PDF Summary:Dark Calories, by Catherine Shanahan

You've probably heard that vegetable oils are a healthier alternative to butter and animal fats. But what if the opposite were true? In Dark Calories, physician Catherine Shanahan argues that vegetable oils—found in everything from salad dressings to restaurant fries—are one of the most toxic substances in our food supply. She explains how these oils contain unstable polyunsaturated fatty acids that oxidize easily, creating harmful compounds that damage your cells and mitochondria.

Shanahan traces how the promotion of vegetable oils became widespread despite weak scientific evidence, and she examines the connections between these oils and chronic inflammation, metabolic dysfunction, and disease. You'll learn why the standard advice about cholesterol may be misguided, how protein deficiency is more common than most people realize, and what dietary changes can help reverse the damage caused by vegetable oils.

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(Shortform note: In an academic paper, researchers summarize experiments that show mitochondria behave differently when they’re made of more polyunsaturated fat. The researchers explain that mitochondria are responsible for converting oxygen into ATP, the energy currency of cells. They note that mitochondria with more polyunsaturated membranes have a different relationship between oxygen consumption and ATP synthesis. This suggests that the type of fat in mitochondrial membranes can influence how efficiently mitochondria produce energy.)

Metabolic Dysfunction: Hormonal & Systemic Consequences

Shanahan explains that resistance to insulin disrupts energy production and may lead to cell death. Ketones are molecules the liver makes from body fat, and ketogenesis is the process by which they are made. Insulin resistance interferes with this process, depriving the brain of adequate fuel. When energy production is insufficient in the mitochondria, cells may begin to perish.

(Shortform note: To understand how insulin resistance interferes with ketogenesis, it’s helpful to understand how the process works. According to a research article, the liver produces ketones from fatty acids when glucose is scarce. However, in insulin-resistant states, the liver’s insulin levels remain high, which blocks the transporter that shuttles fatty acids into mitochondria. This prevents the liver from converting fats into ketones, disrupting the brain’s energy supply.)

Additionally, insulin resistance causes metabolic dysfunction and makes you put on weight. Shanahan describes it as a metabolic issue that leads to suffering. It's how the body reacts to the energy issue that arises when the body contains fat overloaded with PUFA and can't supply energy to cells. Insulin resistance causes you to experience low blood sugar symptoms despite having normal levels.

(Shortform note: Some people have insulin resistance that isn’t caused by fat overloaded with PUFA. Semple et al. describe rare genetic syndromes of severe insulin resistance caused by mutations in the insulin receptor. These patients have severe insulin resistance even when they have little body fat, and they typically have high blood sugar without the symptoms of low blood sugar.)

It increases the body's requirement for blood sugar. As insulin resistance increases, your body requires progressively elevated blood glucose, raising your baseline. If it drops even slightly below your body's needs, you'll experience hypoglycemia. This causes hunger even when your glucose levels are within or higher than the normal range. This hunger may seem urgent, and when you have insulin resistance, it is urgent. Your small cells have energy stores for only twenty seconds. This hunger driven by metabolism can't be conquered by sheer will, and eventually, it leads to weight gain for most people, even athletes.

Limited Energy Reserves in Cells

The phrase “your small cells have energy stores for only twenty seconds” is a bit unclear. It seems to refer to the fact that each cell has a small amount of ATP and other high-energy molecules stored, but these reserves are quickly depleted if not constantly replenished. This highlights how dependent our cells are on a continuous supply of energy from food. When that supply is disrupted, even briefly, it can trigger intense hunger signals as the body tries to restore its energy balance. This mechanism helps explain why people with insulin resistance experience such strong and urgent hunger pangs.

Evidence, Consequences, and Solutions

Shanahan claims that the proof of cholesterol's dangers is weak. Cholesterol is an essential nutrient needed by all the cells in your body to perform basic functions. It's a glossy, fat-like substance. On a molecular scale, its shape is flat and bulky, and its distinctive charge and form allow it to maintain the flexibility of cell membranes—keeping them from becoming solid. The body works hard to produce cholesterol due to its crucial role. Cells are capable of producing it when necessary. We can also obtain cholesterol from our diet, especially through foods such as liver, eggs, butter, and shellfish.

(Shortform note: The European Atherosclerosis Society Consensus Panel disagrees with Shanahan, stating that the evidence for cholesterol’s dangers is strong. In a 2017 paper, the authors argue that the evidence from genetic studies, epidemiological research, and clinical trials consistently shows a causal, dose-dependent relationship between LDL cholesterol levels and the risk of atherosclerotic cardiovascular disease. They emphasize that the totality of this evidence supports the conclusion that LDL cholesterol is a principal cause of atherosclerotic cardiovascular disease. The authors also highlight that lowering LDL cholesterol levels through lifestyle changes and medication can significantly reduce the risk of cardiovascular events.)

The majority of the cholesterol in our blood is produced by our intestinal cells and liver. They require cholesterol to form small lipoproteins, which are vessels that deliver fat into the bloodstream. These lipoproteins carry cholesterol, which doctors assess in blood tests. They act as miniature transporters, carrying fat and fat-soluble vitamins through your arteries, stopping at cells that need the nutrients they're delivering—including cholesterol.

(Shortform note: The term “lipoprotein” refers to a microscopic structure made up of both lipids (fats) and proteins. Lipoproteins are roughly spherical, with a core of cholesterol and triglycerides (a type of fat) surrounded by a shell of phospholipids and proteins. This structure allows them to transport fat molecules through the watery environment of the bloodstream.)

Large epidemiological studies and meta-analyses have conclusively confirmed the lack of correlation between cholesterol you ingest from foods (typically meat and dairy) and cholesterol circulating in your bloodstream. There's so much evidence that the government body responsible for creating the US Dietary Guidelines updated its 2015 report to note that "there is no need to worry about overconsuming cholesterol." Despite this, typical nutritional guidance continues to caution against eating most cholesterol-rich foods. Typical nutritional guidance continues to claim that elevated blood cholesterol leads to artery blockage and cardiac events, and the association between dietary and blood cholesterol is confusing even for experts.

(Shortform note: In an academic paper, nutrition researchers explain that the cholesterol you ingest from foods has little impact on cholesterol circulating in your bloodstream because your body compensates for changes in dietary cholesterol by adjusting how much cholesterol it produces. In other words, when you eat more cholesterol, your body produces less, and vice versa. This means that the amount of cholesterol in your bloodstream only changes slightly. The researchers cite a study in which participants ate 1,000 milligrams of cholesterol per day for 12 weeks. The participants' cholesterol levels only increased by 12%. This is a relatively small increase, especially considering that the participants were consuming a large amount of cholesterol.)

The terms “good cholesterol” and “bad cholesterol” refer to two subtypes of lipoproteins, those tiny amphibious vehicles that carry fats throughout our circulatory system. LDL, or low-density lipoproteins, are known as the "bad" cholesterol. A second type, known as HDL (high-density lipoprotein), is considered "good" cholesterol. These labels are imprecise, as a single cholesterol molecule is present in all lipoproteins. A 2009 study across multiple centers involved 136,905 heart attack patients and showed that just 25 percent had "bad" cholesterol levels—LDL—at or above 130 mg/dL when admitted to the hospital. A little more—35 percent—said they'd been informed that they’d experienced high cholesterol at one time or another in the past. In simple terms, those with normal or low cholesterol were much likelier to have heart attacks compared to those whose cholesterol was high.

Registry Studies Can’t Prove Causation

The paper Catherine Shanahan cites here is a registry study, which means it simply describes the range of LDL values among people who already had heart attacks. It doesn’t compare the risk of future events between people who had heart attacks and those who didn’t. The study’s authors themselves note that the findings don’t mean that people with normal or low cholesterol are more likely to have heart attacks than those with high cholesterol. They simply show that many people who have heart attacks don’t have high cholesterol. This is an important distinction because it means that the study can’t be used to support the claim that lower cholesterol is more hazardous than higher cholesterol. The study’s authors also note that the findings don’t mean that cholesterol-lowering medications are ineffective. They simply show that many people who have heart attacks are already taking these medications. This is an important distinction because it means that the study can’t be used to support the claim that cholesterol-lowering medications are ineffective.

Shanahan argues that we suffer healthwise because of a lack of protein. Protein is vital for all the cells in our body. It helps the mitochondria create enzymes that counteract oxidative stress. One-third of those over fifty and half of those with diabetes aren't consuming enough protein. Lack of protein is more prevalent than people think because doctors lack training in diagnosing it. The USDA's Dietary Reference Intake is 40–50 percent too low. In the 1940s, the government set the Recommended Daily Allowance (RDA) guidelines, which was before we had the understanding of protein metabolism that we do today.

(Shortform note: A 2013 study by the PROT-AGE Study Group, an international panel of nutrition experts, found that the current protein guidelines are too low for older adults. The study reviewed data from nitrogen-balance studies and functional outcomes, concluding that healthy older adults should consume an average daily intake of at least 1.0 to 1.2 g protein per kilogram of body weight, and up to 1.2–1.5 g/kg/day if they have acute or chronic illness, in order to maintain and regain lean body mass and function. This is significantly higher than the current RDA of 0.8 g/kg/day. The authors argue that the current guidelines are based on outdated nitrogen-balance studies that don’t accurately reflect the protein needs of older adults.)

The previous methods for setting the guidelines drastically undercounted our protein requirements. Government guidelines remain unupdated based on new calculations. The daily minimum needed by the majority of individuals is between 60 and 100 g. In the 105 countries studied, men with less protein intake tend to be shorter. Insufficient protein consumption plays a role in the onset of type 2 diabetes and in mortality for individuals with diabetes, particularly for those over age 60. It's assumed that we consume excess protein and that reducing our intake is safe. However, a significant number of people don't consume sufficient protein, particularly those who are thin (including slim kids and pregnant women), health-conscious, aiming for weight loss, or over 50. This negatively affects their health.

(Shortform note: While the author’s argument that we’re underconsuming protein is compelling, it’s important to note that there are exceptions to the rule. For example, people with chronic kidney disease (CKD) are often advised to limit their protein intake to prevent further kidney damage. The National Kidney Foundation recommends that adults with CKD stages 3-5 (not on dialysis) consume 0.55-0.60 grams of protein per kilogram of ideal body weight per day. This is significantly lower than the 60-100 grams per day recommended by the author.)

Shanahan also argues that the industrialization of agriculture harms ecosystems. Regardless of producing animals or plants, it harms the ground. Our well-being is tied to soil health, and our reliance on industrial agriculture is damaging the systems that sustain life. However, agricultural methods that enrich the soil with carbon can increase the soil's fertility and make the ecosystem more diverse, while enhancing the well-being and health of animals.

(Shortform note: Enriching the soil with carbon increases the soil’s ability to absorb and store rainfall, which helps plants grow. This, in turn, gives animals more food and shelter. This makes the ecosystem more diverse and helps animals stay healthy.)

Next, we'll discuss how reducing cholesterol levels by using vegetable oils can increase mortality and cancer risk, and how you can use dietary strategies to reverse dark calorie damage.

The Mechanisms and Proof of Dark Calorie Harm

Shanahan argues that using oils made from vegetables to reduce cholesterol can increase mortality and cancer risk. A 1960s study found that consuming seed oils increased mortality risk by 22% for every 30-point drop in total cholesterol. The study also found that those who consumed margarine and fats from animals had total cholesterol that was 13% higher than individuals whose diets were high in PUFAs, but they had 60% fewer heart attacks and fewer overall deaths. The research was hidden away for decades.

(Shortform note: The study Shanahan refers to is the Minnesota Coronary Experiment, a randomized controlled trial conducted in the late 1960s. The study was designed to test the effects of replacing saturated fats with polyunsaturated fats (PUFAs) on cardiovascular health. The study involved over 9,000 participants from state mental hospitals in Minnesota. The original investigators published limited findings, but the full data remained unpublished for decades. The comprehensive results were only brought to light when researchers revisited the original records and analyzed the data, revealing the unexpected findings.)

In 2016, a group of researchers published the findings, but the medical community showed little response. Additionally, a 2012 article presented the outcomes of three extensive trials in which participants were administered either statins—drugs that reduce cholesterol—or placebos. The trials consistently demonstrated that individuals taking statin medications had cancer development rates 20% to 25% higher compared to those on a placebo. The authors noted that several papers linked low cholesterol with colon, lung, and prostate cancer, as well as with cancer-related mortality. A 2007 BMJ article found a significantly increased likelihood of a new cancer diagnosis in those with the lowest LDL levels. Research from Japan in 2011 discovered a connection between having low cholesterol and dying from cardiovascular events and cancer.

Counterargument: Statins and Low LDL Cholesterol Do Not Increase Cancer and Mortality Risk

The Cholesterol Treatment Trialists’ (CTT) Collaboration, a group of researchers who analyze data from large clinical trials on cholesterol-lowering treatments, disputes the claim that statins and low LDL cholesterol increase cancer and mortality risk. They argue that statin therapy, which significantly lowers LDL cholesterol, does not increase the incidence of cancer or deaths from cancer or other non-vascular causes. Their conclusions are based on a comprehensive analysis of data from over 170,000 participants in 26 randomized trials, which showed no significant increase in cancer incidence or non-vascular mortality among those taking statins, even in individuals with low baseline LDL cholesterol levels or older age groups. The CTT Collaboration emphasizes that the benefits of statin therapy in reducing cardiovascular events outweigh any potential risks, and they recommend statin use for individuals at risk of cardiovascular disease.

Next, we’ll discuss the historical and institutional promotion of unhealthy calories.

Historical and Institutional Promotion of Dark Calories

Shanahan argues that historically, the AHA has advocated for vegetable-based oils over saturated fats. The American Heart Association was founded with a large donation from the makers of vegetable oil, which it used to promote Ancel Keys's cholesterol theory and persuade the public to consume vegetable oils. The AHA still gets funding from companies that sell seed oils, and its practice guidelines continue to back that industry.

(Shortform note: The AHA was founded in 1924 as a small professional society, but by the 1960s, it had become a nationwide public charity. The AHA’s survival depended on its ability to raise funds. In 1961, the AHA launched its first national fundraising campaign, which included a direct mail campaign and a telethon. The campaign was a success, raising over $1 million. The AHA continued to grow in the following decades, and by the 1980s, it was raising over $100 million per year.)

The AHA's current leading corporate donors include Conagra, Monsanto, and LibertyLink, as well as companies like Kellogg’s, Quaker, Tyson, FritoLay, Campbell, and Subway. The AHA employs these funds to assist researchers who want to study how vegetable oils can be beneficial, the detrimental effects of cholesterol, and new applications for medications that reduce cholesterol. The money is also used for lobbyists who shape public health policy on both state and national scales.

(Shortform note: Public-health historians note that the AHA’s reliance on corporate funding began in the 1970s, when the organization sought to expand its educational and outreach efforts. To fund these initiatives, the AHA began to accept sponsorships from food and agricultural companies, which provided significant financial support. This relationship deepened in the 1990s with the introduction of the Heart-Check mark, a paid endorsement program that allowed companies to display the AHA’s logo on their products.)

The AHA publishes or co-publishes 14 medical journals on various subjects related to cardiovascular disease treatment, research, and practice standards. They publish numerous pieces annually. This helps the group prominently feature their message against cholesterol. Since 1949, the AHA has given $5 billion in research donations, granting it considerable sway in the areas of health and nutrition studies. It has the authority to choose which subjects will be researched and what studies appear in its publications. The AHA is now the entity that other groups look to for nutritional guidance due to its long-standing presence, broad impact, and comprehensive publishing efforts. This includes other nonprofits, like the American Diabetes Association and the American Cancer Society, and medical bodies like the American Medical Association and the American College of Physicians.

The Food Industry’s Influence on Nutrition Policy

Catherine Shanahan isn’t the first to examine how organizations like the AHA shape nutrition research and messaging. In her 2002 book Food Politics, Marion Nestle explores how the food industry influences nutrition science and policy. She argues that when health organizations become entangled with food industry funding, even seemingly scientific tasks like writing dietary guidelines can turn into political battles. Nestle details how the process of creating the 1995 US Dietary Guidelines became a battleground for food industry lobbyists. She describes how the meat and dairy industries fought to prevent the guidelines from recommending reduced consumption of their products. Nestle’s work shows that when health organizations rely on industry funding, it can compromise their ability to provide unbiased nutrition advice.

Dietary Strategies for Reversing Damage From Dark Calories

To reverse dark calorie damage, Shanahan suggests avoiding oils from vegetables and refined carbohydrates. She argues that vegetable oils are the most harmful substances for mitochondria in the food supply, and that steering clear of them is the most effective way to protect these cellular powerhouses. Due to their chemistry, vegetable oils are more harmful than animal fats and other oils. For example, consuming a common five-ounce portion of restaurant fries (usually cooked in vegetable oils) is as toxic as smoking twenty to twenty-five cigarettes.

(Shortform note: The US Department of Agriculture and the Department of Health and Human Services recommend that Americans limit their saturated fat intake to less than 10% of their daily calories. They suggest replacing saturated fats with polyunsaturated and monounsaturated fats, which are found in plant oils. This recommendation is based on evidence that saturated fats can raise LDL cholesterol levels, which is a risk factor for heart disease. The guidelines also recommend choosing lean meats and low-fat dairy products to help reduce saturated fat intake.)

Cooking oils derived from vegetables are found in all types of foods that are fried in deep or shallow pans, or in batter. They are used in sauces, condiments for salads, and baked items, as well. Restaurants often use them because they are less expensive than olive oil, butter, and other traditional fats and oils, and they're easy to use. Deep-frying is an easy process that can be applied to many menu items. Deep-fryer oil is reheated repeatedly and used for several days. American regulations mandate fryer oil changes every week, though enforcement is challenging.

How to Know When to Discard Frying Oil

If you operate a restaurant, consider adopting a policy that requires cooking oils derived from vegetables to be replaced when they show signs of degradation, rather than keeping them reheated and reused for several days. In Frying: Improving Quality, J. B. Rossell recommends that restaurants monitor the quality of their frying oils by regularly testing for degradation indicators such as total polar materials (TPM), which increase as the oil breaks down. He explains that oils should be discarded when these values approach the legal or technological limits (typically around 24–27% TPM), even if the oil still appears usable in normal kitchen operations.

Shanahan also recommends considering a traditional diet. This approach relies on the dietary traditions and methods that helped people prosper worldwide. It claims that people have adapted to specific eating patterns and would be healthier by adopting similar habits.

(Shortform note: There are some exceptions to the idea that people would be healthier by adopting the dietary traditions and methods of a traditional diet. For example, epidemiologists have found that people who eat a lot of salted fish and pickled vegetables are at a higher risk of stomach cancer.)