Survival of the Fattest 

An Anthropological Exploration of Obesity, Insulin Resistance & the Devastating Impact It Has Today

Western society is grappling with an impending health crisis: the rampant epidemics of obesity, insulin resistance and diabetes. Despite the remarkable advancements humanity has made in various fields, our health is paradoxically deteriorating. The very progress we've achieved has led to a profound disconnect from our past, leaving us vulnerable to the consequences of our own success. The current state of our health, marked by skyrocketing rates of these chronic conditions, is a direct result of our failure to understand the underlying causes of these conditions. This current health crisis is a self inflicted wound. It’s born from the unintended consequences of our own prosperity, a result of the negative aspects of a modern, affluent lifestyle . We must take responsibility for the consequences of our choices. Despite a wealth of research and published studies, these epidemics continue to spread at an alarming rate, underscoring the urgent need for a deeper understanding of the root causes and effective solutions to combat these interconnected health crises.

The grim statistics are that over 40% of American adults are obese and up to 80% are overweight. That is even greater for certain ethnic groups. As for diabetes, one and nine adults are now diabetic(that doesn’t include those that have underlying insulin resistance). When this is compared to 100 years ago, one in 30 adults were obese and one in 50,000 adults were diagnosed as diabetic. ( although sensitive diagnostic tests were not available) A scary story. Why the dramatic change?

In the 1920s, the first scientific studies (done by the New York City health commissioner) linked diabetes with sugar; the risk factors being older age, sedentary lifestyle, wealthy, Caucasian and those who consumed excess amounts of sugar. In fact, when one looks at sugar intake preceding the 1800s, it was minimal at best. With the onset of World War One , there was an exponential growth of sugar consumption. In the 1950s high fructose corn syrup (HFCS) was introduced, and in the 1960s, scientist learned how to convert the naturally occurring corn sucrose (a combination of glucose & fructose) to pure fructose . The industrialized advantage was that it increased sweetness, improved shelflife, was more economical to produce than sucrose, and increased versatility in its range of applications from beverages to baked goods due to its unique properties and sweetness profile. With the ever-expanding food industry, it was quickly adopted and now appears in almost everything we eat. To further illustrate the role of sugar, the average person’s sugar intake per year in the 1700’s was 4 pounds, in the 1800’s - 18 pounds, in the 1900’s - 90 pounds, and in the year 2000 it was estimated to have reached up to 155 pounds per person. That translates to each one of us eating approximately 17 teaspoons of sugar daily. This exponential rise in the use of sugar, especially artificially produced sugars, was mirrored by the rise of obesity and diabetes. In fact, anthropologist have studied the effects of introducing sugar to a population as was the case of the Nauru people, an isolated indigenous society inhabiting a small island off Australia . Prior to the introduction of the western diet which was high in sugar and processed foods, there was no obesity or diabetes. The diet consisted mainly of coconut, fish and traditional foods. However, in the early 20th century western foods were introduced and by the middle of the century, the country became increasingly dependent on imported goods and processed foods, including sugar, flour and processed meat. By the 1980s, it became very apparent that with the dietary changes came an alarming increase in obesity, diabetes, and non-communicable diseases.

Classically, the calories consumed matched the calories used. Intake equaled output. With the rise in the use of sugary processed foods, our diet became calorie dense while at the same time cars, TV, Internet and elevators replaced energy usage. Before we knew it we were consuming many more calories than were required. The body is never wasteful, storing those extra calories as fat useful for future sources of energy, hence increasing fat deposition ultimately leading to obesity. This process is highly regulated by insulin. This hormone regulates the use of energy in the body; deciding whether to burn fats or sugar. Insulin’s primary role is to store energy, not to burn energy. High insulin levels store energy in the fat cells inhibiting the fat cells from burning those calories. Conversely, low insulin levels allows the fat cells to utilize or burn this stored energy. (Eating carbohydrates greatly increases insulin levels whereas fats don’t. Protein is in between. This explains why a low fat, higher carb diet hinders weight loss not allowing fats to release their stored energy and a high fat, low carb diet promotes fat loss).

Caloric intake fuels the body’s metabolic processes on a cellular level primarily through ATP. Energy is either stored or consumed depending upon the body’s needs. For the most part, the number of fat cells in a body does not increase after your teenage years, although in those populations whose ancestors came from cold climate, there is enhanced ability to produce more fat cells underneath the skin as our ancient ancestors needed a means of insulating themselves against the cold. This increase in the number of fat cells is called lipogenesis.

Insulin instructs the body to store the excess energy in our fat cells and each individual fat cell exponentially gets larger. These fat cells are primarily located around the belly surrounding our internal organs referred to as visceral fat. When the individual fat cells grow to about 4 to 5 times baseline, they became hormonally active, secreting hormones that induced insulin resistance . In that manner, they are protecting themselves from becoming too overloaded; ready to burst. This is akin to the fat cell telling insulin that they are “stuffed, and can’t eat anymore”. Unfortunately, this insulin resistance affects the entire body as all cells have insulin receptors. It ultimately leads to a proinflammatory state, with an elevated stress response, elevated cortisol levels and elevations of adrenaline . The direct result is the development of what we call the ‘metabolic syndrome’. This is characterized by elevated triglycerides, low HDL, fatty liver, insulin resistance, elevated sugars, hypertension, and systemic inflammation. In those individuals that still maintained the ability for lipogenesis, they form more fat cells primarily located beneath the skin. They gained just as much fat but instead of having large fat cells, they have many more smaller fat cells. These smaller fat cells still have plenty of space to grow and thus don’t secrete hormones increasing insulin resistance. This explains why populations whose ancestors evolved from warmer climates develop diabetes and subsequent heart & metabolic diseases at much lower levels of weight gain; a vast difference of risk between those with the big belly (central obesity ‘apple shaped’) and the with big arms, legs and buttocks(so called ‘pear shape’).

The body‘s ability to store excess calories as fat is an integral part of survival. The species is not alone in this ability; it is well known that it exists in many animals. Take for example the grizzly bear. They change behavior in the fall in developing severe hunger, increasingly their food intake and gaining up to 8 to 10 pound daily with significant increase in fat as well as insulin resistance. In that manner, during hibernation over the winter time without a food source , this fat is broken down to provide energy and water. It appears that switch occurs in the fall when the diet changes to ripe fruits and honey, substances high in fructose. Fructose seems to be the key in inducing obesity. When mice from the same litter are fed different diets, one being normal and one high in fructose, the high fructose mouse, while eating the same amount of calories, will become two or three times the size of its sibling. It appears that fructose increases fat and metabolic features, and diets high in fructose are associated with increased fat accumulation, increase glucose levels, and increase fat deposition in the liver.

Glucose is the primary fuel in our bodies and fructose is the sugar found in fruit and honey. Table sugar consists of sucrose, which is a combination of fructose and glucose. Rather than the classical mechanism of ‘too much energy intake coupled with decrease energy expenditure leads to the storage of excessive fat’, new mechanisms have been proposed. It appears that fructose metabolism plays a major role in the development of obesity and insulin resistance. Fructose metabolism on a cellular level affects the mitochondria, the power plant of the cell. It suppresses this by lowering the ATP metabolism and blocking fat breakdown. Fructose simulates a low energy state which is very important for survival, as seen in the bear that needs to hibernate throughout the winter. As part of this survival process, Fructose has been shown to activate hunger & thirst, induce a loss of satiety with Leptin resistance( Leptin is a hormone that regulates appetite by signaling to the brain that the body is no longer hungry while increasing feelings of fullness), lower the body’s resting energy metabolism(somewhat similar to a car that has a slow idle), induces insulin resistance as well as a state of systemic inflammation. The survival advantage is increased fat storage, reduced energy expenditure, protecting the brain from drops in circulating glucose ( the brain requires a steady supply of glucose as it has almost no ability to store glucose), maintains circulation & excretion, reduces oxygen needs, and the activation of systemic inflammation enhances the ability to fight infection. This persistent activation produces obesity and helps protect against most non-communicable diseases. The mechanism by which fructose lowers the metabolism, suppressing mitochondria ATP- the energy factories of the cell, involves uric acid. Uric acid is what causes gout and it has been known for many years that in diabetic individuals and in those with insulin resistance, uric acid levels are higher. So is the incidence of gout. It appears that the elevated levels are linked to our prehistoric ancestors having had a genetic mutation in uricase, the enzyme involved in uric acid metabolism. This has been found to have significant survival advantages. Although this mutation leads to higher uric acid levels in humans compared to other mammals, this mutation may have helped human survive in periods of food scarcity such as during winter months when food sources were limited. Uric acid promotes the conversion of glucose to fructose in the body resulting in increased fructose-induced fat storage and a slower metabolic rate. Studies in rats inhibiting this enzymes led to increased uric acid, fasting blood glucose, body weight, blood pressure, triglycerides and liver fat. In humans, serum uric acid levels have nearly doubled since the 1920s, mirroring the use of added sugars and fructose in the standard diet.

The increase of leptin resistance blocks satiety , the feeling of being full and stimulates weight gain. Similarly, fructose has been shown to increase the bowel absorption of nutrients, maximizing caloric intake. While fructose boosts the body's energy storage, it simultaneously decreases the body's metabolic rate resulting in lower energy expenditure. Notably, this process is not solely driven by caloric intake as fat accumulation and diabetes can develop independently of excess calories. Consequently, a diet high in fructose can increase the risk of obesity, insulin resistance, and diabetes, even if overall caloric intake is moderate.

Fructose comes from fruits such as apples, bananas, and berries. Small amounts can be found in vegetables such as carrots, sweet potatoes, and onions. Honey & agave nectar are high in fructose. Natural fruits remain healthy because fruits contain only small amounts of fructose and the first 3 to 4 grams are initially inactivated in the intestines. In addition, fruits contain antioxidants such as vitamin C, polyphenols, and flavonols(epicatechin) that can block fructose effects. Whole fruits contain significant fiber slowing the absorption of fructose and potassium which has been shown to be beneficial. This is not true of fruit juices. By removing the fiber, juices lead to a concentration of the natural sugars with a more rapid digestion and absorption of these sugars. Juicing frequently removes or reduces the compounds found in whole fruits that help regulate appetite and satiety , including the fiber, water content and certain phytochemicals. The high concentrations of fructose seen in the western diet has overwhelmed the body’s ability to regulate its delicate metabolic energy balance. Sugar and refined carbohydrates markedly increase the serum insulin levels, enhancing its role in energy metabolism. Subsequently it increases the storage of fat with a reduction in the ability to use that fat as an energy source. Diets rich in sugar significantly increase insulin levels while high-protein diets have a relatively modest effect on insulin levels. In contrast, high-fat diets have little to no impact on insulin levels. Interestingly, high-fat diets are associated with low insulin levels, whereas low-fat diets are linked to high insulin levels. However, high insulin level can have a counterintuitive effect, triggering the body to go into survival mode, prioritizing fat storage, and slowing down metabolism. This can lead to the development of the metabolic syndrome and its associated illnesses. Paradoxically eating protein from animal sources rich in saturated fat has been shown to lower blood insulin levels allow for the mobilization of energy from adipose tissue (fat cells) and to stimulate satiety with less hunger. In a sense, the high fat diet is associated with low insulin levels , and the low fat diet with a high level. With high insulin levels seen in low fat diets, the body goes into survival mode, fat storage becomes a priority with a slowing of metabolism, and unfortunately,the metabolic syndrome. Besides dietary sources of fructose, it has been shown that the body can convert its own energy sources, such as glucose and sorbitol (often used as a sugar substitute) into fructose. High glucose concentration stimulates fructose production seen with high carbohydrate diets, high glycemic refined carbohydrates and the markedly elevated glucose levels associated with insulin resistance and diabetes. It is estimated that half of the adverse metabolic effects from glucose are in fact caused by insulin while the other half from fructose.

When the body shifts from relying on glucose to fat for energy, it releases stored fat from adipose tissue and produces ketones. The brain, which requires a constant energy supply, can efficiently use ketones as a primary energy source. This metabolic flexibility allows the brain to adapt to different energy sources, depending on availability. Notably, the brain utilizes 20% of the body's energy requirements, yet unlike other organs, it has little to no capacity to store energy, making a continuous supply of nourishment crucial for proper function.

Research suggests that ketones may provide a more efficient energy source, producing more ATP per molecule than glucose, and potentially reducing oxidative stress and inflammation. This may have neuroprotective effects, potentially benefiting conditions like Parkinson's disease, Alzheimer's disease, and cognitive dysfunction. By reducing the body's reliance on insulin-driven glucose, neuroinflammation can decrease. This is particularly relevant, as neuroinflammation is often linked with systemic inflammation & underlying metabolic issues, which are themselves driven by insulin resistance and a proinflammatory response.

Furthermore, altered glucose metabolism has been observed in individuals with psychiatric disorders such as bipolar disorder, ADHD, depression, and anxiety. Ketones may have mood-stabilizing effects, improving focus and reducing symptoms. Individuals with psychiatric disorders often develop chronic metabolic disorders, which can significantly reduce their life expectancy. While their psychiatric conditions, such as depression or bipolar disorder, can increase the risk of suicide, the actual reduction in lifespan is often driven by related metabolic issues, including insulin resistance, inflammation, and cardiovascular disease. Ketones may offer a potential solution to help mitigate this problem.

From an anthropological perspective, the ability to utilize ketones as an energy source may have provided an adaptive advantage for humans during periods of food insecurity. This adaptation allowed early humans to maintain cognitive abilities and emotional stability so vital in problem-solving and decision-making, necessary for survival. However, with the widespread availability of highly processed and glycemic-dense foods, this adaptation has become a disadvantage, driving insulin resistance, inflammation, and chronic disease.

The discovery that high salt consumption accelerates the body's conversion of glucose to fructose adds another layer of complexity to this process.

Salt increases serum osmolarity and induces the enzyme Aldose reductase- the fructokinase pathway. The result over time is the development of leptin resistance with hyperphagia (increased appetite) causing obesity, insulin resistance and fatty liver. In fact, a high salt diet has been found to predispose to the development of diabetes and non-alcoholic fatty liver disease. This effect that salt has is akin to putting fuel on the fire. Animals are attracted to salt licks as nature has evolved specialized survival instincts.

Processed foods are both high in fructose and high in salt, a deadly yet all too common combination in western diets. Further studies have implicated the fructose metabolism as a driving force of salt induced obesity and elevations of blood pressure. Hydration appears to blunt this negative effect. Its association with the metabolic syndrome has been well documented but recent research has suggested that fructose is also strongly associated with cancer. It appears that fructose transporters are up-regulated in a variety of tumors stimulating cancer growth and metastasis. Blocking fructose metabolism may be a novel approach for the prevention and treatment of cancer.

From an evolutionary point of view, multiple studies have tried to unravel how a survival pathway can go wrong. Could a single mutation in our past have helped survive but today, in times of plenty, cause obesity and diabetes? This helps explain the survival switch, essentially ‘advantage becomes disadvantage’. Fructose is considered the survival nutrient. The ability to obtain fructose by our ancestors in mature fruits and vegetables, as well as the bodies ability to convert glucose to fructose has led to:

1. Increased hunger and foraging to help find food

2. Increase food intake and decrease resting metabolism to increase fat stores

3. Increase in Insulin resistance, preserving the brain’s energy source and reducing overall energy metabolism

4. Increasing systemic inflammation, which help fight against infection

5. Increases blood pressure as well as filtration pressures in the kidney which help support circulation and excretion

6. The shift to glycolysis, the pathway sugar is converted to energy, essential for wound healing, tissue repair, and the immune response.

Humanity is currently grappling with a devastating trio of epidemics: obesity, insulin resistance, and diabetes. The harsh reality is that our modern lifestyles have become a major contributor to these health crises, ultimately working against our own well-being. The link is the exponential growth of sugar consumption, particularly fructose, which has become a ubiquitous ingredient in processed foods. This shift has devastating consequences including insulin resistance, the emergence of the metabolic syndrome and a pro-inflammatory state that contributes to chronic disease. The body's natural response to store excess energy as fat, once a survival mechanism, now drives obesity and related health issues. The metabolism of fructose is a crucial factor, influencing various physiological processes, including mitochondrial function, metabolic rate, hunger and satiety regulation, hormone balance, and overall energy equilibrium.

The Western diet high in processed foods and sugar has overwhelmed the body's innate ability to regulate its metabolic energy balance leading to this myriad of health problems. Understanding the root causes of these epidemics is crucial to developing effective solutions to combat these interconnected health crises. To truly move forward, we must first step back and confront the roots of our very being, for it’s only in understanding what makes us tick that we can forge a future path to health and wellness .