The Benefits of High Cholesterol

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People with high cholesterol live the longest.

This statement seems so incredible that it takes a long time to clear one´s brainwashed mind to fully understand its importance.

Yet the fact that people with high cholesterol live the longest emerges clearly from many scientific papers.

Consider the finding of Dr. Harlan Krumholz of the Department of Cardiovascular Medicine at Yale University, who reported in 1994 that old people with low cholesterol died twice as often from a heart attack as did old people with a high cholesterol.

Supporters of the cholesterol campaign consistently ignore his observation, or consider it as a rare exception, produced by chance among a huge number of studies finding the opposite.

But it is not an exception; there are now a large number of findings that contradict the lipid hypothesis.

To be more specific, most studies of old people have shown that high cholesterol is not a risk factor for coronary heart disease.

This was the result of my search in the Medline database for studies addressing that question.

Eleven studies of old people came up with that result, and a further seven studies found that high cholesterol did not predict all-cause mortality either.

Now consider that more than 90 % of all cardiovascular disease is seen in people above age 60 and that almost all studies have found that high cholesterol is not a risk factor for women.

This means that high cholesterol is only a risk factor for less than 5 % of those who die from a heart attack.

But there is more comfort for those who have high cholesterol; six of the studies found that total mortality was inversely associated with either total or LDL-cholesterol, or both.

This means that it is actually much better to have high than to have low cholesterol if you want to live to be very old.

High Cholesterol Protects Against Infection

Many studies have found that low cholesterol is in certain respects worse than high cholesterol.

For instance, in 19 large studies of more than 68,000 deaths, reviewed by Professor David R. Jacobs and his co-workers from the Division of Epidemiology at the University of Minnesota, low cholesterol predicted an increased risk of dying from gastrointestinal and respiratory diseases.

Most gastrointestinal and respiratory diseases have an infectious origin.

Therefore, a relevant question is whether it is the infection that lowers cholesterol or the low cholesterol that predisposes to infection?

To answer this question Professor Jacobs and his group, together with Dr. Carlos Iribarren, followed more than 100,000 healthy individuals in the San Francisco area for fifteen years.

At the end of the study those who had low cholesterol at the start of the study had more often been admitted to the hospital because of an infectious disease.

This finding cannot be explained away with the argument that the infection had caused cholesterol to go down, because how could low cholesterol, recorded when these people were without any evidence of infection, be caused by a disease they had not yet encountered?

Isn´t it more likely that low cholesterol in some way made them more vulnerable to infection, or that high cholesterol protected those who did not become infected? Much evidence exists to support that interpretation.

Written By: Uffe Ravnskov, MD, PhD

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New Study: Standard American Diet Causes Nearly Half of All Deaths from Heart Disease, Stroke and Type 2 Diabetes

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It should come as no surprise that our diet plays a critical role in our health and longevity, but the sheer level of influence may come as a shock to you.

A new study published in the March 7 issue of JAMA found that poor diet is responsible for an astonishing 45 percent of all deaths from heart disease, stroke and type 2 diabetes in the US. The researchers attributed this high mortality rate to the Standard American Diet (SAD), which is high in sodium, processed meats, sugar-sweetened beverages and unprocessed red meats.

The good news is, just as diet can be our downfall, it’s also just as powerful in promoting exceptional health and longevity — as seen in “Blue Zone” cultures, who are known for their extraordinary lifespan and phenomenal vitality.

A Deadly Trinity of Disease, Directly Linked to Poor Food Choices

According to the newly released JAMA study, which was funded by the National Heart, Lung and Blood Institute (NHLBI), nearly half of all US deaths in 2012 caused by cardiometabolic diseases — like heart disease, stroke and type 2 diabetes — are due to poor diet. Out of the 702,308 adult deaths from cardiometabolic diseases, 318,656 — about 45 percent — were linked with over-consumption of certain unhealthy foods, as well as low consumption of specific nutrient dense edibles.

“Nationally, estimated cardiometabolic deaths related to insufficient healthier foods/nutrients remained at least as substantial as those related to excess unhealthful foods/nutrients,” said lead researcher Renata Micha, RD, PhD, of the Tufts Friedman School of Nutrition Science and Policy, Boston.

Excess consumption of sodium was associated with the highest percentage of death. Consuming high amounts of processed meats, sugar-sweetened beverages and unprocessed red meat were also linked with high mortality. Americans also don’t eat enough of certain health-promoting foods — like fruit, vegetables, nuts and seeds, whole grains, polyunsaturated fats and seafood omega-3 fats.

“Among unhealthful foods/nutrients, the present findings suggest that sodium is a key target,” noted the researchers. “Population-wide salt reduction policies that include a strong government role to educate the public and engage industry to gradually reduce salt content in processed foods (for example, as implemented in the United Kingdom and Turkey) appear to be effective, equitable, and highly cost-effective or even cost-saving.”

According to a press release from the NHLBI:

“The study also shows that the proportion of deaths associated with diet varied across population groups. For instance, death rates were higher among men when compared to women; among blacks and Hispanics compared to whites; and among those with lower education levels, compared with their higher-educated counterparts.”

The findings of the study were based on death certificate data from the National Center of Health Statistics.

With annual US healthcare spending hitting $3.8 trillion in 2014 and $3.2 trillion in 2016 — heart disease and stroke costing nearly $1 billion a day in medical costs along with lost productivity, and diabetes totaling $245 billion annually — the results of this study come as a stark reality check. However, they can also help encourage positive outcomes, such as new public health strategies, public education programs, and revamped industry standards.

For inspiration, we can also look to cultures and communities that have outstanding health and longevity for guidance — and a perfect place to start is with the Blue Zones.

The Island Where People Forgot to Die

Just off the coast of Turkey, very close to Samos, where Pythagoras and Epicurus lived, is a Greek island named Ikaria that is renown as “the island where people forgot to die” because of the exceptional lifespan of its inhabitants. Included in what is referred to as the Blue Zones — five regions in Europe, Latin America, Asia and the US with the highest concentrations of centenarians in the world — the people of Ikaria live about eight years longer than average and have exceedingly good health. These communities are also largely free of health complaints like obesity, cancer, diabetes and heart disease. Moreover, they’re sharp to the very end, whereas in the US, almost half the population over 85 suffers from dementia.

Diet is a key ingredient to their robust health and longevity. In Ikaria, they’re eating a variety of a Mediterranean diet, but with lots of potatoes. They also consume high amounts of beans. One unique foodstuff is called horta, a weed-like green that’s eaten as a salad, lightly steamed or baked into pies. Goat’s milk, wine, honey, some fruit and small amounts of fish are also enjoyed. Other foods include feta cheese, lemons and herbs such as sage and marjoram, which are made into tea.

Lifestyle also comes into play. Plenty of sex (even in old age) and napping are integral aspects of the culture, as is physical activity. There are no treadmills or aerobic classes here. Instead, exercise involves planting and maintaining a garden, manual labor (houses in Ikaria only have hand tools) and walking to run errands.

Another Blue Zone region is Sardinia, Italy where goat’s milk and sheep’s cheese are staples, along with moderate amounts of flat bread, sourdough bread and barley. They also eat plenty of fennel, fava beans, tomatoes, chickpeas, almonds, milk thistle tea and wine from Grenache grapes.

Seventh-day Adventists in Loma Linda, California made the list as well. The community shuns smoking, drinking and dancing, while also avoiding movies, television and other media distractions. Their diet focuses on grains, fruits, nuts, vegetables — and they only drink water. Sugar, except for natural sources found in whole fruit, is taboo. Adventists who follow the religion’s lifestyle live about 10 years longer than those who don’t. Interestingly, pesco-vegetarians in the community, who include up to one serving of fish per day with their plant-based diet, live longer than vegan Adventists. Avocados, salmon, beans, oatmeal, avocados, whole wheat bread and soy milk make up the bulk of their diet.

Nicoya Peninsula in Costa Rica also has a high number of centenarians. Theirs is a traditional Mesoamerican diet of beans, corn and squash — plus papayas, yams, bananas and peach palms (an oval fruit dense in vitamins A and C).

The final Blue Zone is Okinawa, Japan. Their “top longevity foods” are bitter melons, seaweed, turmeric, sweet potato, tofu, garlic, brown rice, green tea and shitake mushrooms.

All Blue Zones share the following characteristics:

  • Only eat until you’re 80 percent full.
  • The smallest meal of the day is always in the late afternoon or evening.
  • Diet consists mostly plants, especially beans. Meat is eaten rarely — on average of just five times a month — and in small portions of about 3 to 4 ounces.
  • Moderate amounts of wine is consumed with 1-2 glasses per day (doesn’t apply to Seventh-day Adventists).
  • A sense of community and close social bonds, often with religious underpinnings.

Although the secret to Blue Zone longevity doesn’t rely exclusively on diet, it’s certainly a core foundation for their exceptional health and vitality. We can take a cue from these regions and integrate their wisdom into our own lives for improved well-being. Have a look at these quick and easy Blue Zone recipes for inspiration.

Written By: Carolanne Wright

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Statin cholesterol drugs are for bread-eaters

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Much of the $23 billion spent each and every year on statin drugs is really targeting the treatment of “high cholesterol”—but actually unhealthy distortions in lipoproteins—created by consuming grains.

Most people, unfortunately, continue to focus on fat consumption, especially saturated fat, as the cause for high cholesterol and have been led to believe that cutting saturated fat and statin drugs are the solution. So let me try and clear up this somewhat confusing issue and show you that 1) there is no real benefit to cutting saturated fat, 2) grains and sugars cause distortions that increase cardiovascular disease, and 3) statin drugs do not fully address the causes of cardiovascular disease, accounting for their relatively trivial benefits.

Here is a typical panel of someone who consumes grains:

Triglycerides 170 mg/dl
LDL cholesterol (calculated) 150 mg/dl
HDL cholesterol 40 mg/dl
Total cholesterol 224 mg/dl

In other words, HDL cholesterol is lowish, triglycerides high, LDL cholesterol and total cholesterol high. What does this mean? Let’s take each, one by one. It’s a bit complex, but stick with it and you will emerge smarter than 95% of doctors who “treat” high cholesterol.

Triglycerides are the byproduct of two digestive processes: 1) De novo lipogenesis or the liver’s conversion of the amylopectin of grains and other sugars into triglyceride-rich VLDL particles that enter the bloodstream, and 2) absorption of dietary fats (which are triglycerides themselves). De novo lipogenesis dominates triglyceride levels in the bloodstream, far outstripping consumption of fat as a determinant of triglyceride levels. This simple fact was only identified recently, as the rise in triglycerides that occurs after consuming fats and oils develops within 2-4 hours, but the much larger rise in triglycerides from carbohydrate-to-triglyceride conversion starts 6-8 hours later, a fact not uncovered in older studies that failed to track this far out in time. (And, in certain genetic types, such as apo E2, the rise from carbohydrates in grains and sugars can last for days to weeks.)

LDL cholesterol is calculated, not measured. The Friedewald calculation, developed in the early 1960s to provide an easy but crude means of estimating the quantity of cholesterol in the low-density lipoprotein fraction of the blood applied several basic assumptions: 1) that everyone consumes an average diet of average macronutrient composition, and 2) that the triglyceride content of all lipoproteins remained constant from person to person (which is not true, but is wildly variable), and 3) that all LDL particles are the same (also not true, as LDL particles vary in size, conformation, surface characteristics, etc.).

Grain consumption, thanks to the process of de novo lipogenesis, increases blood levels of triglycerides and VLDL particles. VLDL particles interact with LDL particles, enriching LDL particle triglyceride content and reducing cholesterol content. This leads to a process of LDL particle “remodeling” that creates small LDL particles–glycation-prone, oxidizable, adherent to inflammatory blood cells, and persistent in the bloodstream for 7 days, rather than the 24 hours of more benign large LDL particles. Grains thereby trigger the process creating persistent and damaging small LDL particles; fats trigger the process that does not.

When we cut out grains and sugars, the Friedewald calculation is therefore no longer valid, as the assumptions–-weak to begin with–-are disrupted. LDL cholesterol, this crude, surrogate effort to indirectly quantify LDL particles, is therefore completely useless—the calculation of LDL cholesterol is INVALID. This has not, unfortunately, dampened enthusiasm among my colleagues nor the drug industry for trying to treat this number with statin drugs to the tune of $23 billion per year.

Better ways to quantify LDL particles: NMR LDL particle number (which includes quantification of small and large LDL particles) or an apoprotein B. (Each LDL particle contains one apo B, which thereby provides a virtual count of LDL particles, but no breakdown into small vs. large.) Lipoprotein testing has been around for over 20 years, is inexpensive and available—but requires an informed doctor to interpret.

HDL cholesterol is, unlike LDL cholesterol, a measured and reliable value. Ironically, it is among the most ignored. Grain-consuming humans tend to have low HDL because the high triglyceride/VLDL particles interact in the bloodstream with HDL particles, enriching HDL particles in triglycerides and reducing cholesterol content. This leads to a reduction in HDL size and HDL quantity, thus low HDL cholesterol values. The lower the HDL, the higher the cardiovascular risk.

Total cholesterol is the sum of all three values: LDL cholesterol + HDL cholesterol + triglycerides/5. (More accurately, LDL cholesterol is the calculated value: LDL = total chol – HDL – trg/5.)

Given the mix of values, total cholesterol is therefore essentially useless. A large increase in HDL, for instance–-a GOOD thing–-will raise total cholesterol; a large reduction in HDL–-a BAD thing–-will reduce total cholesterol: the opposite of what you would think. Total cholesterol can indeed yield useful prognostic information when applied to a population, though the relationship is weak. But it is useless when applied to an individual.

If we reject the silly and simple-minded notions of cholesterol panels, and apply the greater insights provided by advanced lipoprotein analysis, several nutritional observations can be made:

–Saturated fat increases HDL, shifts HDL to larger, more protective, particles, and triggers formation of large LDL particles.
–The amylopectin carbohydrates of grains trigger higher triglycerides, thereby providing more VLDL particles to interact with HDL and LDL particles, the process that leads to triglyceride enrichment and smaller ineffective HDL and smaller atherogenic LDL (heart disease-causing).
–Given the unusual persistence time of small (7 days) vs large (1 day) LDL particles, grain consumption is FAR worse than fat consumption.

You can begin to appreciate how overly simplistic this notion of “reducing cholesterol” using statin drugs really is. You can also appreciate that the real situation is a bit more complicated and beyond the reach of most busy primary care physicians, while being outside the interests of most cardiologists, obsessed as they are with revenue-producing activities like heart catheterizations, stent and defibrillator implantation.

A typical response in the cholesterol panel of someone who has eliminated all wheat, grains, and sugars would look something like this:

Triglycerides 50 mg/dl
LDL cholesterol (calculated) — mg/dl
HDL cholesterol 70 mg/dl
Total cholesterol 200 mg/dl

I left the LDL cholesterol blank because it can do just about anything: go up, go down, remain unchanged—but it doesn’t matter, because it is inaccurate, unreliable, invalid. If you were to measure advanced lipoproteins, however, you would see a dramatic reduction or elimination of small LDL particles and reduction of the total count of LDL particles (since the small LDL component has been reduced or eliminated) with large LDL particles remaining.

Common distortions of cholesterol panels can be easily explained by the chain of events that emerge from a diet rich in “healthy whole grains.” The relatively trivial benefits of statin cholesterol drugs (about a 1% reduction in real risk, not the inflated “relative risks” quoted in ads and statistically-manipulated studies) should come as no surprise, since high cholesterol is not the cause for cardiovascular disease.

Written By: Dr. William Davis

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Iron in Your Blood

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Iron is essential for human life, as it is a key part of various proteins and enzymes, involved in the transport of oxygen and the regulation of cell growth and differentiation, among many other uses.

One of the most important roles of iron is to provide hemoglobin (the protein in red blood cells), a mechanism through which it can bind to oxygen and carry it throughout your tissues, as without proper oxygenation, your cells quickly start dying.

If you have too little iron, you may experience fatigue, decreased immunity or iron-deficiency anemia, which can be serious if left untreated. This is common in children and premenopausal women.

But what many people fail to realize is that too much iron can be equally deadly, and is actually far more common than iron deficiency, thanks to a hereditary disease known as hemochromatosis.

This Health Issue Has Been of Major Importance to Me and My Family

This test saved my dad’s life 20 years ago when I discovered he had a ferritin level close to 1000. It was because he has beta-thalassemia. With regular phlebotomies, his iron levels normalized and now the only side effect he has is type 1 diabetes. The high iron levels damaged his pancreatic islet cells and now he has what is called “bronze” diabetes and so requires the use of insulin.

I also inherited this from him so this is a personal issue. Thankfully, I am able to keep my iron levels normal by removing about a quart of blood a year. This is removed not all at once but over a few dozen deposits.

I screened all my patients with ferritin levels and noticed nearly one-fourth of them had elevated levels. So I would strongly encourage you and your family to be screened annually for this, as it is SO MUCH easier to prevent iron overload than it is to treat it.

Ferritin Screen – One of Your Most Important Health Tests

Checking your iron levels is easy and can be done with a simple blood test called a serum ferritin test. I believe this is one of the most important tests that everyone should have done on a regular basis as part of a preventive, proactive health screen.

The test measures the carrier molecule of iron, a protein found inside cells called ferritin, which stores the iron. If your ferritin levels are low, it means your iron levels are also low.

The healthy range of serum ferritin lies between 20 and 80 ng/ml. Below 20 is a strong indicator that you are iron deficient, and above 80 suggests you have an iron surplus. The ideal range is between 40-60 ng/ml.

The higher the number over 100 the worse the iron overload, with levels over 300 being particularly toxic and will eventually cause serious damage in nearly everyone that sustains those levels long term. It’s important to find out if your levels are high because your body has a limited capacity to excrete iron, which means it can easily build up in organs like your liver, heart and pancreas. This is dangerous because iron is a potent oxidizer and can damage your body tissues contributing to serious health issues, including:

Cirrhosis Liver cancer Cardiac arrhythmias
Type one diabetes Alzheimer’s disease Bacterial and viral infections


Cancer researchers have also found new evidence that bowel cancers are two to three times more likely to develop when dietary iron is too high in your body.1

Risk Factors for Iron Overload

People with hemochromatosis are not the only ones who may accumulate more iron than is healthy. While premenopausal women who are menstruating regularly rarely suffer from iron overload, most adult men and postmenopausal women tend to be at a high risk, as they don’t have a monthly blood loss (one of the best ways you can get rid of excess iron is by bleeding).

Another common cause of excess iron is the regular consumption of alcohol, which will increase the absorption of any iron in your diet. For instance, if you drink wine with your steak, you will likely be absorbing more iron than you need. Other potential causes of high iron levels include:

  • Cooking in iron pots or pans. Cooking acidic foods in these types of pots or pans will cause even higher levels of iron absorption.
  • Eating processed food products like cereals and white breads that are “fortified’ with iron. The iron they use in these products is inorganic iron, not much different than rust and it is far more dangerous than the iron in meat.
  • Drinking well water that is high in iron. The key here is to make sure you have some type of iron precipitator and/or a reverse osmosis water filter.
  • Taking multiple vitamins and mineral supplements, as both of these frequently have iron in them.

Could Reducing Your Iron Level Be a Safer Alternative to Statins?

We may have garnered some valuable information about how iron drives inflammation from studying statins drugs, of all things. Statins are of course, cholesterol drugs. Statins have an anti-inflammatory effect on your body by reducing oxidative stress, which is something the drug companies tend not to disclose. The fact that statin drugs reduce inflammation, and reduce inflammatory markers like C-reactive protein, may explain why statins decrease heart attacks in some people. This benefit has nothing to do with the action of lowering cholesterol, but rather the reduction of inflammation.

In a study published in the April 2013 issue of American Journal of Public Health2, researchers found that statins improved cardiovascular outcomes at least partially by countering the proinflammatory effects of excess iron stores. In this study, the improved outcomes were associated with lower ferritin levels but not with “improved” lipid status. Researchers concluded iron reduction might be a safe and low-cost alternative to statins. An earlier study in the American Heart Journal3 also showed that people with a lower iron burden had less risk for heart attack and stroke.

These studies add credence to what I learned a few years ago from Dr. Steven Sinatra, one of the leading natural cardiologists in the world, that statins’ only health benefit is that of reducing inflammation.

This may be helpful for a small percentage of individuals who have a very high risk of dying from a heart attack, but NOT for those who simply have “high” cholesterol levels. Statin drugs are vastly overprescribed and are not worth the risk for the vast majority of you. In some cases, they may actually increase your risk of stroke. If elevated iron is the driving force behind your inflammation and cardiovascular disease, then it makes far more sense to simply reduce your iron level, as opposed to taking a statin drug that has the potential for many adverse effects.

What to Do if Your Iron Levels Are Too High

The good news if you find out that your iron levels are elevated or you have hemochromatosis is that remedying the condition is relatively simple. Some people advise using iron chelators like phytic acid or IP6, but I tried that with my dad and it failed miserably so I would not recommend it. Donating your blood is a far safer, more effective and inexpensive approach for this problem. If, for some reason, a blood donor center is unable to accept your blood for donation you can obtain a prescription for therapeutic phlebotomy. At the same time, you will want to be sure to avoid consuming excess iron in the form of supplements, in your drinking water (well water), from iron cookware, or in fortified processed foods.


  • Certain phenolic-rich herbs and spices, such as green tea and rosemary, can reduce iron absorption4
  • The primary polyphenol in turmeric known as curcumin actually acts as an iron chelator, and in mice studies, diets supplemented with this spice extract exhibited a decline in levels of ferritin in the liver5
  • Astaxanthin, which has been researched to have over 100 potential health benefits, has been shown to reduce iron-induced oxidative damage6

The Ancient Origins of Iron Overload

How and why hemochromatosis – now one of the most prevalent genetic diseases in the United States – emerged is the subject of numerous theories and speculation – but its true history remains a complex mystery. In a fascinating article on the topic, The Atlantic7 recently highlighted the notion that everyone who inherited the C282Y mutation responsible for the majority of hemochromatosis cases got it from the same person. In other words, one distant ancestor passed on the mutation, which now favors people of Northern European decent.

No one knows the precise identity of the founder, but initial speculation that it was someone of Irish descent has given way to the possibility that it may have actually arisen in a Viking civilization or, even earlier, in a central European hunter-gatherer.

It takes two inherited copies of the mutation (one from the mother and one from the father) to cause the disease (and even then only some people will actually get sick). If you have just one mutation, you won’t become ill but you will absorb slightly more iron than the rest of the population, a trait that may have given people an advantage when dietary sources of iron were scarce.

Did the Hemochromatosis Mutation Emerge to Protect Humans from a Carb-Heavy Agricultural Diet?

There is speculation that the hemochromatosis mutation may have spread in ancient Europe around the time that man transitioned from hunter-gatherer to farmer. Unlike the Paleolithic diet of the “cavemen,” which by necessity included a relatively balanced diet of iron-rich meat, fish and plant foods, farming may have led humans to rely on an overabundance of grain carbohydrates. The featured article reported:

Fossil evidence indicates early European farmers stood roughly 6 inches shorter than their hunter-gatherer ancestors, a possible indication of malnutrition… Average height and life expectancy fell, as bone infections, dental cavities, and skeletal malformations associated with anemia rose. While the exact composition of the Paleolithic plate remains debated, most agree that European hunter-gatherers ate more meat than those in modern farming communities. And this animal protein was an excellent source of one familiar micronutrient: iron.

The World Health Organization estimates that 1.6 billion persons worldwide current suffer from the lack of red blood cells known as anemia — half of which may be caused by iron deficiency. One’s inner paleo might wonder whether this pandemic of iron deficiency began in the Neolithic era as diets bloated with carbohydrates replaced those rich in meat and fish.

Anemia decreases the oxygen carrying capacity of the blood; if marked, this will hinder an individual’s ability to stay healthy, find food, and reproduce. The C282Y mutation increases iron absorption, and it may have inadvertently protected carriers against this threat.”

The Hemochromatosis Link to the Plague

Another intriguing theory suggests that the hemochromatosis mutation may have protected against the Black Death of the 14th century, by preventing the Yersinia pestis bacteria from reproducing inside of human immune cells.

“During the Black Death, mortality may have been highest, up to 50-66 percent, in the British Isles — a future hotbed of hereditary hemochromatosis … In this most unsympathetic environment, minute DNA differences may decide survival or death. A genetic advantage would quickly spread through the island population — it would have less value on the mainland where plague mortality may have been lower,” the featured article reported.

But this theory is challenged by conflicting information that suggests the plague bacteria use iron from its host to enhance its ability to infect cells. People with hemochromatosis may therefore be among the most vulnerable to succumbing to plague infections, which suggests the mutation may have nothing to do with survival. It could, perhaps, be an artifact of natural selection or there may be a different explanation entirely…

Written By: Dr. Mercola

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Moderate Drinking May Slow Decline of ‘Good’ Cholesterol

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Drinking up to two alcoholic beverages daily may slow the decline of high-density lipoprotein cholesterol

Consumption of up to two alcoholic beverages a day may slow the decline of “good” high-density lipoprotein (HDL) cholesterol. New research says that moderate intake of alcohol might benefit HDL levels. However, the data suggests differential effects on the basis of the type of alcoholic beverage and other factors.

There are two types of cholesterol:

A. Low-density lipoprotein (LDL) is referred to as the “bad” cholesterol. It can cause a high-level buildup of plaque in the arteries, known as atherosclerosis, which increases the risk of strokes and heart attacks.

B. High-density lipoprotein (HDL) cholesterol helps to remove the “bad” LDL from the arteries and carries it back to the liver, where it is broken down and is removed from the body. This has earned HDL the title of “good” cholesterol.

A research team  from Pennsylvania State University and China’s Kailuan Hospital recently presented findings at the American Heart Association’s Scientific Sessions 2016 in New Orleans, LA. That event, the world’s premier cardiovascular instructional and research meeting in the world, featured five days of the best in clinical, translational, and population content.

The team analyzed  data from 80,081 Chinese adults who were an average age of 49 years who were free of cancer and cardiovascular disease. The alcohol intake of the participants was assessed at the baseline in 2006, and they were placed in one of five groups: heavy, moderate, light, past, and never. Moderate drinking was 0.5-1 drink daily for women and one to two drinks a day for men.

The HDL levels were also measured in 2006, 2008, 2010, and 2012. During follow-up, the subjects did not take LDL-cholesterol lowering medications. The HDL levels of all participants decreased during follow-up. Moderate drinkers experienced a slower HDL decline when compared to never-drinkers and heavy drinkers.

Further analysis showed that a slower decline in HDL cholesterol depended on the type of alcohol consumed. HDL levels fell slower with the moderate intake of beer. Among those who consumed hard liquor, only moderate and light drinkers had a slower HDL decline. An insufficient number of wine drinkers did not allow determination as to whether wine slowed the reduction of  good cholesterol.

The team admits that further research is necessary in order to determine whether moderate alcohol intake is of benefit for HDL cholesterol among the populations of other countries. Also, it needs to be determined whether slower HDL reduction that goes along with alcohol consumption is associated with outcomes that are clinically relevant.

This research, however, offers additional support for the possible heart health benefits of moderate drinking when it increases HDL levels. Drinking needs to go along with lifestyle interventions such as eating a healthy diet, doing physical activity, and quitting smoking.

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Risk factors for prostate cancer

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New research suggests that age, race and family history are the biggest risk factors for a man to develop prostate cancer, although high blood pressure, high cholesterol, vitamin D deficiency, inflammation of prostate, and vasectomy also add to the risk. In contrast, obesity, alcohol abuse, and smoking show a negative association with the disease. Details are reported in the International Journal of Medical Engineering and Informatics.

Khaled Alqahtani, Shankar Srinivasan, Dinesh Mital and Syed Haque of the Department of Health Informatics, at Rutgers Biomedical and Health Sciences, Newark, New Jersey, USA, explain that prostate cancer is the most common cancer in men with 233000 new cases estimated in the USA during 2014 and almost 30000 deaths. A boy being born today has an almost 1 in 7 chance of developing prostate cancer at some point in their life and a 3% chance of dying from the disease. At this time, however, cancer specialists do not fully understand the underlying causes nor the epidemiology of prostate cancer.

Alqahtani and colleagues have analyzed data from The US Nationwide Inpatient Sample (NIS), the largest database in the USA for all-payer inpatient health care. They focused on the years 2007-2011 amounting to more than 12 million records and looked at men aged 35 to 100 years, finding that approximately 5.35% of them had prostate cancer (642383 men). They then used statistical analyses to look at the independent variables: age, race, family history of prostate cancer, family history of any other cancer, obesity, alcohol abuse, smoking, cholesterol, vitamin D deficiency, inflammation of prostate, vasectomy, and hypertension, to see which factors were critical variables associated with prostate cancer incidence.


Alqahtani, K.S., Srinivasan, S., Mital, D.P. and Haque, S. (2015) ‘Analysis of risk factors for prostate cancer patients’, Int. J. Medical Engineering and Informatics, Vol. 7, No. 4, pp.365-380

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3-4 Egg Yolks per Day May Normalize Your Lipids, Reduce Liver & Abdominal Fat as Well as Your CVD & NAFLD Risk

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Because of their cholesterol content, eggs have long been touted as a driver of heart disease. As a SuppVersity reader, you know that there are multiple reasons why the notion that the consumption of eggs, or rather egg yolks, would increase your cardiovascular disease risk: (a) there’s no mechanistic “if your cholesterol is high, your CVD risk is also high”-link; (b) a causative link between the consumption of dietary cholesterol and serum cholesterol does not exist – at least not in the majority of people; (c) substances in egg yolks, in particular, have been shown to modulate the physical characteristics of your lipoproteins and will thus lower, not increase your CVD risk.

Since you know all that, it may seem less important for you than your doctor and other people who may still believe that cholesterol was a dietary villain you’d better avoid altogether to read about egg yolks recently discovered ability to significantly decrease your blood lipid levels.

k, eventually, this preliminary study confirms the ability of egg yolks to reduce the blood lipid levels in rats, not men. Its results are yet in line with human studies (Fernandez. 2006) and case reports such as Fred Kern Jr’s paper with the telling title “Normal plasma cholesterol in an 88-year-old man who eats 25 eggs a day”, a paper that was published in the New England Journal of Medicine in 1991, a decade during which the number of people, let alone well-known scientists who questioned the detrimental health effects of cholesterol was low, if not zero.

Table 1: Fatty acid profile and cholesterol content of pork belly oil and egg yolk (% of total fatty acid | Park. 2016)

Today, people (including a handful of doctors and scientists 😉 acknowledge that the ingestion of eggs has been reported to lower, not increase blood cholesterol levels. In the absence of a mechanistic explanation for this phenomenon, however, large parts of the medical establishment still doubt that the anti-CVD and anti-cancer effects of eggs are driven by anything but their relatively high content of anti-oxidants. To identify the actual biochemical metabolic mechanisms by which the oral administration of egg yolk affects blood lipid reduction scientists from the Kangwon National University conducted a preliminary rodent study in which they observed similar reductions in ‘bad’ blood triglycerides and total cholesterol, as well as increases in ‘good’ high-density lipoprotein cholesterol as they were observed in the egg eating minority of human subjects in epidemiological studies.

Question: Do the eggs have to be raw? No, probably not. As you’ve learned in my often-cited article on oxysterols (~oxidized cholesterol), it may yet be a bad idea to eat hard-boiled eggs. Why’s that? Learn more in this SuppVersity Classic: “True or False? Butter, Ghee, Lard & Tallow – Are Saturated Animals Fats the Kings and Queens of the Frying Pan?”

This alone may not sound exciting enough for yet another rodent study to make it into theSuppVersity news. What is exciting enough, though, is the fact that the study is the first study to include another high cholesterol product in a control diet: pork belly oil – an “egg yolk analogue” that has a similar, but not identical fatty acid content as egg yolk (see Table 1); and here’s how the study that obviously had a saline control group, as well, worked:

  • rats were fed, ad libitum, a purified pellet diet and drinking water for 6 weeks, and egg yolk or other treatments were orally administered every day at a fixed time;
  • the amount of egg yolk / pork belly oil, namely 5mg/kg, i.e. the human equivalent of approximately 3-4 egg yolks, had been determined based on data from preliminary experiments in which the authors found that this was the amount of egg yolk where the blood lipid lowering effects plateaued (i.e. didn’t increase further, when more egg yolk was fed);
  • feces, blood, weight and food intake were measured and/or analyzed daily / weekly;
  • liver and abdominal fat were determined at the end of the 6-week study

The rats’ food intake was examined every 3 days. Their body weight was measured once per week. Based on this data the so-called “diet efficiency” was calculated as the ratio of the diet intake to the daily average body weight gain (diet intake/body weight gain).

Figure 1: Body weight gain and diet intake of rats after oral dosing of egg yolk (Park. 2016).

As you can see in Figure 1, the latter, i.e. the “diet efficacy”, was significantly higher for the pork-belly oil group (T2) in which the rodents gained significantly more body weight, even though they had a (likewise significantly) reduced food intake.

Beyond cholesterol: weight and body composition improve as well

Against that background, it is not really surprising that the animals “pork belly group” had also accumulated more abdominal and liver fat than those who were fed with egg yolk and ended up being a non-significant 10% leaner (as in having 10% lower abdominal fat masses) than their peers who received nothing but slightly salted water (saline placebo) on top of their std. rodent diet.

Figure 2: Liver weight and abdominal fat weight in gram per 100g body weight (Park. 2016).

The actual news, however, are the health-relevant improvements in triglycerides, HDL-C and LDL-C as well as the reductions in the predictors of selected heart and liver disease, namely the atherogenic index (AI) and the levels of the transaminase enzymes ALT and AST you can see in Figure 3 – changes of which scientists have concluded in other studies that they are indicative of significant metabolic improvements with downstream beneficial effects on your heart and metabolic health; effects for which the study at hand is the first to provide a mechanistic explanation.

What’s the latest on egg yolks: While egg yolk is more and more appreciated “as a source of valuable biologically active substances” (Zdrojewicz. 2016 | learn more in FFT), I am pretty sure that future studies will add to the increasing evidence of the health benefits of egg yolk consumption, such as the recently confirmed anti-NAFLD effects in low protein diets (Erami. 2016), or the previously discussed high amount of ‘active’ vitamin D in egg yolks. Needless to say that theSuppVersity is the place to learn about these studies, first.
Figure 3: Atherogenic index (top, left), liver enzymes (transaminases ALT and AST | top, right) and lipid levels (triglycerides – TG; total cholesterol – TC; HDL; LDL | bottom | Park. 2016).

The explanation revolves around the significant reduction in (compared to pork belly oil) or rather normalization (compared to control and pork belly oil) of HMG-CoA, the enzyme that’s responsible for the endogenous production of cholesterol and the promotion of cholesterol excretion – two potential mechanism, of which Park and Park point out that they are “supported by previous reports that investigated blood lipid reduction in rats that ingested boiled egg and found an increase in LDL-C in the group given pork belly oil (Houston et al., 2011 )” and in line with the fact that “many studies have emphasised that there is no correlation between the amount of egg ingestion and blood cholesterol in humans (Herron et al., 2004; Greene et al., 2005)” as well as studies showing that “lecithin in the egg yolk lowers the level of blood cholesterol, as it is used for the formation of micelles in the small intestine or increases excretion through the reabsorption of cholesterol as bile acids (Yang et al., 2007; Alqasoumi, 2014)”.

You as a SuppVersity reader know that eggs, or more specifically their yolks are nutrient dense superfoods that will improve the structure of your choles-terol molecules, leave your cholesterol levels unchanged and, as I have pointed out only recently in my article “Whole Eggs Can Boost Your Beta-Carotene and Vitamin E Uptake from Veggie Salad W/ Oil Dressing by 400%-700%”, improve the absorption of fat-soluble vitamins sign. more than one would expect if the effect was a result of their fat content, alone | more!

Eggs, cholesterol, CVD and the metabolic syndrome:With statin-like effects on HMG-CoA and their ability to reduce the uptake of dietary cholesterol from the diet, the small egg-shaped cholesterols bombs (eggs also contain sign. more cholesterol than pork-belly oil) come with everything it takes to keep their effect on your cholesterol levels neutral / beneficial.

In fact, the data from the study at hand indicates that the consumption of 3-4 eggs / day is heart healthy and can help you prevent the accumulation of fat in both, the midsection, as well as the subjacent liver. Two good reasons to eat more eggs, especially in view of the fact that the deposition of fat in the liver is supposedly the starting point for the development of diabetes, heart disease and a plethora of other pathological reasons to die prematurely. When you think about it, it would thus not even be hilarious if egg producers put the (non-FDA approved) claim that eggs “may reduce the risk of heart disease” on the boxes of their produce.


  • Alqasoumi, Saleh I. “Evaluation of the hepatroprotective and nephroprotective activities of Scrophularia hypericifolia growing in Saudi Arabia.” Saudi Pharmaceutical Journal 22.3 (2014): 258-263.
  • Cohn, Jeffrey S., et al. “Dietary phospholipids, hepatic lipid metabolism and cardiovascular disease.” Current opinion in lipidology 19.3 (2008): 257-262.
  • Erami, Kazuo, et al. “Dietary Egg Yolk Supplementation Improves Low-Protein-Diet-Induced Fatty Liver in Rats.” Journal of Nutritional Science and Vitaminology 62.4 (2016): 240-248.
  • Fernandez, Maria Luz. “Dietary cholesterol provided by eggs and plasma lipoproteins in healthy populations.” Current Opinion in Clinical Nutrition & Metabolic Care 9.1 (2006): 8-12.
  • Greene, Christine M., et al. “Maintenance of the LDL cholesterol: HDL cholesterol ratio in an elderly population given a dietary cholesterol challenge.” The Journal of nutrition 135.12 (2005): 2793-2798.
  • Herron, Kristin L., et al. “High intake of cholesterol results in less atherogenic low-density lipoprotein particles in men and women independent of response classification.” Metabolism 53.6 (2004): 823-830.
  • Houston, D. K., et al. “Dietary fat and cholesterol and risk of cardiovascular disease in older adults: the Health ABC Study.” Nutrition, Metabolism and Cardiovascular Diseases 21.6 (2011): 430-437.
  • Kern Jr, Fred. “Normal plasma cholesterol in an 88-year-old man who eats 25 eggs a day: mechanisms of adaptation.” New England Journal of Medicine 324.13 (1991): 896-899.
  • Park, Byung-Sung and Park, Sang-O. “Lipid-lowering mechanism of egg yolk in normal rats.” International Journal of Food Science and Technology (2016) – doi: 10.1111/ijfs.13216
  • Yang, Su Young, et al. “Effect of lecithin intake on lipid metabolism and antioxidative capacity in rats fed high fat diet.” Korean Journal of Nutrition 40.4 (2007): 312-319.
  • Zdrojewicz, Zygmunt, Marta Herman, and Ewa Starostecka. “Hen’s egg as a source of valuable biologically active substances.” Postȩpy higieny i medycyny doświadczalnej (Online) 70 (2016): 751.


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