For better skin results with the C60 protocol, you might want to try cutting out all caffeine (including from tea and soda) for a month and eating salmon twice a week to upregulate your beta-adrenergic receptors.
Although the C60 protocol improved the youthfulness of my skin, I still had problems like wounds not healing as fast as I wanted (I have had this problem for over a decade, before I tried either the mito or C60 protocol).
Then, last year when I encountered problems with excess serotonin from years of taking serotonin raising supplements and then (what finally led to a tipping point) combining 5-HTP with the C60 protocol, I took propranolol to upregulate my beta receptors as part of my 7 step serotonin reducing protocol.
I also took Omega 3 later in the protocol and eat 36 mgs of 70% dark chocolate 4-5 days a week (Lindt brand dark chocolate balls) to lower norepinephrine/noradrenaline and epinephrine/adrenaline to further upregulate my beta receptors, and ending all caffeine intake (I used to be a big coffee, green tea, and occasional Nic-vape user).
What I noticed was that the propranolol, surprisingly and unexpectedly, ended the rapid heartbeat and anxiety attacks I had when I ate meat most of last year or took certain supplements (and later the mito protocol which I did 22 times earlier this year entirely eliminated any remaining problems I had eating meat).
Propranolol also had the unexpected effect of making my skin heal noticeably faster.
Apparently both the relief in rapid heartbeat from eating meat and the restoration of skin healing is related to the beta receptors not just controlling responses to adrenaline. It also is involved in glucose metabolism. Presumably my rapid heartbeat from eating meat was caused by my beta receptors so downregulated from serotonin-triggered adrenaline release that there weren't enough beta receptors left to both control normal cardiovascular responses and convert food into glucose.
The mito protocol helped me eat without side effects because the mitochondria (among many other things) are needed to process protein and fat and many supplements, and they are heavily involved in anxiety responses because MAO is directly embedded within mitochondria. But I couldn't take mito protocol until later in my serotonin-reducing protocol.
It also appears that beta receptors are somehow involved in wound healing, probably because of their effect on glucose metabolism -
Docosahexaenoic acid facilitates cell maturation and -adrenergic transmission in astrocytes
https://www.research...lication_detail
The effects of docosahexaenoic acid (DHA; 22:6n-3), a major v-3 PUFA in the mammalian brain, on the structure and function of astrocytes were studied using primary cultures from rat cerebra. Gas-liquid chromatography of methyl esters of FAs isolated from cultures exposed to individual FAs, namely, stearic acid, linoleic acid, arachidonic acid, and DHA, showed alterations in the lipid profiles of the membranes, with a preferential incorporation of the FA to which the cells were exposed. Immuno-fluorescence studies demonstrated that unlike treatment with other FAs, after which the astrocytes remained as immature radial forms, DHA-treated astrocytes showed distinct differentiation, having morphology comparable to those grown in normal serum-containing medium.
Receptor binding studies to determine the concentration of various neurotransmitter receptors showed that DHA selectively increased the number of b-adrenergic receptors (b-ARs) compared with FA-untreated controls, suggesting a greater role of DHA on b-AR expression in membranes. This was also reflected by an increase in downstream events of the b-AR pathways, such as the induction of protein kinase A and glycogen turnover by isoproterenol (ISP), a b-AR agonist in DHA-treated cells.
...
The b-AR system is an important intrinsic regulator of the glycogen turnover of mammalian brain. We determined the glycogen content in specific FA-enriched astrocytic cells under normal and ISP-treated conditions (Fig. 7A). Compared with untreated controls, supplementation of SA and AA had no effect on the glycogen content of the cells, whereas LA and DHA caused significant increases in total glycogen, with average increases 250% and 760%, respectively. When the cells were exposed to ISP, there was significant breakdown in total glycogen content in all FA-treated cells compared with corresponding cells in which no ISP was added. Here also, the maximum breakdown of glycogen by ISP occurred in DHA-supplemented cells, which decreased to the level observed in FA-deficient astrocytes.
Because the observed 7.5-fold increase in total glycogen content in DHA-supplemented cells could be attributable to an effect on the synthesis rate of glycogen, we evaluated the amount of incorporation of [14C]glucose into glycogen in these cells in the presence and absence of ISP (Fig. 7B). In the absence of ISP, treatment with DHA caused an 50% decrease in the newly synthesized glycogen compared with FA-deficient control cells. However, on ISP treatment, there was a 10-fold increase in the incorporation of [14C]glucose into glycogen in the DHA supplemented astrocytes compared with the ISP-treated control cells.
Edited by Kelvin, 30 May 2024 - 11:12 PM.
