Palmitic Acid (palmitate) Is A Fatty Acid Oxidation Inhibitor More Powerful Than Mildronate

[RMJ]

palm oil has a lot of palmitic acid ... unfortunatly a lot of MUFA/PUFA

would hydrogenated palm oil be a good source?

 

[haidut]

palm oil has a lot of palmitic acid ... unfortunatly a lot of MUFA/PUFA

would hydrogenated palm oil be a good source?

I would say any fully hydrogenated oil would be a good fat to consume. Or alternatively - eating plenty of sucrose/fructose.

 

[Wagner83]

I would say any fully hydrogenated oil would be a good fat to consume. Or alternatively - eating plenty of sucrose/fructose.

The post on fructose increasing palmitic acid made me wonder about @tyw thoughts on fructose being processed by the liver and increasing DNL, if DNL is increased but it's mostly palmitic acid the studies you recently posted suggest it could be pretty positive. Do Carbohydrates Turn Into Fat?

 

[haidut]

The post on fructose increasing palmitic acid made me wonder about @tyw thoughts on fructose being processed by the liver and increasing DNL, if DNL is increased but it's mostly palmitic acid the studies you recently posted suggest it could be pretty positive. Do Carbohydrates Turn Into Fat?

Well, let's see what he will say. Based on his previous posts I think he is not fond of palmitic acid and strongly believes it caused insulin resistance or even diabetes. But maybe I am just misremembering...

 

[Terma]

That's what I thought as well, but apparently palmitate acts the same way in liver too. I will post the study later today. So, it does seem to be a genuine FAO inhibitor in tissues other than the heart as well.

Well, for practical purposes I treat liver as a special case just the same (and of course that's partly because it has its own specialized behavior), so whether that changes anything depends on your goals I guess (cancer is not one of my concerns). Appreciate the research nonetheless.

The post on fructose increasing palmitic acid made me wonder about @tyw thoughts on fructose being processed by the liver and increasing DNL, if DNL is increased but it's mostly palmitic acid the studies you recently posted suggest it could be pretty positive. Do Carbohydrates Turn Into Fat?

I think that guy is absolutely right about DNL occurring more easily in liver with fructose, based on what I've read over years. 500g (total carbs, or 250g fructose) would be way too high a (daily) limit for that for that, there's an interpretation issue somewhere with that.

You avoid DNL by spreading your fructose intake over the day. Any single dose of fructose approaching 50g (probably much less, most of the time) has got to produce some (significant) DNL, it's more a question of whether the DNL per se causes any issues, and that's been ridiculously overblown by Lustig and friends (along with VLDL).

(I edited this post about 10 times, it's saturday morning)

 

[haidut]

Well, for practical purposes I treat liver as a special case just the same (and of course that's partly because it has its own specialized behavior), so whether that changes anything depends on your goals I guess (cancer is not one of my concerns). Appreciate the research nonetheless.


I think that guy is absolutely right about DNL occurring more easily in liver with fructose, based on what I've read over years. 500g (total carbs, or 250g fructose) would be way too high a (daily) limit for that for that, there's an interpretation issue somewhere with that.

You avoid DNL by spreading your fructose intake over the day. Any single dose of fructose approaching 50g (probably much less, most of the time) has got to produce some (significant) DNL, it's more a question of whether the DNL per se causes any issues, and that's been ridiculously overblown by Lustig and friends (along with VLDL).

(I edited this post about 10 times, it's saturday morning)

One has to distinguish what portion of fructose's effects on lipids is due to DNL and what portion is simply due to inhibiting fatty acid oxidation and lipolysis. Anything that inhibits lipolysis, FAO, etc will tend to increase triglyceride levels due to the fat from food not being metabolized and being esterified for storage. The well-controlled human studies so far showed that fructose does NOT contribute much to DNL when ingested in doses of 300g or less. That is way more fructose than most people will ingest even on a very carb-heavy diet. So, the trigs-raising effect of fructose is most likely due to fructose causing increased esterification and deposition of fats, and not due to DNL. The gaining of weight many people experience on Peatrian diet initially is likely due to a combination of this effect and also the high stress hormones and insulin resistance many people have due to years of low-carbing or doing exhaustive exercise.
Just my 2c.

 

[Regina]

One has to distinguish what portion of fructose's effects on lipids is due to DNL and what portion is simply due to inhibiting fatty acid oxidation and lipolysis. Anything that inhibits lipolysis, FAO, etc will tend to increase triglyceride levels due to the fat from food not being metabolized and being esterified for storage. The well-controlled human studies so far showed that fructose does NOT contribute much to DNL when ingested in doses of 300g or less. That is way more fructose than most people will ingest even on a very carb-heavy diet. So, the trigs-raising effect of fructose is most likely due to fructose causing increased esterification and deposition of fats, and not due to DNL. The gaining of weight many people experience on Peatrian diet initially is likely due to a combination of this effect and also the high stress hormones and insulin resistance many people have due to years of low-carbing or doing exhaustive exercise.
Just my 2c.

I was pleased to see my own n=1. Coming from nearly zero fruit, low sugar, "safe starch", IF, catabolic body, exhaustive exercise and switching to Peating, I did experience an initial ballooning of weight. For a year, I have beligerently attempted to restrain FFA (niacinamide, aspirin) while eating heaps of fructose and sugar. I don't remember ever eating a piece of fruit in my life before Peating. I posted my recent bloodwork and triglycerides were 52. I can tell my tolerance to fructose and sugar has made a breakthrough with this persistence.

 

[Wagner83]

One has to distinguish what portion of fructose's effects on lipids is due to DNL and what portion is simply due to inhibiting fatty acid oxidation and lipolysis. Anything that inhibits lipolysis, FAO, etc will tend to increase triglyceride levels due to the fat from food not being metabolized and being esterified for storage. The well-controlled human studies so far showed that fructose does NOT contribute much to DNL when ingested in doses of 300g or less. That is way more fructose than most people will ingest even on a very carb-heavy diet. So, the trigs-raising effect of fructose is most likely due to fructose causing increased esterification and deposition of fats, and not due to DNL. The gaining of weight many people experience on Peatrian diet initially is likely due to a combination of this effect and also the high stress hormones and insulin resistance many people have due to years of low-carbing or doing exhaustive exercise.
Just my 2c.

So would you say anything other than low fat when combined with high sucrose/fructose is very bad ?

 

[nikkmm]

I started taking mildronate a few days ago, 250 mg per day in the morning so far, and I can confirm that the effects are pretty incredible. It's like I'm able to breathe again and my body has its energy back without being stimulated, like it finally has access to its energy stores again. I know it's not Peaty but I enjoy running a bit and I can run much faster and longer without becoming out of breath. Sleep hasn't been affected so far either.

But I found this article, not sure if any of you have seen it: https://www.researchgate.net/public...tabolism_in_hyperthyroid_and_hypothyroid_rats

And basically they determined that in hyperthyroid rats, mildronate normalized the thyroid levels (meaning lowered) but in hypothyroid rats who were induced into hyperthyroidism by l-carnitine, it did not improve their thyroid hormone levels. I also noted that even though it lowered T4 and T3 levels, it lowered T4 much more, leading to a more favorable T4/T3 ratio.

Question is, in people who are hypothyroid, is mildronate not a good idea? It's strange because even though that was their conclusion, by the way the tables look to me, it seems like mildronate for 20 days after the induced hypothyroidism from PTU or carnitine actually made them slightly hyperthyroid which from a Peat perspective is a good thing?

 

[haidut]

So would you say anything other than low fat when combined with high sucrose/fructose is very bad ?

If the amount of fat stored (per 24h) exceeds the amount the liver can safely excrete through glucuronidation and the muscles can burn at rest, then yes. If the stored fat is fully saturated then it is probably less bad but still undesirable.

 

[Fractality]

I would say any fully hydrogenated oil would be a good fat to consume. Or alternatively - eating plenty of sucrose/fructose.

What are your thoughts on the concern over industrial processes used to fully hydrogenate oil?

 

[Dr. B]

I started taking mildronate a few days ago, 250 mg per day in the morning so far, and I can confirm that the effects are pretty incredible. It's like I'm able to breathe again and my body has its energy back without being stimulated, like it finally has access to its energy stores again. I know it's not Peaty but I enjoy running a bit and I can run much faster and longer without becoming out of breath. Sleep hasn't been affected so far either.

But I found this article, not sure if any of you have seen it: https://www.researchgate.net/public...tabolism_in_hyperthyroid_and_hypothyroid_rats

And basically they determined that in hyperthyroid rats, mildronate normalized the thyroid levels (meaning lowered) but in hypothyroid rats who were induced into hyperthyroidism by l-carnitine, it did not improve their thyroid hormone levels. I also noted that even though it lowered T4 and T3 levels, it lowered T4 much more, leading to a more favorable T4/T3 ratio.

Question is, in people who are hypothyroid, is mildronate not a good idea? It's strange because even though that was their conclusion, by the way the tables look to me, it seems like mildronate for 20 days after the induced hypothyroidism from PTU or carnitine actually made them slightly hyperthyroid which from a Peat perspective is a good thing?

Any thoughths? Also how can we get mildronate in the us is it prescription only