Advisory: lyrics NSFW
'Track, Smack, Whack Plaque' as HH
always says... extinguish plaque for an eternity.
Forge elite heart fitness...
Chewy boy, doobie with the buddha cess...
So read my mind, the situation's critical...
You think you know me?
Well test your luck and try me out...
Then watch that valium on your dome
I'm putting beary fairy nig*** in a state of shock (shock!)
And I'm a killa whale but nigga check my pit lock
So bust that, crush that, crush that
...I'm harmon like that wolverine
Deadly like that Octagon
Fillmoe to the fu*** heart
Crooked like the Pentagon
...So check my rep, survival tech, and hit man killa tactics
Nig*** get berry faced down on silver plastic...
The fat rat dominator, microphone terminator
Quick to break the neck of an E-40 imitator
Nig*** don't front, you know I got you open
With more Raider in me than they ever had in Oakland
To all you moth*** that juss can't tell
I'm a Pisces but I'd rather be a KILLA WHALE
--increased uric acid (ie, gout)
--prevention of fat from being liberalized for energetic uses
We require only tiny, neglible amounts of insulin for thermogenesis and shuttling of energy (glucose) into muscles and liver for storage.
In fact, increased energy expenditure is exponentially increased when insulin resistance is kept at bay. What is insulin resistance (IR)? It is like being at a rock concert (or Hannah Montana venue with screaming little girls everywhere) where temporary hearing loss is induced by inclement noise pollution. As soon as the volume returns to a low level, hearing resumes. Shut insulin down by going grain-free, carb-restricted, intermittent fasting and exercising, then inflammatory responses and processes are cut off. The same research demonstrated that men and women have blunted energy expenditure when the 'volume of insulin' is dialed exceptionally high. And for us women, we may even have a 'negative' energy output (in other words 'storage') with energy expenditure during the presence of insulin resistance... huhhh??! Talk about an exceedingly 'thrifty' gene... *urgh* Insulin-resistant gals gain weight with exercise... how exceedingly unfair. This actually is a common phenomenon and very discouraging for women trying to lose weight and fight an uphill battle as they eat per conventional medical advice 'low fat'/high-carbohydrate/insulin-inducing diets (USDA 'whole grain' pyramidal nonsense).
Degrees of IR can also be effectively cranked down by (Isharwal S, et al. Dietary nutrients and insulin resistance in urban Asian Indian adolescents and young adults.Ann Nutr Metab. 2008;52(2):145-51.):
--normal BMI achievement
--reduction of pro-inflammatory omega-6 oils
--increase of anti-inflammatory omega-3 EPA+DHA oils (ie, cod liver, fish oil, pasture-fed milk, meat, eggs, etc)
And of course...wheat avoidance, grain elimination, carb restriction, intermittent fasting and exercise.
Excessive insulin (ie, hyperinsulinemia) leads to the below changes (see below diagram):
--generation of TGs and small dense atherogenic LDL
--conversion from fatty streaks to plaque
--increased adipose tissue mass (Obesity, Metablic Syndrome, PCOS)
--accumulation of Triglycerides in non-adipocytes
--nonalcoholic steatohepatitis (fatty liver/NAFLD)
--pancreatic beta-cell failure (fatty pancreas, insulin resistance)
--dilated cardiomyopathy (myocyte (heart cell) stiffening and diastolic dysfunction)
--blood glucose spikes
--expansion of visceral fat (belly fat colonies)
--fatty liver, fatty pancreas, fatty gallbladder, fatty heart
--Diabetes Type 2
--strokes, heart attacks
--cancer (see end)
So... when insulin becomes rampant and uncontrolled like ex-KGB-satellites gaining prominence and power to control global McMafia-like franchises for cocaine, opioid, and crack trafficking, then world and global economies are undoubtedly affected. Whole human systemic organ functions become dominated by hyperinsulinemia, leading to all sorts of dysfunction and energy dysregulation. Why rely on primitive petrol... when nuclear power exists?
Fig 1. Lipotoxicity in humans originates from excessive release of free fatty acids from hypertrophied adipocytes in obese persons. Organ exposure to high levels of free fatty acids causes lipid droplets to accumulate within the cytosol of nonadipose tissues in proximity to mitochondria (white arrows, bottom).By-products of cytosolic triglyceride accumulation and of lipid metabolism may lead to organ dysfunction and failure. McGavock JM, Victor RG, Unger RH, Szczepaniak LS. Adiposity of the heart, revisited. (Full PDF here.) Ann Intern Med. 2006 Apr 4;144(7):517-24. Review. PMID: 16585666
Reversal occurs when insulin is shut down.
The previous review of the research eloquently illustrates the special properties that dictate this ancient 'reactive' hormone. Insulin is one of the few hormones that is controlled by consumed 'substrates'.... What is in charge of turning insulin on and off? What are substrates of insulin?
Found in our daily meals and snacks! What we consume indeed dictates what we are (biochemically speaking).
Food composition directly lowers or raises insulin concentrations. Various other factors of course determine how quick and how sustained hyperinsulinemia occurs (exercise, weight loss, skeletal muscle dominance, size and location of visceral fat colonies (ie, 'belly' is 'bad') but in essence our food controls blood insulin levels.
If what we put in our mouth dictates are insulin levels, then equally powerful is what we don't... In other words, processes like starvation, skipping meals, random eating, intermittent fasting and going low-carb or restricted-carb are ways to reduce and control insulin. Consumption of adequate protein and fats and fiber control insulin release as well.
Take powerful control over plaque and inflammatory processes by shutting insulin secretion off. At Track Your Plaque the Paleo grain-free diet produces the best plaque-busting results. Consider the complete avoidance of all wheat and grains:
Consume most of the carbohydrates from non-starchy vegetables and raw nuts/seeds and low-GI fruit like berries.
Controlling insulin not only controls CAD but also controls cancer... Is 'whole grains' just promoting 'whole C-A-N-C-E-R'? As well as 'whole CORONARY ARTERY DISEASE'?
- Berstein LM. Endocrinology of the wild and mutant BRCA1 gene and types of hormonal carcinogenesis. Future Oncol. 2008 Feb;4(1):23-39. Review. PMID: 18240998
- Hede K.Doctors seek to prevent breast cancer recurrence by lowering insulin levels.
J Natl Cancer Inst. 2008 Apr 16;100(8):530-2. PMID: 18398091
- Barnard RJ.Prostate cancer prevention by nutritional means to alleviate metabolic syndrome. Am J Clin Nutr. 2007 Sep;86(3):s889-93. Review.PMID: 18265484
- Park JH.Inhibition of colon cancer cell growth by dietary components: role of the insulin-like growth factor (IGF) system. Asia Pac J Clin Nutr. 2008;17 Suppl 1:257-60. PMID: 18296350
- Tenenbaum A, et al. Does the lipid-lowering peroxisome proliferator-activated receptors ligand bezafibrate prevent colon cancer in patients with coronary artery disease? Cardiovasc Diabetol. 2008 Jun 19;7(1):18. PMID: 18565233
- Pisani P. Arch Physiol Biochem. 2008 Feb;114(1):63-70. Hyper-insulinaemia and cancer, meta-analyses of epidemiological studies.
Background: A substantial body of evidence links sex hormones, diet, excess body weight and physical activity to the risk of developing cancer at several sites common in affluent countries. The hypothesis that high circulating levels of insulin could be the underlying factor increasing cancer risk has been proposed. Epidemiological studies on markers of hyper-insulinaemia and cancer are reviewed and summarized. Methods: Studies of cancers of the colon and rectum, pancreas, breast, and endometrium examining the association with blood levels of C-peptide, insulin, glucose, glycated haemoblobin (HbA1c) were searched in PubMed. Multivariate, adjusted relative risks (RR) and their 95% confidence intervals were abstracted and summarized by meta-analyses. Results: Most of the studies identified were cohorts that relied on measurements obtained at baseline or assessed in blood stored at low temperature several years before the onset of cancer. The meta-analyses showed excess risks of colorectal and pancreatic cancers associated with higher levels of circulating C-peptide/insulin and with markers of glycaemia. Significant heterogeneity was found among four epidemiological studies of endometrial cancer and C-peptide giving a summary RR compatible with no association. Overall breast cancer risk was significantly higher in the upper categories of C-peptide/insulin, however, the excess derived entirely from retrospective studies. Conclusion: Current evidence suggests that subjects who develop colorectal and pancreatic cancers have increased pre-diagnostic blood levels of insulin and glucose. PMID: 18465360