The Glucose Goddess Is Wrong About Fruit Juice – Here’s Why…

0:00 – My Health Journey Over the Years

4:48– 6 Key Takeaways

The toxicity of seed oils has been gaining traction in the health world. Besides avoiding them, what can we do to protect ourselves from their negative health effects? In this video, I’m gonna summarize some of the core issues with seed oils and provide you with three key solutions that I’ve used with myself and with my clients to protect against these negative effects of seed oils.

So in order to understand why I am recommending these three key solutions. For managing seed oils, I first want to talk about what some of these major problems are with seed oils and one of the big components is that they are high in omega six polyunsaturated fatty acids. So I have four of the major seed oils CH picked out here.

We have soybean oil, corn oil, sunflower oil, and canola oil, and I’ve set them all to a hundred grams. So we could see what percentage omega six polyunsaturated fatty acids that they have or, or polyunsaturated fatty acids in general. So soybean oil is 50.9 grams of omega six, which make about 51% omega six.

And it has about 6.6 grams of Omega-3. This is not long chain omega threes. This is things like alpha and oleic acid. Next we have corn oil. The corn oil is at 51.9 grams of omega six polyunsaturated fatty acids with about one gram of Omega-3. Again, not a long chain EPA or DHA. That’s found typically in fish sunflower oil.

We have 65.7 grams of omega six polyunsaturated fatty acids and no omega threes listed. And the last one is canola oil. Canola oil is about 17.8 grams of omega six and 7.5 grams of Omega-3, which is alpha linoleic acid, which again, is not the long chain D-H-A-E-P-A that we see from fish. And we’ll talk about that in just a little bit.

So stay tuned on why I’m bringing that up. But essentially what we’re seeing is the major seed oils that we see in the diet are quite high in omega six, polyunsaturated fatty acids, much more so if you put. Chocolate, roughly a hundred grams of chocolate. You have only three grams, so 3% omega six polyunsaturated fatty acids with about 0.1, Omega-3 polyunsaturated fatty acids, the omega six polyunsaturated fatty acids and the polyunsaturated fatty acids in general, were.

Considered to be or are considered to be essential fatty acids. This is from the work of the burrs, but the requirement is actually exceptionally low. Some of the newer research actually calls in the question, but essentially what the researchers say here from linoleic acid and regulation of glucose homeostasis is say, well, a daily intake of linoleic acid around one to 2% of total calories.

It’s sufficient to prevent the development of essential fatty acid deficiency. The over tenfold increase in linoleic acid consumption since the mid 20th century has prompted further research as to how linoleic acid impact long-term health. So even with that one to 2%, it’s exceptionally low, but there’s actually quite a few pretty solid arguments that it is even lower that than that, up to about 0.5%.

But let’s just run with 2%. So they’re saying that there’s a a, there’s a requirement for these fats. Around one to 2% of calories. Now the next thing is the consumption of Omega six polyunsaturated fatty acids. Despite the requirement only being one to 2% of calories has exploded from seed oils since 1909.

So we have a graphic here, and what we could see is that from 1909 to 1999, soybean oil and canola oil have gone out of control. These have been two of the biggest. Seed oils and the soybean oil has started to pick up since about 1950s, 1960s. And then the canola oil actually started to pick up around the 1990s or so.

Their intake has drastically increased, and with the increase in this intake, the amount of linoleic acid, which is the Omega six plant citrate fatty acid, has drastically increased as well as a percent of energy in the diet. So in 1909, about 2% of people’s calories. We’re coming from linoleic acid and in 1999 it’s about 8%, and now it’s even higher.

So this has drastically increased over time. We have a very low requirement for polyunsaturated fatty acids, one to 2% of calories, and even then that’s probably higher than is what’s actually true, particularly for the Omega six. But there’s some problems with these fats. They are extremely likely to be damaged by oxidative stress.

They can be per oxidized very easily because of their double bond structure. A table here that shows us. How likely they are to be damaged. We see saturated fats and monounsaturated fats, basically zero. Like their ability to be damaged is very, very low. But when we get to polyunsaturated fats, we have a mega six polyunsaturated fats.

When you look at linoleic acid, it’s significantly higher, many times higher than saturated monounsaturated fats. I know the scale is 2 4 6 a 10, and over here we have onic acid, which is significant. Different even to linoleic acid. And we get to the mega three polyunsaturated fats. They’re even worse than the omega six in terms of their susceptibility to oxidative stress.

So we have alpha linoleic acid here, and then we have DHA here, which is significantly more likely to be damaged than onic acid and linoleic acid, and also alpha linoleic acid. This is basically the more double bonds these fats have, the worse their susceptibility is to actually being damaged. So we have these highly proximal fats, uh, oxidizable fats.

With a very low requirement from them being massively exploded in the diet. Next up, we have the Omega six polyunsaturated Fatty acids, despite being less likely to be damaged, are actually the primary precursors to the inflammatory mediators in the body called the eicosanoids. So we have a graphic here, and what we could see is that omega six fatty acids, this is linoleic acid as an example, but you also have arachidonic acid can be converted to arachidonic acid, multiple steps, and then that can get converted into these inflammatory mediators through the enzymes epoxy oxygenase.

Cycl Oxygenase and Cytochrome P four 50 enzymes, and they create a variety of different inflammatory mediators. Here you can see them listed here. I’m basically laying the groundwork for what strategies we’re gonna use to protect ourselves from these fats by showing you what the actual problems are, or some of the problems.

Just to show this here, that linoleic acid. Acid. They still see in studies that you see increases in these inflammatory mediators with the linoleic acid intake. So the researchers here from a paper titled Linoleic Acid and the Regulation of glucose homeostasis are a view of the evidence, say, while relatively little linoleic acid is metabolized or arachidonic acid, several studies have found that diets rich in linoleic acid can still significantly raise plasma or arachidonic acid derived.

Bioactive lipids, which is important as the arachidonic acid serves as the parent molecule for all inflammatory. I carcinoids. Even though the conversion between linoleic acid and arachidonic acid, it’s not massive. When you increase a linoleic acid content diet, you still see an increase in these inflammatory mediators.

The next thing is, is there are other components. Called oxidized linoleic acid metabolites and linoleic acid directly increase the production of these, and they’re strongly associated with a variety of pathological conditions. The paper titled here is Lowering Dietary linoleic acid reduces bioactive Oxidized linoleic acid metabolites in humans, and the researchers say oxidized linoleic acid metabolites.

Abbreviated ox lambs are pleiotropic bioactive derivatives of linoleic acid. And so we have a graphic here to show you, so you have linoleic acid. The mega six polyunsaturated fat, that’s what we were seeing with the seed oils I showed you in chronometer. And they can convert linoleic acid to these mediators, or they can actually spontaneously through non enzymatic action get converted into these different mediators that we see here.

So that leads me to the next thing. These polyunsaturated fatty acids are directly involved in a variety of pathologic conditions, including Alzheimer’s and dementia. Cardiovascular disease, fatty liver, et cetera. And so we have a quote here from a paper titled Lowering Dietary Linoleic Acid reduces bioactive Oxidized linoleic acid metabolites in humans.

And they say, as a major component of oxidized low density liberal protein and atherosclerotic plaques. Oxidized linoleic acid metabolites are ported to play a central role in foam cell formation and the pathogenesis of atherosclerosis. These metabolites are involved directly in atherosclerosis, oxidized linoleic acid metabolites also can act as endogenous.

TRP V one receptor channel activators facilitating peripheral and central pain sensitization, so they’re involved in increasing the sensitivity to pain. Then you see here circulating oxidized linoleic acid metabolites, which are elevated in Alzheimer’s dementia, and non-alcoholic acetyl hepatitis, which essentially fatty liver disease have been proposed as a mechanism based biomarker useful for indicating the presence.

And severity of both conditions. They’re talking about gauging whether these conditions are present as well as how severe they are just based on these factors alone. What I want to get to is the strategies. These strategies that I’m about to discuss are strategies that I’ve used myself and also strategies that I’ve used with my clients to help improve cardiovascular risk factors and markers in their labs, as well as the liver function markers.

And then also body composition just by adjusting these different components. So strategy number one to manage the polyunsaturated fatty acids, particularly Omega six fatty acids in the diet, is to keep the total omega six content around 2% of calories or less, which is actually quite difficult to do ’cause it’s present in almost all the foods.

Essentially, that works out to be about four grams of omega six polyunsaturated fatty acids. Per 2000 calories. And this is a target that has been directly mentioned by Dr. AP multiple times. But essentially this will be the target to set. And again, this is the absolute minimum threshold. It is actually lower than 2%, so we wanna just at least try to get 2%.

And it’s not that you can’t try to go lower, it just said it gets really hard. So in order to do this. The best way is to shift the fat sources in your diet to be composed of things like olive oil, avocados, macadamia nuts, cocoa butter, dark chocolate, coconut and coconut oil, beef fat, egg yolks that are pasture raised, and then dairy fats if tolerated.

These are gonna help you get closer to that target. Than if you were to incorporate large amount of seed oils, soybean oil, corn oil, sunflower oil, et cetera in the diet is gonna be extremely difficult to actually keep the omega six polyunsaturated fat at that target to keep the total levels low. So you wanna shift these other fat sources now?

I do. I. Have a free video series and PDF guide that shows you how to construct your diet using these fat sources. It’s called a nutrition blueprint, so I’ll drop a link in the description. You could check that out once you keep your total Omega six polyunsaturated fat intake quite low. The next question that I always get from clients is, what do I do with my omega threes?

Mike, what do you think about omega threes? There’s some problems with omega threes. And we’re gonna talk about them. But what I wanna mention here is there is some research talking about ratios of omega threes in the research. What they tend to find is that ratios even at six to one, down to three to one of omega six to Omega-3, they see benefits and they see associations.

So I want to talk about some of these studies. We have a paper here titled Linoleic Acid in the Regulation of Glucose Homeostasis. Our view of the evidence and what they say is historically the ratio of dietary omega six to Omega-3 pufa. Has been used as an indicator to measure risk associated with development of some chronic metabolic disorders.

A greater omega six content in ratio to Omega-3 has generally corresponded with the stimulation of inflammatory pathways that are prothrombotic and pro aggregatory. While lower omega six to Omega-3 ratio is thought to lead to the dominance of anti-inflammatory resolving protectants and mosin evolutionary studies have estimated that the omega six to Omega-3 ratio of the human diet was historically one-to-one.

But advocacy efforts throughout the 20th century by health agencies to increase Omega six polyunsaturated fat consumption have resulted in an increase in modern western diet of omega six to Omega-3 to an average of 10 to one. It used to be one to one is what they’re saying in this paper, and now it’s around 10 to one.

And what they’re gonna talk about here are some better ratios. So what they say here is several views have proposed reducing the Omega six, Omega-3 ratio. As a primary preventative measure to protect against various cancers, cardiovascular disease, type two diabetes, obesity, as well as other chronic metabolic disorders in general.

The studies referenced by these reviews have provided promising data on a variety of benefits associated with a lower omega six to Omega-3 ratio. But it is clear additional research as needed. For example, studies from India evaluating the effects of diets with a different omega six to Omega-3 ratio on insulin action found that a lower omega six to Omega-3 ratio could reduce.

So that was at a six to one ratio, could reduce the prevalence of type two diabetes. And they say similarly, the Lion Heart study, which compared accretion Mediterranean Diet with a four to one ratio to the step one American Heart Association diet. Found that a lower omega six to Omega-3 ratio diet led to a 70% decrease in total mortality.

So even going 10 to one, to four to one led to a significant decrease in overall mortality. What’s the takeaway from this for me? Well, if we have four grams per 2000 calories and we look at maybe a. Four to one ratio of omega six to Omega-3, you’re looking at maybe around a gram or less of Omega-3 per day.

And ideally that’s, that would be coming from at eating adequate seafood in the diet. So my recommendation isn’t even to try to massively intake Omega-3. It’s just incorporate seafood in the diet. So that’s gonna be cod that’s gonna be sold flounder. Shrimp, scallops, mussels, oysters, clams, and then periodically you could have some tuna.

It’s just higher in mercury. Sardines, you could have salmon, except that high amounts of those are gonna give you very high intakes of omega threes, which can be quite problematic. With that in mind, we have a paper here titled Linoleic Acid. And the regulation of glucose homeostasis. A review of the evidence and the authors say here, studies that have reported the overconsumption of Omega-3 proof was indicate both potential deleterious and beneficial effects, such as increased serum glucose, significantly decreased coagulation and reduced blood pressure taken together.

It is possible. That the consumption of specific dietary poof of species may indeed be governed by the Goldilocks principle whereby moderation of omega six pufa or polyunsaturated fats and Omega-3 polyunsaturated fat intake produce optimal metabolic effects. So it’s not about massively increasing Omega-3.

It’s about lowering total omega six and just having an adequate amount of Omega-3 in the diet, ideally from seafood sources. ’cause again, keep in mind, omega threes are even more susceptible to oxidation than the omega sixes are. The next thing is if you’ve been eating seed oils for a long time and you’re loaded up on polyunsaturated fats, these next two strategies are gonna be quite important for you.

The first thing is there’s a variety of antioxidant compounds. That you can stack together to protect yourself from the lipid peroxidation that occurs with the polyunsaturated fats. So the first one is vitamin E. Vitamin E is one of the major lipid-soluble antioxidants, and it’s been known to actually protect against lipid peroxidation.

And so I have a quote here, it’s lipid oxidation that is and is not inhibited by vitamin E. And they say it has been established that vitamin E acts as an essential perial radical scavenging antioxidant. To inhibit free radical mediated lipid peroxidation. So it basically blocks lipid peroxidation, vitamin e scavenges, lipid per oxil radicals before they attack substrate lipid molecules including fatty acids, phospholipids, asal, glycerols cholesterol and cholesterol esters.

So the vitamin E can protect against the different fat components of our bodies from being damaged by lipid oxidation. And we have a graphic here that shows this. So you have a lipid peril radical. It interacts with vitamin E. You get a lipid hydro peroxide, which basically, uh, nullifies this product here.

It’s still not great, but at the same time, it’s not gonna keep driving the lipid peroxidation. And then the, the vitamin E gets recycled by the vitamin C. This is how vitamin E is protecting against lip bit peroxidation. Now, as we can see, vitamin E doesn’t work alone and works with vitamin C. And so we have a clinical trial here.

This is actually a double-blind, placebo controlled randomized crossover study, and what they see is vitamin C supplementation was found to decrease the urinary concentration of lipid peroxidation metabolites by 20 to 30% in support of the notion that vitamin C supplementation exerts antioxidant effect, uh, effects and reduces oxidative stress in vivo.

And we have a paper here and what they show is you have lipid peroxidation occurring here. Vitamin C is basically preventing that the reactive oxygen species or reactive, the free radical from interacting with the lipid. And then basically also vitamin E is per, is managing the lipid peroxidation. The lipid per oxil itself, the vitamin C is recycling the vitamin E.

So basically vitamin C is working to directly manage the the free radicals. While also recycling vitamin E to protect against the lipid peroxidation here. Next up in conjunction with vitamin E and vitamin C, you have glutathione. And the glutathione is a peptide composed of, as we can see here, glutamic, acid, cysteine, and glycine.

And its job is to help recycle vitamin C, vitamin E, and directly, uh, protect against free radicals and reactive oxygen species stress. And so inside this study titled Glycine and an acetylcysteine supplementation in older adults improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, insulin resistance, endothelial dysfunction, gen toxicity, muscle strength, and cognition.

Results of a pilot clinical trial. The researchers gave the, gave people a hundred milligrams per kilogram of glycine per day, and a hundred milligrams per kilogram of cysteine per day. And they did this for 24 weeks. And basically what they found, and we can see this here, we have the plasma T-bar and plasma F two isop SSTs.

These are lipid peroxidation products. And you can see week zero in this column, week 12 in this column, and week 24 in this column for T-Bar, the older adults start at 22.7 micromoles per liter. By week 12, they’re at 14, and then by week 24 they’re at 5.7. So essentially they’re almost four times less Lipid peroxidation products by week 24 with this supplementation.

For the plasma Isop Senes at week, at the beginning, at baseline, they were 185 picograms per milliliter. By week 12, they were 64, and then by week 24 they were 47.8. So again, significant drop in lipid peroxidation products by week 24 with a hundred milligrams per kilogram per day of glycine, and a hundred milligrams per kilogram per day of n-acetylcysteine.

Again, that’s to create glutathione. So you can combine glutathione, vitamin C and vitamin E together to synergize and protect against little bit peroxidation. Then we also have coq 10, and basically we have a, another, uh, double blind, uh, randomized clinical trial here. So basically what they say in a recent double-blind parallel group, randomized clinical trial daily supplementation with 1200 milligrams of coq 10 was proved safe and resulted in a reduction in plasma concentration of S two F two isop tane, a marker of lipid oxidation in patients undergoing maintenance hemodialysis.

So in patients with kidney failure who are on hemodialysis. Giving coq 10 improved or minimized lipid peroxidation. And the, basically the way this works is coq 10 improves mitochondrial function directly. So we have the mitochondria here. On this left side, what we see as complex one is interacting with coq 10 to pass electrons to complex three.

And here you have complex two using coq 10 to pass electrons to complex three. And so basically this helps to make sure that the mitochondrial electron transport chain is functioning well ’cause it’s one of the major drivers to reactive oxygen species stress. And then down here we can see inside the plasma membrane, the cell membrane.

You can see that coq 10 is protecting against lipid peroxidation by recycling as sorbic acid and also, uh, vitamin E. So basically it, it has a variety of benefits and it synergizes again with vitamin E and vitamin C, and then also with glutathione. The last ones here are plant polyphenol compounds. So you have grape seed extract, you have cocoa polyphenols, and then you also have pomegranate juice.

So for the cocoa polyphenols. It. The studies used about 22 grams of cocoa powder and or 16 grams of dark chocolate or 36 grams of cocoa powder, and they say studies on the effects of coco polyphenols have shown that consumption of cocoa decreases. LDL oxidation, lipid peroxidation biomarkers such as F two isop, SANE among healthy subjects.

Then with pomegranate juice, what we can see is that they say malal aldehyde, which is a marker of lipid oxidation. Was reduced by 24.4%. And protein carons, which are a marker of protein damage from, uh, reactive oxygen species stress were reduced by 19.6% and 17.7% at time two and time three respectively.

Supporting the evidence that pomegranate juice consumption enhances the antioxidant status in humans by decreasing lipid peroxidation and protein oxidation. Moreover, glutathione levels were significantly increased at time two, indicating that pomegranate juice consumption improves the antioxidant mechanisms.

And red blood cells by increasing glutathione levels. So basically the pomegranate juice in. Also the coco polyphenols will synergize with the coq 10, the glutathione, the vitamin C and the vitamin E to protect you from excess lipid peroxidation, reactive oxygen species and grape seed extract can also do that as well.

They say here from a meta-analysis, that grape seed extract supplementation caused significant decrease in malal aldehyde. Again, lipid peroxidation product. Oxidize low density liberal protein, so oxidize LDL and high density C reactive protein, and marginally significant increase in total antioxidant capacity.

So essentially the grape seed extract increased antioxidant capacity, lowered the oxidation of LDL and decreased manal aldehyde, while also lowering the inflammatory mediator or signaling compound high sensitivity C-reactive protein. So we’ve set up the diet at this point, right? Your four grams per 2000 calories per day of omega six polyunsaturated fats.

You’re having some seafood in your diet. So your ratio of omega six to mega three is probably somewhere around six to one or four to one or something like this. You have vitamin E on board. You have vitamin C on board. You take, you have adequate glycine intake, you have adequate uh, cystine intake, coq 10, and you’ve incorporated some dark chocolate, some pomegranate juice, and maybe some grape juice or grape seed extract into your diet.

Well, what’s the next thing to look at with the polyunsaturated fats? It’s the inflammatory mediators. ’cause the lipid oxidation is under control and the amount of these things coming in your diet are low. So you should be decreasing your tissue stores of these fats. So now you need to protect against the excessive amounts of, uh, pro-inflammatory mediators.

And now the way to do this is to block those enzymes that we talked about that create them. So you have oxy oxygenase, and you have cycle oxygenase, the C four cytochrome, P four 50 enzymes. You probably don’t wanna block all those because they have a variety of different beneficial effects outside of creating these components.

But cycle oxygenase and oxy oxygenase are the enzymes to look to block if you’re loaded up on polyunsaturated fats and dealing with high levels of inflammation. And there’s two components that can block these enzymes. So NSAIDs, as we see here, but a lot of NSAIDs are problematic. So the major one that has the cardioprotective effects and whatnot is going to be aspirin.

Again, I’m not recommending anybody take aspirin. All I’m saying is that aspirin theoretically is able to actually block. The cycl oxygenase enzyme, which can minimize the production of these inflammatory mediators, prostaglandins, and the thromboxanes. And then the other product is boswellia blocks, not cycl oxygenase, but lipoxygenase to decrease the production of leukotrienes.

So essentially, these components can help to minimize the production of the inflammatory mediators. And so we have a study here, it’s titled Pro-Inflammatory and Pro Resolving Lipid Mediators of Inflammation and HIV Effects of Aspirin, UH, intervention. And they say studies investigating the mechanism of aspirin in general population, whereas used to reduce cardiovascular risks, demonstrate that via the acetylation of cycle oxygenase.

So that’s that inflammatory enzyme we talked about. This potent anti-inflammatory drug not only reduces the production of classic I carcinoids. Namely prostaglandin and thromboxane. It also upregulates the formation of Epi Meric forms of several specialized pro resolving mediators. IE aspirin triggered specialized pro resolving mediators.

So aspirin triggers these, these pro resolving mediators that help to actually resolve inflammation effectively. They say aspirin triggered specialized proso mediators are linked with the regulation of both immune and vascular response to limit the onset and progression of cardiovascular disease and a range of experimental settings including sickle cell disease, atherosclerosis and neointimal hyperplasia.

So essentially what you’re seeing is aspirin blocks the production of pro-inflammatory mediators and shifts towards the production of pro resolving anti-inflammatory mediators. Which again, is helping to shift the balance on those problematic, uh, polyunsaturated fats. And in the subsequent ICOs, andoid inflammatory meteors that are produced.

Next up we have Boswellia. So basically there’s a component in Boswellia. It’s called three oh acetyl, 11 Keto beta boswellic acid. It’s abbreviated as a kba. It is the most active component of boswellia extract and has demonstrated to be a potent inhibitor of five oxy oxygenase. So locks the enzyme that I showed you in the graphic, which is a key enzyme in the biosynthesis of L leukotrienes from arachidonic acid in the cellular inflammatory cascade.

So basically Boswellia can block the oxy oxygenase while block aspirin can block the Cycl cycle oxygenase and shift towards the production of those, those pro resolving anti-inflammatory mediators. So these are components that may potentially protect against some of the, the inflammatory mediators produced.

From the polyunsaturated fats. So with this combination of components, you should be able to to manage the negative effects of the polyunsaturated fats while your body is lowering the amounts that are in your stored tissues because you’ve adjusted your diet. Now with that, if you would like to see how to actually change your diet, or how I’ve changed my diet to keep my polyunsaturated fatty acids very low, I’d recommend you check out these two videos and the cards below.