Beyond Calories: Why Calories In, Calories Out, is not the answer

“The most common form of malnutrition in western world is obesity”  – Mervyn Deitel

Still today a ridiculous paradigm is accepted as fact that you gain weight when the amount of calories you consume exceeds the amount you burn. But, this far underestimates several compounding environmental factors that contribute to the whole story of obesity. This model also lacks the ability to explain many phenomena such as why antibiotics lead to an increase in body fat (1,2,3), or why cesarean babies are at increased risk of storing excess body fat (4,5).

New research is continuing to shed light on why and how our innate metabolic programming shifts into “survival” or “storage” mode. For instance, we now know that excess fat is not just a cosmetic or metabolic issue, it also impacts other systems such as our digestive tract, hormones, and immune system (6). What follows this physiological shift is fat loss becomes more difficult, and overweight people tend to become obese. Accomplishing any shifts in body composition becomes difficult, frustrating, and requires persistence as well as an effective program to break free of this destructive cycle.

What BLOWS my mind more though, is a study of over 900,000 individuals reported in the Lancet suggests that the more fat you have, the more likely you are to straight up die early (7). For every five-point increase in BMI (body mass index), there is a 30% increased risk of all-cause mortality (death for ANY reason at all), 40% increase in death from cardiovascular disease, and 60-120% increase in mortality from diabetes, kidney and liver disease (7). I’m sorry but that’s just messed up (*edited from F*&Ked up to maintain professionalism 😉 but let’s be real).

Calories are NOT KING.

While it is true, overconsuming empty calories and under-exercising can predispose us to weight gain, it does not explain the whole story. We must also consider the many other influences on our bodies energy system such as hormone disruption, alterations to gut bacteria, endocrine disrupting chemicals, inflammation, and of course the number and functioning of our mitochondria. We will cover these factors in more detail below.

Hormone Disruption:

Nutrients, not calories count. Many diet programs are created based on the popular but incorrect belief that one must restrict calories and macronutrients to lose weight. The missing component that these plans do not consider is the impact that foods have on the hormones our body produces. When you restrict calories, hormones called incretins that are secreted by the intestines are disrupted. Incretins prompt the release of insulin when glucose levels rise and help to regulate blood sugar and appetite. When incretins are high weight loss is much more likely, but when they become disrupted, diets fail. Bottom line you should not have to use superhuman willpower to maintain a healthy lean body. This is a tell-tale sign of hormone imbalances.

Gut Bacteria:

A calorie is not just a calorie, they are not created equally and here is the reason why. The calories that we consume can have dramatically different effects on our gut microbiome and thus our hormones and metabolism.  Even the speed in which you consume food, the position you eat (sitting vs on the go), the time of day, the amount of fiber, alcohol, fructose, and the combination of foods can influence what makes up your gut microbiome and how your body processes calories.
For instance, fructose is processed differently than glucose. Fructose blunts satiety signals, alters intestinal bacteria and increases levels of the appetite-stimulating hormone ghrelin (8). To make matters worse, fructose stimulates the reward centers in the brain creating food additions (9). Lastly, fructose has been shown to be able to widen the spaces between intestinal cells increasing the risk of absorbing bacterial endotoxins which then promotes inflammation (10).

Mitochondria & Inflammation:
If you can remember back to high school biology class, our mitochondria are the powerhouse organelles within our cells. You can think of them as little engines that take “fuel” from stored fat or food, combine with oxygen to ignite a “spark” to power our cells. Another way to look at it is our mitochondria take the calories from food and converts them into an energy called adenosine triphosphate (ATP) that our cells can use.  When we consume calories our endocrine system acts as a bank account, designating the foods we eat to “spending money” or to our “savings account” which ends up on your butt, hips, abdomen, and thighs.

The function of the mitochondria is important to fat loss for this reason. Fit individuals have increased mitochondrial function while obese and insulin resistant individuals have not only fewer mitochondria but the ones they do have are sluggish and poorly functioning.  Obese people also have less oxygen reaching their mitochondria and remember oxygen is needed to create ATP or energy from the foods we eat or from our fat stores. Instead of a brightly lit fire within those mitochondria, overweight individuals fire smolders from lack of oxygen and fat burning may come to a halt or at the very least be far less efficient. Creating more of an issue the lack of oxygen triggers inflammation, further hampering fat burning and insulin resistance.  Inflammation can misdirect metabolism into a state of increased sugar burning at the expense of fat burning, certainly not ideal for weight loss. The end result is not only a sluggish metabolism and difficulty losing weight but very low energy and intense cravings for high fat, high carb foods to provide any sort of boost to get through the day.

Not only does the lack of oxygen seen in obesity contribute to inflammation but insulin resistance itself or pre-diabetes is a pro-inflammatory process. Glucotoxicity (sugar toxicity) is a side effect associated with insulin resistance and type 2 diabetes due to unregulated blood sugar levels. AGE, or advanced glycation end products, is the medical term for describing the compound that is produced when excess sugar combines with proteins in the body, such as hemoglobin (11). This is why we use HbA1c (sugar bound to hemoglobin) as a 120-day marker of blood glucose.  The immune system has receptors for AGEs called RAGEs, receptors for advanced glycation end products, which when bound creates inflammation. Fructose and glucose are not the only things that will generate AGEs. Consumption of broiled, deep-fried, grilled and roasted foods are also rich in AGEs which leads to impairments in blood glucose, satiety hormones, and pancreatic function. My recommendation would be to boil and steam whenever possible or when roasting vegetables add the oil after cooking.

Lastly, it is noteworthy to point out the connection between our metabolism and immune system.  Many studies have shown that obese individuals have an increased level of inflammatory T lymphocytes (immune cell). T lymphocytes like to congregate and often behave in a bipolar way flipping between a fun dance party to full-on beast killing mode. Fat cells and inflammatory signals can flip this switch and T Helper cells reprogram their metabolism to favor sugar burning which is incongruent with fat burning (9). What is very concerning is these immune changes are similar to those which are seen in heart disease autoimmunity, and cancer (9).

Key Takeaway: We Need a New Paradigm

Yes, it is true that many will gain weight when they over consume calories and are inactive. However, we can no longer live by the antiquated concept that to lose weight we just need to eat less and exercise more. Research confirms what many yo-yo dieters know, restricting calories triggers hunger and lowers your metabolic rate, sabotaging your attempt to lose any fat. There are many modern ways of living that have contributed to the obesity epidemic such a sitting, sleep deprivation, eating on the go, stress, and endocrine and gut disrupting chemicals in our environment.

Obesity can also be looked at as a double-edged sword as your mitochondria decrease in number and function with every added pound of fat you put on.  With less energy comes less motivation to exercise and thus less oxygen reaching the mitochondria which need oxygen to function and burn fat for fuel. As a result, individuals get stuck in this pro “sugar” burner state and have a very difficult time burning fat for fuel.

The more fat you have the more your fat secretes hormones such as adipokines that attract cells of the immune system called macrophages that release enzymes and cytokines the further drive inflammation. Inflammation disrupts your fat loss efforts and creates a vicious cycle of more inflammation and fat accumulation (12). While the body can normally put out the inflammatory fire, the same hormones secreted from fat cells impair the extinguishing process and contribute to chronic inflammation, more fat gain, and metabolic disruption (13).

We also know that all calories are not created equally. Fructose contributes to fat storage by altering hormones, gut bacteria and creating leaky gut (a recipe for inflammation). Fructose has also been shown to increase fat in the liver, impairs insulin release, raises triglyceride levels all of which increases the risk of type 2 diabetes, fatty liver, cardiovascular disease and obesity (8,9).

What to do next?

If you have enjoyed this blog and are interested in learning more about my approach to sustainable fat loss, please leave a comment below. Also make sure to stay tuned because subsequent blogs will be covering what to do to address the issues that were discussed above such as Hormones, Gut Health, Inflammation, Mitochondria.

<3

Breanne

 

References:

1. Kolehmainen, Marjukka, et al. “Bilberries reduce low‐grade inflammation in individuals with features of metabolic syndrome.” Molecular nutrition & food research 56.10 (2012): 1501-1510.

2. Harte, Alison L., et al. “High fat intake leads to acute postprandial exposure to circulating endotoxin in type 2 diabetic subjects.” Diabetes care 35.2 (2012): 375-382.

3. Erridge, Clett, et al. “A high-fat meal induces low-grade endotoxemia: evidence of a novel mechanism of postprandial inflammation.” The American journal of clinical nutrition 86.5 (2007): 1286-1292.

4. Cani, Patrice D., et al. “Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity.” Gut microbes 3.4 (2012): 279-288.

5. Bäckhed, Fredrik, and Peter A. Crawford. “Coordinated regulation of the metabolome and lipidome at the host-microbial interface.” Biochimica et Biophysica Acta (BBA)-Molecular and Cell Biology of Lipids 1801.3 (2010): 240-245.

6.Van den Bussche, Hendrik, et al. “Which chronic diseases and disease combinations are specific to multimorbidity in the elderly? Results of a claims data based cross-sectional study in Germany.” BMC public health 11.1 (2011): 101.

7. Prospective Studies Collaboration. “Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies.” The Lancet 373.9669 (2009): 1083-1096.

8. Vos, Miriam B., and Craig J. McClain. “Fructose takes a toll.” Hepatology 50.4 (2009): 1004-1006.

9. Purnell, Jonathan Q., and Damien A. Fair. “Fructose ingestion and cerebral, metabolic, and satiety responses.” Jama 309.1 (2013): 85-86.

10. Spruss, Astrid, and Ina Bergheim. “Dietary fructose and intestinal barrier: potential risk factor in the pathogenesis of nonalcoholic fatty liver disease.” The Journal of nutritional biochemistry 20.9 (2009): 657-662.

11. Tahara, Nobuhiro, et al. “Serum levels of advanced glycation end products (AGEs) are independent correlates of insulin resistance in nondiabetic subjects.” Cardiovascular therapeutics 30.1 (2012): 42-48.

12. Jumpertz, Reiner, et al. “Energy-balance studies reveal associations between gut microbes, caloric load, and nutrient absorption in humans.” The American journal of clinical nutrition 94.1 (2011): 58-65.

13. Deopurkar, Rupali, et al. “Differential effects of cream, glucose, and orange juice on inflammation, endotoxin, and the expression of Toll-like receptor-4 and suppressor of cytokine signaling-3.” Diabetes care 33.5 (2010): 991-997.

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