R3 Restoring Cellular Energy ATP Acceleration and Mitochondria Support

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R3 – Restoring Cellular Energy

Restoring cellular energy is essential for optimal bodily function. Without enough energy, our cells cannot carry out their necessary functions like cellular detoxification. If allowed to build up, toxins disrupt cellular energy production, leading to fatigue, decreased cognitive function, thyroid problems, and other health problems.

Mitochondria – The Powerhouse Of The Cell

Mitochondria are often referred to as the powerhouse of the cell, and for good reason. These tiny organelles are responsible for producing adenosine triphosphate (ATP), which is the primary source of energy for cellular processes. Aside from being involved in energy production, mitochondria also play a crucial role in detoxification and epigenetic expression.1

Mitochondria ATP Production And Glutathione Detox The Cell

Glutathione is an essential antioxidant that plays a crucial role in maintaining our overall health. It is often referred to as the “master antioxidant” due to its ability to protect cells from damage caused by free radicals and toxins. It also plays a crucial role in detoxifying harmful substances within the cell.2

Glutathione requires a significant amount of ATP for its production. If we aren’t producing enough ATP, the production of glutathione will also decrease, leading to an imbalance in oxidative stress.3

When there is not enough glutathione to detoxify the cell, toxins and free radicals accumulate and cause damage. This damage leads to inflammation, which triggers the expression of harmful genes. Therefore, maintaining adequate levels of glutathione is crucial for preventing oxidative stress and minimizing the risk of various health conditions.4

Mitochondria – Detox And Epigenetic Expression

Mitochondria have a unique ability to store calcium ions, which are crucial for signaling processes involved in the detoxification of harmful molecules. They also contain enzymes that help break down toxins and other harmful substances.5

In addition to detoxification, mitochondria also have an impact on epigenetic expression. Epigenetics refers to changes in gene expression that do not involve alterations in the DNA sequence. These changes are influenced by various factors, including environmental conditions and lifestyle choices. Mitochondria contribute to this process by releasing signaling molecules that influences the activity of certain genes.6

One such signaling molecule is hydrogen peroxide, which is produced as a byproduct of ATP production. When released from mitochondria, it acts as a messenger to activate specific proteins involved in epigenetic regulation. Additionally, mitochondria also contain their own DNA, known as mitochondrial DNA (mtDNA), which has been shown to play a role in regulating gene expression.7 8

Interestingly, recent research has shown that alterations in mitochondrial function and mtDNA leads to changes in epigenetic patterns, contributing to the development of certain diseases. One of the main consequences of decreased mitochondrial ATP production is the activation of bad genes. These genes are usually turned off in young and healthy individuals but become activated when mitochondria fail to produce enough energy.9

In order to prevent this from happening, it is important to maintain healthy mitochondrial function. This can be achieved through a balanced diet, regular exercise, and avoiding harmful environmental factors such as pollution and toxins.

Restoring Cellular Energy - Mitochondria - Detox And Epigenetic Expression

Blood Hormone Levels Don’t Indicate How Well Hormones Function

The level of hormones in our blood is often used as an indicator of hormonal balance. However, it is important to note that what truly matters is not the blood levels of hormones, but rather, how they attach to receptors and relay messages into cells.10

The process of hormone-receptor binding is highly specific and each hormone can only bind to its corresponding receptor. This precise interaction ensures that the right message is delivered to the right cell at the right time, avoiding any potential errors or confusion.

The number and sensitivity of receptors also play a crucial role in hormone signaling. If there are not enough receptors or if they are less sensitive, the message may not be relayed effectively, leading to hormonal imbalances.11

Additionally, hormones have different effects depending on the target cell's type and location. For example, thyroid hormones may stimulate metabolism in one tissue, while promoting growth and development in another.12

Furthermore, hormonal signaling is not a one-way process, as it involves communication between the hormone-secreting gland and its target organs or feedback loops to maintain homeostasis.13

Cellular Energy And Hormone Dysfunction

When our cellular energy levels are low, it can lead to problems with hormone production and transportation. This means that even if our body is producing adequate amounts of hormones, they may not be able to properly attach to their receptors on cells and carry out their functions effectively.

Studies have shown that chronic inflammation interferes with hormone receptor function. Inflammation in tissues surrounding hormone receptors blocks their ability to bind to hormones, resulting in disrupted signaling and impaired hormone function. This is particularly relevant in conditions such as autoimmune diseases, where chronic inflammation targets specific tissues and causes damage.14

This can result in hormonal imbalances, which can manifest as symptoms like fatigue, weight gain, irregular menstrual cycles, mood swings, and many others. If left unmanaged, these imbalances often worsen over time and lead to serious health issues.15

The Results Of Hormone Dysfunction – Weight Gain

When there is an imbalance or dysfunction in hormones or their receptors, it can result in weight gain and difficulty in losing weight. For instance, studies have shown that individuals with hypothyroidism (an underactive thyroid gland) tend to have a slower metabolism, leading to weight gain. Similarly, imbalances in estrogen levels leads to increased fat storage, especially around the abdomen.16 17

On the other hand, insulin resistance, a condition where the body is unable to respond properly to insulin, leads to weight gain and difficulty in losing weight. This is because insulin plays a vital role in regulating fat metabolism and storing excess glucose as fat.18

In addition, testosterone levels also play a significant role in maintaining an optimal weight. Low levels of testosterone have been linked to an increase in body fat and difficulty in losing weight, particularly in men.19

How Come I Can’t Lose Weight Even Though I Diet And Exercise?

Many people focus solely on diet and exercise when trying to lose weight, but if the hormones are not functioning properly, these efforts are in vain.

As mentioned previously, insulin plays a significant role in weight loss. When we consistently consume a diet high in refined carbohydrates and sugars, our body produces more insulin than necessary, which can eventually lead to insulin resistance. This means that the cells become less responsive to insulin's message, and as a result, the body stores more fat.20

Another hormone that impacts weight loss is cortisol. Cortisol is known as the stress hormone and is released by the body in response to stress. When we experience chronic, ongoing stress, our cortisol levels remain elevated, leading to an increase in appetite and cravings for unhealthy foods. It also causes the body to store more fat, particularly in the abdominal area.21

Furthermore, hormones like leptin and ghrelin, known as hunger hormones, play a role in our appetite and food intake. Leptin signals to the brain when we are full and should stop eating, while ghrelin stimulates our appetite. When these hormones are imbalanced, it leads to overeating and weight gain.22

Restoring Cellular Energy - Hormone Imbalances

Restoring Cellular Energy – Optimizing Mitochondrial Function

There are steps we can take to improve mitochondrial function and restore cellular energy after we have already removed toxins from our life discussed in R1 and regenerated the cellular membrane discussed in R2.

Mitochondria Optimization And The Proper Diet

Mitochondria require a variety of nutrients to function optimally. These include B vitamins, magnesium, iron, and zinc. Eating a balanced diet that includes plenty of fruits, vegetables, grass-fed meat, fish rich in omega-3 fatty acids, nuts, and seeds ensure that your mitochondria have the necessary resources to produce ATP.23

Read more about my Cellular Healing Diet.

Mitochondria Optimization And Exercise

Regular physical activity has been shown to increase mitochondrial biogenesis, which is the creation of new mitochondria in cells. This means more powerhouses in your cells. Aim for at least 30 minutes of moderate exercise per day, such as brisk walking, cycling or swimming.24

Additionally, perform HIIT exercise for maximal mitochondrial biogenesis. HIIT workouts involve alternating periods of intense exercise with short rest periods, challenging the body to work at high intensity levels and promoting improvements in cardiovascular endurance and muscle strength.25

Mitochondria Optimization And Stress Reduction

Chronic stress leads to the production of free radicals, which damage mitochondria and affect their function. Finding ways to manage stress, such as meditation, yoga or deep breathing exercises, helps protect your mitochondria from oxidative damage.26

Mitochondria Optimization And Adequate Sleep

Sleep is crucial for cellular energy production and the repair and maintenance of mitochondria. Aim for 7-9 hours of quality sleep per night to allow your cells enough time to rest and recharge.27

R3 – Restoring Cellular Energy

After R3 – Restoring Cellular Energy, R2 – Regenerating The Cellular Membrane, and R1 – Removing The Source Of Toxins, it’s time to move onto the next step.

R4 – Reducing Cellular Inflammation


1 Cooper GM. The Cell: A Molecular Approach. 2nd edition. Sunderland (MA): Sinauer Associates; 2000. Mitochondria. Available from: https://www.ncbi.nlm.nih.gov/books/NBK9896/

2 Wu G, Fang YZ, Yang S, Lupton JR, Turner ND. Glutathione metabolism and its implications for health. J Nutr. 2004 Mar;134(3):489-92. doi: 10.1093/jn/134.3.489. PMID: 14988435.

3 Minich DM, Brown BI. A Review of Dietary (Phyto)Nutrients for Glutathione Support. Nutrients. 2019 Sep 3;11(9):2073. doi: 10.3390/nu11092073. PMID: 31484368; PMCID: PMC6770193.

4 Perricone C, De Carolis C, Perricone R. Glutathione: a key player in autoimmunity. Autoimmun Rev. 2009 Jul;8(8):697-701. doi: 10.1016/j.autrev.2009.02.020. Epub 2009 Feb 13. PMID: 19393193.

5 Xu Z, Zhang D, He X, Huang Y, Shao H. Transport of Calcium Ions into Mitochondria. Curr Genomics. 2016 Jun;17(3):215-9. doi: 10.2174/1389202917666160202215748. PMID: 27252588; PMCID: PMC4869008.

6 Santos JH. Mitochondria signaling to the epigenome: A novel role for an old organelle. Free Radic Biol Med. 2021 Jul;170:59-69. doi: 10.1016/j.freeradbiomed.2020.11.016. Epub 2020 Dec 1. PMID: 33271282; PMCID: PMC8166959.

7 Fang J, Wong HS, Brand MD. Production of superoxide and hydrogen peroxide in the mitochondrial matrix is dominated by site IQ of complex I in diverse cell lines. Redox Biol. 2020 Oct;37:101722. doi: 10.1016/j.redox.2020.101722. Epub 2020 Sep 14. PMID: 32971363; PMCID: PMC7511732.

8 Kotrys AV, Szczesny RJ. Mitochondrial Gene Expression and Beyond-Novel Aspects of Cellular Physiology. Cells. 2019 Dec 19;9(1):17. doi: 10.3390/cells9010017. PMID: 31861673; PMCID: PMC7017415.

9 Johnson TA, Jinnah HA, Kamatani N. Shortage of Cellular ATP as a Cause of Diseases and Strategies to Enhance ATP. Front Pharmacol. 2019 Feb 19;10:98. doi: 10.3389/fphar.2019.00098. PMID: 30837873; PMCID: PMC6390775.

10 Hiller-Sturmhöfel S, Bartke A. The endocrine system: an overview. Alcohol Health Res World. 1998;22(3):153-64. PMID: 15706790; PMCID: PMC6761896.

11 Hill M, Třískala Z, Honců P, Krejčí M, Kajzar J, Bičíková M, Ondřejíková L, Jandová D, Sterzl I. Aging, hormones and receptors. Physiol Res. 2020 Sep 30;69(Suppl 2):S255-S272. doi: 10.33549/physiolres.934523. PMID: 33094624; PMCID: PMC8603729.

12 Mendoza A, Hollenberg AN. New insights into thyroid hormone action. Pharmacol Ther. 2017 May;173:135-145. doi: 10.1016/j.pharmthera.2017.02.012. Epub 2017 Feb 4. PMID: 28174093; PMCID: PMC5407910.

13 Nussey S, Whitehead S. Endocrinology: An Integrated Approach. Oxford: BIOS Scientific Publishers; 2001. Chapter 1, Principles of endocrinology. Available from: https://www.ncbi.nlm.nih.gov/books/NBK20/

14 Straub RH. Interaction of the endocrine system with inflammation: a function of energy and volume regulation. Arthritis Res Ther. 2014 Feb 13;16(1):203. doi: 10.1186/ar4484. PMID: 24524669; PMCID: PMC3978663.

15 Lund J, Lund C, Morville T, Clemmensen C. The unidentified hormonal defense against weight gain. PLoS Biol. 2020 Feb 25;18(2):e3000629. doi: 10.1371/journal.pbio.3000629. PMID: 32097406; PMCID: PMC7041792.

16 Alidrisi HA, Odhaib SA, Altemimi MT, Mansour AA. Patterns of Bodyweight Changes in Patients With Hypothyroidism, a Retrospective Study From Basrah, Southern Iraq. Cureus. 2021 Jun 2;13(6):e15408. doi: 10.7759/cureus.15408. PMID: 34262799; PMCID: PMC8259075.

17 Vigil P, Meléndez J, Petkovic G, Del Río JP. The importance of estradiol for body weight regulation in women. Front Endocrinol (Lausanne). 2022 Nov 7;13:951186. doi: 10.3389/fendo.2022.951186. PMID: 36419765; PMCID: PMC9677105.

18 Verkouter I, Noordam R, le Cessie S, van Dam RM, Lamb HJ, Rosendaal FR, van Heemst D, de Mutsert R. The Association between Adult Weight Gain and Insulin Resistance at Middle Age: Mediation by Visceral Fat and Liver Fat. J Clin Med. 2019 Sep 28;8(10):1559. doi: 10.3390/jcm8101559. PMID: 31569345; PMCID: PMC6832997.

19 Fui MN, Dupuis P, Grossmann M. Lowered testosterone in male obesity: mechanisms, morbidity and management. Asian J Androl. 2014 Mar-Apr;16(2):223-31. doi: 10.4103/1008-682X.122365. PMID: 24407187; PMCID: PMC3955331.

20 Chiu CJ, Wray LA, Beverly EA. Relationship of glucose regulation to changes in weight: a systematic review and guide to future research. Diabetes Metab Res Rev. 2010 Jul;26(5):323-35. doi: 10.1002/dmrr.1095. PMID: 20578206.

21 Hewagalamulage SD, Lee TK, Clarke IJ, Henry BA. Stress, cortisol, and obesity: a role for cortisol responsiveness in identifying individuals prone to obesity. Domest Anim Endocrinol. 2016 Jul;56 Suppl:S112-20. doi: 10.1016/j.domaniend.2016.03.004. Epub 2016 Mar 31. PMID: 27345309.

22 Hajishizari S, Imani H, Mehranfar S, Saeed Yekaninejad M, Mirzababaei A, Clark CCT, Mirzaei K. The association of appetite and hormones (leptin, ghrelin, and Insulin) with resting metabolic rate in overweight/ obese women: a case-control study. BMC Nutr. 2022 Apr 29;8(1):37. doi: 10.1186/s40795-022-00531-w. PMID: 35484608; PMCID: PMC9052687.

23 Kyriazis ID, Vassi E, Alvanou M, Angelakis C, Skaperda Z, Tekos F, Garikipati VNS, Spandidos DA, Kouretas D. The impact of diet upon mitochondrial physiology (Review). Int J Mol Med. 2022 Nov;50(5):135. doi: 10.3892/ijmm.2022.5191. Epub 2022 Sep 21. PMID: 36129147; PMCID: PMC9542544.

24 Sorriento D, Di Vaia E, Iaccarino G. Physical Exercise: A Novel Tool to Protect Mitochondrial Health. Front Physiol. 2021 Apr 27;12:660068. doi: 10.3389/fphys.2021.660068. PMID: 33986694; PMCID: PMC8110831.

25 Atakan MM, Li Y, Koşar ŞN, Turnagöl HH, Yan X. Evidence-Based Effects of High-Intensity Interval Training on Exercise Capacity and Health: A Review with Historical Perspective. Int J Environ Res Public Health. 2021 Jul 5;18(13):7201. doi: 10.3390/ijerph18137201. PMID: 34281138; PMCID: PMC8294064.

26 Picard M, McEwen BS. Psychological Stress and Mitochondria: A Systematic Review. Psychosom Med. 2018 Feb/Mar;80(2):141-153. doi: 10.1097/PSY.0000000000000545. PMID: 29389736; PMCID: PMC5901654.

27 Melhuish Beaupre LM, Brown GM, Braganza NA, Kennedy JL, Gonçalves VF. Mitochondria's role in sleep: Novel insights from sleep deprivation and restriction studies. World J Biol Psychiatry. 2022 Jan;23(1):1-13. doi: 10.1080/15622975.2021.1907723. Epub 2021 May 6. PMID: 33821750.