Last Friday night after a long week of work, Caveman Cancer Doc was beat. While he strives to constantly avoid chronic stress, there was just too much this week and he couldn’t avoid it. He worked hard all week and needed to relax. He met up with some friends who were eating ice cream. Caveman Doc was intrigued by this magical frozen food. He tried a bite of it. Immediately, he was filled with a feeling of happiness, starting in his tongue and spreading to the rest of his body. Though he only said he would eat a bite, he ended up eating an entire carton. He didn’t understand what was happening, but he couldn’t stop craving more. Caveman Doc really liked this ice cream. An hour after his ice cream binge, he felt tired and sad. He sat down to rest, unsure of why he felt so down. Amazingly, Caveman Doctor craved the ice cream again. He went to the local grocery store and took another carton, clubbing the cashier over the head when she asked if he was going to pay for it (this is a lie, he actually paid her). What was in this food that made him so crazy?
Caveman Doctor Discovers Insulin
What happened to Caveman Doctor? He experienced the ecstatic loss of self-control, annihilating rush of sugary goodness only to be inevitably followed by the valley of fatigue, sadness, and a little self-loathing. Simply put, he found out about insulin the hard way. You have likely had this same experience dozens of times (maybe involving dozens of donuts, if you’re anything like me). However, this is just a tiny example of what happens when we eat sugars and carbs.
Unfortunately, nowadays this encounter is not isolated to a single event as the backbone of our modern diet has morphed into one that is based on carbohydrates1-3. Eating a diet based on carbohydrates works as a detriment to your health in many ways, and the first and most important is the stimulation of insulin release within our pancreas. Insulin serves many purposes in our body and is a vital hormone; however, its main occupation nowadays is to save us from sugar overload as it fights to keep our blood sugar levels low from our carb-laden modern diets.
Is Sugar a Toxin?
What most people don’t realize is that sugar (glucose) in high amounts in our blood is actually a toxin and must be lowered to avoid serious complications. This is where insulin plays it largest part. People with Type 1 diabetes cannot make insulin, and have to take it as a medication multiple times a day to avoid serious complications and death. If they miss a dose of insulin, their blood sugar can rise to such high levels (hyperglycemia) that it can lead to a condition called diabetic ketoacidosis, which is fatal is untreated. FATAL! (Of note, this is not ketosis, which is a normal state in which our bodies make ketones from fat when few carbohydrates are consumed.)
While carbohydrates are often praised as health foods in our society and fats are demonized, the irony is not lost on Caveman Doctor that high blood sugar levels can quickly (acutely) kill us, while fat and cholesterol are vital components of many parts of our body and cell membranes. This is why you will find fat and cholesterol floating in our blood bound to lipoproteins naturally and we don’t have to quickly remove them like blood sugar. In fact, some scientists have questioned whether carbohydrates are even necessary, period4! Caveman Doctor won’t go that far, however, he is still adamantly against basing one’s diet on carbohydrates.
Do anorexia studies provide us with the key to controlling our appetite?
Anorexia is a sad and devastating disorder that can be fatal if left untreated. Patients often have to be hospitalized, and while they cannot be force fed, finding methods to increase their appetite and consumption of food are extremely challenging. One proven method is to give anorexic patients a substance that potently increases appetite. The name of this substance: insulin5,6.
If insulin can increase appetite in a group of anorexic patients, what do you think it will do to you?
Insulin is largely to blame for Caveman Doctor’s ice cream binge and our eating behavior becoming nearly uncontrollable after we eat carbohydrates. Animal studies have confirmed the anorexia data from above and have even showed that insulin actually acts on the part of our brain (the hypothalamus) that causes severe and uncontrollable increases in appetite7. This is the same part of the brain that is disrupted in Prader-Willi syndrome, which results in uncontrollable hunger and obesity in children8. In fact, studies show that:
“insulin causes hunger through a complex feedback system of environmental, behavioral, and biological factors”9
This is likely why once you eat carbohydrates and get a rise in insulin, it is no longer a matter of willpower, but rather a complex mental and physical battle within your body that causes you to become hungrier and eat more. Just like an addictive drug, most people, including myself, have to largely avoid the initial stimulus to avoid the carb cravings.
Dietary Fat Recommendations and Insulin
The double whammy when following the food pyramid and other dietary recommendations from “the experts” are the fat recommendations. Telling people to avoid all fats usually results in their replacement with carbohydrates, causing even more insulin stimulation. Making matters even worse are the recommendations to avoid all saturated fats and instead consume mostly polyunsaturated fats (PUFAs). PUFAs, such as linoleic acid and linolenic acid, which are abundantly found in vegetable oils, actually cause increased insulin secretion in the face of carbohydrate consumption, while saturated fatty acids actually decrease our pancreas’ response and secretion of insulin10. Not to mention the fact that carbs increase your hunger and make you eat more, while fats and proteins keep you feeling satisfied for longer.
This was even shown in a recent study that added a PUFA (soybean oil) or a saturated fat (coconut oil) to the diet of 40 women. Not surprisingly, the women who consumed the coconut oil had a significant decrease in their waist circumference with increased weight loss, as well as increased HDL (“good” cholesterol) and decreased ratios of “bad” to “good” cholesterol (LDL:HDL)11.
It’s almost as though these recommendations were made with the goal of causing the largest stimulation of insulin as possible (…eat a diet of mostly carbohydrates, and when you do eat fat, make sure it’s polyunsaturated!), therefore causing the largest increase in appetite as possible. And we wonder why people have such trouble following dietary recommendations12… Yet, this is the diet that is recommended by most health professionals and, to my knowledge, nearly all government organizations. This diet will undoubtedly enslave its followers to a lifetime of struggling to lose weight. Calories play little to no part here as the constant increase in insulin will do all that is necessary to stop weight loss, keep your hunger high, and your frustration higher.
Insulin and Obesity
While we already know that insulin stimulates appetite and ultimately leads to the consumption of more food and weight gain13-15, carbohydrate-induced rises in insulin actually lead to increased cravings of not only food, but more carbohydrates16!! As discussed in “Cheating the Cheat”, these unhealthy foods actually stimulate our brains to eat…more unhealthy foods!
Unfortunately, the bad doesn’t stop here as insulin turns on several physiological processes down the road within our bodies:
1. Insulin Causes Fat Production:
Studies in humans have shown that high-carbohydrate, low-fat diets actually cause our body to create more fat (fatty acid synthesis)17 as insulin (from carbohydrates) is the hormone that drives this process.
2. Insulin Stops Fat Breakdown:
A similar diet also results in decrease in fat breakdown and oxidation within the human body. Basically, carbohydrate-induced insulin secretion turns on fat production and turns off fat breakdown.This is why Atkins and the initial very low-carbohydrate diets resulted in incredible amounts of weight loss. When no insulin is around, our body turns toward our fat stores for energy and breaks them down. If there is no insulin around to drive fat production, you end up losing weight and losing a lot of it.
High carbohydrate diets also cause elevated levels of triglycerides in our blood18, a risk factor for both heart disease and cancer19-22. Conversely, triglycerides are decreased from low-carbohydrate diets, and this was even shown in several randomized controlled trials23-29. In other words, high-carbohydrate consumption directly increases blood components that can cause heart disease. This is one of the few facts that seems universally accepted by our leaders in medicine, yet fat and cholesterol somehow still get all the blame.
The increase in weight loss on low-carb diets (which by nature means high-fat) as well as the decrease in triglycerides have left religious followers of the “eating fat leads to obesity, clogged arteries, and everything bad” mantra baffled. However, the data speaks for itself. For those of us that know about insulin (the real problem), the entire model fits quite nicely.
Reasons to eat large amounts of carbohydrates (sarcasm noted):
1. You want to gain weight
2. You want to feel hungry again after your blood glucose levels drop
3. You want to feel depressed when your blood glucose levels drop
4. You are in the middle of a marathon and out of glycogen
5. You want to increase your risk of cancer30-38
6. You want to increase your risk of diabetes39
7. You don’t enjoy seeing your abdominal muscles
Conversely, here are reasons to limit your carbohydrates to 100-150 grams per day:
1. You enjoy near-effortless weight loss and maintenance
2. Increased energy level
3. Stable energy without the post-carb highs and lows
4. Avoid obesity
5. Avoid chronic diseases
6. Fight cancer
While 100-150 is set as an easy guideline, dropping lower periodically or even quite often is fine as well. One must have to keep in mind that the lower the carbs, the more weight loss, so if maintenance is a goal, carbohydrates may have to be closer to or over 100 per day on most days. Personally, I tend to however in the middle on most days, with a rare hedge towards 150 on heavy activity days and often towards 50 or lower on non-activity days. If I am trying to go into ketosis, I will keep them around 30 for more than a day. Cavemen likely ate a similar diet and went for days without carbohydrates. Regardless of the level of carbohydrates that we eat, keeping them low will keep insulin low, the weight off, and energy high. Once again, a diet similar to the one that nature laid out for the cavemen appears to be the healthiest. Let’s find simple ways to mimic it for better health.
Another point about this diet that should be inspiring to you if you’re trying to lose weight: it’s not your fault if you’re struggling with hunger and carbs! It’s biology. You can take weight loss into your own hands by avoiding heavy amounts of carbs and limiting them to green leafy vegetables and the fruits that were gathered. Leave the bulk of your diet to eating proteins and fats; the foods that provide us with the health that nature intended.
1. US Department of Agriculture, Center for Nutrition Policy and Promotion. Nutrient content of the U.S. Food supply. Available at: <http://www.usda.gov/cnpp>. Accessed July 14, 2011.
2. Mintz SW. Sweetness and power: the place of sugar in modern history. New York, NY: Penguin Books, 1986.
3. Cite Centers for Disease Control and Prevention, The Obesity Epidemic. Available at: < http://www.cdc.gov/cdctv/ObesityEpidemic/>. Accessed July 27, 2011
4. Westman EC: Is dietary carbohydrate essential for human nutrition? The American journal of clinical nutrition 75:951-3; author reply 953-4, 2002
5. Dally P, Sargant W: Treatment and outcome of anorexia nervosa. BMJ 2:793-795, 1966
6. Munoz MT, Argente J: Anorexia nervosa in female adolescents: endocrine and bone mineral density disturbances. Eur J Endocrinol 147:275-86, 2002
7. Cincotta AH, Luo S, Liang Y: Hyperinsulinemia increases norepinephrine metabolism in the ventromedial hypothalamus of rats. Neuroreport 11:383-7, 2000
8. Swaab DF: Prader-Willi syndrome and the hypothalamus. Acta paediatrica 423:50-4, 1997
9. Rodin J: Insulin levels, hunger, and food intake: an example of feedback loops in body weight regulation. Health psychology : official journal of the Division of Health Psychology, American Psychological Association 4:1-24, 1985
10. Garfinkel M, Lee S, Opara EC, et al: Insulinotropic potency of lauric acid: A metabolic rationale for medium chain fatty acids (MCF) in TPN formulation. Journal of Surgical Research 52:328-333, 1992
11. Assuncao ML, Ferreira HS, dos Santos AF, et al: Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity. Lipids 44:593-601, 2009
12. Burke LE, Dunbar-Jacob J: Adherence to medication, diet, and activity recommendations: from assessment to maintenance. The Journal of cardiovascular nursing 9:62-79, 1995
13. Grossman MI, Stein IF: Vagotomy and the Hunger-producing Action of Insulin in Man. Journal of Applied Physiology 1:263-269, 1948
14. Bulatao E, Carlson AJ: CONTRIBUTIONS TO THE PHYSIOLOGY OF THE STOMACH: Influence of Experimental Changes in Blood Sugar Level on Gastric Hunger Contractions. American Journal of Physiology — Legacy Content 69:107-115, 1924
15. Janowitz HD, Ivy AC: Role of Blood Sugar Levels in Spontaneous and Insulin-Induced Hunger in Man. Journal of Applied Physiology 1:643-645, 1949
16. Geiselman PJ, Novin D: The role of carbohydrates in appetite, hunger and obesity. Appetite;Appetite 3:203-223, 1982
17. Hudgins LC, Hellerstein M, Seidman C, et al: Human fatty acid synthesis is stimulated by a eucaloric low fat, high carbohydrate diet. The Journal of clinical investigation 97:2081-91, 1996
18. Mittendorfer B, Sidossis LS: Mechanism for the increase in plasma triacylglycerol concentrations after consumption of short-term, high-carbohydrate diets. The American journal of clinical nutrition 73:892-899, 2001
19. Cabin HS, Roberts WC: Relation of serum total cholesterol and triglyceride levels to the amount and extent of coronary arterial narrowing by atherosclerotic plaque in coronary heart disease. Quantitative analysis of 2,037 five mm segments of 160 major epicardial coronary arteries in 40 necropsy patients. The American journal of medicine 73:227-34, 1982
20. Freiberg JJ, Tybjærg-Hansen A, Jensen JS, et al: Nonfasting Triglycerides and Risk of Ischemic Stroke in the General Population. JAMA: The Journal of the American Medical Association 300:2142-2152, 2008
21. Goodwin PJ, Boyd NF, Hanna W, et al: Elevated levels of plasma triglycerides are associated with histologically defined premenopausal breast cancer risk. Nutrition and cancer 27:284-92, 1997
22. Hokanson JE, Austin MA: Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies. Journal of cardiovascular risk 3:213-9, 1996
23. Brehm BJ, Seeley RJ, Daniels SR, et al: A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. The Journal of clinical endocrinology and metabolism 88:1617-23, 2003
24. Foster GD, Wyatt HR, Hill JO, et al: A randomized trial of a low-carbohydrate diet for obesity. The New England journal of medicine 348:2082-90, 2003
25. Samaha FF, Iqbal N, Seshadri P, et al: A low-carbohydrate as compared with a low-fat diet in severe obesity. The New England journal of medicine 348:2074-81, 2003
26. Seshadri P, Iqbal N, Stern L, et al: A randomized study comparing the effects of a low-carbohydrate diet and a conventional diet on lipoprotein subfractions and C-reactive protein levels in patients with severe obesity. The American journal of medicine 117:398-405, 2004
27. Stern L, Iqbal N, Seshadri P, et al: The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Annals of internal medicine 140:778-85, 2004
28. Volek JS, Phinney SD, Forsythe CE, et al: Carbohydrate restriction has a more favorable impact on the metabolic syndrome than a low fat diet. Lipids 44:297-309, 2009
29. Yancy WS, Jr., Olsen MK, Guyton JR, et al: A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Annals of internal medicine 140:769-77, 2004
30. Augustin LS, Galeone C, Dal Maso L, et al: Glycemic index, glycemic load and risk of prostate cancer. International journal of cancer. Journal international du cancer 112:446-50, 2004
31. Bianchini F, Kaaks R, Vainio H: Overweight, obesity, and cancer risk. The lancet oncology 3:565-74, 2002
32. Chan JM, Stampfer MJ, Giovannucci E, et al: Plasma Insulin-Like Growth Factor-I and Prostate Cancer Risk: A Prospective Study. Science 279:563-566, 1998
33. Freedland SJ, Mavropoulos J, Wang A, et al: Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis. The Prostate 68:11-9, 2008
34. Ho VW, Leung K, Hsu A, et al: A Low Carbohydrate, High Protein Diet Slows Tumor Growth and Prevents Cancer Initiation. Cancer research 71:4484-4493, 2011
35. Macaulay VM: Insulin-like growth factors and cancer. British journal of cancer 65:311-20, 1992
36. Masko EM, Thomas JA, 2nd, Antonelli JA, et al: Low-carbohydrate diets and prostate cancer: how low is “low enough”? Cancer prevention research 3:1124-31, 2010
37. Pollak M: Insulin, insulin-like growth factors and neoplasia. Best Pract Res Clin Endocrinol Metab 22:625-38, 2008
38. Romieu I, Lazcano-Ponce E, Sanchez-Zamorano LM, et al: Carbohydrates and the Risk of Breast Cancer among Mexican Women. Cancer Epidemiology Biomarkers & Prevention 13:1283-1289, 2004
39. Colditz GA, Willett WC, Rotnitzky A, et al: Weight Gain as a Risk Factor for Clinical Diabetes Mellitus in Women. Annals of internal medicine 122:481-486, 1995
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