Not long ago I wrote an article called “Why Americans Are Fat and Sick”, which attempted to explain why financial and other interests converge on keeping Americans in a state of ill health. I recently came across “Metabolic Syndrome and the Burden on Health Care: Financial Corruption and Lifestyle Solutions” (access it here), which does a tremendous job in explaining the current health crisis in the United States. I offered to publish it here and following is a shorter version edited by the author. I hope everyone will read this, as there’s just no better single, succinct article on the American health care crisis.

Metabolic Syndrome: How Food Companies and Health Officials Made Us Sick

by Alexander Danes, BS Exercise Science, Twitter: “FrownyFace”

In the United States, we are spending $3.2 trillion annually on healthcare. This is more money than any other country on the planet. Pharmaceutical companies hold a monopoly with no competition to incentivize lower prices. At our current rate of spending, healthcare is a financial burden threatening to bankrupt the country. The problem is Metabolic Syndrome: a cluster of conditions including heart disease, diabetes and obesity. Subsidies or programs will not stop this. The solution must come from prevention. There is numerous evidence showing that Metabolic Syndrome is maintained by food companies and health officials. Trillions in profit is maintained on death and suffering. To fight back, we must hit them in the wallet. To reduce or withdraw need of our reliance on medications, which is possible with nothing but lifestyle adjustment.

Metabolic Syndrome is reversible and preventable. You don’t have to be shackled to medications for the rest of your life. You can be free. But, to defeat our enemy, we must understand it.

Blood Money

Insulin

The most expensive chronic diseases are Diabetes and Heart Disease which costs 101 billion and 88 billion annually (Johnson 2016). The price of insulin has sky rocketed from 168% to 325% from 2010 to 2015. The American Diabetes Association is included in the grab for profit, who changed the definition of high blood sugar in 1997 to classify 1.9 million additional Americans as diabetic (Fung 2017). The issue with exogenous insulin is it only manages high blood sugar, it does not address what’s causing it.

Because diabetics are dependent on increasingly expensive insulin, fatal practices have been adopted to conserve it; rationing. In 2018, we lost Alec Raeshawn Smith to diabetic ketoacidosis due to insulin rationing. His mother was not able to afford it in time. She comments that young adults are now resorting to getting married or dropping out of college to keep state funded insurance (Smith 2018). While vital, exogenous insulin has side effects.

Practitioners advise diabetics to lose weight, but the role of insulin is to store high blood sugar as body fat. Injection sites have fat built up (lipodystrophy), side effects include hypoglycaemia, swelling limbs, dizziness and irritability (Chicago Drug Info Group 2018). Medical advice tells patients to consume high carbohydrate meals then manage the blood sugar spike with insulin or diabetic medications.

A popular medication is SGLT-2 inhibitors. The medication increases sugar excretion via urination. The drawback is a raised risk for urinary tract infections and potential bladder cancer (Wick, 2018). The advice given is the equivalent of poisoning yourself and taking the antidote at every meal.

Statins

Heart disease treatment is prevention via cholesterol lowering drugs, but new data shows that high cholesterol is not a consistent marker for heart disease. LDL cholesterol levels and heart disease occurrence show no relationship in comprehensive reviews. Cholesterol and Atherosclerosis show no association in 4 different studies (Carolyn 2018).

A nationwide 2009 study reviewed LDL and 136,905 heart attack patients. The average LDL levels were 104.9, contradicting the “low LDL is protective” narrative (Sachdeva et al 2009). The confusion on cholesterol is deliberate. The boldly titled “Statin Wars” explains that raw data of statin have been manipulated to promote the benefits of cholesterol lowering drugs. The criteria of “at risk” was broadened to increase prescription rates to healthy people. Independent researchers were not allowed to verify results of the drugs. There is little evidence to show statins actually decrease mortality rate. Trials cut out non-responders/side effect patients out of studies to make the medication appear safe (Demasi 2017). Reports on cholesterol medication show muscle and liver damage, memory problems, hyperglycaemia, and accelerated aging (Johnson 2015). Statins have also been documented lowering testosterone in both men and women. Without cholesterol, the body cannot efficiently produce testosterone, which is why statins are commonly co-prescribed with Viagra (Schooling et al 2013). Cholesterol medications incur many side effects, adding to the expensive poly-pharmaceutical costs.

Vegetable (seed) oils

The common advice for preventing heart disease is to avoid saturated fat and use vegetable oil (corn, canola, soy). This too, is a marketing lie. There are no vegetables that can be squeezed and produce significant oil. Seeds and grains have oil, but require extensive heat processing, chemical fat extraction, and chemical odor removal (Gunnars 2018). Vegetable oil has a dark history with the American Heart Association (AHA). In the 1870’s economic depression, William Proctor and James Gamble formed a soap/candle company, saving money by using cheap cotton seed oil. Cotton seed oil is garbage, due to its toxic levels of phytochemical gossypol. Gossypol can cause spikes in potassium, organ damage and even paralysis. In 1907, a new technique solidified cotton seed oil to mimic lard. The newly created hydrogenated oil Cristco was marketed as the healthy alternative to lard. It was not until the 1990’s that hydrogenated oil was documented as harmful for heart disease (Ramsey, Graham 2012). Proctor and Gamble hold deep ties to the AHA, funding and backing them in 1948 ($17 million). In 2017, Bayer (owner of Liberty Link Soybeans) pledged over $500,000 to the AHA. It’s not surprising that the AHA is a supporter of “heart check logo approved vegetable oils”, continually attacking saturated fat. The AHA has held its position on saturated fat since 1961, cherry picking its evidence. The AHA disregards the lack of randomized controlled trials or meta-analyses to support the saturated fat and heart disease hypothesis (Teicholz 2017).

Vegetable oil is harmful, a 2016 review shows vegetable oil and statins increased risk of cardiovascular disease, diabetes and other chronic conditions (Okuyama et al 2016). In perfect demonstration, Israel in 1996 had the highest vegetable oil consumption rates. Paradoxically Israel also had the some of the highest rates of heart disease, hypertension, diabetes, obesity and cancer (Yam et al 1996). The oils we are told is healthy is killing us.

Obesity and metabolic syndrome

Diabetes and heart disease often parallel with high rates of obesity. While obesity is only a symptom of metabolic syndrome, it remains an important warning sign. The CDC estimates the average white male is now over 200 lbs with a 40-inch waist (Fryer et al 2018). Common advice to lose weight is just count calories. When reviewed, this method is a self-destructive failure. A meta-analysis of commercial weight loss programs using calorie deficits noted that 57% of participants only lost about 5% of their starting weight and half of those studies reported 30% difficulty adhering with programs (McEved 2017).

The other half of weight loss is doing cardio. But a low-calorie diet and aerobic exercise causes muscle loss and resting metabolic rate slowdown (Bryner et al 1998). Ever wonder why you feel terrible eating less and exercising more? Your body is wasting away and desperately conserving energy. Ravenous hunger is ongoing and eventually you break and regain the weight (or greater). This phenomena was demonstrated in the weight loss contestants of the “Biggest Loser.” They lost 100s of pounds with low calorie diets and vigorous exercise, but their metabolisms were destroyed. Follow ups showed that the method damaged their metabolisms and they regained their weight (Kolata 2016). Losing weight at the cost of your muscles and proper functioning metabolism is not healthy advice. This hyper focus on calorie counting is destructive to the populace’s mindset as noted in a 2014 review of Calorie Counting. Calorie counts don’t consider important nuance such as metabolic effect or hormone response.

Fast digesting carbohydrates and sugar are consistently noted to trigger fat storage and raise appetite (Lucan, DiNicolantonio 2014). The calorie counting narrative is parroted by sugar and soda companies. In 2019, Coca Cola was caught swaying China’s new obesity policy: Count calories and exercise, you can still have our products! (Boseley 2019). Coca Cola’s backroom funding can be traced back to obscure publicity stunts such as the Twinkie Diet. Researcher Mark Haub was paid by Coca Cola to go on an unverified, non-peer reviewed junk food experiment eating 1800 calories a day to promote calorie counting. Coca Cola spent $2.6 million on other scientists and researchers to spread the calorie narrative (Fung 2016). You don’t have to avoid sugar, just make sure you count calories accurately and you can lose weight. Every calorie counts! Diverting blame away from sugar has a long history, and vast evidence points to sugar as the origin of metabolic syndrome.

Pure, White and Deadly: Sugar

In 1972, one man had perfectly predicted the metabolic syndrome epidemic. Physiologist Dr. John Yudkin published “Pure White and Deadly”, a book chronicling the dangers of sugar. Yudkin showed that sugar damages the eyes, teeth, joints, liver and develops heart disease and cancer (Yudkin 1972, p. 126-141).

Yudkin’s sugar hypothesis was slandered and passed by in favor of the lipid hypothesis. Biochemist Ancel Keys was one of many scientists paid by the Sugar Research Foundation in the 1960s, today’s equivalent of $50,000. The Sugar Research Foundation wanted to find scientists who were interested in publishing research on the supposed dangers of animal fat. This resulted in the creation of the Lipid Hypothesis by Ancel Keys, postulating saturated fat clogged your arteries and high animal fat increases cholesterol and causes heart disease. These claims to this day have not been supported by causal evidence, only partial (weak) correlational evidence. Despite this, governing bodies moved forward with policy changes and told Americans to reduce their animal fat intake and load up on carbohydrate. Sugar was just an empty calorie, it’s harmless.

Professor of Pediatrics and Endocrinology Robert Lustig, M.D. opposes this oversimplification. “Fructose is a toxin.” Lustig explains in his viral YouTube lecture “Sugar the Bitter Truth” the hazardous effects of sugar. Sugar is composed of glucose and fructose; the fructose half can only be metabolized by the liver. Some of the fructose is converted to glucose, but the danger is the primary conversion to triglycerides. Fat continues to build on the liver leading to fatty liver disease. Sugar increases appetite and causes fat storage due to hormone disarray. Sugar triggers ghrelin (hunger), suppresses leptin (satiety) and stimulates insulin (store sugar as body fat). With sugar intake you are always hungry, never satisfied from meals and overweight (Lustig 2016). You’ve been poisoned.

Sugar’s damage to the liver is repeatably documented. Science journal Hepatobiliary Surgery and Nutrition calls sugar a weapon of mass destruction. Along with liver fat build-up, sugar causes oxidative damage and uric acid formation (leading to gout) and VLDL cholesterol, a risk for heart disease (Basaranoglu et al 2015). You can make foie gras of your liver; whether you drink alcohol or eat sugar, the effect is the same. Non-alcoholic fatty liver disease is a silent growing epidemic. Chronic high insulin due to sugar not only fattens the liver, but also deposits fat around your other organs (visceral fat) (Ahmed 2015). A fatty liver epidemic is coming if prevention is not prioritized.

A publication from Open Heart equates sugar as anti-food due to frequent insulin creating a form of internal cellular starvation. When insulin is constantly producing, it blocks body fat release from hormone sensitive lipase. If body fat release is blocked, your stored fat energy is effectively locked off, forcing hunger signals as a compensation (eat more). As long as sugar remains in the diet, fat storage and release will be impaired, leaving you constantly hungry. Frequent consumption builds visceral fat on the liver, fatiguing the pancreas (which makes insulin), and collapsing into metabolic insulin resistance. Insulin is needed to reduce blood sugar, if the brain cannot register the insulin signal, sugar levels stay spiked in the body. Now you’re becoming type 2 diabetic (DiNicolantonio, Berger 2016). This pattern is supported by Diabetes Journal in 2013. Sugar stimulates oxidative stress, creates uric acid, drains ATP (cell energy), and causes body fat formation even without a calorie surplus. A calorie is not a calorie (Johnson et al 2013). This effect is documented in Thailand, monks are becoming obese and diabetic despite eating similar calorie intakes to the population. The key issue is their consumption of sugary drinks/soda, leading some monks to require amputation (Cochrane 2018). We’re not safe either, amputations are on the rise in the US, coming from increasingly younger diabetic 18-44-year olds (Rapaport 2018).

Sugar is heavily associated with heart disease. Open Heart notes that sugar consumption leads to hyperglycaemia, a leading risk factor for heart disease even in non-symptomatic diabetic patients. High insulin is paralleled with myocardial infarctions, obesity, heart disease, hypertension, and hypertriglyceridemia (DiNicolantonio, Okeefe 2017). All chronic conditions are reversible when sugar and refined carbohydrate are low in the diet.

There’s evidence that sugar causes cancer. In 1968, Project 259 was exploring high cholesterol and sugar intake with rats. It was funded by the Sugar Research Foundation until the preliminary results of sugar intake implied a causal relationship with cancer. The findings were kept hidden to avoid investigation from the FDA. Sugar has additional data demonstrating greater cancer rates in endometrial, colon and breast cancer rates (Martin 2017). In 2010 it was discovered that Fructose is a quickly metabolizing energy source for pancreatic cancer growth (Lui et al 2010). People love sugar. Turns out, so does cancer.

If it isn’t plain by now, sugar is a big reason why we’re sick. Sugar spikes insulin, and chronic insulin leads to metabolic syndrome.

So, what happens if you cut out sugar and other insulin spiking foods?

Is the solution as simple and affordable as just changing your lifestyle?

Phoenix Rising

Humans have endured hardships throughout time. We are the apex predators of Earth for a reason. We are smarter and more adaptive than any other creature on the planet. So where did we go wrong? How are we slowly eating ourselves to death? We stopped doing what worked. F1000 Research remarks that humans are built for day/night sleep patterns, periods of fasting, and consuming mostly animal foods. Sugar was rare, humans only ate an occasional bounty of fruit or honey. Sugar is not evil, it is a vital fat storage tool for enduring famine. The problem is sugar is everywhere now, and our survival response is still the same as it was 2.5 million years ago. Eat sugar, build body fat. We don’t exercise, so glycogen (stored sugar) and cortisol (stress hormone) keeps blood sugar high (Klement et al 2018). The solution to metabolic syndrome is go back to what worked; eat mostly animal foods, induce periods of fasting, and exercise to simulate hunting and foraging behaviours.

Ketogenic diet

Reversing metabolic syndrome can be done with diet alone. The ketogenic diet removes insulin-spiking foods (starch and sugar) and emphasizes high animal food and non-starchy vegetables.

Keto works. A 2018 case study placed an obese women who regained weight from her gastric bypass on keto. She successfully lost 100 lbs, reversed her insulin resistance, pre-diabetes, and chronic inflammation in 1 year (Handley et al 2018).

Keto works in larger population studies as well. Virta Health conducted a 1-year continuous care trial with 349 obese diabetic patients. After 1 year on keto, 94% of patients reduced or ceased insulin, and 100% were off sulfonylureas. Chronic inflammation, blood pressure reduced, liver and lipid parameters improved (Halberg et al 2018).

But what about ketoacidosis!? Ketoacidosis and ketosis are 2 different states. Ketosis is a normal state of lipolysis (0.5-5mM) and ketoacidosis is an abnormal state (15-25mM). Keep carbs and sugar out of the diet and ketoacidosis is not a problem (Phinny 2018). Virta’s new health plan states that it will only pay employers if they can get their patients’ A1c down and get them off all medications. These claims are being tested in a 5-year clinical trial with 465 patients. Current results are showing great promise (Robbins 2018). Keto seems preferable to the government approved USDA guide diets. Keto vs USDA diet showed that keto had superior weight, body fat, triglyceride and blood sugar reductions after 32 days. The dropout rate of the 25 diabetic patients was 8% for Keto and 46% for the USDA group (Saslow et al 2017). Keto has a direct effect on metabolic syndrome and is a potent therapeutic tool.

Cholesterol and the lipid hypothesis

We are told to lower our cholesterol, but this advice is killing us. Data shows that higher cholesterol is preferable. A 2005 criticism of the lipid hypothesis showed 19 cohort studies with populations of high cholesterol. They died less, had fewer infections and lived longer (Ravnskov 2005). 10 years later this data is supported again, a Japanese supplementary review absolves cholesterol. Elderly with high cholesterol lived longer, 50-64 year olds showed cholesterol as a negative risk for mortality, high cholesterol decreased rates of heart disease mortality in women, higher LDL showed greater cognition, and high cholesterol protects against liver disease. The issue pleas to abandon the anti-cholesterol hypothesis. Cholesterol is a friend and its witch hunt is the biggest mistake made by the medical establishment in the previous century (Hamazaki et al 2015). Turns out that reducing what your body is composed of is a bad idea. You may as well tell someone to build a house with fewer bricks.

Fasting

Fasting has been rebranded as a new hip dieting trend. This is a disservice to the therapeutic effects of fasting. Fasting reduces chronic inflammation in the arteries. Normal inflammation heals damaged tissue, but chronic over production of inflammation creates blockages (Youm et al 2015). Fasting maintains muscles and blood sugar. Growth hormone levels go up to prompt fat breakdown, which provides fatty acids for glucose conversion and preventing protein breakdown (Moller, Jorgensen 2009). Fasting will cause eating disorders! This concern was tested, a 12-week experiment had obese patients fasting 16 hours a day with an 8-hour eating window. They could eat whatever they wanted in that time. They had no reported signs of disordered eating, maintained their resting metabolisms and lost weight (Kelsey et al 2018). Remember, people drop out of diets, because of resting metabolism slow down, which fasting prevented. How long should one fast? 18-24 hours a day is the most practical and efficient time period. This is when fat breakdown, insulin reduction and autophagy are at a sustainable peak (Mangan 2016).

Exercise

Because cortisol activates from light exposure, it’s important to have daily exercise. The effect of physical exertion is tangible on Non-alcoholic Fatty Liver Disease. Aerobic, moderate and especially high intensity exercise reduced liver mass and ALT (marker indicating liver damage) (Katsagoni 2016). Higher intensity exercise has a profound effect on post-exercise fat breakdown. Obese patients placed on exhaustive exercise regimens had matching fat oxidation with their dietary fat intake. Speaking plainly: the lower your glycogen the greater your fat breakdown (Schrauwen et al 1998). Effective ways to reduce glycogen is high intensity interval training, lifting weights, keto, and fasting. We are often told to “carb load” before exercise, but this advice interferes with weight loss. Overweight men who ate carbohydrates (bread, juice, cereal) and then did treadmill exercise had reduced bodyfat breakdown and reduced gene expression for fat loss compared to overweight fasted men (Chen et al 2017). Consuming carbohydrate gears the metabolism to prefer glucose and dials back fat breakdown in response. The best pre-workout meal may be nothing at all.

Conclusion

The metabolic syndrome epidemic is a paper tiger.

We are spending $3 trillion a year on chronic conditions that are completely reversible and preventable with lifestyle changes. Insulin and diabetic medications can be reduced or eliminated with diets low in insulin spiking diets such as keto. Cholesterol lowering drugs are a pharmaceutical throat slice. They do not meaningfully prevent or aid heart disease, and their side effects are causing unjustifiable harm. Inversely, high cholesterol is more beneficial than low cholesterol. The AHA, ADA, and food companies such as sugar and soda makers are not acting with our interests. Sugar, soda, refined carbohydrates, and vegetable seed oils are all implicit in the development of metabolic syndrome: heart disease, diabetes, obesity, fatty liver and cancer. Keto shows routine success in therapeutic application with metabolic syndrome. Daily fasting 16-24 hours can improve chronic inflammation, obesity and maintain metabolism unlike self-imposed calorie deficits. High intensity exercise combined with carb restriction and fasting liberates body fat.

Humans are one of the most adaptive, enduring species on the planet. We had the perfect game plan for resisting disease and thriving already provided for us in the past. Data shows that these methods work. Let’s show we can do it again.

“Before you heal someone, ask him if he’s willing to give up the things that made him sick.” -Hippocrates

References

Ahmed, M. (2015). Non-alcoholic fatty liver disease in 2015. World Journal of Hepatology. 7(11). Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4462685/ [Accessed 10 Feb 2019]

Basaranoglu, M., et al. (2015). Carbohydrate intake and nonalcoholic fatty liver disease: Fructose as a weapon of mass destruction. Hepatobiliary Surgery and Nutrition., 4(2). Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4405421/ [Accessed 10 Feb 2019].

Bosley S. (2019) Coca-Cola influences China’s obesity policy, BMJ report says. The Guardian. Available at: https://amp.theguardian.com/business/2019/jan/10/coca-cola-influence-china-obesity-policy-protect-sales-bmj-report?__twitter_impression=true [Accessed 9 Feb 2019].

Bryner R, et al (1998). Effects of Resistance vs. Aerobic Training Combined With an 800 Calorie Liquid Diet on Lean Body Mass and Resting Metabolic Rate. Department of Human Performance and Applied Exercise Science. Available at: http://www.itriminternational.com/globalassets/se/pdf/forskningsrapporter/bryner_ja_coll_nutr_1999.pdf [Accessed 9 Feb 2019].

Carolyn, M. (2018). ‘No evidence’ high cholesterol causes heart disease, say doctors. Irish Times. Available at: https://www.irishtimes.com/news/health/no-evidence-high-cholesterol-causes-heart-disease-say-doctors-1.3627093 [Accessed 9 Feb. 2019].

Chen Y, et al. Feeding influences adipose tissue responses to exercise in overweight men. American Journal of Physiology. Available at: https://doi.org/10.1152/ajpendo.00006.2017 [Accessed 11 Feb 2019].

Cochrane L. (2018). Thai Buddhist monks’ health suffering from sugary drinks. ABC News. Available at: https://mobile.abc.net.au/news/2018-05-28/thai-buddhist-monks-health-ruined-by-sugary-drinks/9711412?pfmredir=sm [Accessed 10 Feb 2019].

Connor A. (2016). How the Sugar Industry Shifted Blame to Fat. The New York Times. Available at: https://www.nytimes.com/2016/09/13/well/eat/how-the-sugar-industry-shifted-blame-to-fat.html [Accessed 10 Feb 2019].

Demasi, M. (2017). Statin Wars: have we been misled about the evidence? A narrative review. Br J Sports Medicine. Available at: https://bjsm.bmj.com/content/bjsports/early/2018/01/16/bjsports-2017-098497.full.pdf?ijkey=Rsap0XafljfcOCR&keytype=ref [Accessed 9 Feb 2019].

DiNicolantonio J., Berger A. (2016). Added Sugars Drive Nutrient and Energy Deficits in Obesity: A New Paradigm. Open Heart. Available at: http://openheart.bmj.com/content/3/2/e000469.full [Accessed 10 Feb 2019].

DiNicolantonio J, OKeefe J. (2017). Added sugars drive coronary heart disease via insulin resistance and hyperinsulinaemia: a new paradigm. Open Heart. Available at: https://openheart.bmj.com/content/openhrt/4/2/e000729.full.pdf [Accessed 10 Feb 2019].

Fung J, (2016). Lose Weight on Twinkies? Big Soda‘s Strategy to Make Us Believe That It Is All About Calories. Diet Doctor. Available at: https://www.dietdoctor.com/big-sodas-strategy-make-us-believe-calories [Accessed 9 Feb 2019].

Fung, J. (2017). The Diabetes Payroll. Medium. Available at: https://medium.com/@drjasonfung/the-diabetes-payroll-291649d0e0d2 [Accessed 9 Feb. 2019].

Fryar C, M.S.P.H, Moran D, Sc.M, Gu Q, Ogden C. (2018). Mean Body Weight, Height, Waist Circumference, and Body Mass Index Among Adults: United States,1999–2000 Through 2015–2016. National Health Statistic Reports, CDC. Available at: https://www.cdc.gov/nchs/data/nhsr/nhsr122-508.pdf [Accessed 9 Feb 2019].

Gunnars K. (2018). Are Vegetable and Seed Oils Bad for Your Health? Healthline. Available at: https://www.healthline.com/nutrition/are-vegetable-and-seed-oils-bad [Accessed 13 Feb 2019].

Hallberg, S., McKenzie, A., Williams, P., Bhanpuri, N., Peters, A., Campbell, W., Hazbun, T., Volk, B., McCarter, J., Phinney, S. and Volek, J. (2018). Effectiveness and Safety of a Novel Care Model for the Management of Type 2 Label, Non-Randomized, Controlled Study. Springer Nature. Available at: https://link.springer.com/article/10.1007%2Fs13300-018-0373-9 [Accessed 11 Feb. 2019].

Handley RT et al. (2018) Successful treatment of obesity and insulin resistance via ketogenic diet status post Roux-en-Y. BMJ Case Report. Available at: https://www.ncbi.nlm.nih.gov/pubmed/30121567/ [Accessed 11 Feb 2019].

Hamazaki T, et al. Towards a Paradigm Shift in Cholesterol Treatment. A Re-examination of the Cholesterol Issue in Japan. Annals of Nutrition and Metabolism. Available at: https://www.karger.com/Article/Pdf/381654 [Accessed 12 Feb 2019].

Johnson, C. (2016). The U.S. spends more on health care than any other country. Here’s what we’re buying. Washington Post. Available at: https://www.washingtonpost.com/news/wonk/wp/2016/12/27/the-u-s-spends-more-on-health-care-than-any-other-country-heres-what-were-buying/?utm_term=.d13f6f8ce577 [Accessed 9 Feb. 2019].

Johnson, L. (2015) Statins: Heart disease drug speeds up ageing process, warns new research. Express. Available at: https://www.express.co.uk/life-style/health/608210/statins-age-you-faster-new-research-suggests-long-term-use-warning/amp?__twitter_impression=true [Accessed 9 Feb. 2019].

Johnson R, et al. (2013). Sugar, Uric Acid, and the Etiology of Diabetes and Obesity. Diabetes 62:3307-3315. Available at: http://diabetes.diabetesjournals.org/content/diabetes/62/10/3307.full.pdf [Accessed 10 Feb 2019].

Katsagoni C et al. (2016). Effects of lifestyle interventions on clinical characteristics of patients with non-alcoholic fatty liver disease: A meta-analysis. Metabolism. Available at: https://www.metabolismjournal.com/article/S0026-0495(16)30184-6/pdf [Accessed 11 Feb 2019].

Kelsey G, et al. (2018). Safety of 8-h time restricted feeding in adults with obesity. Applied Physiology, Nutrition, and Metabolism. Available at: https://tspace.library.utoronto.ca/bitstream/1807/92910/1/apnm-2018-0389.pdf [Accessed 11 Feb 2019].

Kolata G. (2016). After ‘The Biggest Loser,’ Their Bodies Fought to Regain Weight. The New York Times. Available at: https://www.nytimes.com/2016/05/02/health/biggest-loser-weight-loss.html [Accessed 9 Feb 2019].

Klement R, et al. (2018). The sedentary (r)evolution: Have we lost our metabolic flexibility? F1000 Research. Available at: https://f1000research.com/articles/6-1787/v2 [Accessed 11 Feb 2019].

McEved, S., Sullivan-Mort, G., McLean, S., Pascoe, M. and Paxton, S. (2017). Ineffectiveness of commercial weight-loss programs for achieving modest but meaningful weight loss: Systematic review and meta-analysis [online] Sage Journals. Available at: http://journals.sagepub.com/doi/abs/10.1177/1359105317705983?fbclid=IwAR24YsiFk_rhc_rwMkE8hMRn2h1f9LQS5K2Mu9 P8LjYr6R590uJFposTxuY [Accessed 9 Feb. 2019].

Lucan S, DiNicolantonio J. (2014). How calorie-focused thinking about obesity and related diseases may mislead and harm public health. An alternative. Public Health Nutrition. Available at: https://journals.cambridge.org/images/fileUpload/documents/PHN2014-007802_1.pdf [Accessed 9 Feb 2019].

Lustig R. (2016). Sugar the Bitter Truth. University of California Television (UCTV). Available at: https://www.uctv.tv/shows/Sugar-The-Bitter-Truth-16717 [Accessed 10 Feb 2019].

Liu H, et al. (2010). Fructose Induces Transketolase Flux to Promote Pancreatic Cancer Growth. Tumor and Stem Cell Biology. Available at: http://cancerres.aacrjournals.org/content/canres/70/15/6368.full.pdf [Accessed 10 Feb 2019].

Mangan, P.D. (2016). The Sweet Spot for Intermittent Fasting. Medium. Available at: https://medium.com/the-mission/the-sweet-spot-for-intermittent-fasting-9aae12a2158c [Accessed 11 Feb 2019].

Martin Y. (2017) Sugar and Cancer: A surprise connection or 50 year cover up? Medical News Today. Available at: https://www.medicalnewstoday.com/articles/320156.php [Accessed 10 Feb 2019].

Moller N, Jorgensen JO. (2009). Effects of growth hormone on glucose, lipid, and protein metabolism in human subjects. The Endocrine Society. Available at: https://www.ncbi.nlm.nih.gov/pubmed/19240267 [Accessed 11 Feb 2019].

Okuyama H, et al. (2016). Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes. Available at: https://www.karger.com/Article/FullText/446704 [Accessed 12 Feb 2019].

Phinny S, et al. (2018). Ketosis vs Ketoacidosis: What is the difference? Virta Health. Available at: https://blog.virtahealth.com/ketosis-vs-ketoacidosis/ [Accessed 12 Feb 2019].

Ramsey D, Graham T. (2012). How Vegetable Oils Replaced Animal Fats in the American Diet. The Atlantic. Available at: https://www.theatlantic.com/health/archive/2012/04/how-vegetable-oils-replaced-animal-fats-in-the-american-diet/256155/ [Accessed 12 Feb 2019].

Rapaport L. (2018). Diabetic Amputations on the rise in the U.S. Reuters. Available at: https://www.reuters.com/article/us-health-diabetes-amputations/diabetic-amputations-on-the-rise-in-the-u-s-idUSKBN1OB2OK [Accessed 11 Feb 2019].

Robbins R. (2018). A startup for diabetes patients rolls out a new model: Insurers only pay if the service works. STATnews. Available at: https://www.statnews.com/2018/11/14/a-startup-for-diabetes-patients-will-only-get-paid-if-the-service-works/ [Accessed 12 Feb 2019].

Ravnskov U. (2008). The fallacies of the lipid hypothesis. Scandinavian Cardiovascular Journal : SCJ. 42. 236-9.10.1080/14017430801983082. Available at: https://www.researchgate.net/publication/5236032_The_fallacies_of_the_lipid_hypothesis [Accessed 12 Feb 2019].

Sachdeva A, et al. (2009). Lipid levels in patients hospitalized with coronary artery disease: An analysis of 136,905 hospitalizations in Get With The Guidelines. Department of Medicine UCLA. Available at: http://epadruginitiative.com/files/Get_With_The_Guidelines_2009.pdf [Accessed 12 Feb 2019].

Schrauwen P. et al. (1998). Fat balance in obese subjects: role of glycogen stores. American Journal of Physiology. Available at: https://www.narcis.nl/publication/RecordID/oai%3Acris.maastrichtuniversity.nl%3Apublications%2F3b82f4d9-158d-440a-b1c7-5bb319f872ba [Accessed 11 Feb 2019].

Schooling M, Yeung S, Freeman G, Cowling B. (2013) The effect of statins on testosterone in men and women, a systematic review and meta-analysis of randomized controlled trials. BMC Medicine. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3621815/ [Accessed 9 Feb 2019].

Slaslow L, et al. (2017). An Online Intervention Comparing a Very Low-Carbohydrate Ketogenic Diet and Lifestyle Recommendations Versus a Plate Method Diet in Overweight Individuals With Type 2 Diabetes: A Randomized Controlled Trial. JMIR Publications. Available at: https://www.jmir.org/2017/2/e36/ [Accessed 11 Feb 2019].

Smith B. (2018). Insulin’s High Cost Leads To Lethal Rationing. NPR. Available at: https://www.npr.org/sections/health-shots/2018/09/01/641615877/insulins-high-cost-leads-to-lethal-rationing [Accessed 12 Feb 2019].

Teicholz N. (2017). Don’t believe the American Heart Assn. — butter, steak and coconut oil aren’t likely to kill you. LA Times. Available at: https://www.latimes.com/opinion/op-ed/la-oe-teicholz-saturated-fat-wont-kill-you-20170723-story.html [Accessed 13 Feb 2019].

University of Chicago, Drug Information Group. (2018) Insulin Regular, Injectable Solution. Healthline. Available at: https://www.healthline.com/health/regular-insulin-injectable-solution#about [Accessed 12 Feb 2019].

Wick J. (2018). These Popular Diabetes Medications Have Horrible Side Effects. CheatSheet. Available at: https://www.cheatsheet.com/health-fitness/popular-diabetes-medications-have-horrible-side-effects.html/ [Accessed 12 Feb 2019].

Yam D, et al. (1996). Diet and disease–the Israeli paradox: possible dangers of a high omega-6 polyunsaturated fatty acid diet. Israel Medical Science. Available at: https://www.ncbi.nlm.nih.gov/pubmed/8960090 [Accessed 13 Feb 2019].

Youm Y, et al. (2015). Ketone body β-hydroxybutyrate blocks the NLRP3 inflammasome-mediated inflammatory disease. Nat Med. Available at: https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC4352123&blobtype=pdf [Accessed 11 Feb 2019].

Yudkin J. (1972). Pure, White and Deadly (p 126-141). Penguin Health. [Accessed 10 Feb 2019].

About the author

Alexander Danes is a graduate of California State University, Fresno.