Tag Archives: cardiovascular risk

Berries, Dark Chocolate and Fruits-Vegetables improve blood vessels within 8 weeks

A recently published study reveals that within 8 weeks of consuming a combination of 70% dark chocolate (50 grams per day), one serving of berries, and four servings of polyphenol rich fruits-vegetables per day, measurable improvements occur in the functioning of arteries in humans with high blood pressure. Just eight weeks and improvement was observed.

So what did the researchers do?

First, they took 102 adults with high blood pressure and instructed them to consume no chocolate, no berries and only 2 portions of fruits-vegetables per day for four weeks. After four weeks on a “low polyphenol diet” they measured forearm blood-flow response to two different vasodilators (a vasodilator increases blood flow by relaxing the muscle in the wall of arteries). Blood and urine samples were also taken.

After the four week period on a low polyphenol diet, 51 patients continued on the same diet (control group). 51 subjects had fruits and vegetables of their own choice (from a list rich in polyphenols), one serving of berries/day and 50 grams/day of 70% dark chocolate delivered free of charge to their homes weekly (intervention group).

All participants kept food diaries, answered food questionnaires, had regular consultations with nutritionists.

After 8 weeks, blood and urine testing demonstrated higher levels of polyphenols in the “high-polyphenol” group, as expected.

Most importantly the subjects consuming dark chocolate, berries and more vegetables-fruits on a daily basis demonstrated measurable and significant improvements in “endothelial function” compared to the other group. Endothelial function reveals the ability of arteries to respond to changes in demand for increased blood flow. “Endothelial” refers to the cells that line the walls of arteries, directly in contact with flowing blood. These cells are endothelial cells.

The maximum forearm blood flow response to the infusion of acetyl-choline (a vasodilator) was the test used to measure endothelial function. The maximum forearm blood flow in the high polyphenol group was TWICE that of the low polyphenol group. This large difference occurred with just eight weeks of a simple dietary intervention.

Before the dietary intervention there was no measurable difference between the two groups of subjects. After the dietary intervention there was a very large and meaningful difference.

Endothelial dysfunction is a major predictor of cardiovascular risk (heart attack and stroke). Endothelial dysfunction is BAD.

You can read about polyphenols here .

Epidemiologic studies demonstrate the health benefits of diets rich in colorful vegetables and fruits. Among the fruits berries appear to have the greatest density of important micro-nutrients on a per calorie basis.

Dark chocolate has a high content of polyphenols and multiple studies suggest significant cardiovascular benefit with just an ounce or two per day. You must be careful though about your source since the dutch method of preparation depletes the polyphenols and some brands have high amounts of cadmium or lead. The richest source of dark chocolate identified by ConsumerLab with the lowest amounts of heavy metal contaminants is 100% (bitter) Bakers Dark Chocolate. Dip it in honey or have it with sweet berries to offset the bitter taste. Avoid in the evenings or late afternoon (the caffeine content can interfere with sleep)

So eat those colorful vegetables, berries and indulge in some dark chocolate.

Here is a suggested list of vegetables, Try to get 8-9 servings per day. I give this recommendation to my patients. I adopted this from the recommendations of Doctor Terry Wahls. (From a Wheelchair to Commuting on a Bicycle: How One Woman Naturally Reversed MS | Terry Wahls MD | Defeating Progressive Multiple Sclerosis without Drugs | MS Recovery | Food As Medicine)

9 SERVINGS OF NON-STARCHY VEGETABLES PER DAY, 3 SERVINGS FROM EACH OF THREE CATEGORIES.

DARK GREEN LEAFY VEGETABLES, 3 SERVINGS PER DAY EQUALS 3 CUPS MEASURED COOKED OR 6 CUPS MEASURED RAW

Arugula, Beet Greens, Bok Choy, Chard all colors, Chicory, Cilantro
Dandelion Greens, Endive, Escarole, Kale-all kinds, Parsley, Radicchio
Radish leaves, Spinach, Turnip Greens, Watercress

Colored vegetables, 3 cups daily:

GREEN: Artichoke, Asparagus, Avocado (FRUIT), Cabbage (red and green) Celery, Cucumber with skin, Okra, Olives, Peppers, Zucchini with skin
RED: Beets, red cabbage, red peppers, cooked tomatoes (fruit)
YELLOW: Carrots, Pumpkin, Squash-summer and winter, Sweet potato,

SULFUR RICH VEGETABLES, 3 CUPS DAILY: Some leafy greens are also sulfur rich so there is overlap in these categories

Arugula, Asparagus, Bok Choy, Broccoli, Brussel sprouts, Cabbage, Cauliflower, Collard Greens, Garlic, Kale, Kholrabi, Leeks, Mushrooms, Onions red-yellow-white, Radishes, Scallions, Shallots, Turnip Greens, Watercress.

Eat the rainbow and enjoy good health.

You can read this study on Medscape but you must first establish a user name and password (free and open access)

Beneficial Effect of a Polyphenol-Rich Diet on CVD Risk

Bob Hansen MD.

STATINS OF NO BENEFIT AGE 80 AND UP, even after a heart attack!

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Finally IT HAS BEEN LOOKED AT AND TRUTHFULLY PUBLISHED, statin drugs for individuals 80 years of age and older WITH DOCUMENTED HEART DISEASE SHOWS NO BENEFIT, EVEN AFTER A HEART ATTACK

Here is the abstract from the study

Statin Therapy and Mortality in Older Adults With CAD
Abstract
Objectives: To examine the effect of statins on long-term mortality in older adults hospitalized with coronary artery disease (CAD).
Design: Retrospective analysis.
Setting: University teaching hospital.
Participants: Individuals aged 80 and older (mean aged 85.2, 56% female) hospitalized from January 2006 to December 2010 with acute myocardial infarction (AMI), unstable angina pectoris, or chronic CAD and discharged alive (N = 1,262). Participants were divided into those who did (n = 913) and did not (n = 349) receive a discharge prescription for a statin.
Measurements: All-cause mortality over a median follow-up of 3.1 years.
Results: Participants treated with statins were more likely to be male, to have a primary diagnosis of AMI, to have traditional cardiovascular risk factors, and to receive other standard cardiovascular medications in addition to statins. In unadjusted analysis, statin therapy was associated with lower mortality (hazard ratio (HR) = 0.83, 95% confidence interval (CI) = 0.71–0.96). After adjustment for baseline differences between groups and propensity for receiving statin therapy, the effect of statins on mortality was no longer significant (HR = 0.88, 95% CI = 0.74–1.05). The association between statins and mortality was similar in participants aged 80 to 84 and those aged 85 and older.
Conclusion: In this cohort of older adults hospitalized with CAD, statin therapy had no significant effect on long-term survival after adjustment for between-group differences. These findings, although preliminary, call into question the benefit of statin therapy for secondary prevention in a real-world population of adults aged 80 and older and underscore the need for shared decision-making when prescribing statins in this age group.

In layman’s terms. This study compared patients aged 80 and older who were hospitalized with documented coronary artery disease and compared those sent home on statins and those sent home without a prescription for statins. There was no difference in death rates between the two groups. The use of statins in this situation (known heart disease) is referred to as secondary prophylaxis. Secondary prophylaxis would be expected to have greater risk reduction when compared to primary prophylaxis (no know heart disease).

I have advocated against the use of statins in primary prophylaxis. Statin Guidelines, one step forward, two steps backwards | Practical Evolutionary Health

The data in this study shows no protection from statins when used for secondary prophylaxis (higher risk group) for age 80 and above.

For more discussions on statins, atherosclerosis, coronary artery disease, go here. Statin Drugs | Practical Evolutionary Health

Live clean, eat clean, sleep well.

Bob Hansen MD

The Obesity Code, a must read book by Dr. Jason Fung.

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Doctor Jason Fung just published a terrific book titled The Obesity Code: Unlocking the Secrets of Weight Loss:

Dr. Fung’s genius excels at simple, direct explanations with clarity and humor. His analogies are often hilarious and through his humor and logic he communicates simple but important truths. The major message is that obesity is a hormonal problem. Obesity is not a disease of excess caloric intake, nor is it a disease of sedentary lifestyle. Dr. Fung cites study after study in which obese patients (young and old alike) consumed less calories and exercised more with dismal results. He reviews the medical literature on the effects of refined carbohydrates and sugar on insulin and other hormones. He explains how sustained high insulin levels cause insulin resistance and weight gain. He clearly and decisively explains how 100 calories of sugar or flour effects the human body in a manner immensely different from 100 calories of broccoli.

“Have you ever seen anyone get fat from eating too much broccoli?”

Most importantly, Dr. Fung provides the solution that has helped hundreds of his patients. The solution is elimination of refined carbohydrates and sugar in combination with intermittent fasting. Intermittent fasting (consuming only water, coffee, tea, broth) for 24 -36 hours a few to several times per month helps to reset the brain’s set point for body weight. When combined with restriction of sugar and refined carbohydrate (foods made with flour) intermittent fasting presents a powerful tool to not only lose weight but to manage diabetes and prevent the many complications of obesity and diabetes.

Intermittent fasting increases the human metabolic rate, Your body actually burns more calories at rest per hour during fasting. The effects of intermittent fasting are distinctly different from what has been referred to as the “starvation response”. The “starvation response” ironically and confusingly refers to human studies that restricted (reduced) caloric intake but continued low calorie meals throughout the day. It is unfortunate that those studies coined the term “starvation response” which is a decrease in resting metabolic rate. Caloric restriction diets reduce the human metabolic rate and therein lies the cause for the failure of all caloric restriction diets.

The confusion of these two approaches and their effects on human metabolism have clouded the discussion of obesity for decades.

Dr. Fung’s communication skills can be enjoyed by reading his book and viewing his many talks on YouTube.

His book and lectures should be mandatory for every medical student, physician, nutritionist and public health official. His book’s exhaustive medical references document the science that supports his theory and his clinical solution.

So take a leap, click on the link above for his book and the links below for some of his videos which are free on-line.

I think that Dr. Fung’s book is the most important book published on this topic in the 21st Century. His work will have profound influence during the next few decades. I encourage you to enjoy his genius.

Bob Hansen MD

Great lecture videos available on line

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In January I attended the annual meeting of Physicians for Ancestral Health. There were great presentations on many topics related to lifestyle and health. Take a look at the website linked below to learn about many topics relating nutrition, exercise, and lifestyle to health.

Open Video Archives | Physicians for Ancestral Health

I presented a lecture titled “The Lipoprotein Retention Model, What’s Missing?” This discusses many factors (root causes) that contribute to the formation of plaque in arteries and what can be done to prevent this insidious process by adopting a “Paleo Lifestyle“.

Why do our tax dollars continue to subsidize death, disability and disease?

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Yesterday I posted a comment on Medscape after reading an article Longtime Dietary Fat Advice Unsupported by Data: Analysis . Medscape is a website with articles and news written for physicians and other health professionals. Anyone can access this information by creating a user name and password, there is no fee.

Here is my comment. It is long and technical. I will provide an explanation in lay terms after quoting myself.

Sugar, especially HFCS (high fructose corn syrup), used in so many foods is more inflammatory than saturated fat. Grass fed meat from ruminants has a fatty acid mix that is exactly the same as wild game, which we evolved to eat, along with tubers, green leafy vegetables, and fruit in season. Excess refined fructose intake AND use of modern refined “vegetable oils” along with non-healthy grains combine to cause excess caloric intake, NAFLD (non-alcoholic fatty liver disease), obesity, metabolic syndrome and CAD (coronary artery disease). N6 PUFA (omega six polyunsaturated fatty acids) are easily oxidized. N3 PUFA (omega 3 fatty acids) despite greater number of double bonds are protected from oxidation in cell and Lipoprotein membranes by plasmalogens as opposed to linoleic acid which is not easily incorporated into plasmalogens. The PUFA in vegetable oils (linoleic acid) is the FA (fatty acid) that is oxidized on LDL particles and remnant particles, stimulating monocytes to transform to macrophages and then foam cells. The USDA, ADA and AHA have had it upside down for decades and they still fail to admit folly. We evolved for > 1 million years without grains and they have contributed to disease. Per calorie fresh vegetables have five times the amount of fiber compared to whole grains. We do not need grains and would be better without them. They contain anti-nutrients and wheat, hybridized in the 1980s to a storm resistant dwarf plant, now has 50 times more gluten/gliadin than the old wheat. This has generated more gluten intolerance and celiac. Our greatest nutritional threats to public health include refined sugar, carbohydrates predominantly from grains and refined vegetable oils. Vegetable oils are not healthy, we did not evolve to eat them. N3 FAs are anti-inflammatory but have been competing in our diets with a sea of inflammatory N6 PUFA from unnatural refined and easily oxidized “vegetable oils”. Even though PUFA can reduce LDL-C they wreak havoc by creating ox-LDL particles which initiate the cascade of atherosclerosis. Substituting SFA (saturated fatty acids) with PUFA results in increased levels of Lp(a) and oxLDL in humans, not a good thing. Close the feed lots, stop government subsidy of corn, wheat, dairy and soy, eat meat from grass fed ruminants, wild seafood, fresh organic vegetables and fruits in season. Nibble on tree nuts. Stop creating carcinogens with high dry heat cooking methods and we will watch obesity, insulin resistance, metabolic syndrome and atherosclerosis melt away.

That was my comment. Here is some explanation.

I have previously discussed the pro-inflammatory nature of refined “vegetable oils”. “Vegetable oils” are actually not from vegetables, they are from grains, seeds and legumes. The two major sources of excess omega six polyunsaturated fats in the American diet are corn oil and soy oil marketed by various brand names such as Wesson. They are major components of margarine and other butter substitutes and are present in most salad dressings. Most salad dressings sold in our supermarkets contain high levels of easily oxidized unhealthy refined “vegetable oils” and HFCS. The use of these salad dressings converts a healthy salad into a vector for disease.

The major source of caloric sweeteners in our food and beverages is high fructose corn syrup. Both corn (oil and sugar) and soy predominate our processed food supply because they are cheap. They are cheap because our tax dollars subsidize their production. This subsidy started during the Nixon administration. Once a food subsidy is put in place it is very difficult to eliminate, Big Agriculture provides a deep pocket for lobby money and our elected officials from the mid-west bread-basket respond to $$.

Another major source of disease causing elements in the standard American diet is highly refined flour from wheat. Doctors Davis and Perlmutter discuss the problems associated with wheat-flour foods in their books Wheat Belly and Grain Brain respectively. The production of wheat has also been subsidized since the Nixon administration.

Wheat is not what it used to be. A new dwarf hybrid wheat has predominated the US market since the 1980s. Bread and pasta are not what they used to be when great grand-mother made her own bread and pasta in the kitchen from coarsely ground whole flour. But even if we all went back to making our own whole-grain bread and pasta from locally ground pre-1980s wheat, bread, pasta and pastry would still present a health risk because of issues related to intestinal permeability, auto-immune disease (now epidemic in the USA), and the presence of nasty lectins and phytates (discussed in my manifesto and previous posts).

The Medscape comment quoted above describes adverse consequences caused by replacing saturated fat in the diet with “vegetable oils”. This is a complex subject and I will try to be brief for now but promise to expand on this in a future post.

Many factors contribute to atherosclerosis, heart attack and stroke. Sedentary lifestyle, stress, inadequate restorative sleep, smoking and poor dietary choices top the list. These factors also contribute to obesity, diabetes, metabolic syndrome, insulin resistance and many cancers.

DIETARY FACTORS:

The combination of sugared foods and beverages (predominantly sweetened with HFCS), refined flour foods, and excess consumption of the PUFA in “vegetable oils” TOGETHER contribute to the formation of plaque in the walls of our arteries (atherosclerosis).

How does this happen?

LDL (low density lipoprotein) is a particle that transports cholesterol and triglycerides through our blood to our organs. This particle is comprised of a core and a surrounding membrane. Here is a picture.

The core contains cholesterol in a storage form (esters) and triglycerides. The outer membrane includes a large protein called apoprotein B-100, “free” cholesterol molecules and phospholipids. The phospholipids contain fatty acids, including PUFA.

LDL has been demonized as “the bad cholesterol” and that demonization has mislead the public.

LDL is the major lipoprotein in our blood but there are others that have different names.

Cholesterol is cholesterol, whether it is carried in LDL or HDL. When carried in the core of a lipoprotein it is carried as a cholesterol ester. 80% of the cholesterol in an LDL particle is carried as an ester in the core. 20% is carried as “free” cholesterol on the outer surface or membrane.

HDL (high density lipoprotein) is smaller and denser. HDL has been called “the good cholesterol”, another misnomer.

HDL particles, when they are functioning correctly can protect us from atherosclerosis but in patients with diabetes, obesity, and insulin resistance, HDL particles do not function well and in fact probably contribute to disease. (More about that in a future post)

But back to LDL.

Although the risk of cardiovascular disease is correlated with the amount of cholesterol carried by LDL in our blood (referred to as LDL-C), the total amount of cholesterol shuttled by LDL particles is much less relevant than one would be led to believe given the great use of statin drugs to lower LDL-C.

The short version is as follows.

Compared to LDL-C, a much better predictor of cardiovascular disease is the amount of “modified” LDL particles circulating in the blood. Oxidized LDL particles are one form of “modified LDL”. LDL can also be modified by excess blood sugar levels (especially from HFCS). This modification is referred to as glycosylated or glycated LDL. In this latter form of modification, the major protein on the outer membrane of the LDL particle (apo B 100 in the picture above) becomes attached to a sugar and the result is an LDL particle that is not easily cleared by normal processes. The modified LDL is not “recognized” by the LDL receptors that act as entry points into our cells for proper processing. The result is that the glycated LDL particles circulate longer and are more likely to use up their anti-oxidants (Vitamin E and Co-enzyme Q 10).

As a result glycated LDL are more likely to become oxidized. That is not good because oxidized LDL sets up a cascade of unhealthy events.

The portion of the LDL particle that becomes oxidized is the fat (fatty acid) from “vegetable oil”, specifically the fatty acid called linoleic acid. This fatty acid has two double bonds making it more likely to be oxidized than for example oleic acid, the major fatty acid in extra virgin olive oil which has only one double bond.

The double bonds between the carbons in the fatty acids are unstable and easily oxidized. The single bonds in saturated fat do not get oxidized.

All other things being equal (and you will see that they are not), the more double bonds in a fatty acid the greater chance for oxidation.

Here is a picture showing the linoleic acid, also called linoleate, on the outer membrane of the LDL particle.

And here is a picture that shows the phospholipids that contain the linoleic acid.

Let’s say it again. The fatty acid found in “vegetable” oil, linoleic acid, is easily oxidized because it has two double bonds.

Saturated fats are not oxidized because they contain no double bonds.

The part of the LDL particle that becomes oxidized is the fatty acid that comes from “vegetable oils”.

A particular kind of immune cell (white blood cells called monocytes) have special receptors for oxidized LDL particles. When ox-LDL are “seen” by these monocytes, the monocytes become transformed into macrophages. Macrophages are designed to destroy bacteria that invade our bodies. The oxidized LDL particles resemble the structures of invading bacteria. The macrophages, with very specialized receptors for oxidized LDL, “swallow” the LDL particles and release toxic chemicals to destroy “the invader”. The macrophages then become “foam cells” in the walls of our arteries, initiating the creation of plaque. Here is a picture.

This picture depicts the oxidation occurring in the wall of the artery after LDL particles have penetrated the wall. However LDL particles can and do become oxidized while still circulating in the blood and these oxidized particles can stimulate monocytes to transform into macrophages and gobble up the oxidized or modified LDL while these particles are still circulating in the blood.

How and whether unmodified LDL particles cross the wall of arteries into the “sub-endothelial” area remains an unsolved complex issue. The picture above implies that LDL particles simply move across the endothelial cells that line the wall of the artery but that is a presumption.

Clearly, macrophages that have “swallowed” modified LDL particles have mechanisms to work their way between the junctions formed by adjacent endothelial cells.

This is an important distinction because many cardiologists believe that what drives atherosclerosis is a mass effect. The greater the number of LDL particles, the more likely they are to cross the endothelial barrier, get oxidized and retained and start the process of plaque formation. However the process is much more complex and not clearly understood.

We do not yet know or understand completely the factors that influence the permeability of the endothelium to Lipoprotein particles. We do know that modified (oxidized and glycated LDL) disrupt the protective surface of endothelial cells which is called the glyocalyx. Other factors that disrupt the glyocalyx include high blood sugars, dramatic fluctuations in blood pressure (too high or too low), oxidative stress, infections, and circulating endotoxin (which is governed by intestinal permeability).

It is clear from several studies that modified (oxidized) LDL as a single variable predicts cardiovascular disease and heart attacks with much greater accuracy than LDL-C (total cholesterol content of LDL particles). It is also clear that monocyte receptors are specific for modified LDL and that the process that initiates the cascade of events that leads to plaque formation involves the interaction between modified lipoprotein particles and the immune system (monocytes).

Now here is another twist.

Omega 3 fatty acids in fish oil are considered “heart healthy”. They help prevent heart attacks and strokes. They also decrease inflammation throughout the body thereby producing many health benefits.

BUT OMEGA 3 FAT HAS MORE DOUBLE BONDS THAN OMEGA 6 FAT (LINOLEIC ACID) YET THEY HELP PROTECT THE HEART. HOW CAN THAT BE?

How do they avoid contributing to atherosclerosis? Are they not even more readily oxidized than linoleic acid?

The simple answer is no.

The major reason is that the omega three fatty acids are protected by “plasmalogens” which are important components of our LDL particle outer membranes. Plasmalogens are found in the membranes of lipoprotein particles and in the membranes of human cells. Because of their chemical structures, omega three fats are easily incorporated into plasmalogens which protect the double bonds of omega three fats from oxidation. Linoleic acid, the predominant component of “vegetable oils” is not easily incorporated into the protective arms of plasmalogens.

This selective protection is well described on pages 141-142 of “The Fats of Life”, written by Dr. Glen Lawrence and published in paperback in 2013. (link below)

I asked Dr. Lawrence about this issue in an email and here was his response.

“The omega-3 fatty acids are preferentially incorporated into plasmalogens, which act as antioxidants due to the double bond adjacent to the ether linkage of these phospholipids. This structure would tend to scavenge free radicals or reactive oxygen species near the surface of the membrane, rather than allowing them to penetrate deeper in the membrane where the double bonds of PUFA are located. This makes any polyunsaturated fatty acids attached to the plasmalogens more resistant to oxidation than they would be in a regular phospholipid. See pp 141-142 of The Fats of Life. The shorter chain and less unsaturated linoleic acid does not tend to be incorporated into plasmalogens.”

In summary:

“Vegetable oil” is actually not oil from vegetables but rather a highly processed and refined oil. This oil contains primarily the easily oxidized omega 6 PUFA (polyunsaturated fatty acid) linoleic acid. Oxidation can occur during manufacture, before consumption while sitting in the bottle, but especially during high heat cooking (fried foods). Oxidation can also in your body as this fat circulates in your blood on the membrane of lipoprotein particles.
LDL particles are the major lipoprotein particles that shuttle cholesterol and fatty acids (in in the form of triglycerides) through our bodies in our bloodstream.
Modified LDL particles (glycated and/or oxidized LDL) stimulate monocytes (immune cells) to transform into macrophages and gobble up the modified LDL. In addition, glycated LDL particles are more easily oxidized because they circulate longer in our blood.
Macrophages become filled with modified LDL. These are called foam cells. Foam cells initiate a cascade of events that lead to the formation of plaque in the walls of our arteries.
The part of the LDL particle membrane that becomes oxidized is the phospholipid that contains linoleic acid which comes from “vegetable oils”
High amounts of sugar, especially HFCS, and highly refined flour foods in our diets cause larger blood sugar fluctuations than whole foods and therefore contribute to the glycation of LDL particles. This glycation leads to more oxidation of LDL. In this manner HFCS and refined flour foods contribute to the process of atherosclerosis.
High amounts of sugar, HFCS and refined flour foods also contribute to obesity, insulin resistance and diabetes which then increase the risk of heart attack and stroke.
Several factors contribute to the disruption of the glycocalyx which is the protective surface of the endothelial cells that line our arteries. These include but are not limited to modified LDL, inflammation, high blood sugars, abnormal fluctuations in blood pressure, circulating endotoxin (associated with increased intestinal permeability), infections. Disruption of the glycocalyx contributes to the formation of plaque (atherosclerosis).
Modified LDL particles might also migrate through the junctions that connect adjacent endothelial cells either inside macrophages or on their own. Many factors, known and unknown likely determine the susceptibility or permeability of these junctions to this migration.

These are the major points, but there is allot more to discuss. Substituting “vegetable oils” for saturated fat in our diets not only increases the amount of oxidized LDL but also increases a dangerous lipoprotein called Lp(a). On third of Americans have an amount of Lp(a) that is considered “high risk” for heart attack and stroke. More about that in a future post.

Then there is the process of an actual heart attack or stroke which involves disruption of plaque and the creation of a blood clot that ultimately disrupts the flow of blood and the death of heart or brain tissue. The susceptibility of plaque to disruption is a huge topic that involves high blood pressure, diabetes, insulin resistance, oxidative stress, inadequate sleep, and stress to name a few. So much more to discuss.

But getting back to the title of this post, why don’t you ask your elected representatives why our tax dollars continue to subsidize nutritional root causes of death, disability and disease?

Here are some links to papers and books that support the discussion above.

Circulating Oxidized LDL Is a Useful Marker for Identifying Patients With Coronary Artery Disease

Cholesterol deposition in macrophages: foam cell formation mediated by cholesterol-enriched oxidized low density lipoprotein.

Erythrocyte fatty acid profiles can predict acute non-fatal myocard… – PubMed – NCBI

Changes in Dietary Fat Intake Alter Plasma Levels of Oxidized Low-Density Lipoprotein and Lipoprotein(a)

Low-density lipoprotein subclass patterns and risk of myocardial in… – PubMed – NCBI

Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis

Oxidative susceptibility of low density lipoprotein subfractions is… – PubMed – NCBI

Effects of linoleate-enriched and oleate-enriched diets in combinat… – PubMed – NCBI

Enhanced oxidative susceptibility and reduced antioxidant content o… – PubMed – NCBI

Susceptibility of small, dense, low-density lipoproteins to oxidati… – PubMed – NCBI

Modulation of Endothelial Glycocalyx Structure under Inflammatory Conditions

Oxidized Lipoproteins Degrade the Endothelial Surface Layer

S1P Control of Endothelial Integrity

Mechanical control of the endothelial barrier. – PubMed – NCBI

Therole of actin-binding proteins in the control of endothelial bar… – PubMed – NCBI

The Fats of Life, Dr. Glen Lawrence

Functions of plasmalogen lipids in health and disease

Grain Brain: The Surprising Truth about Wheat, Carbs, and Sugar–Your Brain’s Silent Killers: David Perlmutter, Kristin Loberg: 9780316234801: Amazon.com: Books

Finally a quote from the Dali Lama (thanks to my cousin Diane for bringing this to my attention).

“Man. Because he sacrifices his health in order to make money. Then he sacrifices money to recuperate his health. And then he is so anxious about the future that he does not enjoy the present, the result being that he does not live in the present or the future, he lives as if he is never going to die, and dies having never really lived.”

Eat clean, live clean, sleep well, exercise wisely, rest often, enjoy the company of loved ones, spend time outdoors and live in the present.

BOB

Low Carb Beats Low Fat Again, Annals of Internal Medicine article

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Once again, a randomized trial demonstrates that a carbohydrate restricted approach is superior to a low fat diet with regards to weight loss, inflammation, body composition and cardiovascular risk factors. This study was recently published in the Annals of Internal Medicine, the official journal for the American College of Physicians.

Men and women aged 22 to 75 years with a body mass index of 30 to 45 kg/m² (obesity defined as BMI > 30, morbid obesity defined as BMI >35) were recruited from the general public by using mailing lists, fliers, work site and community screenings, and television advertisements.

Neither diet included a specific calorie or energy goal. Participants in each group were asked to refrain from changing their physical activity levels during the intervention

Here is the summary cut and pasted from the abstract.

Objective: To examine the effects of a low-carbohydrate diet compared with a low-fat diet on body weight and cardiovascular risk factors.

Design: A randomized, parallel-group trial. (ClinicalTrials.gov: NCT00609271)

Setting: A large academic medical center.

Participants: 148 men and women without clinical cardiovascular disease and diabetes.

Intervention: A low-carbohydrate (<40 g/d) or low-fat (<30% of daily energy intake from total fat [<7% saturated fat]) diet. Both groups received dietary counseling at regular intervals throughout the trial.

Measurements: Data on weight, cardiovascular risk factors, and dietary composition were collected at 0, 3, 6, and 12 months.

Results: Sixty participants (82%) in the low-fat group and 59 (79%) in the low-carbohydrate group completed the intervention. At 12 months, participants on the low-carbohydrate diet had greater decreases in weight (mean difference in change, −3.5 kg [95% CI, −5.6 to −1.4 kg]; P = 0.002), fat mass (mean difference in change, −1.5% [CI, −2.6% to −0.4%]; P = 0.011), ratio of total–high-density lipoprotein (HDL) cholesterol (mean difference in change, −0.44 [CI, −0.71 to −0.16]; P = 0.002), and triglyceride level (mean difference in change, −0.16 mmol/L [−14.1 mg/dL] [CI, −0.31 to −0.01 mmol/L {−27.4 to −0.8 mg/dL}]; P = 0.038) and greater increases in HDL cholesterol level (mean difference in change, 0.18 mmol/L [7.0 mg/dL] [CI, 0.08 to 0.28 mmol/L {3.0 to 11.0 mg/dL}]; P < 0.001) than those on the low-fat diet.

Limitation: Lack of clinical cardiovascular disease end points.

Conclusion: The low-carbohydrate diet was more effective for weight loss and cardiovascular risk factor reduction than the low-fat diet.

Primary Funding Source: National Institutes of Health.

Let’s go through those results again: At 12 months, participants on the low-carbohydrate diet had

greater decreases in weight. This has been demonstrated in multiple previously published studies.
greater decreases in fat mass. This is an important distinction, the low carb group lost more fat, not muscle.
greater decreases in the ratio of total to high-density lipoprotein (HDL) cholesterol. This ratio is a measure of cardiovascular risk (risk for heart attack and stroke). It improved more on low carb than on low fat diets.
greater decreases in triglyceride level. Triglyceride level is also an important cardiovascular risk factor. It went down significantly more as compared to the low fat diet.
greater increases in HDL cholesterol level. This result is considered to be protective against heart attack and stroke.
greater decreases in CRP level than those in the low-fat group. CRP (C-reactive protein) is a blood test for inflammation and is also a cardiovascular risk factor.
significant decreases in estimated 10-year risk for coronary heart disease as measured by the Framingham risk analysis at 6 and 12 months, whereas those in the low-fat group did not. Say again, the low fat group did not decrease their Framingham risk analysis but the low carb group did.

All of these differences were “statistically significant”, meaning they were unlikely caused by accident.
And what about side-effects?

The number of participants who had symptoms, including constipation, fatigue, thirst, polyuria, diarrhea, heartburn, gas, nausea, vomiting, appetite changes, or headache, did not differ significantly between the low-carbohydrate and low-fat groups, except significantly more participants on the low-fat diet reported headaches at 3 months

The authors concluded:

Our study found that a low-carbohydrate diet induced greater weight loss and reductions in cardiovascular risk factors at 12 months than a low-fat diet among black and white obese adults who did not have diabetes, CVD, or kidney disease at baseline. Compared with a low-fat diet, a low-carbohydrate diet resulted in greater improvements in body composition, HDL cholesterol level, ratio of total–HDL cholesterol, triglyceride level, CRP level, and estimated 10-year CHD risk. Because CVD is the most common cause of death in the United States and obesity is a particularly prevalent risk factor, our study has important clinical and public health implications

Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial, A. Bazzano, MD, PhD, MPH et. al., Ann Intern Med. 2014;161(5):309-318. doi:10.7326/M14-0180

Get rid of the sugar-added foods, processed and refined flour foods and vegetable oils. Send a message to corporate America that crap-in-a bag and crap-in-a-box is no longer in demand. Eat only grass-fed meat, wild seafood, fresh vegetables, fresh fruit and tree nuts. Enjoy better health and better food.

Bob Hansen MD.

Stress Reduction and Health

3 Replies

Mindfulness based stress reduction (MBSR) has been demonstrated to have beneficial effects relative to several physiologic measurements in humans. These include improved immune status, decreased inflammation as measured by blood tests, improved DNA repair (increased telomere length), and alterations in metabolic activity in areas of the brain that are viewed as beneficial relative to stress, anxiety and pain as measured by functional MRI scan of the brain (fMRI). Similarly other forms of meditation have been studied relative to cardiovascular risk in humans. The results indicate that stress reduction from meditation can decrease the “composite risk of death, heart attack and stroke” by 48% in patients who have experienced a previous heart attack. (1)

“A selected mind-body intervention, the TM program, significantly reduced risk for mortality, myocardial infarction, and stroke in coronary heart disease patients. These changes were associated with lower blood pressure and psychosocial stress factors. Therefore, this practice may be clinically useful in the secondary prevention of cardiovascular disease.”

This degree of protection exceeds the benefits of statin drugs in patients who have had a heart attack and exceeds the risk reduction accomplished by cardiac rehabilitation exercise programs.

A review of studies on the effects of meditation on cardiovascular disease reported: (2)

Psychosocial stress is a nontraditional risk factor for cardiovascular morbidity and mortality that may respond to behavioral or psychosocial interventions. …. Randomized controlled trials, meta-analyses, and other controlled studies indicate this meditation technique reduces risk factors and can slow or reverse the progression of pathophysiological changes underlying cardiovascular disease. Studies with this technique have revealed reductions in blood pressure, carotid artery intima-media thickness, myocardial ischemia, left ventricular hypertrophy, mortality, and other relevant outcomes. The magnitudes of these effects compare favorably with those of conventional interventions for secondary prevention

Dr. Dean Ornish utilized both meditation and yoga training in his lifestyle intervention program along with moderate exercise, smoke cessation and elimination of junk food (low fat vegan diet). The results demonstrated reduced coronary artery plaque within 2 years. Although many have attributed this to the vegan low fat diet, I have suggested in the past that the beneficial results were accomplished by stress reduction, exercise, smoke cessation, and elimination of junk food (especially refined sugar, flour, trans-fats and refined vegetable oils)

Our culture is not attuned to the regular practice of meditation or yoga. When I recommend stress reduction with these techniques to my patients few pursue it despite providing them with detailed descriptions of the physical benefits demonstrated by medical studies. One does not need to become a Buddhist in order to benefit from the practice of meditation. In the early 1970s the first stress reduction clinic utilizing MBSR(Mindfulness Based Stress Reduction) and Yoga was established at the University of Massachusetts Medical Center by Jon Kabat Zinn PhD. Since then many studies have documented the benefits of stress reduction relative to cardiovascular disease, diabetes, hypertension, chronic pain management, depression and anxiety.

Patients who have experienced their first major depressive episode can reduce the risk of a subsequent major depressive episode by 50% simply practicing MBSR regularly.

Unlike drugs, angioplasty, coronary stents, surgery, and injections, meditation and yoga have no potential negative side effects or complications. They simply require time, practice and a modest amount of training. Inexpensive self-help books, CDs and on-line resources are available to get started. Measurable physiologic benefits are experienced within a few weeks. Blood pressure drops, stress hormones decrease, blood sugars come down, insulin sensitivity improves, immune cells work better, sleep improves, suffering from chronic pain decreases, and functional status improves. That’s a considerable amount of benefit achieved by simply sitting quietly and observing your breath as it moves in and out of your body.

Meditation and yoga are two ways to reduce stress. For a healthy life to achieve stress reduction we must examine many areas. What aspects of daily life can increase and decrease stress and our physiologic response to stress?

Important factors to consider include social isolation, physical and social contact with friends/family/pets, meaningful work, laughter and humor, time spent outdoors, exercise, proper sleep habits and exposure to natural rather than artificial light. These all play significant roles in governing our stress levels, physiologic response to stress and the attendant changes in health.

Social isolation is harmful while regular contact with family and friends is beneficial. Caring for a pet seems to reduce blood pressure and enhance longevity. Engaging in meaningful work for pay or as a volunteer is essential for health, longevity and happiness. Spending time outdoors regularly and cycling your daily activity with the sun (circadian rhythm normalization) are essential to health and stress reduction. Laughter and social interaction provide healing while rumination over problems causes illness. All of these aspects to healthy living deserve attention but if you are ill, overweight, suffer chronic pain, disability or substance abuse then meditation and yoga can have profoundly beneficial effects. When combined with a Paleolithic diet and adequate restorative sleep, stress reduction techniques provide a powerful healing pathway.

Below is a long list of links to articles related to stress reduction, meditation, and yoga in the areas of chronic pain, cardiovascular disease, cancer, pre-natal care, anxiety disorders, depression, insomnia, smoke cessation, burnout, immune function, inflammation, migraine, blood pressure control, traumatic brain injury and even psoriasis.

Read to your heart’s content.

Bob Hansen MD

(1) Stress reduction in the secondary prevention of cardiovascular disease: randomized, controlled trial of transcendental meditation and health education in Blacks.

(2) Psychosocial stress and cardiovascular disease Part 2: effectiveness of the Transcendental Meditation program in treatment and prevention.

Here is the long list of other references. I have tried to group them in categories. There is allot of overlap between categories so my classification is somewhat arbitrary.

Asthma

Yoga intervention for adults with mild-to-moderate asthma: a pilot study.

Cardiovascular Disease:

Stress reduction in the secondary prevention of cardiovascular disease: randomized, controlled trial of transcendental meditation and health education in Blacks.

Usefulness of the transcendental meditation pro… [Am J Cardiol. 1996] – PubMed – NCBI

A randomised controlled trial of stress reduction for hypertension in older African Americans.

Effect of meditation on endothelial function in Black Americans with metabolic syndrome: a randomized trial.

Is there a role for stress management in reducing hypertension in African Americans?

Trial of stress reduction for hypertension in older African Americans. II. Sex and risk subgroup analysis.

Yoga for the primary prevention of cardiovascular disease.

Randomized controlled trial of mindfulness-based stress reduction for prehypertension.

Yoga Nidra relaxation increases heart rate variability and is unaffected by a prior bout of Hatha yoga.

Influence of psychosocial factors and biopsychosocial interventions on outcomes after myocardial infarction.

Trial of relaxation in reducing coronary risk: four year follow up.

When and why do heart attacks occur? Cardiovascular triggers and their potential role.

Emotional stressors trigger cardiovascular events.

How brain influences neuro-cardiovascular dysfunction.

CNS effects:

Short-term meditation training improves attention and self-regulation

Central and autonomic nervous system interaction is altered by short-term meditation

Neruoimaging and EEG

Neural mechanisms of mindfulness and meditation: Evidence from neuroimaging studies.

Short-term meditation induces white matter changes in the anterior cingulate

Mechanisms of white matter changes induced by meditation

Meditation’s impact on default mode network and hippocampus in mild cognitive impairment: a pilot study.

Mindfulness starts with the body: somatosensory attention and top-down modulation of cortical alpha rhythms in mindfulness meditation.

Effects of mindfulness meditation training on anticipatory alpha modulation in primary somatosensory cortex.

Cancer:

Increased mindfulness is related to improved stress and mood following participation in a mindfulness-based stress reduction program in individuals with cancer.

Impact of Mindfulness-Based Stress Reduction (MBSR) on attention, rumination and resting blood pressure in women with cancer: a waitlist-controlled study.

A non-randomized comparison of mindfulness-based stress reduction and healing arts programs for facilitating post-traumatic growth and spirituality in cancer outpatients.

One year pre-post intervention follow-up of psychological, immune, endocrine and blood pressure outcomes of mindfulness-based stress reduction (MBSR) in breast and prostate cancer outpatients.

Impact of mindfulness-based stress reduction (MBSR) on sleep, mood, stress and fatigue symptoms in cancer outpatients.

Keeping the balance–an overview of mind-body therapies in pediatric oncology.

Randomised controlled trials of yoga interventions for women with breast cancer: a systematic literature review.

Mindfulness-based stress reduction in relation to quality of life, mood, symptoms of stress and levels of cortisol, dehydroepiandrosterone sulfate (DHEAS) and melatonin in breast and prostate cancer outpatients.

A pilot study evaluating the effect of mindfulness-based stress reduction on psychological status, physical status, salivary cortisol, and interleukin-6 among advanced-stage cancer patients and their caregivers.

Can diet in conjunction with stress reduction affect the rate of increase in prostate specific antigen after biochemical recurrence of prostate cancer?

Meditation, melatonin and breast/prostate cancer: hypothesis and preliminary data.

Diabetes

Mindfulness-based stress reduction is associated with improved glycemic control in type 2 diabetes mellitus: a pilot study.

Immune System:

Alterations in brain and immune function produced by mindfulness meditation.

Insomnia and Sleep Physiology.

Mind-body interventions for the treatment of insomnia: a review.

Mindfulness-based stress reduction compared with cognitive behavioral therapy for the treatment of insomnia comorbid with cancer: a randomized, partially blinded, noninferiority trial.

Experienced mindfulness meditators exhibit higher parietal-occipital EEG gamma activity during NREM sleep.

I-CAN SLEEP: rationale and design of a non-inferiority RCT of Mindfulness-based Stress Reduction and Cognitive Behavioral Therapy for the treatment of Insomnia in CANcer survivors.

New insights into circadian aspects of health and disease.

Irritable Bowel

Mindfulness-based stress reduction for the treatment of irritable bowel syndrome symptoms: a randomized wait-list controlled trial.

Pain:

A comparison of mindfulness-based stress reduction and an active control in modulation of neurogenic inflammation.

The validation of an active control intervention for Mindfulness Based Stress Reduction (MBSR).

[Mindfulness-based therapeutic approaches: benefits for individuals suffering from pain].

Mindfulness-based stress reduction, mindfulness-based cognitive therapy, and Zen meditation for depression, anxiety, pain, and psychological distress.

Mindfulness starts with the body: somatos… [Front Hum Neurosci. 2013] – PubMed – NCBI

Altered anterior insula activation during anticipation and experience of painful stimuli in expert meditators.

Differential effects on pain intensity and unpleasantness of two meditation practices.

Self-directed Mindfulness Training and Improvement in Blood Pressure, Migraine Frequency, and Quality of Life.

Effectiveness of mindfulness meditation (Vipassana) in the management of chronic low back pain.

Mindfulness meditation in the control of severe headache.

The clinical use of mindfulness meditation for the self-regulation of chronic pain.

An outpatient program in behavioral medicine for chronic pain patients based on the practice of mindfulness meditation: theoretical considerations and preliminary results.

Mindfulness-based stress reduction for chronic pain conditions: variation in treatment outcomes and role of home meditation practice.

Psych, Depression, Anxiety, Burnout, Students

Mindfulness meditation practices as adjunctive treatments for psychiatric disorders.

Reducing psychological distress and obesity through Yoga practice

Yoga and social support reduce prenatal depression, anxiety and cortisol.

Meditation Programs for Psychological Stress and Well-Being [Internet].

Meditation programs for psychological stress and well-being: a systematic review and meta-analysis.

Tai chi training reduces self-report of inattention in healthy young adults.

Mindfulness for teachers: A pilot study to assess effects on stress, burnout and teaching efficacy.

Mindfulness-Based Stress Reduction for Low-Income, Predominantly African American Women With PTSD and a History of Intimate Partner Violence.

Mindfulness-based cognitive therapy for generalized anxiety disorder.

Three-year follow-up and clinical implications of a mindfulness meditation-based stress reduction intervention in the treatment of anxiety disorders.

Effectiveness of a meditation-based stress reduction program in the treatment of anxiety disorders.

Enhanced response inhibition during intensive meditation training predicts improvements in self-reported adaptive socioemotional functioning.

Intensive meditation training improves perceptual discrimination and sustained attention.

Home-based deep breathing for depression in patients with coronary heart disease: a randomised controlled trial.

Mindfulness-based stress reduction lowers psychological distress in medical students.

Yoga and exercise for symptoms of depression and anxiety in people with poststroke disability: a randomized, controlled pilot trial.

The effect of yoga on coping strategies among intensive care unit nurses.

Mindfulness-based stress reduction and health-related quality of life in a heterogeneous patient population.

Developing mindfulness in college students through movement-based courses: effects on self-regulatory self-efficacy, mood, stress, and sleep quality.

Differential effects of mindful breathing, progressive muscle relaxation, and loving-kindness meditation on decentering and negative reactions to repetitive thoughts.

Psychological and neural mechanisms of trait mindfulness in reducing depression vulnerability.

A narrative review of yoga and mindfulness as complementary therapies for addiction.

The acute effects of yogic breathing exercises on craving and withdrawal symptoms in abstaining smokers.

Yoga and massage therapy reduce prenatal depression and prematurity.

Mind-body interventions during pregnancy for preventing or treating women’s anxiety.

Misc. and General

Mindfulness-based interventions for physical conditions: a narrative review evaluating levels of evidence.

Evaluation of a Mindfulness-Based Stress Reduction (MBSR) program for caregivers of children with chronic conditions.

Empirical explorations of mindfulness: conceptual and methodological conundrums.

Mindfulness meditation: do-it-yourself medicalization of every moment.

Becoming conscious: the science of mindfulness.

Meditate to medicate.

Mindfulness in medicine.

Cultivating mindfulness: effects on well-being.

Mind-body medicine. An introduction and review of the literature.

Tai chi chuan in medicine and health promotion.

Tai chi/yoga effects on anxiety, heartrate, EEG and math computations.

Mindfulness Research Update: 2008.

Development and preliminary evaluation of a telephone-based mindfulness training intervention for survivors of critical illness.

A randomized controlled trial of Koru: a mindfulness program for college students and other emerging adults.

Hair Cortisol as a Biomarker of Stress in Mindfulness Training for Smokers.

A review of the literature examining the physiological processes underlying the therapeutic benefits of Hatha yoga.

Body Awareness: a phenomenological inquiry into the common ground of mind-body therapies.

Cortical dynamics as a therapeutic mechanism for touch healing.

Establishing key components of yoga interventions for musculoskeletal conditions: a Delphi survey.

Hatha yoga on body balance.

Yoga might be an alternative training for the quality of life and balance in postmenopausal osteoporosis.

Becoming conscious: the science of mindfulness.

Organ Transplant

Mindfulness meditation to reduce symptoms after organ transplant: a pilot study.

Post Traumatic Brain Injury

A pilot study examining the effect of mindfulness-based stress reduction on symptoms of chronic mild traumatic brain injury/postconcussive syndrome.

Psoriasis

Influence of a mindfulness meditation-based stress reduction intervention on rates of skin clearing in patients with moderate to severe psoriasis undergoing phototherapy (UVB) and photochemotherapy (PUVA).

Telemorase, DNA, Genes

Rapid changes in histone deacetylases and inflammatory gene expression in expert meditators.

Can meditation slow rate of cellular aging? Cognitive stress, mindfulness, and telomeres.

Intensive meditation training, immune cell telomerase activity, and psychological mediators.

Contemplative practice, chronic fatigue, and telomerase activity: a comment on Ho et al.

Toward a unified field of study: longevity, regeneration, and protection of health through meditation and related practices.

Weight Gain, Another Reason to Avoid Statins

2 Replies

Published on line two days ago in advance of print publication, a new study demonstrates an association between statin use and increased caloric intake resulting in weight gain. (1)

A brief editorial (Written by Dr. Rita Redberg, on faculty at UCSF and editor of JAMA: INTERNAL MEDICINE). is worth quoting in entirety as it succinctly reviews many criticisms of statin overuse that I have discussed in previous posts here and here.

“There remains much controversy over the risks and benefits of statins for primary prevention. Besides the risks of muscle aches, diabetes, and cognitive dysfunction, I have observed over the years that for many patients, statins provide a false reassurance, as people seem to believe that statins can compensate for poor dietary choices and a sedentary life. In an elegantly performed analysis of NHANES data from 1999 to 2010, Sugiyama and colleagues have documented exactly such behavior. They found that compared with statin nonusers, statin users significantly increased their fat intake and calorie consumption, along with their BMI, in the last decade. This article raises concerns of a potential moral hazard of statin use, in addition to the already known adverse effects. Focusing on cholesterol levels can be distracting from the more beneficial focus on healthy lifestyle to reduce heart disease risk.” (2)

Of course association does not imply causation, but the editorial above suggests a plausible explanation for the relationship.

I have previously discussed how a carbohydrate restricted whole foods diet (here and here) results in superior weight loss, improved glucose control, reduced blood pressure, reduced triglycerides and improved HDL when compared to a low fat American Heart Association type diet. The former results in spontaneous reduction of caloric intake (improved satiety-no calorie counting required), the latter requires calorie counting in order to reduce caloric intake. The carbohydrate restricted approach does NOT result in increased net fat intake but because carbohydrates are reduced, fat as a % of total calories is increased. On average most studies in adults report a spontaneous reduction of about 400-600 calories per day when carbohydrates are significantly restricted.

A paleolithic diet that eliminates all processed foods, refined vegetable oils, grains, legumes and dairy but includes pastured grass-fed meat, wild seafood, free range poultry and eggs, organic fresh vegetables, fruit and nuts is typically low carbohydrate compared to the standard American diet (SAD). A paleolithic nutritional approach produces similar metabolic improvement within a few weeks. (3)

(1) Sugiyama T, Tsugawa Y, Tseng C-H, Kobayashi Y, Shapiro MF. Different time trends of caloric and fat intake between statin users and nonusers among US adults: gluttony in the time of statins? [published online April 24, 2014]. JAMA Intern Med. doi:10.1001/jamainternmed.2014.1927. PubMed

(2) Statins and Weight Gain: Redberg RF. JAMA Intern Med. 2014 Apr 24. doi: 10.1001/jamainternmed.2014.1994. [Epub ahead of print] PubMed

(3) Metabolic and physiologic improvements from consuming a paleolithic, hunter-gatherer type diet L A Frassetto1, M Schloetter, M Mietus-Synder, R C Morris Jr1 and A Sebastian European Journal of Clinical Nutrition (2009) 63, 947–955; doi:10.1038/ejcn.2009.4; published online 11 February 2009 PubMed

Go in peace

Bob Hansen MD

Fat consumption, Fat circulating in your blood, Heart Disease

1 Reply

Another nail has been driven into the coffin of the diet-heart hypothesis. The Annals of Internal Medicine (the official journal for the American College of Physicians) just published a review article that considered three kinds of studies related to fat and heart disease. (1)

Studies that evaluated the association between dietary consumption of different kinds of fat and cardiovascular disease (heart attack and stroke)
Studies that evaluated the association between levels of different kinds of fat circulating in the blood and cardiovascular disease
Studies that evaluated supplementation with various kinds of fat and cardiovascular disease.

Most importantly, the authors found no statistical association between consumption of saturated fat and cardiovascular disease. I have previously discussed another large meta-analysis published in 2010 with the same finding. (2)

I have discussed the unscientific demonization of saturated fat many times (3,4,5).

This is important because it again speaks against the dietary advice promulgated by the AHA and the USDA to reduce consumption of saturated fat. The low-fat advice has resulted in a proliferation of low-fat high-sugar and high-carbohydrate food products which arguably have contributed to the epidemics of obesity and diabetes in the US.

Similarly, recent studies have correlated dementia with high carbohydrate consumption. (6) If you reduce fat in the diet you must replace it with something else and unfortunately in the US that something else has been sugar and other refined carbohydrates.

Other statistically significant findings in the Annals of Internal Medicine study were an inverse relationship between circulating blood levels of the omega three fats found in seafood (EPA and DHA) and cardiovascular events. The authors pointed out that although higher blood levels of EPA and DHA were significantly associated with lower cardiovascular risk, supplementation with EPA and DHA have had mixed results with many studies showing positive results but some showing no protective effects. My comments on the omega three supplement studies are

supplementation with fish oil (omega three fats) will not benefit most individuals unless excess pro-inflammatory omega six fats (found in refined vegetable oils) are reduced/eliminated and that side of the equation has not been addressed in any of the published studies. In other words, the studies did not reduce omega 6 fats, they just supplemented with omega 3 fat. If an individual is consuming 30-60 grams of omega six fats per day, trying to balance that with 2-3 grams per day of fish oil will not achieve a healthy ratio.
many of the fish oil (omega three) supplement studies used very low amounts of fish oil, well below the amounts used in the studies that demonstrated benefit.

I am not suggesting that everyone should take fish oil supplements. Instead, I support eating a whole foods paleolithic diet based on grass-fed meat, free range poultry, free range eggs, fresh wild seafood, fresh vegetables, fresh fruits and nuts.

Finally, the data on trans-fat consumption demonstrated statistically significant correlation with cardiovascular disease. The biochemistry and physiology of manufactured trans-fats demonstrate a disruptive role of these man-made fats and the elimination of these harmful fats from our food supply will likely provide great health benefits.

The authors comment on the complex relationship between fat consumption and circulating levels of specific fats in the blood as demonstrated by Forsythe et al. (6,7) I will discuss this in future posts. For now consider the paradox that high-fat carbohydrate restricted diets result in lower circulating levels of saturated fat compared to high carbohydrate diets. (6,7), Explanation: excess carbohydrates are immediately converted to fat and stored as saturated fat by humans.

1. Annals of Internal Medicine | Association of Dietary, Circulating, and Supplement Fatty Acids With Coronary Risk: A Systematic Review and Meta-analysis

2. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010; 91:535-46.
PubMed

3. https://practical-evolutionary-health.com/2014/02/16/can-goose-liver-grass-fed-meat-aged-hard-cheese-free-range-eggs-and-cod-liver-oil-prevent-a-heart-attack/

4. https://practical-evolutionary-health.com/2013/11/03/saturated-fat-vs-sugar/

5. https://practical-evolutionary-health.com/2013/11/01/saturated-fat-does-it-matter/

6. Relative intake of macronutrients impacts risk of mild cognitive impairment or dementia. Journal of Alzheimers Dis. 2012;32(2):329-39. doi: 10.3233/JAD-2012-120862.

7. Forsythe CE, Phinney SD, Feinman RD, Volk BM, Freidenreich D, Quann E, et al. Limited effect of dietary saturated fat on plasma saturated fat in the context of a low carbohydrate diet. Lipids. 2010; 45:947-62. PubMed

8. Forsythe CE, Phinney SD, Fernandez ML, Quann EE, Wood RJ, Bibus DM, et al. Comparison of low fat and low carbohydrate diets on circulating fatty acid composition and markers of inflammation. Lipids. 2008; 43:65-77. PubMed

Peace,

Bob Hansen MD

Can goose liver, grass-fed meat, aged hard cheese, free range eggs and cod liver oil prevent a heart attack?

Leave a reply

The data suggests that the answer is yes. The first four of these health foods are rich sources of vitamin K2 and the last food item is packed with Vitamins A and D. The proposed mechanism for their protective effect rests in a wonderful biological quartet. The instruments of this quartet include the fat soluble vitamins D, K2, and A playing harmoniously with a ubiquitous human protein called Matrix gla protein (MGP).

The basic science is exquisite. Vitamins D and A acting together enhance the expression of MGP. In other words, these two fat-soluble vitamins cause our bodies to increase the production of MGP. MGP resides throughout our bodies including the walls of our arteries. Vitamin K2 then activates the MGP which in turn regulates (prevents) the calcification of plaque in the walls of our arteries. MGP masterfully plays this role in many arteries and it’s artistry is particularly effective in the coronary arteries that supply blood and oxygen to heart muscle.

Heavily calcified coronary plaque (the nasty stuff that produces atherosclerosis) as compared to un-calcified plaque is much more likely to rupture and create an acute blockage, thereby causing a heart attack. By inhibiting calcification of coronary plaque activated MGP decreases the risk of a heart attack. The biochemistry and physiology of this process are well accepted and discussed in the opening of several papers that address this topic. (1,2,3)

The data that support this theory includes a lot of basic science that describes the interaction between the four players as well as nutritional studies in humans and rodents.

The first major human study was the Rotterdam study published in the Journal of the American Society for Nutritional Sciences, 2004. Here is a quote from the summary.

“Vitamin K-dependent proteins, including matrix Gla-protein, have been shown to inhibit vascular calcification. Activation of these proteins via carboxylation depends on the availability of vitamin K. We examined whether dietary intake of phylloquinone (vitamin K-1) and menaquinone (vitamin K-2) were related to aortic calcification and coronary heart disease (CHD) in the population-based Rotterdam Study.”

The study followed 4801 adults for over 7 years and analyzed the relationship between Vitamin K intake and incidence of heart attacks, (fatal and non-fatal), death from all causes, and atherosclerosis in the aorta (the major artery of the body). The results were impressive. The analysis divided the 4801 people into three equal groups, 1/3 with the highest consumption of Vitamin K, 1/3 with the lowest consumption, and 1/3 in the middle. The higher and middle groups compared to the group with the lowest consumption had:

significantly fewer non-fatal heart attacks,
significantly fewer deaths from heart attack,
significantly fewer deaths from all causes.

In addition, the group with the highest consumption of Vitamin K2 had significantly less calcified plaque in the walls of their aortas.

Comparing the group of the highest intake of vitamin K2 to the group with the lowest intake, the highest intake group had 41% less risk of non-fatal heart attack, 57% lower risk of death from heart attack and 26% lower risk of death from all causes after adjusting for multiple factors that are believed to play a role in heart attack risk. (Those other factors included age, gender, total energy intake, BMI, smoking status, pack-years smoking, diabetes, education, alcohol consumption. consumption of saturated fat, poly unsaturated fat, flavonoids (anti-oxidants) and calcium.)

Vitamin K2 consumption showed these significant associations whereas Vitamin K1 did not. Vitamin K2 is found most abundantly in animal foods that contain erroneously demonized saturated fat, Vitamin K1 is found in plants that do not contain much if any saturated fat. So this represents not only a strong statistical signal for the health benefit of Vitamin K2, but also supports the health benefit of consuming animal foods with saturated fat. The individuals who consumed more meat and more full fat fermented cheese (the two major sources of vitamin K2 in this study) had dramatically reduced risk of heart attack (both fatal and non-fatal), reduced risk of death from all causes, and less calcified plaque in the major artery of the body, the aorta. Vitamin K2 is a fat soluble vitamin which means it comes with the fat in these foods. Eating low fat foods misses this healthy opportunity.

Five years after the Rotterdam study was published, another study demonstrated similar findings. The title tells the story.

“A high menaquinone (vitamin K2) intake reduces the incidence of coronary heart disease.”

This study followed 16,057 women aged 49-70 years for 8 years. The study participants had no known heart disease at the start of the study. The results:

“After adjustment for traditional risk factors and (other) dietary factors, we observed an inverse association between vitamin K(2) and risk of CHD with a Hazard Ratio (HR) of 0.91 [95% CI 0.85-1.00] per 10 microg/d vitamin K(2) intake.”

Translation: for every increase in daily consumption of vitamin K2 by 10 micrograms per day, there was an average 9% reduction in risk of coronary disease events.

Let’s look at how much Vitamin K2 was consumed in the three groups described in the first study. Going from the lowest to the highest daily consumption the groups averaged 15.1, 26.9 and 40.9 micrograms per day. To put this in perspective, you can view a table of the Vitamin K2 content of various foods produced by Chris Masterjohn, a portion of which appears below. Before you do that, let me explain some facts about Vitamin K2.

Vitamin K2 actually represents a group of very similar vitamins that differ chemically only in the number of specific chemical side chains. The number of these side chains varies from 4 to 10, so these are referred to as MK-4 through MK-10. From Wikepedia:

All K vitamins are similar in structure: they share a “quinone” ring, but differ in the length and degree of saturation of the carbon tail and the number of “side chains”.^[1] The number of side chains is indicated in the name of the particular menaquinone (e.g., MK-4 means that four molecular units – called isoprene units – are attached to the carbon tail) and this influences the transport to different target tissues.

MK-4 is made in the tissue of grass-eating mammals that convert Vitamin K1 (from the green plants) to Vitamin K2 (MK-4). This can be obtained from animal muscle, organ meats, or the milk and milk products of mammals, including human breast milk.

The other forms of Vitamin K-2 (side-chain length > 4) are made by bacteria during the fermentation of foods (such as cheese, sauerkraut, kim chee and Natto). Here is the table from Chris Masterjohn. Go here for the original table.

The percentage of vitamin K₂ present as MK-4 represents that synthesized by animal tissues, while the remainder represents that synthesized by bacteria during fermentation.

FOOD	VITAMIN K2 (MCG/100G)
Natto	1103.4	(0% MK-4)
Goose Liver Paste	369.0	(100% MK-4)
Hard Cheeses	76.3	(6% MK-4)
Soft Cheeses	56.5	(6.5% MK-4)
Egg Yolk (Netherlands)	32.1	(98% MK-4)
Goose Leg	31.0	(100% MK-4)
Curd Cheeses	24.8	(1.6% MK-4)
Egg Yolk (United States)	15.5	(100% MK-4)
Butter	15.0	(100% MK-4)
Chicken Liver	14.1	(100% MK-4)
Salami	9.0	(100% MK-4)
Chicken Breast	8.9	(100% MK-4)
Chicken Leg	8.5	(100% MK-4)
Ground Beef (Medium Fat)	8.1	(100% MK-4)
Bacon	5.6	(100% MK-4)
Calf Liver	5.0	(100% MK-4)
Sauerkraut	4.8	(8% MK-4)
Whole Milk	1.0	(100% MK-4)

Where did our paleolithic hunter-gatherer ancestors get their Vitamin K2? They did not consume dairy products. Vitamin K2 is heavily concentrated in the pancreas, brain and liver of humans and animals. Hunter-gatherers do not waste these valuable fatty organs, in fact offal was deemed the most treasured part of a successful hunt among many hunter-gatherer societies studied during the 19th and 20th centuries.

Not many Americans eat offal such as pancreas, brain and liver so similar to Holland (where these studies were conducted) most Vitamin K2 in the American diet probably comes from hard cheese and egg yolks.

But what is the weakness in drawing conclusions from these two studies?

First they were epidemiological studies, the data was obtained from FFQs (food frequency questionnaires). They were not randomized controlled clinical trials (RCTs). There have been no RCTs that have looked specifically at Vitamin K2 relative to coronary artery disease and deaths. Having said that, you should be aware that most nutrition studies that have been published (in particular those that demonize saturated fat ) fall into the same category, they are epidemiological studies based upon food frequency questionnaires (FFQs) and such studies have been criticized with regards to reliability of data and for lack of controlling the multiple dietary and non-dietary factors that can influence health outcomes.(4)

Unlike the two studies discussed here that statistically adjusted for multiple known or argued risk factors, the epidemiologic studies that are alleged to suggest potential harm from saturated fat did not control or adjust for other statistical “con-founders”. In addition, the review papers that have so overwhelmed our society causing fat-phobia have ignored the large body of evidence that demonstrates the health benefits of consuming animal foods that contain fat soluble vitamins as well as many other vital nutrients. (4)

Regarding randomized controlled trials, there have been many convincing RCTs in rodents that demonstrate not only prevention of calcified plaques in arterial walls but actual reversal of atherosclerosis in rodents with high doses of vitamin K2. (5) Furthermore, a certain breed of experimental rodent that completely lacks MGP suffers from early death caused by severe atherosclerosis further supporting the fundamental role of activated MGP in maintaining vascular health. (6)

1. Dietary Intake of Menaquinone Is Associated with a Reduced Risk of Coronary Heart Disease: The Rotterdam Study

2. A high menaquinone intake reduces … [Nutr Metab Cardiovasc Dis. 2009] – PubMed – NCBI

3. Vitamin K status and vascular calcification: eviden… [Adv Nutr. 2012] – PubMed – NCBI

4. Dietary Fats and Health: Dietary Recommendations in the Context of Scientific Evidence

5. Regression of warfarin-induced medial elastocalcinosis… [Blood. 2007] – PubMed – NCBI

6. Two sides of MGP null arterial disease: chondrogenic lesions dependent on transglutaminase 2 and elastin fragmentation associated with induction of adipsin.

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