Tag Archives: PUFA

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.

LDL 2

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.

hdl_ldl good guy bad guy

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.

LDLand cholesterol molecule

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.

LDL with linoleate

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

LDL 3

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.

ldl_mechanisms oxidation in vessel wall

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:

  1. “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.
  2.  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.
  3. 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.
  4. 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.
  5. The part of the LDL particle membrane that becomes oxidized is the phospholipid that contains linoleic acid which comes from “vegetable oils”
  6. 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.
  7. 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.
  8. 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).
  9. 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

The Dirty Dozen and The Clean Fifteen, from the Environmental Working Group

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I’ve been working on two projects that have kept me from blogging. The first project was a lecture given at the January meeting of Physicians for Ancestral Health. The second project, still on-going, developed out of a new working relationship with Dr. Tommy Wood who I met at the PAH meeting. I will be sharing more about both of these in future posts.

But today I am returning where I left off with my last post about toxins in our babies and our environment. i promised to discuss the The Dirty Dozen and The Clean Fifteen, both trademarks of the Environmental Working Group . So here it is.

The EWG developed these lists to help individuals make informed purchasing decisions  relative to organic vs non-organic vegetables and fruits. The EWG analyzed data from testing for residuals of pesticides. So if you cannot afford to purchase all organic produce, you can get the most benefit from your dollar by limiting your non-organic produce to the “clean” list and purchasing only organic from the “dirty list”.

Highlights of Dirty Dozen™ 2014

Each of these foods contained a number of different pesticide residues and showed high concentrations of pesticides relative to other produce items.

EWG’s Dirty Dozen™ list of produce includes

  1. apples,
  2. strawberries,
  3. grapes,
  4. celery,
  5. peaches,
  6. spinach,
  7. sweet bell peppers,
  8. imported nectarines,
  9. cucumbers,
  10. cherry tomatoes,
  11. imported snap peas
  12. potatoes.

“In particular:

  • Every sample of imported nectarines and 99 percent of apple samples tested positive for at least one pesticide residue.
  • The average potato had more pesticides by weight than any other food.
  • A single grape sample contained 15 pesticides. Single samples of celery, cherry tomatoes, imported snap peas and strawberries showed 13 different pesticides apiece.”

 Dirty Dozen PLUS™

For the third year, EWG expanded the Dirty Dozen™ with a Plus category to highlight two foods that contain trace levels of highly hazardous pesticides. These foods do not meet traditional Dirty Dozen™ ranking criteria but were frequently contaminated with insecticides that are toxic to the human nervous system. EWG recommends that people who eat a lot of these foods buy organic instead.

  1. Leafy greens – kale and collard greens
  2. hot peppers

The Clean Fifteen™ Relatively few pesticides were detected on these foods, and tests found low total concentrations of pesticides.

EWG’s Clean Fifteen™ for 2014 – the produce least likely to hold pesticide residues – are

  1. avocados,
  2. sweet corn,
  3. pineapples,
  4. cabbage,
  5. frozen sweet peas,
  6. onions,
  7. asparagus,
  8. mangoes,
  9. papayas,
  10. kiwis,
  11. eggplant,
  12. grapefruit,
  13. cantaloupe,
  14. cauliflower
  15. sweet potatoes.

 “Notable findings:

  • Avocados were the cleanest: only 1 percent of avocado samples showed any detectable pesticides.
  • Some 89 percent of pineapples, 82 percent of kiwi, 80 percent of papayas, 88 percent of mango and 61 percent of cantaloupe had no residues.
  • No single fruit sample from the Clean Fifteen™ tested positive for more than 4 types of pesticides.
  • Detecting multiple pesticide residues is extremely rare on Clean Fifteen™ vegetables. Only 5.5 percent of Clean Fifteen samples had two or more pesticides.”

At the PAH meeting I spoke with Dr.Tommy Wood and Darryl Edwards , both from England, about food choices in Europe vs the USA.  We had this conversation while eating out and asking the waitress questions about the sources of food. They both commented that when eating in England or the European Union they are not often concerned about food quality because the use of pesticides, hormones, and antibiotics is so reasonably regulated. Most produce is considered organic or close to organic. In addition most meats are grass-fed, free of or low in exogenous hormones and antibiotics, free of excess pro-inflammatory omega six fat and contain more anti-inflammatory and beneficial omega 3 fat, similar to the fat profiles of wild game. Concentrated Animal Feeding Operations (CAFOs) so prevalent in the US are rare in the European Union.

Food for thought and thoughts about food.

Eat clean, live clean and prosper.

Bob

The Ornish Low Fat Vegetarian Diet, does it work?

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Dr. Dean Ornish has done wonderful research in the area of cardiovascular disease and lifestyle intervention. His study on comprehensive lifestyle intervention (1) is often quoted to support a low fat vegetarian diet as treatment for cardiovascular disease. But his “Intensive lifestyle changes for reversal of coronary heart disease” included several components that would be expected to improve health and decrease cardiovascular risk independent of a vegetarian diet as will be discussed below.

Let’s review what this study did.

48 patients with diagnosed moderate to severe coronary artery disease were randomized to one of two treatment groups, an “intensive lifestyle change” (ILC) group or a “usual-care” (UC) control group. 28 patients were allocated randomly to the ILC group and 20 were allocated to the UC group. Out of 48 patients starting the study only 35 completed the study,   20 out of 28 in the ILC group completed the study and 15 out of 20 in the UC group completed the study.

The intensive lifestyle change group followed this program:

  • 10% fat whole foods vegetarian diet
  • daily aerobic exercise
  • stress management training (training in and daily performance of meditation and/or yoga)
  • smoke cessation (they quit smoking)
  • group psychosocial support (3 hour group therapy sessions)

At the start of the study only one patient in the ILC group was smoking and she quit. We do not know how many smokers were in the UC group or how many quit. (I consider that a deficiency of this study. Because smoking is such a significant determinant of cardiovascular outcome, details of smoking at start and end of the study for both groups should have been reported)

At the end of five years the intensive lifestyle change group demonstrated an average 3.1% absolute reduction in the coronary artery blockage as measured by coronary arteriograms (or to put it another way, the diameter of the blocked coronary arteries increased by 3.1%). The usual care group (receiving cholesterol lowering statin drugs) showed an average 2.3% absolute increase in the coronary artery blockage (2.3% reduction in diameter). These are not huge changes or differences but they were measurable and statistically significant.

Twenty five total  “cardiac events” occurred in the 28 patients randomized to the intensive lifestyle change group over the five years and 45 cardiac events occurred in the 20 patients randomized to the “usual care” group (receiving cholesterol lowering statin drugs). But this was due to differences in the number of hospitalizations and angioplasties. There was no statistically significant difference in the number of deaths, heart attacks or coronary artery bypass surgeries.

By the end of the study 2 patients in the ILC group had died compared to 1 death in the usual care group but as mentioned above, this difference was not statistically significant.  We do not know how many deaths occurred in the 8 patients who dropped out of the treatment group or in the 5 patients who dropped out of the usual care group, nor do we know any of the other outcomes for the drop-out patients.

So there were no lives saved by the intensive lifestyle change program and no reduction in the number of heart attacks. In fact the ILC group had 2 deaths compared to 1 in the usual care group.

What does this all mean and why has the Ornish Diet attracted so much attention.?

First, I would suggest that the demonstrated benefits (reductions in the number of angioplasties and hospitalizations) are likely explained by the following parts of the lifestyle changes.

  1. stress reduction training and implementation (meditation and yoga)
  2. elimination of manufactured trans-fats from the diet
  3. elimination of unhealthy pro-inflammatory excess omega six fats (vegetable oils) from the diet
  4. elimination/reduction of processed carbohydrates and sugar.

Although the intensive lifestyle intervention included regular exercise the data show no significant difference in times per week or hours per week of exercise at the end of the study between the two groups.

The big difference was in stress management. The ILC group averaged practicing meditation and/or yoga 5 times per week (48 minutes per day) versus less that once per week (8 minutes per day) in the usual care group.

Stress reduction is a major issue in any disease and in particular in cardiovascular disease.

Several studies have demonstrated that the daily practice of meditation  improves immune function, increases telomerase activity, reduces inflammatory markers, and reduces circulating stress hormones (cortisol and epinephrine) independent of dietary changes.
Meditation has also been observed to improve “endothelial function”, the ability of the cells that line arteries to respond to changes in demand. (2,3,4,5,6,7)

Here is a press release from the American Heart Association 13 November 2012. (8)

“African Americans with heart disease who practiced Transcendental Meditation regularly were 48 percent less likely to have a heart attack, stroke or die from all causes compared with African Americans who attended a health education class over more than five years, according to new research published in the American Heart Association journal Circulation: Cardiovascular Quality and Outcomes.

Those practicing meditation also lowered their blood pressure and reported less stress and anger. And the more regularly patients meditated, the greater their survival, said researchers who conducted the study at the Medical College of Wisconsin in Milwaukee.”

I believe the major benefit of the interventional program was from the stress reduction and the elimination of three major dietary sources of trouble (trans-fats, excess omega 6 fats from processed-refined vegetable oils, and refined carbohydrates-sugar)

I have already discussed in other posts the problems associated with excess omega 6 fats and refined carbohydrates-sugar relative to cardiovascular risk. (9,10,11)

There is little controversy that elimination/reduction in trans-fats produces benefit. (12,13,14)

All three of these changes were essential to the whole foods approach of the intervention group.

I have also discussed the lack of data to support the contention that saturated fat from animal sources of protein contributes to cardiovascular disease. (15, 16))

I remain a strong proponent of a whole foods diet that includes a variety and abundance of organic vegetables and fruits, nuts, pastured grass-fed meat, fresh wild seafood, free-range organic poultry and eggs from that kind of poultry.  This diet represents the foods we have evolved to eat, free from added sugar, hormones, antibiotics, pesticides. This dietary approach also produces a healthy balance of omega 6 to omega 3 fatty acid as well as a significant improvement in the ratio of potassium to sodium.

Stress reduction should be an essential part of our lives and data on this aspect of health will be discussed in future posts. References for this discussion appear below.

Peace,

BOB Hansen MD

REFERENCES:

1. JAMA Network | JAMA | Intensive Lifestyle Changes for Reversal of Coronary Heart Disease

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

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

4. A pilot study of yogic meditation for family dementia caregivers with depressive symptoms: effects on mental health, cognition, and telomerase activity.

5. Meditation Improves Endothelial Function in Metabolic Syndrome, American Psychosomatic Society (APS) 69th Annual Scientific Meeting: Abstract 1639. Presented March 10, 2011.

6. Alterations in brain and immune function produced by mindfulness meditation.

7. Adrenocortical activity during meditation.

8. Meditation may reduce death, heart attack and stroke in heart patients | American Heart Association

9. Polyunsaturated fat, Saturated fat and the AHA

10, Lose weight, control blood sugar, reduce inflammation

11. Sugar, a serious addiction

12. The negative effects of hydrogenated trans fats and what to do about them.

13. Trans fats in America: a review of their use… [J Am Diet Assoc. 2010] – PubMed – NCBI

14. FDA to Ban Trans Fats in Foods – US News and World Report

15. saturated fat | Practical Evolutionary Health

16. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.

Intestinal Permeability, Food and Disease

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In medical school I learned some fundamental concepts about nutrition and digestion that turn out to be wrong. For example, we were taught that proteins in our diet are completely broken down into single amino acids in the gut, then absorbed through the wall of the intestine as individual amino acids. Turns out that not all proteins are completely digested in this manner and that fragments of proteins that are several amino acids long can be absorbed through the gut and enter our blood. Examples of such proteins include wheat gluten and bovine serum albumin (found in cows milk and whey protein) to name a few. The problem with absorbing such nutrients into our bloodstream is that these protein fragments are “foreign” and can be recognized by our immune systems as foreign, triggering an immune (inflammatory) response.

Some peptides (short chains of amino acids) in bovine serum albumin have structural similarity to peptides in human tissues. This foreign protein has been implicated in autoimmune diseases such as Multiple Sclerosis, Rheumatoid Arthritis and Type 1 Diabetes.

Other substances such as bacterial endotoxin similarly can be absorbed into the blood and cause trouble. Endotoxin, also called LPS or  Lipopolysaccharide, is a major component of the outer membranes of certain kinds of bacteria (gram negative bacteria such as E-coli) that live in the  Lumen of our gut. High levels of endotoxin circulating in the blood occur during septicemia and can result in death from septic shock. Lower levels of circulating endotoxin have been demonstrated to contribute to alcoholic and non-alcoholic liver disease, both of which can cause liver failure and death.

Intestinal wall permeability is governed by many factors. There are regulatory proteins that open and close the gaps (tight junctions) between the cells that line the walls of our intestines, thereby allowing more and larger foreign substances to enter our blood. This mode of entry is referred to as “paracellular” since it does not involve the usual absorption mechanism through the walls of the cells that line the intestines.

Substances regularly consumed by Americans known to increase intestinal permeability include gluten (the sticky protein found in wheat, barely, rye, oats), alcohol, non-steroidal anti-inflammatory drugs  like ibuprofen (Motrin, Advil), naprosyn (Alleve), and aspirin.  Refined “vegetable oils” that are high in a specific Polyunsaturated fatty acid called linoleic acid (examples of these vegetable oils include corn oil, soy oil, cottonseed oil) have also been demonstrated to increase intestinal permeability.

Vegetable oils have also been found to enhance the liver inflammation and destruction caused by  alcohol which is at least in part mediated by absorption of endotoxin and ultimately also caused by oxidative stress.

The same applies to non-alcoholic liver fatty liver disease. (Progression of alcoholic and non-al… [Drug Metab Pharmacokinet. 2011] – PubMed – NCBI)

Interestingly, consumption of saturated fat (as found in beef tallow, coconut oil, butter and cocoa butter-the oil of dark chocolate) protects the liver from inflammation and destruction caused by alcohol, while polyunsaturated fat consumption (vegetable oils)  do the opposite. (References above and below)

There is growing evidence for a link between auto-immune disease and Alterations in intestinal permeability. Increased intestinal permeability (IP) has been observed in a substantial percentage of individuals with Type I diabetes. It is commonly observed in populations at high risk of developing Crohn’s disease and has been observed in patients who subsequently develop Crohn’s disease. Patients with ankylosing spondylitis have increased IP and although these patients are typically treated with NSAIDs which increase IP, the effects of NSAIDS have been isolated from a primary defect in IP which is shared by relatives without the disease.

“increased intestinal permeability is observed in association with several autoimmune diseases. It is observed prior to disease and appears to be involved in disease pathogenesis.”

A paleolithic diet avoids all sources of gluten (paleo is grain-free) and it also avoids refined “vegetable oils”. These food items present a double hit relative to inflammation. First, they increase IP which increases circulating levels of various “foreign” proteins and other foreign macromolecules which can stimulate the immune system. The second hit from these food items represents their direct inflammatory effects once absorbed into the body. I have previously discussed the  inflammatory response to excess omega six fats here.

An excellent review of the importance of the ratio of omega six fats found in “vegetable oil”  to omega three fats found in fish oil can also be found here ,  here   and  here.

The potential inflammatory response and anti-nutrient effects of cereal grains and in particular the gliadin portion of wheat gluten has been discussed and reviewed in multiple papers including:

Do dietary lectins cause disease?

Non-Celiac Gluten Sensitivity: The New Frontier of Gluten Related Disorders

BMC Medicine | Full text | Spectrum of gluten-related disorders: consensus on new nomenclature and classification

BMC Medicine | Abstract | Divergence of gut permeability and mucosal immune gene expression in two gluten-associated conditions: celiac disease and gluten sensitivity

Bioactive antinutritional peptides derived from cere… [Nahrung. 1999] – PubMed – NCBI

Antinutritive effects of wheat-germ agglutinin and… [Br J Nutr. 1993] – PubMed – NCBI

This discussion just scratches the surface of the effects of intestinal permeability and health. Future discussion will address how the micro-flora (bacteria and viruses that live in our GI system) affect intestinal permeability, our brains, our immune system and our health.

Avoiding foods that we have not evolved to eat will result in decreased inflammation and will often reduce the symptoms of auto-immune and other inflammatory diseases. Many present day diseases are considered by evolutionary biologists to represent a mismatch between our culture, food, and our evolutionary biochemistry. These diseases were likely rare or non-existent  before the advent of agriculture and the subsequent industrialization of society with highly processed foods.

Eat only pastured meat, free range poultry and eggs, wild seafood, fresh vegetables, fruit and nuts and you will avoid the problems discussed above as well as a host of other problems to be discussed in future posts.

Peace,

Bob Hansen MD

Saturated fat, does it matter?

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Recommendations to reduce saturated fat consumption have pervaded our media since the AHA published its first dietary guidelines for the American public in 1961. The AMA at first opposed the recommendations but the AHA pushed on. The guidelines encouraged substitution of polyunsaturates for saturated fat. The guidelines were presented in a two page report with 1/2 page of references. A subsequent independent review of those references revealed that 1/2 of them did not support the recommendations, details, details.

My last blog looked at a meta-analysis of the major studies subsequently published on this topic and found that implementation of that recommendation does not reduce heart attacks or cardiac deaths and in fact there was a trend (not statistically significant) for worse outcomes associated with substituting PUFA (polyunsaturated fatty acids, primarily linoleic acid) for SFA (saturated fatty acids).

Please note that we are talking hard endpoints here, death and heart attack. So much of the literature that consumes this issue only looks at the effect on so called risk factors. When you actually look at the clinical outcomes (death, heart attack, stroke)  there is no benefit demonstrated when saturated fats are reduced.

In 1966 the makers of Mazola Corn Oil and Mazola Margarine sponsored publication of Your Heart Has Nine Lives, a book advocating the substitution of vegetable oils for butter and other “artery clogging” saturated fats.

The history of this campaign to demonize SFA and glorify PUFA is well described in Gary Taubes Good Calories, Bad Calories, as well as in Mary Enig’s essay The Oiling of America. I would encourage you to read both.  The latter is available on line as is Gary Taubes’ famous essay What if its all a big fat lie?

http://www.westonaprice.org/know-your-fats/the-oiling-of-america

http://www.nytimes.com/2002/07/07/magazine/what-if-it-s-all-been-a-big-fat-lie.html?pagewanted=all&src=pm

In 2010 a highly respected lipid research group published what should have been a wake-up call study for the medical profession.

Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.

The data included 5 to 23 years follow up on 347,747 subjects. 11,006 developed coronary heart disease or stroke. Intake of saturated fat was not associated with an increased risk of coronary heart disease (CHD), stroke, or  cardiovascular disease (CVD =CHD plus stroke).

“there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”

To be clear, association (statistical correlation) does not prove or disprove causation, but if such a large amount of data from prospective studies shows no statistically significant correlation, than a causative theory should be rejected until and unless randomized controlled clinical trials suggest otherwise.

This study should have created a tsunami in the media and in the medical community but it hardly caused a ripple in the pond. Michael Eades explains why in an excellent post here.

http://www.proteinpower.com/drmike/lipid-hypothesis/eat-less-move-die-anyway/

The editors of the journal published a scathing rebuke of the authors but could not find anything wrong with the data and conclusions except that the data refuted their belief system. Busy physicians tend to read the editorials and place more credence in an editorial than in a study that questions or refutes a major thesis.

Lets look at some other studies that considered hard clinical endpoints.

Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial.

The objective of this study was:

“To test the hypothesis that a dietary intervention, intended to be low in fat and high in vegetables, fruits, and grains to reduce cancer, would reduce CVD risk.”

This study was a randomized controlled trial of 48,835 postmenopausal women aged 50-79 years of diverse backgrounds and ethnicity.

“RESULTS: By year 6, mean fat intake decreased by 8.2% of energy intake in the intervention vs the comparison group, with small decreases in saturated (2.9%), monounsaturated (3.3%), and polyunsaturated (1.5%) fat; increases occurred in intakes of vegetables/fruits (1.1 servings/d) and grains (0.5 serving/d).”

Did this decrease heart attacks or strokes? NO

“The diet had no significant effects on incidence of CHD (hazard ratio [HR], 0.97; 95% confidence interval [CI], 0.90-1.06), stroke (HR, 1.02; 95% CI, 0.90-1.15), or CVD (HR, 0.98; 95% CI, 0.92-1.05).”

Now lets look at a study where women were followed after a heart attack to see if reducing saturated fat helped.

Dietary fats, carbohydrate, and progression of coronary atherosclerosis in postmenopausal women. Am J Clin Nutr. 2004 Nov;80(5):1175-84.

In this study quantitative coronary angiography was performed at baseline and after mean follow up of 3.1 years. 2243 coronary artery segments in 235 women were studied.

Here is what they found.

  • a higher saturated fat intake was associated with a smaller decline in mean minimal coronary diameter (P = 0.001) and less progression of coronary stenosis (P = 0.002) during follow-up
  • Carbohydrate intake was positively associated with atherosclerotic progression (P = 0.001), particularly when the glycemic index was high
  • Polyunsaturated fat intake was positively associated with progression (of coronary atherosclerosis) when replacing other fats (P = 0.04) but not when replacing carbohydrate or protein
  • Monounsaturated and total fat intakes were not associated with progression. (extra virgin olive oil and macadamia nuts are rich in monounsaturated fat)

The P values cited demonstrate unequivocal statistical significance for all of these associations.

So intake of carbohydrate and polyunsaturated fat was positively associated with progression of coronary atherosclerosis. Conversely, saturated fat intake was associated with less progression of coronary stenosis.  Again, I must point out that association does not prove or disprove causation. Nevertheless, there have been no prospective studies that demonstrate an association between saturated fat consumption and cardiovascular events (real clinical endpoints). Here we have data that show a negative association with saturated fat but positive association with carbohydrate and polyunsaturated fat consumption.

The logic has always been that substituting PUFA for SFA reduces cholesterol levels (short term studies) and therefore it should reduce heart attacks and strokes. But if you search the medical literature you find that the overwhelming body of data shows no reduction in hard clinical outcomes by reducing saturated fat, in fact just the opposite is true as in the two Ramsden studies cited in my previous post.

Uffe Ravnskov has pointed out that the proponents of the dietary  saturated fat-cholesterol theory often times misrepresent the data from published studies and cite those studies in support of the theory when in fact the data actually refute the theory. (as was the case for the AHA’s first dietary recommendations demonizing saturated fat in 1961) Uffe’s letters to the editor have been a nuisance to the proponents of that theory for decades.

An exhaustive review of the literature by Ravnskov was published in 1996. The summary deserves a complete quotation here.

J Clin Epidemiol. 1998 Jun;51(6):443-60.

The questionable role of saturated and polyunsaturated fatty acids in cardiovascular disease.

Source

uffe.ravnskov@swipnet.se

Abstract

A fat diet, rich in saturated fatty acids (SFA) and low in polyunsaturated fatty acids (PUFA), is said to be an important cause of atherosclerosis and cardiovascular diseases (CVD). The evidence for this hypothesis was sought by reviewing studies of the direct link between dietary fats and atherosclerotic vascular disease in human beings. The review included ecological, dynamic population, cross-sectional, cohort, and case-control studies, as well as controlled, randomized trials of the effect of fat reduction alone. The positive ecological correlations between national intakes of total fat (TF) and SFA and cardiovascular mortality found in earlier studies were absent or negative in the larger, more recent studies. Secular trends of national fat consumption and mortality from coronary heart disease (CHD) in 18-35 countries (four studies) during different time periods diverged from each other as often as they coincided. In cross-sectional studies of CHD and atherosclerosis, one group of studies (Bantu people vs. Caucasians) were supportive; six groups of studies (West Indians vs. Americans, Japanese, and Japanese migrants vs. Americans, Yemenite Jews vs. Yemenite migrants; Seminole and Pima Indians vs. Americans, Seven Countries) gave partly supportive, partly contradictive results; in seven groups of studies (Navajo Indians vs. Americans; pure vegetarians vs. lacto-ovo-vegetarians and non-vegetarians, Masai people vs. Americans, Asiatic Indians vs. non-Indians, north vs. south Indians, Indian migrants vs. British residents, Geographic Study of Atherosclerosis) the findings were contradictory. Among 21 cohort studies of CHD including 28 cohorts, CHD patients had eaten significantly more SFA in three cohorts and significantly less in one cohort than had CHD-free individuals; in 22 cohorts no significant difference was noted. In three cohorts, CHD patients had eaten significantly more PUFA, in 24 cohorts no significant difference was noted. In three of four cohort studies of atherosclerosis, the vascular changes were unassociated with SFA or PUFA; in one study they were inversely related to TF. No significant differences in fat intake were noted in six case-control studies of CVD patients and CVD-free controls; and neither total or CHD mortality were lowered in a meta-analysis of nine controlled, randomized dietary trials with substantial reductions of dietary fats, in six trials combined with addition of PUFA. The harmful effect of dietary SFA and the protective effect of dietary PUFA on atherosclerosis and CVD are questioned.

That was published in 1998, since then the evidence remains as Uffe described it 15 years ago. More studies show no relationship between saturated fat consumption and cardiovascular death, heart attack, or stroke.

Finally, multiple autopsy studies around the world have been conducted to investigate an association between diet and atherosclerosis. None of these studies have demonstrated a positive association between degree of atherosclerosis and saturated fat intake.

Yet the AHA continues to recommend lower levels of saturated fat consumption while showing little concern for the problem of sugar and refined carbohydrates.

In my next post I will discuss why sugar and refined carbohydrates are major players in the physiology of atherosclerosis. Future posts will address the China Study, Forks Over Knives, the Ornish Diet and related topics. Additionally I will discuss why an egg a day keeps the doctor away.

Go in peace.

Bob Hansen MD.

Polyunsaturated fat, Saturated fat and the AHA

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The present paradigm among physicians and cardiologists presents saturated fat as a disease producing component of animal foods. Dietary recommendations include the reduction of saturated fat and replacement with carbohydrates and/or monounsaturated and polyunsaturated fats. In fact, the American Heart Association (AHA) updated its recommendations to increase the consumption of polyunsaturated fats as a percentage of total caloric intake in January 2009.

This was met by protests from three NIH scientists who had done extensive research in the area of fat consumption and health. Those scientists wrote letters to the editor of Circulation, the scientific journal of the AHA. Those protest letters were not published in print but were published on-line (where only geeks like me would find them,  the vast majority of physicians would never lay eyes on them)

The authors of those letters subsequently produced a brilliant study that involved forensic research. They conducted interviews with principal investigators who directed the studies upon which the AHA had based it’s recommendations. They discovered important data that had been collected but not mentioned in those study publications by painstakingly sleuthing multiple sources. They then produced a meta-analysis of the data from the studies. Their meta-analysis was published in the British Journal of Nutrition Dec 2010.

http://www.ncbi.nlm.nih.gov/pubmed/21118617

What they found was astonishing. The AHA had based it’s recommendations on faulty data. A major point of refutation involved  omega 3 fatty acids (fish oil which is arguably cardio- protective) vs omega 6 fatty acids. Both are poly-unsaturated fatty acids (PUFA). The AHA paradigm has been that replacing saturated fat with omega 6 PUFA results in reduction of cholesterol (short term studies) and therefore should reduce heart attacks and stroke. But the studies they used to support their recommendations were not “clean”.

Only three of the nine studies were “pure” omega 6 interventions, which increased omega-6 FA without a concurrent rise in omega-3.

Four of the studies increased both omega 3 and omega 6 PUFA. In one of those four studies the patients were given the equivalent of 16 fish oil capsules per day.

The control diets had an estimated 3% manufactured trans fats in the diet. This unquestionably increases risk of heart attack and creates a confounding factor.

The Omega 6 diets increased the risk of heart disease and death compared to the mixed omega 3 and omega 6 studies. The risk of cardiac death was increased by 28% in the omega 6 diets compared to the mixed diets.

The mixed omega 6 omega 3 diets showed an 8% risk reduction of death from all causes and a 22% risk reduction from cardiac death.

So the AHA had made recommendations that could possibly be harmful and certainly not helpful. Despite this great piece of investigative science, the AHA did not change it’s recommendations.

Since that time Christopher Ramsden and colleagues have published a sequel “to evaluate the effectiveness of replacing dietary saturated fat with omega 6 linoleic acid, for the secondary prevention of coronary heart disease and death”.

http://www.ncbi.nlm.nih.gov/pubmed/23386268

In their summary they stated:

“substituting dietary linoleic acid in place of saturated fats increased the rates of death from all causes, coronary heart disease, and cardiovascular disease. “

There you have it. The AHA has not withdrawn it’s dietary recommendations to increase n-6 fat despite the compelling evidence to the contrary. This is unfortunately a consistent pattern.

Why would an increase in omega 6 fats and a reduction in saturated fat increase cardiovascular events?

Here is one explanation which is supported by basic science. Omega 6 fats are PUFA (polyunsaturated). PUFA are easily oxidized but saturated fat is not. When PUFA sit in the membrane (outer wall) of LDL particles they become oxidized and the oxidized LDL particle stimulates macrophages (white blood cells) to become foam cells and create plaque in the walls of your arteries. Saturated fats are not easily oxidized. Saturated fats do not contribute to the formation of oxidized LDL.

The AHA encourages us to consume “vegetable oils” (oils made from corn, soy, cottonseed, safflower, etc) instead of saturated fat. The predominant fat in “vegetable oil” is linoleic acid, the major omega 6 fat in the American diet. Linoleic acid is not the hero in this story and saturated fat is not the villain that the AHA portrays it to be.

Having said that, one might ask the following. If PUFA are easily oxidized and omega 3 fats are are also PUFA, then how could omega 3 fats be “cardio-protective” while omega 6 fats are damaging?

Good question. That will be addressed in  future posts.

But before we get to that, there are other data on saturated fats that must be discussed in order to dispel the fear of saturated fat.  That data and discusion will come in the next post.

Go in peace, the post is ended.

Bob Hansen MD