The World’s Most Powerful Science Backed Ingredient.
ElevATP®
ElevATP has made claims that the combination of Ancient Peat and Apple Polyphenols can significantly raise ATP levels in mitochondria (via the assumption that changes in ATP blood levels translate directly into increases in mitochondrial ATP) from a dose of 150mg. The key issue here is how does it do that since neither Ancient Peat nor Apply Polyphenols can be directly converted into ATP, the primary energy molecule in cells. They don’t even contain the necessary chemical structure to follow that conversion pathway.
In order for Ancient Peat or Apply Polyphenols to increase ATP levels, it would need to be through indirect influence on some other pathway that would require the utilization of some other ATP generating substrate to create the ATP. Those pathways were never identified and to date there is no credible scientific evidence to support claims that Ancient Peat or Apple Polyphenols can directly stimulate ATP production in any significant way. While some Company sponsored study evidence suggests some potential indirect benefits to energy metabolism, Ancient Peat and Apply Polyphenols are far from a direct ATP source like ketones (BHB).
This leads us to the conclusion that Ancient Peat and Apply Polyphenols are not macronutrients, contain no significant caloric energy and their ability to increase ATP levels is at best through a very indirect means.
Here’s a bit more detail:
- Lack of Direct ATP Energy Source: While peat and apple extracts do contain a variety of compounds, the primary carbohydrates of peat are cellulose, hemicellulose and lignin. These are long chain molecules that do not breakdown easily and what limited simple sugars that do remain are very small. Even if you were capable of extractions of simple sugars, harsh chemicals would be required to do the extraction.
Apple polyphenols themselves don’t contain glucose as part of their molecular structure. While apple polyphenols don’t directly yield glucose, they might have a very minor and indirect influence on blood glucose levels, while apple polyphenols aren’t a source of glucose themselves.
The key question is whether these specific compounds in ElevATP® have unique effects well beyond the substrate itself on triggering energy metabolism because the extracts themselves don’t have ATP producing capabilities. That pathway has not been discussed or shown in any of the company sponsored results.
ElevATP is not a direct ATP fuel source, leaving only the claim that somehow the extracts stimulate increased ATP production blood cells translating directly to mitochondrial ATP through an unknown pathway.
- Inability for Mitochondrial ATP Measurement: Increases in blood or general cellular ATP levels don’t necessarily translate into higher ATP within power-generating mitochondria of muscle cells. To definitively support that claim of improving mitochondrial ATP performance, researchers would need to measure ATP directly in muscle tissue during exercise. That was not shown. Since Ancient Peat and Apple Polyphenols contain no direct ATP generative pathway, it literally makes it impossible to calculate any level of comparable ATP yield that can easily be calculated from direct ATP macronutrient generative molecules like glucose, BHB and fatty acids.
- Unclear Mechanism of Action: The claim that it supports the body’s own ATP production is very vague. There is no support for this claim on how it supposedly achieves this in order to make a convincing scientific case. As of now, this remains speculative at best.
The reliance on company-sponsored studies without strong independent research raises validity concerns. Here’s what’s available:
- Company-Sponsored Studies: Most readily available studies on ElevATP are sponsored by the company that produces it (FutureCeuticals). While these studies might show some positive results, they inherently carry a potential bias and require a more critical lens.
- Lack of Independent University Research: We could not find independent, peer-reviewed University sponsored studies specifically focusing on the mechanism by which ElevATP supposedly increases mitochondrial ATP production.
- Vague Marketing Materials: ElevATP’s marketing materials are vague about how the combination of ancient peat and apple polyphenols achieve their claimed increases in mitochondrial ATP. Without a clearly stated, scientifically supported mechanism of action, it’s impossible to find targeted research from any universities on this subject matter.
BHB (Beta-Hydroxybutyrate)
BHB is the main powerhouse ketone body. Ketones convert directly to ATP with known metabolic and measurable pathways. It provides energy for the body, especially the brain, and it has been shown in numerous research papers how much brain energy impacts the improvement in physical performance and reduces disease. 1 BHB has a very different metabolic pathway than glucose.
Here is BHB:
- Direct Mitochondrial ATP Fuel: BHB can be directly used by mitochondria to generate ATP. This offers a potential advantage over glucose-dependent pathways during periods of high energy demand and low oxygenation, exhibited during high intensity exercise.2
- Potential Benefits: Some studies suggest that ketones also improve mitochondrial efficiency and cellular signaling pathways3, which could positively impact energy production, utilization and performance, while reducing Reactive Oxygen Species (ROS)4. This offers potential to put athletes into “The Zone” and enhance recovery.
- Growing Research Landscape: Research on BHB and athletic performance is massive and ongoing, with promising results. Just compare how many studies focus today on BHB versus ancient peat and apple polyphenols to get a glimpse where the scientific community is focused.
Where Things Stand
- ElevATP®: Peat and Polyphenols are not direct sources of ATP. The potential mechanism of action for ElevATP® is unclear and would require clarification in order to be seen as credible. Its claimed real-world performance benefits in athletes also would require validated third party study results to be considered conclusive.
Further, it isn’t appropriate to assume that increased blood level ATP translates to increased mitochondrial ATP, or in this case even muscle ATP under exercise conditions. There is a lack of scientific evidence demonstrating the product has a direct impact on actually boosting mitochondrial ATP production.
- BHB: BHB produces mitochondrial ATP directly. That statement of fact might be enough in comparing the capabilities of these two ingredients. The verified, large body of clinical research on BHB offers an authenticated and straightforward metabolic picture suggesting BHB is a preferred macronutrient fuel that produces measurable ATP energy directly in mitochondria.
BHB’s ability to produce mitochondrial ATP is definite and calculable. Its metabolic pathways are known. This is what makes BHB the impressive and unique molecule it is, and why it is considered the gold standard of cellular energy.
References:
- Ketone Bodies and Brain Metabolism: New Insights and Perspectives for Neurological Diseases, Wilfredo López-Ojeda , Ph.D., M.S., and Robin A. Hurley, M.D., F.A.N.P.A.Published Online:14 Apr 2023https://doi.org/10.1176/ appi.neuropsych.20230017
- Metabolism of Exogenous D-Beta-Hydroxybutyrate, an Energy Substrate Avidly Consumed by the Heart and Kidney Front. Nutr., 19 February 2020 Sec. Nutrition and Metabolism Volume 7 – 2020 | https://doi.org/10.3389/fnut.2020.00013
- Beta-Hydroxybutyrate: A Dual Function Molecular and Immunological Barrier Function Regulator Jiancheng Qi, 1 , † Linli Gan, 1 , † Jing Fang, 1 , † Jizong Zhang, 1 Xin Yu, 1 Hongrui Guo, 1 Dongjie Cai, 1 Hengmin Cui, 1Liping Gou, 1 Junliang Deng, 1 Zhisheng Wang, 2 and Zhicai Zuo 1 , https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC9243231/
- Ketones inhibit mitochondrial production of reactive oxygen species production following glutamate excitotoxicity by increasing NADH oxidation. Maalouf M 1, Sullivan PG, Davis L, Kim DY , Rho JM Author information Neuroscience, 18 Jan 2007, 145(1):256-264 https://doi.org/10.1016/j.neuroscience.2006.11.065 PMID: 17240074 PMCID: PMC1865572