Why Omega 3 should be avoided and what to use/do instead

Hopefully this article will ruffle some feathers…or scales…

I’ll start with the core negative functions of omega 3 and then discuss some of its other “benefits” such as creating different prostaglandins, leukotrienes as well as a look into resolvins, etc.

Table of Contents

Basics on fats

Saturated fat contains no double bonds (such as stearic acid above), which makes them very rigid and unable to be damaged by ROS.

Monounsaturated fats contain 1 double bond and can make the cell membrane a little more fluid compared to saturated fat. They are also mostly resistant to oxidative stress. There are many different kinds of MUFAs, with the most common being oleic acid (C18:1n9; found in meat, olive oil, macadamia nut oil, etc.), followed by palmitoleic acid (C16:1n7; found in macadamia nut oil and avocadoes), and vaccenic acid (C18:1,trans7 (trans fat found in dairy)). The body can elongate and unsaturated saturated and monounsaturated fat. For example, palmitic acid can be elongated to stearic acid, which can then be unsaturated to oleic acid. It can then be further elongated and unsaturated to Mead acid (C20:3n9).

Polyunsaturated fats, those that are obtained through the diet or that are made in the body, contain more than two double bonds. The addition of more double bonds makes these fats more fluid, but also more unstable (reactive to ROS) and chaotic. The most common PUFA in the diet is linoleic acid (C18:2n6) which can be elongated and unsaturated to arachidonic acid (C20:4n6). Arachidonic acid contains 4 double bonds compared to 2 double bonds found in linoleic acid, which makes arachidonic acid a lot more reactive and unstable/fluid than linoleic acid.

If we switch our attention to omega 3, alpha-linolenic acid (ALA;18:3n3) is the predominant one found in plants, whereas EPA (20:5n3) and DHA (22:6n3) are the predominant ones found in fish and seafood.

The longer they get, the more unsaturated they become. EPA and especially DHA are the most unstable and chaotropic of them all. When they are incorporated into the lipid structures of cells, they make those structures very fluid and unstable. Unstable structures aren’t very effective at stabilizing complexes and optimizing their function.

It’s like riding your car but the bolts you’re using to fasten the wheels are made of silicone instead of metal. Would you feel safe? Most likely not. You’ll have to drive a lot slower and not do anything crazy or those wheels will come flying off.

Saturated fats equals metal bolts and omega3s equal silicone bolts.

Omega 3 and longevity and health

Many people take omega 3 because it has been marketed to extend lifespan. However, tissue unsaturation is inversely correlated with longevity (the Membrane Theory of Aging proposes that lifespan is inversely related to the degree of unsaturation of membrane phospholipids (R)).

And it’s not the accumulation of omega 6, but also omega 3 (R). And it’s also the omega 3 to omega 6 ratio that plays a role (R). A higher omega 3:omega 6 ratio is inversely correlated with longevity, more so than a high omega 6 ratio.

Also, DHA levels increase with aging. All the long chain highly unsaturated fats (arachidonic acid, EPA and DHA) increase with aging, not just omega 6.

The life-extension “benefits” of omega 3 are completely abolished by caloric restriction (calorie restriction is frequently used in animal models to extend lifespan). What the research actually found is that saturated fat enhances longevity additive to calorie restriction. “Lifespan was increased in CR mice consuming lard > soybean oil > fish oil-containing diets.” (R). Many of the benefits of calorie restriction are actually because of reduced intake of things that promote inflammation, such as PUFAs, iron, inflammatory amino acids, etc.

The increase in PUFAs with aging makes cells unstable, reduces energy production, enhances ROS production and promotes the formation of lipid peroxides, which are potent oxidants. And this all contributes to aging.

Other studies, however, have indicated that lifespan is decreased in both diabetic rats fed fish versus corn oil (Berdanier 1992) and senescence-accelerated mice fed fish oil (Tsuduki et al. 2011) or perilla oil (source of 18:3 n-3) (Umezawa et al. 2000) versus safflower oil. Moreover, a recent longevity study carried out with long-lived, male, B6C3F1 mice fed diets supplemented with krill oil and Lovaza, a pharmaceutical grade fish oil, beginning at 12 months of age, has demonstrated a 6.6% lifespan shortening relative to controls (Spindler et al. 2014).” (R)

Omega 3 and the mitochondria

The mitochondria is where all the magic happens. The better the mitochondria works, the more energy we have, the faster we recover, the higher our IQ and mental function, the deeper our sleep, the more gracefully we age and much more.

We want the mitochondria to work optimal, not create a lot of reactive oxygen species, have optimal ATP and CO2, induce mild uncoupling (to protect us from ROS and lipid peroxides).

For that to happen our mitochondria must be solid (relative rigid) and organized and not too fluid and chaotic.

The part of the mitochondria I specifically want to focus on is the electron transport chain.

Omega 3 and the electron transport chain

Fats, and in this case, EPA and DHA, are incorporated in cardiolipin, which is basically one of the most important cellular lipid structures.

Cardiolipin is a lipid structure that consists of 4 fatty acids.

These fats in the cardiolipin can change based on our diet. About 60-80% of cardiolipin consists of linoleic acid (C18:2n6), whereas the others are a mix of saturated, mono and polyunsaturated fat.

The more PUFAs your diet contains, the more PUFAs will be incorporated into cardiolipin. The less PUFAs are in the diet, the more linoleic acid, saturated and monounsaturated fat there will be in the cardiolipin.

The less unsaturated the cardiolipin is, the better it works. Linoleic acid > arachidonic acid > DHA.

Cardiolipin’s function

The picture below demonstrates the formation of a supercomplex consisting of complex I, III and IV. Each individual complex, as well as the supercomplex, is stabilized by cardiolipin.

Optimizing cardiolipin function has been a major part of research this last couple of years and that lead to the birth of the cardiolipin protective peptide called SS-31.

The main function of cardiolipin is to stabilize various complexes of the electron transport chain and to “create”/stabilize supercomplexes. “…cardiolipin (CL) is particularly important because it binds tightly to proteins (810) and increases substantially their propensity to cluster and to form supercomplexes“, such as complex I + III and II + III and III + IV (R).

Supercomplexes are more effective at producing energy and reduces the production of ROS.

These complexes can also be seen as a highway. Saturated fat makes sure these complexes are well aligned for the electrons to be passed through effectively, sort of like the autobahn in Germany.

PUFAs, with omega 3 being the worse, turn the autobahn into a mudder road. Much less effective and dangerous.

Omega 3 reduces energy production efficiency

Let me share with you multi studies that show that omega 3 has a negative impact on energy production.

Dietary supplementation of EPA or DHA increases the levels of n–3 PUFA acyl chains within mitochondrial membranes, which leads to membrane disorganization and potentially increased electron leakage. Several studies show that an increase in the polyunsaturation of phospholipids, particularly cardiolipin, increases the production of ROS (153159).” (R)

DHA reduces complex function:

Moreover, DHA lowered enzyme activities of respiratory complexes I, IV, V, and I+III. Mechanistically, the reduction in enzymatic activities were not driven by a dramatic reduction in the abundance of supercomplexes. Instead, replacement of tetralinoleoyl-CL with tetradocosahexaenoyl-CL in biomimetic membranes prevented formation of phospholipid domains that regulate enzyme activity” (R)

Omega 3 reduces genes that regulate the ETC in brown adipose tissue. It reduces uncoupling, thyroid hormone activation and ATP production.

Expression of mitochondrial electron transportation chain (ETC)-regulated genes were significantly inhibited (P < 0.05) by n-3 PUFAs, including ATP5J2, COX7a1, and COX8b. Mass spectrometric and western blot evaluation showed protein levels of enzymes which regulate the ETC and Krebs cycle, including ATP synthase α and β (F1F0 complex), citrate synthase, succinate CO-A ligase, succinate dehydrogenase (complex II), ubiquinol-cytochrome c reductase complex subunits (complex III), aconitate hydratase, cytochrome c, and pyruvate carboxylase were all decreased in the n-3 PUFAs group (P < 0.05). Genomic and proteomic changes were accompanied by mitochondrial dysfunction, represented by significantly reduced oxygen consumption rate, ATP production, and proton leak (P < 0.05). This study suggested that EPA and DHA may alter the BAT fate of myoblasts by inhibiting mitochondrial biogenesis and activity and induce white-like adipogenesis, shifting the metabolism from lipid oxidation to synthesis” (R)

Fish oil, because it causes destabilization, fluidness and leakiness, enhances proton leak, which is like water falling from the bucket due to holes. Saturated fat gives you a solid bucket with no holes, whereas PUFAs give you a leaky bucket.

The CR (calorie restriction)-lard group showed the lowest proton leak compared with the other CR groups. …Moreover, the CR-fish group also had lower Complex II activity compared with the other CR groups.” (R)

Cellular dysfunction and death are caused by oxidation of the PUFAs in cardiolipin. Once the cardiolipin is damaged, it can’t stabilize the complexes anymore and cytochrome C releases from the mitochondrial membrane and this initiate the whole process of cell death.

Cytochrome C release is reduced in sucrose-fed rats (saturated fat is converted to saturated fat; so the cardiolipin contained mostly saturated and monounsaturated fat and also linoleic acid, with very little to no very long-chain PUFAs)” (R)

Feeding saturated fat (SF) has the same effect as feeding sugar.

However, cytochrome c release from SF kidney mitochondria was lower than from control. In addition, cardiolipin, a mitochondria-specific phospholipid, was found increased in SF mitochondria due to the enhanced amount of both cardiolipin synthase and tafazzin. Cardiolipin was also found enriched with saturated and monounsaturated fatty acids, which are less susceptible to peroxidative stress involved in cytochrome c release.” (R). 

As previously mentioned, long-chain PUFAs accumulate with aging and this reduces mitochondrial function. Feeding the old animals hydrogenated peanut oil (a process that saturates the PUFAs) restores the functions of the complexes of the ETC.

Even supplementing old animals with hydrogenated peanut oil restores mitochondrial respiration to about 80% of normal. … The fatty acid composition of muscle homogenates of old rats differed from that of young animals by a reduced content of myristic, oleic, linoleic, and α-linolenic acids and enhanced content of dihomo-γ-linolenic, arachidonic, and docosahexaenoic acids. Per oral supplementation of the old rats with hydrogenated peanut oil completely restored the activity of complex IV and increased the activity of complex I to 80% of the value observed in muscles of young animals, reducing the content of stearic, dihomo-γ-linolenic, arachidonic, eicosapentaenoic, docosapentaenoic, and docosahexaenoic acids relative to that in the groups of old and young rats.” (R)

Omega 3 and lipid peroxidation

Each double bond in the fat makes it more unstable and prone to oxidation. Holman reported the relative oxidation rates for unsaturated fatty acids to be 0.025 (1 double bond), 1 (2 double bonds), 2 (3 double bonds), 4 (4 double bonds), 6 (5 double bonds), and 8 (6 double bonds) (R). Thus, DHA (containing 6 double bonds) has an oxidation rate 320 times higher than oleic acid (1 double bond).

Since consumption or ingestion of fish oil (EPA and DHA) causes electron leak and ROS production, this makes them even more dangerous. These fats are the most susceptible to oxidation and then they increase ROS production as well. It’s like a bomber dropping his bombs in the hanger where all the other bombs are stored. A vicious loop of destruction.

“Luckily”, the body sees this as a “hormetic stress” and upregulates superoxide dismutase, catalase and glutathione peroxidase, which detoxes superoxide, hydrogen peroxide and lipid peroxides. But it’s like filling your pool with water until it runs over. Then you build a ridge around the pool about 1 foot higher so that the water can keep on accumulating. At the end of the day, your pool is equally “full” but contains more water. It doesn’t mean you have more leeway. Although omegas upregulate these detox enzymes, these enzymes will only be detoxing the ROS created by the omegas in the first place. So your back to 0 benefits, but you’re actually in the minus because these fats still reduce complex function, which reduces ATP and CO2 production. It’s a net loss.

It is hypothesized (according to this study) that n-3 PUFA induced lipid peroxidation may be beneficial in unstressed individuals by up-regulation of anti-oxidant systems while it may exaggerate oxidant damage in patients with severe oxidant stress (R). But like I mentioned, the upregulation of anti-oxidant systems is like when you’re single, you have 1 car. Now you get married and your spouse has a car. Now you get children and they too get cars. Everyone still has 1 car and no one has 2 cars. No net gain.

As the study continues to say: “n-3 PUFA are highly susceptible to oxidation due to multiple double bonds. Oxidation of lipids may induce cell damage and stimulate the inflammatory response. Thus, it is unclear whether n-3 PUFA are antioxidative or pro-oxidative.” Let me be clear…they are pro-oxidant.

Another example is that you’re training the same muscle group every day all day, but you’re eating more protein to compensate. Will you grow more because you’re eating more or will your body use the protein to regenerate the damage you’re continuously causing?

Let me show you some research:

We observed that skeletal muscle mitochondria from the CR-Fish group had increased lipid peroxidation compared with both control and CR-Lard groups, despite consuming a diet containing twice the amount of the antioxidant t-butylhydroquinone as the other groups.” (R)

peroxidized cardiolipin, from fish oils, in the mitochondrial membrane can inactivate cytochrome oxidase by mechanisms similar to those of hydrogen peroxide. Phospholipase A2 activity and mitochondrial damage are enhanced when mitochondrial membranes are enriched with n-3 fatty acids” (R).

The study of Miloudi et al. [96] is an example of why measuring the appropriate oxidation products is important for interpreting studies of lipid oxidation. Miloudi investigated oxidation of a variety of parenteral nutrition formulations containing a soybean oil-based lipid emulsion or a fish oil-based lipid emulsion (Omegaven, Fresenius Kabi, Bad Homburg, Germany). Oxidation was evaluated both in vitro and in vivo (guinea pigs infused with the formulations). Oxidation was assessed using hydroperoxides, two aldehydes, and F2α-isoprostanes. n-6 PUFA peroxidation was assessed using 4-hydroxynonenal (HNE) and F2α-isoprostanes while n-3 PUFA peroxidation was assessed using 4-hydroxyhexenal (HHE). Total PUFA content of the two lipid emulsions were not equivalent; total PUFA content was twice as high in the soybean lipid emulsion formulation compared with the fish oil emulsion formulation (approximately 25 vs. 12 mM). When comparing peroxidation between different lipid emulsions it is very important to administer comparable quantities of fatty acids. Despite higher PUFA administration with the soybean emulsion, total hydroperoxides were comparable between the two lipid emulsions. As expected, HNE levels were higher in the soybean emulsion compared to the fish oil emulsion while HHE levels were higher in the fish oil emulsion compared to the soybean lipid emulsion. However, the sum of HNE and HHE were higher with the fish oil emulsion compared to the soybean emulsion (approximately 15.3 µM vs. 4.1 µM). A fatty acid oxidation index was calculated and indicated that n-3 PUFA were more susceptible to oxidation than n-6 PUFA. Hepatic levels of F2α-isoprostanes (reflecting peroxidation of n-6 PUFA) were slightly (but not significantly) higher in the soybean lipid group.” (R)

Results indicated that DHA enhanced susceptibility of the liver and kidney to lipid peroxidation concomitant with higher levels of DHA in the tissues. Vitamin E was unable to protect membranes of the liver and kidney rich in DHA from lipid peroxidation.” (R)

Allard et al. [107] demonstrated that supplementation of the diet with n-3 fatty acids from fish oil (Menhaden oil, National Marine Fisheries Service, Charleston, SC, USA; DHA + EPA = 5.3 g/d) in healthy men resulted in an increase in lipid peroxidation (measured with malondialdehyde (MDA) and lipid peroxides) compared to olive oil supplementation. Lipid peroxidation was not altered by vitamin E supplementation (900 IU/d dL-alpha-tocopherol).” (R)

McGrath et al. [115] administered fish oil (MaxEPA, Scherer, Troy, Michigan; 10 g/d; DHA + EPA = 3 g/d; 10 IU alpha-tocopherol) or olive oil to individuals with non-insulin dependent diabetes mellitus in a double-blind randomized cross-over study. Treatment with olive oil did not change plasma MDA or vitamin E levels while treatment with fish oil resulted in elevated MDA and decreased vitamin E levels, compared to baseline and olive oil treatments.” (R)

Grundt et al. [117] administered n-3 PUFA supplements (Pronova, Oslo, Norway; 3.5 g/d) or corn oil supplements (4 g/d) containing 16 mg/d alpha-tocopherol for 1 year to 255 subjects following myocardial infarction. Serum thiobarbituric acid-malondialdehyde complex levels increased significantly in both groups. However, the increase in the n-3 PUFA group was significantly greater than in the corn oil group.” (R)

Rice et al. [118] randomized 272 adults with acute lung injury to enteral nutrition supplemented with fish oil, gamma-linolenic acid, and antioxidants (Oxepa, Abbott, Columbus, OH, USA) or an isocaloric control enteral diet. Fish oil supplementation increased plasma EPA levels 8 fold compared to controls. Fish oil supplementation was associated with significantly poorer clinical outcomes (ventilation days, ICU stay, organ failure days, and mortality). F3-isoprostane excretion in the urine, an index of EPA peroxidation, was significantly higher in the fish oil supplemented group.” (R)

Wu et al. [119] reported superoxide radical and total oxygen radical levels in gastrointestinal surgery patients randomized to a fish oil containing intravenous lipid emulsion (SMOFlipid, Fresenius Kabi, Bad Homburg, Germany; containing soybean oil, medium chain triglycerides (MCT), olive oil, fish oil) or soybean MCT lipid emulsion. Despite superoxide radical levels being lower in the fish oil lipid emulsion group at day 1 (1234 vs. 2004 counts/10 s), maximal levels on day 2 (2260 vs. 1745 counts/10 s) were higher in the fish oil emulsion group. The change in superoxide levels from day 1 to day 6 increased in the fish oil lipid group (+95 counts/10 s) while levels decreased in the soybean MCT emulsion group (−403 counts/10 s). Total oxygen radical levels were comparable in both lipid groups on day 1 (18 counts/10 s soybean MCT vs. 24 counts/10 s mixed fish oil lipid). Levels on day 6 increased in both groups but were much higher in the fish oil containing lipid group (288 vs. 42 counts/10 s).” (R)

Antebi et al. [112] randomized 20 patients to a mixed soybean MCT olive fish intravenous lipid emulsion (SMOFlipid, Fresenius Kabi, Bad Homburg, Germany) or soybean intravenous lipid emulsion following abdominal surgery. After 5 days of parenteral nutrition with the lipid emulsions, low density lipoproteins were isolated and subjected to in vitro oxidation. Oxidation of the low density lipoproteins from the fish oil containing lipid emulsion group was greater than from the soybean emulsion group. The investigators speculated that n-3 PUFA incorporation into low density lipoproteins increased its oxidizability.” (R)

If you look at cardiovascular disease and you see lots of oxidized LDL, keep in mind that the majority of that could be due to fish oil if you were supplementing it.

Omega 3 is “anti-inflammatory” and creates resolvins

Another major reason why people take fish oils is because it lowers inflammation, supposedly. It’s claimed to be anti-inflammatory.

However, the use of the term “anti” may not be the best description of these effects. “Anti” means opposed to. Most effects of n-3 PUFA on inflammation result from suppression rather than opposition of inflammation. n-3 PUFA suppresses the production of transcription factors and cytokines involved in inflammation (discussed below) and produce less-inflammatory eicosanoids. They do not produce mediators which oppose the actions of inflammatory cytokines. Examples of the anti-inflammatory effects of DHA and/or EPA include suppression of the production of numerous inflammatory mediators that include leukotriene-B4 (LTB4), prostaglandin E2 (PgE2), interleukin-1β (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF), and reactive oxygen species.” (R)

So as you can see it’s not anti-inflammatory, but only produces less inflammatory metabolites compared to omega 6. But still, because it’s so highly reactive and creates very inflammatory lipid peroxides, it’s actually highly inflammatory itself.

But what about pro-resolvins?

Both omega 3 and 6 can produce specialized pro-resolving mediators (SPMs) resolvins, protectins, maresins, and their metabolic precursors.

SPMs possess both immune suppressive effects upon inflammation and immune-stimulating effects (clearance of dead cells and microbes).

However, SPM synthesis is often dysfunctional in ill people. So those that need it the most, often get it the least.

For example, LPS (endotoxin from the gut) decreases SPM levels which is consistent with impaired SPM synthesis following an acute inflammatory state.

Let me show you some examples in humans

These results suggest an impairment in the metabolism of 17-HDHA to resolvins in patients with peripheral vascular disease. Interestingly, the increase in HEPEs and resolvins E1 and E3 with fish oil was extremely heterogeneous. Although 18-HEPE showed consistent increases with fish oil, the change in resolvin E levels ranged from a small decrease or no effect to an increase in levels. For example, resolvin E1 decreased in 1 patient, was unchanged in 1 patient, and demonstrated a small or larger increase in the remaining patients. In the placebo group, resolvin E1 decreased in 2 patients and increased in the remainder. The 2 patients with the largest increases in resolvin E1 were in the placebo group (the increase being 3 fold greater than any patient in the fish oil group). Similar heterogeneous responses were found for resolvin E3.” (R)

Fish oil increased plasma EPA and DHA levels and 18-HEPE levels in both groups, although the increase in 18-HEPE was lower in the metabolic syndrome patients. 17-HDHA and 14-HDHA increased in the control group. However, there was no change in 17-HDHA and 14-HDHA levels in the metabolic syndrome patients. Resolvins E1-E3 increased similarly in both groups following fish oil. However, there was no increase or a slight decrease in resolvins D1-D2, 17R-resolvin D1, protectin D1, and maresin-1 in both groups. Addition of aspirin was without effect. This study demonstrates impaired metabolism of EPA and DHA to 18-HEPE, 17-HDHA, or 14-HDHA in patients with metabolic syndrome. It also demonstrates the ineffectiveness of fish oil for increasing production of resolvins D1-D2, protectin D1, and maresin-1 in healthy and metabolic syndrome patients.” (R)

The investigators compared survivors (n = 13) with non-survivors (n = 9). Higher levels of pro-inflammatory cytokines (i.e., TNFα, IL-6, IL-8), prostaglandin F2α, leukotriene B4, and SPMs (resolvin D5, resolvin E1, 17-epi-resolvin D1, and 17-epi-protectin D1) correlated with higher mortality. The investigators speculate that failure of resolution (i.e., response to the SPMs) contributed to the mortality. Thus, in this study higher SPM levels failed to improve outcome but may reflect upon defects in action rather than synthesis.” (R)

This premise is supported by the study of Sordi et al. [82] using an animal model of pulmonary sepsis (intratracheal Klebsiella pneumoniae). LXA4 levels increase early in this infectious model, along with the inflammatory response. Treatment with LXA4 receptor antagonists (antagonizes SPM action) early during sepsis decreased bacterial dissemination and improved survival. Early treatment with LXA4 (increased SPM action) worsened infection and failed to improve survival. In contrast, treatment with LXA4 during late sepsis improved inflammation and survival while LXA4 receptor antagonists had no effect.” (R)

SPMs are produced in many, if not all, tissues. Their actions are believed to be local and short lived. It is unclear if levels in the blood accurately reflect upon levels in the tissues. SPMs also appear to be tissue and disease specific. Not all SPMs are produced in each tissue [83]. It is essential that studies evaluate the tissue specificity of SPM actions and tissue-specific SPM production in a variety of human diseases.” (R)

Now that we discussed all the “benefits” of omega 3s, let’s discuss more of its side effects.

Other side effects

Omega 3 and cardiovascular and heart disease

Fish oils are heavily marketed for lowering cholesterol and prevention of cardiovascular disease.

However, many studies actually found that it doesn’t help at all and that it can actually have negative effects.

This clinical trial showed that daily treatment with omega 3s did not decrease the prevalence of cardiovascular mortality or morbidity in patients with multiple cardiovascular risk factors (R).

This meta-analysis included 20 randomized controlled trials with a total of 68,680 patients. The median age was 68 years, with a range from 49 to 70 years. Thirteen of the studies evaluated omega 3 for secondary prevention of cardiovascular outcomes, 4 assessed both primary and secondary prevention, and 3 looked at outcomes in patients with implantable cardioverter defibrillators. All lasted longer than one year, and most were high quality, with a low risk of bias. Prespecified subgroup analysis found no association between treatment effect and omega-3 fatty acid dose for cardiovascular health. And in the 2 trials involving dietary supplementation with omega-3 PUFAs, the results for all-cause mortality and cardiac death were conflicting, with one showing an increase in all-cause mortality and cardiac death and the other showing a decrease in both outcomes compared with the control group (R).

This study found that oleic acid, linoleic acid, and eicosapentaenoic acid (EPA) were positively related to coronary risk factors, while nervonic acid (C24:1n9) exerted negative effects on these risk factors (R).

The oxidation of proteins (from lipid peroxides and peroxyl radical from omega 3) generating plaque formation involves only the LOO* radical-sensitive functional groups in side chains of the protein backbone and is therefore a rather late event in the development of Alzheimer disease and atherosclerosis.” (R)

 “When the level of free PUFAs generated by phospholipases (usually PLA2) exceeds a certain limit, lipoxygenases (LOX) commit suicide, causing liberation of iron ions. The latter react with LOOHs (lipid hydroperoxides) and thus induce a switch from enzymatic to nonenzymatic generation of lipid peroxidation (LPO) products. Although the LOO. radicals produced in enzymatic reactions are deactivated within the enzyme complex, LOO. radicals generated in nonenzymatic reactions are able to attack any biological compound, inducing severe damage. Apparently, iron ions and LOOH molecules at the surface of injured cells transfer the nonenzymatic LPO reactions to the phospholipid layer of bypassing lipoproteins, thus explaining why inflammatory diseases, such as diabetes, are combined with atherogenesis.” (R)

Accumulation of omega 3 in the heart leads to marked impairment of alpha 1-adrenoceptor-induced positive inotropic effects and induction of arrhythmias (R).

Although n-3 fats are considered beneficial for cardiovascular health, they appear to reduce endurance times, and their side effects need to be further investigated.” (R) Meaning they reduce the work capacity of the heart.

As a side note, consumption of the “essential fatty acids”, at the expense of saturated fatty acids, does not lower the risk of death from cardiovascular diseases (R).

Keep in mind that saturated fat isn’t bad. Even high-fat diets consisting of lard or milk fat don’t contribute to the development of cardiovascular disease and cardiac dysfunction. High fat diets, obesity, or hyperglycemia don’t necessarily induce cardiac dysfunction in mice (R). What causes the problems is the impairment of glucose oxidation and an increase in fat oxidation. That’s why meldonium, which inhibits fat oxidation, is so therapeutic for heart disease. Check out this article where I discuss the benefits of inhibiting fatty acid oxidation.

Of all the high-fat diets tested in this study, menhaden (fish) oil decreased the sensitivity of CPT I (the enzyme that transports long-chain fats into the mitochondria, and the enzyme that’s inhibited by meldonium) to inhibition by malonyl CoA the most. This means that fat-rich in EPA and DHA promotes fat oxidation at the expense of glucose and this leads to mitochondrial dysfunction and eventually heart problems (R).

On the other hand, sugar (which creates saturated and monounsaturated fat through lipogenesis) or lard or a combination of both doesn’t promote cardiac remodeling with a predisposition to heart failure under conditions of obesity or excess sucrose (R).

And the harmful effects of omega 3 aren’t just because it is highly oxidizable, but also because it’s so fluid as being too fluid impairs proper cellular function (R).

Fish are rich in n-3 PUFAs; thus, it was deduced that the protective properties of a fish diet are due to n-3 PUFAs. Fish, fish oils, and vegetables contain besides n-3 PUFAs as minor constituents furan fatty acids (F-acids). These are radical scavengers and are incorporated after consumption of these nutrients into human phospholipids, leading to the assumption that not n-3 PUFAs, but F-acids are responsible for the beneficial efficiency of a fish diet.” (R)

Omega 3 and the immune system

Another reason why omega 3 is “anti-inflammatory” is because it is immunosuppressive. Some people might think that’s a good thing, but it’s not. You want your immune system to be able to kill pathogens in the body, but also not to react to your own body. It should be balanced.

Unsaturated fats, with GLA and DGLA being the most potent and EPA and arachidonic acid being modest, inhibit specific aspects of cytotoxic T cell function by making the membranes too fluid (R). This increase in fluidity allowed more calcium to leak in and disrupt its function. “Although no change was observed with the saturated palmitic acid, maximal effects were observed with GLA and DGLA and modest effects with EPA and AA.”  

“n-3 PUFA are also reported to suppress cellular immune responses (Table 1) that include leukocyte chemotaxis, adhesion, proliferation, transmigration, phagocytosis, activation, antigen processing, T-lymphocyte functions, and production of natural killer cells [6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26]. Thus, immunosuppressive rather than immunomodulatory is a more accurate scientific term to describe the effects of DHA and EPA.” (R)

The reason why immunosuppression is bad is because it makes it susceptible to cancer and infections.

Check out the research on omega 3 and risk for infections here

Schwerbrock et al. [30] reported that fish oil (Research Diets, New Brunswick, New Jersey) fed mice had impaired resistance to influenza infection. The fish oil group had lower natural killer (NK) cells, neutrophils, and inflammation in the lung and higher mortality compared to the control group. Cruz-

Chamorro et al. [31] administered diets based upon olive oil, fish oil (unspecified fish oil), and hydrogenated coconut oil (20% lipid diets) or a low fat diet (2.5%) to mice. Mice were treated with cyclophosphamide to induce an immunosuppressed state or saline (control) and infected with Listeria monocytogenes. Splenocyte proliferation was suppressed by fish oil in response to conconavalin A and lipopolysaccharide compared to the other diets in normal and immunosuppressed groups. The fish oil group also had higher levels of bacteria in the spleen and liver compared with the other diets. Mortality was highest with the fish oil diet and lowest with the olive oil diet.

Interestingly, Zapata-Gonzalez et al. [16] speculate that the high incidence of tuberculosis in Eskimo populations may result from fish oil-induced alterations in antigen presenting cells.

Xia et al. [43] demonstrated that fish oil supplementation (fish oil, Bioserv F5424, Flemington, NJ, USA) increased growth of subcutaneously implanted melanoma cells in mice.

Woodworth et al. [35] found that fish oil supplementation (fish oil, Ocean Nutrition, Newark, CA, USA) in mice infected with Helicobacter hepaticus led to the development of colonic adenocarcinoma and significantly increased mortality compared with control and corn oil-based diets (18% vs. 0%).

Mannini et al. [44] compared fish oil supplemented (unspecified fish oil) to maize oil supplemented (high in linoleic acid) diets in mice transplanted with T-lymphoma cells. Fish oil supplementation increased metastasis, cancer organ infiltration, and cachexia.

In support of an immune suppressive effect, Grimm et al. [45] demonstrated that fish oil supplementation (fish oil emulsion, unspecified source) prolonged graft survival in an animal heart transplant model (impaired rejection). Interestingly, the immunosuppressive effects of fish oil were similar to those of soybean oil in this model.

This is a very important finding, so I’m going to show it here. Fish oils, because of their immunosuppressive effects, enhances the severity of the bacterial infection and have reduced ability to detox endotoxins. “While, ω-3 PUFA supplementation protected against severe colitis, these mice suffered greater mortality associated with sepsis-related serum factors such as LPS binding protein, IL-15 and TNF-α. These mice also demonstrated decreased expression of intestinal alkaline phosphatase and an inability to dephosphorylate LPS.” (R)

And this is very bad for those that have COVID, because: “In obese or diabetic individuals, there is an increase in the abundance of either Gram-negative bacteria in the gut or their product, endotoxin, in systemic circulation. We speculate that when the COVID-19 infection localizes in the intestine and when the permeability properties of the intestinal membrane are compromised, an inflammatory response is generated when proinflammatory endotoxin, produced by resident Gram-negative bacteria, leaks into the systemic circulation.” (R) Sepsis is caused by infection from endotoxin, and fish oils can significantly worsen this. Stay far away.

Omega 3 and cancer

Omega 3 intake has been shown to increase the risk for melanoma, basal cell carcinoma, colon cancer (R, R, R) and promote the growth of tumors (as the n-3/n-6 ratios increase, the total number and weight of tumors increased gradually (R)).

Increasing LCn3 (NNTH 334, RR1.10, 95% CI 0.97–1.24) and ALA (NNTH 334, RR1.30, 95% CI 0.72–2.32) may slightly increase prostate cancer risk; increasing total PUFA may slightly increase risk of cancer diagnosis (NNTH 125, RR1.19, 95% CI 0.99–1.42) and cancer death (NNTH 500, RR1.10, 95% CI 0.48–2.49) but total PUFA doses were very high in some trials.” (R)

Omega 3 and mental disorders

The amount of DHA in the brain (and other tissues) increases with aging, and its breakdown products, including neuroprostanes, are associated with dementia and higher levels of DHA and total PUFA are found in the plasma of demented patients (R, R).

When the brain is injured, DHA and arachidonic acid contribute to brain edema, weakening the blood-brain-barrier, increasing protein breakdown, inflammation, and peroxidation, while a similar amount of stearic acid in the same situation caused no harm (R).

AA and DHA aggravated cerebral ischemic injury, which manifested as enlargement of areas of cerebral infarction and increased impairment of motor activity, in a concentration-dependent manner. However, there were no remarkable differences in post-ischemic alterations between the SA and saline groups. The post-ischemic augmentation of injury in AA and DHA treatment groups was accompanied by increases in the permeability of the blood-brain barrier (BBB), brain edema, metalloproteinase (MMP) activity, inflammatory cell infiltration, cyclooxygenase 2 (COX-2) expression, caspase 3 activity, and malondialdehyde (MDA) production, and by a decrease in the brain glutathione (GSH) content. Furthermore, we found that either AA or DHA alone had little effect on free radical generation in neuroglia, but they greatly increased the hydrogen peroxide-induced oxidative burden.” (R)

Omega 3 has been said to be good for ADHD, but it actually just makes the cells insensitive to external stimuli. Both DHA and EPA inhibit calcium-ATPase (which keeps intracellular calcium low to allow normal neurotransmission) in the cerebral cortex; this suggests “a mechanism that explains the dampening effect of omega-3 fatty acids on neuronal activity” (R). An excess dampening can lead to brain fog and anhedonia.

DHA (more strongly even than arachidonic acid) inhibits the uptake of the excitotoxic amino acid aspartate, and in some situations glutamate, prolonging their actions (R). Glutamate, acting on NMDA, can promote insulin resistance and lipid accumulation (R) and has also been linked to anxiety, brain over-excitation, overthinking, OCD, etc.

One major side effect of omega 3 is that it displaces cholesterol from lipid rafts. Excess omega 3 can lead to too low levels of cholesterol and this significantly reduces the transport rate and affinity of serotonin for the transporter. Meaning, more serotonin will be floating around in the brain, causing all kinds of issues, such as vascular constriction, vascular leakage, low libido, brain fog and almost all other cognitive degenerative condition (R).

Furthermore, depleting cholesterol (with omega 3) lowers both agonist and antagonist binding to serotonin receptors 1A and 7 and alters responses of serotonin 2A receptors (R). And this isn’t just serotonin, but also dopamine and other neurotransmitters. Too much omega 3 can cause neurotransmitter dysfunction and that’s the last thing you want if you want to feel good.

Lastly, the cognition promoting effects of omega 3 may be related to vitamin E levels. This study found that when vitamin E was sufficient, omega 3s didn’t have any benefits (R). But on the flip side, omega 3 depletes vitamin E faster than omega 6 does.

Omega 3, diabetes and fat gains

Many studies find that omega 3 might improve insulin sensitivity, which is logical if overall inflammation is lowered. Aspirin can do this as well.

However, many other studies have found that omega 3 is actually not effective and even harmful. In certain studies, it’s been shown to worsen insulin sensitivity, reduce the metabolic rate, accumulate with aging and disease (which then further worsens it through oxidative stress, metabolic breakdown and inflammation), and can actually lead to weight gain.

Check out the research

Omega-3 fatty acid treatment (5.5 g of omega-3 fatty acids (3.3g EPA and 2.2 g DHA)) in type II diabetes leads to rapid but reversible metabolic deterioration, with elevated basal hepatic glucose output and impaired insulin secretion but unchanged glucose disposal rates.” (R)

Fish oil in doses of 5g per day decreased the metabolic rate by 5%. “There was a main effect of time with decrease in RMR (5%) and fat oxidation (18%) in both the supplementation groups.” (R)

A high serum DGLA (dihomo-γ-linolenic acid (created from alpha-linolenic acid and found in evening primrose, blackcurrant and borage)) level was associated with obesity, body fat accumulation, a high ALT level, and insulin resistance in patients with type 2 diabetes.” (R)

Here, we first confirmed that cardiac DHA levels are elevated in diabetic humans relative to controls.” (R)

EPA and DHA, may trigger myoblast reprogramming into certain adipocyte phenotypes, since their ligand PPARg, the key regulator of adipogenesis. For instance, Saraswathi et al. (2007) reported that mice fed diets enriched with EPA and DHA exhibited significant change in lipid composition to the favor of increasing perigonadal fat mass when compared to control group (Saraswathi et al., 2007). Moreover, offspring born from dams fed maternal diet high in DHA throughout the period of gestation and lactation (5% total fat; 0.95% DHA) showed increased total and subcutaneous fat mass when adjusted to total body weight at 6 weeks of age. Furthermore, n−3 PUFAs consumption has been recently linked to increase body fat composition in adult mice with genetically induced diabetes (Todoric et al., 2006). These changes in mitochondrial function were concurrent with increased lipid droplets size and number.” (R)

Large lipid droplet size creates more inflammation than normal lipid droplets, and saturated fat creates smaller, less inflammatory lipid droplets compared to omega 3 and 6. Mitochondrial dysfunction is the cause of the drop in metabolic rate and fat gain.

Fasted blood samples were taken at baseline and after 12 weeks of supplementation. There were significant increases in the EPA (413%) and DHA (59%) levels in red blood cells after FO supplementation, with no change of these fatty acids in the OO group. RMR and substrate oxidation did not change after supplementation with OO or FO after 6 and 12 weeks. Since there was no effect of supplementation on metabolic measures, we pooled the two treatment groups to determine whether there was a seasonal effect on RMR and substrate oxidation. During the winter season, there was an increase in FA oxidation (36%) with a concomitant decrease (34%) in carbohydrate (CHO) oxidation (p < 0.01), with no change in RMR. These measures were unaffected during the summer season. In conclusion, FO supplementation had no effect on RMR and substrate oxidation in healthy young males. Resting FA oxidation was increased and CHO oxidation reduced over a 12 week period in the winter, with no change in RMR.” (R)

Although the above study didn’t find a decrease in RMR from fish oils, it did find a drop in glucose oxidation during the winter. This is how animals go into hibernation. They gain a lot of fat and slow their metabolism a lot by eating PUFAs, and then go into hibernation and burn mostly fat. Humans are not meant to do this, and it’s the ability to oxidize fat that makes us smart, warm, stress-resilient, fast, strong, etc. Anything that messes with proper glucose oxidation is best avoided.

It’s commonly touted that sugar is responsible for an increase in advanced glycation end-products (AGEs) and an increase in Hb1Ac, but it’s actually PUFAs.

In the first step of a response, lipid hydroperoxide molecules are generated. An increasing impact switches the enzymatic reaction to a nonenzymatic one by generation of lipid peroxyl radicals, which attack sugars by oxidation. In the course of these reactions, hydrogen peroxyl radicals are generated, resembling lipid peroxyl radicals in their reactivity. The reactions induced by these radicals are not under genetic control, they attack nearly all types of biological molecules (such as proteins, lipids, and sugars), and are responsible for the deleterious cell alterations in aging and age-related diseases (such as diabetes, Alzheimer’s disease, or atherosclerosis) and probably also in autoimmune diseases, which involve sugars at the cell membranes.” (R)

Omega 3 and gut inflammation

Omega 3 is said to have a positive effect on the gut, but if there is already a lot of inflammation going on, then adding highly reactive lipids, can easily make the problem worse.

In mice, n-3-PUFAs have induced a more paradoxical response. Several studies have shown improved inflammatory scores in n-3-PUFA supplemented rodents (5053), whereas others have noted worsening of intestinal inflammation severity (5254). In one study, attenuation of spontaneous ileitis in SAMP1/Yit mice by n-3 PUFA was due to inhibition of monocyte recruitment in the inflamed tissues (55), while two other studies in C57BL/6 mice showed that n-3-PUFAs exacerbated DSS-colitis due to decrease of adiponectin expression, one of which noting no change with n-6-PUFA or control diets (5254). In another study, 2,4,6-trinitrobenzenesulfonic acid (TNBS)-colitis rats given n-3-PUFA orally showed inhibition of pro-inflammatory eicosanoids, prostaglandin E2 (PGE2), and leukotriene, similar to treatment with 5-aminosalicylic acid (Peroxisome proliferator-activated receptor gamma; PPARγ agonist) (53), whereas others have suggested a decreasing effect over time, due to T-cell apoptosis/regrowth (56).” (R)

The proportion of unsaturated FA in the cell membranes influences the susceptibility to oxidative stress. Oxidative stress accompanies infectious diseases, and the development of lipid peroxides and other reactive oxygen products may be harmful to the epithelial barrier function. Fatty acid peroxides from the feed may also be absorbed with other lipid-solubles and thereby harm the intestinal function.” (R)

excessive intake of n-3 fatty acids is suspected to increase apoplexy, the higher incidence of apoplexy (intestinal bleeding) observed in Greenland natives compared with Danes.” (R)

Omega 3 and lipofuscin

Lipofuscin, also called the age pigment, has been supposed to be cellular debris derived from lipid peroxides by free radical-induced oxidative stress, and thus regarded as one of the indices of lipid peroxidation in tissues. As oxidative stress and lipid peroxidation increase (especially in the presence of metals such as iron, copper, mercury, cadmium, etc.) so does the formation of lipofuscin.

Lipofuscin accumulation in the eye, is a major risk factor implicated in macular degeneration, a degenerative disease,[15] and Stargardt disease, an inherited juvenile form of macular degeneration.

In the peripheral nervous system, abnormal accumulation of lipofuscin known as lipofuscinosis[1] is associated with a family of neurodegenerative disorders – neuronal ceroid lipofuscinoses, the most common of these is Batten disease.

Also, pathological accumulation of lipofuscin is implicated in Alzheimer’s diseaseParkinson’s diseaseamyotrophic lateral sclerosis, certain lysosomal diseasesacromegaly, denervation atrophylipid myopathychronic obstructive pulmonary disease,[16] and centronuclear myopathy. Accumulation of lipofuscin in the colon is the cause of the condition melanosis coli.”

This study found that monkeys fed fish oil has x3 more lipofuscin in their livers compared to those receiving corn oil. Also, basal levels of thiobarbituric acid reactive substances (TBARS) (a measure of oxidative damage), was x4 greater in the fish oil group. The researchers found that even a 10 fold increase in alpha-tocopherol, a potent antioxidant, was not fully able to prevent the peroxidative damage from fish oil (R).

Summary

So to wrap it all up, omega 3s in excess can cause mitochondrial dysfunction (reduce ATP production, increase electron leak, oxidative stress and inflammation), lipid peroxidation, DNA damage, lipofuscin formation, depression of the immune function, bleeding and increased risk of hemorrhagic stroke, as well as increased lipid peroxidation resulting in oxidative damage to various tissues (R).

A voluminous literature developed largely in Scandinavia prior to the time that EFA and tocopherol were discovered. Agduhr investigated the effects of cod liver oil upon several animal species and described abnormalities such as suppression of growth, leucopenia, haemorrhage of the myocardium, degeneration of the heart muscle, edema of the lungs, and necrosis of the liver. Slagsvold observed that cod liver oil poisoned cattle, with stiffness and muscle lesions as symptoms. In another study the toxicity of cod liver oil in calves was manifested as a severe muscular dystrophy…. The rats fed cod liver oil were sterile.” (R)

In the 1940s, some of the toxic effects of fish oil (such as testicular degeneration (PUFAs accumulate there), softening of the brain (PUFAs accumulate there as well, and it’s the depletion of cholesterol that contributes to this effect), muscle damage, and spontaneous cancer) were found to result from an induced vitamin E deficiency (R).

Everywhere PUFAs (omega 3) accumulate, there is can cause destruction and require massive amounts of vitamin E to partially block its harmful effects.

Side effects of omega 3s

  • Inhibit ETC complex function
  • Enhances cell membrane fluidity and allows more calcium to enter the cell. This is the first step to cell death and fibrosis.
  • Promotes electron leak which causes oxidative stress.
  • Is highly reactive and creates harmful lipid hydroperoxides and peroxyl radicals.

Benefits of omega 3s

  • Creates less inflammatory mediators compared to omega 6
  • Create resolvins (although that pathway is dysfunctional in people with inflammation, and yet they are the ones that need it the most).

But let me just give a disclaimer here. I’m not against eating oysters, mussels or the occasional dish out of fear of omega 3. Fish, shellfish and other seafood contain anti-oxidants that protect the omega 3 from oxidation, and as shown by the study above (R), it’s the furan in the fish that has the benefits and that’s protecting against oxidative damage. It’s the overconsumption of omega 3 supplements that I’m opposed to. Leave the supplements altogether and just eat good food.

Additionally, be sure to check out the side effects of omega 6:

What to do instead

Exercise

This study found that omega 3 didn’t enhance the benefits of resistance exercise in older individuals.

No significant effects were noted for the 2 inflammatory cytokines measured (P > .05). We conclude that progressive resistance training exercise is an excellent method to enhance parameters of body composition, skeletal muscle strength, and functional ability in older men, whereas omega-3 supplementation did nothing to enhance these parameters or influence inflammatory biomarkers. …In the present study, we found no difference in the levels of inflammatory biomarkers between groups despite a significant difference in omega-6 to omega-3 ratio.” (R)

Another reason to be careful with omega 3 is because a decrease in cardiolipin with age is associated with sarcopenia. And as you can see, omega 3 enriched cardiolipin can quickly lead to reduced cardiolipin content (R).

So just by doing exercising alone, with proper nutrition for recovery, will offer a lot more health benefits than what omega 3 is touted to give you.

Coconut oil

Coconut oil has been shown to be great at boosting the metabolism without interfering with glucose oxidation and lowering inflammation even in very small doses of 1g per day (just a few studies for example: R, R, R, R, R, R, R). Few people take only 1g fish oil, but more like 3-5g of fish oils daily. So instead of taking very harmful fish oils, rather take 1 tsp of coconut oil daily for much better benefits without any of the side effects.

Coconut oil is mostly saturated fat, which can’t oxidize, so it can’t harm the body in any way.

Also, coconut oil has antibacterial, antifungal, antiviral, antiparasitic, antidermatophytic, antioxidant, and immunostimulant activities, as opposed to omega 3 fatty acids (R). “The medium chain fatty acids and monoglycerides found primarily in coconut oil have miraculous healing power which act as natural antibiotic and also help modulate immunity.” (R)

Avoid inflammatory foods

One of the main reasons why people have inflammation is because they consume inflammatory foods. Foods such as grains, starches (this depends on the person), iron-fortified foods, moldy food, omega 6 rich oils or food prepared in those oils (rapeseed, canola, sunflower, safflower, etc.), lectin, excess phosphate, etc.

So just by avoiding those inflammatory foods and replacing them with anti-inflammatory foods, such as coconut oil, fruits, dairy, etc., will take your health to a much better place. And add in exercise when your health permits.

If you want to learn more on how to eliminate inflammation and what foods to eat to improve your health, which includes easy-to-digest food, micronutrient dense foods, how to pair certain foods for maximal energy production and satiety, then check out The Alpha Energy Nutrition Course.

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6 Replies to “Why Omega 3 should be avoided and what to use/do instead”

    1. Hey man,
      It’s just an association. Most people that take fish oils are relatively health-conscious, so that can also contribute. But I’d say that by displacing omega 6, they can be “beneficial”.

  1. Hey Hans,

    what about keto krill oil? ( i use the dr mercola brand).

    best,

    Sami

    1. My approach would just be to reduce omega 6 intake, perhaps take 1/2 tsp coconut oil and some vitamin E daily and then eat some seafood once or twice a week. That should take care of it. How much PUFAs does the krill oil contain? I think it should be fine though, but if you’re in decent health, why use it at all? If you’re not in decent health, then the recs I made should be even better than taking krill oil.

      1. Hi Hans! thanks for the reply. I basically have a stack and I wasn’t aware of the issues ( to such an extent) with PUFA’s. I’ve started transitioning to only saturated and Monosaturated fats. Im generally on a carnie diet. I cook with grass fed tallow and ghee for the most part. however, but i eat berries(and some other fruits) and use basmati rice as my carb of choice. I have an issue which I intend to discuss with you in a consult IF my next plan of action doesn’t work. I’ve used your advice as a guide. I won’t be able to buy the products for a while though ( terrible transit heat). If it fails, I’ll be booking a consult sometime in autumn. Continue with the great work!

      2. Thanks man, will do. I hope your next plan of action works out, if not, you know where to find me. 🙂

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