Click Here if you want to upgrade your account
If you were able to post but cannot do so now, send an email to admin at raypeatforum dot com and include your username and we will fix that right up for you.
I ate some meat fried in cocoa butter yesterday, and had very vivid dreams last night.
Oleic acid is a membrane lipid, and the saturated fats less so. While true that stearic and palmitic acids are found on the membrane, they exist in lower concentrations. Stearic acid can become oleic acid through Δ⁹-desaturase, so you'd think that oleic acid could spare this to some degree. This fact might appear exononerate olive oil but it does not, or at least not completely, as olive oil also contains widely variable amount of linoleic acid (so you could get a 'cancer batch' by choosing olive oil from the wrong region pressed in the wrong season). This is further complicated by the fact that commercial olive oil is the most adulterated oil, with the cheaper seed oils often added by unscrupulous profiteers. Oleic will further become Mead acid (20∶3·ω−9), exclusively a membrane lipid further distinguished by being the only 20-carbon polyunsaturated fatty acid which cannot form an eicosanoid. The other 20-carbon membrane lipid having three double bonds—dihomo-γ-linolenic acid (20∶3·ω−6)—has one if its double bonds in a different position, lending it the proper cyclooxygenase geometry to be transformed into 1-series prostaglandins. The more common arachidonic acid (20∶4) forms the 2-series prostaglandins and the α-linolenic acid-derived EPA (20∶5) is the progenitor of the 3-series. Twenty carbon monounsaturated fatty acids exist and are minor constituents of foods, and these likewise are not prostaglandin precursors without prior desaturation; one of these is an ω−9 fatty acid found in certain tropical seeds, one is an omega − 11 fatty acid found in fish, and the other is an omega minus seven fatty acid found in certain plants. The fully-saturated near-mythological arachidic acid (20∶0·ω−∅) lacks all double bonds, and is thus is an omega minus nothing fatty acid.
I would be careful with trying to activate the cannabinoid receptors. They seem to be connected with estrogen, stress, and addiction.
Yes there is. You can edit a post for up to ~2–4 hours afterwards (I think it's 300 minutes, but not 100% certain.) I am going to coffee/tea/water-fast for one day as a routine cleansing procedure. Muscles aren't autolyzed on very short fasts and can even grow using the amino acids liberated from autolysis elsewhere with glucose liber-
How often do you perform such fasts, and what benefits have they given to you?
I'm curious about recipes too.
I think Xisca must be talking about me. If you remember, I developed T1D after starting Peating.
That's a shame.
I just started again. I had read many of the classic books about ten years ago, but then had went through a period where I't thought they were somewhat sensationalized for book sales—perhaps being a bit 'woo.' But now it's actually being studied using molecular biochemistry, results of which have largely verified the older claims written before even DNA had been discovered. The keywords are different, although similar. The 21st century scientific terms found in the literature correspond to the classic macro-observational terms penned roughly 100 years ago: The terms 'fasting' and 'caloric restriction,', 'autolysis' and 'autophagy,' and 'cleansing' vs 'autosomal proteolysis' are nearly superimposable. Ray Peat has written about lipofuscin in his website articles, and fasting—or 'caloric (leucine) restriction'—seems to be the only way to influence the process besides and limiting iron, polyunsaturated fatty acids, and avoiding Al³⁺ completely. The autophagic vesicles which can induced in the neurons by leucine restriction—or mTOR downregulation—can be expected to reduce absolute lipofuscin, neurofibrillary tangle, and misfolded β-amyloid aggregate volume through initial isolation and subsequent proteolysis using lysosomal caspases. According to classic authors such as Herbert Shelton and John Tilden, fasting can bring about mental clarity after the initial phase of foggy-headedness and confusion; perhaps it does so by clearing the intra-neuronal space? Histologists have long recognized that in the very old, and often very demented, the ostensibly-undegradable lipofuscin can account for up to 75% of a neuron's internal cytosolic volume.
I went from a low-carb "paleo" diet (for lack of a better word) to a typical Peat diet. Basically added fruit, fruit juices, milk and Peaty supplements to an already good, whole food diet. Butter and coconut oil were the only fats I used. But I used to consume a lot of nuts and PUFA before, and of course it can take some time to be rid of that.
FWIW I went from a similar diet to peating and mol cured my T2D. I don't think this negates your experience. But I do think it should draw attention to the individuality of this effort.
I guess I don't blame low-carb paleo because I didn't have any symptoms on low-carb paleo. The symptoms only started about 5 months after switching to a Peat diet.
Yes, I've read his theories on auto-immune diseases, and they made a great deal of sense to me. I'm fully aware of his views on estrogen as the root of all evil. It was after reading his writings that I stopped taking estrogen.
Yes, I agree, and Peat makes a compelling case for this. All I can say is that in practice. in vivo, for me, it didn't work out well.
Until it's not. Until your body's cells can't take it in as energy any more, and it dumps it into your blood and urine, causing ketoacidosis. I lived this way for over a year, in denial of what was happening. Ended up in the emergency room with blood sugar over 500. Sugar was not my friend.
I think the thing that was lucky for me was that I still was wary of sugar when I discovered RP, and continued to be for some time. I brought sugar on very slowly. I believe this resensitized me slowly. Going from low carb to RP must be a shock to the system. There is a lot of speculation in this all of course, but it worked out for me.
