How to deplete yourself of PUFA quickly and safely

Eliminating nut and seed oils are one of the best things you can do for health and longevity.

By doing so, you not only improve health in the long run, but it also has an almost immediate beneficial effect that translates to faster recovery in the gym or from physical activity, faster healing, having more energy, being less predisposed to disease, etc.

Seed and nut oils, such as soy, canola, rapeseed, sunflower, safflower, linseed, cottonseed, sesame seed, peanut oil, etc. are all very high in polyunsaturated fats (PUFAs) and are best avoided.

Safe (low PUFA) nut oils/butters include coconut, cocoa, macadamia, and olive.

Watch this article here

Let me first show you why it’s best to avoid PUFAs and then I’ll show you how to do so.

Why to avoid PUFAs and harms done by excess

3 big reasons to avoid PUFAs

#1 PUFAs are rapidly oxidized/damaged.

This scales with unsaturated bonds. So omega 3 is much worse than omega 6. This is a big problem because these fats are incorporated into cell membranes and fatty structures that are needed to stabilize energy production (i.e. cardiolipin), and when they spontaneously oxidize, ATP production drops. And once energy production goes, so does health and longevity.

And apart from reducing ATP, these lipid peroxides are inflammatory in themselves. So once these fats are oxidized, the blood is flooded with lipid peroxides and proteins from the dead/damaged cell, to which the body mounts an immune response. Over time this can lead to autoimmune conditions.

Any insult, whether it comes from inside the body or outside (e.g. sun (UV) or exercise), can damage these fats and cause lots of problems, such as mitochondrial damage, lipofuscin, a drop in energy production, cell death, etc. That’s why aspirin is anabolic for old people (they usually have an excess of stored PUFAs).

A quick word on lipofuscin.

Lipofuscin is a cell gone bad. Meaning, when a cell gets damaged, normal cell turnover such as mito- and autophagy, breaks the cell down and recycles it, preventing the damaged cell from accumulating. Lipofuscin is damaged cells that accumulate iron that hasn’t been/can’t be properly broken down and recycled.

Lipofuscin doesn’t aid in energy production, but it’s actually destructive. Lipofuscin’s ability to incorporate different metals contributes to reactive oxygen species (ROS) generation through the Fenton reaction (ROS reacting with iron) and this causes even more protein and lipid oxidation, leading to more lipofuscin formation (R).

Lipofuscin was considered a harmless hallmark of aging, but its presence is detrimental as it continually accumulates (R). And it would seem that the accumulation is exponential if excess iron and PUFA are not removed from the diet.

As we get older and more PUFA accumulates, the slower and more “dirty”/dysfunctional energy production becomes. This leads to a hypoanabolic and hypercatabolic state, leading to an increase in oxidative stress—lipid peroxidation protein insolubilizing with waste-trash products accumulating, such as ceroid lipofuscin (R).

Considering that PUFAs represent the main underlying elements behind lipofuscin formation, an impairment of lipid metabolism proved to be the starting point of lipofuscin accumulation and synthesis. Also, very importantly, lipofuscin is “immune” to cellular proteostasis (breakdown) and PUFAs itself actually inhibit proteolytic enzymes. More precisely, there is an impediment to the degradation of the folded proteins and thus results in complexes formed with other perinuclear/centrosomal-proximal proteins with the risk to aggregate into aggresomes (R).

And the reason I’m talking about both PUFA and iron here, is because they work in concert to create lipofuscin; these dysfunctional cells that create ROS and no ATP.

Furthermore, lipid peroxides, created when PUFAs are oxidized, can inhibit proliferation and cell cycle progression by the down-regulation of D1, D2, and A cyclin expression (R).

Lastly, lipid peroxides (from both omega 3 and 6) active the enzyme heme oxygenase (HO) (R, R). Heme breakdown, create free iron (Fe2+) and carbon monoxide.

Iron then reacts with free radicals and PUFAs to create even more damage. Carbon monoxide on the other hand inhibits cytochrome c oxidase of the electron transport chain, thus reducing ATP production.

Keep in mind that many of this cell turnover machinery/enzymes are ATP-dependent. Without enough ATP, proper cleanup can’t occur.

Also, increasing studies have shown a dark side of HO-1, in which HO-1 acts as a critical mediator in ferroptosis induction and plays a causative factor for the progression of several diseases. Ferroptosis is a newly identified iron- and lipid peroxidation-dependent cell death (R). HO-1 expression is associated with neuronal damage and neurodegeneration especially in Alzheimer’s and Parkinson’s diseases (R).

#2 PUFAs are used by COX and LOX to create inflammatory mediators.

COX and LOX stand for cyclooxygenase and lipoxygenase. These enzymes create inflammatory eicosanoids.

Yes the COX enzyme can also create SPMs (specialized pro-resolving mediators), but that’s not a good reason to supplement omega 3. If you want to know why, check out my omega 3 article and check the section on SPMs.

The inflammatory mediators are involved in many, if not most, of the degenerative conditions mentioned above.

#3 Inhibit cellular energy production.

PUFAs are incorporated into cell membranes, which determine the function of the cell and the stability of various enzymes and complexes. PUFAs reduce the stability of the energy-producing complexes, thus promoting ROS production and lowers ATP production. More ROS in the presence of PUFAs creates lipid peroxides and lipofuscin. It’s just awful.

So all in all, PUFAs reduce energy production and most processes in the body are energy-dependent.

Theory is all good and well, but let’s look at the evidence

Clinical and experimental evidence has indicated that 2-series PGs (created from PUFAs) are involved in the initiation and progression of numerous diseases, including diabetes mellitus (34), hypertension (35), obesity (36), fatty liver disease (37), vascular diseases (38), carcinoma (39), inflammatory bowel disease (40), rheumatoid arthritis (41), asthma and allergic diseases (42) and Alzheimer’s disease (43).” (R)

Furthermore, PUFAs has been shown to lower androgens and can cause sterility (R, A), is catabolic (saturated fat is mildly anabolic) (R), anti-metabolic (reduces ATP production via many mechanisms) (R, A), suppresses the immune system (immunosuppressive; this enhances the risk of dying from infections and cancer), shortens lifespan (R, R, A) and much more.

Related articles

It’s impossible to show all the mechanisms and negative effects all in one post, so hope this serves are a sufficient brief intro on the harms of PUFAs.

Getting rid of it

#1 Eliminate dietary sources of PUFA

The way you accumulate PUFAs is by consuming them. So the best way to get rid of them is to stop consuming them. You don’t have to go on a zero PUFA diet (which is hard and not necessarily the best way to go about it).

You can simply eliminate all high PUFA foods, e.g. nut and seed oils (nut and seeds in general), grain-fed chicken and pork, fatty fish (if the fatty fish isn’t super fresh, it contains a fair amount of lipid peroxides) and grain-fed chickens’ eggs,

Good foods include lamb, beef and bison meat, dairy (preferably low fat to limit calories), shellfish, coconut oil, cocoa butter, fruit and vegetables.

You’d be surprised how good you feel just by making these switches. If you start to nourish your body properly, it will thank you and you’ll start to feel better real soon.

#2 Optimize mitochondrial function

Fats are burned through beta-oxidation in the mitochondria. No matter if you eat zero fat or take lipolysis inhibitors, you’ll always be burning fat. So optimizing cellular function is key.

A few ways to do that are to eliminate PUFA, donate blood if iron is too high, improve thyroid function, fix gut problems and keep aldosterone and parathyroid hormone low with salt and calcium. Exercise is also great for improving mitochondrial function and reducing inflammation.

#3 Increase brown fat

Thyroid hormone T3 is the best way to increase brown fat. T3 also increases mitochondrial density and uncoupling proteins, all of which helps to get rid of PUFA without causing inflammation.

Have your thyroid hormones checked and then perhaps get on an NDT supplement if your levels are low just to get everything kickstarted.

#4 Inhibit excess lipolysis

Fat/adipose tissue is one of the biggest storage spaces of PUFA. Lipolysis is the process where fats in the adipose tissue are released into the general circulation. Lipolysis often times becomes overactive in an inflamed state, which leads to fat accumulation in the liver, muscle, heart, visceral area, etc.

Lipolysis is also not the rate-limit step in fat oxidation, so boosting lipolysis doesn’t really mean much. Inhibiting it will also not prevent fat loss, because inhibitors don’t block it 100%. Perhaps only 30% or so. Many of the lipolysis inhibitors only inhibit excess lipolysis.

Niacin, ginger and aspirin are great supplements for inhibiting excess lipolysis and prevent the body from being flooded with PUFA all the time (R).

#5 Optimize liver function

The liver can get rid of PUFAs through glucuronidation, which is a detox process. But for that to happen, your liver needs to be in good condition. It needs vitamins and minerals and carbs from the diet in order to work optimally, so making sure your food is easy to digest and nutrient-dense will be very helpful here.

Protect against excess PUFA

#1 Inhibit ROS production

ROS damages PUFAs, and while excess PUFAs increase ROS, reducing excess ROS in the meanwhile will protect the PUFAs and prevent excess inflammation. This should only be a temporary solution as you reduce tissue levels of PUFAs so that you don’t need supplemental anti-oxidants anymore. And this is because ROS are needed in certain amounts and clinical trials with anti-oxidants fail to prevent disease.

90% of ROS is created in the mitochondria, specifically the electron transport chain. So optimizing that is key. The electron transport chain is complex and requires many vitamins and minerals and other compounds to work properly.

Biosynthesis of the component of mitochondrial respiratory chain, coenzyme Q, is dependent on vitamins B2, B6, B12, folic acid, pantothenic acid, niacinamide and vitamin C.” (R)

So all comes down to eating a nutrient dense diet… And this is not whole grain this and natural that. It’s milk, eggs, oysters, meat, organ meat, fruit and tubers.

Certain compounds that assist the ETC, such as methylene blue, vitamin K2 + vitamin C, red light, thymoquinone, PQQ, beta-lapachone, etc., will all help to reduce ROS, increase NAD and ATP and prevent lipid peroxidation.

There are many other sources of ROS which I will not go into here, but will only point out the importance of optimizing endogenous antioxidant enzymes, such as superoxide dismutase (SOD), catalase, glutathione. These enzymes, and the regeneration of glutathione, require zinc, selenium, manganese, riboflavin and magnesium. I recommend getting it all from the diet.

#2 COX inhibitors

PUFAs are used by the COX and LOX enzymes to produce inflammatory eicosanoids.

A few good inhibitors include aspirin, ginger, boswellia, berberine and turmeric.

#3 PUFA dilation

When someone has a lot of PUFA stored in their fat, then their body is often flooded with PUFA all the time. Diluting the PUFA with lots of medium-chain fats from coconut oil, will help against excess inflammation.

Medium-chain fats can enter the mitochondria without the carnitine transporter and are very rapidly burned as fuel. This is a very clean fuel source. This helps to prevent excess PUFA accumulation in the cell which is highly inflammatory.

I got the idea from Dr Peat. Here was his experience with it:

Although I had stopped using the unsaturated seed oils years ago, and supposed that I wasn’t heavily saturated with toxic unsaturated fat, when I first used coconut oil I saw an immediate response, that convinced me my metabolism was chronically inhibited by something that was easily alleviated by “dilution” or molecular competition. I had put a tablespoonful of coconut oil on some rice I had for supper, and half an hour later while I was reading, I noticed I was breathing more deeply than normal. I saw that my skin was pink, and I found that my pulse was faster than normal–about 98, I think. After an hour or two, my pulse and breathing returned to normal. Every day for a couple of weeks I noticed the same response while I was digesting a small amount of coconut oil, but gradually it didn’t happen any more, and I increased my daily consumption of the oil to about an ounce. I kept eating the same foods as before (including a quart of ice cream every day), except that I added about 200 or 250 calories per day as coconut oil. Apparently the metabolic surges that happened at first were an indication that my body was compensating for an anti-thyroid substance by producing more thyroid hormone; when the coconut oil relieved the inhibition, I experienced a moment of slight hyperthyroidism, but after a time the inhibitor became less effective, and my body adjusted by producing slightly less thyroid hormone. But over the next few months, I saw that my weight was slowly and consistently decreasing. It had been steady at 185 pounds for 25 years, but over a period of six months it dropped to about 175 pounds. I found that eating more coconut oil lowered my weight another few pounds, and eating less caused it to increase.” (R)

In my omega 3 article, I posted a study showing that as little as 1g coconut oil can significantly reduce inflammation and I also proposed that it would be a better idea to take coconut oil instead of fish oil for lowering inflammation.

#4 Saturated fat consumption

Since PUFAs are incorporated into cell membranes, it makes sense to displace them via the consumption of long-chain saturated fat, such as palmitic (C16), stearic acid (C18) and arachidic acid (C20).

Studies show that feeding old animals hydrogenated peanut oil (which contains only saturated fat) restores mitochondrial function close to youthful levels. Many other studies show that vegetable oil causes disease, and just adding in cocoa butter or fat with long-chain saturated fat, protects against the harmful effects of PUFA.

Dairy fat is also great for improving health. If you want to read more on that, check out my dairy fat article.

The best sources of these long-chain fats include suet, cocoa butter and dairy fat.

#5 Optimize gut function and prevent leaky gut

If you had to pick one organ to optimize for longevity, it has to be the gut.

Related article:

The gut has an influence on the whole body. If you don’t look after it, your whole body will suffer, but if you look after it, your whole body will thank you.

The gut is a significant source of toxins, and if you have leaky gut, those toxins enter into the body. And gut toxins and PUFAs are not a nice combination.

Here are a few articles on how to optimize your gut function


You can also check out my Instagram post on this by clicking on the icon below.

Eating and storing a bunch of PUFAs are not good for you. The best way to fix it is to eliminate high PUFAs foods from your diet and use some aspirin, vitamin E and coconut oil. Simple as that.

Also, be sure to eat a nutrient-dense diet (cronometer is very helpful here) and optimize gut health.

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