Membrane Unsaturation & Aging

Membrane Unsaturation & Aging

Unsaturation of Your Membranes Affect Aging

What is yet another cause of aging?? It has to do with the structure of your cell membranes (unsaturation is worse).

This is Part 2 of the triology of the topic on aging. Understanding is the first step in figuring out how to mitigate it.

Fat in Food

Let’s start off with some basic principles here.

You probably know that the fat you eat breaks down and changes when it goes into your body. It metabolizes, moves around, and ends up going somewhere.


As a matter of fact, the fat you eat is correlated with the fat that ends up in your mitochondrial membranes. It doesn’t just go straight there, but it does end up there after some processing.

Saturated fat turns into saturated fat (or a lesser degree of unsaturation) for the membranes. Likewise, unsaturated fat ends up as more unsaturated fat. [1 , 2 , 3 , 4]

However, the unsaturated fats come in various degrees and come from various kinds of unsaturated fats.

The types of fats in your membrane are categorized by their “degree of unsaturation.”

Essentially, that is fancy talk for how many double bonds the lipids have:

Saturation vs Unsaturation

==> Saturated means no double bonds.

==> Unsaturated means double bonds.

But how do we keep track of the unsaturated fats? They can have multiple double bonds, right?

Scientists keep track of them by designating a degree of unsaturation.

When we look at double bonds on the larger scale of a cell, we call it the “double bond index” (DBI). A higher DBI means there are more double bonds in the membrane.

If you are interested in more info on dietary fats and what they do to your membranes, check out our blog post on lipids and mitochondrial membranes.

In this week’s research, we didn’t look at how your membranes have different levels of unsaturation.

Rather, we look at what the implications are with different levels of unsaturation.

Summary of Part 2

  1. Lower DBI = more longevity
  2. Higher DBI = more peroxidation
  3. More peroxidation = breaking down of membranes
  4. Breaking down of membranes = harmful products

[Remember, this is a review article, so there won’t be an emphasis on presentation of data here. Mainly, it is just commentary by the researchers who looked at all the data from numerous studies.]

They’ve done an excellent job by including a wide variety of studies and animals for this section of the article. We give a summary of their findings below.


The piece of research is the same, and in case you want to see it again, the link is below!

==> The Cell Aging Regulation System (CARS) – conducted by Gustavo Barja at the University of Madrid.[5]

[This Week’s Research File]

This blog post is a continuation from the last one. Review it here.

Tortoise -- Long Living Animal

Pretty much, we said that longer living animals have less ROS production.

The ROS cause a lot of problems that lead to cell aging. The cell aging and dying leads to your aging and ultimate death.

Doesn’t that just lighten up the mood? The point is that your body is breaking down, and we want to figure out why.

For this next part of the research, we will focus on the implications of the types of fat your membranes are composed of.

The Double Bond Index

The researchers set out to look at the factors contributing to why some animals living longer than others.

One of the points of significance was the amount of double bonds in the membranes of long-lived animals.

They found some interesting points here.

Having more saturated fat than unsaturated fat did not correlate to any significant increase in the longevity.

Rather, it was the severity of the unsaturated fat alone.

Having unsaturated fat with more doubles bonds was the unifying finding.

To rephrase: having more unsaturated fat in your membranes doesn’t mean shorter lives unless those unsaturated fats happened to be really polyunsaturated.

Unsaturation in Your Membranes

Specifically, fats with 1, 2, or 3 double bonds correlated with longer lives versus having 4, 5, or 6 double bonds.

==> Having unsaturated lipids with 1, 2, or 3 double bonds is okay.

==> Having unsaturated lipids with 4, 5, or 6 double bonds is bad.

This is reiterate the fact that more unsaturated fats than saturated fats isn’t necessarily worse. It is the degree to which those fats are unsaturated that matters.

Below is an excerpt of the article that summarizes this point:

“Interestingly, the final result is that the total percentage of of unsaturated and saturated fatty acids does not change among species with different longevities. It is the unsaturation degree of the polyunsaturated fatty acids present that decreases from short- to long-lived animals.” [5]

Why is Unsaturation a Problem?

That is a great question…

It’s one thing to know a correlation. It is a whole other thing to understand the mechanism behind it.

Is it a causal relationship, or is it a simple coincidence?

The researchers discovered and theorized it is not a coincidence.

And looking at it in closer detail, this makes sense. At least, it makes sense enough to continue looking into it.

ROS Products Don’t Just Mess with Your DNA

First of all, double bonds are very reactive.

They are more susceptible to changes than single bonds. Other reactive species come by and react with them.

And what might those reactive species be??

Why yes, it is the ROS mentioned in the last blog post!

Reactive Oxygen Species

The same ROS that are causing DNA damage are also causing the breakdown of your membranes.

It’s a double whammy:

==> Your membranes are breaking down and losing structural integrity.

==> They break down into other harmful products. They don’t just go away.

The harmful and mutagenic products are called “lipid peroxidation products.”

They include nasty things like hydroxynonenal and malondialdehyde. [5 , 6 , 7]

So, you are not just harming your membranes with ROS. You are also creating more bad compounds in your cells.

Seems to be a bit of a problem. Let’s take a look.

Peroxidation Products Harm DNA and Proteins

We are getting a bit technical with the chemistry here, so we hope to make it easy.

Oxidation of double bonds causes carbonyl groups to form.

Peroxidation Products Affect DNA

These groups have a very specific kind of chemistry. The oxygen groups happen to “line up” well with amino acids (in proteins) and nucleic acids (in DNA).

They react with the proteins and DNA to cause more damage and mutation. [6 , 7]

The main point is: lipid peroxidation products are bad.

They are also involved in the mechanisms of aging.

Next Hypotheses

More information on these correlations is needed.

But it is fair to say that the degree of unsaturation is causal of shorter lives.

It is not just a correlation – more double bonds actually cause the aging.

That’s our hypothesis. It makes sense, and this article confirms our thinking.

Summary of the article:

  1. Lower DBI = more longevity
  2. Higher DBI = more peroxidation
  3. More peroxidation = breaking down of membranes
  4. Breaking down of membranes = harmful products

Next week, we will look at the last topic of this trilogy. It is Part 3 of the aging mechanisms.

We will go over the topic of dietary (and protein) restriction and it’s role in aging…

To health, love, and happiness!.


[1] Geiser, F. 1990. Influence of polyunsaturated and saturated dietary lipids on adipose tissue, brain and mitochondrial membrane fatty acid composition of a mammalian hibernatorBiochimica et Biophysica Acta (BBA) – Lipids and Lipid Metabolism 1046:159–166.

[2] Mcmurchie, E. J., Gibson, R. A., Charnock, J. S. & Mcintosh, G. H. 1986. Mitochondrial membrane fatty acid composition in the marmoset monkey following dietary lipid supplementationLipids. 21(5):315–323.

[3] Guderley, H., Kraffe, E., Bureau, W. & Bureau, D. P. 2008. Dietary fatty acid composition changes mitochondrial phospholipids and oxidative capacities in rainbow trout red muscleJournal of Comparative Physiology B 178(3):385–399.

[4] Schenkel, L., Bakovic, M. 2014. Formation and Regulation of Mitochondrial Membranes. International Journal of Cell Biology 2014:1-13.

[5] Barja, G., et. al. 2017. The Cell Aging Regulation System (CARS)Reactive Oxygen Species 3(9):148–183.

[6] Romero, F. J., et. al. 1998. Lipid peroxidation products and antioxidants in human disease. Environmental Health Prospect 106(Suppl 5): 1229–1234.

[7] Ramana, K., Srivastava, S., Singhal, S. 2017. Lipid Peroxidation Products in Human Health and Disease. Oxidative Medicine and Cellular Longevity 2017: 2163285.

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