Healthy aging in dogs and cats:
hallmarks of aging, kidney jing weakness and the integrative protocol
Aging is not an inevitable decay but a process that you can understand and support. From telomere shortening and mitochondrial depletion to inflammaging and microbiome dysbiosis. And how traditional Chinese medicine has described the aging process for centuries as Kidney Jing weakness. Two perspectives on the same biological fact.
By Stefan Veenstra DVM
Aging as a biological process: the hallmarks of aging
Biologically speaking, aging is not a disease but a progressive decline in cellular repair capacity, mitochondrial efficiency, and immune regulation. In 2013, López-Otín et al. described the hallmarks of aging: the molecular and cellular characteristics that universally underlie aging. In 2022, this framework was expanded to twelve hallmarks, with explicit addition of microbiome dysbiosis and chronic inflammation. In dogs and cats, these hallmarks are identical to those in humans, with one striking difference: dogs lose telomeric DNA about ten times faster than humans, corresponding to the ratio of average lifespan between the two species.
Starting support early is more effective than waiting for visible complaints. In large breeds, cellular aging starts around three to four years of age. In small breeds around five to six years. Biology does not wait for visible symptoms.
The twelve hallmarks explained
Telomeres are the protective end pieces of chromosomes that shorten slightly with each cell division. Once telomeres reach a critical length, the cell stops dividing or goes into senescence. Telomere length correlates strongly with average lifespan across different dog breeds. Resveratrol activates SIRT1, a NAD+-dependent enzyme that supports telomere integrity and stimulates telomerase production. Ergothioneine protects telomere DNA from oxidative damage by ROS, the primary cause of accelerated telomere shortening.
Mitochondria are the cell’s energy factories. With age, mitochondrial efficiency decreases due to accumulation of mutations in mitochondrial DNA, decrease in mitophagy (clearance of damaged mitochondria), and decrease in NAD+ levels. NAD+ is essential as a cofactor for the mitochondrial respiratory chain and for sirtuins, the longevity proteins that regulate metabolism, DNA repair, and mitochondrial biogenesis. Cellular senescence and NAD+ depletion are both well-established molecular hallmarks of aging and manipulation of both processes has been shown to improve or worsen the aging phenotype. CoQ10 is the essential electron carrier in complex I and II of the respiratory chain and declines significantly with age.
Senescent cells are cells that have stopped dividing but are also not cleared through apoptosis. They accumulate with age and produce the Senescence-Associated Secretory Phenotype (SASP): a cocktail of pro-inflammatory cytokines that damage surrounding healthy cells and fuel systemic inflammation. Quercetin is a plant-derived flavonoid that acts as a senolytic via inhibition of anti-apoptotic proteins (BCL-2 family), selectively clearing senescent cells. Senolytics are a promising anti-aging strategy by targeting senescent cells; reduction in senescence reduces age-related pathology and extends lifespan in vivo in multiple models.
Inflammaging is the term for the chronic, low-grade inflammatory state associated with aging and was explicitly included as a hallmark in 2022. It is not acute inflammation but a permanent background activation of the immune system that accelerates all aging processes: it feeds SASP from senescent cells, damages mitochondria, increases the risk of cancer and neurodegeneration, and accelerates joint breakdown. Curcumin inhibits NF-kB, the central transcription factor of inflammaging, on multiple levels at once. MSM/quercetin inhibits additional pathways via NF-kB and direct antioxidant activity.
The epigenome, methylation patterns, and histone modifications that determine which genes are active change systematically with age. SIRT1 is a NAD+-dependent histone deacetylase with multiple protein substrates and a key epigenetic regulator; it regulates DNA repair, apoptosis, mitochondrial biogenesis, and cellular stress response. Resveratrol activates SIRT1 instantly. NAD+ precursors in Longevity Support increase the NAD+ availability that SIRT1 needs as a cofactor. Loss of proteostasis, the quality control of proteins, leads to accumulation of misfolded proteins that drive neurodegenerative processes.
Microbiome dysbiosis was explicitly added in 2022 as a hallmark of aging. With age, microbiome diversity structurally declines: commensal, protective strains decrease while pro-inflammatory, opportunistic bacteria increase. This enhances inflammaging via increased LPS production and decreased production of protective short-chain fatty acids. The gut-brain axis and the gut immune axis are both affected. In older animals with chronic complaints, the Intestinal Protocol is therefore the structural basis on which the aging protocol has the most effect.
DNA damage accumulates with age as repair mechanisms become less efficient. Each cell experiences tens of thousands of DNA lesions per day. In young cells, these are largely repaired via basal excision repair, homologous recombination, and other DNA repair pathways. As NAD+ levels drop, PARP enzymes (which use NAD+ as a cofactor) lose efficiency as DNA repairers. SIRT1 and SIRT6 are NAD+-dependent sirgardens that stabilize chromatin structure and coordinate DNA repair. Longevity Support increases NAD+ availability and activates sirtuins via resveratrol that monitor genomic stability. Glutathione neutralizes reactive oxygen species that are the main cause of oxidative DNA damage.
Tissue repair relies on stem cells that can replace damaged cells. With age, both the number and the function of tissue’s own stem cells in bone marrow, intestine, muscles and brain decrease. NAD+ depletion and mitochondrial dysfunction are direct causes of stem cell depletion: stem cells have a high energy expenditure and are particularly susceptible to mitochondrial decline. Resveratrol and NAD+ precursors activate mitochondrial biogenesis in stem cells via SIRT1 and SIRT3 and improve their self-renewal capacity. This is partly the explanation why older animals recover more slowly from illness, surgery or tissue damage.
Cells communicate through hormones, cytokines, growth factors, and extracellular vesicles. With aging, this communication network is disrupted: pro-inflammatory signals dominate (SASP of senescent cells), protective growth factors such as IGF-1 and NGF decrease, and endocrine coordination between organs weakens. This directly contributes to inflammaging and to the systemic deterioration caused not by one organ but by the failure of intercellular coordination. Curcumin inhibits SASP signaling via NF-kB. Myco Immune Complex modulates macrophage polarization via beta-glucans and restores the balance between pro- and anti-inflammatory intercellular signals.
Cells have systems that detect nutritional status and coordinate cell growth, metabolism, and maintenance: mTOR (stimulates growth in food abundance), AMPK (activates catabolism and maintenance in energy deficit), and the IGF-1 signaling pathway. With aging, mTOR becomes chronically overactivated, even with calorie restriction, which suppresses autophagy (cellular clearing process) and promotes protein accumulation. Resveratrol activates SIRT1 and AMPK and indirectly inhibits mTOR, which stimulates autophagy. Calorie reduction and intermittent fasting are the most powerful interventions for mTOR modulation. Curcumin directly inhibits mTOR via PI3K/Akt inhibition. A protein-rich but low-carbohydrate diet also supports these nutrient systems at the nutritional level.
Joint breakdown in older animals results from multiple aging processes at once: inflammaging activates MMP enzymes that break down cartilage, mitochondrial depletion in chondrocytes reduces repair capacity, and senescent cells in the joint tissue feed chronic synovial inflammation. Stiffness, difficulty getting up and reluctant movement are the most visible signs of aging in dogs and one of the main reasons why owners seek help.
Canine cognitive dysfunction syndrome (CDS) is the veterinary equivalent of Alzheimer’s in humans and shares the same neuropathological features: amyloid-beta deposition, tau pathology, and mitochondrial depletion in neurons. Lion’s Mane (Hericium erinaceus) stimulates the production of Nerve Growth Factor (NGF), the neurotrophin that supports neuronal plasticity, survival and synaptic connections. NGF decline is an early feature of neurodegeneration. Adaptogen Complex modulates the HPA axis and cortisol reactivity that is chronically dysregulated in CDS and accelerates hippocampal atrophy.
Simon et al. (2024) — Double-blind placebo-controlled RCT in 70 senior dogs with mild to moderate cognitive decline: combination of NAD+ precursor and senolytics (quercetin) resulted in significant improvement in owner-reported cognitive function on the CCDR scale. Nature Scientific Reports, doi:10.1038/s41598-024-63031-w.
Stress, anxiety and aging: the HPA axis as an accelerator
Chronic stress accelerates aging at every level. Cortisol damages the hippocampus, the brain region essential for learning, memory, and emotion regulation. Chronically elevated cortisol levels accelerate telomere shortening, increase inflammaging via NF-kB activation, and damage the gut barrier. Older animals that are also anxious or chronically stressed age faster than peers in a low-stress environment. The HPA axis becomes a self-reinforcing cycle: anxiety increases cortisol, cortisol accelerates hippocampal atrophy, hippocampal atrophy decreases cortisol regulation and increases anxiety reactivity.
Adaptogen Complex in the cognition block of the aging protocol addresses exactly this pathway: ashwagandha modulates the HPA axis via GABA-A receptor activation in the hypothalamus and structurally lowers cortisol reactivity. This protects the hippocampus and slows down the stress-related component of cognitive aging.
The Perspective of Traditional Chinese Medicine: Kidney Jing and Kidney Yin Weakness
Traditional Chinese medicine (TCM) describes aging as a progressive depletion of the life essence stored in the Kidney. This is not a metaphor but a clinically useful diagnostic framework that has been refined for more than two thousand years and that is receiving renewed attention in integrative veterinary medicine.
The kidney in TCM is not the same as the anatomical kidney. The Kidney is the organ system that stores Jing (essence), manages growth and reproduction, nourishes bones, produces the marrow (including spinal cord and brain), nourishes the hair, and forms the energetic foundation of all other organ systems. Aging is primarily seen in TCM as exhaustion of Kidney Jing: the innate life essence that is present at birth and progressively decreases.
Kidney Jing weakness: the essence is running out
Kidney Jing is the deepest layer of vital essence. It determines constitutional strength, vitality, reproductive capacity and longevity. Jing runs out slowly and can be partially replenished through diet, rest, and a regular life. Excessive stress, chronic illness, improper diet, and too little rest accelerate Jing’s exhaustion. Clinically, we see weakness in a Kidney Jing: early aging, premature gray hair, bone and cartilage weakening, hearing loss, mental decline, reduced vitality and reproductive capacity, and in cats often premature renal insufficiency. The parallel with the Western hallmarks of aging (telomere shortening, mitochondrial exhaustion, cognitive decline) is unmistakable.
Kidney Yin weakness: the cooling essence is depleted
Kidney Yin represents the cooling, nourishing and moisturizing function of the Kidney system. Exhaustion of Kidney Yin leads to relative heat patterns: internal heat, dryness, agitation, panting with no apparent cause, restless sleep at night, thirsty animals, dry fur and skin, and a red tongue. Kidney Yin weakness manifests as internal heat, dryness, anxiety, and panting and is common in senior animals with kidney problems. In Western biology, this corresponds to chronic oxidative stress, inflammaging, and ANS dysregulation that disrupts thermoregulation. In senior cats, Kidney Yin weakness is one of the most common TCM patterns, closely intertwined with chronic renal insufficiency.
Kidney Yang weakness: the fire is going out
Kidney Yang is the warming, activating force. Exhaustion of Kidney Yang leads to cold patterns: fatigue, lethargy, cold limbs, slow metabolism, tendency to gain weight, diarrhea with undigested food and a pale tongue. In Western terms: mitochondrial exhaustion, thyroid suppression and autonomic dysregulation. Yang weakness and Jing weakness overlap in older animals: the fire (Yang) that keeps the Jing essence warm and moving also becomes depleted as Jing descends.
Kidney Jing was weak in Western biology: the parallels are remarkably accurate. Jing depletion = telomere shortening + NAD+ depletion + loss of stem cell reserves. Renal Yin weakness = oxidative stress + inflammaging + ANS dysregulation (relative sympathetic activation). Kidney Yang weakness = mitochondrial dysfunction + metabolic slowdown + thyroid hypoactivity. TCM provides an integrated diagnostic framework for what Western biology describes as separate hallmarks.
Fowler M. (2020) — Traditional Chinese Veterinary Medicine to Treat Kidney Jing Deficiency: Clinical Case and Theoretical Framework for TCVM Treatment of Kidney Jing Weakness via Nutritional Therapy and Herbal Medicine. American Journal of Traditional Chinese Veterinary Medicine.
When to start? Age Timeline by Race
Starting early is the most effective principle in longevity medicine. Preventive use in middle age gives more results than curative use in advanced age-related complaints. Biologically speaking, this makes sense: telomeres are easier to protect than to repair, mitochondria are easier to maintain than to rebuild, and inflammaging is easier to inhibit than to reverse.
Starting from 3 years old. Biological aging starts early due to high growth factor exposure and short lifespan.
Starting from 4-5 years. Combine base coat with joint protocol in breeds with dysplasia predisposition.
Starting from 7-8 years. In cats, extra attention is paid to Kidney Yin weakness signs such as panting and thirst.
Start immediately regardless of age. Add a cognitive layer to CDS drawings. Bowel protocol as a basis for chronic complaints.
The protocol: base layer and additional layers
Base layer: always start
Longevity Support provides NAD+ precursors for mitochondrial energy production and sirtuin activation, resveratrol for SIRT1 activation and telomere protection, and ergothioneine for oxidative protection of mitochondrial DNA. Liposomal Coenzyme Q10 supports the mitochondrial respiratory chain synergistically with Longevity Support: NAD+ and CoQ10 act at complementary points in the electron transport chain. Liposomal Curcumin inhibits inflammation via NF-kB on multiple levels. Histamine Balance provides quercetin as senolytics for senescent cell clearance and MSM for cartilage and collagen building. Liposomal Glutathione protects cells and liver from oxidative aging damage and supports mitochondrial redox balance.
Supplement for joint complaints
Mobility Support, PEA Complex and O-Mega Blend. This is the complete Joint Protocol in addition to the base layer.
Supplementation in case of cognitive decline
Myco Adaptogen Complex delivers Lion’s Mane for NGF stimulation and neuronal plasticity, and Reishi for immune modulation and calming of the chronically stressed hippocampus. Myco Immune Complex modulates the immune system via beta-glucans: in CDS, systemic inflammation is a direct driver of neurodegeneration. Adaptogen Complex modulates the HPA axis and protects the hippocampus from cortisol damage.
“Aging in dogs is not a different biology than in humans. The same hallmarks, the same mechanisms, the same story, only told faster.” — Stefan Veenstra DVM
View the full NGD Care Aging Protocol
The base layer, additional layers per complaint and the comparison table with standard approach are on the product page. Personal advice via an intake with Stefan Veenstra via NatuurlijkGezondeDieren.nl.
Literature
- López-Otín et al. (2013/2022). The hallmarks of aging. Cell, doi:10.1016/j.cell.2022.11.001.
- Simon et al. (2024). RCT NAD+ Precursor and Senolytics in Senior Dogs: Improving Cognitive Function. Nature Scientific Reports, doi:10.1038/s41598-024-63031-w.
- Fick et al. Telomere length correlates with average lifespan across dog breeds. Cited in: Canine aging review 2024. MDPI Cells, doi:10.3390/cells13242101.
- Canine aging review (2024). Dog aging: molecular, cellular and physiological processes. MDPI Cells, doi:10.3390/cells13242101.
- Revisiting hallmarks of aging in dogs (2024). PMC, doi:10.3390/cells13242101 — sirtuins, NAD+ and epigenetic regulation in dogs.
- Mori et al. (2021). Lion’s Mane and NGF Stimulation: Mechanistic Overview. International Journal of Medicinal Mushrooms.
- Gugliandolo et al. (2022). PEA in dogs with osteoarthritis. Veterinary Sciences, doi:10.3390/vetsci9020059.
- Fowler M. (2020). TCVM treatment for Kidney Jing weakness in dogs. American Journal of Traditional Chinese Veterinary Medicine.
- AHVMA (2023). Use of TCVM in chronic kidney disease dogs and cats: four cases. Journal AHVMA.
- McGowan et al. (2018). Cortisol and Hippocampal Function in Chronically Stressed Dogs. Physiology and Behavior, doi:10.1016/j.physbeh.2018.06.002.
- Dramard et al. (2023). Ashwagandha in anxious dogs: RCT eight weeks. Journal of Veterinary Behavior, doi:10.1016/j.jveb.2023.02.004.
- Romay et al. (2003). C-phycocyanin: antioxidant and NF-kB inhibiting properties. Current Protein and Peptide Science.
This article is educational in nature and does not replace a veterinary consultation. The Old Age Protocol is preventive and supportive in nature. For a personalized protocol based on age, breed and complaints: intake via NatuurlijkGezondeDieren.nl.