What’s the Fuss about Seed Oils

As public concern rises over mounting health problems in younger and younger people, associated with the unrelenting obesity and diabetes epidemics, the spotlight of attention has turned to the components of the ultra-processed foods that line the shelves of our grocery stores. The foods have the benefit of being cheap (relatively speaking) and convenient, with remarkably long shelf lives. At first suspicions, were confined to the nature of the grains and the amount of sugar, especially in the form of high-fructose corn syrup in so many products. Could we blame them for weight gain and insulin resistance, especially since carbohydrates had become the base of the FDA recommended dietary pyramid in the 1970s, a change made to reduce saturated fat intake because of concerns about its relationship to heart disease? But since the early 2000s, food research has uncovered trouble with the other major component of so many packaged and processed foods – the vegetable oils that hold them together, and, more specifically, the category of vegetable oils derived from plant seeds.

By now, the average American diet includes 5-10 tablespoons of vegetable oil a day. While we need certain fats and fatty acids and a proper in the diet, with a proper balance between different types such as omega 3 and omega 6 fatty acids, their consumption in the form of vegetable oils is very different from their consumption in the form of whole foods. Prior to the development of vegetable oils in the early 20^th C, the dietary requirements for essential fats were easily met by the consumption of nuts, seeds, and animal products like lard, butter and tallow – the only fats available for eating and cooking. As whole foods though, 5-10 tablespoons of corn oil would require eating 98 ears of corn. The same amount of sunflower oil would take 2800 sunflower seeds.

Seed oils are particularly rich in one fat called linoleic acid which is now known to cause weight gain, and a host of metabolic abnormalities including insulin resistance and oxidation of LDL-cholesterol, the so called “bad” cholesterol associated with heart disease. Oxidation is a chemical process that adds oxygen easily to unstable molecules and interferes with their function. It is thought to be related to many inflammatory processes associated with illness. There is also recent research suggesting that in order to participate in the development of plaques in arteries, LDL-cholesterol must be in an oxidized state.

Given the concentration of oils such as linoleic acid, as well as a host of other fatty acid and breakdown products in vegetable oils, it is conceivable that they do contribute to health problems like obesity and diabetes. Moreover, the chemical process used to make the vegetable oils into the solid oils that resist spoilage, increase shelf life and give foods nice textures, the process that introduced these oils into the human diet, was shown by the 1990s to increase rather than decrease heart disease, prompting legislation to cut the use of these substances in foods and sending food scientists back to the lab to find adequate substitutes. Combined with other observations suggesting that the massive change in dietary fats over the last 100 years also also contributed to cancer, gall stones and mood disorders it is reasonable to ask how such a striking change in diet came about and what to do about it now.

Two major events created and expanded the vegetable oil industry. The first was the industrial revolution that demanded lubricating oil. Just as the whaling industry was collapsing at the end of the 19^th C , machines made oil extraction from seeds efficient, and cottonseeds were plentiful. The second was the dietary advice given by the medical profession in the mid 1900s to avoid saturated fats and to replace them with the polyunsaturated fats in vegetable oils in an effort to curb the rising number of heart attacks. This advice came after the dietary cholesterol heart hypothesis won out over a sugar/insulin hypothesis as the cause of heart disease, and after polyunsaturated oils were shown to lower total cholesterol levels in studies that compared them to dietary saturated fat. In terms of safety ratings, vegetable oils were grandfathered in under the GRAS (generally recognized as safe) category in food safety rules introduced in 1958, because by then they had been in use for half a century. They clearly were not toxic in the short term, but safety is measured over time in real world use.

By the 1990s, when the vegetable comprised 9-10% of American caloric intake, the nature of the “trans fats” produced by hydrogenation of vegetable oils emerged. Instead of cutting heart disease, they had increased it. Subsequent work in the 2000s showed that large numbers of poorly characterized and studied fats are produced by the hydrogenation process, with some contributing to insulin resistance and weight gain, prompting warning labels and sending food scientists back to the lab to find other methods of reducing oxidation of seed oils and make them structurally suitable for baked goods. The methods include genetic modification of seed crops (currently 90% of soybean crops are sown with GMO seeds), chemical processes known as interesterification, and attempts to make oils by fermentation of sugar cane or algae. The expense involved may erase any economic reasons for replacing animal fats, and the efforts are taking place on a background of serious questioning of the dietary heart hypothesis that prompted the shift away from saturated fats in the first place.

So what should you do in his unsettled time when much of what we thought was settled science is in question, and when you want to do the best you can for your own health? First, recognize that there is truth in the statement that you are what you eat. Autopsy studies have shown that the laboratory made fats are found in cell membranes, which are the guardians of cell function. In addition, the chemical makeup of LDL cholesterol reflects the amount of vegetable oil in the diet and may be a crucial factor in the development of arterial plaques

Second, read labels and avoid products with hydrogenated or partially hydrogenated oils, as well as poorly defined oils. Know the names of the most common seed derived oils: soybean, corn, sunflower, safflower, grapeseed, peanut, cottonseed, rice bran, and canola (Canadian oil low acid, from the rapeseed). Olive oil and avocado oils are derived from plant fruits and are better choices. They contain mainly mono-unsaturated fats which are less prone to oxidation. In addition, they have higher heat points and therefore produce fewer toxic byproducts such as aldehydes in the cooking process. Coconut oil and palm oil, also made from the pulp of the plants, are saturated fats. They have made a comeback from the days when they too were considered risky for heart disease despite thousands of years of consumption by populations who did not develop the problem.

Third, be aware that the introduction of seed oils into the human diet parallels the rise in heart attacks that prompted the dietary attempts to cure the disease in the mid 20^thC, which in turn accelerated vegetable oil consumption. And significant declines in saturated fat consumption did not solve heart disease. There are, to be sure, other factors such as smoking involved, and many possible reasons for the health dilemmas facing us now, two decades into the 21^st C. But it is possible that the vegetable oils and more specifically the poly unsaturated seed oils that are modified in laboratory processes are a significant part of the problem. So it seems reasonable to try to understand them, to return to whole food sources of essential fats, and to keep consumption of these oils and the processed foods that rely on them as low as possible.

Posted by medical plaintalk

Physician turned medical writer.

Cholesterol Phobia

Cholesterol research is difficult, esoteric and accessible in journals that seldom make it beyond their target audience – other people doing the same type of work. One theory about the relationship of cholesterol and heart disease has dominated medical practice for over half a century, but there has always been dissension in the ranks of scientists, some of whom labor away in obscurity, slowly building a case that may one day topple the current dogma. I have attempted to make this subject accessible to a non-medical audience because the current paradigms for thinking about heart disease and treating it affect everyone who sees a doctor, listens to the news or reads the popular press – even children, because they eat what their parents believe is healthy for them.
Cholesterol phobia: is the end in sight?

Cholesterol earned a villain’s reputation because it got caught at many criminal scenes where victims succumbed to heart attacks. It was found lurking in the walls of arteries too narrowed by “plaques” to allow blood passage. Even in young healthy men, cholesterol- laden “fatty streaks” were surprise findings at autopsy after accidental or war-related death. Experimentally, fat choked arteries were easy to produce in experimental animals by feeding them food pellets saturated with fat – even olive oil worked. The laboratory work bolstered attempts to show that different populations consuming different amounts of fat had different rates of heart disease. Though both the laboratory and epidemiology studies were fraught with contradictory results, and the dietary cholesterol theory of heart disease was initially rejected by the American Heart Association, the personalities and scientific politics involved eventually catapulted the theory into the lives of all Americans, over 20 million of whom are now on potent drugs to combat the evil substance.

The dietary theory of heart disease

After more than half a century of war on cholesterol, the dietary theory remains just that – a theory – no matter how many commercials remind you that you need to lower your cholesterol. You may be surprised to hear that cholesterol could be absolved of its villainous status, within your lifetime. But don’t expect your doctor to agree, at least not yet. The cholesterol theory has a grip on our culture that is almost religious. The current dogma, advertised everywhere, is simple: there is good cholesterol, labeled HDL, and bad cholesterol, labeled LDL and anyone who cares a whit about his health will do whatever it takes to get those numbers in line with the current recommendations of the American Heart Association –eat a low fat diet, exercise, and take the right drugs.

Inconvenient facts

Inconvenient facts have always dogged the theory. Cholesterol levels plummet in seizure patients treated with high fat, no carbohydrate diets. Heart attacks occur despite normal cholesterol levels. Low fat diets raise cholesterol levels -President Eisenhower was one of the most famous examples. And buried in the literature of the last half century are many clues pointing a blaming finger away from cholesterol and toward the complex lipoproteins that ferry it around the body. As more and more questions are raised about the efficacy and dangers of drugs that reduce cholesterol, more attention may turn to these lipoproteins. After all, like cholesterol, they have been part of the statistic most closely associated with heart disease – the LDL (low-density lipoprotein) cholesterol.

What are lipoproteins?

Total cholesterol measures cholesterol attached to lipoproteins. Lipoproteins are combinations of phospholipids (fats that dissolve in water) and specialized proteins that fit like keys into receptors on cells. Lipoproteins function like cargo ships, carrying fats to cells for fuel, to fat tissue for storage, and back to the liver for reprocessing when demanded. More or less cholesterol crowds aboard each boat depending on the number of boats available. The size of the fleet, in turn, depends on the amount of triglycerides (another type of fat), awaiting shipment – not on the amount of cholesterol.

Triglycerides rule

Triglycerides and cholesterol are very different fats. Triglycerides provide the fatty acids that fuel most cells and are stored in fat tissue for later energy demands. Cholesterol yields no energy at all. It is a building block, used in the construction of all cell membranes and in the making of hormones and bile. Not all cholesterol comes from fat in the diet. The brain makes its own, and the liver and skin make whatever the body needs – raising production whenever dietary intake is low. Cholesterol and triglycerides attached to lipoproteins are like citizens of two different countries travelling together on one of the country’s boats. That country that builds the boats belongs to the triglycerides. The more triglycerides present in the body, the more lipoproteins in the fleet.

The varying density of lipoproteins

Lipoproteins fully loaded with cholesterol and triglycerides are fluffy and buoyant (fat floats) and called very low density lipoproteins, VLDL for short. They dock at cells in need of fuel or cholesterol, unload some cargo, lose some buoyancy, and become a little denser. Eventually they become low-density lipoproteins (LDL) and , with no energy or building material left to give up, they return to the liver for recycling. Another particle type called high-density lipoprotein (HDL) is even less buoyant – and less well understood. In contrast to cholesterol bound to LDL and VLDL, the cholesterol carried by HDL particles, like the cholesterol carried away from the intestines by chylomicrons (very large lipoproteins) does not contribute to the storage of fat in any tissues so is not associated with plaque formation in arteries. Normal to high levels of HDL cholesterol are associated with lower risk of heart disease.

What do the anti-cholesterol drugs do?

The widely prescribed statin drugs block the body’s ability to make cholesterol, which makes less cholesterol available to be loaded on to the lipoprotein boats. But boat making proceeds apace because it is driven by the amount of triglyceride awaiting transport- and the triglycerides, remember, come from dietary carbohydrates. Lowering cholesterol manufacture does not lower lipoprotein production – the lipoprotein boats will simply carry less cholesterol per lipoprotein particle, making each particle smaller and denser. Will this magically keep cholesterol out of artery walls? Not a good bet. Lipoprotein research labs have identified seven different particle types within the LDL fraction of total cholesterol. Heart risk appears to be correlated with the smallest and densest sub-fraction – the kind carrying the least amount of fat per molecule. (The anti-cholesterol drugs do have an independent anti-inflammatory effect which may be the way they diminish risk of a cardiac event in people with heart disease.)

Take-away message

So how does this complicated information change your life? Triglycerides, the stimulus for VLDL and LDL production, are a product of carbohydrate processing – especially of sugars and refined grains. Lowering VLDL production and hence LDL production requires lowering dietary carbohydrates – not fat, not cholesterol. Blood cholesterol isn’t even a good marker for total body cholesterol, which includes cholesterol squirreled away in artery walls. Cholesterol in arteries behaves much like cholesterol stored in fat tissue. It is responsive to the entire array of interconnected feedback loops involving not only fats, but carbohydrates and insulin and all the other hormones. It is time to respect its complexity and quit expecting that coaxing the body to make less cholesterol by taking drugs to block its production, or by eliminating it from the diet will end the scourge of heart disease.

Posted by medical plaintalk

Physician turned medical writer.

The Sweet Tooth: Pathway to a Broken Heart?

For the last half a century or more we have believed the dietary cholesterol theory about heart disease, a hypothesis (idea to be tested by experiment) that found favor with researchers, grant makers, doctors and drug makers. What if this theory is wrong? What if cholesterol in artery walls has less to do with dietary fat than with the way the body processes carbohydrates? What if refined sugars and grains are the dietary culprits? Could insulin, the master hormone at the center of all energy processing, be a better marker than cholesterol for heart disease?

What is blood sugar?

The first thing to understand about sugar is that the blood sugar is not the same thing as the sugar in your pantry. Or the sugar in soft drinks or the sugar in fresh fruit. Blood sugar is a simple molecule called glucose – a product of plants’ ability to convert the energy of the sun into starches, long chains of glucose linked together. When you eat a starch, the digestion process breaks down the chains into simple glucose molecules which circulate in your blood. Glucose is used by every cell in the body for energy, and is also made into glycogen for storage in liver and muscle.The sugar in your pantry is sucrose extracted from plants, specifically cane grasses and beets, by a refining process that concentrates and crystallizes it. Each sucrose molecule is a combination of one glucose molecule with another of fructose, a chemically different plant sugar molecule.

The taste for sweetness is innate and possibly addictive. Before the advent of refined sugar, indulging the sweet tooth was difficult. The only edible sources were berries and fruits and small amounts of honey guarded by nasty bees – all confined by climate and geography. Sugar made its way into the human diet slowly, spreading from the East to the West as the secret of this “liquid gold” made its way along routes of commerce.

Sugar and the diseases of civilization

With time and commerce, consumption of sugar and refined grains skyrocketed. The diseases of civilization – diabetes, heart disease and obesity – followed refined sugar, flour and rice around the world, appearing wherever old dietary staples were replaced by these “white” foods. By the 1920s, the Americans averaged 110-120 pounds of sugar per person per year. We inched up to 124 pounds by the late 1970s. Then came the Japanese chemical innovation that made high-fructose corn syrup (HFCS) a dietary staple. By 2000, HFCS bumped sugar consumption up to 150 lbs. per year, largely in the form of sweetened drinks.

High fructose corn syrup

HFCS differs from sucrose because the ratio of fructose to glucose in corn syrup is 10% higher than in table sugar – 55:45 instead of 50:50. Some scientists believe that it is the remarkable increase in fructose consumption in modern times that correlates with the appearance of the metabolic syndrome – abdominal obesity, high fasting blood sugar, high triglycerides, abnormal lipoprotein levels and high blood pressure. If so, a 10% increase in fructose combined with a recent, large jump in overall sugar consumption may spell real trouble.
How can fructose cause trouble? Isn’t it the primary sugar of fruits? Yes, but eating an apple with a small amount of fructose combined with absorption-slowing fiber hardly nudges blood sugar up – a far cry from the blood sugar spike after 20 ounces of an HFCS sweetened beverage. Drink a coke, and about 60% of the glucose in the HFCS goes directly into the blood for immediate use, and 40 % into the liver for storage as glycogen. The fructose all goes to the liver for conversion into fat – released into the blood as triglycerides. The higher the fructose in the diet, the higher the triglycerides in the blood. Fructose is a “lipogenic” or fat-producing sugar, and long term consumption also raises LDL or bad cholesterol.

The problems with too much sugar

Once sugar consumption exceeds the small amounts nature provides without refining techniques, trouble begins. The different ways the body processes fructose and glucose combine to produce very efficient fat production. A rise in blood glucose prompts the pancreas to put out insulin to help ferry glucose into cells for energy use or storage. Insulin, like fructose, is “lipogenic” because it helps move fats into storage depots in three areas – the liver, fat tissue, and the walls of arteries. And as triglycerides are formed from fructose, insulin busies itself shuttling them around the liver and out into the blood. The pancreas then produces even more insulin to take care of the glucose – this is the phenomenon known as insulin resistance, part of the metabolic syndrome associated with heart disease.

Is it the cholesterol or the sugar?

The theory that cholesterol in dietary fat is the direct cause of cholesterol deposits in arteries requires a leap over the metabolic pathways that process simple sugars and are intimately involved in fat formation and storage – and over the fact that many people with low cholesterol levels have heart disease. Over the last half century, many researchers and doctors made the leap because they believed the theory. Just as important to widespread acceptance, though, were less scientific influences like the cheap availability of a test for blood cholesterol, the difficulty and expense of measuring insulin, and the dominance of researchers devoted to the dietary cholesterol theory over those who questioned it.

Medical history books contain an embarrassing array of once-unassailable theories and practices that have fallen by the wayside. Despite a modern sense of scientific invincibility, current medical ideas are not immune from error. Sugar and refined carbohydrates are not yet the poster children for the scourge of heart disease, but they may be a far better target than cholesterol. If the dietary fat theory gives way to the sugar theory, the massive push to lower cholesterol by diet and drugs may go into the books as one of those once-unassailable ideas that eventually fell.

Posted by medical plaintalk

Physician turned medical writer.

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