Love Handles In a Box
Fact: The unhealthiest foods you could possibly eat often have the most health claims on the label. Ironic, isn't it? Think about most breakfast cereals. You're basically eating a bowl of sugar and flour. But the front of the box is packed with health claims:
- Low fat!
- Heart healthy!
- High fiber!
- Reduced sodium!
- Made with whole grains!
Flip that box around like a smart grown-up and take a look at the ingredient list: sugar, flour, sugar in another form, sugar in a different color, sugar with a pretty name, etc. It's Type-2 diabetes in a bright box featuring a cartoon character selling love handles and loneliness.
And now they have a new marketing angle: a clever blend of childhood nostalgia and "fat acceptance." They tell us to eat what we want and love our body no matter what it looks like. Presumably, this is because they've finally recognized that the only people still eating cereal for breakfast have already given up on their health and body composition.
Funny thing is, when looking at the evidence, it's clear that there were never really health benefits in the first place to back up all these "healthy" labels. Here's how many of them originated and why they're wrong.
1 – Low Fat
It's taken over 40 years to officially call BS on the fraudulent claims about fat. The fear of dietary fat started in the 60's and 70's and immediately moved breakfast cereal into the "healthy" category. Hey, sugar is fat free! Bacon, eggs, and butter were out. Low-fat indigestible roughage was in because the research of the time was suggesting that saturated fat was clogging our arteries and increasing our risk of heart disease.
And despite the various top-notch review studies disproving this myth today, the cereal killers, sugar-water sellers, and big pharma phonies continue to lobby government officials, pay off medical and fitness professionals, and fund bogus research studies to keep it alive.
A low-fat diet isn't a benefit because eating fat doesn't cause disease. NOT eating it probably does, and we now know the body even needs some saturated fat to function optimally.
2 – High Fiber
Once you understand the origins of the low-fat guidelines it's easy to see how the advice to eat more fiber came about.
Denis Burkitt was the man behind the 1970's research linking high-fiber diets to lower rates of disease (colorectal cancer specifically). Just like Ancel Keys (the fat fraud), his evidence was awful. He basically claimed that African tribesman were healthier than Westerners because they ate their grains whole (with the fibrous outer shell). He conveniently failed to include a number of disease-free tribes thriving on starch-less diets high in saturated fat and animal protein, like the Masai.
Nonetheless, the bran we were throwing in the garbage became a prized possession, Burkitt wrote a best-selling book, and the "high-fiber" stamp fit perfectly next to the "low-fat" one on our breakfast bowl of blood sugar and body fat. It remains there today, right along with the misconception that whole grains are healthier than refined grains and that more fiber is a good thing, regardless of the source.
Meanwhile, the only study looking at the long-term impact of eating a high-fiber diet (DART, 1989) found an INCREASED risk of heart disease (23%) and mortality (27%). Those studies looking at colorectal cancer saw no benefit to upping our fiber intake:
"Our data do not support the existence of an important protective effect of dietary fiber against colorectal cancer or adenoma." (Fuchs CS et al. NEJM, 1999)
"In this large pooled analysis... high dietary fiber intake was not associated with a reduced risk of colorectal cancer." (Park Y et al. JAMA, 2005.)
3 – Cholesterol
The "lipid hypothesis" suggests that elevated cholesterol is associated with heart disease. And when we add it to what high-fiber, low-fat fanatics tell us, it's no wonder we think the way we do and fall for bogus health claims.
Right around the time all this low-fat, high-fiber evidence was surfacing, doctors and scientists were convinced they'd found the underlying cause of atherosclerosis – the narrowing and hardening of arteries. Nearly every doctor was on board with the theory. In the early 80's the National Institute of Health gathered 14 experts who voted unanimously that, "Lowering elevated blood cholesterol levels will reduce the risk of heart attacks caused by coronary heart disease."
They did so despite the fact that a causal relationship was never established, there's a library of evidence disproving it, and the original experiments used rabbits (herbivores that can't process dietary cholesterol) and a chemically prepared bare-cholesterol, which tends to oxidize.
But along came the prescription statins, and all of a sudden the questions and doctors aggressively opposing the theory disappeared. This created an environment where we dish out damaging side effects to more than 32 million Americans to lower the thing that's NOT associated with heart disease and does nothing to prevent it.
If cholesterol were associated with heart disease, there would be fewer heart attacks in those on statins and those with lower cholesterol, but there aren't. And there would be more heart attacks in those not on statins with higher cholesterol, but there aren't. The two variables aren't even related.
What we do see is statins causing mitochondrial and hormonal dysfunction, and lower cholesterol levels associated with cognitive and neurological impairment (Alzheimer's, Parkinson's, depression). This shouldn't come as a surprise when you understand that cholesterol is a building block for cell membranes, precursor to steroid hormones and essential nutrients, and fuel provider to neurons who can't generate it on their own.
"Our finding that low plasma cholesterol is associated with depressive symptoms in elderly men is compatible with observations that a very low total cholesterol may be related to suicide and violent death." (Morgan RE, et al. 1993, Lancet.)
Cereal fiber's ability to lower cholesterol is more of a detriment than a benefit. And realistically, the people getting heart attacks are the ones with elevated triglycerides, low HDL cholesterol, and excess small-dense (oxidizable) LDL particles – the same thing eating less saturated fat, more high-glycemic carbs, and vegetable oil-filled boxes of stuff claiming to "lower cholesterol" provides.
4 – Sodium
Heard the one about the obese, pre-diabetic guy with high triglycerides? Doc told him to eat less salt!
That's a joke. Or at least it should be. Salt doesn't make you fat and it's probably the last thing the average person needs to be worrying about when it comes to health.
High blood pressure is the fourth and final phase that turns Syndrome X into the Deadly Quartet. When you have metabolic syndrome, eating less salt won't do anything to solve the real problem.
- 2 weeks – insulin resistance (hyperinsulinemia)
- 2 months – elevated triglycerides (hyperlipidemia)
- 6 months – obesity (high bodyfat)
- 12 months – high blood pressure (hypertension)
People with high blood pressure don't need to eat less salt. They need to stop drinking liquid fructose and start driving-past instead of driving-thru.
More importantly, trying to abide by the FDA and AHA's recommendations to keep salt intake below 2400 mg per day (1tsp) increases cardiovascular disease risk and mortality from a heart attack or stroke. Ironically, this appears to be the result of elevated triglycerides and reductions in insulin sensitivity – the same thing driving the high blood pressure in the first place.
"The inverse association of sodium to CVD mortality seen here raises questions regarding the likelihood of a survival advantage accompanying a lower sodium diet." (Cohen HW, et al. AJM, 2006)
Therefore, one could say that your low-salt food is a double-whammy since you're consuming the food that's elevating the cause of high blood pressure and opting for the "lowers blood pressure" variety that's making it worse.
5 – Gluten
The gliadin proteins in wheat can be damaging to many people because of those proteins' ability to induce inflammation and increase intestinal permeability. Wheat itself may also cause cravings and interfere with your appetite-regulating mechanisms.
However, this doesn't mean all products with a "gluten-free" stamp of approval are suddenly health foods. Pizza is still pizza, pancakes are still pancakes, and a slab of pound cake beside your coffee is and always will be a bad choice... gluten-free or not. This should be common sense, but millions are willingly fooled every day because it's pretty easy to convince us that a delicious junk food is fine when it has an official-looking health claim on the box.
Just like we were tricked into selecting low-fat and low-sodium packaged products because of their apparent health benefit, food marketers have simply found another way to convince you that their bag or box of garbage is healthy.
Gluten-free cereal may be better than gluten-filled cereal, but it's still cereal. And you'd be better off leaving both for the birds.
Related: The 10 Dumbest Diet Myths
Related: You're Fat. Asians Aren't. Here's Why.
- La Berg AF. 2008. How the Ideology of Low Fat Conquered America. J Hist Med Allied Sci 63(2):139-177.
- Siri-Tarino PW, et al. 2010. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr 91(3):535-46.
- Skeaff CM and Miller J. 2009. Dietary fat and coronary heart disease: summary of evidence from prospective cohort and randomised controlled trials. Ann Nutr Metab 55(1-3):173-201.
- Yamagishi K, et al. 2010. Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese: the Japan Collaborative Cohort Study for Evaluation of Cancer Risk (JACC) Study. Am J Clin Nutr 92(4):759-65.
- Mente A, et al. 2009. A systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease. Arch Intern Med 169(7):659-69.
- Limb M. 2014. Tougher action is needed to address "alarming" levels of overweight and obesity, says England's chief medical officer. BMJ 348:g2438.
- Burkitt DP. 1971. Epidemiology of cancer of the colon and rectum. Cancer 28(1):3-13.
- Mann GV, et al. 1971. Atherosclerosis in the Masai. Am J Epidemiol 95 (1): 26-37.
- Burr ML, et al. 1989. Diet and reinfarction trial (DART): design, recruitment, and compliance. Eur Heart J 10(6):558-67.
- Fuch CS, et al. 1999. Dietary fiber and the risk of colorectal cancer and adenoma in women. N Engl J Med 340(3):169-76.
- Park Y, et al. 2005. Dietary Fiber Intake and Risk of Colorectal Cancer: A Pooled Analysis of Prospective Cohort Studies. JAMA 294(22):2849-2857.
- Steinberg D. 2006. Thematic review series: the pathogenesis of atherosclerosis. An interpretive history of the cholesterol controversy, part V: the discovery of the statins and the end of the controversy. J Lipid Res 47(7):1339-51.
- Kellner A. 1952. Lipid Metabolism and Atherosclerosis: The Ludwig Kast Lecture. Bull N Y Acad Med 28(1):11-27.
- Stehbens WE. 2001. Coronary heart disease, hypercholesterolemia, and atherosclerosis. I. False premises. Exp Mol Pathol 70(2):103-19.
- Golomb BA and Evans MA. 2008. Statin adverse effects : a review of the literature and evidence for a mitochondrial mechanism. Am J Cardiovasc Drugs 8(6):373-418.
- Krumholz HM, et al. 1994. Lack of Association Between Cholesterol and Coronary Heart Disease Mortality and Morbidity and All-Cause Mortality in Persons Older Than 70 Years. JAMA 272(17):1335-1340.
- Braunwald E. 1997. Cardiovascular Medicine at the Turn of the Millennium: Triumphs, Concerns, and Opportunities. N Engl J Med 337:1360-1369.
- Prior IA. 1981. Cholesterol, coconuts, and diet on Polynesian atolls: a natural experiment: the Pukapuka and Tokelau island studies. Am J Clin Nutr 34(8):1552-61.
- Superko HR, et al. 2002. Small LDL and its clinical importance as a new CAD risk factor: a female case study. Prog Cardiovasc Nurs 17(4):167-73.
- Kendrick M. 2007. The Great Cholesterol Con: The Truth About What Really Causes Heart Disease and How to Avoid It. John Blake.
- Corona G, et al. 2010. The effect of statin therapy on testosterone levels in subjects consulting for erectile dysfunction. J Sex Med 7(4 Pt 1):1547-56.
- West R, et al. 2008. Better memory functioning associated with higher total and low-density lipoprotein cholesterol levels in very elderly subjects without the apolipoprotein e4 allele. Am J Geriatr Psychiatry 16(9):781-5.
- Huang X, et al. 2008. Low LDL cholesterol and increased risk of Parkinson's disease: prospective results from Honolulu-Asia Aging Study. Mov Disord 23(7):1013-8.
- de Lau LM, et al. 2006. Serum cholesterol levels and the risk of Parkinson's disease. Am J Epidemiol 164(10):998-1002.
- Shin JY, et al. 2008. Are cholesterol and depression inversely related? A meta-analysis of the association between two cardiac risk factors. Ann Behav Med 36(1):33-43.
- Perez-Rodriguez MM, et al. 2008. Low serum cholesterol may be associated with suicide attempt history. J Clin Psychiatry 69(12):1920-7.
- Seneff S. 2009. APOE-4: The Clue to Why Low Fat Diet and Statins may Cause Alzheimer's
- Morgan RE, et al. 1993. Plasma cholesterol and depressive symptoms in older men. Lancet 341(8837):75-9.
- Brown L, et al. 1999. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr 69(1):30-42.
- Swain JF, et al. 1990. Comparison of the Effects of Oat Bran and Low-Fiber Wheat on Serum Lipoprotein Levels and Blood Pressure. N Engl J Med 322:147-152.
- Barnard RJ, et al. 1998. Diet-induced insulin resistance precedes other aspects of the metabolic syndrome. J Appl Physiol 84(4):1311-1315.
- Alderman MH, et al. 1998. Dietary sodium intake and mortality: the National Health and Nutrition Examination Survey (NHANES I). 351(9105):781-785.
- Jurgens G and Graudal NA. 2003. Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterols, and triglyceride. Cochrane Database Syst Rev 1:CD004022.
- Garg R. 2011. Low-salt diet increases insulin resistance in healthy subjects. Metabolism 60(7):965-968.
- Cohen HW, et al. 2006. Sodium Intake and Mortality in the NHANES II Follow-up Study. Am J Med 119(3):275e7-275e14.
- Fasano A, et al. 2003. Prevalence of celiac disease in at-risk and not-at-risk groups in the United States: a large multicenter study. Arch Intern Med 163(3):286-92.
- Troncone R and Jabri B. 2011. Coeliac disease and gluten sensitivity. J Intern Med 269(6):582-590.
- Fasano A. 2011. Zonulin and its regulation of intestinal barrier function: the biological door to inflammation, autoimmunity, and cancer. Physiol R 91(1):151-75.
- Fasano A. 2012. Zonulin, regulation of tight junctions, and autoimmune diseases. Ann N Y Acad Sci 1258(1):25-33.