By Dave Asprey
A friend in the field of aging recently floated the idea that permanently reducing your body temperature might extend lifespan. I’m not calling him out personally here because playing the takedown game is for angry people…if he wants a polite and curious discussion, I’m game.
Permanently reducing your body temperature is entirely different from cryotherapy, which I have been doing as a part of my advanced longevity practice for the last 15 years (And I offer it at UpgradeLabs.com).
This article is based on the last 25 years I’ve worked in the field of longevity. I dropped my body temperature to 96.8 when I was younger, fatter, and had chronic fatigue. Once I brought it back up to 98.6, my health improved a lot.
True, there are studies showing that a lower metabolic rate could slow cellular aging, mimicking calorie restriction. While this might sound appealing in theory, there is a clear case that maintaining an optimal body temperature is essential for longevity. Why?
Because your body is a finely tuned biochemical system, and key enzymes that control energy, repair, and metabolism function poorly at lower temperatures. You need those to work properly so your body will repair itself. Short bursts of intense cold make you stronger. Chronic cold is a stressor. Here’s why reducing your body temperature—even to 97°F (36.1°C)—could do more harm than good. Some proponents even target 95°F!
The Temperature-Sensitive Enzymes That Keep You Alive and Thriving
Your body relies on enzymes for every biological process. These enzymes work best at a core body temperature of 98.6°F (37°C) [1], and even small temperature reductions can significantly impact their efficiency. Here are the most critical enzymes for longevity and why they need you to stay warm.
1. Deiodinases: The Key to Thyroid Hormone Activation
- Role: Convert the inactive thyroid hormone (T4) into active T3, which regulates your metabolism
- Optimal Temperature: 98.6°F (37°C)
- Efficiency Drop at 97°F: 20–50%
- Why This Matters for Longevity: Without sufficient T3, your metabolic rate slows, leading to fatigue, weight gain, and impaired cellular repair. At just 97°F, your deiodinases can lose half their efficiency, meaning your cells won’t get the energy signals they need to repair damage and maintain youthfulness. Reduced thyroid function also increases oxidative stress, a major contributor to aging [2].
2. Cytochrome c Oxidase: Your Energy Factory
- Role: Powers the final step of mitochondrial energy production (ATP synthesis). You probably read about this in my NYT bestseller longevity book Super Human.
- Optimal Temperature: 98.6–99°F (37–37.2°C)
- Efficiency Drop at 97°F: 15–20%
- Why This Matters for Longevity: Mitochondria are the engines of your cells, and cytochrome c oxidase drives energy production. Lowering your body temperature reduces mitochondrial output, leaving cells energy-starved and less capable of maintaining peak function. Energy deficits in mitochondria are strongly linked to aging and neurodegenerative diseases [3].
3. Sirtuins: The Longevity Guardians
- Role: Regulate DNA repair, mitochondrial function, and inflammation [4]. If you read Super Human, I went deep in activating these for longevity. One of the reasons you take NAD is to activate sirtuins!
SIRT3, a mitochondrial sirtuin, regulates enzymes involved in energy production and protects mitochondria from oxidative stress [5].
SIRT1 and SIRT6 help repair DNA damage and maintain genomic stability [6].
SIRT1 suppresses pro-inflammatory pathways by deacetylating NF-?B (a key inflammatory regulator) [7].
SIRT1 and SIRT2 influence insulin sensitivity, fat metabolism, and glucose homeostasis [8][9].
- Optimal Temperature: 98.6°F (37°C)
- Efficiency Drop at 97°F: 15–20%
- Why This Matters for Longevity: Sirtuins rely on NAD?, which is already limited with age [10]. Lower temperatures can further slow their activity, reducing DNA repair and mitochondrial output. Sirtuins are a cornerstone of longevity science, and impairing their function with chronic cold may accelerate cellular aging.
4. Proteasomal Enzymes: Cellular Trash Collectors
- Role: Break down damaged proteins to maintain cellular health [11]. In the Super Human aging framework, I wrote about extracellular junk. These enzymes fix that.
- Optimal Temperature: 99°F (37.2°C)
- Efficiency Drop at 97°F: 10–15%
- Why This Matters for Longevity: At lower temperatures, proteasomal activity declines, allowing toxic protein aggregates to accumulate. This is a hallmark of aging and diseases like Alzheimer’s and Parkinson’s [12]. (See my NYT bestseller on cognitive function, Head Strong, for more on Alzheimer’s)
5. DNA Repair Enzymes (e.g., PARP)
- Role: Repair DNA damage from oxidative stress [13].
- Optimal Temperature: 98.6°F (37°C)
- Efficiency Drop at 97°F: 10–20%
- Why This Matters for Longevity: DNA damage is inevitable, but enzymes like PARP repair it to maintain genomic stability. At 97°F, repair rates drop, leading to mutations and accelerated aging. If you plan to extend your life beyond the normal limits, you are going to have to be able to repair your DNA. Decades of being too cold is going to lead to excessive DNA damage.
6. Lipases: The Fat Burners
- Role: Break down stored fat into usable energy [14].
- Optimal Temperature: 98.6°F (37°C)
- Efficiency Drop at 97°F: 10–15%
- Why This Matters for Longevity: Efficient fat metabolism is essential for sustained energy and reducing inflammation. Cold body temperatures impair lipase function, leading to fat storage and metabolic sluggishness. As a part of my long-term longevity plan, I reduced my body fat down to 5% and clinical scans show my liver is as healthy as a 10-year-old’s. Carrying extra fat, especially visceral fat (the kind around your organs), decreases your chances of living a long time [15]. Brief exposure to cold burns fat. Chronic exposure to cold causes your body to store more.
What About Being “Cold Most of the Time”? Eastern Perspectives on Warmth and Health:
Traditional Chinese Medicine (TCM) and Ayurvedic medicine play a major role in biohacking and longevity. After all, these practices are some of the oldest longevity practices on the planet. Biohacking proves that they work because it provides so much data. It also shows when ancient practices don’t work. In this case, it’s worth looking at those perspectives to see if there is a historical practice for being cold often.
TCM and Ayurveda have long recognized the importance of maintaining warmth in the body. TCM associates constant coldness with weakened “yang energy,” which is responsible for vitality, digestion, and immune strength. Similarly, Ayurveda warns that excess “cold” disrupts the digestive fire (Agni), leading to sluggish metabolism and toxin buildup.
It’s almost like you could predict those observations by knowing enzyme temperature ranges!
In both systems, chronic coldness is seen as a root cause of low energy and accelerated aging—a perspective now supported by this new research identifying how suboptimal body temperature impairs enzyme function.
The Takeaway
Reducing your body temperature may seem like a shortcut to longevity, but the science says otherwise. Enzymes critical to your energy, metabolism, and cellular repair simply don’t work as well at lower temperatures. Even a drop to 97°F can reduce their efficiency by 20–50%, leaving your cells less equipped to repair damage, produce energy, and fight aging.
Instead of cooling your body, focus on strategies that support enzyme activity:
- Keep your thyroid healthy with adequate iodine and selenium.
Consider microdose (7.5-15mg) thyroid glandular supplementation if your TSH is above one and does not respond to minerals and tyrosine supplements - Support mitochondrial function with nutrients like CoQ10 and PQQ.
- Maintain optimal NAD? levels to fuel sirtuins. I use Qualia NAD+.
Staying warm is a proven way to ensure your body operates at its best—for energy today and longevity tomorrow.
References
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- Chakrabarti SK, Ghosh S, Banerjee S, Mukherjee S, Chowdhury S. Oxidative stress in hypothyroid patients and the role of antioxidant supplementation. Indian J Endocrinol Metab. 2016 Sep-Oct;20(5):674-678. doi: 10.4103/2230-8210.190555. PMID: 27730079; PMCID: PMC5040049.
- Bratic I, Trifunovic A. Mitochondrial energy metabolism and ageing. Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):961-7. doi: 10.1016/j.bbabio.2010.01.004. Epub 2010 Jan 11. PMID: 20064485.
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- Weir HJ, Lane JD, Balthasar N. SIRT3: A Central Regulator of Mitochondrial Adaptation in Health and Disease. Genes Cancer. 2013 Mar;4(3-4):118-24. doi: 10.1177/1947601913476949. PMID: 24020003; PMCID: PMC3764467.
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- Yeung F, Hoberg JE, Ramsey CS, Keller MD, Jones DR, Frye RA, Mayo MW. Modulation of NF-kappaB-dependent transcription and cell survival by the SIRT1 deacetylase. EMBO J. 2004 Jun 16;23(12):2369-80. doi: 10.1038/sj.emboj.7600244. Epub 2004 May 20. PMID: 15152190; PMCID: PMC423286.
- Zhou S, Tang X, Chen HZ. Sirtuins and Insulin Resistance. Front Endocrinol (Lausanne). 2018 Dec 6;9:748. doi: 10.3389/fendo.2018.00748. PMID: 30574122; PMCID: PMC6291425.
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