PUFAs Role On Skin

T

tobieagle

Guest
You'll find parrots, which have extremely high metabolic rates and long longevity, fare better off (live longer) by eating MORE seeds and grains, aka: more PUFA, but also more Vitamins found in the seeds. The net effect is actually less PUFA on mitochondrial membranes; these animals can use the compounds in seeds and grains specifically to exclude PUFAs from their mitochondria membranes, despite a high PUFA diet.

I doubt you will find high concentrations of PUFA in seeds of tropical plants. Their fat composition is highly dependant on the ambient temperature.
 

tyw

Member
Joined
Nov 19, 2015
Messages
407
Location
Cairns, Australia
I doubt you will find high concentrations of PUFA in seeds of tropical plants. Their fat composition is highly dependant on the ambient temperature.

??? o_O tropical plants can still have lots of PUFA -- peanuts, brazil nuts, cashews, pumpkin (seeds), mongongo, candlenut, etc .... all require high temperatures (ie: "tropical") to grow, are commonly found in the tropics.

Then of course, there's the actual study to which the positive longevity effects of grains and seeds on parrot lifespan -- DIET INFLUENCES LIFE SPAN IN PARROTS (PSITTACIFORMES)

....
 

bistecca

Member
Joined
Feb 6, 2016
Messages
191
Location
maryland, USA
@James IV and @schultz

I personally do not find it that useful to compare differences in metabolic between species, for the reasons that I've discussed here -- Some Thoughts On Avocadoes

You'll find parrots, which have extremely high metabolic rates and long longevity, fare better off (live longer) by eating MORE seeds and grains, aka: more PUFA, but also more Vitamins found in the seeds. The net effect is actually less PUFA on mitochondrial membranes; these animals can use the compounds in seeds and grains specifically to exclude PUFAs from their mitochondria membranes, despite a high PUFA diet.

Ref: 'Metabolic rate and membrane fatty acid composition in birds: a comparison between long-living parrots and short-living fowl', (Montgomery et. al, 2011)

And then you'll find rats who deplete their PUFA get much larger mitochondria, with more cristae, and higher rates of substrate flux:

- Effect of polyunsaturated fatty acids deficiency on oxidative phosphorylation in rat liver mitochondria
- MITOCHONDRIAL CHANGES IN THE LIVER OF ESSENTIAL FATTY ACID-DEFICIENT MICE


The differences worth comparing are from dietary manipulation within the same type of organism, and watching for effects. So far, the only effect that seems to universally increase metabolic rate in the same organism, is reduction of overall mitochondrial membrane PUFA levels.

----

Also, let's not ignore the higher level effects, like Thyroid hormones and Gluthathione, all of which are boosted by carbohydrates.

Also, let's not make the mistake of saying that just because some carbs are needed for a well-functioning thyroid, that more is better ;)

....


Hi TYW.. You're posts always intrigue me.. I know this is a late response... It occurred to me as i was reading this, aren't parrots tropical? Aren't nuts and seeds in the tropics likely to have lower proportions of PUFA? And probably very high levels of vitamin E? I can think of so many tropical fruits with that amber hue.
 

tyw

Member
Joined
Nov 19, 2015
Messages
407
Location
Cairns, Australia
Hi TYW.. You're posts always intrigue me.. I know this is a late response... It occurred to me as i was reading this, aren't parrots tropical? Aren't nuts and seeds in the tropics likely to have lower proportions of PUFA? And probably very high levels of vitamin E? I can think of so many tropical fruits with that amber hue.

Firstly:
- all grains are going to have some PUFA
- all seeds are going to have some PUFA, even in the tropics
- the only nuts that are low PUFA are macadamias, and those still are MUFA dominated (ie: not saturated)

- And most importantly, the more granivorous a parrot was, the better their longevity.

ie: we are comparing a relative increase in unsaturated fat consumption, and finding a positive outcome.

Then, when we make a comparison to humans and other animals:

- whether or not a grain or seed has high quantities of vitamin E (or any compound that could "defend against PUFA accumulate")

- it is observed that excess PUFA consumption trumps any other factor in how much PUFA accumulates on the mitochondrial membranes in these other animals (including humans). Whereas in these long-lived birds, there is no such thing as excess PUFA consumption (endogenous regulatory pathways prevent accumulation no matter how much PUFA they eat)

.....
 

Ideonaut

Member
Joined
Sep 20, 2015
Messages
499
Location
Seattle
Factors for amount and morphology of mitochondrial growth are unknown.
In his article "Protect the Mitochondria" Peat says," Environmental enrichment, learning, high altitude, and thyroid hormone promote the formation of new mitochondria . . . ".
 

tyw

Member
Joined
Nov 19, 2015
Messages
407
Location
Cairns, Australia
In his article "Protect the Mitochondria" Peat says," Environmental enrichment, learning, high altitude, and thyroid hormone promote the formation of new mitochondria . . . ".

Increase in Mitochondrial number may happen via Biogenesis or Fission. This is also just one of many factors that account for mitochondrial activity. Some factors regarding increase in mitochondrial number are known, but many are not.

Next, increase in mitochondrial number is not always a good thing. Regarding mitochondrial fission, I quote from Dave Valentine's book, 'Human Longevity', from chapters 17 and 18:

There is increasing evidence discussed below that cells, especially neurons, must constantly adjust the ratio of fission to fusion during aging.

Mitochondria present in, say, a neuron can be divided into three classes, as follows:
  1. Normal mitochondria fulfilling their role as ATP machines
  2. Mitochondria destined to be or being rejuvenated by fission
  3. Unhealthy, unwanted, or toxic mitochondria marked for mitophagy, as discussed in Chapter 18
Toxic mitochondria are defined in more detail in Chapter 18. But a key point made here is that the highly beneficial role for polyunsaturated membranes seen in normal mitochondria might be switched in mini-mitochondria into a harmful or toxic state.

There is increasing evidence that the balance between fission and fusion can be tipped during neurodegeneration when toxic proteins/peptides, such as in the case of mutant huntington (mHtt), bind to fission machinery (Johri et al., 2011).

....

During energy stress, when ATP levels drop, AMPK is activated and phosphorylates ULK1 and ULK2 (both Atg1 homologs) in turn activate mitophagy and general autophagy.

A decrease in mitochondrial membrane potential (ψm) can be induced by ROS and by targeting a-synuclein to the mitochondria. A depression in mitochondrial membrane potential serves as a signal for mitophagy.

Mitophagy occurs, with the first benefit is the availability of nitrogen from recycled mitochondrial proteins needed for protein synthesis, and the second benefit is a drop in levels of ROS, which might otherwise kill the cell.​

Regarding Mitochondrial biogenesis, it is clear that it is indiscriminately increased in the face of excessive stress, when more energy is needed:

- Diabetes regulates mitochondrial biogenesis and fission in neurons
- Mitochondrial biogenesis in the metabolic syndrome and cardiovascular disease
- Transcriptional control of mitochondrial biogenesis: the central role of PGC-1α | Cardiovascular Research | Oxford Academic
- The Interaction of Mitochondrial Biogenesis and Fission/Fusion Mediated by PGC-1α Regulates Rotenone-Induced Dopaminergic Neurotoxicity. - PubMed - NCBI

Context is key -- "What are we upregulating mitochondrial count for?" is a question that each cell asks itself. It has to ask this because maintenance of existing mitochondria is not a cheap task, and if the balance is wrong, the cell will kill itself ..... This becomes hugely complicated, and requires the cell to match mitochondrial function and number to perceived demands. Depending on the tissue, that demand may fluctuate a lot.

It is never a case of "more mitochondria is better".


This is made only more complicated by Morphological changes. An example: Douglas Wallace was co-author to this paper on "Trans-mitochondrial junctions" -- Trans-mitochondrial coordination of cristae at regulated membrane junctions : Nature Communications

As an aside, if the reader of this post is unfamiliar with Douglas Wallace, his talks about mitochondrial function and disease are very good.​

This is a specific type of alignment behaviour exhibited by certain mitochondrial, and the authors show just how significant a change in membrane potential this alignment has ..... It is literally mitochondrial Tug-of-War, with aligned mitochondrial cristae working together to allow for energetic flow.

What allows for this to happen? What degrades this function? Does degradation permit disease? (which is likely, given just how big an energetic boost is created) .... All questions to which we have no clue how to answer.


Also, how do we measure mitochondrial capacity? 10 mitochondria working at 2x speed are as good as 20 mitochondria working at 1x speed. ECT flow rates are determined by everything from mitochondrial cristae folding patterns, to membrane unsaturation, to substrate delivery rates into mitochondria, to relative oxygenation at Cyt-c oxidase, etc ...., ALL of which are governed by Nuclear DNA (ie: tissue-level differences), by mtDNA, by mtDNA-to-nuclear-DNA interactions, to what you just decided to put into your mouth an hour ago .....



Hugely complicated business .... I stand by my statement: Factors for amount and morphology of mitochondrial growth are unknown.

Unfortunately, focusing on these sorts of mitochondrial mechanics doesn't lead to useful conclusions. I personally rather focus on more actionable mechanics that I've been discussing in this other thread -- How The Sugar Industry Shifted Blame To Fat

.....
 

LeeLemonoil

Member
Joined
Sep 24, 2016
Messages
4,265
Unsaturated fatty acids induce calcium influx into keratinocytes and cause abnormal differentiation of epidermis. - PubMed - NCBI

Unsaturated fatty acids induce calcium influx into keratinocytes and cause abnormal differentiation of epidermis.

Katsuta Y, et al. J Invest Dermatol. 2005.

Abstract
Abnormal follicular keratinization is involved in comedogenesis in acne vulgaris. We recently demonstrated that calcium influx into epidermal keratinocytes is associated with impaired skin barrier function and epidermal proliferation. Based on these results, we hypothesized that sebum components affect calcium dynamics in the keratinocyte and consequently induce abnormal keratinization. To test this idea, we first observed the effects of topical application of sebum components, triglycerides (triolein), saturated fatty acids (palmitic acid and stearic acid), and unsaturated fatty acids (oleic acid and palmitoleic acid) on hairless mouse skin. Neither triglyceride nor saturated fatty acids affected the skin surface morphology or epidermal proliferation. On the other hand, application of unsaturated fatty acids, oleic acid, and palmitoleic acid induced scaly skin, abnormal keratinization, and epidermal hyperplasia. Application of triglycerides and saturated fatty acids on cultured human keratinocytes did not affect the intracellular calcium concentration ([Ca(2+)](i)), whereas unsaturated fatty acids increased the [Ca(2+)](i) of the keratinocytes. Moreover, application of oleic acid on hairless mouse skin induced an abnormal calcium distribution in the epidermis. These results suggest that unsaturated fatty acids in sebum alter the calcium dynamics in epidermal keratinocytes and induce abnormal follicular keratinization.
 

LeeLemonoil

Member
Joined
Sep 24, 2016
Messages
4,265
Skin Aging and Photoaging Alter Fatty Acids Composition, Including 11,14,17-eicosatrienoic Acid, in the Epidermis of Human Skin


Study states that an Omega-3 acid is photoprotective and anti-age.
Also: Saturated fats decrease in aging skin while, as does PUFA linoleic acid (the latter to a smaller degree)

Curiously, both MUFAs Oleic acid and Palmitoleic acid increase substantially in aging skin, in line with the findings of the previous post that these FAs are highly excitatory in the skin.
A metabolite of Palmitoleic acid, 2-decanol is supposedly also the scent-molecule most associated with the odour of "old people"


So highly praised skin oils high in both MUFAs like Olive, Macadamia and Avocado might not be such a good choice after all?
 

Similar threads

Back
Top Bottom