Can Cold Exposure Help to Prevent Weight Gain?

Reviews the literature on temperature control and adaptive thermogenesis; concludes that cold exposure can help to prevent weight gain, and that central heating may have contributed to the rise in obesity

The proportion of people who are overweight or obese has risen dramatically in economically developed countries since the late 1970s. For example, as the chart below indicates, the proportion of Americans who are overweight increased by ~30 percentage points between 1980 and 2015. A number of different societal changes are likely to have contributed to this trend. One such change, which has received comparatively little attention in the popular press, is increased use of central heating.

Why might increased use of central heating have contributed to the rise in overweight and obesity? This post outlines the explanation, drawing on recent evidence from the literature on temperature control and adaptive thermogenesis.

There are three main ways by which the body returns to its homeostatic set point under conditions of positive energy balance: reducing energy intake (eating less), increasing energy expenditure through exercise, and increasing energy expenditure through non-exercise activity. The last of these three is termed adaptive thermogenesis (i.e., facultative production of heat to maintain body temperature or burn off excess energy.)

Many animals achieve adaptive thermogenesis through activation of so-called brown adipose tissue (brown fat). Unlike white adipose tissue, brown fat contains a much higher density of iron-rich mitochondria, which gives it a brown appearance. As Schrauwen et al. (2015) note, “It was over 400 years ago that Conrad Gesner wrote about a fat depot in the neck of marmots that could be called neither fat nor flesh, but something in between”. The thermogenic capacity of brown fat was first reported in a 1961 paper entitled, ‘Thermogenic activity of the hibernating gland in the cold-acclimatized rat’. Specifically, signals from the SNS simulate the mitochondria within brown fat cells to produce heat via activation of UCP-1––a process known as non-shivering thermogenesis.

Until recently, brown fat was not thought to be present in human adults. (In infants, it appears to make up about 30% of fat by volume). But then in 2009, three studies were published in the New England Journal of Medicine (a journal with an impact factor of 72), which used a new method called FDG-based positron-emission tomography to detect metabolically active brown fat in adults. Interestingly, significant levels of brown fat activity were only observed when subjects were exposed to cold. In addition, two of the studies observed correlations between brown fat activity and body fat percentage or BMI. For example, Figure 3B from van Marken Lichtenbelt et al.’s paper is shown below:

(Incidentally, it is not clear whether brown fat activity was lower in subjects with higher body fat because such individuals carry less metabolically active brown fat, because their core temperature fell less due to greater thermal insulation, or because of some combination of the two.)

As van Marken Lichtenbelt et al. (2014) explain, the process of non-shivering thermogenesis occurs when temperature falls below what is called the thermoneutral zone: “the range of ambient temperatures that do not induce regulatory changes in metabolic heat production or evaporative heat loss.” This can be distinguished from the so-called thermal comfort zone: “the range of ambient temperatures… within which a human in specified clothing expresses satisfaction with his thermal environment.” The thermal comfort zone is believed to be wider than the thermoneutral zone, and may widen further as one’s level of cold acclimatisation increases. Of course, when temperature falls sufficiently far below the thermoneutral zone, shivering occurs. These dynamics are illustrated in the chart below (LCT denotes lower critical temperature; UCT denotes upper critical temperature):

In short, exposure to mild cold burns excess energy through non-shivering thermogenesis, while exposure to extreme cold burns excess energy through both non-shivering thermogenesis and actual shivering. As Keith et al. (2006) note, these effects have long been exploited in the livestock industry, “where selecting the environment to maximise weight gain is critical”.

Since exposure to mild cold does not induce shivering, most people may not find it too uncomfortable. Indeed, there are a number of lines of evidence suggesting that mild cold exposure could be an effective strategy for preventing weight gain. These are reviewed in detail by Johnson et al. (2011).

First, inhibition of SNS activity via the use of beta-andrenoceptor blocking agents leads to reduced energy expenditure and weight gain in both humans and animal models (recall that non-shivering thermogenesis is activated by signals from the SNS).

Second, individuals carrying genetic variants associated with low UCP-1 expression exhibit weaker thermogenic responses to overfeeding, and such individuals had higher BMI in one Czech population study (recall that activation of UCP-1 produces non-shivering thermogenesis).

Third, experimental studies using respiratory chambers have found that energy expenditure is negatively correlated with ambient temperature over a range of temperatures from 15°C to 28°C––the lower end of which does not induce shivering.

Fourth, the level of brown fat activity observed in Americans varies according to season, being lower in the summer and higher in the winter. For example, Figure 1E from Au-Yong et al.’s (2009) paper is shown below:

Fifth, in animal models, cold acclimatisation leads to darkening of the adipose tissue, corresponding to an increase in the proportion of brown fat cells. And in one Finnish study, outdoor workers had larger brown fat deposits than their counterparts who worked indoors.

How large an effect could intermittent exposure to mild cold have on body-weight? According to a recent experimental study by Luo et al. (2016), average metabolic rate is ~16% higher at a temperature of 16°C than at a temperature of 26°C for individuals wearing “light clothing” (underwear, T-shirt, shorts, socks and sport shoes), and is ~6% higher for individuals wearing “medium clothing” (underwear, T-shirt, sweater, trousers, socks, and sport shoes). These results are shown in the chart below (0.42clo corresponds to light clothing; 0.91clo corresponds to medium clothing):

The evidence adduced above suggests that the increased use of central heating may have contributed to the obesity epidemic. What other evidence is there that supports this hypothesis?

First and most importantly, there has been a considerable increase in average indoor temperature in developed countries over the last half century. As Johnson et al. (2011) note, “Since the 1960s, a cultural shift in norms of thermal comfort and expectations of ‘thermal monotony’ have been driven by the widespread uptake of central heating and air conditioning”. In the UK for example, mean living room temperatures increased from 18.3°C in 1978 to 19.1°C in 1996, while mean bedroom temperatures increased from from 15.2°C in 1978 to 18.5°C in 1996. Additional figures can be found in Mavrogianni et al. (2011).

Second, a number of studies have investigated whether measures like bodyweight, BMI or waist circumference are associated with temperature across geographical areas. Admittedly, the evidence here is somewhat mixed. Studies in Tibet, Spain, the US, South Korea and Japan found positive associations. But other studies in the Netherlands, and the US did not find any association. In addition, none of the preceding studies looked at the impact of central heating itself.

Third, available data from the UK indicates that calorie consumption per capita has fallen since the mid-1970s, and that sugar consumption per capita has fallen since the early 1990s. Sugar consumption per capita also appears to have declined in Australia. In addition, a 2014 study in the United States––which examined trends in obesity, caloric intake and physical activity from 1988 to 2010––observed no change in caloric intake, but a substantial decline in physical activity. On the other hand, a 2011 US study did find an increase in caloric intake between 1975 and 2006. The preceding findings suggests that reduced energy expenditure may have contributed more to the obesity epidemic than increased energy intake.

In conclusion, exposure to mild cold induces non-shivering thermogenesis in humans, at least partly via activation of brown adipose tissue. It may therefore be an effective strategy for preventing weight gain. Furthermore, average indoor temperatures have risen considerably in developed countries over the last half century, due to increased use of central heating. Given that humans burn more energy when cold then when at thermal comfort, this trend may have contributed to the rise in overweight and obesity.

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