Tag Archives: cardiovascular disease

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

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

Paleolithic Diet Reversed Osteoporosis and Fatty Liver in an 82 year old man

Joe (not his real name) is an 82 year old man who presented to me in 2009 with severe degenerative arthritis of the spine, debilitating chronic pain,  osteoporosis, coronary artery disease, congestive heart failure and fatty liver. When I first met him in 2009 he weighed 265 pounds (6 foot), had just undergone multi-vessel coronary artery bypass surgery. He could not walk more than 30 feet without feeling short of breath and severe low back pain. He was referred to me for interventional pain management. At that time the only way he could sleep was in a hospital bed with his head elevated to a 90 degree angle. Otherwise he experienced “orthopnea” (shortness of breath lying flat caused by congestive heart failure). His osteoporosis (demineralization of bone) was so bad it was difficult to do pain blocks using X-RAY because the bone did not show up well on X-Ray due to the osteoporosis. He had also suffered compression fractures in the lumbar spine. Compression fractures are caused by weak bones where just the weight of the body can cause one or more vertebrae to partially collapse.

I recommended a paleolithic-carbohydrate restricted diet. He lost 90 pounds and on the paleo diet was able to get off some of his medication for congestive heart failure.

I saw Joe yesterday for an interventional pain management procedure (radio-frequency ablation of nerves to his painful arthritic lower lumbar facet joints). He gets these about every 6 months to treat chronic pain.

I recalled the first time I did this procedure. It was a struggle because his bones were so demineralized. But yesterday it was a breeze, his bones looked 30 years younger and had enough calcium and other minerals to provide beautiful fluoroscopic (live X-ray) images.

Joe is now sleeping with just 10 degrees elevation at the head of his bed (previously 90 degrees). His fatty liver disease is gone.

The Paleo diet allowed this elderly gentleman to lose 90 pounds, improve his exercise tolerance dramatically (he just won a metal detecting contest competing against young adults) and significantly improve his bone strength. It also cured his fatty liver disease.

Not bad for just limiting food to fresh vegetables, fresh fruits, meat, seafood, nuts and eggs.

Joe’s improvement is not a surprise. A study done at UCSF on the metabolic ward demonstrated improved calcium metabolism (reduced urinary excretion of calcium)  within 2 weeks of placing young “couch potato” adults on a paleolithic diet. It also demonstrated improvements in blood pressure, glucose tolerance, decreased insulin secretion, increased insulin sensitivity and improved lipid profiles in just a few weeks. This occurred without an exercise program (exercise will enhance bone strength, reduce blood pressure, improve insulin sensitivity and improve lipid profiles) and without weight loss. The subjects were “force fed” to avoid weight loss so the beneficial effects of the dietary change alone could be analyzed without the con-founder of weight loss. You can read the abstract of this study here.

The improvements in calcium metabolism are not mentioned in the abstract but appear in the full article in Table 1.

Joe is very grateful for the tremendous improvement in his quality of life, primarily achieved by adopting a Paleo-diet.

Until next time.

BOB Hansen MD

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

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

  1.  greater decreases in weight. This has been demonstrated in multiple previously published studies.
  2.  greater decreases in  fat mass. This is an important distinction, the low carb group lost more fat, not muscle.
  3.  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.
  4.  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.
  5.  greater increases in HDL cholesterol level. This result is considered to be protective against heart attack and stroke.
  6. 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.
  7. 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

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.

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.

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.

 

Carbohydrate Restriction for Diabetes I and II

A great review article challenging the current low fat dogma has been published. This should be required reading for all physicians. It brings clarity, data, and perspective to the discussion.

Here is the abstract:

Abstract

“The inability of current recommendations to control the epidemic of diabetes, the specific failure of the prevailing low-fat diets to improve obesity, cardiovascular risk or general health and the persistent reports of some serious side effects of commonly prescribed diabetic medications, in combination with the continued success of low-carbohydrate diets in the treatment of diabetes and metabolic syndrome without significant side effects, point to the need for a reappraisal of dietary guidelines.”

Here are the opening paragraphs.

“The benefits of carbohydrate restriction in diabetes are immediate and well-documented. Concerns about the efficacy and safety are long-term and conjectural rather than data-driven. Dietary carbohydrate restriction reliably reduces high blood glucose, does not require weight loss (although is still best for weight loss) and leads to the reduction or elimination of medication and has never shown side effects comparable to those seen in many drugs.

Here we present 12 points of evidence supporting the use of low-carbohydrate diets as the first approach to treating type 2 diabetes and as the most effective adjunct to pharmacology in type 1. They represent the best-documented, least controversial results. The insistence on long-term random-controlled trials as the only kind of data that will be accepted is without precedent in science. The seriousness of diabetes requires that we evaluate all of the evidence that is available. The 12 points are sufficiently compelling that we feel that the burden of proof rests with those who are opposed.

“At the end of our clinic day, we go home thinking, ‘The clinical improvements are so large and obvious, why don’t other doctors understand?’ Carbohydrate restriction is easily grasped by patients: because carbohydrates in the diet raise the blood glucose, and as diabetes is defined by high blood glucose, it makes sense to lower the carbohydrate in the diet. By reducing the carbohydrate in the diet, we have been able to taper patients off as much as 150 units of insulin per day in eight days, with marked improvement in glycemic control – even normalization of glycemic parameters.”

— Eric Westman, MD, MHS [1].

Here is the link to the whole article.

Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base

Peace and good health.

Bob Hansen MD

Amputations, Gangrene and Carbohydrates

As an anesthesiologist I have spent more than 60,000 hours in the operating room and cared for over 30,000 patients. I often observe the end-results of bad dietary advice. I am referring to the liberal carbohydrate allowance that the American Diabetes Association and other agencies offer diabetics.

Today was a particularly poignant day as I cared for two diabetics who required amputations for complications of diabetes type II. These complications could have likely been avoided if our supermarkets were not stocked with high carb nutritionally deplete “food” AND if the ADA, physicians and nutritionists counseled diabetics to significantly reduce their carbohydrate intake. Instead, the low fat narrative has so predominated our culture, that we have taken our eyes off of the major dietary threats during the past 40 years, excessive carbohydrates and especially refined carbohydrates.

The leading cause of amputations in modern society are the complications of diabetes including peripheral arterial disease (atherosclerosis in the arteries to our limbs) and peripheral neuropathy (loss of sensation in the feet and hands). The combination of these two, or just one alone can lead to non-healing wounds and ulcers in the feet, then chronic infections and ultimately gangrene. Futile efforts to restore circulation to the legs with vascular bypass surgeries or arterial stents usually just briefly delay the inevitable series of amputations that start in the toes and progress up the leg, step by step until only a stump is left above the level once occupied by the knee.

Gangrene is an ugly thing. During the Civil War the major cause was trauma. Today the major cause is diabetes and indirectly, excess carbohydrate consumption.

The visual experience of gangrene results in a visceral reaction, even after more than 30 years of observation. The knowledge that most of these complications could be avoided by simply eating whole fresh foods instead of crap in a bag or crap in a box is frustrating. The human suffering and economic costs (lost wages, disability, medical expenses) are staggering. Diabetes type II is largely a disease of lifestyle. The lifestyle elements involved include poor dietary habits, lack of exercise, inadequate sleep, and stress. All of these contribute and all are modifiable and avoidable.

Type II diabetes is arguably reversible early in the disease process. As it progresses a patient reaches an irreversible point of no return where the pancreas has been exhausted and the insulin producing cells are no longer efficient and effective. Equally important,  the cells in the rest of the body do not respond in a normal fashion to what little insulin is produced. But even at this stage carbohydrate restriction can mitigate complications if only healthy fresh whole-foods are consumed and modest exercise is practiced on a daily basis.

Other complications of diabetes including blindness, painful neuropathy, kidney failure requiring dialysis, heart attack and stroke all are arguably avoidable with a whole foods paleolithic carbohydrate restricted diet and modest amounts of regular exercise.

What a pity, what a shame, what a waste.

Below are some links and research articles to back up my statements.

Peace, health, and harmony.

BOB

1. Type 2 Diabetes

2. American Diabetes Association Embraces Low-Carbohydrate Diets. Can You Believe It? | Richard David Feinman

3. Nutrition Science on Pinterest

4. Low-Carb for You: Low-Carb versus Low-Fat

And Many More:

Jenkins DJ, Kendall CW, McKeown-Eyssen G, Josse RG, Silverberg J, Booth GL, Vidgen E, Josse AR, Nguyen TH, Corrigan S et al: Effect of a low-glycemic index or a high-cereal fiber diet on type 2 diabetes: a randomized trial. JAMA 2008, 300(23):2742-2753.

Westman EC, Yancy WS, Mavropoulos JC, Marquart M, McDuffie JR: The Effect of a Low-Carbohydrate, Ketogenic Diet Versus a Low-Glycemic Index Diet on Glycemic Control in Type 2 Diabetes Mellitus. Nutr Metab (Lond) 2008, 5(36).

Gannon MC, Hoover H, Nuttall FQ: Further decrease in glycated hemoglobin following ingestion of a LoBAG30 diet for 10 weeks compared to 5 weeks in people with untreated type 2 diabetes. Nutr Metab (Lond) 2010, 7:64.

Gannon MC, Nuttall FQ: Control of blood glucose in type 2 diabetes without weight loss by modification of diet composition. Nutr Metab (Lond) 2006, 3:16.

Gannon MC, Nuttall FQ: Effect of a high-protein, low-carbohydrate diet on blood glucose control in people with type 2 diabetes. Diabetes 2004, 53(9):2375-2382.

Forsythe CE, Phinney SD, Feinman RD, Volk BM, Freidenreich D, Quann E, Ballard K, Puglisi MJ, Maresh CM, Kraemer WJ et al: Limited effect of dietary saturated fat on plasma saturated fat in the context of a low carbohydrate diet. Lipids 2010, 45(10):947-962.

Jakobsen MU, Overvad K, Dyerberg J, Schroll M, Heitmann BL: Dietary fat and risk of coronary heart disease: possible effect modification by gender and age. Am J Epidemiol 2004, 160(2):141-149.

Siri-Tarino PW, Sun Q, Hu FB, Krauss RM: Saturated fat, carbohydrate, and cardiovascular disease. Am J Clin Nutr 2010, 91(3):502-509.

Int J Cardiol. 2006 Jun 16;110(2):212-6. Epub 2005 Nov 16. Effect of a low-carbohydrate, ketogenic diet program compared to a low-fat diet on fasting lipoprotein subclasses. Westman EC, Yancy WS Jr, Olsen MK, Dudley T, Guyton JR.

Mol Cell Biochem. 2007 Aug;302(1-2):249-56. Epub 2007 Apr 20.Beneficial effects of ketogenic diet in obese diabetic subjects. Dashti HM, Mathew TC, Khadada M, Al-Mousawi M, Talib H, Asfar SK, Behbahani AI, Al-Zaid NS.

 

 

Stomach bacteria can cause and worsen heart disease

A recent study from Italy (1) has identified a relationship between the bacteria that causes stomach ulcers and heart disease. H Pylori is a bacteria that can colonize the lining of the stomach and remain there for a lifetime unless diagnosed and eliminated with antibiotics. This bacteria was demonstrated to be a major cause of stomach ulcers by two physicians ( Dr. Barry Marshall and Dr. Robin Warren) who won the Nobel Prize for their finding.

Atherosclerosis the formation of plaque in the walls of arteries, is in large part an inflammatory process (2,3). The coronary arteries supply oxygenated blood to heart muscle and heart valves. A heart attack (myocardial infarction) occurs when a plaque  ruptures or tears, sending debris downstream in a coronary artery. That debris and/or the exposed ruptured plaque causes  a blood clot that obstructs blood flow to a portion of the heart and if the clot remains untreated a heart attack (muscle damage) occurs within minutes to hours. This process can also result in a fatal abnormal heart rhythm (ventricular fibrillation).

A major source of inflammation that is known to contribute to atherosclerosis and heart attacks is infection (2). Many patients suffer heart attacks following an acute infection or severe emotional stress.  Inflammation is involved in forming plaques, creating unstable plaques, causing plaque to tear or rupture and inflammation is involved in the dynamic process that leads to a heart attack (3). To quote the authors of this study:

Ischaemic heart disorders are the consequence of an atherosclerotic process. A concomitant cause of atherosclerosis is inflammation. Infections represent the single most frequent determinant of inflammation. In case of H pylori infection, the organism colonises the human stomach for life (if infection is not properly treated); therefore, the trigger is continuous and inflammation lasts for a lifetime.

The authors of this study found that a certain subset of H Pylori bacteria carry a protein that is similar to two or more very important and essential proteins in heart muscle. Those proteins are called human tropomyosin and cardiac ATPases. Both types of proteins are essential to the ability of the heart muscle to pump blood through the heart.

The authors postulate a mechanism called molecular mimicry. Because H Pylori proteins are very similar to certain proteins in the heart, colonization or infection in the GI tract by H Pylori results in an immune response directed against these foreign proteins which are very similar to proteins in heart muscle. The immune system”mistakes” these heart muscle proteins for the foreign proteins in H Pylori and mounts an immune response against the heart muscle. The study found that patients infected with certain H Pylori strains had higher circulating levels of inflammatory markers and BNP . BNP is associated with heart failure, (loss of heart muscle contracting ability) and loss of heart muscle function results in a poorer prognosis in patients with coronary artery disease.

Thus this study supports a direct link between bacterial infection in the GI tract and heart disease, mediated through the immune system.

This sort of molecular mimicry has been recognized in medicine as it relates to two very well known diseases caused by infections with a species of streptococcus (as in strep throat). Those diseases are rheumatic heart disease (also called rheumatic fever)  and glomerulonephritis, Either of these can occur as a complication of strep infections, ergo the importance of diagnosing and treating strep throat.

H Pylori represents one of many examples of the interplay between bacteria in our GI tract, the immune system and disease causation. Intestinal dysbiosis (imbalance between healthy and disease causing bacteria that reside in our gut) has been associated with a  multitude of disease processes including obesity, diabetes, psychiatric disorders and cancer (5,6,7,8,9,10).

An essential component of this process is the entry of foreign proteins or other antigens (immune stimulants) across the gut wall into the body where the immune system gets activated. Intestinal Permeability is a term that describes the ability of substances to cross the GI barrier (intestinal wall) and enter the circulation (blood or lymph glands). I have discussed this before. There are many potential causes of increased intestinal permeability (leaky gut) including small intestinal bacterial overgrowth (a specific kind of dysbiosis) dietary sources such plant lectins and saponins found in grains and legumes, stress, sleep deprivation and medications such as NSAIDS. When an individual suffers from leaky gut (increased intestinal permeability) the probability that toxic substances can enter the blood stream increases. Endotoxin (produced by pathogenic bacteria in the gut) has been related to many inflammatory disease processes wreaking havoc when it penetrates the intestinal barrier.

Intestinal permeability, auto-immune disease, molecular mimicry, and gut dysbiosis are topics often discussed in the Paleo community. These topics represent physiologic processes that relate to humans deviating from our evolutionary habits, diets and lifestyles.

References are below.

Peace.

BOB

(1)  Cross-sectional Study: CagA–positive Helicobacter pylori Infection, Acute Coronary Artery Disease and Systemic Levels of B-type Natriuretic Peptide Journal of Clinincal Pathology. 2014;67(3):251-257.

(2) 11. Epstein SE, Zhou YF, Zhu J. Infection and atherosclerosis: emerging mechanistic paradigms. Circulation 1999;100:e20–8.

(3)  Ross R. Atherosclerosis: an inflammatory disease. N Engl J Med 1999;340:115–26

(4)  Mayr M, Kiechl S, Mendall MA, et al. Increased risk of atherosclerosis is confined to CagA-positive Helicobacter pylori strains: prospective results from the Bruneck study. Stroke 2003;34:610–5.

(5) Diabetes, obesity and gut … [Best Pract Res Clin Gastroenterol. 2013] – PubMed – NCBI

(6) Involvement of gut microbiota in the de… [Gut Microbes. 2012 Jul-Aug] – PubMed – NCBI

(7) Crosstalk between the gut microbiota a… [Clin Microbiol Infect. 2012] – PubMed – NCBI

(8) [The role of gut microbiota in… [Postepy Hig Med Dosw (Online). 2013] – PubMed – NCBI

(9) [Research advances in th… [Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2013] – PubMed – NCBI

(10) The gut microbiota, obesity and insulin resi… [Mol Aspects Med. 2013] – PubMed – NCBI