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Longevity isn't about living to 100. It's about living fully at 60, 70, 80 with energy, clarity, and a body that still feels like yours.
Here's what I've come to believe after years of health coaching, evidence-based nutrition and health science, and my own deep dive into functional nutrition medicine: most people are fighting aging at the surface level. They're optimizing sleep, hitting the gym, eating well—and those things absolutely matter. But underneath all of that, there are cellular processes quietly deteriorating that no amount of kale or cardio can fully address on their own.
This is my personal suggested framework for longevity: eight pillars, some cutting-edge, some beautifully boring, all working together.
Pillar 1: Cellular energy
NAD+: The cellular currency you're running low on
If I had to pick one molecule at the center of the longevity conversation, it's NAD+ (nicotinamide adenine dinucleotide). It drives energy metabolism, DNA repair, mitochondrial health, and the activation of sirtuins, which are proteins that are essentially nature's longevity regulators.
Here's the problem: you're losing it. By age 50, most people have roughly half the NAD+ they had in their 20s. By age 80, levels can fall to as low as 1–10% of youthful concentrations. And it's not just aging doing the damage; a sedentary lifestyle, highly processed foods, chronic stress, environmental toxins, and oxidative stress all accelerate that decline. In other words, the way most people live modern life is actively depleting the one molecule most responsible for how well their cells function and repair themselves.
Shed offers NAD+ in multiple forms—nasal spray, tablet, and injectable—because delivery is important and the right format depends on the person. What I personally love using alongside NAD+ is my own co-formulated supplement built around NAD+ and the cofactors that make it work harder:
- TMG (trimethylglycine) to support methylation and protect against homocysteine buildup
- Alpha GPC for cognitive support and acetylcholine production
- Methylated B12 and methylated folate because these are the bioavailable forms your cells can actually use
Most NAD+ supplements skip the upstream methylation support entirely. That's the gap I co-formulated Shed’s NAD+ Vitality Complex to fill.
At Shed, we offer NAD+ in the format that fits your lifestyle. Talk to your care team about what's right for you.
Pillar 2: Master antioxidant
Glutathione: Your body's primary defense against cellular aging
If NAD+ is the fuel that powers your cells, glutathione (GSH) is the shield that protects them. It's the most abundant endogenous antioxidant in the human body—and like NAD+, it declines with age, stress, and environmental load.
Aging is, in large part, a story of oxidative stress, an imbalance between the free radicals your cells generate and your body's capacity to neutralize them. When that balance tips, you get DNA damage, mitochondrial decay, and accelerated cellular aging. Glutathione is your primary defense mechanism against all of it.
Beyond fighting free radicals, glutathione recycles vitamins C and E, supports liver detoxification, modulates immune function, and protects against neuroinflammation. Research shows that glutathione deficiency in aging occurs not because the body stops wanting to produce it, but because the synthesis machinery slows down. The goal is to support that system consistently, not reactively.
Glutathione is available through Shed as part of our longevity support. Paired with NAD+, both products address cellular aging at the source.
Pillar 3: Metabolic and neuro longevity
Microdose GLP-1: The most underrated longevity tool in the conversation
Most people associate GLP-1 medications with weight loss. But what the research is revealing about low-dose GLP-1 receptor activation is genuinely compelling for anyone invested in their healthspan, regardless of where they are on their weight journey.
Microdosing GLP-1, which is roughly one-fifth of a standard therapeutic dose, isn't about appetite suppression or weight loss. It's about activating metabolic and neurological pathways that directly influence how we age. Insulin resistance is one of the most consistent hallmarks of aging, and low-dose GLP-1 activation has been shown to improve insulin sensitivity and stabilize blood glucose, both of which are critical for preserving cellular health over decades.
The brain piece might actually be the most exciting part. GLP-1 receptors aren't just in your gut, they're all over your brain. Early research suggests that GLP-1 activity may help clear out the sticky protein buildup linked to cognitive decline, calm inflammation in the brain, and strengthen the connections between neurons that keep your thinking sharp as you age.
And here's what makes the microdose angle interesting: because GLP-1 is originally a gut hormone, keeping low levels of it consistently active may also support a healthier gut microbiome and turn down the body's overall inflammatory "volume" over time, two things that matter enormously for long-term health.
The research in healthy adults is still developing. But the biology is sound, and the potential is real.
GLP-1 microdosing is always done under medical supervision with monitoring, not as a DIY biohack. Shed's microdose GLP-1 program is built for longevity and metabolic optimization. If you've hit your goals and you're asking what's next, this may be the answer.
Pillar 4: Environmental load
Audit your environment: The longevity variable we don’t talk about enough
You can do everything else on this list and still accelerate your biological age if you're living in a high-toxin environment. Not dramatically toxic—the quiet, cumulative kind most of us don't think about.
Endocrine disruptors, heavy metals, mold, pesticide residues, and synthetic off-gassing directly deplete glutathione, impair mitochondrial function, and drive the chronic inflammation that accelerates aging. The audit starts at home: your cookware, your cleaning products, your personal care products, your water, your air—especially the air in the room where you sleep eight hours a night.
Start here: filtered water, stainless or cast iron cookware, fragrance-free personal care, and an air purifier in your bedroom. These aren't biohacks. They're the unglamorous foundation that makes everything else work better. Check out https://www.ewg.org/ to learn more about your current environmental load.
Pillars 5–8: The non-negotiables
Exercise, sleep, water, and food: Where everything else lands or falls apart
The advanced tools work because the foundations are solid. NAD+ performs better when mitochondria aren't suppressed by dehydration. Glutathione is more available when the liver isn't overwhelmed. The GLP-1 signal lands more cleanly in a well-fed, well-rested body.
Exercise: Resistance training preserves muscle, the most underrated longevity organ. Zone 2 cardio builds mitochondrial density. Consistent, intentional movement activates many of the same longevity pathways as caloric restriction.
Sleep: This is when your brain clears metabolic waste via the glymphatic system, when growth hormone peaks, and when cellular repair happens. Chronic poor sleep accelerates cortisol, inflammation, insulin resistance, and cognitive decline. Seven to nine hours isn't a preference; it's a biological requirement.
Hydration: Every enzymatic reaction, every detox pathway, and every nutrient transport mechanism requires water. Dehydration at the cellular level accelerates every aging marker we track. Prioritize it with electrolytes if you're active.
Nutrition: Colorful vegetables deliver the polyphenols and phytonutrients that support your antioxidant pathways from the inside out. Protein preserves muscle and drives repair. Fermented, fibrous, prebiotic-rich foods keep the microbiome diverse, which influences everything from inflammation to brain health.
“Longevity isn't a destination—it's the cumulative result of daily decisions that either work for your biology or against it,” said Roseanne Schnell, Lead Dietitian and Nutritionist. “At the core is a simple but powerful premise: when you reduce chronic inflammation and support metabolic function, you're not just adding years to your life—you're adding life to your years. The Restore and Balance Anti-inflammatory Nutrition Plan is built around this reality. By prioritizing whole foods, a diversity of phytonutrients, a thriving gut microbiome, adequate omega-3 intake, and stable blood sugar, you're giving your body the raw materials it needs to repair, adapt, and perform—today and decades from now.”
This is what a longevity practice looks like
Not a single supplement. Not a 30-day fix. A layered, intentional approach, where foundations amplify the advanced tools, and the advanced tools protect what the foundations have built.
At Shed, our longevity offerings—NAD+, glutathione, and microdose GLP-1—are here because your health journey doesn't end at the goal. It deepens there.
Ready to explore what a longevity protocol looks like for you? Connect with your Shed care team or visit tryshed.com today to learn more.
This information is for educational purposes only and is not a substitute for medical advice. Please consult your healthcare provider before starting or changing any medication or supplement.
These statements have not been evaluated by the FDA. These products are not intended to diagnose, treat, cure, or prevent any disease.
Compounded medications are prepared by licensed pharmacies to meet individual patient needs. While they are not reviewed or approved by the FDA for safety or effectiveness, they are made in accordance with strict regulatory guidelines. Prescription is only available after consultation with a licensed provider to determine if treatment is appropriate.
References
Pillar 1: NAD+
Abdellatif, M., Sedej, S., Carmona-Gutierrez, D., Madeo, F., & Kroemer, G. (2021). NAD+ metabolism and its roles in cellular processes during ageing. Nature Reviews Molecular Cell Biology, 22(2), 119–141. https://doi.org/10.1038/s41580-020-00313-x
Braidy, N., Guillemin, G. J., Mansour, H., Chan-Ling, T., Poljak, A., & Grant, R. (2012). Age related changes in NAD+ metabolism, oxidative stress and SIRT1 activity in Wistar rats. PLOS ONE, 7(4), e42357. https://doi.org/10.1371/journal.pone.0042357
Camacho-Pereira, J., Tarragó, M. G., Chini, C. C. S., Nin, V., Escande, C., Warner, G. M., Puranik, A. S., Schoon, R. A., Reid, J. M., Galina, A., & Chini, E. N. (2016). CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metabolism, 23(6), 1127–1139. https://doi.org/10.1016/j.cmet.2016.05.006
Costford, S. R., Bajpeyi, S., Pasarica, M., Albarado, D. C., Thomas, S. C., Xie, H., Church, T. S., Jubrias, S. A., Conley, K. E., & Smith, S. R. (2010). Skeletal muscle NAMPT is induced by exercise in humans. American Journal of Physiology — Endocrinology and Metabolism, 298(1), E117–E126. https://doi.org/10.1152/ajpendo.00318.2009
Imai, S., & Guarente, L. (2014). NAD+ and sirtuins in aging and disease. Trends in Cell Biology, 24(8), 464–471. https://doi.org/10.1016/j.tcb.2014.04.002
Massudi, H., Grant, R., Braidy, N., Guest, J., Farnsworth, B., & Guillemin, G. J. (2012). Age-associated changes in oxidative stress and NAD+ metabolism in human tissue. PLOS ONE, 7(7), e42357. https://doi.org/10.1371/journal.pone.0042357
Rajman, L., Chwalek, K., & Sinclair, D. A. (2018). Therapeutic potential of NAD-boosting molecules: The in vivo evidence. Cell Metabolism, 27(3), 529–547. https://doi.org/10.1016/j.cmet.2018.02.011
Trammell, S. A., Schmidt, M. S., Weidemann, B. J., Redpath, P., Jaksch, F., Dellinger, R. W., Li, Z., Abel, E. D., Migaud, M. E., & Brenner, C. (2016). Nicotinamide riboside is uniquely and orally bioavailable in healthy humans. Nature Communications, 7, 12948. https://doi.org/10.1038/ncomms12948
Yoshino, J., Mills, K. F., Yoon, M. J., & Imai, S. (2011). Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metabolism, 14(4), 528–536. https://doi.org/10.1016/j.cmet.2011.08.014
Pillar 2: Glutathione
Lizzo, G., Migliavacca, E., Lamers, D., Frézal, A., Corthesy, J., Vinyes-Parès, G., Bosco, N., Karagounis, L. G., Hövelmann, U., Heise, T., von Eynatten, M., & Gut, P. (2022). A randomized controlled clinical trial in healthy older adults to determine efficacy of glycine and N-acetylcysteine supplementation on glutathione redox status and oxidative damage. Frontiers in Aging, 3, 852569. https://doi.org/10.3389/fragi.2022.852569
Sekhar, R. V., Patel, S. G., Guthikonda, A. P., Reid, M., Balasubramanyam, A., Taffet, G. E., & Jahoor, F. (2011). Deficient synthesis of glutathione underlies oxidative stress in aging and can be corrected by dietary cysteine and glycine supplementation. American Journal of Clinical Nutrition, 94(3), 847–853. https://doi.org/10.3945/ajcn.111.014498
Suh, J. H., Shenvi, S. V., Dixon, B. M., Liu, H., Jaiswal, A. K., Liu, R. M., & Hagen, T. M. (2004). Decline in transcriptional activity of Nrf2 causes age-related loss of glutathione synthesis, which is reversible with lipoic acid. Proceedings of the National Academy of Sciences, 101(10), 3381–3386. https://doi.org/10.1073/pnas.0400282101
Ursini, F., Bosello Travain, V., Cozza, G., Miotto, G., Roveri, A., Toppo, S., & Maiorino, M. (2023). Glutathione and glutathione-dependent enzymes: From biochemistry to gerontology and successful aging. Ageing Research Reviews, 91, 102066. https://doi.org/10.1016/j.arr.2023.102066
Viña, J., Sastre, J., Pallardó, F. V., & Borrás, C. (2003). Mitochondrial theory of aging: importance to explain why females live longer than males. Antioxidants & Redox Signaling, 5(5), 549–556. https://doi.org/10.1089/152308603770310194
Pillar 3: Microdose GLP-1
Alharbi, S. H. (2024). Anti-inflammatory role of GLP-1 receptor agonists. Therapeutic Advances in Endocrinology and Metabolism, 15. https://doi.org/10.1177/20420188231222367
Drucker, D. J. (2016). The cardiovascular biology of glucagon-like peptide-1. Cell Metabolism, 24(1), 15–30. https://doi.org/10.1016/j.cmet.2016.06.009
Grieco, M., Days, A., Sergi, D., & Lau, D. (2019). Glucagon-like peptide-1: A focus on neurodegenerative diseases. Frontiers in Neuroscience, 13, 1112. https://doi.org/10.3389/fnins.2019.01112
Holst, J. J. (2007). The physiology of glucagon-like peptide 1. Physiological Reviews, 87(4), 1409–1439. https://doi.org/10.1152/physrev.00034.2006
Whitley, H. P., Trujillo, J. M., & Neumiller, J. J. (2023). Special report: Potential strategies for addressing GLP-1 and dual GLP-1/GIP receptor agonist shortages. Clinical Diabetes, 41(3), 461–464. https://doi.org/10.2337/cd23-0036
Pillar 4: Environment and toxins
Landrigan, P. J., Fuller, R., Acosta, N. J. R., Adeyi, O., Arnold, R., Basu, N. N., Baldé, A. B., Bertollini, R., Bose-O'Reilly, S., Boufford, J. I., Breysse, P. N., Chiles, T., Mahidol, C., Coll-Seck, A. M., Cropper, M. L., Fobil, J., Fuster, V., Greenstone, M., Haines, A., … Zhong, M. (2018). The Lancet Commission on pollution and health. The Lancet, 391(10119), 462–512. https://doi.org/10.1016/S0140-6736(17)32345-0
Pizzorno, J. (2016). Environmental toxins and their role in aging. Integrative Medicine: A Clinician's Journal, 15(4), 8–10.
Sears, M. E., & Genuis, S. J. (2012). Environmental determinants of chronic disease and medical approaches: Recognition, avoidance, supportive therapy, and detoxification. Journal of Environmental and Public Health, 2012, 356798. https://doi.org/10.1155/2012/356798
Pillars 5–8: Foundations
Garatachea, N., Pareja-Galeano, H., Sanchis-Gomar, F., Santos-Lozano, A., Fiuza-Luces, C., Morán, M., Emanuele, E., Joyner, M. J., & Lucia, A. (2015). Exercise attenuates the major hallmarks of aging. Rejuvenation Research, 18(1), 57–89. https://doi.org/10.1089/rej.2014.1623
Sonnenburg, J. L., & Bäckhed, F. (2016). Diet–microbiota interactions as moderators of human metabolism. Nature, 535, 56–64. https://doi.org/10.1038/nature18846
Speakman, J. R., & Hambly, C. (2007). Starving for life: What animal studies can and cannot tell us about the use of caloric restriction to prolong human lifespan. Journal of Nutrition, 137(4), 1078–1086. https://doi.org/10.1093/jn/137.4.1078
Van Cauter, E., Leproult, R., & Plat, L. (2000). Age-related changes in slow wave sleep and REM sleep and relationship with growth hormone and cortisol levels in healthy men. JAMA, 284(7), 861–868. https://doi.org/10.1001/jama.284.7.861
Xie, L., Kang, H., Xu, Q., Chen, M. J., Liao, Y., Thiyagarajan, M., O'Donnell, J., Christensen, D. J., Nicholson, C., Iliff, J. J., Takano, T., Deane, R., & Nedergaard, M. (2013). Sleep drives metabolite clearance from the adult brain. Science, 342(6156), 373–377. https://doi.org/10.1126/science.1241224
