Beyond thyroid: Iodine and PUFA interaction, greater protection than vitamin E?

TexugoDoMel

tl;dr - Iodinating (or halogenating) the double bounds of unsaturated fatty acids makes them behave more like saturated fats than unsaturated fats.

My goal is a slightly prolific introduction for those who are interested, since I feel that this side ends up losing a bit of potential by limiting iodine only to the thyroid (or more timidly to iodocasein). The great affinity of molecular iodine (I2) for the double bounds of PUFAs should cause some curiosity, since the affinity is such that unsaturation is usually determined by the iodine value. The idea that the complexity of today's organisms originated in the ocean, where the more unsaturated PUFAs such as EPA, DHA and ARA predominate, in my opinion only reinforces that this affinity is not random.

My interest in this subject began when I read Travis from the old forum mentioning that iodinated PUFAs behaved more like saturated fatty acids; an iodinated PUFA couldn't even be used to produce eicosanoids.

Since the double bond is obliterated by added iodine atoms, the lipids' geometry shifts from sp²- to the sp³-hybridization and straightens. Iodinated lipids are more like saturated lipids than unsaturated ones, and can be viewed as being 'saturated by iodine' and not hydrogen—or partially-saturated by both.

The in vitro inhibition of breast cancer cells by iodine (I₂)—yet not iodide (I⁻)—has been explained by the reduction of prostaglandin E₂ synthesis consequent of membrane arachidonic acid iodination. I'd bet that I could find that study again if you'd like to read it.

'Prostaglandins are produced from AA [arachidonic acid] by the enzyme cyclooxygenase, indicating the presence of high levels of AA in breast tumors. It is possible that these high levels of AA, and the iodolipids formed from them, may explain the specific effect of I₂ in tumoral cells. This hypothesis is being explored in our laboratory.' ―Arroyo-Helguera

I didn't find much about iodinated PUFAs (apart from AA with 6-iodolactone), but considering that iodine is a halogen then Chlorine, Fluorine, Bromine, etc. would have similar binding capacities, and it really is much easier to find content about them.

So back to the topic, does a PUFA that has its double bounds iodinated/halogenated really start to behave more like a saturated fatty acid? Apparently so! If we use Linoleic Acid, with its 2 double bounds and melting point at -5°C, and saturate the double bounds with bromine, Linoleic Acid is now called tetrabromostearic acid, with a melting point of 115°C, and if we do this with Oleic Acid and its single double bound, we would get dibromostearic acid(9-10 dibromostearic acid).

The name is “converted” according to the number of carbons and the halogen present, so 18C UFAs would be known as somethingstearic, while if it were 16C it would be somethingpalmitic (such as dibromopalmitic). If we used iodine, as in the bromine examples, linoleic would become tetraiodostearic and oleic would become diiodostearic.

The theory is interesting, but what about in practice? Luckily for me, there's a study in which they compared a fat-free diet and a fat-free diet with the addition of tetrabromostearic acid (brominated linoleic acid) in terms of their ability to generate the classic symptoms of essential fatty acid deficiency(scaly paws, scaly or necrotic tails, and decreased growth). What were the results?

Skin symptoms appeared somewhat earlier but were not more severe in the adults receiving the 3 per cent tetrabromostearic acid than in the animals receiving only the basal(fat-free) diet
At the time of sacrifice, all rats receiving the basal diet(fat-free) or the diet containing 3 per cent tetrabromostearic acid exhibited the signs of essential fatty acid deficiency: scaly paws, scaly or necrotic tails, and decreased growth.
Although the animals fed the tetrabromostearic acid (Table I) showed symptoms of fat deficiency, these animals had only a slight increase in cytochrome oxidase activity. This increase becomes evident when expressed on the basis of liver nitrogen, but the low number of observations does not allow the assignment of any significance to this oxidase activity. With this exception, however, liver enzyme activity in the animals fed the tetrabromostearic acid was almost exactly the same as that in animals fed the basal(fat-free) diet
The addition of 9, 10,12,13-tetrabromostearic acid to the basal diet appears to have little effect on the development of fat deficiency, except possibly to reduce cytochrome oxidase activity.

This is just one study that I found interesting to mention because it involved a deficiency of essential fatty acids, but apparently confirms the idea that halogenated fatty acids behave more like saturated fats.

Cunningham, H. M., & Lawrence, G. A. (1977). Absorption and metabolism of chlorinated fatty acids and triglycerides in rats. Food and Cosmetics Toxicology, 15(2), 101–103

H O KUNKEL, J N WILLIAMS Jr. The effects of fat deficiency upon enzyme activity in the rat

LucH

@TexugoDoMel said in Beyond thyroid: Iodine and PUFA interaction, greater protection than vitamin E?:

halogenated fatty acids behave more like saturated fats.

Thanks for posting. I didn't even know iodine could do the same job as tocopherols.
Explanation on this link (ScienceBuddies):
https://www.sciencebuddies.org/science-fair-projects/ask-an-expert/viewtopic.php?t=20745#:~:text=As for unsaturated fats%2C the,into single-bonded saturated fats.
"iodine atoms add to the carbon to carbon bonds in a fatty acid chain (MUFA or PUFA), so the color disappears when the atoms are added into a bond."

TexugoDoMel

@LucH
I don't know if it does the same job as vitamin E, I think it has a greater potential for protection since iodine practically converts the PUFA into a “saturated fat”. Vitamin E also has a great affinity for PUFAs and protects against lipid peroxidation by limiting damage, but it continues to behave like a PUFA in all aspects, and if vitamin E is not regenerated after some attack, lipid peroxidation will happen in the same way.

Explanation on this link (ScienceBuddies):

https://www.sciencebuddies.org/science-fair-projects/ask-an-expert/viewtopic.php?t=20745#:~:text=As for unsaturated fats%2C the,into single-bonded saturated fats.

"iodine atoms add to the carbon to carbon bonds in a fatty acid chain (MUFA or PUFA), so the color disappears when the atoms are added into a bond."

Interesting link, I tried an experiment like this once but I tried to look at it from another angle, I'm going to do it again based on the explanation in the link.

albion

I wonder if this could make Iodine a good topical treatment for cellulite

gg12

So is it as simple as just using iodized salt. How much iodine for how much PUFA? I admire your smarts

LucH

@gg12 said in Beyond thyroid: Iodine and PUFA interaction, greater protection than vitamin E?:

So is it as simple as just using iodized salt. How much iodine for how much PUFA?

Hi
I won’t trust iodized salt because you can’t be sure of what you get. Why? This salt contains potassium iodure (KI). KI is a salt with iodine. OK
But, taken on a regular base, “potassium iodide acts as a thyroid blocker, meaning it stops your thyroid from releasing thyroid hormone.” Cleveland clinic.
Excerpt (1)
Potassium iodide blocks thyroglobulin, promotes the appearance of antibodies that the body secretes to block the progression towards cancer (2).
Another study published in August 2017 in China compared the action of organic iodine supplementation in the form of algae with intake in the form of potassium iodide; seaweed rich in iodine had a positive effect on the thyroid without harmful effects. While potassium iodide causes oxidative damage in the thyroid and increases the risk of autoimmune thyroiditis (3).
Sources ad References

Interesting link (in French; translator needed)
http://nutraceutic.org/iodure-de-potassium/
Iodure de potassium : danger
Docteur Paul Dupont ancien chef de clinique d’endocrinologie nutrition
Faudrait-il interdire l’iodure de potassium ?
Fiore E1, Latrofa F1, Vitti P1. Iodine, thyroid autoimmunity and cancer. Eur Thyroid J. 2015 Mar;4(1):26-35.
Gao CH1, Qu JQ1, Zhou XY1, Gao TS2,3. Iodine-Rich Herbs and Potassium Iodate Have Different Effects on the Oxidative Stress and Differentiation of TH17 Cells in Iodine-Deficient NOD.H-2h4 Mice. Biol Trace Elem Res. 2017 Aug 12.
Excerpt:
When compared with potassium iodate (PI => KIO3), iodine-rich herbs had a positive effect on the recovery of goiter resulting from iodine deficiency without any obvious harmful effects.
Excessive intake of PI cause oxidative injury in the thyroid gland and increase the risk of autoimmune thyroiditis, while iodine-rich herbs cause less oxidative injury, significantly enhancing antioxidant capacity, and inhibit the high differentiation of Th17 cells in the thyroid glands of NOD.H-2h4 mice.
NB: Potassium iodate is used in some countries instead of potassium iodide to iodize table salt because it is more stable in humid conditions, in porous packaging and in low purity salt; but unlike the latter (iodine potassium), it is an intestinal irritant.
NB: I take Kelp, an iodine tablet of 150 mcg, from Now Foods, one another day. I’d begin slowly; 2x/wk. For people having immune problem, it’s advised to take selenium 100 mcg first, 3x/wk, then 2x/wk afterwards, to avoid side effects. Why? Too much of a good thing is bad. =>I can post a link if more details are wanted, to give examples.
Examples

Water if not compensated with trace elements (hyponatremia by athletes in T° above 40° C / 104° F)
HD niacin (B3) with NAC
HD Vit E
Not HD Vit E and HD K at the same time.
Frequent HD selenium (without Vit E)
Note: HD = High Dose.

visalibero

@LucH
What source of iodine would you consume?

LucH

@visalibero said in Beyond thyroid: Iodine and PUFA interaction, greater protection than vitamin E?:

What source of iodine would you consume?

I take kelp (seaweed), 150 mcg tablet, when I don't eat white fish or shrimps.
Now foods.
See NB above (last paragraph.)