Since the days after Ancel Keys’ Seven Countries Study, people have been loath to the idea of eating cholesterol containing foods fearing it would lead to accumulated fat in our arteries and demise.
In addition to causing atherosclerosis, Keys thought that fat must make people fat. Because fat contains a little more than 9 calories per gram, whereas protein and carbohydrates contain only about 4 calories per gram, nutrition experts have long reasoned that a low-fat diet enables weight loss due to its reduced calorie content. In other words, if we eat fat, we will be fat…Cutting back on calories was one of several competing theories at this time about how people should lose weight, and since fat packed more calories, many doctors advised their patients to cut back on this part of the diet. Since then, fat in all forms has simply come to be commonly understood as something to be avoided.
Teicholz, N. (2014). The Big Fat Surprise: Why Butter, Meat and Cheese Belong in a Healthy Diet Simon & Schuster. (p. 29).
Overeating and eating fat makes you fat? From what I understand now, it’s not that simplistic. At a recent presentation, 'The quality of calories: Competing paradigms of obesity pathogenesis,’ Gary Taubes elaborates that this idea remains the prevailing logic. He explains that Tautology is the repetition and redundancy of Circular Logic (and is at the core of fat shaming - which this blog is not in any way shape or form - about). For example:
Why do we get fat? Because we are overeating.
How do we know we’re overeating? Because we’re getting fatter.
And why are we getting fatter? Because we’re overeating.
From this same presentation, Taubes reveals at least four of the top medical schools in the U.S. (Standford, Cornell, Harvard, & Chicago) and one in England (Oxford) were already promoting Diets for Obesity based on low carbohydrate foods. In fact, in 1951 from The Practice of Endocrinology, Raymond Greene, University of Oxford, England wrote:
Foods to be avoided:
1. Bread, and everything else made with flour
2. Cereals, including breakfast cereals and milk puddings
3. Potatoes and all other white root vegetables
4. Foods containing sugar
5. All sweets
Foods to eat as much as you like:
1. Meat, fish, birds
2. All green vegetables
3. Eggs
4. Cheese
5. Fruit (except bananas & grapes)
Of note, even before these low carbohydrate diet recommendations from these leading medical schools in the 1940s and 50s (suggesting that this way of eating has been around and recommended for decades), Vance Thompson wrote “Eat and Grow Thin” in 1914, touted as the first-ever low carbohydrate diet recommendations in the early 20th century. Thompson based the menus in his book on the “dietary charts issued by the United States Department of Agriculture…prepared by Mr. C.F. Langworthy, expert in charge of Nutrition Investigations” (p.94). Interestingly, the forbidden foods listed on the USDA ‘avoid’ chart in his book include the very same foods on the ‘Foods to be avoided’ list above – all due to the high sugar/carbohydrate content in these foods leading to their addictive, obesogenic effects on the body.
So, how do the foods we eat promote either weight gain/illness or good health?
It’s vital that we understand the metabolic processes a body goes through when it ingests certain macro-nutrients (protein, fat, carbohydrates). Chief among the vanguards in this arena is Jason Fung (The Obesity Code) and Gary Taubes (Why We Get Fat) who postulate that weight gain is a hormonal metabolic process driven by insulin. This is key because the current belief is that weight gain (or loss) is simply a CICO (calories in/calories out), eat less/move more issue and that we all just need to simply eat less, avoid fat (especially saturated fat), and eat lots of ‘heart healthy foods’ (translation: whole grains, legumes, polyunsaturated oils/fats, fruits, veg & limited lean only poultry/fish) and exercise a lot to stay fit, trim and healthy.
So the question that needs to be asked is, How’s that working for you?
Not well…not well at all.
Let’s consider the metabolic processes your body exhibits with respect to certain macro-nutrients (proteins, carbohydrates, fats). It’s important to note that the body’s hormonal physiology with regard to weight gain is no secret and has been well known for more than 100 years.
DR. ALFRED FROHLICH from the University of Vienna first began to unravel the neuro-hormonal basis of obesity in 1890; he described a young boy with the sudden onset of obesity who was eventually diagnosed with a lesion in the hypothalamus area of the brain. It would be later confirmed that hypothalamic damage resulted in intractable weight gain in humans. This established the hypothalamic region as a key regulator of energy balance, and was also a vital clue that obesity is a hormonal imbalance. Neurons in these hypothalamic areas were somehow responsible for setting an ideal weight, the body set weight. Brain tumors, traumatic injuries and radiation in or to this critical area cause massive obesity that is often resistant to treatment, even with a 500-calorie-per-day diet.
Fung, J. (2016). The Obesity Code: Unlocking the Secrets of Weight Loss. Greystone Books. (p. 65).
But in the absence of brain injury or disease, what mitigating factor(s) could help with regard to satiety in terms of preventing weight gain?
Discovered in 1994, this factor was leptin, a protein produced by the fat cells. The name leptin was derived from “lepto,” the Greek word for thin. The mechanism was very similar to that proposed by [Romaine] Hervey in 1959. Higher levels of fat tissue produce higher levels of leptin. Traveling to the brain, it turns down hunger to prevent further fat storage….Leptin is one of the primary hormones involved in weight regulation in the normal state. However, in obesity, it is a secondary hormone because it fails the causality test. Giving leptin doesn’t make people thin. Human obesity is a disease of leptin resistance, not leptin deficiency.
(Fung, pp. 65-66)
So the body’s hormonal response with regard to satiety requires a nod from leptin. In the absence of satiating foods that include natural fats for example, leptin resistance ensues, resulting in almost constant hunger. But what triggers hunger in the first place? Ghrelin. Ghrelin is the hormone that regulates hunger, and is triggered when insulin is routinely high/low, and especially out of control due to the ingestion of carbohydrates (especially processed carbs) and protein (especially lean protein).
Briefly, insulin is a fat storing hormone, and its opposite is glucagon, the fat burning hormone. Both hormones serve as signals to either store or burn fat. In other words, when insulin is low by reducing or eliminating sugar and carbohydrates from the diet, glucagon is secreted to shore up low blood sugar and burn fat for fuel.
But how does glucagon get the “signal” to burn fat? In the absence of insulin surging through the body to store incoming sugar and carbohydrate foods, glucagon is secreted (with the help of a fat-burning enzyme called hormone sensitive lipase, aka, HSL) and goes into the cells that are storing fat, and releases it breaking down triglycerides into fatty acids and glycerol for fuel. So when the glucagon to insulin ratio is high, you burn your body fat (Bikman). In other words, insulin tells your body to store away nutrients, and glucagon signals to your body to mobilize them out of storage for energy. When this happens, fat burning and subsequent weight loss occurs.
The crucial point to understand, however, is not how insulin causes obesity, but that insulin does, in fact, cause obesity. Once we understand that obesity is a hormonal imbalance, we can begin to treat it. If we believe that excess calories cause obesity, then the treatment is to reduce calories. But this method has been a complete failure. However, if too much insulin causes obesity, then it becomes clear we need to lower insulin levels. The question is not how to balance calories; the question is how to balance our hormones. The most crucial question in obesity is how to reduce insulin.
(Fung, pp. 87-88)
In other words… reduce the foods in your diet that spike insulin, and stop eating all the time. When you do eat, make sure the foods you eat are very nutrient dense. If you can do that, you’ll be satiated for longer periods, and your body will burn its stored fat for energy.
But why is this basic metabolic, hormonal response to food (fat storage v. fat burning) not widely known and accepted as basic human physiology in the nutrition world, let alone from our doctors?