apart form PUFA break down) to increase exposure to many of these substances (like smoking for instance), but this does not detract from the significance of enormous increases in consumption of PUFA, over the last few decades.

“…results of this study provide some intriguing new leads with respect to the possible role of the α,β-unsaturated toxicants acrolein and crotonaldehyde in lung cancer…”

“Several studies have documented the involvement of oxidative stress represented by lipid peroxidation in the pathogenesis of Alzheimer’s disease (AD)…Our results suggest that increased oxidative stress and CRA [crotonaldehyde] formation in glial cells is implicated in the disease processes of AD.”

The fish oil breakdown products, isoprostanes and neuroprostanes, have also been shown to play a role in the development of inflammation and oxidative stress, as well as the progression of a variety of disease states, including the neurodegenerative diseases multiple sclerosis, Alzheimer’s disease, Huntington’s disease, Creutzfeldt-Jakob disease and Amyotrophic lateral sclerosis (ALS).

Look, I’m not claiming to know the ins and outs of every single possible biological reaction to fish oil consumption (or PUFA consumption in general), but these are some arguments that make sense to me in the light of what I have seen and read and experienced.

Have a look for yourself, and if you can find someone who can explain away all of these glaring contradictions to the ‘fish oil is protective’ hypothesis, let me know. In the meantime, do you really want to be adding more PUFA into the mix than is absolutely necessary?

Avoiding consumption of fish oil (and all other PUFAs), is a rational approach to protection from type II diabetes, cancer and Alzheimer’s. Sufficient ingestion of sugar can be protective, in part by preventing the release of stored PUFA into the blood, limiting exposure to stress substances, and by promoting exposure to the anti-inflammatory saturated and omega-9 fats.

Although the saturated fats released into the bloodstream (either from storage in the tissue or from the consumption of fatty food), can also interfere (at least temporarily) with the ability of the cell to oxidize sugar, they are stable. Because of this they do not easily break down (like PUFA) into the toxic chemicals, thereby allowing the cell to return to the proper use of sugar for fuel, when it becomes available again.

Oxidative stress resulting from exposure to the breakdown products of fish oil and other PUFAs promotes inflammation and interferes with thyroid energy metabolism. Suppressed thyroid function encourages the release of the stess substances nitric oxide and serotonin, and has been shown to be involved in the progression of the inflammatory illnesses, including diabetes, cancer and Alzheimer’s.

“…a group of patients with primary hypothyroidism…found high plasma levels of malondialdehyde (MDA), an OS [oxidative stress] marker that is formed by lipid peroxidation, and NO [nitric oxide]…Elevated MDA levels were also shown in subclinical hypothyroidism…OS seems to be an important mechanism underlying the progress of inflammation. A vicious circle creates a link between these two conditions. Thyroid hormones can have a protective role…on the other side…hypothyroidism can worsen OS.”

Sugar promotes thyroid function and protects against the excessive release of nitric oxide and serotonin, and so in this sense alone it can be undertood to be a truly anti-inflammatory, anti-stress, disease protective substance. All of this adds further weight to arguments against fish oil (and PUFA in general) being something you want to have more of when you are unwell, or at any time for that matter. But if you are still looking at disease through the eyes of mistaken biological results or interpretations, it’s understandeable that you might see things in the exact opposite way.

Restricting sugar, and increasing exposure to the breakdown products of PUFA of any kind, (interfering with the ability of the cell to oxidize glucose), causes many inflammatory stress substances to be released (including cortisol and adrenalin) in greater amounts than would normally be the case, some of which promote the release of more PUFA out of storage, and this can create a vicious circle type scenario of gradually worsening metabolic function.

These kinds of stressful circumstances encourage the progression of diabetes related symptoms, worsening hyperglycemia, insulin resistance and other blood sugar dysregulation issues, leading to misconceived ideas which make it seem logical to place the blame upon sugar. If you think your health practitioner has looked into these subjects deeply, think again.

One possible therapeutic approach involves experimentation with the gradual increase in use of white sugar and honey, (in combination with protein, minerals and other nutrients necessary for a properly functioning metabolism), from sources such as sweet ripe juicy fruits and fruit juice, and milk, cheese and gelatin, whilst at the same time avoiding as much as possible, the consumption of the polyunsaturated fish and seed oils, and too much of the difficult to digest stress promoting grains, seeds, nut, beans and many kinds of vegetables.

Such a diet can potentially help to protect against stress and inflammation, preventing the excessive release of PUFAs held in storage, and promoting exposure to the anti-inflammatory, pro-metabolic fats. An increase in production of the saturated and omega-9 fats (due to increased sugar consumption and decreased exposure to PUFA) can also assist in protecting against the by-products of the breakdown of fish oil and other PUFAs, and can improve the ability of cells to come back to the proper utilization of glucose for fuel, allowing the body to slowly rid itself of toxic substances via safer means, helping metabolism improve.

See more here

Adverse metabolic effect of omega-3 fatty acids in non-insulin-dependent diabetes mellitus

Dietary supplementation with n-3 fatty acids may impair glucose homeostasis in patients with non-insulin-dependent diabetes mellitus

Polyunsaturated fatty acids may impair blood glucose control in type 2 diabetic patients

Fish-oil supplementation reduces stimulation of plasma glucose fluxes during exercise in untrained males

No Effect of Added Sugar Consumed at Median American Intake Level on Glucose Tolerance or Insulin Resistance

No Change in Oral Glucose Tolerance Tests As a Result of Ten Weeks of Consumption of Various Fructose Containing Sugars or Glucose

Effects of Fish Oil Supplementation on Glucose and Lipid Metabolism in NIDDM

Elevated 4-hydroxyhexenal in Alzheimer’s disease (AD) progression

Effects of maternal acrolein exposure during pregnancy on testicular testosterone production in fetal rats

The Effects of Fructose-Containing Sugars on Weight, Body Composition and Cardiometabolic Risk Factors When Consumed at up to the 90th Percentile Population Consumption Level for Fructose

Fructose replacement of glucose or sucrose in food or beverages lowers postprandial glucose and insulin without raising triglycerides: a systematic review and meta-analysis.

Exotic Fruits as Therapeutic Complements for Diabetes, Obesity and Metabolic Syndrome

Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid-deficient diet alters the response to endotoxin in rats.

Isoprostanes and Neuroprostanes as Biomarkers of Oxidative Stress in Neurodegenerative Diseases

Relationship between Added Sugars Consumption and Chronic Disease Risk Factors: Current Understanding

Skeletal muscle insulin resistance is induced by 4-hydroxy-2-hexenal, a by-product of n-3 fatty acid peroxidation.

Association Between Thyroid Hormones, Lipids and Oxidative Stress Markers in Subclinical Hypothyroidism

A Prospective Study of Sugar Intake and Risk of Type 2 Diabetes in Women

Acrolein Metabolites, Diabetes and Insulin Resistance

Effect of dietary linoleate content on the metabolic response of rats to Escherichia coli endotoxin.

Hepatocyte ALOXE3 is induced during adaptive fasting and enhances insulin sensitivity by activating hepatic PPARγ

Oxidative stress in hypothyroid patients and the role of antioxidant supplementation

Serotonin as a New Therapeutic Target for Diabetes Mellitus and Obesity

Lipid Peroxidation Products in Human Health and Disease

High dietary fish oil alters the brain polyunsaturated fatty acid composition.

Structural and functional changes in human insulin induced by the lipid peroxidation byproducts 4-hydroxy-2-nonenal and 4-hydroxy-2-hexenal.

Mechanism of acrolein-induced vascular toxicity.

Mercapturic Acids Derived from the Toxicants Acrolein and Crotonaldehyde in the Urine of Cigarette Smokers from Five Ethnic Groups with Differing Risks for Lung Cancer

Thyroid Hormones, Oxidative Stress, and Inflammation

Crotonaldehyde accumulates in glial cells of Alzheimer’s disease brain.

Role of dietary fish oil on nitric oxide synthase activity and oxidative status in mice red blood cells.

Reactive Carbonyl Species Derived from Omega-3 and Omega-6 Fatty Acids.

Acute fructose administration decreases the glycemic response to an oral glucose tolerance test in normal adults.

Dietary oxidized n-3 PUFA induce oxidative stress and inflammation: role of intestinal absorption of 4-HHE and reactivity in intestinal cells.

Trans‐4‐hydroxy‐2‐hexenal is a neurotoxic product of docosahexaenoic (22:6; n‐3) acid oxidation

Dietary fish oil augments nitric oxide production or release in patients with type 2 (non-insulin-dependent) diabetes mellitus.

DNA damage by lipid peroxidation products: implications in cancer, inflammation and autoimmunity

Protein-bound acrolein: a novel marker of oxidative stress in Alzheimer’s disease.

Acrolein induced both pulmonary inflammation and the death of lung epithelial cells.

Reactive Carbonyl Species Derived from Omega-3 and Omega-6 Fatty Acids.

Glucose-stimulated acrolein production from unsaturated fatty acids.

Free fatty acids and insulin resistance.

Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes.

Oxidative and Nitrosative Stress in the Metastatic Microenvironment

Advanced glycoxidation and lipoxidation end products (AGEs and ALEs): an overview of their mechanisms of formation

A Potential Role for Acrolein in Neutrophil-Mediated Chronic Inflammation.

Consumption of sucrose and high-fructose corn syrup does not increase liver fat or ectopic fat deposition in muscles.

Acrolein produces nitric oxide through the elevation of intracellular calcium levels to induce apoptosis in human umbilical vein endothelial cells: implications for smoke angiopathy.

Malondialdehyde and 4-hydroxy-2-hexenal are formed during dynamic gastrointestinal in vitro digestion of cod liver oils.

Effect of fructose on glycemic control in diabetes: a systematic review and meta-analysis of controlled feeding trials.

Moderate amounts of fructose- or glucose-sweetened beverages do not differentially alter metabolic health in male and female adolescents.

Acrolein Induces Endoplasmic Reticulum Stress and Causes Airspace Enlargement

Malondialdehyde epitopes are sterile mediators of hepatic inflammation in hypercholesterolemic mice

Misconceptions about fructose-containing sugars and their role in the obesity epidemic.

Acrolein Decreases Endothelial Cell Migration and Insulin Sensitivity Through Induction of let-7a

Challenging the Fructose Hypothesis: New Perspectives on Fructose Consumption and Metabolism

Proinflammatory effects of malondialdehyde in lymphocytes.

Decreased total antioxidant levels and increased oxidative stress in South African type 2 diabetes mellitus patients

Pathological correlations between traumatic brain injury and chronic neurodegenerative diseases

Adipose tissue metabolism in essential fatty acid deficienty. Effects of prostaglandin e1, epinephrine, and ACTH

A low-carbohydrate high-fat diet increases weight gain and does not improve glucose tolerance, insulin secretion or β-cell mass in NZO mice

Involvement of Interleukin-6-Regulated Nitric Oxide Synthase in Hemorrhagic Cystitis and Impaired Bladder Contractions in Young Rats Induced by Acrolein, a Urinary Metabolite of Cyclophosphamide

Dietary intake of carbohydrates and risk of type 2 diabetes: the European Prospective Investigation into Cancer-Norfolk study.

Role of by-products of lipid oxidation in Alzheimer’s disease brain: a focus on acrolein.

Acrolein Exposure Is Associated With Increased Cardiovascular Disease Risk

Lipid peroxidation in Rheumatoid arthritis; consequences and monitoring.

Oxidation of Marine Omega-3 Supplements and Human Health

Interaction of aldehydes derived from lipid peroxidation and membrane proteins

Elevated malondialdehyde levels in sepsis – something to ‘stress’ about?

High Serum Levels of Malondialdehyde and 8-OHdG are both Associated with Early Cognitive Impairment in Patients with Acute Ischaemic Stroke

A Possible Role of Acrolein in Diabetic Retinopathy: Involvement of a VEGF/TGFβ Signaling Pathway of the Retinal Pigment Epithelium in Hyperglycemia

Acrolein is increased in Alzheimer’s disease brain and is toxic to primary hippocampal cultures.

Serum malondialdehyde level: Surrogate stress marker in the Sikkimese diabetics

Acrolein acts as a neurotoxin in the nigrostriatal dopaminergic system of rat: involvement of α-synuclein aggregation and programmed cell death

Lipidomic analysis for carbonyl species derived from fish oil using liquid chromatography-tandem mass spectrometry.

Alterations in Acrolein Metabolism Contribute to Alzheimer’s Disease.

Changes in nitric oxide, prostaglandins and myeloperoxidase activity in acrolein-induced cystitis in rats.

Acute Acrolein Exposure Induces Impairment of Vocal Fold Epithelial Barrier Function

Role of salivary malondialdehyde in assessment of oxidative stress among diabetics

Plasma malondialdehyde levels and risk factors for the development of chronic complications in type 2 diabetic patients on insulin therapy.

Gene pathways associated with mitochondrial function, oxidative stress and telomere length are differentially expressed in the liver of rats fed lifelong on virgin olive, sunflower or fish oils.

Dietary omega-3 polyunsaturated fatty acids promote colon carcinoma metastasis in rat liver.

Metabolic effects of dietary sucrose in type II diabetic subjects

Molecular Mechanisms of Acrolein Toxicity: Relevance to Human Disease

Acrolein-induced vasomotor responses of rat aorta

Effect of Carcinogenic Acrolein on DNA Repair and Mutagenic Susceptibility

Associations of Omega-3 Fatty Acid Supplement Use With Cardiovascular Disease Risks

TRPA1 regulates gastrointestinal motility through serotonin release from enterochromaffin cells

Janus-faced Acrolein prevents allergy but accelerates tumor growth by promoting immunoregulatory Foxp3+ cells: Mouse model for passive respiratory exposure

Mechanisms of acrolein-induced myocardial dysfunction: implications for environmental and endogenous aldehyde exposure

Acrolein as a Major Volatile in the Early Stages of Fish Oil TAG Oxidation.

4-Hydroxyhexenal Is a Potent Inducer of the Mitochondrial Permeability Transition

Acrolein involvement in sensory and behavioral hypersensitivity following spinal cord injury in the rat

Plasma malondialdehyde (MDA) levels in breast and lung cancer patients.

Acrolein Inhalation Suppresses Lipopolysaccharide-Induced Inflammatory Cytokine Production but Does Not Affect Acute Airways Neutrophilia

Induction of endothelial iNOS by 4-hydroxyhexenal through NF-kappaB activation.

Oxidative toxicity in diabetes and Alzheimer’s disease: mechanisms behind ROS/ RNS generation

Formation of Acrolein in the Autoxidation of Triacylglycerols with Different Fatty Acid Compositions

Acrolein induces Alzheimer’s disease-like pathologies in vitro and in vivo.

Endogenous generation of reactive oxidants and electrophiles and their reactions with DNA and protein

Effect of fish oils containing different amounts of EPA, DHA, and antioxidants on plasma and brain fatty acids and brain nitric oxide synthase activity in rats

Carnosine protects against the neurotoxic effects of a serotonin-derived melanoid.

Levels of F2-isoprostanes, F4-neuroprostanes, and total nitrate/nitrite in plasma and cerebrospinal fluid of patients with traumatic brain injury.

Long chain omega-3 fatty acid immunomodulation and the potential for adverse health outcomes

Trans-4-hydroxy-2-hexenal, a product of n-3 fatty acid peroxidation: make some room HNE…

Diabetogenic impact of long-chain omega-3 fatty acids on pancreatic beta-cell function and the regulation of endogenous glucose production.

4-Hydroxynonenal (HNE) modified proteins in metabolic diseases.

Eicosapentaenoic acid enhances nitric oxide production by cultured human endothelial cells.

Formation of Malondialdehyde, 4-Hydroxynonenal, and 4-Hydroxyhexenal during in Vitro Digestion of Cooked Beef, Pork, Chicken, and Salmon.

Involvement of interleukin-6-regulated nitric oxide synthase in hemorrhagic cystitis and impaired bladder contractions in young rats induced by acrolein, a urinary metabolite of cyclophosphamide.

Acrolein is a major cigarette-related lung cancer agent: Preferential binding at p53 mutational hotspots and inhibition of DNA repair

Formation of malondialdehyde (MDA), 4-hydroxy-2-hexenal (HHE) and 4-hydroxy-2-nonenal (HNE) in fish and fish oil during dynamic gastrointestinal in vitro digestion.

Potential role of acrolein in neurodegeneration and in Alzheimer’s disease.

#omega3nightmare
#sugarblaming

Image: Allcinema: “Vampire Fish River Monsters”
Artist: Unknown

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