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THE CURSE OF COTTONSEAD

The risk of [cottonseed] toxicity has aroused worldwide attention due to the consumption of agricultural by-products such as cottonseed oil, milk, and meat from the affected animals.¹ Poducts derived from cottonseed (oil, cellu­lose, flour and meal), and meat and milk from farm animals fed cottonseed, have served as food since the 1800s. However, the seeds of the cotton plant² are very toxic. They can produce acute poisoning, as well as cumulative effects over weeks or years of eating very small amounts. Cottonseeds are so toxic that nineteenth-century laws prohibited dumping them near rivers. Yet by the 1860s, cottonseed oil was commonly mixed into lard or olive oil and eaten by both humans and animals,³ and by the early 1900s, both people and animals were consuming straight cottonseed oil.

Cottonseed poisoning produces a wide-ranging list of symptoms in humans and animals, including fatty liver, arterial plaques, anemia, labored breathing (from pulmonary edema), depression, anxiety, kidney disease, poor vision and infertil­ity.⁴ Given this lengthy list, it is somewhat ironic that a famous 1977 commercial for Chiffon margarine, made from 100 percent cottonseed oil, scolded, “It’s not nice to fool Mother Nature!” It is consumers who are fooled, because few have made the connection between cottonseed consumption and the ensuing symptoms of cottonseed toxicity; instead, “experts” have blamed the symptoms on bacteria, genes, stress or overconsumption of red meat and saturated fat—anything but the true culprit. As a result, most people and farmers don’t realize that they should be making a concerted effort to avoid cottonseed in human and animal food.

In this article, I will describe the main poisons in cottonseed and their effects, discuss cottonseed poisoning in farm animals and re­view the association between human exposure to cottonseed poisons and infertility, atheroscle­rosis, dementia and violence. I will also discuss a profitable alternative product for cotton farmers.

COTTONSEED POISONS AND SOME OF THEIR EFFECTS

The major poison in cottonseeds is gos­sypol, a yellow polyphenol pigment that serves as the cotton plant’s natural pesticide. In a 2020 paper, Chinese researchers acknowledged that “[e]xcessive intake of gossypol induces severe pathological signs of toxicity in livestock and wildlife.”¹ The same group of researchers also discussed gossypol toxicity in humans via the food chain and has sounded the alarm about potential adverse impacts on fetal neurodevel­opment.⁵

In humans and animals, gossypol binds to lysine, and this is a serious problem. As I wrote in my article titled “Why We Need a High- Lysine Diet” (Wise Traditions, Summer 2023),⁶ lysine activates so many enzymes, hormones and other proteins that researchers titled a 2015 study, “Why Always Lysine?”⁷ Describing ly­sine as “one of the most modified amino acids,” those researchers argued that lysine is probably the “major means” by which signaling pathways modify protein molecules.⁷

Lysine is critical for cardiac muscle strength and energy; strong arterial walls; a healthy liver; healthy cholesterol; absorption of calcium, iron and zinc; production of hormones (including sex hormones, insulin, thyroid, cortisol, blood pressure hormones and IGF-1); collagen; anti­oxidants; and much more. Lysine is also anti-inflammatory and is important for pain relief, autophagy, anti-aging and cancer prevention. Importantly, lysine limits problems associated with the amino acid arginine,⁶ including ex­cessive inflammatory nitric oxide, which is a driving force of cell death.8 Thus, by binding to lysine, gossypol causes far-reaching destruction.

Gossypol also causes harm by binding to the essential amino acids threonine (needed for collagen production) and methionine (which plays many roles in metabolism and oxidative stress). In addition, it binds to vitamins A and D, several minerals (iron, calcium and zinc) and the circulating protein albumin.

One major example of the damage caused by gossypol involves its interference with red blood cells and oxygen-carrying hemoglobin. When gossypol binds to lysine and iron in hemo­globin, breaking apart the red blood cells, this releases the iron. The iron is oxidized to ferric iron, which forms hydroxyl radicals—the most dangerous type of free radical. Additionally, the freed-up iron feeds pathogens. Bilirubin, an end product of red blood cell and hemoglobin breakdown, can lead to jaundice if it accumu­lates in excess.

As gossypol binds to lysine and iron in the hemoglobin and breaks apart the red blood cells, depleting oxygen, it sets into motion a cascade of effects that can lead to non-cardiogenic pul­monary edema (build-up of fluid in the lungs). The immune response is to make more blood via bradykinin (a mediator of inflammation). Ordi­narily, angiotensin-converting enzymes (ACE and ACE2) control how much blood is made by breaking down bradykinin, but gossypol blocks ACE. As a result, bradykinin makes too much blood, which leaks from the capillaries into the alveolar spaces of the lungs, causing a dry cough with no mucus to cough up—a condition often blamed on smoking. This form of pulmonary edema is distinct from both cardiac pulmonary edema and bacterial pneumonia.

Gossypol also interferes with a wide range of other enzymes, including lactate dehydro­genase enzymes, which supply energy during hypoxia (low oxygen levels in the tissues); alde­hyde dehydrogenase enzymes, which detoxify alcohol and formaldehyde; HMGCR enzymes, which break down cholesterol; and enzymes (sialyltransferase and 5-alpha reductase [5AR]) and luteinizing hormone, which are important for fertility. Additionally, gossypol disturbs the thyroid, sex hormones, infection-fighting lymphocytes, GLUT1 (a glucose transporter that recycles vitamin C), potassium balance and the important antioxidant glutathione. It also causes mitochondrial dysfunction!

Another example of gossypol-linked harms is related to a sialic acid called Neu5Gc, ordinar­ily not found in humans. If humans end up with free Neu5Gc in their body, it causes problems. In animals, in normal circumstances, sialic acids (which are acidic monosaccharides) are incorporated into proteins in the animal’s flesh via the sialyltransferase enzyme; for this reason, even though meat contains Neu5Gc, it is not a problem. Recently, free Neu5Gc has been linked to and used as an argument against meat-eating, but it appears that the real culprit is consumption of meat from animals fed cottonseed; people who eat meat from cottonseed-fed animals are likely ingesting free Neu5Gc that has not been safely incorporated into proteins, because gos­sypol has blocked the animal’s sialyltransferase.⁹

In addition to gossypol, cottonseed contains another major poison: foul-smelling fats called cyclopropene fatty acids. The only other food source of these fats are the pits of lychee fruit. Cyclopropene fats block three critical fat- and cholesterol-metabolizing enzymes: stearoyl- CoA desaturase (SCD), lecithin-cholesterol acyltransferase (LCAT) and delta-6 desaturase (D6D). Cyclopropene fats also break down apolipoprotein A1 and A2, which are needed for HDL cholesterol. All of this causes high LDL and VLDL—but low HDL—cholesterol, the type of lipoprotein that clears cholesterol out of the cells. Cholesterol then accumulates through­out the body in red blood cells, bone marrow, the cornea, the spleen (enlarging it) and the liver, causing liver damage and inflammation. Liver problems, low oxygen, pulmonary edema and infections are all signs of cottonseed poisoning in animals. I will return to the problems associ­ated with cyclopropene fats when I discuss heart disease and dementia. Notably, cottonseed also contains a high level of the unstable omega-6 fatty acid, linoleic acid, which forms the free radicals found in nearly all diseases and blocks ketosis, critical for a healthy heart.

In addition to the poisons already discussed, there are chemical solvents in cottonseed oil. The oil was formerly extracted using a chlo­rinated compound (trichloroethylene), found to cause heart defects. Now, it is extracted and bleached by hexane. Cottonseed oil—like other seed oils—is also genetically modified.^10,11

COTTONSEED POISONING OF FARM ANIMALS

As early as 1899, a veterinarian noted that cows given too much cottonseed suffered from signs of pulmonary edema and anemia, dis­playing symptoms such as labored breathing internal bleeding, convulsive movements, swol­len legs, corneal lesions and ocular discharge— with the optic nerve one of “the most seriously and frequently affected organs.”¹² Yet over one hundred years later, not only are cattle still dying from cottonseed poisoning, but the incidence of gossypol toxicity has increased.¹³

The sidebar on the previous page lists the many symptoms of cottonseed poisoning that occur in farm animals.^4,12-18 Studies show that cottonseed poisoning can affect a wide variety of organ systems and organs, including the heart and circulatory system, liver, kidneys, gallblad­der and thyroid gland, as well as metabolism, oxygenation, fertility, vision and more.

Mature ruminants are less susceptible to gossypol poisoning than other farm animals.13 This is because, during digestion, the gossypol is detoxified as it binds to lysine; however, the cyclopropene fats in cottonseeds still end up in the milk.¹⁹ Moreover, even very small amounts of these poisons accumulate in the liver, kidney, heart, other muscles, nerves and the spleen, since one of gossypol’s effects is to hinder detoxification.

Hundreds of studies conducted over the past century have sought to determine how much cottonseed ruminants, pigs, poultry and fish can eat before they show symptoms of poisoning, and countless numbers of animals have died in this process. Nonetheless, cottonseed meal is still included in feedstuff designed to fatten animals, including young beef cattle in feed lots, dairy cows, sheep and goats in large dairy operations and farmed fish. Mature ruminant animals, fish and shellfish can consume large quantities of cottonseed meal before they show ill-effects, possibly because lysine is also an ingredient in their feed.

Some advise against giving cottonseed to pigs or poultry, which suffer the same—or worse—symptoms of gossypol toxicity as ru­minants.16 According to a physiological chemist writing in 1921, “of all the farm livestock these animals [pigs] are the most sensitive to the del­eterious effects of cotton seed meal.”²⁰ A 2016 report by Polish researchers argued that poultry can be fed cottonseed meal as long as lysine and iron are included in the feed.²¹ However, lysine and iron supplementation serve to ameliorate only the effects of gossypol and not the other toxic ingredients in cottonseed.

There is no test for gossypol toxicosis, so making a diagnosis of illness in animals requires a veterinarian to test the exact feed the animals were eating. However, symptoms occur several weeks to a month after feeding cottonseed, and by then, the exact feed is already eaten. As a result, vets are unlikely to diagnose cottonseed poisoning—even if the animal had been eating cottonseed and then died from typical cotton­seed poisoning symptoms!

In 1989, Oklahoma veterinary scientist S E Morgan acknowledged the frequent misdiagno­sis of cottonseed poisoning.²² She wrote:

“Field necropsies in which pulmonary congestion and edema were attributed to shipping-fever pneumonia, failure to exam­ine the heart either grossly or microscopi­cally, failure to believe that 200 ppm free gossypol could kill a calf, failure to believe that any age of sheep could suffer gossypol toxicity, and failure to believe that just because you fed the same thing last year, it will not cause a problem this year, all were factors in causing the misdiagnosis of this toxicity.”²²

Importantly, the conditions labeled as “bovine respiratory disease,” “avian cholera,” “swine flu” and “bird flu” all have symptoms that match cottonseed poisoning. Bovine re­spiratory disease (BRD) and bovine congestive heart failure (BCHF) are described as the most common and costly diseases affecting beef cattle. BRD is blamed on the stress of ship­ment to a feedlot, and because bacteria such as Pasteurella multocida are found with BRD, vets treat it with antibiotics and vaccines. Notably, the hypoxia caused by cottonseed suppresses the immune system and lowers lymphocyte levels, which allows bacteria to accumulate. Symptoms of BRD—such as labored breath­ing internal bleeding, convulsive movements, swol­len legs, corneal lesions and ocular discharge— with the optic nerve one of “the most seriously and frequently affected organs.”¹² Yet over one hundred years later, not only are cattle still dying from cottonseed poisoning, but the incidence of gossypol toxicity has increased.¹³

The sidebar on the previous page lists the many symptoms of cottonseed poisoning that occur in farm animals.4,12-18 Studies show that cottonseed poisoning can affect a wide variety of organ systems and organs, including the heart and circulatory system, liver, kidneys, gallblad­der and thyroid gland, as well as metabolism, oxygenation, fertility, vision and more.

Mature ruminants are less susceptible to gossypol poisoning than other farm animals.¹³ This is because, during digestion, the gossypol is detoxified as it binds to lysine; however, the cyclopropene fats in cottonseeds still end up in the milk.¹⁹ Moreover, even very small amounts of these poisons accumulate in the liver, kidney, heart, other muscles, nerves and the spleen, since one of gossypol’s effects is to hinder detoxification.

Hundreds of studies conducted over the past century have sought to determine how much cottonseed ruminants, pigs, poultry and fish can eat before they show symptoms of poisoning, and countless numbers of animals have died in this process. Nonetheless, cottonseed meal is still included in feedstuff designed to fatten animals, including young beef cattle in feed lots, dairy cows, sheep and goats in large dairy operations and farmed fish. Mature ruminant animals, fish and shellfish can consume large quantities of cottonseed meal before they show ill-effects, possibly because lysine is also an ingredient in their feed.

Some advise against giving cottonseed to pigs or poultry, which suffer the same—or worse—symptoms of gossypol toxicity as ru­minants.¹⁶ According to a physiological chemist writing in 1921, “of all the farm livestock these animals [pigs] are the most sensitive to the del­eterious effects of cotton seed meal.”²⁰ A 2016 report by Polish researchers argued that poultry can be fed cottonseed meal as long as lysine and iron are included in the feed.²¹ However, lysine and iron supplementation serve to ameliorate only the effects of gossypol and not the other toxic ingredients in cottonseed.

There is no test for gossypol toxicosis, so making a diagnosis of illness in animals requires a veterinarian to test the exact feed the animals were eating. However, symptoms occur several weeks to a month after feeding cottonseed, and by then, the exact feed is already eaten. As a result, vets are unlikely to diagnose cottonseed poisoning—even if the animal had been eating cottonseed and then died from typical cotton­seed poisoning symptoms!

In 1989, Oklahoma veterinary scientist S E Morgan acknowledged the frequent misdiagno­sis of cottonseed poisoning.²² She wrote:

“Field necropsies in which pulmonary congestion and edema were attributed to shipping-fever pneumonia, failure to exam­ine the heart either grossly or microscopi­cally, failure to believe that 200 ppm free gossypol could kill a calf, failure to believe that any age of sheep could suffer gossypol toxicity, and failure to believe that just because you fed the same thing last year, it will not cause a problem this year, all were factors in causing the misdiagnosis of this toxicity.”²²

Importantly, the conditions labeled as “bovine respiratory disease,” “avian cholera,” “swine flu” and “bird flu” all have symptoms that match cottonseed poisoning. Bovine re­spiratory disease (BRD) and bovine congestive heart failure (BCHF) are described as the most common and costly diseases affecting beef cattle. BRD is blamed on the stress of ship­ment to a feedlot, and because bacteria such as Pasteurella multocida are found with BRD, vets treat it with antibiotics and vaccines. Notably, the hypoxia caused by cottonseed suppresses the immune system and lowers lymphocyte levels, which allows bacteria to accumulate. Symptoms of BRD—such as labored breath­ing, coughing, ocular and nasal discharge and depression—correspond closely to symptoms of cottonseed poisoning. BRD and BCHF affect calves weeks after they arrive at a feedlot, where many are given cottonseed meal. In young cattle with an immature rumen, there is ample reason to suspect cottonseed as the cause of pulmo­nary edema with follow-on bacterial infection, which leads to death in many. BRD survivors, interestingly enough, have permanent lung damage. Ironically, a 2020 study investigating BRD fed the cattle both cottonseed meal and cottonseed oil!²³

The same Pasteurella multocida bacteria are found with a similar bird respiratory disease called “avian hemorrhagic septicemia” or “avian cholera.” Symptoms include green and yellow diarrhea, lung lesions, hemorrhage, a spotted, enlarged and necrotic liver and spleen, lame­ness, depression, anorexia, infertility and eye discharge. Although avian cholera is said to be “highly contagious,” the gastrointestinal symp­toms could indicate food poisoning. Despite the declared contagiousness, chicks under six weeks old are actually less susceptible²⁴—and six weeks is when they become old enough to eat cottonseed.

The first case of avian cholera reported in the U.S. occurred in 1867, and Louis Pasteur isolated his first bacterium (Pasteurella mul­tocida) in 1880—the exact same time period during which animals were first getting cot­tonseed in America. Avian cholera is also called “Indian cholera,” and substantial amounts of cottonseed have poisoned animal feed in India for centuries. In some areas of India, cattle re­ceive cottonseed as 100 percent of their protein requirement, which could render Indian beef very high in cottonseed poisons. This practice may have influenced the decision by some in India never to eat beef. In fact, the Indian state of Gujarat—the state that produces the most cotton—has attempted to legally turn Gujarat into a “vegetarian state,”²⁵ including through implementation of the toughest cattle slaughter ban in the country,²⁶ although in practice, many people still eat meat.

“GOOD HEAVENS, WE’RE ALL EATING COTTON!”

Humans consume cottonseed in a variety of forms, including as cottonseed oil and fiber. It’s unknown how much gossypol occurs in modern cottonseed oil, which today is processed to par­tially remove it. However, gossypol is likely to still remain at toxic levels because, as recently as 2012, a toxicologist recommended fortifica­tion of cottonseed oil with vitamin A, which gossypol depletes, to protect against its toxic effects.²⁷ Notably, early-twentieth-century stud­ies showed that large amounts of vitamin-A-rich cod liver oil helped protect against gossypol.²⁸

Thirty-five percent of the cottonseed oil produced in the U.S. goes into baking and frying oils,²⁹ so it is essential to check labels. Cottonseed oil appears in products as varied as granola, salad dressings and honey-roasted peanuts, and in the blended oils and shortening in which doughnuts, French fries and chips are fried. If a product lists cottonseed oil grouped with other oils, it’s safe to assume that it contains cottonseed oil, which is the least expensive of all the industrial seed oils. An early hydrogenated cottonseed-oil shortening that rivaled Crisco, called Kream Krisp, likely served as frying oil for the first Krispy Kreme doughnuts, which are still fried in cottonseed oil today.³⁰ Tragically, cottonseed oil may have contributed to the heart attack death of a man running in a marathon sponsored by Krispy Kreme to raise money for a local hospital; the runners had to eat twelve doughnuts in sixty minutes—while jogging!³¹

Unfortunately, you can’t always read labels to identify cottonseed oil in your food. For ex­ample, cottonseed oil is commonly used in fast food restaurants—even Olive Garden, a higher-end restaurant chain, uses cottonseed oil in some of its food. In addition to its use in restaurants, cottonseed oil is likely included as a prominent ingredient in deli and food truck food.

Much of the fiber in foods may also come from cotton; cotton has the “virtue” of contain­ing 90 percent cellulose (versus 40 percent for wood). Thus, cotton fiber regularly serves as an additive to stabilize, emulsify and thicken, and for anti-caking purposes. Food manufacturers also add cottonseed fiber to sausages (and their casings!) and other processed meats and meat patties, as well as to sauces, soups, gluten-free baked goods, seasoning mixes, meatless prod­ucts, cheese, yogurt, ice cream, high-fiber diet foods, beverages and even pet food. In addition, pharmaceutical companies often add cottonseed fiber to laxatives, pain relievers (such as oxyco done), amphetamines and other drugs.

Microcrystalline cellulose (MCC) is a cellulose powder produced by acid hydrolysis of (mainly) cotton linter. Manufacturers use it in processed foods to control viscosity, texture and consistency, as well as to replace fat; it also functions as a preservative. Manufacturers add MCC to vegetarian capsules for supplements and drugs. Fast food chains depend on MCC to create the right consistency in buns, cheese, shakes, sauces, fries, onion rings and meats—in other words, in just about everything. Discussing one MCC product, the PharmaCentral website explains that the “native cellulose. . . is completely indigestible, and its hydrolysis during the production of microcrystalline cellulose does not alter its behaviour in the intestine.”³² Sounds like a recipe for gut problems!

Hydroxypropyl methylcellulose (HPMC), also shortened to hy­promellose, is a vegetarian substitute for gelatin and gluten used in plant-based vegan meats, gluten-free foods and many other products. Scientists explain that in processed foods, HPMC functions “as a film former, emulsifier, stabilizer, or thickening agent”; for the pharmaceuti­cal industry, it provides a “drug delivery matrix.”³³ In both applications, manufacturers appreciate HPMC for “its ease of use, wide availability, superior film-forming capability, good biocompatibility and biodegrad­ability.”³³ HPMC also serves as a fat replacer (acting as a lubricant to provide a creamy mouthfeel) and extends shelf life.

COTTONSEED POISONS IN MEAT AND MILK

Chinese researchers have reported that gossypol “has a strong ten­dency to accumulate in animal tissues” and “is not easily cleared from the animal body,” generating “considerable concern” about the safety of cottonseed meal.34 They describe research dating back to the 1960s showing that “levels of gossypol in pig organs were directly related to the level of gossypol in the diet and to the length of time the diet was fed,” with “[l]arger amounts of gossypol. . . found in the liver, kidney, heart, and spleen,” and “lesser amounts found in brain and muscle.”³⁴ In trout fed cottonseed meal, researchers have detected gossypol in body tissues twelve months later, mainly in the liver and kidneys.³⁵

According to a website that markets cottonseed feed to dairy farmers, “Typical rations include up to 15% cottonseed on a dry matter basis,”³⁶ amounting to eight pounds of cottonseed per day. In a 2012 study as­sessing the effects “of different sources and levels of dietary gossypol on gossypol residues in plasma and milk of lactating cows,” Chinese researchers reported that at the 15 percent dry matter level, “gossypol was detected in plasma and milk,” but, they alleged, “not at harmful levels.”³⁷ However, just as gossypol builds up in the tissues of cows eat­ing cottonseeds, gossypol also builds up in human body tissue. Bound gossypol found in heat-treated cottonseed oil byproducts is less toxic than the free gossypol found in whole cottonseed, but in recent years, cattle rations have increasingly included whole cottonseed, especially in feed lots and larger dairy operations. The Weston A. Price Foundation is working with a lab to measure gossypol in milk.

As mentioned, cyclopropene fats are also found in conventional milk.19 The explanation generally offered is that this is the result of feeding cows silage, because lactobacilli (which play a role in silage fermen­tation³⁸) produce cyclopropene fats.³⁹ However, cottonseed also contributes to cyclopropene fats in milk. In an interesting 1985 study of two groups of cattle—in which both groups ate silage, corn and soybeans, but only one group was fed cottonseed—no cyclopropene fats were found in the non-cottonseed group, despite the silage, but the fatty acids were detectable in the milk of the cottonseed-fed cows.¹⁹ As the researchers cautioned:

“Total lipid in plasma, total serum choles­terol, serum gossypol, and apparent liver gossypol concentrations were greater in cows fed whole cottonseed. Gossypol and cyclopropenoid fatty acids appeared to be absorbed from the gut of cows fed whole cottonseed. Small amounts of gossypol in serum and liver tissue and small amounts of cyclopropene fatty acids in adipose tis­sue lipids and milk fat indicate a need to elucidate the significance of these physi­ologically active compounds in the human diet and their biological effects on lactating dairy cows.”¹⁹

When, in 2017, the European Food Safety Authority (EFSA) assessed the human health implications of feeding cottonseed to farm animals, it claimed there were almost no quan­titative data available regarding “carry-over into animal derived products,” even though elsewhere the authors admitted that “gossypol is transferred to edible parts, muscle and of­fal of ruminants and poultry, and is probably transferred to cow’s milk.”⁴⁰ Nevertheless, they concluded that feeding cottonseed to farm animals did not pose a health risk for humans!

COTTONSEED AND INFERTILITY

Over the decades, public and private enti­ties have displayed considerable interest in the antifertility effects of cottonseed. In the first half of the 1980s, China, the Rockefeller Foundation and the World Health Organization (WHO) studied the use of small doses of gossypol for male contraception.⁴¹ In 1986, after some study participants reported a lack of reversibility and others developed low blood potassium levels (hypokalemia), China discontinued the re­search.⁴² Products containing cottonseed meal are currently fed to feral pigs for contraceptive purposes.⁴³

Gossypol causes infertility in farm animals and humans by blocking luteinizing hormone (needed for synthesis of all sex hormones) and, as mentioned earlier, the enzymes 5AR and sialyltransferase. 5AR converts a percentage of testosterone in males into dihydrotestosterone (DHT), which is needed for genital maturation and facial hair. Blocking 5AR thus causes infer­tility while also increasing testosterone, which increases sex drive and erections, bone length, muscle strength and acne, and deepens the voice. Sialyltransferase, for its part, is what attaches the sialic acid N-acetylneuraminic acid to its acceptor to enable the union of sperm with egg.

Gossypol also interferes with female sexual development, causing infertility and “irregular and longer estrous cycles, lower levels of estra­diol, reduced number of ovarian follicles, and decreased pregnancy rate.”⁴⁴

COTTONSEED AND ATHEROSCLEROSIS

As noted above, small amounts of the cot­tonseed poisons gossypol and cyclopropene fats—even tiny doses—accumulate over time in the heart, liver, kidneys and spleen (which pro­duces both red and white blood cells and recycles our iron), damaging the cardiovascular system and causing fatty liver and atherosclerosis. It is an interesting fact that coronary artery disease first appeared in the U.S. after Americans began to eat Crisco and Wesson oil, both of which would have contained a significant amount of these poisons (see timeline, next page). As early as 1954, researchers noted that feeding chickens cottonseed oil, along with 2 percent cholesterol, would cause atherosclerosis!⁴⁵

How do chronic small doses of cottonseed poisons cause atherosclerosis? First, cyclopro­pene fats cause fatty liver and necrosis, which weakens heart muscle and leads to arrhythmia, the main risk factor for strokes. Second, cot­tonseed, as noted, is high in linoleic acid, which “drives” heart disease. Third, gossypol-created lysine deficiency causes calcification in the arteries and excessive inflam­matory nitric oxide (NO), which is “the major driving force for cell death” in the inflammatory cell death pathway.⁴⁶ Nitric oxide (as made in the body from citrulline) is essential for artery health, but lysine deficiency causes the production of inflammatory NO from arginine. Low lysine also causes low niacin, and gossypol depletes vitamin C. This may be why Linus Pauling found that vitamin C plus lysine brought rapid relief from angina, and why some practitioners recommend niacin to lower cholesterol.

Finally, gossypol blocks HMGCR, the enzyme that degrades cho­lesterol (thus raising cholesterol levels). Lysine is one of the catalytic, or regulating, amino acids of HMGCR. Because gossypol binds to lysine, it also binds to the lysine on HMGCR, which disables the enzyme. Notably, it is this lysine that is the target of statin drugs.⁴⁷ In familial hypercho­lesteremia, HMGCR is faulty, so fetal exposure to gossypol (which is mutagenic) could cause this condition. Gossypol may also block human Niemann-Pick cholesterol transporter, which allows macrophages to dis­pose of damaged cholesterol. In a study of moths, gossypol blocked this transporter by binding to lysine; it may also do so in humans. Notably, in a 1983 study discussing gossypol’s potential use for male contraception, the researcher mentioned “the fear of atherosclerosis in the ongterm.”⁷⁹

Cyclopropene fats are found with heart disease, kidney disease, high triglycerides and pancreatic cancer—and all of these problems are related to atherosclerosis. The cyclopropene fats block the SCD enzyme that is needed to convert excess carbohydrate into fat, thereby raising cholesterol, causing fatty liver and liver damage and contributing to osteoarthritis. Cyclopropene fats also block the D6D enzyme necessary for converting linoleic acid to gamma-linolenic acid (GLA), which has downstream effects on the heart. Under ordinary circumstances (that is, if D6D is not blocked), GLA (via D5D) is converted into arachidonic acid (ARA), the precursor to prostacyclin, a “powerful cardioprotective hormone,”⁴⁸ which lowers high blood pressure and inhibits the progression of atherosclerosis.⁴⁹ D6D regulates conversion of the omega-3 fat alpha-linolenic acid (ALA) to EPA (eicosapentaenoic acid) and, via D5D, to DHA (docosahexaenoic acid). DHA is low in people with heart disease.

The very high amount of linoleic acid (55 percent of total fats) con­tained in cottonseed oil compounds the problems already described. Phos­phatidylcholine, cells and LDL—which normally would contain ARA (for prostacyclin) and/or anti-inflammatory DHA—now instead contain linoleic acid and ALA, fats that are very unstable and easily oxidized (damaged). Inflammation from toxins causes LDL that contains linoleic acid to become oxidized LDL (oxLDL). A macrophage then engulfs the oxLDL and, normally, the enzyme lecithin–cholesterol acyltransferase (LCAT) removes the cholesterol for disposal. However, cyclopropene fats also block LCAT, and if LCAT is blocked, the over-filled macrophage turns into a stationary foam cell in the artery as arterial plaque. This is the basic problem in atherosclerosis.

People with LCAT deficiency have hemolytic anemia (caused by red blood cells breaking apart), kidney failure, atherosclerosis, enlarged liver and spleen, enlarged lymph nodes and corneal opacities.⁵⁰ It should come as no surprise by now to learn that these symptoms of low LCAT are also symptoms of cottonseed poisoning. Low LCAT, together with vitamin A depletion, may be the mechanism behind the vision problems linked to cottonseed poisoning.

The high linoleic acid content of cottonseed oil adds to the problem of blocking D6D. Moreover, linoleic acid is oxidized only into unstable free radicals, including lipid derivatives called HODEs, rather than into cardioprotective prostacyclin. HODEs are found in large quantities with fatty liver and heart disease, diabetic kidney disease, cataracts and Al­zheimer’s and also play a major part in diabetes. In fact, HODEs from linoleic acid are so prevalent in diabetes that they have been flagged as early biomarkers of the disease.⁵¹ HODEs are also found with chronic pain, asthma, pancreatitis, rheumatoid arthritis and various cancers.^52,53

Destructive aldehydes are associated with many of the same chronic conditions as HODEs.^54,55 Thus, it is a major problem that gossypol blocks the enzyme (aldehyde dehydrogenase) that detoxifies aldehydes,⁵⁶ because when heated, cottonseed’s linoleic acid forms a toxic aldehyde called acrolein. Acrolein can become a leuko­toxin (exerting toxic effects against the white blood cells called leukocytes) and, in sufficient quantity, will cause acute respiratory distress syndrome (ARDS),⁵⁷ disseminated intravascular coagulation (tiny blood clots) and death. Dis­seminated intravascular coagulation is found with farm animals.

Consumption of cottonseed products likely makes people more vulnerable to a brain parasite called Toxoplasma gondii. This is because cot­tonseed oil contains not only cyclopropene fats but also another rare fat called arachidic acid, both of which occur in the parasite’s membranes. Toxoplasma also requires arginine for growth, which is excessive with the lysine deficiency created by gossypol. Toxoplasma is found with autism (in one study, in up to 81 percent of blood samples),⁵⁸ Alzheimer’s and mental health con­ditions such as obsessive-compulsive disorder (OCD), anxiety, schizophrenia and dysphoria. Researchers report that “serologic evidence of previous Toxoplasma infection is present” in up to 70 percent of the U.S. population!⁵⁹ It is, therefore, vital to avoid both cottonseed and Toxoplasma for mental health.

COTTONSEED’S HIDDEN ROLE IN HEART DISEASE

Interestingly, deaths from heart disease peaked in the late 1960s concurrently with the peak in Crisco consumption. When Crisco consumption fell (Figure 1), heart disease deaths also fell. In the U.S., the death rate from coro­nary heart disease (CHD) declined from two hundred sixty-two deaths per hundred thousand people in 1970 to just over one hundred sixteen deaths per hundred thousand in 2009.⁸⁰ So, the 2009 death rate was 44 percent of the death rate in 1970, which was near the height of Crisco consumption. The drop in the death rate from CHD in the UK was even more striking, as Figure 2 illustrates.

In a 2018 article describing five decades of researcher “confusion” and incorrect “or­thodoxy” about the causes of coronary heart disease, a Canadian researcher suggested that the role of saturated fat had been “much exag­gerated”⁶⁰ and that high-carbohydrate diet plays a role in heart disease. In a study that measured blood levels of saturated fat in people eating either a high-carbohydrate diet or a high-saturat­ed-fat diet, the group on the high-carbohydrate diet had higher levels.⁶¹ This is because when you eat a low-carbohydrate diet, saturated fat is made into ketones to be burned for heart energy, whereas excess carbohydrates, in any form, are converted into the saturated fat palmitic acid and triglycerides for energy storage. Rather than conversion into energy, these fats accumulate in the blood, liver and body fat.

Decreased cigarette smoking often re­ceives the credit for the decline in heart disease deaths.⁶² Interestingly, cottonseed oil may encourage smoking. This is because gossypol lowers lysine, and low lysine causes anxiety. Lysine plus methionine are also components of acetylcholine, which is critical for the heart and nervous system, regulating heartbeat, blood pressure and heart contractions. Nicotine relieves anxiety by binding to an acetylcho­line receptor. Low acetylcholine—from low lysine—and the anxiety that this causes could create a desire for nicotine.

Smoking increased significantly starting in 1920, after the introduction of Crisco in 1911. Stated another way, the desire for nicotine began its increase with Crisco and then went down when Crisco consumption went down. Even if smoking cessation did have an effect on deaths from heart disease, lowering Crisco consumption likely lowered the desire and need to increase the effects of acetylcholine by smok­ing cigarettes.

DEMENTIA AND VIOLENCE

In both animals and humans, depression and dementia are symptoms of cottonseed poi­soning. Gossypol blocks production of DHT, and low DHT is linked to depression, anxiety and schizophrenia. Studies also indicate that the effects of gossypol are passed on to the next generation. When researchers fed gossypol to pregnant mice, the offspring’s brainstem cells were faulty; the gossypol also caused hip­pocampal hemorrhage, changes in membrane permeability and interference with microtubule assembly.¹ Even though the mothers showed no symptoms, the offspring, with fewer neurons, displayed anxiety, depression, and behavior and learning abnormalities. The cyclopropene fats in cottonseed also play a role in dementia by blocking APOA 1 and 2.⁶³ In addition, fatty liver, as caused by cyclopropene fats, is linked to anxiety and depression.

Cottonseed poisons cause strokes, and stroke is the main risk factor for Alzheimer’s. In contrast, lysine protects against stroke. Gos­sypol blocks the cholesterol transporter NPC1, which is impaired in Alzheimer’s, and Al­zheimer brains display calcification and neuron growth that is unprotected by myelin.⁶⁴ Also, the lysine in the tau protein is modified with Alzheimer’s, preventing autophagy and caus­ing the accumulation of the tau protein. Lysine activates the glucose and vitamin C transporter in the brain, GLUT1. Some doctors suggest that a diet higher in lysine than arginine may prevent Alzheimer’s.⁶⁵

Furthermore, gossypol crosses into the brain. In rodent studies, mice and rats fed tiny amounts of gossypol developed the tangles of Alzheimer’s⁶⁶ and “Swiss cheese” holes in their brains.67 Wisconsin physician Dr. Bruce Semon argues that small amounts of cottonseed poisons, accumulated throughout the years, may be a major cause of Alzheimer’s and other psychoses.⁶⁷

With adequate lysine, tryptophan can be made into metabolites such as niacin and serotonin, but even a simple lysine deficiency can lead to anxiety and depression. With lysine deficiency, there is less tryptophan and, therefore, less niacin and serotonin. Low serotonin is linked to dementia, with research suggesting “serotonin loss may be a key player in cognitive decline, rather than a side-effect of Alzheimer’s disease.”⁶⁸ Low serotonin also means low melatonin (the sleep hormone), and people with Alzheimer’s are low in night-time melatonin.

The human brain is nearly 60 percent fat, so potentially harmful dietary fat can affect brain function in a number of ways. Researchers have linked high consumption of linoleic acid to violent behavior.⁶⁹ Widespread consumption of cottonseed oil, especially in the South, may partly explain why, in the early 1900s, the South was plagued with unrest and violence in the form of lynchings and other atrocities. Notably, the Ku Klux Klan revival occurred in 1915 in Georgia, where Wesson Oil first came on the market (in 1900) and four years after Crisco made its first appearance; this is also where pellagra dementia was first diagnosed, in 1902. The cause of pellagra is niacin deficiency, but lack of lysine can result in niacin deficiency and cause pellagra. Pellagra was endemic in the cotton mill villages, where residents ate substantial amounts of cottonseed oil mixed into lard, and even con­sumed extremely toxic, fresh unprocessed cottonseed oil.^70,71 In fact, the way scientists induce pellagra is to feed an animal corn or peas and— cottonseed oil!^72,73

Cottonseed oil hydrogenation, used for both Crisco and cottonseed oil margarine, was invented in Germany, and the first Alzheimer’s diagnosis occurred in Germany in 1901. In impoverished post-WWI Germany, cheap cottonseed oil from the U.S. was substituted for the large amount of lard Germans had previously consumed.

In the Atlanta Constitution in 1917, one read:

“Germany and Austria have suffered hunger more on account of their separation from the cotton fields of the United States. . . than from the lack of bread. . . . Oleomargarine was all the ‘butter’ that many Teutons knew, and vegetable fats the only ‘lard’ many of them used, and ‘olive oil’ made from. . . cotton seed. . . most of the ‘olive oil’ they consumed.”⁷⁴

Certainly, Adolph Hitler and Benito Mussolini, who were both veg­etarians, would have eaten a considerable amount of cottonseed. Thus, a combination of toxins and unusual fats in cottonseed oil likely contributed to “the most violent century.”

OTHER CONTRIBUTORS

Although Crisco and Wesson Oil no longer contain cottonseed oil, and our consumption of cottonseed oil has fallen, infertility, heart disease dementia persist. Saturated fat, grass-finished beef and high-quality cured meats are not to blame. Instead, these conditions likely result from a combination of excessive carbohydrates; meat, processed meats and milk containing a significant amount of cottonseed poisons; and pesticides on fruits and vegetables.

Many pesticides currently in use are associated with infertility, heart disease and dementia. These include organophosphates, which bind to lysine, and chemicals that act as estrogens, contributing to infertility. Discussing implications for the heart, the authors of a study published in 2020⁷⁵ described increased heart disease risks associated with a wide variety of pesticides:

• Chlorpyrifos, coumafos, carbofuran, ethylene bromide, manco­zeb, ziram, metalaxyl, pendimethalin and trifluralin: Increased risk of acute myocardial infarction (1.8–3.2)
• Primaphos, fenitrothion, malathion and deltamethrin: Risk of increased blood pressure
• Tetrachlorodibenzo-p-dioxin: Increased cardiovascular disease risk (1.09–2.78)
• Organochlorine: Increased cardiovascular disease risk (1.19– 4.54)
• Heavy metals and arsenic: Increased risk of atherosclerosis and arterial hypertension

A WAY FORWARD

Cottonseed purveyors continue to promote cottonseed as an inexpen­sive and healthy source of protein and fat for both humans and animals, even as the cottonseed given to humans and animals has directly caused or indirectly contributed to untold suffering, death and economic hardship. At the same time, the cotton industry is under fire for major pollution and water use at every stage of production, from cotton processing to the finished product. Mountains of cotton clothing are also thrown away every year—largely the result of greatly increased cotton production since 2000 and from “fast fashion” clothing companies, which feature many new styles every month.

The time has come to acknowledge that no matter how it is processed or how small the quantity, foods that contain cottonseed come with very dangerous poisons. Therefore:

1. We need to stop thinking of, and using, cottonseed as food for humans and animals.
2. As consumers, we must carefully avoid foods containing cot­tonseed. This requires public education, and it requires testing for gossypol and cyclopropene fats in milk, meat and fish.
3. We also need limits placed on the use of cottonseed oil and other cottonseed food additives, which, moreover, should be clearly labeled.
4. When humans or animals show signs of cottonseed poisoning— whether infertility, heart disease or mental illness—and they have been exposed to cottonseed poisons, they need to be treated for cottonseed poisoning. For example, it’s critical to replenish the many nutrients that cottonseed depletes. These include lysine, iron (ferrous sulfate), vitamins A, C and D, zinc, copper, calcium, potassium, selenium (sodium selenite), arachidonic acid, DHA and the amino acids threonine, methionine and glycine.

Also recommended is a higher-protein diet, with emphasis on foods that are high in lysine, methionine and zinc, such as organic dairy, wild-caught fish and grass-finished meat.

In addition, whenever possible, we need to transition land that produces cotton to real food production instead. Todd Boykin, a for­mer cotton farmer, offers one example.⁷⁶ After Boykin, seeded land destroyed from cotton farming to grass, and fenced it for managed grazing, he reported “dramatic evidence of change. . . in the years soon after the conver­sion.” There was a big rain followed by strong wind. Boykin reported, “despite the fact that it had just rained—the neighbor’s cotton ground was blowing a huge cloud of dust across the field onto our grass. But where we were standing, no soil was moving.”⁷⁶ This is a solution that could and should be implemented because, according to Boykin, “The profitability of grazing cattle on converted ground runs neck and neck with growing cotton.” In short, Boykin’s switch from cotton farming to cattle ranching shows that there is a way forward—out of some of the most devastating illnesses of our time to healthy food production!

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SIDEBARS

DOCUMENTED SYMPTOMS OF COTTONSEED POISONING IN FARM ANIMALS

GASTROINTESTINAL: Fever, abdominal pain, intestinal inflammation (gastroenteritis), vomiting, bloody diarrhea,
nasal discharge
RED BLOOD CELLS: Leaky capillaries, pulmonary edema, hemorrhage, red blood cell fragility, disseminated intravascular
coagulation, petechiae, breakdown of hemoglobin/free bilirubin (jaundice), anemia/oxygen deficiency, shortness of breath, dry cough, respiratory failure
HEART: Atherosclerosis, heart failure/heart attack, myocardial breakdown, necrosis
LIVER: Fatty liver, damaged liver, necrosis (with red-brown spots), bloody vomit
GALLBLADDER: Damaged bile ducts (bile needed to absorb the fat-soluble vitamins A, D, E and K)
KIDNEYS: Kidney damage, hemorrhage, tubule degeneration, blood in urine, interstitial nephritis
EYES: Red eyes, watery eyes, blindness from corneal opacity, optic nerve damage
INFERTILITY: Both sexes (blocks steroid synthesis)
MENTAL HEALTH: Depression, dementia
ENERGY: Listlessness, disruption of energy metabolism, thyroid dysfunction
GROWTH AND DEVELOPMENT: Cachexia (wasting syndrome), breakdown of muscle, bone and fat
INFECTIONS: Low lymphocytes (white blood cells)
POTASSIUM-SODIUM BALANCE: Imbalance (low potassium and high sodium), arrhythmia, lameness, convulsions,
flaccid paralysis
BONE MARROW: Reduction in bone marrow cells
JOINTS: Swelling

TIMELINE OF COTTONSEED OIL USE AND HEART DISEASE

In the early years, cottonseed oil was probably more toxic than today because the cottonseed was not as heav­ily processed to remove the gossypol. It also had a bad odor from the trichloroethylene solvent, the rancid linoleic acid and the “foul-smelling” cyclopropene fats. For these reasons, manufacturers did not initially sell it as straight cottonseed oil but instead secretly added it to olive oil or lard, selling it in the U.S., Europe and Russia.

1899: David Wesson invents a deodorization process, and manufacturers begin selling straight cottonseed oil.

1911: Using a hydrogenation process invented in Germany, Procter & Gamble markets Crisco as a “pure” product (as opposed to lard adulterated with cottonseed oil!).

1913: The Story of Crisco: 615 Tested Recipes and a Calendar of Dinners becomes a popular cookbook, first marketed to Jewish people who keep kosher.⁷⁷ Around this time, genetic diseases that may be connected to the cholesterol and bleeding effects of cottonseed (such as familial hypercholesteremia, Niemann-Pick disease, hemophilia A and anxiety) begin to affect many Jewish people.

1930s: My mother told me about shopping for Crisco when she was growing up during the Depression, describing shelf after shelf filled with large canisters of Crisco, with just a small section for lard. A clipping in the recipe box of my grandmother reads: “Donʼt waste your deep-frying Crisco. Strain it clear and use it for frying again and again.”

1939: Cottonseed oil sales fall when soybean oil takes over the market thanks to a new process that made a better hydrogenated product from soybean oil.

1948: A Crisco ad campaign—a contest that airs on Truth or Consequences—generates $1.7 million for the American Heart Association (AHA). This donation by Procter & Gamble enables the AHA to become nationally recognized as the source of heart disease expertise, even though that “expertise” likely is influenced by Procter & Gamble. Cotton­seed oil is now made by Cargill, and Cargill is on the Nutrition Forum of the AHA, along with McDonald’s, PepsiCo, Mars (chocolate), the United Soybean Board, Canola Info and General Mills.⁷⁸

1954: The first tub-style margarine, Chiffon, is manufactured, containing 100 percent partially hydrogenated cot­tonseed oil and thus, containing trans fats in addition to other poisons.

1956-1957: The AHA goes on television to present the “diet-heart hypothesis,” telling Americans that saturated fat is unhealthy because it increases cholesterol, which clogs arteries, thus causing coronary artery disease. Consumption of meat, eggs and butter goes down, and cottonseed oil consumption increases. Importantly, the opposite of what the AHA expects occurs: deaths from coronary artery disease skyrocket.

1959: In a study of hens, the animals are given what is called an “atherogenic diet,” consisting of 5 percent cot­tonseed oil and 2 percent cholesterol, revealing the fact that researchers already know that cottonseed oil causes “clogged arteries.”

1969: Crisco consumption in the U.S. peaks and then decreases rapidly. Interestingly, deaths from heart disease also peak in 1969 and then rapidly decrease. This decline is attributed to statins. However, because statins increase all-cause mortality, the fewer deaths from heart disease may be the result of lower Crisco consumption.

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This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly journal of the Weston A. Price Foundation, Summer 2024

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