The US is fat, very fat. The CDC National Center for Health Statistics found, “more than one-third (36.5%) of U.S. adults have obesity”(1). Here are a few images to give you an inside look at what this means:
As of 2014, a trend found by Flegal et al. demonstrated “…the prevalence of overall obesity and of class 3 obesity showed significant linear trends for increase between 2005 and 2014″(3). So, we are not only fat, but are getting fatter. If you are like me, you may also be wondering, “what is another currently expanding disease in the US?” The answer is type 2 diabetes. The CDC states, “more than 30 million Americans have diabetes (about 1 in 10), and 90% to 95% of them have type 2 diabetes”(6). These are now simple facts of 2018 and are great. So, what is my problem with them? It seems federal agencies, like the CDC are more interested in the reductionistic symptoms (obesity being one for example) rather than the holistic cause. There was a Ted Talk given by Dr. Peter Attia that I think hit the nail on the head. He did a nice job demonstrating how little we know about metabolism’s link to obesity/type 2 diabetes, then spoke about how the healthcare industry as a whole has failed obese/diabetic people.
This bring us to the heart of this post: I want to redefine the term(s) “obesity” and “type 2 diabetes”, then offer my hypothesis on the cause.
Redefining Obesity and Type 2 Diabetes
In order to redefine the term(s) obesity and type 2 diabetes, I think it is first important to look at the independent definitions. Obesity is defined as “an excessive accumulation of fat in the body” and type 2 diabetes is defined as, “non-insulin-dependent diabetes mellitus”(5). Now, lets begin to take a more holistic view of these arbitrary terms with a more current key word that combines these two terms: “diabesity”(7). I like diabesity because it stresses the interdependence of these two terms. This aggregate word also begs us to ask the important question, what is the link between the two? The answer is: the two are intimately linked because they are both symptoms of a much larger pathology, hyperglycemia.
Therefore, a simple definition of diabesity is: a complex, progressive cascade of symptoms resulting from hyperglycemia. Now comes a bit of biochemistry to describe the mechanism of this pathology.
Biochemistry of Glucose Metabolism
Dating back to 1941, R.D Lawrence published an article in the Proceedings of the Royal Society of Medicine journal, eloquently stating, “plants and animals build up reserves of fat from carbohydrate[s]”(8). Without understanding the complex biochemistry of glucose metabolism, Lawrence summarized the entirety of it. What does this mean? The symptoms of diabesity stem from eating too many carbohydrates (sugars). Here is my hypothesis of the mechanism that leads to the symptoms of diabesity.
- Consume copious amounts of refined sugars
- Beta cells of the pancreas respond to the high levels of blood glucose and secrete insulin
- Insulin binds the glut-4 receptor on muscle and adipose tissue, allowing for the influx of glucose
- Glucose undergoes glycolysis, which increases the amount of cytoplasmic pyruvate
- *Pyruvate is transported into the mitochondria and enters the Krebs Cycle as acetyl-CoA, yet only undergoes the first oxidation-reduction reaction to citrate because the downstream allosteric enzyme isocitrate dehydrogenase is down regulated in the energetic environment (inhibited by ATP and NADH).
- As citrate accumulates, it exits the mitochondria into the cytosol where it will eventually be converted to malonyl-CoA (a building block of fat) by another allosteric enzyme, acetyl-CoA carboxylase (promoted by citrate, insulin, and a high carbohydrate/low fat environment). We will come back to this, for it is very clinically relevant step
- Skipping several steps (you’re welcome) triacylglycerides (TAG) will be produced and stored in your adipocytes (fat storing cells)
- Increased TAG storage leads to the symptom of obesity. People tend to store fat in the apple or pear pattern
- People who store fat in apple pattern, tend to develop insulin resistance (7)
- Blood insulin levels rise, along with blood glucose levels, resulting in type 2 diabetes
- From here the mechanism is less agreed upon, but the generally accepted, big picture cascade of events goes: tunica intima damage of blood vessels, atherosclerosis, cardiomegaly, pulmonary edema, hypoxia, tachycardia/tachypnea, angina, cardiac infarction, death.
It is important to note that this mechanism does not occur overnight, it happens over many years and is the body’s natural adaptation to the stress of hyperglycemia. From a pathology perspective, the only way to heal a disease is to alleviate the stressor causing it; therefore, the treatment of this specific disease calls for decreasing the amount of carbohydrate intake. I believe the US population is smart, we are just miseducated. There needs to be an educational movement teaching us that processed foods and refined carbohydrates are very bad for you. Then, providing us with a healthy, alternative diet plan (insert plug here for future article). The cool thing is mother nature already has packaged foods in the proper macronutrient ratios; we just need to eat them.
What would I do if I had diabesity?
- WWJE: What Would Jesus Eat? I would only eat food that have been on this earth for 2000 years and shop USDA Organic.
- Ketogenic diet. Eliminate all refined carbohydrates (grains, potatoes, sugars) and decrease my complex carbohydrate intake exponentially; while at the same time increase the amount of healthy unsaturated fats with each meal. I would eat a lot of fat. This will down-regulate the acetyl-CoA carboxylase enzyme, so the body will make less endogenous TAGs. I will cover this diet in depth in my future lipid metabolism post (10,11).
- Get into a state of zen (AKA decrease cortisol). Easier said than done.
- Increase my muscle mass by compound barbell movements. This will help turn the tide of the fuel partitioning battle and is a vital piece to the puzzle (12).
- Make sure I had no nutrient deficiencies. This topic calls for an entire article on its own right.
What I wouldn’t do.
I would not take biguanides like Metformin, statins like Lipitor, smoke (if I did), eat fast food, eat refined carbohydrates or eat fruit. I also would not follow the choose my plate diet, given out by the CDC (1).
The human metabolism is extremely complex and has been simplified for the clinical purpose in this article. From a physiological perspective, we are constantly adapting to the stresses placed on our body. These adaptation algorithms have been selected for since the dawn of evolution. At what point did our physiology break down and we require drugs to be healthy? It deeply upsets me when I see a conflict of interest in people writing the AMA guidelines; the same people who would rather treat symptoms with drugs to keep people sick, than treat a food problem with food. There’s no money to be made in the ‘no carbohydrate industry’. I dream of a future where doctors practice with a high level care-factor and treat the cause of a patients disease. It is imperative to recognize that these are not overnight treatments; a good rule of thumb is the treatment adaptation could take as much time as the pathological adaptation. Hopefully one day, people with diabesity will stop being victims of the system and reach true health. I believe there is hope.
I leave you with two nuances: 1. There is a significant amount of people with type 2 diabetes with a lean body mass (13). What does this fact do to mechanism of insulin resistance? 2. There is a laundry list of adiposopathy’s associated with diabesisty, most important being pathological hunger hormones and corrupt circuitry signals causing excess hunger (14). Thus, there is no cookie cutter treatment plan.
- Centers for Disease Control and Prevention. Overweight and 0besity. https://www.cdc.gov/obesity/index.html . Accessed May 13, 2018.
- Comparison of BMI using MRI . Digital Image. N.p., 2 Aug. 2016. Web. 13 May 2018.
- Flegal, Katherine M, et al. “Trends in Obesity Among Adults in the United States, 2005 to 2014.” JAMA: Journal of the American Medical Association 315.21 (2016):2284-2291. Web.
- “Obesity, the Metabolic Disease.” Obesity, the Metabolic Disease | Ethicon, Ethicon US, LLC, 13 May 2018, http://www.ethicon.ethicon.com/healthcare-professionals/specialties/obesity/obesity-overview#!defined.
- Stedman’s Medical Dictionary for the Health Professions and Nursing. Philadelphia :Lippincott Williams & Wilkins, 2005. Print.
- Centers for Disease Control and Prevention. (2018). Diabetes. Retrieved from https://www.cdc.gov/diabetes/basics/type2.html
- Golay, A, and J Ybarra. “Link between obesity and type 2 diabetes.” Baillière’s best practice & research. Clinical endocrinology & metabolism 19.4 (2005):649-663. Web.
- Lawrence, R D. “Interactions of Fat and Carbohydrate Metabolism-New Aspects and Therapies: (Section of Therapeutics and Pharmacology).” Proceedings of the Royal Society of Medicine 35.1 (1941):1-10. Web.
- Gnoni, Gabriele V, et al. “The mitochondrial citrate carrier: metabolic role and regulation of its activity and expression.” Iubmb Life 61.10 (2009):987-994. Web.
- Bhanpuri, Nasir H, et al. “Cardiovascular disease risk factor responses to a type 2 diabetes care model including nutritional ketosis induced by sustained carbohydrate restriction at 1 year: an open label, non-randomized, controlled study.” Cardiovascular Diabetology 17.1 (2018):56-56. Web.
- Hallberg, Sarah. “‘Reversing type 2 diabetes starts with ignoring the guidelines’: education from Dr Sarah Hallberg’s TEDx talk.” British journal of sports medicine (2018). Web.
- Codella, Roberto, et al. “May the force be with you: why resistance training is essential for subjects with type 2 diabetes mellitus without complications.” Endocrine (2018). Web.
- Barma PD, Ranabir S, Prasad L, Singh TP. Clinical and biochemical profile of lean type 2 diabetes mellitus. Indian Journal of Endocrinology and Metabolism. 2011;15(Suppl1):S40-S43. doi:10.4103/2230-8210.83061.
- López Jaramillo, Patricio, et al. “The role of leptin/adiponectin ratio in metabolic syndrome and diabetes.” Hormone molecular biology and clinical investigation 18.1 (2014):37-45. Web.