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Starvation Is NOT Healthy. Stop counting calories & go #SANE w/me at http://SANESolution.com

How Much Fat Should I Eat While Going SANE?

“Simply lowering the percentage of energy from total fat in the diet is unlikely to…reduce coronary heart disease incidence.” – F.B. Hu, Harvard University Overcoming the fear of fat is critical to eating a natural, balanced ratio of nutrients. We should never again skip SANE sirloin steak and non-starchy vegetables in favor of inSANE […]

2018-02-17/0 Comments/by SANE

Simple Science: How Excess Insulin Makes Us Fat

SANE Science

“…obesity is impossible in the absence of adequate tissue concentrations of insulin.” – M. Goldberg, in Journal of the American Medical Association In the last post we touched on how hormones control the metabolic conversation that determines if we are storing or burning body fat. Let’s now dig into the hormone insulin’s role in this […]

2018-02-17/0 Comments/by SANE

How Much Fat Should I Eat While Going SANE?

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2018-02-17/0 Comments/by SANE

Simple Science: How Excess Insulin Makes Us Fat

SANE Science

2018-02-17/0 Comments/by SANE

How Much Fat Should I Eat While Going SANE?

Uncategorized

“Simply lowering the percentage of energy from total fat in the diet is unlikely to…reduce coronary heart disease incidence.” – F.B. Hu, Harvard University

Overcoming the fear of fat is critical to eating a natural, balanced ratio of nutrients. We should never again skip SANE sirloin steak and non-starchy vegetables in favor of inSANE whole wheat spaghetti with whole wheat garlic bread. Fat is delicious, Satisfying, unAggressive, and almost impossible to overeat unless combined with starch or sweeteners. That is why most people end up losing weight on low-carbohydrate, high-fat diets like Atkins. Basically, any diet discouraging fat encourages weight gain.

You and I have already reviewed research disproving that foods containing fat are fattening, but let’s quickly recap: If we set aside the myths we’ve been told for the past forty years, there is no reason to think fat is bad for us. Natural foods contain fat. Natural foods were the only thing our ancestors ate for 99.8% of our evolution. How could the only foods available to us for 99.8% of our evolution harm us? If anything, we must have evolved to thrive on foods containing fats. Furthermore, the theory that fat is fattening has never been proven, despite over a billion dollars’ worth of research attempting to do so. Finally, a decline in fat in our diet has been accompanied by the largest spike in obesity and disease rates in history.

A great many scientific studies show that worrying about fat is at best a distraction, and at worst, harmful and fattening. Consider the research done just at the Harvard Medical School:

“Among European countries, no association was observed between the national percentage of energy from fat and median body mass index in men…a clear inverse relation was observed in women.”
“Limiting unsaturated fats, which is usually done by increasing carbohydrate…is detrimental. This is consistent with metabolic studies indicating that replacing unsaturated fats with carbohydrate increases triacylglycerol and decreases HDL cholesterol. Furthermore, low-fat, high-carbohydrate diets provide a higher glycemic load, aggravate hyperinsulinemia [clogging], and may thus increase the risk of diabetes and coronary artery disease.”
“Studies and…trials have provided strong evidence that a higher intake of [omega-3] fatty acids from fish or plant sources lowers risk of coronary heart disease.”

Next, let’s cover specifically how to eat SANE, natural, not necessarily fat-free foods, while easily avoiding inSANE foods that facilitate fat gain and feeling more satisfied and energized than ever.

Fat FAQs
1. The Smarter Science of Slim cites dozens of international research studies that show natural fats aren’t bad, but then goes on to recommend lean meats, a blend of egg whites with whole eggs, and low-fat or fat-free plain Greek yogurt and cottage cheese. Is this a contradiction?

2. Why should I eat egg whites vs. whole eggs? Why should I eat low-fat cottage cheese and low-fat plain Greek yogurt vs. the full fat variants?

Hu FB, Willett WC. Optimal diets for prevention of coronary heart disease. JAMA. 2002 Nov 27;288(20):2569-78. Review. PubMed PMID: 12444864.
Apoundert CM, Campos H, Stampfer MJ, et al. Blood levels of long-chain n-3 fatty acids and the risk of sudden death. N Engl J Med 2002;346:1113-1118.
Siscovick DS, Raghunathan TE, King I, Weinmann S, Wicklund KG, Apoundright J, Bovbjerg V, Arbogast P, Smith H, Kushi LH, Cobb LA, Copass MK, Psaty BM, Lemaitre R, Retzlaff B, Childs M, Knopp RH. Dietary intake and cell membrane levels of long-chain n-3 polyunsaturated fatty acids and the risk of primary cardiac arrest. JAMA 1995;274:1363-1367.
Hu FB, Manson JE, Willett WC. Types of dietary fat and risk of coronary heart disease: a critical review. J Am Coll Nutr. 2001 Feb;20(1):5-19. Review. PubMed PMID: 11293467.
Willett WC. Is dietary fat a major determinant of body fat? Am J Clin Nutr. 1998 Mar;67(3 Suppl):556S-562S. Review. Erratum in: Am J Clin Nutr 1999 Aug;70(2):304. PubMed PMID: 9497170.
Willett WC. Dietary fat plays a major role in obesity: no. Obes Rev. 2002 May;3(2):59-68. Review. PubMed PMID: 12120421.
Willett WC, Leibel RL. Dietary fat is not a major determinant of body fat. Am J Med. 2002 Dec 30;113 Suppl 9B:47S-59S. Review. PubMed PMID: 12566139.
McCullough ML, Feskanich D, Stampfer MJ, Rosner BA, Hu FB, Hunter DJ, Variyam JN, Colditz GA, Willett WC. Adherence to the Dietary Guidelines for Americans and risk of major chronic disease in women. Am J Clin Nutr. 2000 Nov;72(5):1214-22. PubMed PMID: 11063452
Hu FB, Manson JE, Willett WC. Types of dietary fat and risk of coronary heart disease: a critical review. J Am Coll Nutr. 2001 Feb;20(1):5-19. Review. PubMed PMID: 11293467.

2018-02-17/0 Comments/by SANE

Simple Science: How Excess Insulin Makes Us Fat

SANE Science

“…obesity is impossible in the absence of adequate tissue concentrations of insulin.” – M. Goldberg, in Journal of the American Medical Association

In the last post we touched on how hormones control the metabolic conversation that determines if we are storing or burning body fat. Let’s now dig into the hormone insulin’s role in this conversation as it is known in scientific circles as, “The most important hormonal factor influencing lipogenesis [body fat creation].”

Insulin’s job is to get energy into cells. For example, after we eat lunch, our body digests it and then releases insulin to carry those freshly digested calories into our cells. Since insulin is activated only when we need to get fuel into our cells, our metabolism “hears” insulin in the bloodstream “communicating” that we have energy on its way to our cells and therefore do not need to use any stored energy—aka burn body fat. So the hormone insulin—not the calories we ate—blocks the burning of body fat. That point is extremely important.

“[Insulin signals an] abundance of [external] energy, [and]…fat breakdown is suppressed and its synthesis promoted…” – researcher G. Wilcox, Mepoundourne Pathology

Our metabolism does not decide to burn or store body fat based on calories. It makes these decisions based on the hormones those calories trigger. That is why the quality of calories matters so much. As we have already seen, higher-quality calories trigger body-fat-burning hormones while low-quality calories trigger body-fat-storing hormones.

“Fat is mobilized [burned] when insulin secretion diminishes.” – The American Medical Association

We can cut calories all day and will not burn body fat effectively if we are eating low-quality calories which trigger excess body-fat-storing hormones such as insulin. Why? Hormones like insulin remove our ability to burn body fat regardless of whether or not we need to according to calorie quantity. That is why scientists refer to the hormone insulin as the “principal regulator of fat metabolism.”

Here is the sad part. Calories from inSANE starch and sweets trigger the release of ridiculous amounts of insulin. All that insulin gets those inSANE starch and sweets’ calories into our cells, but then we still have insulin left over in our bloodstream. That excess insulin clogs us up and removes our ability to burn body fat.

Where the Average American Gets Calories

(Insulin-spiking starch and sweeteners make up 43% of what we eat)

“…obesity [is characterized by] defects in insulin action, whole-body insulin resistance, and hyperinsulinemia” – researcher D.A. York, Pennington Biomedical Research Center

Things go from bad to worse if this inSANEity keeps up for too long. Not only does all the excess insulin destroy our ability to burn body fat, it makes the metabolism resistant to insulin. How does this process work? Compare becoming resistant to the effects of insulin with becoming resistant to the effects of alcohol. When people drink alcohol in moderation, everything is fine. It takes relatively little alcohol to generate the desired effect, so people don’t drink too much of it. However, if people drink too much alcohol, they become resistant to alcohol’s effects. Then they have to drink more alcohol to get the desired effect. This volume of alcohol eventually destroys their liver and makes them gain body fat. This leaves heavy drinkers in an unfortunate place where they have become resistant to alcohol and have to drink an unhealthy amount of it to get the desired effect.

Similarly, when people eat mostly SANE foods and just a little inSANE starch and sweets, everything is fine. It takes little insulin to get energy into cells, so the body doesn’t produce too much of it. However, if people eat mostly starch and sweets, their bodies become resistant to insulin’s effects. Then their body has to produce more insulin to get energy into cells. This volume of insulin eventually destroys their pancreas and makes them gain body fat.

“Foods made from wheat flour account for about 20% of the calories in the American diet…” –Marion Nestle, New York University

Even more unfortunate, at least one in four Americans are insulin resistant. All this excess insulin forms the backbone of the hormonal dysfunction causing us to gain fat. Not only does it crush our ability to burn body fat, it also increases the rate at which we store body fat because excess insulin preferentially puts calories into our fat tissue. This happens because no matter how resistant other tissues become to insulin, our fat tissue is always receptive. And while that is technically good because it keeps insulin resistance from killing us, it can crush any dreams of losing weight. We end up with more body fat and no ability to burn it. This sad state is know as internal starvation and will be the subject of the next post.

American Medical Association Council on Foods and Nutrition. A critique of low-carbohydrate ketogenic weight reduction regimens. A review of Dr. Atkins’ diet revolution. JAMA. 1973 Jun 4;224(10):1415-9. PubMed PMID: 4739993.
“Diabetes mellitus.” Belinda Rowland., Teresa G. Odle., and Tish Davidson, A. M. The Gale Encyclopedia of Alternative Medicine. Ed. Laurie Fundukian. 3rd ed. Detroit: Gale, 2009. 4 vols.
Blüher M, Michael MD, Peroni OD, Ueki K, Carter N, Kahn BB, Kahn CR. Adipose tissue selective insulin receptor knockout protects against obesity and obesity-related glucose intolerance. Dev Cell. 2002 Jul;3(1):25-38. PubMed PMID: 12110165.
Cordain, Loren, and Joe Friel. The Paleo Diet for Athletes: A Nutritional Formula for Peak Athletic Performance. Emmaus, Pa.: Rodale Books, 2005. Print.
E.A. Newsholme and C. Start. Regulation of Metabolism. 173 ISBN: 0471635308
Flatt, Jen-Pierre. Tremblay, Angelo. Energy Expenditure and Substrate Oxidation. In: Bray GA, Couchard d, James WP, eds. Handbook of Obesity. New York: Marcel Dekker, 1997: 513-538.
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Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA. 2002 May 8;287(18):2414-23. Review. PubMed PMID: 11988062.
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Obesity and leanness. Basic aspects. Stock, M., Rothwell, N., Author Affiliation: Dep. Physiology, St. George’s Hospital Medical School, London Univ., London, UK.
Schenk S, Saberi M, Olefsky JM. Insulin sensitivity: modulation by nutrients and inflammation. J Clin Invest. 2008 Sep;118(9):2992-3002. Review. PubMed PMID: 18769626; PubMed Central PMCID: PMC2522344.
Whitehead, Saffron A.; Nussey, Stephen (2001). Endocrinology: an integrated approach. Oxford: BIOS. pp. 122. ISBN 1-85996-252-1.
Wilcox G. Insulin and insulin resistance. Clin Biochem Rev. 2005 May;26(2):19-39. PubMed PMID: 16278749; PubMed Central PMCID: PMC1204764.
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York DA, Hansen B. Animal models of obesity. In: Bray GA, Couchard d, James WP, eds. Handbook of Obesity. New York: Marcel Dekker, 1997: 191-221

2018-02-17/0 Comments/by SANE

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