19 replies to this topic

[QuestforLife]

What to make of C60 fullerenes in olive oil for life extension?

 

The famous Baati study, The prolongation of the lifespan of rats by repeated oral administration of [60] fullerene [1] is now mired in controversy; ignored by most serious scientists. In this monograph, I’ll try and unpick what this paper really found in an attempt to shed some light on the enduring mystery.

To be upfront, I don’t suspect fraud. I think that Baati stumbled upon something extraordinary. But like so many papers, the authors didn’t understand their results, they made some errors in presentation, and others failed to replicate the results [2]. So their results get dismissed. Another non-replicating paper for the dustbin?

 

I’m going to put forward an alternative explanation for the mechanism of action for C60 in olive oil and its effect on the lifespan of rats. It by no means is a complete explanation. But it does suggest an angle for further investigation.

 

Firstly, the lifespan study ’design’ was ad hoc. It actually wasn’t intentional, as they stopped it early due to the death of one of the controls; attributed to oral gavaging (forced feeding via a tube). For the 7 months of treatment, they gavaged two of the three groups of rats with 1ml of olive oil a day (the control was gavaged with water). That might not sound like much, but for an animal the weight of a human that scales up to 9 or 10 tablespoons. Quite a lot! The rats probably weren’t hungry after having that quantity of olive oil rammed down their throats. In fact, I wonder if this could have triggered a state of keto genesis.

 

I’ve been ketogenic for extended periods. There are significant changes to the body when it switches to burning fats for energy. Extended lifespan from keto is possible as it replicates many of the effects of calorie restriction, including weight loss [3]. Now you may counter that the olive oil treated rats had the same weight as controls. But they were only treated for 7 months of their life. And there is precedent for temporary diets to have lasting effects when powerful, mitochondrial antioxidants are involved (as C60 is supposed to be [4]).

 

For example, Dietary lipoic acid supplementation can mimic or block the effect of dietary restriction on life span is instructive [5]. In one of the experiments, ALA locked-in the (shorter) lifespan of ad libitum fed mice, even when ALA dosing ceased and food was subsequently restricted. In another group, switching from dietary restriction to ad libitum plus ALA caused a restoration of normal weight, but preserved the lifespan benefits of calorie restriction.

 

To sum up, it is at least plausible that large quantities of olive oil could put mice into a ketogenic state, and that the dosing of C60 in that oil could extend the effects of that diet beyond its cessation. This explanation indicates why replication may have failed. No one else has gavaged large quantities of olive oil into their animals. Other experiments also used mice[2], not rats - and interestingly mice are not as well adapted to fat burning as rats, as evidenced by this paper where they showed murine ability to uncouple mitochondria is worse than rats across multiple tissues [6].

 

Whilst on the subject of uncoupling, it is interesting to note that C60 is hypothesised to absorb protons from mitochondria [4], which reduces the potential energy available to drive ATP production, enabled by the re-entry of those protons to the mitochondria. This is similar to what uncoupling does, whereby protons are permitted re-entry via the pore rather than the ATP complex. Either way, you decrease mitochondrial efficiency and increase respiration rate. This is very useful when you are trying to absorb lots of fats [7], and the poor mitochondria can’t go fast enough.

 

This is interesting for understanding keto, but why exactly would this extend life? I’ve got some tentative ideas. The functionality of the mitochondrial network sets the optimal cell size [8], and beyond this cell size growth is accomplished by increased glycolysis in the cytoplasm, not increased respiration. Many regard cell size as central to aging [9], with large cells being old cells and driving organism level aging. Making cells rely on mitochondria is a good way to stop cell growth beyond the optimum size; fat burning requires working mitochondria. 

 

There is a whole life extension community devoted to stem cell rejuvenation using C60 [10]. This popular protocol combines C60 with stearic acid. Stearic acid is a long, saturated fat. It requires lots of rounds of beta oxidation, with lots of FADH₂ made to feed into mitochondria. Stearic acid is known to trigger mitochondrial fusion in vitro and in vivo [11],[12] and I suspect other mitochondrial adaptations like uncoupling as well. I predict that eating stearic acid is a powerful inducer of ketogenesis. As to the claimed stem cell benefits, it is well known that saturated fats trigger stem cell renewal, for example in the intestine [13]. This is likely a fasting mimicking effect; the body is drawing down on reserves so flicks cellular switches to self-renewal rather than differentiation.. 

 

I leave you with a final thought: didn’t Jean Calment consume large quantities of chocolate, olive oil (and wine)?

 

References:
1. Baati T, Bourasset F, Gharbi N, Njim L, Abderrabba M, Kerkeni A, Szwarc H, Moussa F. The prolongation of the lifespan of rats by repeated oral administration of [60]fullerene. Biomaterials. 2012 Jun;33(19):4936-46. doi: 10.1016/j.biomaterials.2012.03.036. Epub 2012 Apr 10. Erratum in: Biomaterials. 2012 Sep;33(26):6292-4. PMID: 22498298. 

 

2. Grohn KJ, Moyer BS, Wortel DC, Fisher CM, Lumen E, Bianchi AH, Kelly K, Campbell PS, Hagrman DE, Bagg RG, Clement J, Wolfe AJ, Basso A, Nicoletti C, Lai G, Provinciali M, Malavolta M, Moody KJ. C60 in olive oil causes light-dependent toxicity and does not extend lifespan in mice. Geroscience. 2021 Apr;43(2):579-591. doi: 10.1007/s11357-020-00292-z. Epub 2020 Oct 29. PMID: 33123847; PMCID: PMC8110650.

 

3. Kennedy AR, Pissios P, Otu H, Roberson R, Xue B, Asakura K, Furukawa N, Marino FE, Liu FF, Kahn BB, Libermann TA, Maratos-Flier E. A high-fat, ketogenic diet induces a unique metabolic state in mice. Am J Physiol Endocrinol Metab. 2007 Jun;292(6):E1724-39. doi: 10.1152/ajpendo.00717.2006. Epub 2007 Feb 13. Erratum in: Am J Physiol Endocrinol Metab. 2007 Dec;293(6):E1846. Roberson, Russell [added]. Erratum in: Am J Physiol Endocrinol Metab. 2009 May;296(5):E1179. PMID: 17299079.

 

4. Chistyakov VA, Smirnova YO, Prazdnova EV, Soldatov AV. Possible mechanisms of fullerene C₆₀ antioxidant action. Biomed Res Int. 2013;2013:821498. doi: 10.1155/2013/821498. Epub 2013 Oct 8. PMID: 24222918; PMCID: PMC3816026.

 

5. Merry BJ, Kirk AJ, Goyns MH. Dietary lipoic acid supplementation can mimic or block the effect of dietary restriction on life span. Mech Ageing Dev. 2008 Jun;129(6):341-8. doi: 10.1016/j.mad.2008.04.004. Epub 2008 Apr 22. PMID: 18486188.

 

6. Andrews ZB, Horvath TL. Uncoupling protein-2 regulates lifespan in mice. Am J Physiol Endocrinol Metab. 2009 Apr;296(4):E621-7. doi: 10.1152/ajpendo.90903.2008. Epub 2009 Jan 13. PMID: 19141680; PMCID: PMC2670629.

 

7. Maassen JA, Romijn JA, Heine RJ. Fatty acid-induced mitochondrial uncoupling in adipocytes as a key protective factor against insulin resistance and beta cell dysfunction: a new concept in the pathogenesis of obesity-associated type 2 diabetes mellitus. Diabetologia. 2007 Oct;50(10):2036-41. doi: 10.1007/s00125-007-0776-z. Epub 2007 Aug 22. PMID: 17712547; PMCID: PMC2039833.

 

8. Miettinen TP, Björklund M. Cellular Allometry of Mitochondrial Functionality Establishes the Optimal Cell Size. Dev Cell. 2016 Nov 7;39(3):370-382. doi: 10.1016/j.devcel.2016.09.004. Epub 2016 Oct 6. PMID: 27720611; PMCID: PMC5104693.

 

9. Lengefeld J, Cheng CW, Maretich P, Blair M, Hagen H, McReynolds MR, Sullivan E, Majors K, Roberts C, Kang JH, Steiner JD, Miettinen TP, Manalis SR, Antebi A, Morrison SJ, Lees JA, Boyer LA, Yilmaz ÖH, Amon A. Cell size is a determinant of stem cell potential during aging. Sci Adv. 2021 Nov 12;7(46):eabk0271. doi: 10.1126/sciadv.abk0271. Epub 2021 Nov 12. PMID: 34767451; PMCID: PMC8589318.

 

10. https://www.longecit...with-c60/page-1

 

11. Senyilmaz D, Virtue S, Xu X, Tan CY, Griffin JL, Miller AK, Vidal-Puig A, Teleman AA. Regulation of mitochondrial morphology and function by stearoylation of TFR1. Nature. 2015 Sep 3;525(7567):124-8. doi: 10.1038/nature14601. Epub 2015 Jul 27. PMID: 26214738; PMCID: PMC4561519.

12. Senyilmaz-Tiebe D, Pfaff DH, Virtue S, Schwarz KV, Fleming T, Altamura S, Muckenthaler MU, Okun JG, Vidal-Puig A, Nawroth P, Teleman AA. Dietary stearic acid regulates mitochondria in vivo in humans. Nat Commun. 2018 Aug 7;9(1):3129. doi: 10.1038/s41467-018-05614-6. PMID: 30087348; PMCID: PMC6081440.

 

13. Barisas DAG, Stappenbeck TS. Intestinal Stem Cells Live Off the Fat of the Land. Cell Stem Cell. 2018 May 3;22(5):611-612. doi: 10.1016/j.stem.2018.04.018. PMID: 29727673.

[QuestforLife]

Correction, rats weren't dosed daily for 7 months, but...

As biodistribution studies after daily gavages showed that C60
accumulates in livers and spleens, in order to avoid the negative effects of prolonged olive oil administration such as obesity, excessive steatosis, liver lipid degeneration, and insulin resistance, we treated the rats daily only during 7 days and weekly during the first two months, then every two weeks until one control rat died

[1]

[Mind]

Thanks for the informative post and theory.

 

However, from a high-level view, I would tend to think that a super high-calorie ketogenic diet would be detrimental, as compared to a low-calorie ketogenic diet, considering the evidence for calorie restriction and intermittent fasting.

[QuestforLife]

The keto theory could easily be wrong, but not based on that objection - as there is no evidence that the rats were on 'super high-calorie ketogenic diet'.

If anything, I was suggesting a dose of olive oil first thing would reduce feeding and overall cause a deficit.

[Turnbuckle]

The keto theory could easily be wrong, but not based on that objection - as there is no evidence that the rats were on 'super high-calorie ketogenic diet'.

If anything, I was suggesting a dose of olive oil first thing would reduce feeding and overall cause a deficit...

 

 

Firstly, the lifespan study ’design’ was ad hoc. It actually wasn’t intentional, as they stopped it early due to the death of one of the controls; attributed to oral gavaging (forced feeding via a tube). For the 7 months of treatment, they gavaged two of the three grou

 

Comparing the EVOO rats with the EVOO+C60 rats, the first lived 15% longer than the controls, while the C60 group lived 90% longer. C60 has no calories, thus there was indeed a big difference with C60 that is not explainable by a caloric intake hypothesis. As for the controls, they all died before any of the C60 rats. All three treatment protocols were stopped when one control rat developed tumors and died. (All three groups had been gavaged, but the control got only water.) I have heard -- and I don't know if it is true -- that the last two C60 rats were euthanized as they needed to proceed with the paper, but by that time the group had lived nearly twice as long as the controls, so that wouldn't change the conclusions. As for the study being ad hoc, I saw no evidence of that, except with the decision to stop treatments when a control rat developed tumors, and (if true) to euthanize the last two surviving rats.

Edited by Turnbuckle, 19 October 2022 - 10:08 PM.

[QuestforLife]

Comparing the EVOO rats with the EVOO+C60 rats, the first lived 15% longer than the controls, while the C60 group lived 90% longer. C60 has no calories, thus there was indeed a big difference with C60 that is not explainable by a caloric intake hypothesis. As for the controls, they all died before any of the C60 rats. All three treatment protocols were stopped when one control rat developed tumors and died. (All three groups had been gavaged, but the control got only water.) I have heard -- and I don't know if it is true -- that the last two C60 rats were euthanized as they needed to proceed with the paper, but by that time the group had lived nearly twice as long as the controls, so that wouldn't change the conclusions. As for the study being ad hoc, I saw no evidence of that, except with the decision to stop treatments when a control rat developed tumors, and (if true) to euthanize the last two surviving rats.

 

The fact the olive oil only rats lived longer than controls, is evidence that there is merit in what I am saying. The fat angle is important. 

 

Looking at the lifespan curve (original and corrected), the last 2 olive oil rats died together, and the last 2 C60oo rats died together. All these might have been euthanised if they were suffering.

 

As to my comment - dosing the rats once per day, then weekly for 2 months, then every 2 months, then stopping when a control died, seems 'ad hoc' to me. But I didn't mean any offence by it. The study is clearly of great importance.  

[Turnbuckle]

Note that after the first control rat died  —

 

...the growths of all surviving animals showed no significant difference until M30 (Fig. 3b) indicating that the treatment did not alter their food intake...

 

At M38 all water-treated control rats were dead (Fig. 3a). This agrees with the expected lifespan of this animal species that is thirty to thirty six months. At this time 67% of olive-oil-treated rats and 100% of C60-treated rats were still alive.

 

 

Also note that all treatments were stopped at M17, and the weights of the control rats fell below that of the other two groups only 13 months later, when half the control rats were dead.

 

Ketosis cannot explain why the rats continued to live on in spite of no further treatments. The same objection can be made to the paper’s antioxidant hypothesis. It doesn’t work, as even the paper suggested that C60 disappears fairly rapidly. And neither hypothesis can explain the multiple failures to replicate this experiment. Three tries have been made so far, two published in reputable journals, and all failed to show this remarkable improvement in longevity, either for EVOO alone (18% improvement) or for EVOO+C60 (90% improvement).

 

The better explanation is that there was an undisclosed variable in the first experiment, such that C60 boosted stem cell numbers and thus gave the treated rats a new lease on life. The variable was in how the rats were fed.

 

The paper was unfortunately silent on how they were fed during the treatments, but if they were fed as in the acute toxicity study, fasted overnight but with access to water, they would have entered a state of mitochondrial fusion, as rodents have a metabolic rate six times that of humans, and fusion is a metabolic response to fasting. There is no suggestion in the papers of the subsequent researchers that they fasted the rats, and fasting makes this important but unappreciated difference --

 

Nutrient scarcity in organisms is linked to an increase in circulating glucagon and other stress hormones, such as norepinephrine, which generally increase intracellular cAMP levels and PKA signaling (Fig 2A). Under these circumstances, mitochondrial fusion is typically observed.

https://www.ncbi.nlm...les/PMC4023882/

 

 

Mitochondrial fusion makes all the difference between stem cell (SC) proliferation and SC differentiation. So the better hypothesis is that the Baati rats experienced an SC stimulant effect that required mitochondrial fusion for SC proliferation. This also explains why olive oil alone improved longevity, as some of the polyphenols in olive oil stimulate SC activity. That olive oil has this property is now known —

 

Additionally, olive oil and its components positively modulated different stem cell populations...

https://www.ncbi.nlm...cles/PMC6904865

 

 

Edited by Turnbuckle, 20 October 2022 - 11:37 AM.

[QuestforLife]

 

Mitochondrial fusion makes all the difference between stem cell (SC) proliferation and SC differentiation. So the better hypothesis is that the Baati rats experienced an SC stimulant effect that required mitochondrial fusion for SC proliferation. This also explains why olive oil alone improved longevity, as some of the polyphenols in olive oil stimulate SC activity. That olive oil has this property is now known —

 

It might be the polyphenols, but more likely in my assessment it is the fats in the olive oil that stimulate the various adaptations - mitochondrial fusion, uncoupling, etc - that trigger SC self-renewal, as I referenced quite thoroughly in my post.

 

This would explain how a temporary treatment - with temporary ketogenic adaptions - could have a lasting effect. And, indeed, C60 clearly enhances this effect.    

[Turnbuckle]

...but more likely in my assessment it is the fats in the olive oil that stimulate the various adaptations - mitochondrial fusion, uncoupling, etc ...

 

 

If that were true, the attempts to replicate would have succeeded. 

[QuestforLife]

If that were true, the attempts to replicate would have succeeded. 

 

No other attempt gavaged a 'large' quantity of olive oil. The Moody study fed them a smaller quantity voluntarily via pipette [1]. So adaptions to fat would have been muted.

 

No other attempt used rats. Mice have a reduced UCP response in comparison to rats, as I referenced above. In fact, a recent attempt at replication found olive oil actually reduced lifespan of mice [2] in comparison to controls.

 

 

[1] Grohn KJ, Moyer BS, Wortel DC, Fisher CM, Lumen E, Bianchi AH, Kelly K, Campbell PS, Hagrman DE, Bagg RG, Clement J, Wolfe AJ, Basso A, Nicoletti C, Lai G, Provinciali M, Malavolta M, Moody KJ. C60 in olive oil causes light-dependent toxicity and does not extend lifespan in mice. Geroscience. 2021 Apr;43(2):579-591. doi: 10.1007/s11357-020-00292-z. Epub 2020 Oct 29. PMID: 33123847; PMCID: PMC8110650.

 

[2] Shytikov D, Shytikova I, Rohila D, Kulaga A, Dubiley T, Pishel I. Effect of Long-Term Treatment with C60 Fullerenes on the Lifespan and Health Status of CBA/Ca Mice. Rejuvenation Res. 2021 Oct;24(5):345-353. doi: 10.1089/rej.2020.2403. Epub 2021 May 19. PMID: 33849306.

[Turnbuckle]

You are quickly running afoul of Occam's razor. 

[QuestforLife]

You clearly agree with me that fat burning is important, or you wouldn't be using stearic acid.

 

 

 

 

 

[Turnbuckle]

You clearly agree with me that fat burning is important, or you wouldn't be using stearic acid.

 

An unwarranted assumption. I use stearic acid because it creates mitochondrial fusion--

 

We show here that C18:0 ingestion rapidly and robustly causes mitochondrial fusion in people within 3 h after ingestion. 

https://pubmed.ncbi....h.gov/30087348/

 

 

DHM may be used in addition to or in place of stearic acid, as it also causes mitochondrial fusion and can penetrate the BBB, unlike stearic acid.

 

DHM also modulated mitochondrial dynamics of fusion and fission by increasing mitofusins 1 and 2, while decreasing fission-related, dynamin-related protein 1 and mitochondrial fission 1.

https://pubmed.ncbi....h.gov/24637344/

 

[QuestforLife]

An unwarranted assumption. I use stearic acid because it creates mitochondrial fusion--

 

 

No, perfectly warranted. SA causes fusion BECAUSE it is a fat that REQUIRES mitochondria to fuse to deal with it. 

 

 DHM may be used in addition to or in place of stearic acid, as it also causes mitochondrial fusion and can penetrate the BBB, unlike stearic acid.

 

I wonder why DHM causes fusion? BECAUSE it upregulates SIRT3 [1], which allows FAT BURNING.

 

See where I am going with this..?

 

What you are saying is correct, but you are missing WHY. 

 

[1] Akindehin S, Jung YS, Kim SN, Son YH, Lee I, Seong JK, Jeong HW, Lee YH. Myricetin Exerts Anti-Obesity Effects through Upregulation of SIRT3 in Adipose Tissue. Nutrients. 2018 Dec 12;10(12):1962. doi: 10.3390/nu10121962. PMID: 30545041; PMCID: PMC6316341.

[Turnbuckle]

No, perfectly warranted. SA causes fusion BECAUSE it is a fat that REQUIRES mitochondria to fuse to deal with it. 

 

 

 

 

I wonder why DHM causes fusion? BECAUSE it upregulates SIRT3 [1], which allows FAT BURNING.

 

See where I am going with this..?

 

What you are saying is correct, but you are missing WHY. 

 

[1] Akindehin S, Jung YS, Kim SN, Son YH, Lee I, Seong JK, Jeong HW, Lee YH. Myricetin Exerts Anti-Obesity Effects through Upregulation of SIRT3 in Adipose Tissue. Nutrients. 2018 Dec 12;10(12):1962. doi: 10.3390/nu10121962. PMID: 30545041; PMCID: PMC6316341.

 

 

Stearic acid acts very differently from the similar palmitic acid. It acts as a signaling agent. From the paper --

 

 

In this study, we identify stearic acid (C18:0) as a metabolite that is sensed in our diets and regulates human physiology, in particular mitochondrial morphology and function. Intriguingly, our data imply that when we eat, the C18:0 in our food causes our mitochondria to fuse within a few hours of eating. This response is impressively robust: we obtained statistically significant results with only 10 healthy subjects. Unlike C18:0, C16:0 does not have this effect. This could explain part of the difference between C16:0 and C18:0 observed epidemiologically, whereby C16:0 increases the risk for cancer and cardiovascular risk whereas C18:0 reduces both: if dietary C18:0 signals the intake of lipids to the human body, to activate a physiological response for lipid handling which includes fatty acid beta-oxidation, whereas C16:0 does not, this would imply that C16:0 ingestion will lead to more fat accumulation in the body than C18:0 ingestion. Fat accumulation, in turn, is a risk factor for both cardiovascular disease and cancer. Hence the balance of C16:0 to C18:0 in our diets may be important.  could be particularly bad because it provides lipids to the body without activating the mitochondrial response that C18:0 does.

 

...our previous work in cell culture showed that mitochondrial fusion is very specifically induced by C18:0 and not by any other fatty acid such as C16:0, C18:1, or C20:0, because there is a dedicated signaling pathway that senses C18:0.

https://www.ncbi.nlm...les/PMC6081440/

 

 

Also

 

Here we identify the metabolite stearic acid (C18:0) and human transferrin receptor 1 (TFR1; also known as TFRC) as mitochondrial regulators. We elucidate a signalling pathway whereby C18:0 stearoylates TFR1, thereby inhibiting its activation of JNK signalling. This leads to reduced ubiquitination of mitofusin via HUWE1, thereby promoting mitochondrial fusion and function. We find that animal cells are poised to respond to both increases and decreases in C18:0 levels, with increased C18:0 dietary intake boosting mitochondrial fusion in vivo.

https://pubmed.ncbi....h.gov/26214738/

 

 

Stearic acts as a fusion agent, and then fusion acts as a functional regulator of SC fate --

 

We now uncover that the state of an organelle, namely mitochondria, has the capacity to coordinate self-renewal versus differentiation of stem cells. Mitochondria are dynamic organelles that undergo morphological changes through fission and fusion. Although major changes in mitochondrial structure have been generally attributed as a cellular response to stress, we now present evidence that mitochondrial dynamics can act as a functional regulatory factor...

 

The ability of stem cells to continuously self-renewal is key to preventing stem cell depletion and aging. Although it is clear that aging results in stem cell depletion, the underlying reasons for this decline remain unclear. Given our findings, we propose that disruption of mitochondrial dynamics, as observed during aging and in degenerative diseases, is an important factor in the eventual depletion of the stem cell pool. Though mitochondrial fragmentation is generally perceived as a sign of mitochondrial dysfunction and oxidative stress, data presented in this study modify this view and present changes in mitochondrial morphology as a means to induce intracellular signaling. Within the biological setting of development or regeneration, mitochondrial fragmentation is required for the transient passage of cells to committed progenitors. However, ... a chronically fragmented state, such as that observed during aging and many neurodegenerative diseases, impair the self-renewal capacity of stem cells and lead to depletion of the stem cell pool.

https://pubmed.ncbi....h.gov/27237737/

 

[QuestforLife]

Stearic acid acts very differently from the similar palmitic acid. It acts as a signaling agent. From the paper -

Stearic acid seems to occupy an important position as a signalling molecule, granted. And yet, palmitic acid also triggered self renewal in intestinal stem cells as reviewed here [1]

[size=5]Stearic acts as a fusion agent, and then fusion acts as a functional regulator of SC fate --

This paper is rather weak. Just because you sabotage really important mitochondrial fusion proteins and this impairs neural progenitor self-renewal, doesn't mean mitochondrial state is the only arbiter of self renewal decisions. It just means you broke an important part of the machine.

Sure, mito fusion must have an impact but most likely it's part of a wider regulation that involves the cells detecting growth factors and feeding state and this is what fatty acid metabolism is allowing us to manipulate.


[1] Barisas DAG, Stappenbeck TS. Intestinal Stem Cells Live Off the Fat of the Land. Cell Stem Cell. 2018 May 3;22(5):611-612. doi: 10.1016/j.stem.2018.04.018. PMID: 29727673.

Edited by QuestforLife, 20 October 2022 - 06:27 PM.

[QuestforLife]

Only an association study, but still interesting...[1]

After adjusting for demographic and lifestyle factors, the OOC (olive oil consumption) was
associated with a lower risk of all-cause, CVD and cancer mortality. Compared
to the less than once per month consumption, the consumption of up to
one tablespoon per day was associated with a 9% lower risk of all-cause
mortality (HR: 0.91; 95%CI: 0.68-1.22) and the consumption of 2 or more
tablespoons with a 31% lower risk of all-cause mortality (HR: 0.69; 95%CI:
0.50–0.93; p-trend = 0.011).

[1] Torres-Collado L, García-de la Hera M, Lopes C, Compañ-Gabucio LM, Oncina-Cánovas A, Notario-Barandiaran L, González-Palacios S, Vioque J. Olive oil consumption and all-cause, cardiovascular and cancer mortality in an adult mediterranean population in Spain. Front Nutr. 2022 Aug 30;9:997975. doi: 10.3389/fnut.2022.997975. PMID: 36110407; PMCID: PMC9468703.

Attached Files

•  fnut-09-997975-g001-2.jpg   64.06KB   0 downloads

Edited by QuestforLife, 20 October 2022 - 09:21 PM.

[QuestforLife]

You lose the ability to burn fats if you lack proper anti-oxidants, as seen by the benefits of the GlyNAC trial [1]

 

In our earlier studies, we discovered and reported that inducing GSH deficiency results in impaired mitochondrial fatty-acid oxidation. This suggests that
GSH adequacy is critically necessary for adequate mitochondrial fatty-acid oxidation (17). The OA in our RCT had both impaired mitochondrial fatty-acid oxidation and elevated mitochondrial glucose oxidation. This indicates mitochondrial dysfunction. The full extent of the age-associated mitochondrial impairment only became
clear when the molecular data were examined. Mitochondrial function was severely compromised on multiple levels, including ab-
normalities in mitochondrial biogenesis (PGC1α), nutrient sensors regulating fatty-acid entry into mitochondria (pAMPK/AMPK,
SirT3, CPT1b), mitochondrial β-oxidation of fatty-acids (HADHA, PPARα), electron transport chain complexes (I, II, III, V), ATP syn-
thesis (ATP5A), and mitophagy (PINK1). GlyNAC supplementation began to rapidly improve these defects in 2-weeks, but a longer dur-
ation of 16-weeks was needed to correct these defects.

 

Probably why C60 is so beneficial in Turnbuckle's protocol.

 

[1] Kumar P, Liu C, Suliburk J, Hsu JW, Muthupillai R, Jahoor F, Minard CG, Taffet GE, Sekhar RV. Supplementing Glycine and N-Acetylcysteine (GlyNAC) in Older Adults Improves Glutathione Deficiency, Oxidative Stress, Mitochondrial Dysfunction, Inflammation, Physical Function, and Aging Hallmarks: A Randomized Clinical Trial. J Gerontol A Biol Sci Med Sci. 2022 Aug 17:glac135. doi: 10.1093/gerona/glac135. Epub ahead of print. PMID: 35975308.

[Rocket]

Don't believe the studies. Trust me, they lie lie lie all the time. Anything beneficial is squelched with studies saying you'll die or there's no effect.

I am having great results with high dose c60.

I recently added methelyne blue.

[joesixpack]

Correction, rats weren't dosed daily for 7 months, but...
[1]

If my recollection is correct, the rats on C60 EVOO did the best, But the rats on just EVOO did pretty well too. I do not know if anyone ever followed up on the EVOO study, but I bet it would have been positive. The olive oil seems to be a big factor.