Spending Valentine’s Day with your sweetheart might just take on a new meaning … an evolutionary one. Even though we live in an era in which endless opportunities for a mate are just a swipe left or right, science suggests that maybe we all have that one special someone out there.
Social monogamy is the practice of forming pair bonds in a two-partner relationship. One explanation for monogamy is to protect offspring—one partner takes care of the baby while the other hunts for food. Another more gruesome theory is that animals living in pairs evolved to prevent rival males from killing a female’s baby in order for the male to then sire his own. But why many different species became monogamous remained unanswered. For a long time, all scientists knew was that certain brain regions and hormones (like the “love hormone” oxytocin) played a role.
Humans haven’t mutated this much…yet. Credit: iStock
The word “mutation” may conjure up images of fictional monsters, Marvel X-Men and creatures with non-human characteristics. It’s true that mutations are often associated with disease: something that has gone wrong in the body to produce an oddly shaped body part or sometimes cancer. However, mutations can’t be categorized as “good” or “bad” so easily. In fact, some mutations turn out to be a good thing, such as the human affinity for long distance running. More on that in a bit, but first a lesson in mutations …
A mutation is a permanent alteration in the DNA sequence that makes up a gene. In other words, the DNA—genetic material that contains information about inherited characteristics—changes in a way that makes the gene different than how it normally appears in most people. Because of this change, certain proteins and their functions change…
Unlikely or not, it is interesting to ponder the physiological and technical challenges of a Martian marathon. Read our post from last week to learn why runners will be moving in giant leaps. Stride aside, how will the freezing cold, lack of oxygen, calorie requirements, and protective clothing affect the runners?
Cons of the Mars environment:
Temperature: beyond chilly
Race day conditions can be quite unpredictable even on Earth, and Mars will be no exception. Temperatures can vary from a moderate 70˚ F (20˚ C) around noon to an unbearable -195˚ F (125˚ C) at night. For the sake of this thought experiment, let’s assume that race day temperatures hover around the average of -67˚ F (-55˚ C).
At this temperature the blood vessels in many organs and leading to the skin will undergo profound constriction, reducing blood flow to areas where the runners…
Carb-loading for the Red Planet marathon might prove more difficult than simply gorging on a pre-race pasta dinner. Since they will be shivering and burning a lot more calories not only during, but before the race, runners will simply have to eat more on Mars during the pre-race period to fully saturate their muscles with glycogen.
Just getting plates of pasta to Mars will be a major issue. After years in transit, many of the nutrients in any food shipped to Mars will have been lost, and deep-space radiation will have degraded much of a food’s chemical and physical structure. Preparing and shipping food to Mars for the runners to eat requires special methods. Anyone care for high-pressure processed, microwave sterilized, freeze-dried spaghetti and meatballs…anyone?
Use of critical fuels such as carbohydrate and fat will drastically increase on mars due to the extreme cold
Humans have successfully conquered herculean feats of endurance in some of the most unbearable conditions on Earth. Such conquests as the Badwater Ultramarathon, 135 miles (217 km) through Death Valley, where temperatures can reach 130˚ F (54˚ C), or the 100k Antarctic Ice Marathon (average wind-chill -4˚F (-20˚ C)) not only require a certain amount of mental fortitude (some might call it insanity), but also careful consideration of human physiology and its inherent limits. Unpreparedness for such harsh climates can spell disaster; Mother Nature isn’t merciful to those who are ill-prepared. In tests of extreme endurance, environmental conditions, and the body’s response to those conditions, can be the dividing line between successful completion of the race and a certain meltdown.
It is unlikely that humans will ever lose their aspiration to push the limits of human physiology through feats of endurance. Given humanity’s recent…
This study was published by researchers at Taipei Veterans General Hospital (Taiwan) in the American Journal of Physiology Endocrinologoy and Metabolism
Obesity is associated with a variety of immune and metabolic problems, that are in large part related to the increased inflammatory state. Chronic inflammation in obesity results from immune cells, adipose tissue, muscle, and liver all having an “inflammatory profile.” Eventually, this can lead to development of insulin resistance and lower metabolic rates.
Caffeine has been shown to “downregulate” many markers of inflammation in animals and humans such as tumor necrosis factor-alpha (TNF), interleukin-6 (IL6), and monocyte chemoattractant protein-1 (MCP-1). Additionally, caffeine is said to inhibit lopigenic genes (“fat making”) and improve blood lipids, lower fat mass, and increase insulin sensitivity. All of these would be highly beneficial to obesity-related metabolic abnormalities.
What did they study?
Researchers wanted to know if caffeine, in doses similar to what someone might consume in 2-3 cups of coffee per day, could perhaps modulate some of the inflammatory and metabolic dysfunction in an obese rat model. To do this, they investigated what happened on a molecular level after chronic caffeine treatment in tissues from the circulatory, immune, and metabolic systems.
How did they do it?
To get the “fat rats”, researchers fed rats what is known in research as a “high fat diet”, or HFD. This diet contains ~34.9% fat (mostly saturated) by weight and had 60% of calories from fat. After 6 weeks on this diet, rats experienced fatty liver, obesity, and insulin resistance.
In addition to the obese rats, the researchers also had a “control” group of rats who were fed a normal chow diet (NCD).
Next, the HFD and NCD fed rats were assigned to one of two groups: either a 6 week caffeine treatment group (20 mg/kg/day of caffeine orally) or a control (vehicle) group who consumed no caffeine.
So, there were 4 groups in total. Obese rats who were both treated with caffeine and not treated, and a control group who was also treated with caffeine or not.
What did they measure?
A LOT. (Major players discussed below)
In addition to measures of inflammation such as TNF, IL-6, and MCP (discussed above), researchers also did two measures which assess metabolic health: a glucose tolerance test (GTT) and an insulin tolerance test (ITT). What these allow us to see is how sensitive to insulin (higher is better, in most cases) a certain animal/human is. A glucose tolerance test similarly tests the body’s ability to “handle” a load of glucose. Both of these give an idea of the “metabolic health” of the rats.
Metabolic rate (whole body oxygen consumption over 24 hours), liver triglycerides, and muscle/adipose tissue biopsies were also performed to analyze.
What were the results?
It is important to discuss, before each result, what changes happened in the high-fat diet fed mice. This allows us to get a sense of the deleterious effects the diet had, so we can then see how caffeine “therapy” may have had a beneficial effect.
The high-fat diet increased levels of inflammatory markers and induced fatty liver in the diet induced obese mice. The HFD fed rats also had lower levels of anti-inflammatory markers, and a higher white blood cell count (signaling immune activation).
Notably, Caffeine treatment for 6 weeks was able to suppress the inflammatory profiles of the HFD fed mice compared to those who received the “vehicle” (i.e. NO caffeine). Basically, caffeine “normalized” inflammatory markers like TNF AND IL-6 to levels seen in the normal chow fed rats.
The HFD + no caffeine group experienced significant insulin resistance. The HFD + caffeine group had greater insulin sensitivity parameters; they were essentially “protected” from developing insulin resistance on this diet.
After HFD induced obesity, the rats had higher triglycerides, serum free-fatty acids, and indicators of fatty liver, as well as a decreased metabolic demand, increased fat mass, liver weight, and size/proportion of fat cells.
Chronic treatment with caffeine lowered the body weights of the HFD fed rats, and increased their metabolic rate. The changes in markers of fatty liver, levels of triglycerides, free fatty acids were all reversed in the caffeine-treated rats, suggesting protection from metabolic dysfunction.
Higher muscle, adipose, and liver inflammatory ICAM-1, TNF-alpha, IL-6, MCP-1 are associated with systemic/local inflammation in HFD rats – these were inhibited in caffeine treated HFD rats, suggesting caffeine is “anti-inflammatory” and can lower inflammatory mediators in cells.
Normalizing the circulating levels of the metabolic hormones adiponectin and the glucose transporter GLUT4 suggests that inflammation-associated insulin resistance was prevented in caffeine treated rats.
Caffeine treatment caused a change in “energy utilization” in the HFD rats – increasing metabolic rate and preventing the lowered metabolism resulting from the HFD. The formation of fat cells (de novo lipogenesis) was decreased in caffeine treated rats.
Caffeine, present in many beverages and consumed for centuries, may be a potential treatment, whereby it acts via multiple molecular mechanisms and pathways to inhibit obesity-related abnormalities. This is important in a time when diet-induced obesity/metabolic syndrome is a growing issue. Any therapy with a potential to even marginally inhibit deleterious effects of diet and environment should be explored.
If you enjoyed this post, check out my Medium page, where I talk more in depth about research studies, the research process, and generally wonder about issues in exercise, science, and nutrition today.
Chances are, if you have taken any interest in the topic of diet and nutrition recently, you are well aware that there is a “debate” going on between sides that seem diametrically opposed to one another. The debate emphasizes the question of how we (and by “we” I mean America, but now many other developed countries as well) arrived at our current epidemic of obesity, diabetes, and the metabolic syndrome; diseases with ties to modernization but to which no known “cause” is yet attributed. This “cause” is the center of our current debate.
The steps leading to the obesity epidemic, at facevalue, seem simple. The theory (based on the law of thermodynamics) that “calories in = calories out” dictates whether one gains or loses weight is as used to explain why we get fat.
Simply put, we eat too much, exercise too little, and thus throw the equilibrium off balance, in favor of the “calories in” side, and gain weight. In the vaguest sense, this concept still holds up observationally, but we now know that there is much more to the story than simple caloric balance. For instance, basal metabolic rate (how many calories we expend just being alive) greatly influences our energy needs – and this is furthermore influenced by our spontaneous physical activity, our sleep levels, our hormones, and even the different macronutrient composition of our diets from day-to-day (higher protein intake usually results in a higher BMR, since it takes more energy to digest protein than either carbohydrate or fat).
The previous point, that the macronutrient composition of our diet is HIGHLY influential in terms of body weight and metabolic regulation, is the source of our ongoing dietary “debate.” Instead of arguing that “how much” we eat has created the rise in obesity, the argument now put forth is that “what” we eat (carbohydrates, protein, fat, sugar) is more influential. In this regard, sugar, and refined carbohydrates (think white carbs) are the prime suspects. In a sense, sugar is on trial.
As will be brought up later when referencing two recent papers on the topic; the idea for a long time was that sugar, just being calories, was essentially equal to a calorie from any other source. In this regard, it didn’t matter if you ate 2,500 calories of pasta and potatoes or steak and broccoli – a calorie is a calorie is a calorie. This idea is, for the most part, discredited. With knowledge of how different nutrients effect hormones such as insulin, and our ability to conduct well-controlled feeding studies – it is now accepted that carbohydrates and sugar have a detrimental metabolic effect when consumed in excess (some will argue when consumed at all) and that fat and protein, as dietary constituents, should be emphasized.
The idea that carbohydrates (namely, refined sugars) are bad is supplemented by the accusation that not only did our diets make us fat, but that the recommendations from our own government emphasizing “low fat” eating were what led to our over consumption of refined carbohydrates. This adds up, since many low-fat packaged foods are consequently loaded with sugar in order to retain their flavor. Some go as far as to say that the government conspired to hide the detrimental effects of sugar from the public to benefit industry, and funded research to support one dietary dogma over another.
To get a better picture of the story – I think it is necessary to discuss the issue from both sides. We must see supporters of the “sugar caused obesity” camp as well as those who, while not deniers of this fact, seem to think there is more underneath the surface of our modern-day health epidemic. Those on this side of the debate argue that sugar, while not healthy in its own right, is only one part of a larger story of a declining quality food environment. In this argument also lies the insistence that the government guidelines did not lead to a drastic change in eating habits nor did they drastically alter the nutritional landscape and cause the proliferation of obesity. Maybe, it is argued, we have suffered an overall decline in food quality and physical activity, and thus arrived at our current dilemma.
The other camp prefers that we isolate one single perpetrator – sugar.
In this camp, we have Gary Taubes. Taubes, a science journalist, falls into many camps – including the “anti-carb” camp, as well as the camp that accuses the government of dietary guideline manipulation and proliferation of metabolically-disadvantageous advice. The main target of Taubes’ criticism is sugar, which, he argues, is worse than simply “empty calories”.
The following arguments appear in his recent essay in the British Medical Journal titled “What if sugar is worse than just empty calories?” Following presentation of his essay, I will provide evidence-based arguments “against” Taubes’ incrimination. We may never have definitive proof of how we got fat and how we stop getting fatter – but continuing debate may move us closer.
Sucrose: Guilty as charged
Much of Taubes’ evidence relies on anecdotal data from which he uncovers a link – one between sugar, sugar industry, and diabetes/obesity. Taubes cites researchers Haven Emerson and Louise Larimore who, in the 1840’s, observed that “rises and falls in sugar consumption are followed with fair regularity…by similar rises and falls in the death rates from diabetes.” This observation largely went unnoticed by researchers and the concept that sugar should be incriminated as the sole cause of the increase in metabolic diseases fell out of favor.
Taubes wants the concept to make a comeback. He argues that we “understand” the cause of our predicament in theory (although I would argue that we do not). I’m not sure what he means by this – but it seems like the fact that he “thinks” he knows the answer to our diabetes/obesity epidemic (sugar) is good enough. His “theory” is that our “theory” of obesity and diabetes is incorrect. Why can’t we cure this epidemic? Because, Taubes argues, our thinking is flawed.
It stands to reason that our understanding may be flawed about what causes obesity. While merely repeating points I outlined above, it should be noted again that it was and is still thought that “over consumption of calories causes obesity – too much food, rather than the wrong kind.” A renewed interest in “calorific sweeteners” having major roles in obesity and diabetes is claimed by Taubes to be insufficient – since they are still placed in the context of over consumption of calories and thus their unique metabolic effect is under-emphasized.
Sugar = excess calories. Placed in our Newtonian balancing act, sugar adds calories to the “intake” side such that…
Calories in >> Calories out.
What do we get? Obesity.
But, this balancing act doesn’t always work in the opposite direction, meaning that a caloric deficit doesn’t always = weight loss. Why this is, the argument goes, is due to the fact that sugar has “deleterious effects on the human body independent of its calorific content” and that a unique pathway exists between sugar consumption and disease.
The above diagram, in simple terms, describes the unique effects of sugar (primarily fructose, a component of sucrose) in the body. Fructose, only cleared in the liver, leads to accumulation of fat (lipogenesis) which then leads (eventually) to insulin resistance, the hallmark pathophysiological disturbance in Type II diabetes.
This is fact. The biochemical properties of fructose are unique, and perhaps uniquely toxic, as shown in experimental studies. In this regard, we “know” what causes fatty liver disease, and what might contribute to obesity and diabetes.
According to the essay, we ignored these findings in support of the “saturated fat” model that was used to explain heart disease and postulated to explain diabetes and obesity. However, the correct answer, Taubes argues, is not found in this explanation. The reason we haven’t found the answer is due to “exoneration” of sugar by the sugar industry’s PR campaign which “set research on any link between sugar, heart disease, and diabetes, back by 20 years.” While Stanford University researchers were doing elaborate studies demonstrating that they could induce metabolic syndrome and insulin resistance in animals by feeding them sugar-rich diets, the US was busy focusing in on the apparent link between saturated fat and disease. Metabolic alterations in response to high sugar consumption: insulin resistance, type II diabetes, fatty liver disease, dyslipidemia, ectopic and visceral fat accumulation, were all overlooked and under-appreciated.
Finally, Taube’s presents his own theory. IF sugar (fructose) is uniquely toxic and leads to the cluster of metabolic abnormalities in humans, like it does in animals (this has yet to be demonstrated experimentally in humans), THEN the past 40 years of dietary prescription have been wrong – and dangerously so. We have spent nearly $750 million dollars investigating the saturated fat-disease hypothesis while neglecting any investigation into sugar. All That Taubes can conclude is that “his” hypothesis could be true and that, in the meantime, our best bet is to set upper limits to sugar consumption, communicate the “dangers” of sugar, and set research priorities that establish further knowledge on this subject that is currently in its infancy. I agree with Taubes in this respect, but the fact that sugar is unhealthy is far from a novel hypothesis.
Taubes’ take is valid, and his prestige as an investigative journalist allows him to make such assumptions and accusations with certainty and credibility. However, the way he uniquely targets one singly dietary aspect, accusing it in isolation of causing the twin-epidemics of obesity and diabetes radically oversimplifies the issue. As we will see, even some of the data do not support Taubes’ accusations that our dietary recommendations were flawed. Vindicating sugar as a harmful part of any diet is supported and worthy of recommendation. Criminalizing it for single handedly causing a worldwide epidemic of disease is reductionist.
Taking this reductionist approach ignores several other putative explanations for what may have caused the obesity and diabetes epidemic – explanations covered by Kevin Hall in his perspective paper titled “Did the Food Environment Cause the Obesity Epidemic?” Included in these explanations are questions of dietary causation. “Is it the Protein?” “Is it the fat?” “Is it the carbohydrate?” “Is it the calories?” “Is it the food quality?” Hall delves into each of these possible explanations for “why we got fat” and concludes whether sufficient evidence points to a positive relationship, or possibility of one in theory.
Since we are focusing on the subject of carbohydrate, we will deal in these terms only and draw from hall’s conclusions on the matter. Reiterating models used by Taubes, Hall explains the “carbohydrate-insulin model” of obesity; that carbohydrates are uniquely obesogenic because they elevate insulin secretion and direct fat toward storage in adipose tissue and away from oxidation as fuel sources in active tissue. Carbohydrates decrease energy expenditure (compared to equal calories of fat or protein) and increase hunger, leading to weight gain.
The caveat: the data don’t support this hypothesis – at least experimentally.
Hall cites studies (his own) which “fail to support key model predictions regarding changes in energy expenditure and body fat.” In these studies, simply put, diets that are otherwise isocaloric (that is, contain equal amounts of calories) but differ in their composition of fat, protein, and carbohydrate, fail to show differences in weight gain. According to the carbohydrate-insulin model, and Taubes et al, a diet higher in carbohydrate but otherwise equal calories should result in weight GAIN. While some studies have demonstrated unique metabolic effects of a high-carbohydrate/refined sugar diet, current conclusions based on experimental evidence are that it is “possible that the increased carbohydrate in the food supply, particularly refined carbohydrates, contributed to the obesity epidemic by augmenting (increasing) calorie intake.”
We can all anecdotally relate to this. Food containing high amount of refined carbohydrates are often calorie-laden, and similarly contain high amount of fat, sugar, and artificial ingredients, all a “recipe” for negative health consequences. It is difficult to manipulate carbohydrate intake by itself, especially in real-life context and not in an isolated lab environment (and not in animal models, which restrict the ability to generalize of any experimental manipulation of diet). Furthermore, any data driven from observational studies are purely that, observational. Who seems to consume the most refined carbohydrates and sugar? Individuals who exercise less and tend to have other negative lifestyle risk factors that confound any conclusions regarding diet alone. Thus, the carbohydrate-insulin model will remain, for the time being, just that – a model.
Hall states in his conclusions that while it is hard to scientifically demonstrate one “cause” of the obesity epidemic, it is “easy” to rule out simple explanations such as one macronutrient or dietary component (sugar).
What is plausible, in Hall’s opinion (and mine)? Complex changes in our food environment overall, as well as alterations in our normative eating behavior, have led to profound physiological changes on the individual and population level. It is not just that we are eating more sugar, that fact is indisputable, but we are eating more of EVERYTHING. Taking food out of the equation, it is also clear that changes in our lifestyle (decreased physical activity, bot exercise and occupational) are very likely playing an important role in obesity and other diseases of modern living. Sedentary behavior is now being increasingly recognized as an independent risk factor for many diseases.
Verdict: Evidence Inconclusive
I do not think the argument for the cause of obesity, as Hall states, can be simplified to one source. Gary Taubes presents some fascinating historical data, tight correlations, and even experimental studies supporting his opinion that sugar is the cause of diabetes and obesity. Taking this handpicked evidence for what it is – he is right. However, as with everything in life, human physiology is complex, and complex may be an understatement. If we really look at the myriad of factors that influence body weight – energy expenditure, fat deposition, physical activity – it is truly impossible to isolate specific mechanisms that regulate it. While we mostly know what causes diabetes, and have probable explanations about what generally leads to obesity, heart disease, etc…they are all still generalizations and probably will be for a long time.
Luckily, we know what we must do in order to live healthy and long lives. Phrases like “eat a balanced diet” and “get plenty of exercise” are unhelpful and I will avoid their use here (or ever). There probably IS a better way to eat and IS an optimal amount of exercise for each one of us. Too much sugar, and too many carbohydrates are probably not great. Fats, we now know, are generally healthy and we no longer (or probably shouldn’t) recommend against them in a general sense. Science will increasingly let us in on the secret of how our bodies work best, but until that time comes, it seems like general dietary and lifestyle advice should follow a pattern fitting with our evolution: movement, diversity of healthy eating, and more movement.
1. TaubesGary. What if sugar is worse than just empty calories? An essay by Gary TaubesBMJ2018; 360