Cold Exposure and Weight Loss 


“Cold Exposure, Weight Loss, and Thermogenesis Taking ice baths has been popularized, in part, due to the effects of the cold on weight loss.
One of the body’s ways of responding to cold is to increase metabolism, not to produce energy in the form of adenosine triphosphate (known as ATP), but to produce heat to warm the body and, in the process, burn fat. This process is referred to as cold thermogenesis.

There are two types of thermogenesis that occur as a biological response to cold exposure. The
first kind of cold induced thermogenesis occurs in muscle tissue and involves ramping up
metabolism in order to produce heat. This works because metabolism is not 100% efficient and
produces heat as a byproduct. This is referred to as shivering thermogenesis, because the
muscle contractions are what actually increases the energy metabolism.
The second type of cold induced thermogenesis occurs in adipose tissue (fat) and does not involve shivering. It is called nonshivering thermogenesis . This type of thermogenesis is what is really responsible for the “fat burning” effect that cold exposure can have and usually happens after the body has adapted to cold exposure.

Let’s talk about nonshivering thermogenesis and brown adipose tissue . This process is partly regulated by norepinephrine, which we already know is robustly induced by cold exposure by anywhere from 2 to 5fold,depending on the intensity of the cold and length of the exposure.
Cold induced norepinephrine increases the expression of protein known as uncoupling protein 1
(UCP1) , which has the effect of uncoupling the mitochondria, the energy producing
powerhouses of the cell.

But what does it mean for mitochondria to be uncoupled? When it is said that the mitochondria
are coupled, we are referring to the coupling of the generation of a unit of energy (ATP) to the
transport of electrons ( which have been derived from the food you eat ), that create an
electrochemical gradient across mitochondria which is negatively charged on the inside and
positively charged on the outside. Mitochondria are a little bit like batteries in that sense.
When cold exposure activates the uncoupling protein 1 (UCP1), this uncouples the
electrochemical gradient, meaning there is no longer a negative or positive terminal to the
mitochondria. In response, the mitochondria try and reestablish
the electrochemical gradient by
transporting electrons which are derived from stored fat (called fat oxidation) and producing heat
as a byproduct of this process.

One of the ways uncoupling protein 1 (UCP1) ramps up metabolism is by producing more
mitochondria in adipose tissue, which causes a “browning effect” by converting or
“transdifferentiating” the more common white adipose tissue into it’s more metabolically active
counterpart, brown adipose tissue (BAT). You can think about this in simple terms: the more
brown adipose tissue your body has, the more fat your body will burn. The reason it is called
brown adipose tissue is because each fat cell has more mitochondria per cell and the
mitochondria make the fat appear brown when looking at it under a microscope.
Cold exposure increases nonshivering
thermogenesis in humans .

It was thought for some time that human adults had negligible amounts of brown adipose tissue (BAT). Increasingly,

however, studies are showing that adult humans do have this special type of adipose tissue that
is metabolically active . The fact that we have brown adipose tissue at all in adulthood actually
overturns old dogma that once stated that BAT was mostly found during infancy in humans. In
fact, it’s now been shown that brown adipose tissue (BAT) shows an inverse correlation to
percent body fat in an individual . Therapeutically enhancing the transdifferentiation or
production of brown adipose tissue (BAT) from white adipose tissue (WAT) is a promising and
active field of clinically applicable research for the treatment of obesity.
The good news is that repeated intermittent cold exposure has been shown to both increase
brown adipose tissue (BAT) in humans and increase our capacity for nonshivering
thermogenesis. Healthy young men and women that were exposed to air temperatures of
5961°F (1516°C) for 6 hours a day for 10 consecutive days increased their brown adipose
tissue by around 37% , and after acclimating also increased nonshivering
thermogenesis by1118%.

It is also interesting to note that if the BAT was sampled during the summer it was only
detected in ~25% participants compared to 50% if BAT was sampled during winter.
If having more brown adipose tissue, which becomes more active in cold, helps us stave off
obesity then it might reasonably be surmised that being cold would boost our metabolism. In
fact, it does! One study done in a small sample of young men showed that cold water
immersion(head out) in 68°F (20°C) for one hour increased metabolic rate by 93% and 1 hour at 57°F
(14°C) increased metabolic rate by 350% .

I’d like to discuss one mechanism by which cold exposure may increase the concentration of
brown adipose tissue. One study found that the sympathetic nervous system may be playing an
intimate role in the production of brown adipose tissue in rats: experimentally blocking
beta adrenergic receptors, which norepinephrine acts on, prevented the production of brown
adipose tissue . This relationship is interesting, because it might imply that the greater the
release of norepinephrine that we can induce from cold, the more browning of our adipose
tissue we might expect to occur.

Our diet may also be a way we can therapeutically brown our adipose tissue. One study
recently showed that consumption of fish oil actually increased the metabolism of mice , reduced
the fat accumulation between 15 to 25%, and was shown to likely be doing this by a brown
adipose tissue mediated mechanism.

Cold exposure increases activity of antioxidant enzymes . One of the side effects of ramping
up fat oxidation to burn stored fat for energy is the production of those damaging reactive
oxygen species (ROS) that damage nearly everything inside cells, including DNA. This is
actually a normal product of energy metabolism and, in a way, is a natural part of being alive.
How we respond to this damage and mitigate it is ultimately what’s important.

Reactive oxygen species (ROS), by contributing to things like DNA damage and cellular
senescence, are a huge component of the very process of aging. They are also a sign of
mitochondrial dysfunction. Being able to prevent that damage from occurring or being able to
repair it after it does occur is extremely important to staying healthy, and for one thing, cancer
free. Interestingly enough, it appears as though the exposure to cold, by functioning as a hormetic
stressor, actually activates very potent genetic antioxidant systems which are exponentially
more powerful than supplemental antioxidants. For example, young men exposed to
cryotherapy for 3 minutes at 202°F (−130°C) everyday for 20 days doubled the activity of one of
the most potent antioxidant enzyme systems in the body called glutathione reductase, and
increased another potent antioxidant enzyme called superoxide dismutase by ~43%.
Similarly, elite kayakers that engaged in whole body cryotherapy (248 to 284°F or 120 to140°
C) 3 minutes a day for 10 days increased the activity of superoxide dismutase by 36% and
glutathione peroxidase by 68% .

That is pretty stout. For those of you not familiar with superoxide dismutase, this enzyme is in your mitochondria cleaning up all that damage that is
being produced every second of every day. In other words, it is awesome. It is also important to note that the increase in antioxidant enzyme activity, in this case, took multiple sessions of the whole body cryotherapy…meaning the more frequent cryotherapy was done, the more robust of an increase in activating these powerful antioxidant enzymes.”


Reference – Excerpt from Rhonda Patrick’s Cold Stress Report. https://www.foundmyfitness.com/reports/cold-stress.pdf