Are you the guy with the wrinkled brow? Are you thinking of starting a ketogenic or paleolithic diet? Having second thoughts because of the high fat content of the ketogenic diet or the paleolithic diet? Are you worried about the results of your latest lipid panel? Did your doctor just tell you, “Might need to start you on medication to control your “bad cholesterol”?
I’ll tell you my story. Maybe my attempt to understand the fat content of the ketogenic diet will help you decide whether eating a ketogenic or paleolithic diet is the right choice for you. For proportions of macronutrients in ketogenic and other diets, follow the links. https://carbohydrateconfessions.com/what-is-a-ketogenic-diet/
The Cardiovascular Risk Factor Dilemma
This post started, as many of my posts do, as an attempt to unravel a personal dilemma, one which kept buzzing about in my brain. My dilemma, which I suspect I share with many of you, is whether to follow my doctor’s advice and worry about my cholesterol levels or to reduce my carbohydrate intake and increase my fat intake so I can lose weight. (My weight loss journey is described in my book.) https://carbohydrateconfessions.com/
I had several questions. Will eating more fat hurt me in the long run? Does the fat in a ketogenic diet increase my risk of heart disease or stroke? What’s going to happen to my blood lipids when I increase my fat intake?
Cardiovascular Disease and Me
I first heard about cardiovascular risk factors and diet during a routine employee health examination. The doctor told me that my blood pressure was a little high, but my concerns grew when another doctor mentioned the cholesterol levels in my blood were also worrisome. I should stop eating so much red meat and saturated fat.
Haunted by Cholesterol
After that the question of my cholesterol levels haunted every doctor’s visit. No matter what the reason for my appointment, the blood lipids in my blood leaped to the top of the list. Sometimes “my numbers” were off, and sometimes they were okay. Doctors warned that I would soon need to take medication to control my blood lipids.
I Begin to Worry About My Lipid Panel
At other visits my doctors pointed knowingly to a table of indecipherable blood test results and rattled on about the ranges of a lot of stuff I’d never thought about before. The table had information on LDL-C, HDL-C, and other intimidating acronyms. I later learned I was looking at my lipid panel.
My doctors were so earnest because they truly believed that my blood cholesterol needed attention.
I couldn’t dispel the sensation that I’d been displaced into a 1930’s Tarzan movie and was watching my personal witch doctor conjure up a magical cure for something I couldn’t see and didn’t understand.
Fear and Loathing
Coincidentally, diagrams of cholesterol clogged arteries bombarded my consciousness. These were everywhere—in my doctor’s office, in magazines, and on the screen of my television.
In and of themselves, the images were ugly, but they were also tainted by a sense of menace. Something that ugly had to be bad, so I was getting the message. Be afraid of cholesterol. Be very afraid because some cholesterol is “bad”, very bad.
Image of a dissected artery clogged by masses of yellow goo was taken from the Science magazine website.
The Cholesterol Hypothesis
When I don’t understand something, I read. I learned that my doctors based their treatment recommendations upon the “cholesterol hypothesis”. Then, I found Malcom Kendrick’s book, The Great Cholesterol Con (Kendrick, 2007). He demolished the cholesterol hypothesis. https://www.amazon.com/Great-Cholesterol-Really-Causes-Disease/dp/1844546101/
The Syllogism Which Is the Cholesterol Hypothesis
- Having plaques composed of cholesterol and other stuff in the coronary arteries is bad for the cardiovascular system.
- Foods which contain saturated fats raise the cholesterol levels in our blood.
- So, eating saturated fat is bad because it causes plaques and heart disease.
Kendrick quipped that the cholesterol hypothesis is “extra-super straightforward—suitable for children from the age of five upwards, no parental guidance required (Kendrick, 2007).”
How Did Cholesterol Become a Bad Guy?
The cholesterol hypothesis started in the 1950’s after a number of well-known senators had life ending heart attacks. Simultaneously, heart disease among middle aged men skyrocketed.
Scientists found a problem requiring a solution, and they sought a cause for the attacks. Scholars considered many dietary factors including cholesterol, phytosterols, eating too much, amino acids, fats, carbohydrates, and minerals (Kearns, Schmidt, & Glantz, 2016).
The possible causative factors were winnowed down to two—sugar and fat. Two physiologists led a pitched and ugly battle for their candidate. John Yudkin believed that sugars caused heart disease, but Ancel Keys argued that fat, saturated fat, and dietary cholesterol had a significant role in coronary heart disease.
Keys’ theory won, and the cholesterol hypothesis was on its way to dominating medical and dietary practice.
Very Basic Lipid Physiology
A few basic definitions are needed here. Cholesterol and the fats and oils we eat are lipids. Cholesterol is necessary for life. The liver manufactures large amounts of cholesterol each day, and cholesterol forms the basis of cell membranes, the synthesis of Vitamin D, some hormones, and bile salts.
Cholesterol doesn’t dissolve in water. Thus, our bodies use lipoprotein carrier molecules to transport the cholesterol manufactured by the liver each day through the bloodstream to sites throughout our bodies.
The Popular View of Lipid Physiology
Like me, you may have seen an diagram like this in a magazine or in the doctor’s waiting room.
The complex of cholesterol and the low-density lipoprotein is termed “LDL-C”, and the complex of cholesterol with high-density lipoprotein is called HDL-C”.
LDL-C or low-density lipoprotein takes the cholesterol from the liver to the cells, but high density lipoprotein or HDL-C takes the excess cholesterol from cells and returns it to the liver. The liver breaks down the excess cholesterol and produces bile salts.
LDL-Cholesterol Isn’t Bad
If you’ve been an industrious student, you think you’re pretty sharp. You’ve figured out which of these cholesterols on your lipid panel is “good” and which is “bad”. You know that LDL-C is “bad” and HDL-C is “good”. You know this because your doctor smiles approvingly your LDL-C and HDL-C panel numbers are in healthy ranges.
This value-laden notion of good and bad cholesterol is only partly true, so watch the informative videos in order.
The Illogical Leap of Faith
Pharmaceutical companies, the medical community, and the public wanted to believe in their extra-super straightforward cholesterol hypothesis. Pharmaceutical company representatives, briefcases loaded with samples of cholesterol lowering medications, loitered in doctors’ offices. Doctors dutifully wrote prescriptions, and we consumers jumped off the statin cliff like demented lemmings.
In 1996, two Nobel laureates confidently predicted that the recent cholesterol hypothesis breakthroughs might “end coronary disease as a major public health problem early in the next century.”From Kearns et al. (2016)
We Want to Believe
Everyone wanted to believe in the cholesterol hypothesis, but the ever-cynical H. L. Mencken was right again.
For every complicated problem, there is a solution that is simple, direct, understandable and wrong.—H. L. Mencken
How Did We Go Astray?
We didn’t get into this state of unreality on our own. We had help. Big Sugar industriously chipped away at our collective consciousnesses for more than 75 years! A desire to get a larger market share drove their efforts.
Knowing how the public perceptions and medical practices of a generation were shaped and molded by financially motivated sugar and pharmaceutical manufacturers can make us better consumers.
Enter the Puppet Masters
When a dedicated group of researchers found and reviewed many internal sugar industry documents, these records proved that the sugar industry led a prolonged, malicious, and ongoing assault upon the health of a generation.
The blueprint used to foist the economically advantageous “lie” of the cholesterol hypothesis began in 1954 with a seminal speech by the president of the Sugar Research Foundation (Kearns et al., 2016)
The Sugar Research Foundation’s Master Plan
Set Strategic Goal
Henry Hass, president of the Sugar Research Foundation, identified a strategic opportunity to increase the sugar industry’s share of the market by getting Americans to eat a lower-fat diet.
The Sugar Research Foundation spent today’s equivalent of 5.3 million dollars on advertising that sugar keeps us alive and gives the energy we need to face our daily problems.
Challenge and Undermine
Discredit scientists who believed that sugar rather than fat was at the root of cardiovascular problems.
Manipulate Public Opinion
Use opinion poll data to develop advertising campaigns which will increase acceptance of the dangers of fat and the beneficial properties of sugar.
Find Susceptible Scientists
Pay scientists at prestigious institutions to write and publish papers which are favorable to the cholesterol hypothesis and unfavorable to the growing body of research on the cardiovascular dangers of sugar. These paid “scientists” concluded that there was “no doubt” that reducing dietary cholesterol and substituting polyunsaturated fat for saturated fat was all that was necessary to prevent coronary heart disease.
Conceal the financial relationship between the Sugar Research Foundation and corrupt scientists.
Persuade governmental agencies and medical practitioners to adopt policies favorable to the Sugar Research Foundation point of view by commissioning a review which influenced the 1976 US Food and Drug Administration’s evaluation of the safety of sugar.
Guilt and Manipulative Tactics
One example of how far the sugar industry was willing to go in its attempts to sway public opinions was the fear tactics used in their advertisements. The photo was taken from a Sugar Institute advertisement. In the ad, mothers who might be using artificial sweeteners to lose weight are guilt tripped, and these thoughtless mothers were advised that depriving their child of sugar would make him or her more vulnerable to illness and would deprive the child of needed energy.
“Make sure they get sugar every day”, the Sugar Institute advised.
Sugar Institute Skullduggery
The Sugar Institute is now the Sugar Association. Some other fascinating Sugar Institute skullduggery is noted in a U. S. Supreme Court decision. https://www.law.cornell.edu/supremecourt/text/297/553
The Cholesterol Hypothesis Is Simple, Direct, Understandable and Wrong
The emperor has no clothes!
Cartoon depiction of R. Nixon & cabinet in 1970. From the Library of Congress
Despite the concerted efforts of the sugar and the pharmaceutical industries to prove otherwise, the cholesterol hypothesis is an emperor without clothes.
Ways the Cholesterol Hypothesis Has Failed
- Amount of cholesterol in your blood should predict heart disease incidence.
- Lowering blood cholesterol levels of individuals to healthier patterns should reduce the number of people who die from heart disease and stroke.
- Eating a diet high in fat and low in carbohydrates should increase the risk of heart disease.
- Taking medication to lower cholesterol levels in the blood should increase life expectancy and reduce cardiovascular illness.
Lipid Levels as Predictors of Mortality
When it comes to the lipid levels in our blood, we weren’t created equal. Some of us are born with low levels of LDL-C. The cholesterol hypothesis predicts that these individuals would be healthier and live longer, but they don’t (DuBroff, 2017; Naude et al., 2014).
How much saturated fat you eat and the amount of cholesterol in your blood don’t predict heart disease or stroke. The evidence against these significant premises of the cholesterol hypothesis is “strong and systematic” (Chiu, Williams, & Krauss, 2017).
Very Low Ketogenic Diets Improve Cardiovascular Risk Markers
Bueno and colleagues summarized the results of 13 studies which examined the impact of a ketogenic diet on body weight and cardiovascular risk factors including HDL-Cholesterol, LDL-Cholesterol, blood pressure, and diabetes markers (Bueno, de Melo, de Oliveira, & da Rocha Ataide, 2013; Krauss, Blanche, Rawlings, Fernstrom, & Williams, 2006; Mangravite et al., 2011; McDonald & Cervenka, 2018; Santos, Esteves, da Costa Pereira, Yancy, & Nunes, 2012). Individuals on a low carb high fat diet lost more weight than those on a low-fat diet. Their blood pressures were reduced and their blood markers such as HDL-C were improved.
Cholesterol Lowering Drugs Don’t Increase Life Expectancy
Taking a medication such as a statin to lower cholesterol levels in the blood doesn’t change the number of cardiovascular events or deaths.
The ACCELERATE trial evaluated a new cholesterol lowering medication designed to reduce low-density lipoprotein and increase high density lipoprotein (DuBroff, 2017). Although the drug did its job and LDL-C dropped by 37% and HDL increased by 130%, there was no change in cardiovascular events or deaths.
The Strength of The Data On Cholesterol Lowering Drugs
This conclusion is not biased or isolated. Dubroff provides a table listing 44 randomized control studies showing no meaningful change in life expectancy when we take cholesterol lowering medications (DuBroff, 2017).
Statins and Life Expectancy
Let’s look at the studies on cholesterol lowering drugs which claim a statistical benefit for taking cholesterol lowering medication. How much longer can the average person taking statins expect to live?
In the first study to systematically evaluate the efficacy of statin or cholesterol lowering medication by using an average postponement of death as an outcome measure, Kristensen et al. (2015) examined 11 well designed studies. A range of “postponement values” was found. The median postponement for primary and secondary prevention trials were 3.2 and 4.1 days, respectively (Kristensen, 2015).
How Many Days??
Let those numbers sink in. You take statin medications and expose yourself to drug-related health risks, you pay enormous sums to get these drugs, and your payoff is what? 3 to 4 days!
Would you take a statin if you knew that you would only have 3 or 4 more days to live?
Are We Gaining on Heart Disease?
The next century has long since arrived, and 50% of men and 38% of women over the age of 60 are taking cholesterol lowering drugs such as statins. The American Council on Science and Health noted that “Anytime we see half of an entire population being prescribed a drug, it might be time to ask if we’re overdoing it.” https://www.acsh.org/news/2018/07/18/are-doctors-overprescribing-statins-13208
The confident predictions of the 1990’s haven’t been realized. In fact, cardiovascular disease remains a “pandemic” (DuBroff, 2017).
Why Do We Cling to the Cholesterol Hypothesis?
Pharmaceutical and sugar companies cling to the cholesterol hypothesis because they’re making money, lots of money. Some scientists cling to the cholesterol hypothesis because they’re invested or corrupted.
Medical practitioners cling to the hypothesis because it’s safe and easy. Practitioners can go to industry-funded workshops and get a dose of reassurance. No nasty scientific articles to read.
Patients are reassured that they are protected against heart disease with the stroke of a pen so all the patient must do is swallow a pill or two each day. Easy!
Legend Versus Fact
Finally, we cling to the cholesterol hypothesis because it has achieved the status of a myth or legend. We like legends.
“When legend becomes fact, print the legend.”Carlton Young as Maxwell Scott in Who Shot Liberty Valance?
The Long View
Due to the legendary status of the original cholesterol hypothesis, the hypothesis will die with a whimper rather than a bang. Legends simply don’t die. They can only wither.
Eventually, we’ll be able to turn back the clock to the 1950’s, take a hard look at the role dietary sugar has in our collective cardiovascular woes, and start all over again.
If I’ve done my job, you are less afraid of fat because you know that fat per se isn’t bad, and I hope you understand that preventing heart disease is more complicated than giving up eggs and butter. I hope you’re more open to dietary choices beyond the ill-conceived food pyramid.
I choose to believe that the fat in the ketogenic diet will not increase my risk of cardiovascular illness. That’s how I interpret the scientific studies and arguments. Your choice may be different. Make your choice a reasoned and considered one and make it in conjunction with your family and medical practitioner.
Bueno, N. B., de Melo, I. S., de Oliveira, S. L., & da Rocha Ataide, T. (2013). Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. Br J Nutr, 110(7), 1178-1187. doi:10.1017/S0007114513000548
Chiu, S., Williams, P. T., & Krauss, R. M. (2017). Effects of a very high saturated fat diet on LDL particles in adults with atherogenic dyslipidemia: A randomized controlled trial. PLOs One, 12(2), e0170664-e0170664. doi:10.1371/journal.pone.0170664
DuBroff, R. (2017). Cholesterol paradox: a correlate does not a surrogate make. Evidence Based Medicine, 22(1), 15. doi:10.1136/ebmed-2016-110602
Kearns, C. E., Schmidt, L. A., & Glantz, S. A. (2016). Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Internal Medicine, 176(11), 1680-1685. doi:10.1001/jamainternmed.2016.5394
Kendrick, M. (2007). The Great Cholesterol Con. London: John Blake.
Krauss, R. M., Blanche, P. J., Rawlings, R. S., Fernstrom, H. S., & Williams, P. T. (2006). Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia. Am J Clin Nutr, 83(5), 1025-1031; quiz 1205. doi:10.1093/ajcn/83.5.1025
Kristensen, M. L., Christensen, P. M.,Hallas, J. . (2015). The effect of statins on average survival in randomised trials, an analysis of end point postponement. BMJ Open, 5(e007118).
Mangravite, L. M., Chiu, S., Wojnoonski, K., Rawlings, R. S., Bergeron, N., & Krauss, R. M. (2011). Changes in atherogenic dyslipidemia induced by carbohydrate restriction in men are dependent on dietary protein source. The Journal of Nutrition, 141(12), 2180-2185. doi:10.3945/jn.111.139477
McDonald, T. J. W., & Cervenka, M. C. (2018). Ketogenic Diets for Adult Neurological Disorders. Neurotherapeutics, 15(4), 1018-1031. doi:10.1007/s13311-018-0666-8
Naude, C. E., Schoonees, A., Senekal, M., Young, T., Garner, P., & Volmink, J. (2014). Low carbohydrate versus isoenergetic balanced diets for reducing weight and cardiovascular risk: a systematic review and meta-analysis. PLOs One, 9(7), e100652. doi:10.1371/journal.pone.0100652
Santos, F. L., Esteves, S. S., da Costa Pereira, A., Yancy, W. S., Jr., & Nunes, J. P. (2012). Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors. Obes Rev, 13(11), 1048-1066. doi:10.1111/j.1467-789X.2012.01021.x