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“Plagues Of Modern Times”

INSULIN RESISTANCE

WORLDWIDE, WE’RE SUFFERING FROM DISEASES THAT WERE ONCE UNHEARD OF. EACH YEAR, ROUGHLY 10 MILLION PEOPLE DIE FROM CANCER, ALMOST 20 MILLION DIE FROM HEART DISEASE, OBESITY IS AT EPIDEMIC LEVELS, AND UP TO HALF A BILLION PEOPLE ARE DIAGNOSED WITH TYPE 2 DIABETES.


ALMOST 4 FOLDS ARE PRE-DIABETIC AND ALMOST 70% OF THE WORLD ADULT POPULATION ARE ALREADY “INSULIN RESISTANCE.”


Today’s “Plagues of Modern Times” have one thing in common—Insulin Resistance.


All of these disorders (and many others) have one thing in common… To varying degrees, each is caused or made worse by the inability of the hormone insulin to perform as it should; A condition largely within our control called Insulin Resistance. Odds are high, if you’re suffering from one or more of these disorders that you’re significantly affected by this condition. Insulin resistance is the thread that runs through many chronic afflictions of modern times—obesity, heart disease, and, most conspicuously, type 2 diabetes. All are entangled with diet, and all are linked causally to a dysfunctional response to insulin, the hormone that orchestrates the body's use and storage of nutrients. Elucidating the causes of insulin resistance is one of the most critical endeavours in modern medicine, and two competing theories have now gained wide support. One is that cells essentially become poisoned by fat. This lipotoxicity or lipid overload hypothesis holds that normal processes break down when fat (adipose) tissue cannot store excess fat, and fat accumulates inappropriately in muscle and liver cells. The main rival to this idea, the inflammation hypothesis, holds that as fat cells increase in size with the accumulation of fat, they release inflammatory cytokines and molecules known as adipokines. It's these molecules, so this theory goes, that cause insulin resistance elsewhere in the body. Researchers are now confident that these inflammatory mechanisms play some role in insulin resistance.


Are you Insulin Resistant? Answer these questions:

• Do you have more fat around your belly than you’d like?

• Have you been frustrated by failed attempts to loose weight with a low-fat diet?

• Do you have high blood pressure or a family history of heart disease?

• Do you have high levels of blood triglycerides?

• Do you retain water easily?

• Do you have “gout”?

• Do you have patches of dark-coloured skin?

• Do you have family member with Insulin Resistance or Type 2 Diabetes?

• Do you have a family member have/had gestational diabetes or PCOS (women)?

• Do you constantly crave sugary or starchy foods?


If you answered “Yes” to two or more of these questions, we invite you to read on…


How to assess if you are Insulin Resistance or Sensitive? ( Through blood marker reading of Cholesterol Reading of Triglyceride/HDL-c ratio ) Your TG:HDL ratio is calculated on a fasting lipid profile.


A calculator is here: Simply take the Triglyceride and divide by the HDL; the closer to ONE, the better.

For example: TG = 120 mg/dL and HDL=40 mg/dL. 120 / 40 = 3.0, and indicates an elevated risk of heart attack and stroke.


Therefore, in adults, the triglyceride/HDL-"good" cholesterol ratio should be below 2 (just divide your triglycerides level by your HDL). In other words, the lower your triglycerides, or the higher your HDL, the smaller this ratio becomes.


#Lipid Conversion Factors:


To Convert From mmol/L to mg/dL

For total, HDL, and LDL cholesterol multiply mmol/L by 38.67

e.g. 3.5 mmol/L = 3.5 mmol/L * 38.67 = 135 mg/dL

For triglycerides multiply mmol/L by 88.57

e.g. 1.9 mmol/L = 1.9 mmol/L * 88.57 = 168 mg/dL


To Convert From mg/dL

For total, HDL, and LDL cholesterol divide mg/dL by 38.67

e.g. 135 mg/dL = 135 mg/dL/38.67 = 3.5 mmol/L

For triglycerides divide mg/dL by 88.57

e.g. 168 mg/dL = 168 mg/dL/88.57 = 1.9 mmol/L


Perm J. 2015 Fall; 19(4): 4–10.doi: 10.7812/TPP/14-237 PMCID: PMC4625988 PMID: 26517432 Study of the Use of Lipid Panels as a Marker of Insulin Resistance to Determine Cardiovascular Risk Ruth Ann Bertsch, MD, PhD, FACP

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