Hello, I’m Dr. Hocheol Shin, or “Dr. Shin.” I study feline kidney health and aging at Greycoat Research.

I earned my Ph.D. studying cancer and immunology, and I’m now building on that experience to explore how we can help cats stay healthier for longer.

In “Reading Papers with Dr. Shin,” we’ll explore research related to feline health together. We’ll look a little deeper into how things work, what the studies actually found, and what those findings might mean for our cats. I’ll explain any unfamiliar terms as we go.

Ready to open today’s paper with Lulu? 

< Three-Sentence Summary >

1. CoQ10 is an essential electron carrier in mitochondria, the cell’s power plants. Human studies have reported lower levels in some tissues with aging and lower circulating levels in patients with CKD.

2. In a human CKD trial, CoQ10 did not significantly change kidney function or exercise capacity, but it did alter some blood lipid markers. The researchers interpreted these findings as possible changes in fat metabolism; whether they translate into health benefits remains to be established.

3. CoQ10 is one of the ingredients in the Greycoat Research formulation. Alongside its role in energy metabolism, differences in absorption between forms and formulations deserve attention.

< Introduction >

So far in this series, we have explored how resveratrol and quercetin may influence inflammatory signaling and oxidative stress. Today, we start with how cells produce energy. Coenzyme Q10 (CoQ10) is an essential part of that process, carrying electrons through the cell’s power plants.

Most cells produce a substantial share of their energy in tiny power plants called mitochondria, and CoQ10 is one of the components they need. Your cat’s body makes it naturally, and it plays an important role in energy-demanding organs such as the heart and kidneys.

Two findings make CoQ10 interesting here. First, human studies have reported lower CoQ10 content in some tissues with aging. Second, lower circulating levels have been observed in people with CKD. That raises a natural question: could supplementation help? Today, we’ll look at what actually changed in the studies.

One point to flag upfront: direct clinical evidence for CoQ10 supplementation in cats with CKD is limited. This article mainly draws on human and mouse research, so we’ll distinguish what those studies found from what still needs to be established in cats.

< Background >

1. Mitochondria and CoQ10 — the cell’s power plant and its electron carrier

If a cell were a factory, mitochondria would be its power generators, using oxygen to turn energy from food into a form the cell can use: ATP. The electron transport chain is part of this process. CoQ10 carries electrons from complexes I and II, among other sources, to complex III. Think of it as a courier that keeps electrons moving through the plant. A shortage can disrupt energy production and the control of oxidative stress.

2. Why age and kidney disease matter

Tissue CoQ10 content does not stay constant throughout life. Human studies have found lower levels in older age than in early adulthood in organs such as the heart and kidneys. Lower circulating CoQ10 and mitochondrial dysfunction have also been reported in people with CKD. These findings give us a reason to investigate CoQ10 in older cats, but whether the same changes occur in cats needs to be established separately.

3. The connection back to our earlier switches

Interestingly, CoQ10 is also being studied in connection with the pathways that regulate cellular energy metabolism. These include SIRT1, which we met in the resveratrol and quercetin articles, and PGC-1α, which helps regulate mitochondrial biogenesis and function. A mouse study we’ll discuss below offers one example of this connection.

< Main Study: CoQ10 in Human CKD  >

Ahmadi A et al. Randomized crossover clinical trial of coenzyme Q10 and nicotinamide riboside in chronic kidney disease. JCI Insight 2023.

Our main paper is a randomized, double-blind, placebo-controlled trial of CoQ10 supplementation in people with CKD.

Study Design

This was a randomized, double-blind, placebo-controlled crossover trial (the “CoNR” trial) in 25 patients with CKD (mean eGFR 36.9 mL/min/1.73 m²). Each participant went through three 6-week phases — placebo, CoQ10 (1,200 mg/day), and nicotinamide riboside (NR, an NAD+ precursor, 1,000 mg/day) — separated by washout periods. Researchers measured exercise capacity, kidney function, inflammation, and detailed plasma metabolomics and lipidomics. These were the doses used in this human trial, not feeding doses for cats.

Key Results

It helps to separate the exercise and kidney-function results from the exploratory metabolic and lipid findings.

Measures with no significant change compared with placebo:

• Aerobic exercise capacity (VO₂peak), total work, and total work efficiency
• Kidney-related markers — eGFR, serum creatinine, cystatin C, and urine albumin-to-creatinine ratio (UACR)
• Inflammatory marker — CRP

Changes observed in the exploratory metabolomics and lipidomics analyses:

• Compared with placebo, some free fatty acid species increased by roughly 19% to 40%, while some triglyceride species decreased by roughly 19% to 66%. The triglycerides that decreased tended to have long chains and a high degree of unsaturation. These percentages do not describe a change in the total triglyceride concentration measured on a routine blood panel.
• The ketone body 3-hydroxybutyrate, which is associated with fatty acid oxidation, was numerically about 41% higher, but the difference was not statistically significant (p=0.07).
• The researchers interpreted these patterns as suggesting possible improvement in β-oxidation, the process of breaking down fatty acids for energy. This was an inference from circulating markers, however, and the lipidomics analysis was not adjusted for multiple comparisons. The findings need further confirmation.

Plasma CoQ10 increased significantly. Supplementation was generally well tolerated during the study, with no serious adverse effects reported. A rise in blood levels does not, by itself, establish that a tissue-level shortage has been corrected.

Why This Matters

This is the key distinction. Six weeks of CoQ10 did not produce a significant improvement in kidney function or exercise capacity. Some circulating metabolic and lipid markers did change. Those findings give us clues about how CoQ10 might influence energy metabolism, but a change in markers alone does not establish a healthier internal environment or a kidney-protective effect. 

< Supporting Evidence: Aging and Delivery  >

1. CoQ10 declines with age in some human tissues

Kalén A, Appelkvist EL, Dallner G. Age-related changes in the lipid compositions of rat and human tissues. Lipids 1989.

This classic study measured CoQ10 in several organs from people of different ages, from infancy to old age. In the heart, kidneys, and several other organs, the highest values were observed around age 20, with lower values in older age groups. This supports investigating the relationship between aging and CoQ10, but does not establish that supplementation necessarily benefits older individuals.

2. Not all CoQ10 is absorbed equally — the delivery problem 

Langsjoen PH, Langsjoen AM. Comparison study of plasma CoQ10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clin Pharmacol Drug Dev 2014.

CoQ10 is fat-soluble and can be difficult to absorb. It comes in two forms: ubiquinone (oxidized) and ubiquinol (reduced). In this study, 12 healthy adults took each form at 200 mg/day for four weeks. Using softgel formulations with matched excipients, plasma total CoQ10 rose from a baseline of about 0.9 µg/mL to about 2.5 µg/mL after ubiquinone and 4.3 µg/mL after ubiquinol. Ubiquinol produced a larger rise under these study conditions. That gives us a reason to pay attention to form and formulation, but does not establish the same difference for every product or in cats.

3. The link to SIRT1 and mitochondrial regulation

Tian G et al. Ubiquinol-10 supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice. Antioxid Redox Signal 2014.

This study supplemented ubiquinol-10 in SAMP1 mice, a model of accelerated aging. The researchers observed that age-related declines in the expression of SIRT1, PGC-1α, and related factors in the liver were attenuated in supplemented mice. They also examined changes involving mitochondrial function and antioxidant defenses. This provides a link between CoQ10 and the regulatory pathways discussed in our earlier articles. It remains a finding from a specific form of CoQ10 in an accelerated-aging mouse model, not evidence of the same effects in feline kidneys.

< Limitations >

There are several limits to keep in mind when relating these studies to cats.

• Direct clinical evidence for CoQ10 supplementation in cats with CKD is limited. The kidney-related clinical results discussed here come from humans.
  
  
• This human CKD trial found no significant changes in kidney function, exercise capacity, or CRP. Whether the metabolic and lipid changes translate into health benefits remains unclear.
  
  
• The trial was small (25 participants), and each treatment period lasted only six weeks, limiting conclusions about longer-term effects.
  
  
• Human and feline physiology differ. Evidence is also insufficient to establish an effective dose, pharmacokinetics, or long-term safety in cats with CKD.
  
  
• The lipidomics findings were exploratory and not adjusted for multiple comparisons. Changes in human blood levels or mechanisms observed in mice do not directly establish tissue-level effects in cats.
  
  

< Personal Thoughts >

CoQ10 is essential to cellular energy production. For someone studying kidney health and aging, that naturally raises an appealing question: if the body depends on it, could providing more be helpful? In this human trial, however, supplementation did not significantly improve kidney function. Being essential to the body does not, by itself, establish the benefits of taking more.

What caught my attention nonetheless was the shift in certain blood lipid measures. The researchers interpreted this pattern as a possible sign of changes in how the body uses fat for energy. It is too early to say whether those changes translate into better health, but they offer a reason to look more closely at CoQ10’s effects on energy metabolism. The mouse study involving SIRT1 and PGC-1α adds another piece to that discussion. What interests me is when, and under what conditions, these metabolic changes might lead to meaningful benefits—and whether similar possibilities exist in cats.

There is another question worth asking: how much of the CoQ10 we give actually reaches the body? The amount listed on a label is a starting point. Its form and formulation can also influence absorption, which is why I included the human study comparing different forms of CoQ10.

We take the same perspective on the CoQ10 included in the Greycoat Research formula. I believe our questions should extend beyond why an ingredient belongs in a formula to how it is delivered and what role it might play in a cat’s body. The human and mouse studies discussed here do not establish the absorption or efficacy of our formula. They do, however, help make the next research questions more specific. Those are the questions I want to follow as we explore where CoQ10 might fit into supportive care for cats.

The findings discussed in this article reflect associations, mechanisms, and early translational evidence rather than confirmed efficacy in cats with kidney disease. Please consult a veterinarian before starting any supplementation protocol.

< References >

1.  Ahmadi A, Begue G, Valencia AP, et al. Randomized crossover clinical trial of coenzyme Q10 and nicotinamide riboside in chronic kidney disease. JCI Insight. 2023;8(11):e167274.

2.  Kalén A, Appelkvist EL, Dallner G. Age-related changes in the lipid compositions of rat and human tissues. Lipids. 1989;24(7):579-584.

3.  Langsjoen PH, Langsjoen AM. Comparison study of plasma coenzyme Q10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clin Pharmacol Drug Dev. 2014;3(1):13-17.

4.  Tian G, Sawashita J, Kubo H, et al. Ubiquinol-10 supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice. Antioxid Redox Signal. 2014;20(16):2606–2620. doi:10.1089/ars.2013.5406.

 < About the Author >

Hocheol Shin, Ph.D.

B.S./M.S./Ph.D. in Biological Sciences, KAIST (Korea Advanced Institute of Science and Technology)

Research background in cancer immunology, tumor microenvironment, and translational oncology. Currently engaged in companion animal health and longevity research.

[Educational Disclaimer]

This article is for educational purposes only and is not a substitute for professional veterinary advice, diagnosis, or treatment. It is not intended to diagnose, treat, cure, or prevent any disease.

Please consult your veterinarian before making changes to your cat’s diet, supplements, or care routine.