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My mitochondria protocol: Feeding Mito it's two favorite foods

mitochondria alcar cocoa butter

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#1 Phoebus

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Posted 05 January 2022 - 01:38 AM


This is my Mitchondria protocol that I have been using for a while. I love it. Gives me a really nice boost of energy and seems like it has anti aging properties. It basically consists of ALCAR and stearic acid in the form of cocoa butter, but they need to be taken in the proper manner. 
 
 
First as most of you know, we find that mitochondria are literally destroyed as we age. 
 

 

Why NAD+ Declines during Aging: It’s Destroyed

 
Eduardo Chini and colleagues address an open question in biogerontology: why do NAD+ levels fall as we age? They show that the major culprit is an NADase called CD38 whose levels rise during aging. Their results also add to the body of evidence indicating that loss of SIRT3 activity in mitochondria is a cause of age-related metabolic decline
 

 

So as SIRT3 falters, the mitochondria die. However evidence shows ALCAR is able to restore SIRT3 expression. 

 

 

 

Treatment with the AMPK agonist AICAR or the antioxidant agent acetyl-l-carnitine (ALCAR) restored SIRT3 expression and activity, improved renal function, and decreased tubular injury in WT animals, but had no effect in Sirt3-/- mice. 

In cultured human tubular cells, cisplatin reduced SIRT3, resulting in mitochondrial fragmentation, while restoration of SIRT3 with AICAR and ALCAR improved cisplatin-induced mitochondrial dysfunction. Together, our results indicate that SIRT3 is protective against AKI and suggest that enhancing SIRT3 to improve mitochondrial dynamics has potential as a strategy for improving outcomes of renal injury.      

https://pubmed.ncbi....h.gov/25607838/

 

Not only that but carnitine is literally the key to mitochondria being able to recieve nourishment. It is carnitine's job to shuttle nutrients in and waste products out of the mitochondria. 

 

 

 

 

L-Carnitine is a naturally occurring substance required in mammalian energy metabolism that functions by facilitating long-chain fatty acid entry into cellular mitochondria, thereby delivering substrate for oxidation and subsequent energy production. It has been purposed that L-carnitine may improve and preserve cognitive performance, and may lead to better cognitive aging through the life span, and several controlled human clinical trials with L-carnitine support the hypothesis that this substance has the ability to improve cognitive function. We further hypothesized that, since L-carnitine is an important co-factor of mammalian mitochondrial energy metabolism, acute administration of L-carnitine to human tissue culture cells should result in detectable increases in mitochondrial function. Cultures of SH-SY-5Y human neuroblastoma and 1321N1 human astrocytoma cells grown in 96-well cell culture plates were acutely administered L-carnitine hydrochloride, and then, mitochondrial function was assayed using the colorimetric 2,3-bis[2-methoxy-4-nitro-5-sulfophenyl]-2H-tetrazolium-5-carboxyanilide inner salt cell assay kit in a VERSAmax tunable microplate reader. Significant increases in mitochondrial function were observed when human neuroblastoma or human astrocytoma cells were exposed to 100 nM (20 μg L-carnitine hydrochloride/L) to 100 μM (20 mg L-carnitine hydrochloride/L) concentrations of L-carnitine hydrochloride in comparison to unexposed cells, whereas no significant positive effects were observed at lower or higher concentrations of L-carnitine hydrochloride. The results of the present study provide insights for how L-carnitine therapy may significantly improve human neuronal function, but we recommend that future studies further explore different derivatives of L-carnitine compounds in different in vitro cell-based systems using different markers of mitochondrial function.

 https://pubmed.ncbi....h.gov/24005823/

 

But what nutrients does the mitochondria need? As it turns out it burns fatty acids, but a specific fatty acid is it favorite food - stearic acid. 

 

 

 

Dietary stearic acid regulates mitochondria in vivo in humans
Abstract

 

Since modern foods are unnaturally enriched in single metabolites, it is important to understand which metabolites are sensed by the human body and which are not. We previously showed that the fatty acid stearic acid (C18:0) signals via a dedicated pathway to regulate mitofusin activity and thereby mitochondrial morphology and function in cell culture. Whether this pathway is poised to sense changes in dietary intake of C18:0 in humans is not known. We show here that C18:0 ingestion rapidly and robustly causes mitochondrial fusion in people within 3 h after ingestion. C18:0 intake also causes a drop in circulating long-chain acylcarnitines, suggesting increased fatty acid beta-oxidation in vivo. This work thereby identifies C18:0 as a dietary metabolite that is sensed by our bodies to control our mitochondria. This could explain part of the epidemiological differences between C16:0 and C18:0, whereby C16:0 increases cardiovascular and cancer risk whereas C18:0 decreases both.

 

 

So mito love C:18 fatty acid, ie stearic acid. The food highest in concentration of stearic acid is cocoa butter.

 

So my protocol consists of ALCAR and cocoa butter for the above reasons. So just gobble down some ALCAR caps right? Wrong. 

 

First off all amino acids compete with each other for absorption. For highest absorption you must take aminos alone with no other protein intake. Secondly there is a way to greatly increase the penetration of ALCAR into the muscle tissues - insulin. when you take ALCAR with carbs, it create an insulin spike. The insulin then drives the ALCAR deep into the tissues. 

 

 

http://citeseerx.ist...=rep1&type=pdf      

 

 Carbohydrate ingestion augments L-carnitine retention in humans

 

The present study aimed to investigate whether an increase in whole body carnitine retention can be achieved through L-carnitine feeding in conjunction with a dietary-induced elevation in circulating insulin. On two randomized visits (study A), eight men ingested 3 g/day L-carnitine followed by 4 500-ml solutions, each containing flavored water (Con) or 94 g simple sugars (glucose syrup; CHO). In addition, 14 men ingested 3 g/day L-carnitine followed by 2 500 ml of either Con or CHO for 2 wk (study B). Carbohydrate ingestion in study A resulted in a fourfold greater serum insulin area under the curve when compared with Con (P 0.001) and in a lower plasma TC concentration throughout the CHO visit (P 0.05). Twenty-four-hour urinary TC excretion in the CHO visit was lower than in the Con visit in study A (155.0 10.7 vs. 212.1 17.2 mg; P 0.05). In study B, daily urinary TC excretion increased after 3 days (65.9 18.0 to 281.0 35.0 mg; P 0.001) and remained elevated throughout the Con trial. During the CHO trial, daily urinary TC excretion increased from a similar basal value of 53.8 9.2 to 166.8 17.3 mg after 3 days (P 0.01), which was less than during the Con trial (P 0.01), and it remained lower over the course of the study (P 0.001). The difference in plasma TC concentration in study A and 24-h urinary TC excretion in both studies suggests that insulin augmented the retention of carnitine in the CHO trials.

 

NOw in that study they use simple syrup for carb source. I don't drink that stuff, instead I use high carb fruits like dates, bananas or apples. 

 

The Protocol 

 

On empty stomach take 

 

3 - 5 grams ALCAR 

 

High carb fruit (date/banan/apple) 

 

1 gr Cocoa butter 

 

Then wait for that to absorb before eating any protein source at all. Wait at least 20 - 30 minutes. 

 

Thats it! that is the protocol. I do that about 2 - 3 times a week and believe it really gives me great energy. My skin seems to have improved since starting this formula, less line and wrinkles look smoother. I also take nicotinamide most day of the week.  I have been on this protocol for about 3 months so far and love it. I plan to continue indefinitely. 

 


Edited by Phoebus, 05 January 2022 - 02:36 AM.

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#2 Phoebus

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Posted 05 January 2022 - 04:08 AM

 

 

An important antiaging use of l-carnitine has been to increase the rate of mitochondrial oxidative phosphorylation that naturally declines as a result of aging. This decline impairs energy production while it increases production of ROS/RNS. Feeding old rats acetyl-l-carnitine was found to reverse age-related decreases in l-carnitine levels while it increased fatty acid metabolism. It also reversed the age-related decline in cellular glutathione levels and improved the complex IV activity of muscle mitochondria.89

https://www.ncbi.nlm...les/PMC4566449/

 

that is why its a good idea to take the cocoa butter along with the carnitine. The ALCAR increases the Mito's rate of fatty acid consumption, so you need to feed it its favorite fatty acid - stearic acid - when you increase ALCAR levels. 

 

ALCAR is like stepping on the gas of your mitos and stearic acid is like filling up the gas tank 


Edited by Phoebus, 05 January 2022 - 04:10 AM.

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#3 stephen_b

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Posted 05 January 2022 - 07:39 AM

Interesting. Just 1 g of cocoa butter? That should be about 370 mg of stearic acid. I'm just wondering what the best amount might be.


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#4 Phoebus

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Posted 05 January 2022 - 04:00 PM

Yeah there is no real data on this protocol, its flying by the seat of your pants 

 

1 gram is the amount that seems to work for me, thats all I can say. Wish I could be more scientific but when no data exists there is nothing you can do about it. 


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#5 Phoebus

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Posted 01 February 2022 - 02:25 AM

more on carnitine 

 

A recent study found 2 blood proteins have a major effect on longevity, one of them being Lipoprotein A 

 

 

 

Blood proteins could be the key to a long and healthy life, study finds Peer-Reviewed Publication

UNIVERSITY OF EDINBURGH

Two blood proteins have been shown by scientists to influence how long and healthy a life we live, research suggests. 

Developing drugs that target these proteins could be one way of slowing the ageing process, according to the largest genetic study of ageing.

As we age, our bodies begin to decline after we reach adulthood, which results in age-related diseases and death. This latest research investigates which proteins could influence the ageing process.

Many complex and related factors determine the rate at which we age and die, and these include genetics, lifestyle, environment and chance. The study sheds light on the part proteins play in this process.

Some people naturally have higher or lower levels of certain proteins because of the DNA they inherit from their parents. These protein levels can, in turn, affect a person’s health.

University of Edinburgh researchers combined the results of six large genetic studies into human ageing – each containing genetic information on hundreds of thousands of people,

Among 857 proteins studied, researchers identified two that had significant negative effects across various ageing measures.

People who inherited DNA that causes raised levels of these proteins were frailer, had poorer self-rated health and were less likely to live an exceptionally long life than those who did not. .

The first protein, called apolipoprotein(a) (LPA), is made in the liver and thought to play a role in clotting. High levels of LPA can increase the risk of atherosclerosis – a condition in which arteries become clogged with fatty substances. Heart disease and stroke is a possible outcome.

The second protein, vascular cell adhesion molecule 1 (VCAM1), is primarily found on the surfaces of endothelial cells – a single-cell layer that lines blood vessels. The protein controls vessels’ expansion and retraction – and function in blood clotting and the immune response.

Levels of VCAM1 increase when the body sends signals to indicate it has detected an infection, VCAM1 then allows immune cells to cross the endothelial layer, as seen for people who have naturally low levels of these proteins.

Blood proteins could be the key to a long and | EurekAlert!

 

this study found that just 2 grams of carnitine a day dramatically lower Lipoprotein A 

 

https://pubmed.ncbi....h.gov/11213533/

 

if anyone knows how to reduce  vascular cell adhesion molecule 1 (VCAM1) please chime in 


Edited by Phoebus, 01 February 2022 - 02:26 AM.

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#6 stephen_b

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Posted 07 February 2022 - 08:11 PM

For me, ALCAR on an empty stomach before a run causes what feels like low blood sugar or glycogen depletion, perhaps more of the former. I haven't tried taking it with carbs right before a run. It might be good to compare that experiment with taking it away from a run, like with after a meal to time it with the post prandial insulin release, and then running the next day.

 

I have found a great benefit to endurance to taking 500 mg each of niacinamide and d-ribose, followed by 4g or so of stearic acid (I use 4 of these cocoa butter pucks to make a pancake).


Edited by stephen_b, 07 February 2022 - 08:11 PM.


#7 Phoebus

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Posted 18 February 2022 - 04:07 AM

 

One type of saturated fatty acid may be good for mitochondrial health.

A new study shows a saturated fatty acid called stearic acid improved mitochondrial structure and function after oral ingestion in both healthy and diabetic people. There was also an increase in the utilization of stearic acid by the mitochondria.

Interestingly, another saturated fatty acid called palmitic acid did not improve mitochondrial health and has been associated with an increased risk for cardiovascular disease and cancer whereas stearic acid has been linked to reduced risk of those diseases.

This data seems to suggest that stearic acid activates a physiological response for lipids including fatty acid beta-oxidation, whereas palmitic acid does not. This could mean that palmitic acid may lead to fat accumulation in the body which could have adverse effects.

https://www.foundmyf...m/news/s/vj4bwq



#8 Phoebus

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Posted 18 February 2022 - 04:40 AM

 

First, some fatty acids (e.g., stearic acid) may prevent mitochondrial dysfunction in PD by promoting mitochondrial fusion [142] Stearic acid acts a signalling molecule which stearoylates transferrin receptor thereby inhibiting the activation of JNK signalling pathway [142]. This leads to ubiquitination of mitofusin promoting mitochondrial fusion and function. Interestingly, stearoylation of the transferrin receptor has been shown to be specific to stearic acid.

Second, saturated fatty acids may bind to leaky mitochondrial membranes promoting mitochondrial function. Stearic acid is known to be converted to oleic acid [164], which is incorporated into the mitochondrial phospholipid membrane in rats [165]. Plausibly, oleic acid derived from stearic acid may be integrated into these leaky membranes promoting mitochondrial respiration and function. Phospholipids make up the characteristic outer and inner membranes that give mitochondria their shape [166]. Leaky membranes are indicative of lower membrane potential, which in turn can reduce ATP generation [82,83]. Dysfunctional and leaky mitochondria also produce more ROS [84], which can cause an imbalance that can compromise the ability of an organism to detoxify these reactive intermediates causing oxidative stress. So, incorporation of saturated fatty acids likely results in increased membrane potential, improved ATP generation, and reduced oxidative stress.

https://www.mdpi.com...7/20/8/1850/htm

 

we see here that stearic acid promotes mito fusion (as opposed to fission) 


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#9 Phoebus

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Posted 18 February 2022 - 04:44 AM

 

The key element in this control mechanism is the transferrin receptor, which binds stearic acid. "For the first time in biological research, we have found out that stearic acid, which up until now has been believed to be simply a metabolic product, also has signaling function," says Teleman. The researchers demonstrated that mitochondrial control via stearic acid works not only in flies but also in the HeLa human cancer cell line.

When the researchers added stearic acid to fly food, the animals' mitochondria fused; when they kept fatty acid levels low, the organelles fragmented. "If using stearic acid as a food additive improves the performance of normal mitochondria, then it might do the same in pathogenically dysfunctional mitochondria," Teleman explained, describing their experimental approach.

https://www.scienced...50728101220.htm



#10 JPY

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Posted 04 April 2022 - 10:44 AM

Are you cycling this protocol at all with “fission” days, similar to Turnbuckle’s mitochondrial protocol? I notice you said you are taking nicotinamide most days so perhaps that is taking care of it.

#11 Helios

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Posted 14 April 2022 - 03:20 PM

How did you come up with the dosing?

 

ALCAR seems kinda of high, Stearic acid kinda low.


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#12 Gal220

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Posted 24 June 2022 - 06:30 AM

@Phoebus have you tried adding alpha lipoic acid to this protocol?

 

https://www.amazon.c...s/dp/B000AR8PUU






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