
What techniques are out there to reduce glucose spikes?
This blog explores how individuals can conduct their own experiments to maintain a steady blood glucose and avoid potentially unhealthy glucose spikes above 7.8 mmol/L (140 mg/dL).
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Posted on Saturday December 6, 2025 in Muscle, Protein and Metabolic Resilience

An article written by Dr Edward Leatham, Consultant Cardiologist ©Edward Leatham 2025
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For most of human history, the human thermogenic system — particularly brown adipose tissue (BAT) — was activated daily through environmental cold exposure. BAT is a mitochondria-rich, calorie-burning organ whose activation increases resting metabolic rate, improves insulin sensitivity, and reduces visceral adipose tissue (VAT).
Modern, temperature-controlled lifestyles suppress BAT activation, reduce D2-mediated conversion of T4→T3 within BAT, and promote VAT accumulation and metabolic inflexibility.
Multiple human studies show that mild daily cold exposure (e.g., 17°C for 2 hours/day, 6 weeks) produces:
These benefits are reversible when ambient temperatures rise.
BAT activation can also be stimulated by certain foods, notably capsaicin and capsinoids (non-pungent compounds found naturally in sweet pepper varieties), offering a potential dietary adjunct to cold-based thermogenic strategies.
This short unreviewed paper consolidates the mechanistic, clinical, and translational evidence supporting cold exposure — and selected dietary compounds — as tools for VAT reduction and metabolic health.
Brown adipose tissue (BAT) is present in adult humans and plays a critical role in:
By contrast, visceral adipose tissue (VAT):
Stimulating BAT counteracts the metabolic burden imposed by VAT.
Cold exposure initiates a tightly coordinated physiological cascade:
This mechanism increases glucose uptake, improves insulin sensitivity, and stimulates fat oxidation — all of which oppose VAT accumulation.
Contemporary indoor environments (21–23°C year-round) suppress cold-induced thermogenesis by:
Humans are no longer routinely exposed to the cold stimulus required to recruit and maintain BAT activity.
Yoneshiro et al., J Clin Invest 2013 (1)
Daily exposure to 17°C for 2 hours/day for 6 weeks resulted in:
Lee et al., Diabetes 2014 (2,3)
Cold acclimation:
van der Lans et al., J Clin Invest 2013 (4) Just 10 days of mild cold exposure increased:
Schrauwen & van Marken Lichtenbelt, Diabetologia 2016 (5)
This review establishes that chronic mild cold exposure improves glycaemic control and may be a physiological adjunct therapy for preventing and managing type 2 diabetes.(6)
Beyond cold exposure, certain dietary compounds can stimulate BAT activation.
The most extensively studied are capsaicin (from chilli peppers) and capsinoids, non-pungent analogues found in certain sweet pepper varieties.
Mechanism:
Key Human Study:
Yoneshiro et al., AJCN 2012 (capsinoid trial) (7)
This demonstrates that capsaicin and capsinoids can mimic mild cold exposure, making them a valuable dietary adjunct to improve metabolic rate and reduce VAT accumulation.
Non-shivering thermogenesis increases baseline energy use.
Reducing hyperinsulinaemia reduces VAT deposition.
BAT acts as a glucose sink.
BAT oxidises fatty acids rapidly during thermogenesis.
Obesity reduces D2 activity → low intracellular T3
Cold exposure increases D2 → restores T3 signalling
Cold exposure synergises with:
Cold exposure is:
It represents an underutilised metabolic tool with potential population-level benefits for reducing VAT, obesity, insulin resistance, and diabetes.
BAT is a powerful metabolic organ capable of improving insulin sensitivity, increasing metabolic rate, and reducing VAT. Modern living suppresses BAT activation, but mild daily cold exposure and certain dietary compounds (capsaicin, capsinoids) can safely restore this ancient metabolic pathway.
Turning the thermostat down is a simple, evidence-based, physiologically grounded intervention to improve metabolic health, reduce VAT, and support cardiometabolic prevention.
7. Yoneshiro T, Aita S, Matsushita M, Kayahara T, Kameya T, Kawai Y, et al. Recruited brown adipose tissue as an antiobesity agent in humans. J Clin Invest. 2013 Aug;123(8):3404–8.
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