^ Jump up to: a b Gatta-Cherifi, Blandine; Cota, Daniela (2015). "Endocannabinoids and Metabolic Disorders". Endocannabinoids. Handbook of Experimental Pharmacology. 231. pp. 367–91. doi:10.1007/978-3-319-20825-1_13. ISBN 978-3-319-20824-4. PMID 26408168. The endocannabinoid system (ECS) is known to exert regulatory control on essentially every aspect related to the search for, and the intake, metabolism and storage of calories, and consequently it represents a potential pharmacotherapeutic target for obesity, diabetes and eating disorders. ... recent research in animals and humans has provided new knowledge on the mechanisms of actions of the ECS in the regulation of eating behavior, energy balance, and metabolism. In this review, we discuss these recent advances and how they may allow targeting the ECS in a more specific and selective manner for the future development of therapies against obesity, metabolic syndrome, and eating disorders.
These calorie counting fanatics are either unaware, or don’t want you to know about what we call the law of metabolic compensation. This law dictates that your metabolism is not like a calculator at all but more like a thermostat or see-saw. You eat less and exercise more to burn calories, and your body compensates by making you more hungry while at the same time decreasing the amount of calories you burn at rest (resting energy expenditure or REE).

Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.


Thanks to your sales push, I finally committed and bought the Lift Weights Faster library. I look forward to using your ramp up method since I'm post injury and can't jump right back into high octane workouts. How do I get your manual? Thanks for great referral to Jen's stuff. I've received her newsletters forever but hadn't committed to the workouts because they were BEASTLY HARD.
Bhasin et al, as part of the Framingham Heart Study, found that sex hormone-binding globulin is independently associated with the risk of metabolic syndrome, whereas testosterone is not. Age, body mass index (BMI), and insulin sensitivity independently affect sex hormone-binding globulin and testosterone levels. [48] More recent studies have raised the possibility of an association between testosterone deficiency and metabolic syndrome. [49]
The word diabetes (/ˌdaɪ.əˈbiːtiːz/ or /ˌdaɪ.əˈbiːtɪs/) comes from Latin diabētēs, which in turn comes from Ancient Greek διαβήτης (diabētēs), which literally means "a passer through; a siphon".[111] Ancient Greek physician Aretaeus of Cappadocia (fl. 1st century CE) used that word, with the intended meaning "excessive discharge of urine", as the name for the disease.[112][113] Ultimately, the word comes from Greek διαβαίνειν (diabainein), meaning "to pass through,"[111] which is composed of δια- (dia-), meaning "through" and βαίνειν (bainein), meaning "to go".[112] The word "diabetes" is first recorded in English, in the form diabete, in a medical text written around 1425.
MRT, a.k.a. "metabolic resistance training," might as well be called "madman training." It's no-holds-barred, haul-ass, maximum-effort, build-muscle, heave-weight, torch-fat, absolutely insane huff-n-puff training. It'll spike your metabolism, crush calories like beer cans, lift your lactate threshold, boost your ability to make muscle, and maximize your body's capacity for change.

^ Feinman, R. D; Pogozelski, W. K; Astrup, A; Bernstein, R. K; Fine, E. J; Westman, E. C; Accurso, A; Frassetto, L; Gower, B. A; McFarlane, S. I; Nielsen, J. V; Krarup, T; Saslow, L; Roth, K. S; Vernon, M. C; Volek, J. S; Wilshire, G. B; Dahlqvist, A; Sundberg, R; Childers, A; Morrison, K; Manninen, A. H; Dashti, H. M; Wood, R. J; Wortman, J; Worm, N (2015). "Dietary carbohydrate restriction as the first approach in diabetes management: Critical review and evidence base". Nutrition. 31 (1): 1–13. doi:10.1016/j.nut.2014.06.011. PMID 25287761.
Diabetes mellitus is classified into four broad categories: type 1, type 2, gestational diabetes, and "other specific types".[11] The "other specific types" are a collection of a few dozen individual causes.[11] Diabetes is a more variable disease than once thought and people may have combinations of forms.[37] The term "diabetes", without qualification, usually refers to diabetes mellitus.
The good news is that committing to living a healthier life over the long-haul can make a difference. Lifestyle changes—for example, getting exercise, losing weight, eating a heart-healthy diet and not smoking—can help delay or even prevent the development of serious health problems. It’s important to partner with your health team to map out steps to manage your risk.
There is debate regarding whether obesity or insulin resistance is the cause of the metabolic syndrome or if they are consequences of a more far-reaching metabolic derangement. A number of markers of systemic inflammation, including C-reactive protein, are often increased, as are fibrinogen, interleukin 6, tumor necrosis factor-alpha (TNF-α), and others. Some have pointed to a variety of causes, including increased uric acid levels caused by dietary fructose.[18][19][20]

Metabolic syndrome promotes coronary heart disease through several mechanisms. It increases the thrombogenicity of circulating blood, in part by raising plasminogen activator type 1 and adipokine levels, and it causes endothelial dysfunction. [14] Metabolic syndrome may also increase cardiovascular risks by increasing arterial stiffness. [15] Additional mechanisms include oxidative stress, [16] which has been associated with numerous components of metabolic syndrome. [17]
A person who weighed 180 pounds who diets down to 150 pounds burns significantly less energy than another person of the same height who also weighs 150 pounds who did not diet. Something about dieting causes an exaggerated slow down in metabolic rate that goes beyond what would be predicted based on tissue loss. And, as pointed out previously, this comes along with strong and unrelenting biological sensations to seek food. That is a recipe for compensatory weight regain.
High blood glucose sets up a domino effect of sorts within your body. High blood sugar leads to increased production of urine and the need to urinate more often. Frequent urination causes you to lose a lot of fluid and become dehydrated. Consequently, you develop a dry mouth and feel thirsty more often. If you notice that you are drinking more than usual, or that your mouth often feels dry and you feel thirsty more often, these could be signs of type 2 diabetes.
Being undiagnosed celiac for decades definitely played into my weight loss struggles. This is counter to what current medical literature says but I see it all of the time. Food allergies, food sensitivities and the like can have a huge impact on weight loss resistance! They do this through inflammatory processes in the body but also through altering gut hormones and the types of bacteria that live in the gut. Study after study has shown that the blood sugar and insulin response to a food is incredibly individual BUT it can be predicted by the type of bacteria that are living in your gut. Yes, in the future we will be sequencing everyone’s gut bugs and using them to alter the course of every disease. I am sure of it!

Emerging data suggest an important correlation between metabolic syndrome and risk of stroke. [58] Each of the components of metabolic syndrome has been associated with elevated stroke risk, and evidence demonstrates a relationship between the collective metabolic syndrome and risk of ischemic stroke. [59] Metabolic syndrome may also be linked to neuropathy beyond hyperglycemic mechanisms through inflammatory mediators. [60]
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