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If you’re taking Fish Oil… Your Arteries are Quickly Changing.

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If you’re taking Fish Oil… Your Arteries are Quickly Changing.

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284 segments

0:00

What if fish oil were changing your

0:02

arteries? Well, it's not even a question

0:05

because there are multiple studies

0:06

indicating that to be the case.

0:08

Technically, it's not limited to fish

0:10

oil, but to really any omega-3 fat

0:13

supplement or just omega-3s as a whole.

0:15

While we've gone over the ways that

0:17

omega-3 fats affect our heart, we've

0:20

never gone into how they affect our

0:22

arteries. Specifically, the plaque in

0:24

your arteries change when you consume

0:27

omega-3s. According to an array of

0:29

studies, we know that atherosclerosis,

0:32

so the plaque that develops in your

0:33

arteries, are a major cause of heart

0:36

attack, stroke, and much more directly

0:38

and indirectly. But the issue is far

0:42

more complex because the quality or type

0:44

of plaque makes a massive difference on

0:47

your risk. For example, soft plaque,

0:49

also known as non-calcified plaque, is

0:51

especially dangerous because it's

0:53

susceptible to rupturing and lodging in

0:55

finer blood vessels. stopping blood flow

0:58

to downstream areas, killing those

1:00

areas. On the other hand, calcified or

1:02

even fibrodic plaque is less dangerous

1:05

because it's considered stable or

1:07

semi-stable, meaning it generally has a

1:09

cap on the top of the soft plaque that

1:12

protects from erupting into the

1:14

bloodstream. To be clear, it's still not

1:17

ideal, but between the two, it's

1:19

preferred. So, what happens to this

1:22

plaque when we consume omega-3s, fish

1:24

oil, or otherwise? In this study, the

1:27

researchers are using non-invasive

1:29

imaging called CT angography to measure

1:33

the plaque within the arteries of two

1:35

groups of people. One group consuming

1:36

omega-3s, and the other was not

1:39

supplementing the control group. As seen

1:41

by these data, the left is the control

1:43

group, so the non-supplementers, and the

1:45

right are the omega-3 group. This

1:47

measurement is of houndsfield units,

1:50

meaning the higher it goes, the more

1:53

fibrous and possibly calcified the

1:55

plaque is. Generally, values reaching

1:57

100 and above indicate more fibrous

2:00

plaque, and values into the higher

2:02

hundreds and even thousands indicate

2:04

calcified plaque. So, knowing what we

2:06

know about plaque, we can clearly see

2:08

that the omega-3 condition is reaching

2:10

into those higher thresholds, indicating

2:12

more solid fibroic plaque. Similarly, if

2:16

we look at another metric Gcore, which

2:18

tells us on a scale the type of plaque

2:21

burden, it looks like this. Notice the

2:23

blood vessel. Then notice the four cate

2:26

categorization. So, one is calcified

2:28

plaque. Uh, good in this context. Two is

2:32

mostly calcified plaque, three is mostly

2:34

non-calcified plaque, and four is

2:36

largely non-calcified plaque, the soft

2:39

plaque that we've been trying to avoid.

2:41

If uh you're looking for a deeper

2:43

explanation on what uh to look for here,

2:45

you've got the wrong guy. I too have no

2:48

idea what we're looking at here, aside

2:49

from what I just outlined. But if we

2:52

focus in on the data, we see a

2:54

statistically significant effect

2:56

indicated by a p value below 0.05 for

2:59

the omega-3 group. Those individuals

3:01

have lower Gcore around 4.5 while those

3:05

not supplementing have a 7.4 four well

3:09

into that soft plaque categorization and

3:11

likely widespread. Now to be clear, both

3:14

of these indicate increased

3:15

cardiovascular risk, but relative to one

3:18

another, the omega-3 group is doing

3:20

better. In short, omega-3s are changing

3:22

the composition of the plaque that we

3:24

have in our arteries. I think this

3:26

finding is absolutely fascinating, but

3:28

it leaves me wondering exactly how it

3:31

does that, as well as if we can even

3:33

trust these results. Why can't we trust

3:36

these results? Well, I'm not going to

3:38

jump to the conclusion that we can't,

3:40

but this type of study has flaws because

3:42

it's a cohort study, meaning we're

3:45

discussing associations here. The

3:47

researchers did match participants

3:49

across groups for a number of important

3:51

factors here. Even so, this is a small

3:54

study, and the participants still didn't

3:56

get the omega-3s as an intervention. So,

4:00

an actual capsule given by the

4:01

researchers. So, there's a high chance

4:03

for misleading interpretations. As a

4:06

result, we can only say that there's an

4:08

association between omega-3 consumption

4:10

and favorable arterial plaque changes.

4:13

But we don't need to stop there because

4:16

there have been randomized control

4:17

trials performed like this one, and they

4:20

reveal two fascinating findings.

4:22

Remember, the title of the video says

4:25

quickly, which is odd when we're

4:27

discussing something like heart disease,

4:29

which takes years, if not decades, to

4:32

develop. However, this randomized

4:34

control trial only lasted an average of

4:37

5 weeks, and yet it provides some cool

4:40

data. So, this type of data is

4:42

interventional, meaning that it brings

4:44

us with much more certainty to actually

4:47

implicating omega-3s in changing our

4:49

arterial plaque. People were randomly

4:52

assigned to the omega-3 group or the

4:54

control group given a placebo or a third

4:57

condition given sunflower oil. Then they

4:59

measured the plaque in the arteries and

5:02

they didn't just classify the plaques

5:04

based on the calcification and so on

5:06

like in the last study. They looked at

5:08

the composition of that plaque. Remember

5:10

arterial plaque is filled with

5:12

cholesterol molecules, fat molecules,

5:14

and even proteins. But it's also filled

5:16

with something else that makes it more

5:19

or less dangerous. We'll come back to

5:21

that in just a minute. For now, I'm

5:24

going to scare you with the data. Yeah,

5:27

it's a lot. And instead of straining

5:30

your eyes and boring you, I'll just

5:31

point out this one line across the

5:34

board. This is an omega-3 fat. And these

5:37

data tell us that this omega-3 is

5:41

enriched in the arterial plaque when

5:43

people consume more omega-3s. That part

5:46

is pretty self-explanatory. The more you

5:48

eat, the more you could have

5:49

incorporated into the plaque. But what

5:52

is it doing there? Well, my friend,

5:55

that's where we get to look at another

5:57

table. But before you groan and say, "I

6:00

didn't sign up to this to look at

6:02

numbers, you nerd." I'll promise to make

6:04

this extremely simple by bringing in

6:06

some images to explain the happenings.

6:09

Here's the table. And here we're looking

6:12

at the three conditions up top. I just

6:15

realized I didn't explain that in the

6:16

last table. Sorry about that. But we

6:19

have three different comparisons.

6:21

difference between sunflower oil and

6:24

control, which we don't care about in

6:26

this story. Then fish oil versus

6:28

control, we care. And fish oil versus

6:31

sunflower oil, we kind of care about

6:33

that, too. Then there's two groups of

6:36

cells found inside the plaque. That's

6:38

right, cells inside the plaque of your

6:40

arteries. They're macrofasages and TE-C

6:43

cells. Both of these cells come from

6:45

different families. One is part of your

6:48

normal defense system called the innate

6:50

immune system and the other the tea

6:52

cells come from a more specialized

6:54

immune system called the adaptive. The

6:56

big point being that they are different

6:58

immune cells. Then we have three

7:00

categories of staining. So 0 1 and two.

7:03

And the zero score stands for no

7:05

staining detected. Therefore no immune

7:07

cells present. The one indicates

7:09

moderate staining. So some immune cells

7:12

are there. And the two is the heavy

7:14

staining indicating the greatest number

7:16

of immune cells. By the way, by staining

7:19

I mean this we're using fluorescent

7:21

proteins that attach to these immune

7:23

cells specifically allowing us to

7:25

identify them. Okay, that explained. If

7:28

the number goes down like here, that

7:30

means there's less staining. And if they

7:33

go up over 1.0, that typically indicates

7:36

more of that staining group. This is all

7:39

then confirmed by the statistics the p

7:41

values which should be below 0.05 to

7:44

indicate an identified effect. So in

7:46

short there are no differences for tea

7:49

cells across any of the groups and there

7:51

are reductions in the group two staining

7:54

for the macrofasages in both omega-3

7:57

comparisons. In addition, there's more

7:59

of group one staining for the same

8:02

groups. That suggests to me that the

8:04

number of macrofasages in the plaque is

8:06

reducing although not completely

8:09

disappearing. That all matters because

8:11

macrofasages are abundant in the plaque

8:13

and they accentuate the inflammatory

8:15

response inside the plaque exacerbating

8:18

the problems coming from plaque. More

8:20

specifically, they're usually involved

8:22

in unstable forms of plaque and increase

8:25

the risk of rupture. This could be a

8:27

mechanism by which omega-3s help the

8:29

plaque stability by removing these cells

8:31

that destabilize the plaque. How

8:34

freaking cool is that? In fact, we see

8:36

that further evidenced in other data

8:38

that I won't plague you with, but it

8:39

shows that more unstable plaques have

8:42

fewer macrofasages in them, which also

8:45

associates with omega-3 levels in the

8:47

plaque. There's more that we need to get

8:49

into, including what this means for you

8:52

and how to contextualize this because

8:54

there's some nuances to be aware of, but

8:57

this is actually a pretty bare bones

8:58

analysis considering there's more data

9:01

on everything that we just went over, as

9:03

well as a brand new study on omega-3's

9:05

ability to reverse plaque in our

9:07

arteries and the differences between

9:09

omega-3 types. I'm covering all of that

9:12

in the full analysis included with the

9:14

Physionic Insiders, which also includes

9:17

access to all my analyses in article and

9:19

video format, a private podcast, a

9:22

private community that I'm highly

9:23

engaged in, and even live sessions with

9:26

me and the rest of the insider

9:27

community. And there's more, but I've

9:30

been talking about this for too long.

9:31

So, if you're interested, check out the

9:33

description and join the Physionic

9:35

Insiders. I hope to see you there. Now,

9:37

to context. We've covered two studies

9:39

and this third corroborates a lot of

9:41

what we just went over and we did

9:44

include a randomized control trial which

9:46

is important and impressive considering

9:48

the results. However, even so, it should

9:51

be noted that we could really use some

9:53

longerterm studies and just more

9:56

evidence as a whole. But that context

9:59

applied, we also have multiple

10:01

intervention studies that indicate

10:03

omega-3s are generally beneficial for

10:05

heart health by reducing heart disease

10:08

related events. So although that doesn't

10:10

speak to these specific artery effects,

10:13

it speaks to the overall trend of

10:15

omega-3 fats improving cardiovascular

10:17

health. So where does that leave us?

10:20

Well, one quick thing that I need to get

10:22

off my chest. Why don't fish do well in

10:26

school?

10:28

Because they work below sea level.

10:33

This has been entirely too serious of a

10:36

video, so I had to throw one in there.

10:38

Okay, on to the takeaways. I think

10:40

overall consuming omega-3 fats have weak

10:42

to moderate evidence indicating one of

10:44

the ways that they improve our

10:45

cardiovascular health is by remodeling

10:47

the plaque in our arteries to be less

10:49

inflamed and to be more stable. This

10:52

paired with outcome data offers evidence

10:55

that we should be consuming omega-3s. If

10:57

that's through algae, fish, krill oil,

11:00

or by eating fatty fish. See, the joke

11:03

was related. You know what else is

11:07

related? This Omega-3 video right here.

11:10

Thanks for hanging out with me and I'll

11:12

see you over there.

Interactive Summary

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The video discusses how omega-3 fatty acids, commonly found in fish oil, may positively affect arterial plaque. It explains the difference between soft, dangerous plaque and stable, calcified plaque. Studies suggest that omega-3 consumption can lead to a shift towards more stable plaque composition, indicated by changes in Hounsfield units and G-scores. While initial studies are observational, randomized controlled trials show that omega-3s are incorporated into plaque and may reduce the number of inflammatory cells (macrophages) within the plaque, which are associated with unstable plaque. This suggests a potential mechanism for omega-3s in stabilizing arterial plaque and improving cardiovascular health. However, the video also notes the need for longer-term studies to confirm these findings and provides context by mentioning broader evidence of omega-3s benefiting heart health.

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