Cottonseed Oil: America’s Original Vegetable Oil

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Warning: This oil comes with potentially damaging side effects due to the ingredient it’s made from or the manufacturing process used to extract it. Because these negative effects overshadow the potential benefits, I do not recommend this oil for therapeutic use. Always be aware of the potential side effects of any herbal oil before using.

Among the many crops grown in the United States is cotton. According to the National Cotton Council, roughly 162 pounds of cottonseed are produced for every 100 pounds of fiber.1

The raw cottonseed actually consists of three commodities: linters, which are cotton fibers still clinging to the harvested seeds and which are used to make a variety of products, from paper money to cosmetics to photography film; the hulls, which are pressed into a meal or used as a bulk food in the livestock feed industry; and the kernels inside the hulls, which are crushed to produce the oil.2

As an agriculture product in the U.S., cottonseed oil is considered to be “one of the country’s most important sources for vegetable oil,” according to the Agricultural Marketing Resource Center.3 While cottonseed oil is also touted by the industry to be “cholesterol-free with a high level of antioxidants,” making it a “premium oil” for cooking, baking and use by the processed (snack) food industry,4 fine food magazines such as Bon Appetit warn that it’s one of the top three “least healthy” oils for you.5

This is one reason why I would not recommend it as part of your diet. Before I explain my stand, here is what mainstream recommendations say about this vegetable oil.

What Is Cottonseed Oil?

Cottonseed oil is a fairly common vegetable oil in the U.S. and was used as early as the 1800s.6 It was called “America’s original vegetable oil” and created a high demand among its consumers.7 Cottonseed oil is similar to canola, corn, safflower, soybean and sunflower in terms of its polyunsaturated fat oil composition.8 In its nonhydrogenated form, it can be used for deep frying to lower the amounts of trans fat in fried foods.9

Uses of Cottonseed Oil

Cottonseed oil is known for its culinary purposes. It’s used for frying or baking, and added to salad dressings,10 baked goods, cereals and mayonnaise.11 Because of its neutral taste, cottonseed oil will not mask or overpower the other flavors in your dish, unlike other oils.12 It’s a familiar feature of processed foods,13 like potato chips14 and French fries,15 which I absolutely recommend you avoid if you want to achieve optimal health.

Cottonseed oil is added to margarines, icings and whipped toppings because of its potential to help form beta prime crystal, which gives these food products a smooth and creamy appearance and consistency.16

Cottonseed oil is also added to personal care products such as soap and cosmetics,17 lubricants, nail polish removers, fertilizers18 and laundry detergents.19 This oil is even added to soaps used in washing wool. In the first half of the 20th century, cottonseed oil was also used as an excipient in drugs like penicillin and vaccines, but was replaced by peanut oil after cotton seed allergy reactions began being reported.20

Today cottonseed oil is one of many used as emulsifiers and excipients approved for use in a range of drugs and vaccines.21,22

Composition of Cottonseed Oil

Cottonseed oil is mainly composed of polyunsaturated fatty acids (PUFAs), with linoleic acid making up a majority of its PUFA content.23 Other fatty acids that can be found in cottonseed oil include palmitic acid, myristic acid, palmitoleic acid, stearic acid, oleic acid and linolenic acid. The fatty acid composition of nonhydrogenated cottonseed oil is:24

  • Saturated fat — 27%
  • Monounsaturated fat — 18%
  • Polyunsaturated fat — 55%

When partially hydrogenated, cottonseed oil’s fatty acid profile is altered and its monounsaturated fatty acid (MUFA) concentrations increase:

  • Saturated fat — 29%
  • Monounsaturated fat — 50%
  • Polyunsaturated fat — 21%

How Is Cottonseed Oil Made?

Although cotton farming goes back centuries — with the cultivation of it being evident even in prehistoric times — cottonseed oil production is relegated to more recent history, when it became part of a milling process.25 This is different from mills seen today, which are either screw press or solvent extraction facilities.26 Modern processing of cottonseed oil involves numerous steps, and the main techniques include:27

  • Alkali refining
  • Bleaching
  • Winterization

Because it’s naturally stable, cottonseed oil requires less hydrogenation compared to other oils, and this results in lower trans fat levels.28

Does Cottonseed Oil Have Any Health Benefits?

Some of the health benefits you may have heard about cottonseed oil is that it’s “healthy” because of its high unsaturated fat levels that exhibit total cholesterol-, low-density lipoprotein (LDL)- and triglyceride-lowering properties.29 It’s also touted for producing low levels of trans fats when used for deep-frying foods30 and for its low amounts of saturated fat.31

From a nutrition standpoint, cottonseed oil, along with almond oil and wheat germ oil,32 also has high concentrations of vitamin E,33 a nutrient that may play a role in lowering your risk for diseases, such as Alzheimer’s disease, cardiovascular disease and prostate cancer.

Conventional health experts advise getting vitamin E from vegetable oils like cottonseed oil, because people do not eat foods rich in this nutrient on a daily basis.34,35 It is also believed that vitamin E contributes to the long shelf life of cottonseed oil.36

However, I disagree with these health claims. As much as possible, don’t use vegetable oils like cottonseed oil, whether it’s hydrogenated or not, and whether it’s unrefined or processed. It can negatively impact your health in multiple ways, as explained in the remaining sections. There is only one truly stable and healthful oil to use, and that is high-quality organic coconut oil.

The Drawbacks of Unrefined and Refined Cottonseed Oil

Initially, cottonseed contains gossypol that’s responsible for the oil’s yellowish color.37 This substance can be toxic to nonruminant animals (only adult cattle and sheep are known to metabolize it38) and reacts with protein and lessens the oil’s nutritional value.39

Increased amounts of gossypol have been linked to adverse effects like breathing problems, anorexia and heart, lung, liver and blood cell problems.40 This compound also triggered reproductive health problems among female nonruminant animals, particularly by disturbing “estrous cycles, pregnancy and early embryo development,” and among male animals by causing infertility, sperm immotility and reduced sperm counts.41

In attempts to make this oil less damaging to your health, manufacturers came up with the following areas of improvement for cottonseed oil production:42

  • Lowering or eliminating gossypol in cottonseed oil
  • Increasing the yield of cottonseed oil extraction
  • Increasing the oil’s PUFAs and vitamin E concentrations
  • Reducing saturated fatty acids

Another step the industry took as far back as 2007 was to implement “educational” marketing campaigns stressing the nutritious aspects of the nonhydrogenated oil, including the fact that “it does not require hydrogenation, the process that produces trans fatty acids,” thus making it “trans fat free.”43,44

And while the U.S. Food and Drug Administration (FDA) banned trans fats and partially hydrogenated oils in May 2018,45,46 the makers of Crisco shortening, a hydrogenated product, was already prepared, having introduced a new trans fat-free version of its product, made from sunflower, soy and cottonseed oils, in 2008.47

Even though being trans fat-free is a good thing, USDA data from July 2018 still show that 94% of the cotton crop grown in American soil is actually genetically engineered, which could leave questions as to how safe or nutritious cottonseed oil really is.48

Although GE proponents dismiss the concerns,49,50GE crops have been linked in the past to possible reproductive problems, organ disruption,51 digestive problems52 and questions about possible allergic reactions.53 Some published reports have also highlighted that cottonseed oil contains a high pesticide load54 and is susceptible to mold contamination.55,56

If You’re Looking for a Healthy Cooking Oil, Here Are the Best Choices

Remember that saturated fat is important for many of your bodily functions, and will not cause heart disease as mainstream recommendations have led you to believe. One of the foods most abundant in saturated and other high-quality healthy fats that is an excellent substitute for cottonseed oil is organic coconut oil.

Coconut oil is ideal for cooking because it’s resistant to high heat damage, and at the same time provides benefits for your overall well being. The article, “Use Coconut Oil Daily” outlines some of the reasons you should make the switch to this oil.

Olive oil is another option you can try, but it must be used cold and drizzled over your favorite foods. It shouldn’t be heated because of its low smoke point, which can cause toxic smoke when used at high heats. For more information on some of the most ideal sources of healthy fats, read “Top 13 Reasons to Replace Dangerous Oils With Healthy Fats.”


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The Healthy Longevity Global Grand Challenge at the National Academy of Medicine

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The institutions of the world are slowly waking to the potential of treating aging as a medical condition, thereby postponing, reversing, and ultimately entirely preventing age-related disease. The side-effect will be greatly extended lives, lived in good health, in youthful vigor. Aging is the accumulation of cell and tissue damage, and rejuvenation is the periodic repair of this damage. The research and development communities are only just starting on the road of damage repair in medicine. The first rejuvenation therapies, in the form of senolytic treatments to selectively destroy senescent cells, are only now emerging. They will make a sizable difference, far more than has been achieved by any other approach to medicine for age-related disease, but this is just the first step on a long road.

Alongside progress towards rejuvenation therapies and methods of modestly slowing aging, advocates for the treatment of aging have been working energetically at the task of steering the agendas at large research and medical institutions. This has been going on for something like two decades now. It is a slow process, but is finally starting to bear fruit, as illustrated by today’s news regarding the recently established Healthy Longevity Global Grand Challenge organized by the National Academy of Medicine. That very conservative organizations are now willing to talk in public about treating aging, and the ability to significantly alter the trajectory of human aging, is a sizable advance over the state of affairs even as recently as a decade ago.

Yet there is more to accomplish: the representatives of these organizations are still unwilling to talk about extending human life spans, in good health, for as long as possible. They talk about healthspan and prevention of age-related disease, and skip over the point that, for so long as health is maintained, people will live for longer. Aging is damage, health is the absence of that damage. Extended life span and extended health are bound together; you can’t have one without the other.

When radical life extension is not on the table as a goal, the inevitable result is that significant funding and attention goes towards projects that are capable of only small degrees of influence over aging. Take mTOR inhibitors, or metformin, or any of the other approaches to calorie restriction mimetics that upregulate stress responses, for example. These are an improvement over most older approaches to age-related disease, but that is a very low bar to pass. They are an exceptionally poor choice when compared with repairing the underlying damage that causes aging, such as by destroying senescent cells. But there is enormous enthusiasm for objectively worse strategies in the treatment of aging at the present time. I have to think that the mainstream rejection of the goal of adding decades or more of healthy life, extending the human life span far beyond its present limits, has something to do with this poor strategic prioritization.

National Academy of Medicine: Healthy Longevity Global Grand Challenge


Dramatic breakthroughs in medicine, public health, and social and economic development have resulted in unprecedented extensions of the human lifespan across the world over the past century. This triumph for humanity provides new opportunities as well as new challenges. Globally, we are facing a major demographic shift. Today, 8.5% of people worldwide (617 million) are aged 65 and over. By 2050, this percentage is projected to more than double, reaching 1.6 billion. The global population of the “oldest old” – people aged 80 and older – is expected to more than triple between 2015 and 2050, growing from 126 million to 447 million.

At the current pace, population aging is poised to impose a significant strain on economies, health systems, and social structures worldwide. But it doesn’t have to. We can envision, just on the horizon, an explosion of potential new medicines, treatments, technologies, and preventive and social strategies that could help transform the way we age and ensure better health, function, and productivity during a period of extended longevity. Multidisciplinary solutions are urgently needed to maximize the number of years lived in good health and a state of well-being. Now is the time to support the next breakthroughs in healthy longevity, so that all of us can benefit from the tremendous opportunities it has to offer.

The National Academy of Medicine is launching a Global Grand Challenge for Healthy Longevity – a worldwide movement to increase physical, mental, and social well-being for people as they age. The initiative will have two components: a prize competition to catalyze breakthrough innovations from any field, and an evidence-based report authored by an international commission.

Johnson & Johnson Innovation Announces Collaboration with National Academy of Medicine to Help People Live Longer, Healthier Lives


Johnson & Johnson Innovation today announced the signing of a sponsorship agreement with the National Academy of Medicine (NAM) to be the principal corporate partner of the Healthy Longevity Catalyst Awards in the United States. Part of the Healthy Longevity Global Grand Challenge1 founded by the NAM, the Catalyst Awards are a global prize competition to launch later this year, designed to stimulate innovation to transform the field of healthy longevity. The program will culminate in one or more Healthy Longevity Grand Prizes for major breakthroughs in increasing human healthspan.

The NAM Grand Challenge will roll out over three distinct phases and employ a tiered model of awards and prizes to stimulate new research and solutions around healthy longevity. Under the agreement, Johnson & Johnson Innovation will provide funding for the foundational Healthy Longevity Catalyst Awards in the U.S., to identify innovative, entrepreneurial proposals that have the greatest chance of being translatable into solutions to prevent, intercept and/or cure disease or deficits related to aging. “We envision a world in which widespread disease is a historical artifact and people enjoy longer, healthier lives, promoted by technological and medical advances. To achieve this, we need to shift the paradigm from today’s widespread focus on ‘disease care’ – where we wait for people to get sick, to only then do something about it – towards true health care, by keeping people well in the first place, eliminating disease and restoring people to full health.”

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Visualizing the Cost of Age-Related Disease as Disability Adjusted Life Years

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Disability adjusted life years (DALYs) are a statistical construct used in epidemiology to assess the harms caused by disease, particularly the chronic diseases of aging, as these are by far the greatest burden of disease that is inflicted upon the population as a whole. The costs of aging are huge, however they are measured. It is the greatest single cause of human suffering and death, and the economic effects of this constant destruction of human lives and capabilities are sized to match. The greatest good any of us can do in the world as it stands today is to work towards bringing aging under medical control.


Disability-adjusted life years (DALYs) are used globally to quantify the number of healthy years of life lost from the presence of a disease, disability, or injury. The burden of chronic, non-fatal health loss and early mortality is evaluated separately and compared across populations. More studies are needed for understanding how aging is linked with disease. Calculating the years lived with a disease (YLDs) and years of life lost (YLLs) from premature mortality will provide insights into the burden of common health conditions for the growing aging adult population. This information can help to identify which health conditions contribute most to the number of healthy years of life lost for aging adults, thereby informing how healthcare providers and interventions prioritize treatment and prevention efforts. The purpose of this study was to determine the burden of 10 common health conditions for a nationally-representative sample of middle-aged and older adults in the United States.

The principal findings of this investigation revealed that over 1-million years of healthy life were lost for middle-aged and older Americans from the 10 health conditions evaluated over the 16 year study period. Although aging adults were impacted by each health condition, hypertension accounted for the greatest burden; whereas, hip fractures had the lowest number of DALYs. There were 30,101 participants included. Sex stratified DALY estimates ranged from 4092 (fractured hip) to 178,055 (hypertension) for men and 13,621 (fractured hip) to 200,794 (hypertension) for women. The weighted overall DALYs were: 17,660 for hip fractures, 62,630 for congestive heart failure, 64,710 for myocardial infarction, 90,337 for COPD, 93,996 for stroke, 142,012 for cancer, 117,534 for diabetes, 186,586 for back pain, 333,420 for arthritis, and 378,849 for hypertension. In total, there were an estimated 1,487,734 years of healthy life lost from the 10 health conditions examined over the study period.

Link: https://doi.org/10.1186/s12877-019-1110-6

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Cholesterol Managers Want to Double Statin Prescriptions

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Cholesterol is found in nearly every cell in your body. This waxy substance is vital for optimal functioning of cell membranes, regulating protein pathways and supporting brain health, hormone levels and reducing your heart disease risk. Your body also uses cholesterol to manufacture vitamin D after being exposed to the sun.

As Zoe Harcombe, Ph.D., has noted,1 “It is virtually impossible to explain how vital cholesterol is to the human body. If you had no cholesterol in your body you would be dead.” The majority of the cholesterol in your body, approximately 80%, is manufactured in your liver,2 suggesting your body cannot survive without it.

The remaining 20% is absorbed from the foods you eat but only at a rate of 20 to 60% of what’s in your food. As Alice Lichtenstein, senior scientist and director of the cardiovascular nutrition laboratory at Tufts University, told Eating Well, the absorption rate depends on the individual,3 and if you consume less, your body compensates by making more.

In other words, there is a level at which your body attempts to maintain your cholesterol by manufacturing more or less in response to your dietary intake. Since animals use cholesterol in much the same way as humans, beef, pork and chicken have similar levels of cholesterol in the meat.

In the past decades cholesterol has been vilified as a primary culprit in heart disease. Merck brought the first statin drug, Lovastatin, aka Mevacor, to market in 1987.4,5 Since then, statins have gone on to become the biggest selling class of pharmaceutical compounds of all time, with annual sales in excess of $19 billion in 2017 and projected to reach $24.4 by 2022.6,7 Although the growth has been rapid, recent data demonstrate physicians are not prescribing statins to all eligible patients.8

Physicians Not Offering Statins to Eligible Patients

According to research from the Centers for Disease Control and Prevention (CDC),9 36.7% of U.S. adults over the age of 21 met the eligibility requirements in 2015 for cholesterol lowering treatment with statins as defined by the 2013 guidelines issued by the American College of Cardiology and the American Heart Association.

These guidelines define four groups said to benefit from statins,10 including those with atherosclerotic cardiovascular disease, diabetes and low-density lipoprotein (LDL) cholesterol levels between 70 and 189 milligrams per deciliter (mg/dL). According to the CDC, 55% (43 million American adults)11 who fit the criteria are currently taking statin medication.

Despite these extraordinary numbers, a new study12 from Duke University Medical Center finds 26.5% of U.S. adults who fit the current criteria to use cholesterol-lowering drugs are not taking them. The study is suggesting this occurs since doctors do not offer the drugs to their patients or the patients express concern over the side effects.13

The guidelines were expanded by the U.S. Preventive Services Task Force14 to include individuals who did not have a prior history of heart disease but who had concurrent health conditions that may place them at higher risk for heart attack in the future, such as obesity, high blood pressure, diabetes, high cholesterol and age.

According to the current survey, 59.2%15 who were not taking the drug said their physician had not offered them a prescription. This was most common among women, black people and uninsured patients.

In an email to Reuter’s, Dr. Ian Kronish, associate director of the Center for Behavioral Cardiovascular Health at Columbia University Irving Medical Center, commented on the findings, saying some physicians may not have been completely behind the changes to the guidelines published in 2013, particularly for patients who didn’t have extremely high cholesterol levels or a previous history of heart disease.16

How Do Statins Work?

Statins don’t stop your body from absorbing cholesterol from your food, but rather prevent your liver from making the cholesterol it was designed to produce by blocking an enzyme in the mevalonate pathway called HMG-CoA reductase, used to make cholesterol in the liver.

Essentially, this classification of drugs blocks the mevalonate pathway, which plays a key role in multiple cellular processes, not just the production of cholesterol. Although studied with regard to cholesterol synthesis, the extent of the impact of the mevalonate pathway is not fully understood.17

The drugs also deplete your body of coenzyme Q10 (CoQ10), which may in part account for many of its devastating long-term results. A black box warning was proposed to warn patient and physicians about this reduction in CoQ10,18 but in 2014 the FDA decided against it.19

CoQ10 is used in energy production by every cell in your body and is vital for optimal health and longevity. In its reduced form, ubiquinol, it’s a crucial component of cellular respiration and the production of adenosine triphosphate (ATP), a coenzyme used as an energy carrier in every cell in your body. Since your heart is the most energy demanding organ, depleting this energy supply can have devastating consequences.

Former FDA Commissioner Had Strong Ties to Big Pharma

The featured study was performed at Duke University by scientists with a history of producing research supporting statin use and calling for a greater number of prescriptions in patients who may not have had a previous history of heart disease,20,21,22,23,24 continuing a legacy of pharmaceutical support left by Dr. Robert Califf,25 who served as U.S. Food and Drug Administration (FDA) commissioner from February 2016 until January 2017.26

In May 2014, Califf, a Duke cardiologist and study chairman, gave a presentation27 to a group of experts, describing ways to increase the pace of innovation through the transformation of the research process. Specifically, his last slide called for a plan to simplify the regulatory systems governing research, believing it may have slowed biomedical innovation.

This was near the end of his association with Duke University, as he was soon to be nominated by then President Barack Obama as the FDA commissioner.28 During his confirmation hearings he defended his position in accepting drug industry funding and promised to not lower the agency’s safety standards.

When questioned by senators, Califf attempted to disarm his previous statement that regulations governing research were too complicated and slowed innovation by saying,29 “I’ve never been a proponent of lowering standards. If anything, I’ve argued for raising them.”

According to The New York Times,30 Califf had been associated with scientific papers produced by pharmaceutical company researchers, he’d been paid by seven drug companies and a device maker for consulting services, and his university salary was partially supported by drug companies, including Merck, Novartis and Eli Lilly.

In a conflict of interest section at the end of one paper, he declared financial support from more than 20 companies and research entitites.31 Daniel Carpenter, a Harvard political science professor with an expertise in the FDA calls him the “ultimate industry insider.”32

Califf also resigned from the board of directors at Portola Pharmaceuticals on January 26, 2015, just prior to his nomination as FDA commissioner, having received compensation of $259,623.33

Recently, Duke Clinical Research Institute paid $112.5 million to settle claims that bogus research data34 were submitted to the National Institutes of Health to acquire grant money for research.35 Seven years of data were determined to be unreliable.

Risks Associated With Statins Supported by Science

Among those who were offered but declined statins in the featured study,36 the most common reason stated was fear of side effects from the drugs.37 Senior study author Dr. Ann Marie Navar from the Duke Clinical Research Institute38 believes public perception of side effects is unrealistic. She commented:

“Although there are risks associated with statins, the public fear of side effects is out of proportion to the actual risks. Misconceptions about statins are everywhere and are fueled by false information on the internet.”

However, despite Navar’s attempt to downplay the side effects of statin medications, the risks are well-documented and supported by scientific evidence, so the fears are well-founded. According to the FDA:39

  • There have been rare reports of serious liver problems. Patients should notify their health care professional right away if they have the following symptoms: feeling unusually tired or weak; loss of appetite; upper belly pain; dark colored urine; yellowing of the skin or the whites of the eyes.
  • Memory loss and confusion have been reported. The conditions are generally non-serious and reversible after stopping statin use.
  • Increases in blood sugar levels have been reported.
  • Before starting a statin, patients should inform their health care professional about all medicines that they are taking or plan to take. Some medicines may interact with statins, increasing the risk for side effects.

However, these are only the side effects acknowledged by the FDA and not the full scope of the effects supported by research. A reduction in CoQ10 triggered by this classification of drugs may increase your risk of acute heart failure40 and atherosclerosis, as found in data published in Expert Review of Clinical Pharmacology.41

The study addressed several physiological mechanisms, including how the drug inhibits the synthesis of vitamin K2, which is responsible for protecting your arteries from calcification. One of its biological roles is to move calcium out of your blood and into the proper areas of your body, such as your bones and teeth.

Since statins inhibit the function of vitamin K2,42 it may place you at risk of deficiency, which may contribute to osteoporosis, heart disease, brain disease and inappropriate calcification. The same enzyme used by your liver to produce cholesterol that is inhibited by statins is also involved in the production of ketone bodies.

The depletion of CoQ10 and the inhibition of vitamin K2 also increases your risk of other serious diseases including cancer. Long-term statin use more than doubles a woman’s risk of two types of breast cancer,43 and significantly increases a man’s risk for prostate cancer.44 Research has also associated statin use with an increased risk of diabetes,45,46,47 neurodegenerative diseases,48 cataracts49,50 and musculoskeletal disorders.51

How to Evaluate Your Risk of Heart Attack

As you consider whether taking statins make sense for your health, it’s important to understand what your cholesterol numbers mean. Your total cholesterol is not a strong indicator of your risk of heart disease. Better indicators are:

  • The ratio of your high-density lipoprotein (HDL) to total cholesterol — To get this number, divide your HDL level by your total cholesterol and multiply by 100 to get the answer. Ideally, your HDL to cholesterol ratio would be 24% or above.
  • Your triglyceride to HDL ratio — Your triglyceride to HDL ratio should ideally be below 2.

Two tests that are even more important for assessing your cardiovascular disease risk are your serum ferritin and gamma glutamyl transpeptidase (GGT). The GGT is used as a screening marker for excess free iron and a great indicator of your risk of sudden cardiac death. The recommended and ideal levels of ferritin and GGT are as follows. For more information about these tests, read my previous article, “Cholesterol Does Not Cause Heart Disease.”

Ferritin — Adult men and non-menstruating women: 30 to 40 nanograms per milliliter (ng/mL) or 75 to 100 nanomoles per liter (nmol/L).

The most commonly used threshold for iron deficiency in clinical studies is 12 to 15 ng/mL (30 to 37 nmol/L). You do not want to be below 20 ng/mL (50 nmol/L) or above 80 ng/mL (200 nmol/L). High iron during pregnancy is also problematic; having a level of 60 or 70 ng/mL (150 or 175 nmol/L) is associated with greater odds of poor pregnancy outcomes.

GGT — Below 16 units per liter (U/L) for men and below 9 U/L for women. Above 25 U/L for men and 18 U/L for women, your risk of chronic disease increases significantly.

Protect Your Heart and Lower Your Risk of Heart Disease

Here are a number of suggestions to help protect yourself against heart disease. For further discussion of how lifestyle factors impact your risk, see my previous article, “Nearly Half of American Adults Have Cardiovascular Disease.”

Avoid environmental pollutants and toxins, including smoking, vaping, heavy metals, herbicides and pesticides, especially glyphosate.

Minimize your exposure to electromagnetic fields and wireless radiation from cellphones, Wi-Fi, routers, smart meters and more, as this kind of radiation has been shown to cause serious free radical damage and mitochondrial dysfunction.

Eat an unprocessed whole food-based diet low in net carbs and high in healthy fats. A ketogenic diet — which is very low in net carbohydrates and high in healthy fats — is key for boosting mitochondrial function.

When your body is able to burn fat for fuel, your liver creates water-soluble fats called ketones that burn more efficiently than carbs, thereby creating fewer reactive oxygen species and secondary free radicals. Ketones also decrease inflammation and improve glucose metabolism.52

Eat nitrate-rich foods to help normalize your blood pressure. Good sources include arugula, cilantro, rhubarb, butter leaf lettuce, mesclun mixed greens, beet greens, fresh beet juice, kvass (fermented beet juice) and fermented beet powder.

Get plenty of nonexercise movement each day; walk more and incorporate higher intensity exercise as your health allows.

Intermittently fast. After you’ve become accustomed to intermittently fasting for 16 to 18 hours, you may try a stricter fast once or twice a week, when you eat a 300- to 800-calorie meal loaded with detox supporting nutrients, followed by a 24-hour fast. So, in essence, you’re then only eating one 300- to 800-calorie meal in 42 hours.

If you have heart disease, consider enhanced external counterpulsation (EECP). To find a provider, see EECP.com.53

If you have heart disease, you may also consider taking g-strophanthin, an adrenal hormone helping to create more parasympathetic nervous system neurotransmitters, thereby supporting your parasympathetic nervous system. It also helps flush out lactic acid. Strophanthus is the name of the plant, the active ingredient of which is called g-strophanthin in Europe, and ouabain in the U.S.

Get sensible sun exposure to optimize your vitamin D status and/or take an oral vitamin D3 supplement with magnesium and vitamin K2.

Implement heart-based wellness practices such as connecting with loved ones and practicing gratitude.

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Electrostimulation Improves Working Memory in Old People

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Researchers here report on a demonstration in which they used electrostimulation to improve the working memory of old people to put it on a par with young people. It will be interesting to watch the investigation into the underlying mechanisms in the years ahead, though I expect it will be quite difficult to work backwards from such a non-invasive stimulus focused on brain waves, and into the underlying biochemistry of the brain.


Researchers have demonstrated that electrostimulation can improve the working memory of people in their 70s so that their performance on memory tasks is indistinguishable from that of 20-year-olds. The research targets working memory – the part of the mind where consciousness lives, the part that is active whenever we make decisions, reason, recall our grocery lists, and (hopefully) remember where we left our keys. Working memory starts to decline in our late 20s and early 30s, as certain areas of the brain gradually become disconnected and uncoordinated. By the time we reach our 60s and 70s, these neural circuits have deteriorated enough that many of us experience noticeable cognitive difficulties, even in the absence of dementias like Alzheimer’s disease.

Researchers asked a group of people in their 20s and a group in their 60s and 70s to perform a series of memory tasks that required them to view an image, and then, after a brief pause, to identify whether a second image was slightly different from the original. At baseline, the young adults were much more accurate at this, significantly outperforming the older group. However, when the older adults received 25 minutes of mild stimulation delivered through scalp electrodes and personalized to their individual brain circuits, the difference between the two groups vanished. Even more encouraging? That memory boost lasted at least to the end of the 50-minute time window after stimulation – the point at which the experiment ended.

Coupling occurs when different types of brain rhythms coordinate with one another, and it helps us process and store working memories. Slow, low-frequency rhythms – theta rhythms – dance in the front of your brain, acting like the conductors of an orchestra. They reach back to faster, high-frequency rhythms called gamma rhythms, which are generated in the region of the brain that processes the world around us. But when the theta rhythms lose the ability to connect with those gamma rhythms to monitor them, maintain them, and instruct them, then the melodies within the brain begin to disintegrate and our memories lose their sharpness. Meanwhile, synchronization, when theta rhythms from different areas of the brain synchronize with one another, allows separate brain areas to communicate with one another. This process serves as the glue for a memory, combining individual sensory details to create one coherent recollection. As we age, our theta rhythms become less synchronized and the fabric of our memories starts to fray.

The present work suggests that by using electrical stimulation, we can reestablish these pathways that tend to go awry as we age, improving our ability to recall our experiences by restoring the flow of information within the brain. And it’s not just older adults that stand to benefit from this technique: it shows promise for younger people as well. In the study, 14 of the young-adult participants performed poorly on the memory tasks despite their age – so the researchers called them back to stimulate their brains too. “We showed that the poor performers who were much younger, in their 20s, could also benefit from the same exact kind of stimulation. We could boost their working memory even though they weren’t in their 60s or 70s. Coupling and synchronization exist on a continuum. On one end of the spectrum, someone with an incredible memory may be excellent at both synchronizing and coupling, whereas somebody with Alzheimer’s disease would probably struggle significantly with both. Others lie between these two extremes-for instance, you might be a weak coupler but a strong synchronizer, or vice versa.”

Link: https://www.bu.edu/research/articles/electrostimulation-can-improve-working-memory/

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Even Early Stage Kidney Disease Causes Cognitive Impairment

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The link between age-related kidney dysfunction and cognitive impairment is an interesting one, particularly in the context of research into klotho, which has functions in both the kidney and the brain, and has been shown to extend life and improve cognitive function in animal studies. It isn’t completely clear as to which of these areas of the body is most important to the noted benefits to cognitive function in animal models, produced via various strategies for klotho overexpression. The most recent research on this topic tends to suggest that the mechanisms are indirect, involving many organ systems, rather than being a direct effect in the brain. Klotho in the brain might not be as important as initially thought.


The link between brain dysfunction and chronic kidney disease (CKD) was first noted in 1930, so it is not a new finding. Experts spoke of “dialysis dementia” or “uremic encephalopathy“. What is new, however, is the finding that mild cognitive impairment (MCI) may already be present in earlier stages of CKD, affecting approximately one in two CKD patients (prevalence varies in studies between 30% and 60%). In contrast to “normal” dementia, CKD-related MCI is not age-related, meaning the cognitive impairment exceeds that expected of the normal aging process. It usually worsens with declining glomerular filtration rate (GFR) of patients – the lower the GFR, the higher the risk of being affected by cognitive impairments.

The pathogenesis appears complex, involving a variety of factors besides vascular disease – the most frequent trigger for “standard” dementia in elderly people. Dialysis does not help or stop the process of cognitive decline, thus experts believe that factors which are not corrected completely by dialysis, for example the clearance of middle molecules, uncontrolled secondary hyperparathyroidism and anemia, may further the process of cognitive impairment. One interesting finding, though, is that kidney transplantation appears to slow cognitive decline.

The paucity of intervention strategies is the reason why there is no routine screening for MCI in CKD patients. Cognitive decline is one of many manifestations of brain damage that clearly accompany the decline of kidney function. Other manifestations include sleep disorders and depression, both of which are also common in CKD patients. “Chronic kidney disease is an illness that obviously affects the body and the brain. The latter has been neglected by research, but new tools in neuroscience, such as tractography or two-photon microscopy hold out the promise of gaining further insights in the pathogenesis of MCI so that we might identify therapy targets and be able to treat it one day. Until then, we have to be aware that CKD is a severe disease which affects not only the kidneys, but also other organs systems and the brain – even in early stages. This is why we should strengthen CKD prevention strategies and raise awareness for this illness that is much more severe than most people think.”

Link: https://www.eurekalert.org/pub_releases/2019-04/e-kdt041019.php

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Evidence for Age-Related Epigenetic Changes to Increase Cancer Risk

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Researchers here use organoid models of tissue to recapitulate some of the epigenetic changes that occur in the bodies of old individuals, as a way to investigate how those changes alter the risk of cancer. There are of course numerous factors involved in the fact that cancer risk is age-related: rising levels of mutational damage; the above mentioned epigenetic changes that diminish protective anti-cancer mechanisms inside cells; inflammatory tissue environments that support the very early growth of precancerous cells; the declining ability of the immune system to find and destroy cancerous cells. Evidence suggests that the latter item, the aging of the immune system, is the most important factor over the course of the present human life span, but until the research community can repair or reverse that process, it will be hard to say in certainty.


Most cancers contain epigenetic and genetic alterations, but how they work together to cause cancer was not well understood. Researchers have found that epigenetic alterations characterized by changes in DNA methylation – a process by which cells add a tiny methyl group to a beginning region of a gene’s DNA sequence, often silencing the gene’s activation – are a key component of cancer initiation. In their laboratory model, known cancer-driving gene mutations did not cause colon cancers to form unless epigenetic methylation changes to the DNA were also present.

Cancer is primarily a disease of aging, with the majority of cancers occurring in people over age 60. To study colon cancer in the setting of aging, researchers used a mouse colon organoids derived from six- to eight-week old mice. Organoids are lab-grown cells that clump together and resemble specific normal organs, such as the colon in this case, and can grow indefinitely. The researchers compared colon organoids with and without mutations in the BRAFV600E, a known cancer-driving gene mutation common particularly to human right sided colon cancer. As the organoids aged, they remained genetically stable but became epigenetically unstable, even without the BRAF mutation being introduced. The scientists found that acquired DNA methylation during “aging” of the organoids, silenced cancer protective genes in a pattern similar to human aging that associates with risk for colon cancer by decade.

The team engineered the colon organoids to contain a transgenic BRAF mutation they could activate on demand. In all of the BRAF-activated organoids, DNA methylation was necessary for the mutation to initiate tumor development. Without this epigenetic change, the mutation did not initiate cancer in mice. “Essentially, we ‘aged’ young cells to become old, methylation-wise. In general, the risk of cancer increases with age, but if we can shift the epigenetic landscape through lifestyle changes to limit the impact of methylation fluctuations, we might be able to prevent cancer from developing. Although these studies were done to examine BRAFV600E-mediated tumorigenesis, we believe our findings apply to the cancer driver roles of other oncogenic mutations.”

Link: https://www.hopkinsmedicine.org/news/newsroom/news-releases/johns-hopkins-researchers-create-novel-cell-model-of-aging-related-colon-cancer-risk

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What Air Pollution Does to Your Body

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In April 2019, London launched an ultralow emission zone in central London, which will charge motorists more than $16 a day to drive into the area, unless they meet certain strict emissions standards. The move is expected to cut emissions from motor vehicles by about 45 percent in central London.1

Seventy-two percent of London adults said they supported the measure to charge vehicles that pollute, as London mayor Sadiq Khan described air pollution in the city as a “public health emergency.”2 In the U.K., air pollution causes about 40,000 deaths annually,3 echoing death rates from air pollution across the globe.

Research published in The Lancet revealed that 9 million premature deaths were caused by pollution in 2015, which is 16 percent of deaths worldwide — “three times more deaths than from AIDS, tuberculosis and malaria combined and 15 times more than from all wars and other forms of violence,” the researchers wrote.4

Damage From Air Pollution Starts in the Womb

Breathing polluted air causes insidious damage that starts in the womb and adds up over your lifetime. In the U.S. alone, more than 3% of premature births haven been attributed to air pollution, specifically particulate matter (PM 2.5).5

PM 2.5 refers to dust, dirt, soot, and smoke — particles smaller than 2.5 micrometers in diameter. It’s the most studied type of air pollution. These particulates can enter your system and cause chronic inflammation, which in turn increases your risk of a number of health problems, from cancer to heart and lung disease.

Costs attributed to the 3.32% of premature births linked to air pollution were estimated at $5.09 billion. As researchers noted, “Reducing rates of PTB [preterm birth] is important to prevent not only neonatal complications such as respiratory distress syndrome, sepsis and intraventricular hemorrhage, but also adverse psychological, behavioral, and educational outcomes in later life, mostly related to cerebral palsy and neurodevelopmental delay.”6

Exposure to air pollution has also been linked to low birth weight babies, intrauterine growth retardation, stillbirth, congenital anomalies and problems with fetal brain growth.7

It’s long been questioned how developing babies could be harmed by their mother’s air pollution exposure, but research presented at the European Respiratory Society International Congress revealed that pollution particles may enter the placenta and possibly harm the developing baby in utero.

The study was small, involving placentas from five London women, but revealed what researchers believe to be carbon particles in some placental macrophage cells. Study author Dr. Norrice Liu of Queen Mary University of London explained:8

“Our results provide the first evidence that inhaled pollution particles can move from the lungs into the circulation and then to the placenta. We do not know whether the particles we found could also move across into the fetus, but our evidence suggests that this is indeed possible.

We also know that the particles do not need to get into the baby’s body to have an adverse effect, because if they have an effect on the placenta, this will have a direct impact on the fetus.”

Air Pollution Is Deadly to Children

Air pollution is responsible for respiratory diseases that kill 543,000 children aged 5 years and younger each year, according to the World Health Organization (WHO). Breathing polluted air also causes asthma in 14% of children around the globe.9

“Polluted air is poisoning millions of children and ruining their lives,” said Tedros Adhanom Ghebreyesus, WHO Director-General. “This is inexcusable. Every child should be able to breathe clean air so they can grow and fulfil their full potential.”10 Sadly, WHO estimates that about 93% of the world’s children (or 1.8 billion) live in areas that have such polluted air their health and development are at risk.

Even in children living in one of London’s low-emission zones, researchers found their lung capacity was reduced by about 5 percent when pollution rose above legal levels — and no improvements in lung capacity were seen even when small improvements in air quality occurred. “Interventions that deliver larger reductions in emissions might yield improvements in children’s health,” the researchers concluded.11

Researchers in London are now giving air-monitoring backpacks to 250 London schoolchildren, who will wear the bags for one week. The scientists are trying to determine where children are exposed to the most air pollution in order to make recommendations to curb their exposure and hopefully improve lifelong health.

“Air pollution has been found to restrict lung growth in children. Low lung function in childhood can persist into adulthood and is often associated with other health problems including chronic obstructive lung disease in later life, said Ben Barratt of King’s College London in a news release.12

How Corn Is Polluting the Air

Vehicle emissions are a commonly referred to culprit in air pollution, but corn, a major agricultural crop used for animal feed, ethanol biofuel and food, is another, often-overlooked source. Air pollution that results from growing corn is associated with 4,300 premature deaths per year in the U.S. alone, researchers wrote in Nature Sustainability — with associated damages estimated at $14 billion to $64 billion.13

Most of the pollution is due to emissions of ammonia from the heavy use of nitrogen fertilizer. “Ammonia from fertilizer application accounted for about 70 percent of attributable deaths,” study author Jason Hill of the University of Minnesota told NPR. “Some of that nitrogen washes into waterways, and some of it gets released into the atmosphere as ammonia.”14

As nitrogen fertilizers break down into their component parts, ammonia is released into the air. When the ammonia in the atmosphere reaches industrial areas, it combines with pollution from diesel and petroleum combustion, creating microparticles. Concentrated animal feeding operation (CAFO) workers and neighboring residents alike report higher incidence of asthma, headaches, eye irritation and nausea.

Research published in the American Journal of Respiratory and Critical Care Medicine also revealed that markers of lung function were related to how far they lived from CAFOs.15

The closer they lived to the factory farms, and the greater the density of livestock, the more impairments in lung function were revealed. Lung function of neighboring residents declined in concert with increased levels of CAFO-caused ammonia air pollution, the study revealed.16

Corn is a double-edged sword, polluting the air not only on the farm but also at the CAFOs where it’s used for animal feed. There are other trickle-down effects as well. “Growing corn in Minnesota results in emissions in Florida, where phosphate fertilizer is produced,” Hill said.17

Agriculture Is the No. 1 Source of Air Pollution

The No. 1 cause of air pollution in much of the U.S., China, Russia and Europe is linked to farming and fertilizer — specifically to the nitrogen component of fertilizer used to supposedly enrich the soil and grow bigger crops.

In fact, research published in the journal Geophysical Research Letters demonstrated that in certain densely populated areas, emissions from farming far outweigh other sources of particulate matter air pollution.18

Researchers have long known soil microbes convert nitrogen-based fertilizers to nitrogen oxides and release them into the air. However, it was estimated that only 1 kilogram of gas was produced per 100 kilograms of fertilizer, or roughly 1 percent. Researchers thought the amount of gas would increase linearly, or stay at 1 percent of the amount of fertilizer used.

However, further experimentation found the increase was exponential and not linear, as the original research didn’t account for conversion when excess nitrogen fertilizer was applied to the fields. In California, agricultural lands may be responsible for as much as 51 percent of nitrogen oxides off-gassing across the state, especially in areas that use synthetic nitrogen-based fertilizers.19

CAFOs are also highly problematic, as they vent manure-laden air into the surrounding environment 24/7.20 In addition to ammonia, other toxic compounds commonly released by CAFOs include:21

  • Hydrogen sulfide, which has a rotten egg odor and can cause inflammation of eye and respiratory tract membranes, loss of olfactory neurons and even death
  • Methane, an odorless but highly flammable greenhouse gas
  • Particulate matter, including particles from feed, bedding, dry manure, soil, animal dander and feathers, which can cause chronic bronchitis and respiratory symptoms, declines in lung function and organic dust toxic syndrome, a severe flu-like illness

Air Pollution Linked to Diabetes, Damage to Brain and Heart

Breathing polluted air is detrimental to your health at all ages, including in adulthood. While lung function is known to decline gradually with age, there is evidence that air pollution accelerates this decline. Living in an area with higher levels of air pollution is also linked to the development of Type 2 diabetes in adults, as well as decreased cognitive function22 and sleep disturbances.23

“Evidence that exposure to air pollution affects brain structure was found by magnetic resonance imaging (MRI) of participants in the Framingham Offspring Study, indicating that higher exposure to PM2.5 is associated with a reduction in total brain volume,” according to a Royal College of Physicians report.24 As for the damage air pollution does to your heart, researchers explained:25

The evidence for the effects of both short- and long-term exposures to air pollution on cardiovascular disease in adults is strong. Exposure to air pollution can exacerbate existing heart conditions and contribute to the development of cardiovascular disease, resulting in increased hospital admissions and deaths from cardiovascular disease.”

Ways to Combat Air Pollution’s Drain on Your Health

In an ideal world, we’d all live in an environment with fresh, clean air to breathe. Unfortunately, this is far more the exception than the rule. In your home, indoor air can be a major source of contaminants, so I recommend taking steps to keep your indoor air clean, including opening windows to let fresh air in and avoiding the use of known air pollutants like chemical cleaning products, air fresheners and scented candles.

Purifying your home’s air is also a wise step, as is leading a healthy lifestyle. What you eat can help combat air pollution’s health effects, for instance, including anti-inflammatory omega-3 fats, which may help protect your heart from air pollution.26

Other nutrients to eat plenty of, especially if you live in a polluted area, include vitamins C and E, which may be beneficial to children with asthma,27 and B vitamins, which in high doses have been show to completely offset damage caused by very fine particulate matter in air pollution.28

At a more foundational level, the researchers of the corn study suggested “strategic interventions” in corn production, “including changing the fertilizer type and application method, improving nitrogen use efficiency, switching to crops requiring less fertilizer, and geographically relocating production.”29

On a personal level, be sure to choose organic, biodynamic grass fed foods as much as possible, and avoid those from industrial farms, which are making air pollution problems worse instead of better.

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Calorie Restriction Affects the Plasticity of Fat Tissue, Not Just the Amount of Fat Tissue

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The practice of calorie restriction, a reduction of up to 40% below the usual ad libitum calorie intake, while still obtaining optimal levels of dietary micronutrients, is well known to slow aging and extend life in near all species and lineages tested to date. Calorie restriction produces sweeping changes in the operation of cellular metabolism, such as upregulation of a range of cellular stress responses, including the maintenance processes of autophagy. It also, however, has the obvious outcome of greatly reducing body fat, particularly the visceral fat that clusters around the organs of the abdomen.

Visceral fat tissue is metabolically active and quite harmful over the long term, so there is always the question of the degree to which the benefits of calorie restriction derive from loss of fat tissue versus upregulated autophagy and the like, and how that balance is different between species. Visceral fat tissue creates chronic inflammation via a variety of mechanisms: cell signaling that is similar to the results of infection; the immune response to debris from dead fat cells; increased numbers of senescent cells in fat tissue. Chronic inflammation then accelerates the development and progression of all common age-related disease. We can see this in the epidemiology of the obese and overweight, as these individuals suffer a shorter life expectancy, a greater risk of age-related disease, and higher lifetime medical costs, with these disadvantages scaling in size with ever greater excess fat tissue.

Yet, on the other hand, if autophagy is disabled through genetic manipulation, calorie restriction no longer functions to extend life span in mice. This data strongly argues for the primacy of upregulated cellular housekeeping over loss of visceral fat tissue as the primary driver of slowed aging via calorie restriction. Yet again, consider that researchers have also shown that surgical removal of visceral fat from mice has a significant effect on life span, though not as great as calorie restriction, which argues an opposite conclusion. It is a challenging phenomenon to investigate.

The open access paper noted here discusses another fat-related aspect of the calorie restriction response, which is to enhance the plasticity of fat deposits, their ability to transform from harmful to beneficial forms of fat tissue. Taken at the high level, white fat is harmful, while brown fat is beneficial – the real picture is somewhat more complex, but this will do as a starting point. As we age the browning of white fat is diminished, but calorie restriction helps to maintain this function, with consequent benefits to health over the long term, distinct from those related to the amount of fat present in the body.

Long-term caloric restriction ameliorates deleterious effects of aging on white and brown adipose tissue plasticity


Aging is associated with an increased risk of metabolic disorders such as obesity, insulin resistance (IR), and other manifestations of metabolic syndrome in both humans and rodents. In parallel with these alterations, a low grade of inflammation has also been described in several tissues associated with aging. Aging is typically associated with increased adiposity and redistribution of adipose tissue (AT), characterized by a loss of subcutaneous adipose depot mass and a gain of fat in the abdominal visceral compartment.

Caloric restriction (CR) is the most efficient intervention to delay the deleterious effects of age-related metabolic diseases. Previous studies in several animal models have shown that CR has physiological effects on lifespan, and reduces body weight and glucose and insulin serum levels. Whether CR interventions in humans slow aging is not yet known. Accumulating data indicate that moderate CR with adequate nutrition has numerous beneficial effects against obesity, diabetes, inflammation, and cardiovascular diseases. However, the mechanisms involved in the amelioration of aging effects by CR are not well understood. Accretion of AT has been related to the development of age-associated metabolic alterations such as IR. Moreover, reduction of adiposity by CR or fat removal have demonstrated to ameliorate age-associated IR. The improvement of the metabolic status achieved by CR may well be due, at least in part, to the decreased adiposity.

Furthermore, increased adiposity by hypertrophy and/or hyperplasia has been demonstrated to increase macrophage infiltration. This circumstance, together with changes in adipocyte physiology that includes hypoxia, reticulum, and oxidative stress, leads to an inflammatory state which is a key factor in the AT expandability capacity. Nevertheless, AT is a complex organ with different localizations and functions beyond its traditional role as a fat storage unit.

A complete understanding of CR effects on AT biology requires the elucidation of whether these effects are preferentially mediated by white AT (WAT) and/or brown AT (BAT), the contribution of specific WAT depots, and the relevance of differentiation/trans-differentiation to beige AT. WAT also has an important endocrine role by secreting different peptide hormones (adipokines) including adiponectin, which regulates insulin sensitivity, as well as glucose and energy homeostasis. In contrast to WAT, BAT plays a central role in energy expenditure via expression of uncoupling protein 1 (UCP-1). BAT is the major site for both cold- and diet-induced thermogenesis, and its atrophy has been observed in obese and older individuals in association with increased visceral fat and hyperglycemia. Consequently, defective WAT and BAT function may exacerbate the development of metabolic complications of obesity/aging.

Here, we aimed to investigate whether the plasticity of the WAT and BAT depots (hypertrophy and/or hyperplasia, extracellular matrix remodeling, inflammation, and browning or whitening capacity) is differentially affected at middle age, and whether moderate CR results in beneficial metabolic effects regulating the functionality of these AT depots. We show that several metabolic alterations of old animals are already being developed in middle-aged animals. These alterations include development of IR, altered WAT and BAT plasticity, as well as alteration of thyroid axis status, which can be mitigated, at least to some extent, by moderate and long-term CR.

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Don’t Be Fooled by New Egg Warnings

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While the consumption of chicken as a source of protein has become popularized in recent decades, eggs have been unfairly vilified, in part because of misconceptions regarding their cholesterol content. For decades, the American public was told that eggs, as a source of cholesterol and saturated fats, promote heart disease.

However, in recent years, studies have clearly shown that eggs — particularly egg yolks — are one of the healthiest foods you can eat, and even though egg yolks are relatively high in cholesterol, numerous studies have confirmed eggs have virtually nothing to do with raising your cholesterol, having only a minimal impact on plasma lipoprotein levels.1 As previously reported by NPR:2

“[E]ating cholesterol can raise levels of it in the blood, but, as a growing body of research has shown, not by that much. Consuming sugar, trans fats or excessive saturated fat (from unhealthy sources) can be more harmful to cholesterol levels than dietary cholesterol itself.

Most of the cholesterol in our bodies we make ourselves in the liver, and total body levels are heavily influenced by genetics, gender and age. As more and more research suggests that some degree of cholesterol consumption is harmless, if not healthy, the egg’s reputation is gradually returning.”

In 2015, dietary cholesterol (and egg restriction) was finally eliminated from the U.S. dietary guidelines, and the controversy appeared to have settled. Now, a new study is again urging people to avoid eggs, linking egg consumption and dietary cholesterol to an increased risk of cardiovascular disease and death.

New Study, Old Arguments

The study3,4,5 in question, published in the journal JAMA on March 19, 2019, analyzed data from 29,615 American adults pooled from six prospective cohort studies with a median follow-up of 17.5 years, and claims to have found a dose-dependent relationship between egg consumption and cardiovascular disease (CVD) and all-cause mortality.

The researchers calculated two risk ratios: an adjusted hazard ratio (HR) and an adjusted absolute risk difference (ARD). According to this study:

Each 300 milligrams (mg) of dietary cholesterol consumed per day (equating to approximately one and a half eggs) had a:

HR of 17 percent and an ARD of 3.24 percent for CVD

HR of 18 percent and an ARD of 4.43 percent for all-cause mortality

Even each additional half an egg consumed per day was associated with higher risk of incident CVD and all-cause mortality

Eating three to four eggs per week was associated with a:

HR of 6 percent and an ARD of 1.11 percent for CVD

HR of 8 percent and an ARD of 1.93 percent for all-cause mortality

According to lead researcher Wenze Zhong, Ph.D.,6 a postdoctoral fellow at the Feinberg School of Medicine at Northwestern University in the Department of Preventive Medicine, the results suggest there’s no safe amount of egg consumption, and the team believes the results should be taken into consideration when the U.S. dietary guidelines are updated.

“Any level of egg consumption is associated with increased risk of cardiovascular disease and mortality, because we found a dose-response association. Greater consumption means higher risk,” he told Runner’s World.7

What’s Wrong With This Egg Study?

A number of health and nutritional experts have already weighed in on the study, pointing out its multiple flaws. As noted by Runner’s World:8

“’For one, the amount of risk, or hazard, that’s reported here is trivial —and the way in which they calculated it doesn’t exactly lend itself to an easy determination of someone’s true risk,’ [Stuart] Phillips [Ph.D., director of the McMaster Centre for Nutrition, Exercise, and Health Research] said …

[T]he researchers noted there may be measurement error because the diet data was based on recall … Not only can this type of self-reported data be unreliable, but also, researchers assessed this only once … and assumed it didn’t change in an average of 17 years of follow-up.

Also, they stated that all cohorts used different dietary assessment tools, leading them to implement their own methodology to harmonize diet data. Finally, the study findings are observational, so while they can suggest a relationship, they can’t prove that one thing caused the other.”

Andrew Mente, Ph.D., principal investigator for the Epidemiology Program at the Population Health Research Institute, pointed out a clear contradiction in the data, telling Runner’s World:9

“The primary hypothesis here is that eggs increase your bad cholesterol, and the more you eat, the worse it gets. But buried way down in the appendix is a note that they found higher egg intake is related to a reduction in LDL, your bad cholesterol. So, what’s driving the association in this research? It seems like there’s a contradiction with the findings.”

I interviewed Dr. Malcolm Kendrick, author of “Doctoring Data: How to Sort Out Medical Advice From Medical Nonsense,” right after the study was published and he echoed Mente’s concerns above. Below is a slice of my upcoming interview with him.

Zoe Harcombe, who has a Ph.D., in public health nutrition, went a step further, listing no less than 10 different problems, including the following:10,11

The study found an association between egg consumption and CVD, but not coronary heart disease, which is a major part of CVD.

The meta-analysis included six studies, one of which was dominant, and all of which looked at American populations only, which means findings are not applicable to non-Americans, as dietary patterns are not generalizable between populations.

Association does not mean causation, and according to Harcombe, “17 percent is too small to get off the ground for Bradford Hill criteria,” also known as Hill’s criteria for causation.12

This refers to a set of nine principles commonly referred to when trying to establish evidence of a causal relationship between a proposed cause and an observed effect. The nine criteria include effect size (strength of association), reproducibility of effects, specificity, temporality, biological gradient, plausibility, coherence, experimental evidence and analogous evidence.

Harcombe explains the 17 percent relative risk saying, “It would equate to an absolute risk difference of 17 versus 15 events (i.e., two events) per 1,000 person years to use the event rate from the dominant study” of the six studies included in the analysis.

The study did not evaluate pure egg consumption. “It was a study of ‘Ingredients in mixed dishes,’” Harcombe says, “which — for eggs — means a long list of junk food from cakes to ice cream.”

They also did not adjust for significantly different CVD risk factors. Instead, it was assumed that different characteristics could have been caused by eggs and/or cholesterol.

Interestingly, people reporting the lowest intake of dietary cholesterol also had significantly lower energy intake overall — a mere one-third of the energy intake of those with the highest cholesterol intake. Harcombe suggests, “Maybe people weren’t eating more eggs or dietary cholesterol — they were just more honest about, or better at recalling, their food intake!”

The researchers also resorted to a strangely random selection when it came time to calculate the risk of harm from each additional half egg. “[S]ub-group analysis revealed that this only applied to specific, but random, groups of participants, e.g., women, but not men; slim, but not overweight people.”

And now for the BIG one — conflicts of interest — Harcombe points out they’re “the who’s who of statin manufacturers,” adding, “The paper appears to have as its core purpose resurrection of the diet-cholesterol-heart myth — the dietary cholesterol part of which was rejected … at least 65 years ago.”

Several Studies Have Confirmed Eggs Are Good for Your Heart

It’s also worth noting that several meta-analyses have refuted the claim that egg consumption raises your risk for CVD. Among them:

  • Research13 published in 2009 discovered that the proteins in cooked eggs are converted by gastrointestinal enzymes, producing peptides that act as ACE inhibitors (common prescription medications for lowering blood pressure) — a finding that supports the stance that eggs are in fact part of a heart-healthy diet.
  • A 2013 meta-analysis that found eating up to one egg per day “is not associated with increased risk of CVD or stroke.”14
  • A 2016 meta-analysis, which concluded that “Overall, summary associations indicate that intake of up to one egg daily may be associated with reduced risk of total stroke.” With regard to coronary heart disease, there was no clear association between egg intake and risk.
  • A 2017 analysis “reviewed the evidence of egg consumption on major CVD risk factors in individuals with or at risk for Type 2 diabetes (prediabetes, insulin resistance or metabolic syndrome),” finding “consumption of six to 12 eggs per week, in the context of a diet that is consistent with guidelines on cardiovascular health promotion, has no adverse effect on major CVD risk factors in individuals at risk for developing diabetes or with Type 2 diabetes.”
  • A 2018 meta-analysis looking at observational and interventional studies published within the past 10 years that addressed cholesterol intake and risk of CVD and Type 2 diabetes concluded that “Dietary patterns, physical activity and genetics affect the predisposition of CVD and T2D [Type 2 diabetes] more than a single food item such as eggs. In conclusion, up to seven eggs per week can safely be consumed, but in patients with established CVD or T2D only with special emphasis on a healthy lifestyle.”

Eggs Are an Important Part of a Healthy Diet

Instead of focusing on the faulty science that made you worry unnecessarily about consuming too much cholesterol, there are numerous reasons to go ahead and enjoy them. They’re loaded with valuable vitamins and minerals, including selenium, vitamins B2 (riboflavin), B5 (pantothenic acid), B7 (biotin) and B12, high-quality protein, iodine, vitamin D, zinc, omega-3 fats and more.15

Eggs are also an important source of lutein and zeaxanthin, two antioxidants known to play a role in healthy vision and the prevention of cataracts and macular degeneration.

Egg Yolks Are the Highest Source of Dietary Choline

Importantly, eggs are one of the best sources of choline available. Choline was officially recognized as an essential nutrient by the Institute of Medicine (IOM) in 1998. Egg yolks are the most concentrated source of choline in the American diet, providing 680 milligrams per 100 grams.16

Choline helps keep your cell membranes functioning properly, plays a role in nerve communications and prevents the buildup of homocysteine in your blood, which is good because elevated levels are linked to heart disease. Choline also helps reduce chronic inflammation.

This vital nutrient is also prized because it enables your body to make the brain chemical acetylcholine, which is involved in storing memories. In pregnant women, choline helps prevent birth defects such as spina bifida, while also playing a role in your baby’s brain development.

According to a study17 published in the journal Nutrients, only 8 percent of U.S. adults are getting enough choline — including only 8.5 percent of pregnant women. Among egg consumers, however, more than 57 percent meet the adequate intake levels for choline. Based on the outcomes, the study authors concluded that “it is extremely difficult to achieve the adequate intake for choline without consuming eggs or taking a dietary supplement.”18

Some of the symptoms associated with low choline levels include lethargy, memory problems and persistent brain fog. Because your body can only synthesize small amounts of this nutrient, you must get it from your diet on a regular basis.

Choline and Nonalcoholic Fatty Liver Disease (NAFLD) 

The two major fates for choline are to be phosphorylated and used to make phospholipids, or to be oxidized and used as a donor of methyl-groups. An especially important choline metabolite in the liver is phosphatidylcholine, which is necessary for the packaging and export of triglycerides in very low density lipoprotein (VLDL).

It has only recently been appreciated that you need choline to help remove triglycerides from your liver. So if you have insulin resistance from a poor diet and high triglycerides it will be vital to make sure that you increase your choline intake or you will radically increase your risk of nonalcoholic fatty liver disease (NAFLD). This is largely related to its role in phosphatidyl choline and transporting fats out of your liver.19

If you have normal triglycerides, choline augmentation is not as important for NAFLD but still plays a vital role in the other benefits described in the previous section. 

Also choline is an important part of the mitochondrial membrane and mitochondrial dysfunction is a central mechanism in the pathogenesis of NAFLD.20 Choline deficiency likely plays a major role in NAFLD because it disturbs mitochondrial bioenergetics21 and fatty acid oxidation.22

Not All Eggs Are Created Equal

When it comes to eggs, quality is important. Most of the eggs you find at your local grocery store come from concentrated animal feeding operations (CAFOs), which are known to be hotbeds for Salmonella infection.23 Eggs can become contaminated while they are being formed if the Salmonella bacteria exist inside a chicken’s ovaries.

As noted in the report,24,25 “Food Safety and Cage Egg Production” by the Humane Society, published in 2011, “All 16 scientific studies published in the last five years comparing Salmonella contamination between caged and cage-free operations found that those confining hens in cages had higher rates of Salmonella, the leading cause of food poisoning-related death in the United States.” Today, we also have antibiotic-resistant strains of salmonella to contend with, which makes potential contamination even more worrisome.

While there’s no way to guarantee 100 percent safety at all times, the benefits of free-range poultry are becoming more well-recognized, and reduced disease risk is definitely part of that benefits package. Unfortunately, loopholes abound, allowing CAFO-raised chickens and eggs to masquerade as “free-range” and “organic.”

It’s worth noting that “cage-free” still does not mean the chickens were raised under ideal conditions. They’re not raised in cages, but they may still not have access to the outdoors, and the organic label simply means the hens have been raised on organic feed. It is not an indication that they’ve been humanely or sustainably raised.

So, there are still significant differences even between “cage-free” and “free-range” (or “pastured”) eggs. With so many loopholes and lack of transparency, it can be very confusing to sort through it all. The Cornucopia Institute addresses these issues in its egg report and organic egg brand scorecard, which ranks 136 egg producers according to 28 organic criteria.

As noted by Mark A. Kastel, The Cornucopia Institute’s co-director and senior farm policy analyst, “The organic egg scorecard enables concerned consumers to select authentic brands delivering the very best quality eggs regardless of the hyperbole on the label.”

Best Certifications to Look for When Buying Milk, Meat and Produce

On a final side note, organic misdirection and outright fraud are also rampant in dairy and meat production, and dedicated organic leaders have struggled to come up with newer, stricter rules for true organics.

At present, two of the absolute best certifications are the American Grassfed Association (AGA) certification26 and the Demeter certification,27 which is biodynamic certification that goes far beyond mere organics.

The AGA certification covers meat and dairy from animals raised on a diet of 100 percent forage. The animals are never confined to a feedlot; never treated with antibiotics or hormones; and are born and raised on American family farms. These two certifications presently offer the absolute best assurances that the food you buy has been sustainably produced, without toxic chemicals or inhumane treatments.

Find out more about Nitric Oxide and Cardiovascular health.

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