Dandruff or scalp irritation? Try BLOO.
Iodine is very important but remember that iodine displaces bromide and fluoride and can cause unpleasant symptoms precisely because of this. It's a good idea to adjust the amount of selenium too, as there's a good chance you'll feel unwell when supplementing with iodine if you're deficient in selenium.
You said here:
AFAIK, only T4 Can be converted into rT3.
You're right, but T3 can be converted to diiodothyronine.
There's a guy who "dissolves" t3 and t4 in water and drinks it during the day. If that's possible, it might be smoother and easier to monitor the effects
No, I was just interested in the information and looked it up. I didn't know that food had such an influence on T4 absorption
@GreekDemiGod said in Personal Log - Digestion, energy, vitality:
@TexugoDoMel During.
I made the mistake of switching my doses way too often.
I should have stayed on a dose for a minimum of 2 weeks, ideally 4-6 weeks.This time, 'm going to try 50mcg T4 + 25/ 50 mcg T3 for a month.
I don't know your background (apart from what you said in your post) or your diet in general, but I would consider that something is wrong with your diet or routine, especially if supplementing thyroid with a stable dose doesn't help you and you "feel worse on a long-term basis" just like before, since thyroid increases the need for nutrients.
Thyroid supplementation has to be a support for a higher state, not a mask
You said:
Thinking of trying exogenous thyroid again, but on all the combinations I've tried in the past I've felt worse on a long-term basis.
When you say that, is it during or after you stop using it?
You're right!
T3
T4
And youngsinatra wrote:
Fasted bioavailability of LT4 is 80%, with food it’s 40-60%.
Fasted bioavailability of LT3 is 90% and apparently it’s absorption is not influenced by food consumption.So if I take 100mcg of T4 and 20 mcg of T3 a day with food. I probably end up with 40-60mcg of bioavailable T4 and 18 mcg of T3, theoretically changing the T4/T3 ratio from 5:1 >>> 2:1 or 3:1.
Perhaps by taking only T4, which has a long half-life, you need to maximize absorption in those cases where the person's absorption is probably already very impaired. Most of the time, after a while, T4 alone makes things worse with rT3.
I don't remember the context but I think Ray was talking about T3+T4 together with food to somehow "mimic the natural release of T3". Too much hormone at once activates mechanisms to return to balance (such as conversion to rT3, excretion, etc...).
@VehmicJuryman said in New "Mission" of RPF:
@AkJono said in New "Mission" of RPF:
Wow, deal offer for the RPF name, but no dice says the lion.
I know Charlie reads this thread, so I want to ask him, what exactly does he think gives him the right to profit off of Peat's name while constantly insulting him and banning anyone who agrees with or defends his theories? What a pathetic man.
@insufferable said in Can eicosanoids be formed from mead acid?:
I skimmed this and I may be misunderstanding but it looks like the answer is yes, mead acid forms all the same stuff as EFA, just its own versions of those things.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10576882/
You're right, eicosanoids are formed from mead acid, and mead acid derivatives are different.
@insufferable said in Can eicosanoids be formed from mead acid?:
It does mean that you're not getting away without forming eicosanoids though! Which is a good thing cause I guess you'd die without them, without inflammation.
All in all I don't agree with a very low PUFA diet. If your body just forms its own PUFA (mead acid) when dietary PUFA isn't present, then what's the point of fighting it?
You basically answered in your conclusion by looking at the article you cited, Mead Acid derivatives are different versions and therefore the actions occur in a different way/intensity than "EFAs". Here is an example of rats exposed to endotoxic shock, if the type of PUFA makes no difference, why are the results so different?
Mortality of rats exposed to endotoxic shock:
EFA-deficient: 24%(in other studies that kept them on EFAD for longer it was as low as 0)
DHA: 40%
Control: 100%
Other study:
Their resistance to endotoxic shock is the same reason why they are resistant to basically all autoimmune diseases, from lupus to type 1 diabetes, and inflammation. The point of limiting them in the diet is to limit the maladaptations of an organism saturated with "EFAs", with which the whole "process" is corrupted.
Type 1 diabetes:
Lupus:
Ray Peat never said anything about no eicosanoids:
Linoleic acid, linolenic acid, arachidonic acid: Their toxicity is potentially prevented by the Mead acids, and their eicosanoid derivatives, which behave very differently from the familiar prostaglandins, as far as they have been compared; can be drastically reduced by dietary changes.
Are you fasting to reduce fatty liver? If so, take a look at the relationship with choline, maybe it will help you
I'd keep an eye on choline, which is very important for liver health(alcoholic liver disease or not).
@Norwegian-Mugabe said in Concentric only exercises:
Is intercourse concentric only?
HAHAHA
"Babe! This position is degenerating my mitochondria"
Hypertrophy between concentric and eccentric seems to be basically the same when you match the mechanical tension. What's different is the type of hypertrophy (diameter vs. fiber length). So I would add:
Benefits of avoiding eccentric / concentric only
-Less muscle damage, so you can exercise more days, recovery is very fast and you don't have to divide muscle protein synthesis too much between hypertrophy and muscle repair(not the same thing).
-Same hypertrophy potential(but in a different way)
-Apparently reset of repeated bout effect
But I agree if you approach it in the standard mindset of 6-8 reps or more per set you'll look weird and it's quite difficult.
As my background is in Olympic lifting and I always liked working with singles/doubles, it was quite easy to apply. The same results or better compared to my colleagues at the time without getting too debilitated
Interesting! They say that NSAIDs can damage the kidneys, do you think it can help in these cases, since aspirin also helps with basically the same things (AMPK, blood sugar)?
I have this study here but I have no idea of the dosage to get these numbers.
Sodium salicylate was given orally to three nephrotic children. Two of these patients had evidence of glomerular lesions. They were treated with increasing doses of sodium salicylates for twenty-two and twenty-three days respectively and their plasma-salicylate concentration rose to 250 and 350 γ per cubic centimeter. The proteinuria decreased in both children to half of the pretreatment level. No further benefit was noted. The third child suffered from lipemic nephrosis without apparent glomerular involvement. Salicylates were given for thirty-seven days and a plasma level of 200 to 300 γ per cubic centimeter was maintained for nineteen days. Complete elimination of edema and ascites occurred, the proteinuria stopped, the blood chemistry and sedimentation rate returned to normal, and this patient has thus far remained free of symptoms for over nine months.
https://www.translationalres.com/article/0022-2143(50)90034-5/fulltext
@araclavie said in Concentric only exercises:
@TexugoDoMel I've followed Peter Attia for a while before discovering Ray Peat, and Attia said something like old people lose their "breaks" i.e. eccentric strength first (following off the stairs as a common cause of death, etc), so it's more important to incorporate eccentric mov't into training. What are your thoughts on this? I'm quite new to Ray Peat and hoping to learn more about how to exercise properly.
I think that for an older person you want to focus (or should) on a stimulus that is strong enough to generate adaptations but weak enough not to cause too much muscle damage, since an old person doesn't have the same metabolic vigor as a young person (for this reason aspirin hinders the gains of a young person but helps the gains of an old person), and that's why the emphasis on the concentric is the most appropriate, even more so if you consider the most current studies that it's not physical movement that causes muscle damage, but that muscle damage is "caused by inflammation" (calcium ion-related fatigue).
I agree with @JulofEnoch that it's more of a reflex thing combined with general muscle weakness. You also don't have to completely eliminate eccentric movements.
@araclavie said in Concentric only exercises:
@TexugoDoMel So training for concentric strength should also lead to gains in eccentric strength as well?
Yes, because in both concentric and eccentric movements you are using the actin-myosin myofilaments, and the production of force in this case happens in the "same way".
The advantage of the eccentric movement compared to the concentric in relation to your question is that the force in the concentric part is predominantly a result of the actin-myosin cross-bridges, whereas in the eccentric part you have the action of the "active" actin-myosin cross-bridges AND the "passive part" titin.
Depending on what you eat and the amount of calories you'll still be digesting after the workout, but I don't know if it'll be enough, I think you'd have to pay attention to how you feel after the workout and the next day and adjust accordingly
That being said, if eating disrupts your sleep why don't you try a "liquid meal"? Milk + gelatin/collagen(or whey/casein) + sugar and salt
From a "workout perspective" the importance of the post-workout meal is to stop muscle protein breakdown(MPB) and stimulate muscle protein synthesis(MPS):
"Indeed, in addition to the 3-fold rise in MPS from essential amino acids(EAA), there is also a significant anti-proteolytic (∼40–50%) effect of feeding on skeletal muscle which is apparently entirely attributable to insulin."
"It follows that increasing dietary EAA availability after exercise enhances both the magnitude and duration of the increase in MPS."
No, but seeing vitamin A as poison is
Why didn't you use aspirin for the inflammation?
"...In those studies, the most potent steroids demonstrated almost complete inhibition of the TAT enzyme and, in fact, inhibition of TAT has been proposed as an alternative metric of “anabolism” in addition to the well-known measurement of the levator ani muscle since it provides a much easier method for measuring the anabolic effects of steroids and comparing them to each other."
"In those early studies, progesterone (and to a lesser degree DHEA) was also shown to almost fully block TAT induction by cortisol, but unlike Trenbolone it also raises the metabolic rate and if the animals do not get extra food they do not gain muscle. That’s what led to progesterone being labelled as either “ineffective” or even a “catabolic” steroid when in fact if the caloric/protein intake is increased to match the metabolic rate progesterone may be as “anticatabolic” as Trenbolone."
