Researchers at Stanford University, according to analysis of data going back to the 1800s, found that average body temperature has decreased (Myroslava Protsiv et al, Decreasing human body temperature in the United States since the Industrial Revolution). Other data supports the present lower norm (J.S. Hausmann et al, Using Smartphone Crowdsourcing to Redefine Normal and Febrile Temperatures in Adults: Results from the Feverprints Study).
They considered that increased health and so decreased inflammation could be the cause, but it’s not clear that inflammation overall has decreased. The modern industrial diet of sugar and seed oils is highly inflammatory. Inflammation has been linked to epidemic of diseases of civilization: obesity, diabetes, heart disease, arthritis, depression, schizophrenia, and much else. In some ways, inflammation is worse than it has ever been. That is why, as a society we’ve become obsessed with anti-inflammatories, from aspirin to turmeric.
The authors of the paper, however, offer other data that contradicts their preferred hypothesis: “However, a small study of healthy volunteers from Pakistan—a country with a continued high incidence of tuberculosis and other chronic infections—confirms temperatures more closely approximating the values reported by Wunderlich”. Since these were healthy volunteers, they should not have had higher inflammation from infections, parasites, etc. So, why were their body temperatures higher than is seen among modern Westerners?
It also has been suggested that there are other potential contributing factors. Ambient temperatures are highly controlled and so the body has to do less work in maintaining an even body temperature. Also, people are less physically active than they once were. The more interesting explanation is that the microbiome has been altered, specifically reduced in the number and variety of heat-producing microbes (Nita Jain, A Microbial-Based Explanation for Cooling Human Body Temperatures).
I might see a clue in the Pakistan data. That population is presumably more likely to be following their traditional diet. If so, this would mean they have been less Westernized in their eating habits, which would translate as fewer refined starchy carbs and sugar, along with fewer seed oils high in omega-6 fatty acids. Their diets might in general be more restricted: fewer calories, smaller portions, less snacking, and longer periods between meals. Plus, as this would be an Islamic population, fasting is part of their religious tradition.
This might point to more time spent in and near ketosis. It might be noted that ketosis is also anti-inflammatory. So why the higher body temperature? Well, there is the microbiome issue. A population on a traditional diet combined with less antibiotic usage would likely still be supporting a larger microbiome. By the way, ketosis is one of the factors that supports a different kind of microbiome, related to its use as treatment for epilspsy (Rachael Rettner, How the Keto Diet Helps Prevent Seizures: Gut Bacteria May Be Key). And ketosis raises the basil metabolic rate which in turn raises temperature. Even though fasting lowers body temperature in the short term, if it was part of an overall ketogenic diet it would help promote on average higher body temperatures.
This is indicated by the research on other animals: “An increased resistance to cold assessed by the rate of fall in body tem-perature in the animals as well as human beings on a high-fat diet has been reported by LEBLANC (1957) and MITCHELL et al. (1946), respectively. LEBLANC (1957) suggested that the large amount of fat accumulated in animals fed a high-fat diet could not explain, either as a source of energy reserves or as an insulator, the superiority of high-fat diet in a cold environment, postulating some changes induced by a high-fat diet in the organism that permits higher sustained rate of heat production in the cold.” (Akihiro Kuroshima, Effects of Cold Adaptation and High-Fat Diet On Cold Resistance and Metabolic REsponses To Acute Exposure In Rats).
And: “Rats on a corn oil diet convert less T4 to active T3 than rats on a lard diet. Rats on a safflower oil diet have a more greatly reduced metabolic response to T3 than rats on a beef fat diet. Rats on a high-PUFA diet have brown fat that’s less responsive to thyroid hormone. Remember, brown fat is the type that generates heat to keep us warm. Rats on a long-term diet high in soybean oil have terrible body temperature regulation, which thyroid function in large part controls” (Mark Sisson, Is Keto Bad For Your Thyroid?). A 1946 study found that a high-fat diet had less of a drop in body temperature in response to cold (H.H. Mitchell, The tolerance of man to cold as affected by dietary modification; carbohydrate versus fat and the effect of the frequency of meals).
Specifically about ketosis, in mice it increases energy expenditure and causes brown fat to produce more heat (Shireesh Srivastava, A Ketogenic Diet Increases Brown Adipose Tissue Mitochondrial Proteins and UCP1 Levels in Mice). Other studies confirm this and some show an increase of brown fat. Brown fat is what keeps us warm. Babies have a lot of it and, in the past, it was thought adults lost it, but it turns out that we maintain brown fat throughout our lives. It’s just that diets have different affects on it.
Bikman points out the relationship between insulin and ketones — when one is high the other is low. Insulin tells the body to slow down metabolism and store energy, that is to say produce fat and to shut down the activity of brown fat. Ketones do the opposite, not only activating brown fat but causing white fat to act more like brown fat. This is what causes the metabolic advantage of the keto diet, in losing excess body fat and maintaining lower weight, as it increases the burning of 200-300 calories per day (metabolizing 10 lbs of body fat a year). By the way, cold exposure and exercise also activate brown fat, which goes back to general lifestyle factors that go hand in hand with diet.
Some people attest to feeling warmer in winter while in ketosis (Ketogenic Forums, Ketosis, IF, brown fat, and being warmer in cool weather), although others claim to not handle cold well which might simply be an issue of how quickly people become fully fat-adapted. A lifetime of a high-carb diet changes the body. But other than permanently damaged biological functioning, the body should be able to eventually shift into more effective ketosis and hence thermogenesis.
In humans, there is an evolutionary explanation for this. And humans indeed are unique in being able to more easily enter and remain in ketosis. But think about when ketosis most often happened in the past and you’ll understand why it seems to be inefficient in wasting energy as heat, what is a slight metabolic advantage if you’re trying to lose weight. For most of human existence, carb restriction was forced upon the species during the coldest season when starchy plants don’t grow. That is key.
It was an advantage to not only be able to survive off of one’s own body fa but to simultaneously create extra heat, especially during enforced fasting when food supplies were low as fasting would tend to drop body temperature — an argument made by the insulin researcher Benjamin Bikman (see 9/9/17 interview with Mike Mutzel on High Intensity Health at 20:34 mark, Insulin, Brown Fat & Ketones w/ Benjamin Bikman, PhD; & see Human Adaptability and Health). Ketosis is a compensatory function for survival during the harshest time of the year, winter.
Maybe modern Westerners have lower body temperature for the same reason they are plagued with diseases of civilization, specifically those having to do with metabolic syndrome and insulin resistance. If we didn’t take so many drugs and other substances to manage inflammation, maybe our body temperature would be higher. But it’s possible the lack of ketosis by itself might be enough to significantly keep it at a reduced level. And if not ketosis, something else about the diet and metabolism likely are involved.
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What is the relevance? Does it matter that average body temperature has changed? As I pointed out above, it could indicate how the entirety of physiological functioning has been altered. A major component has to do with the metabolism which relates to diet, gut health, and microbiome. About the latter, Nita Jain wrote that,
“A 2010 report observed that 36.7° C may be the ideal temperature to ward off fungal infection whilst maintaining metabolism. In other words, high body temperatures represent optimization in the tradeoff between metabolic expenditure and resistance to infectious diseases. Our reduced exposure to potentially pathogenic fungi in developed countries may therefore be another possible factor driving changes in human physiology” (A Microbial-Based Explanation for Cooling Human Body Temperatures).
That would be significant indeed. And it would be far from limited to fungal infections: “In general, a ketogenic diet is useful for treating bacterial and viral infections, because bacteria and viruses don’t have mitochondria, so a ketogenic diet starves them of their favorite fuel source, glucose” (Paleo Leap, Infections and Chronic Disorders). Ketosis, in being anti-inflammatory, has been used to treat gout and autoimmune disorders, along with mood disorders that often include brain inflammation.
The inflammatory pathway, of course, is closely linked to the immune system. Reducing inflammation is part of complex processes in the body. Opposite of the keto diet, a high-carb diet produces inflammatory markers that suppress the immune system and so compromises prevention of and healing from infections. Indeed, obese and diabetic patients are hospitalized more often and get worse symptoms of influenza infections (flu).
But it’s not merely the reduction of inflammation. As an energy source, ketones are preferred over glucose by immune cells that fight infections, although maybe some bacteria can use ketones. It’s a similar pattern with cancer, in which ketosis can help prevent some cancers from growing in the early stages, but the danger is once established particular kinds of cancers can adapt to using ketones. So, it isn’t as simple as ketosis curing everything, even if it is a overall effective preventative measure in maintaining immunological health and general health.
What interests us most here are infections. Let’s look further at the flu. One study gave mice an influenza infection (Emily L. Goldberg et al, Ketogenic diet activates protective γδ T cell responses against influenza virus infection; Abby Olena, Keto Diet Protects Mice from Flu). The mice were on different diets. All of those on standard chow died, but half survived on the keto diet. To determine causes, other mice were put on a diet high in both fat and carbs while others were given exogenous ketones, but these mice also died. It wasn’t only the fat or the ketones in the keto diet. Something about fat metabolism seems to have been key, that is to say not only fat and not only the ketones but something about how fat is turned into ketones during ketosis, although some speculate that protein restriction might have been important.
The researchers were able to pinpoint the mechanisms for fighting off the infection. Turning fat into ketones allows the gamma delta subset of T cells in the lungs to be activated in response to influenza. This was unexpected as they haven’t been a focus in previous research. These T cells increase mucus production in epithelial cells in the lungs. This creates a protective barrier that traps the virus and allows it to be coughed up. At the same time, the keto diet blocks the production of inflammasones, multiunit protein complexes activated by the immune system. This reduces the inflammation that can harm the lungs. This relates to the T cell stimulation.
From an anecdotal perspective, here is an interesting account: “I have been undergoing a metabolic reset to begin the year. I have been low carb/keto on and off for the last 4.5 years and hop in and out of ketosis for short periods of time when it benefits me or when my body is telling me I need to. Right now, I decided to spend the first 6 weeks of 2018 in ketosis. I check my numbers every morning and have consistently been between 1.2 and 2.2 mmol/L. I contracted a virus two days ago (it was not influenza but I caught something) and my ketone levels shot through the roof. Yesterday morning I was at 5.2 (first morning of being sick) and this morning I was at 5.8 (although now I am in a fasted state as I have decided to fast through this virus.)” (bluesy2, Keto Levels with Virus/Flu).
Maybe that is a normal response for someone in ketosis. The mouse study suggests there is something about the process itself in producing ketones that is involved in the T cell stimulation. The ketones also might have a benefit for other reasons, but the process of fat oxidation or something related to it might be the actual trigger. In this case, the ketone levels are an indicator of what is going on, that the immune system is fully engaged. The important point, though, is this only happens in a ketogenic state and it has much to do with basil metabolic rate and body temperature regulation.
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98.6 Degrees Fahrenheit Isn’t the Average Anymore
by Jo Craven McGinty
Nearly 150 years ago, a German physician analyzed a million temperatures from 25,000 patients and concluded that normal human-body temperature is 98.6 degrees Fahrenheit.
That standard has been published in numerous medical texts and helped generations of parents judge the gravity of a child’s illness.
But at least two dozen modern studies have concluded the number is too high.
The findings have prompted speculation that the pioneering analysis published in 1869 by Carl Reinhold August Wunderlich was flawed.
Or was it?
In a new study, researchers from Stanford University argue that Wunderlich’s number was correct at the time but is no longer accurate because the human body has changed.
Today, they say, the average normal human-body temperature is closer to 97.5 degrees Fahrenheit.
“That would be a huge drop for a population,” said Philip Mackowiak, emeritus professor of medicine at the University of Maryland School of Medicine and editor of the book “Fever: Basic Mechanisms and Management.”
Body temperature is a crude proxy for metabolic rate, and if it has fallen, it could offer a clue about other physiological changes that have occurred over time.
“People are taller, fatter and live longer, and we don’t really understand why all those things have happened,” said Julie Parsonnet, who specializes in infectious diseases at Stanford and is senior author of the paper. “Temperature is linked to all those things. The question is which is driving the others.” […]
Overall, temperatures of the Civil War veterans were higher than measurements taken in the 1970s, and, in turn, those measurements were higher than those collected in the 2000s.
“Two things impressed me,” Dr. Parsonnet said. “The magnitude of the change and that temperature has continued to decline at the same rate.” […]
“Wunderlich did a brilliant job,” Dr. Parsonnet said, “but people who walked into his office had tuberculosis, they had dysentery, they had bone infections that had festered their entire lives, they were exposed to infectious diseases we’ve never seen.”
For his study, he did try to measure the temperatures of healthy people, she said, but even so, life expectancy at the time was 38 years, and chronic infections such as gum disease and syphilis afflicted large portions of the population. Dr. Parsonnet suspects inflammation caused by those and other persistent maladies explains the temperature documented by Wunderlich and that a population-level change in inflammation is the most plausible explanation for a decrease in temperature.
Decreasing human body temperature in the United States since the Industrial Revolution
by Myroslava Protsiv, Catherine Ley, Joanna Lankester, Trevor Hastie, Julie Parsonnet
This substantive and continuing shift in body temperature—a marker for metabolic rate—provides a framework for understanding changes in human health and longevity over 157 years.
Very interesting paper. Well done. However, a hypothesis still remains to be tested. The decline of the infectious burden well corresponds to the decrease of the body temperatures between the XIXth and XXth century cohorts (UAVCW vs NHANES), but it does not explain the further and much more important reduction between the XXth and XXIth century studies (NHANES vs STRIDE); see Figure 1 (distributions gap) and Figure 1 / Supp 1 (curve gap), where the impact seems to be twice as large between 1971 and 2007 than between 1860 and 1971.
Besides regulating the ambient room temperature (through winter heating in the early XXth century and summer air conditioning in the late XXth and early XXIth century), another hypothesis was not discussed here ie the significant decline in daily physical activity, one of the primary drivers of physiological heat production.
Regular physical activity alters core temperature even hours after exercising; 5h of moderate intensity exercise (60% VO2max) also increase the resting heart rate and metabolic rate during the following hours and night with a sympathetic nervous system activated until the next morning (Mischler, 2003) and higher body temperatures measured among the most active individuals (Aoyagi, 2018).
As in most developed countries, the North American people – who worked hard in agriculture or industry during the XIXth century – lost their active daily habits. We are now spending hours, motionless in front of our screens, and most of our adolescents follow this unsettling trend (Twenge, 2019); such an effect on temperature and energy regulation should also be considered as it may have an important impact on the potential progresses of their life expectancy and life duration.
Jean-François Toussaint Université de Paris, Head IRMES
Mischler I, et al. Prolonged Daytime Exercise Repeated Over 4 Days Increases Sleeping Heart Rate and Metabolic Rate. Can J Appl Physiol. Aug 2003; 28 (4): 616-29 DOI: 10.1139/h03-047
Aoyagi Y, et al. Objectively measured habitual physical activity and sleep-related phenomena in 1645 people aged 1–91 years: The Nakanojo Community Study. Prev Med Rep. 2018; 11: 180-6 DOI: 10.1016/j.pmedr.2018.06.013
Twenge JM, et al. Trends in U.S. Adolescents’ media use, 1976–2016: The rise of digital media, the decline of TV, and the (near) demise of print. Psychol Pop Media Cult, 2019; 8(4): 329-45. DOI: 10.1037/ppm0000203
(edited Feb 15) Feb 14
Although there are many factors that influence resting metabolic rate, change in the population-level of inflammation seems the most plausible explanation for the observed decrease in temperature over time.
Reduced body temperature measurements may also be the result of loss of microbial diversity and rampant antibiotic use in the Western world. Indeed, the authors mention that a small study of healthy volunteers from Pakistan reported higher mean body temperatures than those encountered in developed countries where exposure to antimicrobial products is greater.
Rosenberg et al. reported that heat provision is an under-appreciated contribution of microbiota to hosts. Previous reports have estimated bacterial specific rates of heat production at around 168 mW/gram. From these findings, we can extrapolate that an estimated 70% of human body heat production in a resting state is the result of gut bacterial metabolism.
Consistent with this idea are reports that antibiotic treatment of rabbits and rodents lowers body temperature. Germ-free mice and piglets similarly displayed decreased body temperatures compared to conventionally raised animals and did not produce a fever in response to an infectious stimulus.
Although heat production by symbiotic microbes appears to be a general phenomenon observed in both plants and animals, its significance in humans has hardly been studied. Nonetheless, the concomitant loss of diversity and heat contribution of the gut microbiota may have far-reaching implications for host metabolic health.
I would like to propose that our reduced body temperature measurements may be the result of loss of microbial diversity and rampant antibiotic use in the Western world. Indeed, a small study of healthy volunteers from Pakistan reported higher mean body temperatures than those encountered in developed countries where exposure to antimicrobial products is greater.
Heat provision is an under-appreciated contribution of microbiota to hosts. Microbes produce heat as a byproduct when breaking down dietary substrates and creating cell materials. Previous reports have estimated bacterial specific rates of heat production at around 168 mW/gram. From these findings, we can extrapolate that an estimated 70% of human body heat production in a resting state is the result of gut bacterial metabolism.
Consistent with this idea are reports that antibiotic treatment of rabbits and rodents lowers body temperature. Germ-free mice and piglets similarly displayed decreased body temperatures compared to conventionally raised animals and did not produce a fever in response to an infectious stimulus. The relationship also appears to be bi-directional, as host tolerance to cold has been shown to drive changes in the gut microbiomes of blue tilapia.
Heat production in goats was found to decrease by about 50% after emptying the rumen to values similar to what would be expected during a fasting state. These observations suggest that during fasting, microbial fermentation is responsible for half of the animal’s heat production while host metabolism accounts for the other half. The warming effect of microbes has also been reported in plants. Yeast populations residing in floral nectar release heat when breaking down sugar, increasing nectar temperature and modifying the internal flower microenvironment.