Category Archives: obesity

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.

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

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

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

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

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

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

But back to LDL.

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

The short version is as follows.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Now here is another twist.

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

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

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

The simple answer is no.

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

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

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

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

In summary:

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

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

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

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

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

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

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

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

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

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

Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis

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

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

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

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

Modulation of Endothelial Glycocalyx Structure under Inflammatory Conditions

Oxidized Lipoproteins Degrade the Endothelial Surface Layer

S1P Control of Endothelial Integrity

Mechanical control of the endothelial barrier. – PubMed – NCBI

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

The Fats of Life, Dr. Glen Lawrence

Functions of plasmalogen lipids in health and disease

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

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

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

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

BOB

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

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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

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

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

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

Here is the summary cut and pasted from the abstract.

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

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

Setting: A large academic medical center.

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

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

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

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

Limitation: Lack of clinical cardiovascular disease end points.

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

Primary Funding Source: National Institutes of Health.

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

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

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

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

The authors concluded:

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

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

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

Bob Hansen MD.

Carbohydrate Restriction for Diabetes I and II

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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

Chronic Pain Reduced by the Paleo Lifestyle

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I spend 50% of my clinical time treating chronic pain patients. A paleolithic diet which consists of pastured grass-fed meat, free range poultry and eggs, fresh seafood, fresh vegetables, fruits and nuts decreases inflammation by eliminating major sources of dietary induced inflammation.

Yesterday I saw a patient one month after he started a paleolithic lifestyle (paleo diet, 8 hours of sleep per night- cycling with the sun, regular exercise including a prescribed spine rehab program).

Within 30 days his pain has decreased by more than 50%, He feels more energetic. He stated “I have started to dream again and get a full night’s sleep”. He has lost 12 pounds in one month and his blood pressure is down. He is ready to return to work after not working for eight months (with some activity restrictions). He is not taking any opiate pain medication.

His MRI scan and X-rays of the spine will not demonstrate any improvement. He still has degenerative disc disease, one or more tears in a disc annulus (outer wall of the disc) and arthritis in the facet joints of his neck (cervical spine) and lower back (lumbar spine). But the lifestyle elements that have contributed to his chronic inflammation have been significantly reduced in just 30 days and he has benefited “tremendously” in his own words.

There are many mechanisms involved with chronic inflammation. Most patients with chronic pain have an inflammatory component. Many patients with chronic pain are overweight or obese. Excess visceral adiposity (fat around the internal organs) creates a state of chronic inflammation by constantly producing inflammatory chemicals called chemokines and cytokines. These inflammatory mediators are produced by the fat cells and by the white blood cells (macrophages) that reside alongside the fat cells. They contribute to a process called central sensitization where the brain and spinal cord nerves that mediate pain become sensitized and over-react to sensory input. Interleukin 6 is one of these mediators. Increased levels are associated with fatigue, depression and a state of hyperalgesia where painful stimuli are amplified. Tumor necrosis factor alpha is another important inflammatory mediator produced in excess when excess fat accumulates around the internal organs. Weight loss is essential to decease systemic inflammation, particularly in the setting of chronic pain when someone is overweight or obese.

Pro-inflammatory foods can also increase inflammation by altering intestinal flora and increasing intestinal permeability. These mechanisms have been discussed in previous posts and in the manifesto page of this website.

Few patients follow my dietary and lifestyle advice. Most seem to prefer taking pills, getting injections and other interventional pain procedures. In other words, they prefer to “be-fixed” rather than take lifestyle initiatives that are likely to not only decrease their pain but also improve their general health. As an interventional pain practitioner I encourage patients to take full advantage of the pharmacology and interventional procedures that are likely to help. But without significant changes in bad dietary habits, poor sleep hygiene and without adopting a rehabilitation exercise program the pills and injections/procedures are much less effective and the prognosis is poor.

Stress reduction is also essential for health in general and for pain reduction in particular. Yet despite repeated recommendations to utilize an inexpensive stress reduction workbook, few patients ever bother to take this important step to reduce pain, anxiety and suffering.

Our culture is one in which patients expect to “be fixed” rather than to be led down a path which leads to healing and functional improvement by actively participating in their own rehabilitation and healing. Our culture is also one in which major organizations provide bad dietary advice, particularly with respect to encouraging increased consumption of grains and legumes which have pro-inflammatory components and anti-nutrients. We evolved over a few million years without consuming grains, legumes, refined vegetable olis or dairy. Our evolutionary biology and physiology thrive when these foods, particularly processed foods are eliminated from the diet and we consume only those whole natural foods we have evolved to eat.

Modern medicine provides many remarkable drugs, surgeries and procedures that can be life saving and life altering. But application of this technology without addressing the fundamental determinants of health (proper nutrition, restorative sleep, judicious exercise, stress reduction, and restoration of circadian rhythm) yields much less benefit. Ultimately, unless we remove from our lives the destructive components of modern society and culture we cannot heal and instead continue to suffer from chronic degenerative diseases that cause pain, loss of intellect and loss of mobility.

No references tonight, just comments and reflection. References have been provided in previous posts.

Peace, health, and happiness.

Dr. Bob

The bacteria in your gut are essential to your health Part II, obesity, metabolic syndrome and dysbiosis

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I have discussed the evidence linking the mix of bacteria in your gut (gut flora) to health and disease in Part I. The Bacteria in your Gut are essential to your health Part I | Practical Evolutionary Health

Today I will discuss the evidence related specifically to obesity and metabolic syndrome (the constellation of obesity, insulin resistance, high blood pressure, and abnormal blood lipids). My discussion will follow closely the evidence and theory presented in research and review papers authored by Dr. Cani and colleagues. The first one is titled:

“Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics.”

You can find the full text of this article here .

I have had the pleasure of corresponding with Dr. Cani by e-mail regarding her many publications investigating the relationship between gut flora, obesity, and metabolic syndrome.

“Recently, we and others have identified several mechanisms linking the gut microbiota with the development of obesity and associated disorders (e.g. insulin resistance, type 2 diabetes, hepatic steatosis).”

Explanation: The gut microbiota are the bacteria, viruses and other “bugs” that reside in our intestines. Insulin resistance can occur in various parts of the body, wherever insulin has an effect including fat cells, liver, muscle, brain. When higher amounts of insulin are required to achieve an effect this is called insulin resistance. In Type 2 diabetes, the pancreas is still able to make insulin but insulin is less effective in controlling blood sugar. In Type I diabetes the pancreas no longer produces insulin. Hepatic Steatosis means fatty liver disease. The liver accumulates fat and this can lead to cirrhosis, liver failure and death. Alcohol consumption can cause this but when alcohol is not involved this is called Non-Alcoholic-Fatty-Liver Disease (NAFLD). Our nation presently has an epidemic of not just obesity but also NAFLD. Evidence points to excess carbohydrate consumption and excess consumption of vegetable oils (linoleic acid) as contributing factors in NAFLD. Carbohydrate restriction and consumption of saturated fat, particularly medium chain fats (as found in coconut) can protect against NAFLD. But the gut flora also play a role. The mechanisms involved are many.

“Among these, we described the concept of metabolic endotoxaemia (increase in plasma lipopolysaccharide levels) as one of the triggering factors leading to the development of metabolic inflammation and insulin resistance.”

Endotoxemia occurs when a toxin from certain kinds of bacteria circulates in the blood. This endotoxin enters our blood through our intestines under conditions in which the protective barrier of the intestines is compromised. The compromise of the intestinal barrier is variously referred to as ” leaky gut” or “increased intestinal permeability”. Wheat gluten-gliadin causes increased intestinal permeability (especially in celiac disease) as can other plant lectins. In this discussion, the gut bacteria also contribute in the setting of “dysbiosis” (the beneficial effects of helpful bacteria are overwhelmed by the harm-causing bacteria when a healthy balance is not present)

Lipopolysaccharide (LPS) comes from the outer wall membrane of certain bacteria. Blood plasma is the liquid part of blood in which the blood cells circulate. So an “increase in plasma lipopolysaccharide” simply means that there is more LPS circulating in the blood. That is a bad thing. Depending on how much is circulating this alone can cause organ failure and death and is a major part of the physiologic changes involved in septic shock. But lower levels of LPS circulating in the blood can cause chronic low grade inflammation and insulin resistance. Obesity is associated with chronic inflammation and increased LPS circulating in the blood and being distributed to various organs where it wreaks havoc.

“Growing evidence suggests that gut microbes contribute to the onset of low-grade inflammation characterizing these metabolic disorders via mechanisms associated with gut barrier dysfunctions.”

“We have demonstrated that enteroendocrine cells (producing glucagon-like peptide-1, peptide YY and glucagon-like peptide-2) and the endocannabinoid system control gut permeability and metabolic endotoxaemia.”

That is a mouth-full. Over thirty different kinds of hormone producing cells have been found in the human intestine. These cells are called enteroendocrine cells. The hormones produced by these cells have many effects. You can find a great review of these cells and their effects here .

In Dr. Cani’s review article she describes how some of these hormones produced in the gut can increase intestinal permeability and allow more of the toxic, inflammation producing LPS to enter the bloodstream. But these hormonal effects are just part of the picture. Another part relates to endocannabinoids.

The Endocannabinoid system in humans is complex and relates to hunger, satiety, energy metabolism, and yes gut permeability. Endocannabinoid refers to our internal (endo) production of cannabis like substances. Pot smoking people get the munchies because of the appetite stimulating effects of marijuana. But endocannabinoids have many other physiologic effects including the modulation of pain, mood, immune function and memory.

Dr. Cani describes in great detail the evidence supporting the roles that the gut flora play in influencing intestinal permeability mediated through the effects of various hormones and endocannabinoids. In animal and human studies changing the gut flora produces changes in these hormones and endocannabinoids which in turn can increase or decrease intestinal permeability and increase or decrease circulating LPS.

It turns out that specific Prebiotics can produce growth of beneficial gut bacteria and through the series of steps outlined above, reduce inflammation in the body, improve blood sugar, improve insulin sensitivity, and decrease fat,

Oh, and similar to the endocannabinoid system, there is an “apelinergic system” in our bodies that also plays a role. If you want to read more about these systems you should read the original article and the other links below to related articles.

I have discussed in the past that fecal transplants have been used to treat the specific dysbiosis that occurs with C Difficile colitis. But fecal transplants have many potential beneficial uses.

The Fatlose 2 trial is presently studying the effects of fecal transplants on insulin resistance and related problems in human volunteers. I will let you know when the results are published, Studies conducted in rodents have demonstrated significant weight loss and improved insulin sensitivity when obese rodents receive fecal transplants from lean rodents.

In summary: dysbiosis represents an unhealthy mix of bacteria in the gut

dysbiosis causes increased intestinal permeability (leaky gut)
increased intestinal permeability leads to increased circulating LPS, which is bad
elevated levels of circulating LPS create a chronic state of inflammation which contributes to obesity and metabolic syndrome
the mechanisms that link dysbiosis to intestinal permeability include hormonal disruption (enteroendocrine cells) and the endocannabinoid system. Other mechanisms are also likely in play.
prebiotics and probiotics can mitigate dysbiosis, reduce intestinal permeability, reduce inflammation, and offer potential therapy for obesity and metabolic syndrome
fecal transplantation offers a potential for treatment for obesity and metabolic syndrome, research is underway

Our ancestors lived and evolved for a few million years prior to the relatively brief ten thousand years of agriculture and one hundred years of industrialization. The overuse of antibiotics in medicine and animal husbandry have contributed to dysbiosis. Other factors include stress, disruption of circadian rhythm, sleep deprivation. Cesarean delivery and avoidance of breast feeding conspire to dysbiosis. Processed foods feed unfriendly bacteria in our guts at the expense of beneficial bugs. Agricultural foods have introduced dietary lectins which also increase intestinal permeability and thereby contribute to chronic inflammation. The further we stray from our evolutionary niche, the more problems we experience.

This discussion just touches the surface of gut flora, dysbiosis, health and disease. We have yet to explore the gut-brain axis. Our gut and microflora communicate with and effect the function of our brain and other organs as well.

We will continue to explore health and disease from an evolutionary perspective.

Below are links to articles related to our discussion.

Peace, health and happiness.

BOB

Gut microbiota controls adipose tissue expans… [Benef Microbes. 2014] – PubMed – NCBI

Glucose metabolism: Focus on gut microbiota, … [Diabetes Metab. 2014] – PubMed – NCBI

Probiotics, prebiotics, and the host microb… [Ann N Y Acad Sci. 2013] – PubMed – NCBI

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

Gut microbiota and its possible relationship … [Mayo Clin Proc. 2008] – PubMed – NCBI

Enteroendocrine Cells: Neglected Players in Gastrointestinal Disorders?

Not all calories are the same.

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The old school teaching about obesity went like this. Consume more calories than you burn and you gain weight. Consume less calories than you burn and you lose weight. Obesity is just a problem of self control. All calories are the same.

This way of thinking has been dis proven but still pervades many discussions.

Ample evidence supports the following facts that should be considered in choosing foods and mitigating the obesity epidemic.

High glycemic high carbohydrate foods and beverages such as bread, pasta, potatoes, crackers, chips, granola bars, breakfast cereal, soda, energy drinks produce a rapid rise in blood sugar and insulin levels, stimulate hunger, enhance further carbohydrate cravings, and drive people to overeat. Thus, what kind of food you eat affects how much you eat. (1,2)
High carbohydrate diets result in decreased calorie burning (decreased metabolic rate) compared to high fat high protein diets. Thus, a diet with carbohydrate restriction not only limits hunger (improves satiety) but also results in burning more calories for the same level of activity and at rest. I have previously discussed weight loss studies that consistently demonstrate that carbohydrate restriction results in spontaneous reduction in caloric consumption. At the same time this approach results in burning more calories while you watch TV or go for a walk. (3)
The human body does not absorb all of the calories present in food. A higher % of the calories present in highly processed refined foods (which represent 70% of the American diet) are absorbed compared to whole unprocessed foods such as tree nuts. (4)
Whole foods, especially non-starchy vegetables, provide much more satiety producing fiber (non-starchy vegetables have five to seven times as much fiber compared to whole grain bread on a per calorie basis)
Food choices produce different effects on the gut flora. A diet consisting of whole hunter-gatherer type foods (grass fed meat, free range poultry and eggs, wild seafood, fresh fruits, vegetables and nuts) enhance and support the development of “good bacteria” in the gut. As discussed before , the gut flora have a major impact on the risk of obesity and other diseases.
High carbohydrate diets produce higher insulin levels. Insulin results in conversion of carbohydrate into fat and storage of fat. Insulin inhibits the burning of fat. Carbohydrate restriction results in burning fat for energy.
The process of protein digestion consumes more calories compared to the digestion of carbohydrate. Protein has a higher thermogenic effect compared to carbohydrate.

THE BOTTOM LINE: not all calories are the same. The quality of the food we consume affects our metabolic rate, our absorption of calories, how quickly we feel full and therefore how many calories we consume, and the mix of good bacteria and bad bacteria that live in our GI tract.

Good health, peace and tranquility to all

BOB

1. Fed Up Asks, Are All Calories Equal? – NYTimes.com

2. Changes in diet and lifestyle and long-term wei… [N Engl J Med. 2011] – PubMed – NCBI

3. Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study

4. Impact of Peanuts and Tree Nuts on Body Weight and Healthy Weight Loss in Adults

Weight Gain, Another Reason to Avoid Statins

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

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

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

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

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

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

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

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

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

Go in peace

Bob Hansen MD

The Bacteria in your Gut are essential to your health Part I

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Our human body consists of about 100 trillion cells but we carry about 1000 trillion bacteria in our intestines, that represents 10 times the amount of our own cells. (1) These bacteria are variously called our micro-flora, microbiome, gut flora, etc, along with viruses and other organisms that co-exist and co-evolved with us. Advances in rapid gene identification have enabled an explosion of knowledge related to our micro-flora, health and disease. We each carry an estimated 500 to 1000 different species of bacteria in our intestines and the balance/mix of these bacterial species can have profoundly positive or negative affects on our health. Patterns of micro-flora have been identified for a variety of human disorders including obesity, diabetes type I, several kinds of cancer and inflammatory bowel disease to name a few. The issue of association vs. causation remains to be resolved but the beneficial and therapeutic effects of pro-biotics and fecal transplant (in rodent and human studies) in a variety of situations along with the observed deleterious effects of interrupting our micro-flora speak in favor of a causative or contributory role. (2) (3)

Accumulating evidences indicate that some diseases are triggered by abnormalities of the gut microbiota. Among these, immune-related diseases can be the promising targets for probiotcs. Several studies have proved the efficacy of probiotics for preventing such diseases including cancers, infections, allergies, inflammatory bowel diseases and autoimmune diseases. Lactobacillus casei strain Shirota (LcS) is one of the most popular probiotics, benefits of which in health maintenance and disease control have been supported by several science-based evidences.(2)

Early microbial colonization of the gut reduces the incidence of infectious, inflammatory and autoimmune diseases. Recent population studies reveal that childhood hygiene is a significant risk factor for development of inflammatory bowel disease, thereby reinforcing the hygiene hypothesis and the potential importance of microbial colonization during early life. (3)

Early-life environment significantly affects both microbial composition of the adult gut and mucosal innate immune function. We observed that a microbiota dominated by lactobacilli may function to maintain mucosal immune homeostasis and limit pathogen colonization. (3)

The human GI tract starts with the mouth and ends with the rectum. In between lay the esophagus, stomach, and intestines which consist of the duodenum, jejunum, ileum, and colon.

The surface area of the intestines equals that of a tennis court providing a huge area for absorption, digestion and interaction between our immune system and the micro-flora. This large surface area is the result of the intestinal micro-villi which produce an undulating surface resembling a series of peaks and valleys. The constant interplay between our immune system (4) and our micro-flora from birth to death along with the signaling and communication that occurs between our micro-flora and our nervous system (5,6,7) present two physiologic mechanisms for potential symbiosis (mutually beneficial interaction) vs dysbiosis (disease causing relationship).

Before birth the mouth, skin and intestine of the fetus is sterile. The first major introduction of bacteria to the infant occurs with birth when the infant swallows bacteria in the mother’s birth canal and the infant’s skin becomes colonized by the mother’s bacteria. Infants born by cesarean section lack this initial exposure and they suffer increased risk of allergic and auto-immune disease (8). The rate of cesarean section in the US is now about 30 % and along with that increase there has been an observed increase in allergy, auto-immune and other diseases.

The second major addition to human gut and skin flora occurs with breast feeding and again breast-fed infants show decreased rates of allergy and auto-immune disease as well as decreased infections compared to bottle fed infants.

The interaction between the micro-flora and the immune system presents many complex relationships and interactions. Immune tolerance allows the immune system to recognize “self” and “friendly bacteria” limiting the development of auto-immune disease and enhancing anti-inflammatory processes. At the other extreme recognition of “non-self” allows for the recognition and disposal of “foreign” invaders such as infections or mutated cancer cells.

“The Old Friends Hypothesis”
Common organisms interact with dendritic cells in the GI tract, leading to increased maturation of dendritic cells. When there is interaction with these organisms again, the dendritic cells increase Treg maturation; not Th1 or Th2. This increases the baseline amount of anti-inflammatory cytokines, producing a Bystander Suppression. Another consequence of the increased number of mature dendritic cells is as they interact with self antigens, they increase the number Treg specific to these antigens. This is referred to as Specific Suppression. Together these two arms lead to tolerance of both self antigens as well as those of helpful gut organisms. (8)

Translation: Treg or Regulatory T cells regulate the immune system and help prevent auto-immune disease and allergic reactions. Th1 and Th2, T helper cells , on the other hand, increase inflammation and help our bodies defend against infection. The balance between Tregs and Th1, Th2 cells governs inflammatory responses.

Premature infants have an increased risk of a developing a very severe illness called necrotizing enterocolitis. Human studies have demonstrated significant risk reduction for this problem with the administration of pro-biotics to infants in neonatal intensive care units. (9)

Similarly, administration of pro-biotics during the first few years of life (to mother and child) have been associated with decreased risk of eczema in children. While some studies suggest reduction of allergies and asthma in children, the regular use of probiotics remains undecided relative to preventing food allergies or asthma (10, 11).

Due to the recent exponential increase in food allergies and atopic disorders, effective allergy prevention has become a public health priority in many developed regions. Important preventive strategies include the promotion of breastfeeding and vaginal deliveries, judicious use of perinatal antibiotics, as well as the avoidance of maternal tobacco smoking. Breastfeeding for at least 6 months and introduction of complementary solids from 4-6 months are generally recommended. Complex oligosaccharides in breast milk support the establishment of bifidobacteria in the neonatal gut which stimulate regulatory T lymphocyte responses and enhance tolerance development…Perinatal supplementation with probiotics and/or prebiotics may reduce the risk of atopic dermatitis, but no reliable effect on the prevention of food allergy or respiratory allergies has so far been found. A randomized trial on maternal fish oil supplementation during pregnancy found that atopic dermatitis and egg sensitization in the first year of life were significantly reduced, but no preventive effect for food allergies was demonstrated. (10)

Thus birth by cesarean section increases risk and breast feeding decreases risk of immune related problems (allergies, auto-immune disease and infection ). Use of probiotics for mother and child decrease the risk of eczema but the use of probiotics in preventing asthma or food allergy remains unsettled. There are a host of possible probiotics available that include various combinations of “healthy bacteria”. Future posts will discuss some of these.

Our micro-flora are constantly exposed to potential changing agents. Known influences include antibiotics (as medications or in the foods that we eat), stress, sleep, and diet. Because of the ubiquitous use of antibiotics in agriculture and animal husbandry, and the sometimes excessive use of antibiotics in medicine our microbiome is frequently changed by external factors. Many experts on the microbiome consider these influences harmful and attribute the rising rates of several diseases as consequences of disruption in our gut flora.

Clostridium Difficile Colitis , a serious infection or overgrowth of the bacterium Clostridium difficile in the intestine occurs most commonly as a result of antibiotic administration to treat infections. This serious problem responds to anti-biotic treatment (ironically both the cause and cure) 90% of the time with the first round of treatment but there is a high incidence of recurrence due to the fact that C-difficile spores are resistant to antibiotics and can cause recurrent infection. In refractory or recurrent C-difficile cases a fecal transplant (FMT or fecal microbiota transplant) from a healthy human results in a 90 to 95% cure rate with the first treatment.

Antibiotic usage disrupts the normal gut flora and leads to an increased predisposition to CDI. The risk of recurrent CDI after initial treatment of the first infection is approximately 20–25% [Kelly and Lamont, 2008; Khanna et al. 2012g] and is further increased up to 60% with the use of additional systemic antibiotics and subsequent CDI recurrences [Hu et al. 2009]. The pathophysiology of recurrent CDI involves ongoing disruption of the normal fecal flora and an inadequate host immune response. Standard CDI treatment with antibiotics such as metronidazole and vancomycin further disrupts colonic microbial communities that normally keep expansion of C. difficile populations in check. Since C. difficile spores are resistant to antibiotic therapy for CDI, they can germinate to vegetative forms after treatment has been discontinued and lead to recurrent CDI. (12)

The authors of this study review the data for fecal microbiota transplant and summarize by stating:

Therefore, existing literature suggests that fecal transplant is safe and effective with over 500 cases of recurrent CDI with no serious adverse events reported to date. FMT appears to be an appropriate treatment option for multiple CDI recurrences and may be considered for refractory moderate to severe C. difficile diarrhea, failing standard therapy. The FDA had recently announced that an Investigational New Drug Application would be required for use of FMT for CDI, but this was later changed to the use of an informed consent process to ensure communication of potential risks.

In the area of obesity rodent studies have demonstrated that fecal transplants from thin to obese subjects results in significant weight loss. Measurable differences in the microbiome of obese vs thin humans have been identified.

The prevalence of obesity and related disorders such as metabolic syndrome has vastly increased throughout the world. Recent insights have generated an entirely new perspective suggesting that our microbiota might be involved in the development of these disorders. Studies have demonstrated that obesity and metabolic syndrome may be associated with profound microbiotal changes, and the induction of a metabolic syndrome phenotype through fecal transplants corroborates the important role of the microbiota in this disease. (13)

The issue of gut flora and obesity deserves a dedicated post. Multiple research articles and review articles have been published on the topic of fecal transplantation in relation to obesity, diabetes, metabolic syndrome, autoimmune disease and cancer. (14,15,16)

Diabetes, obesity, allergy, auto-immune disease, infections, psychiatric disorders and cancer represent examples of the potential interplay between the human microbiome, human health and disease. Multiple sources of information suggest a cause and effect relationship. The results of fecal transplantation in human and rodent studies, manipulation of the gut flora with pro-biotics and pre-biotics, data on the effects of vaginal vs cesarean delivery, and the benefits of breast feeding all proclaim the importance of our micro-flora.

Most traditional cultures have one or more forms of fermented foods. Examples include yogurt, kefir, sauerkraut, kim chee, beet kvass, kombucha. Almost any food can be fermented to produce health promoting probiotics and there is a growing movement for home-fermentation and/or consumption of purchased fermented foods. In addition to the pro-biotic nature of fermented foods and beverages, fermentation offers other potential health benefits. These include reduction of the anti-nutrients found in various neolithic foods (such as mineral binding phytic acid found in grains and legumes, digestive enzyme inhibitors found in soy and other legumes). Other potential health benefits include the production of Vitamin K2 found in many fermented foods.

This discussion barely scratches the surface of gut flora, health and disease. Future posts will address how our gut bacteria produce essential nutrients and affect mental health as well as physical health. Other important topics include how our activity, food, sleep and stress affect the our gut ecology. The system is dynamic with effects going in both directions.

Following the references below you will find links to NPR discussions of related topics. You can choose to read the articles and/or listen to the NPR interviews and reports.

Peace, happiness and longevity.

BOB

(1) Microbes in Gastrointestinal Health and Disease

(2) Probiotics as efficient immunopotentiators: Translational role in cancer prevention

(3) Environmentally-acquired bacteria influence microbial diversity and natural innate immune responses at gut surfaces.

(4) Has the microbiota played a critical role in the evolution of the adaptive immune system?

(5) It’s a Gut Feeling – how the gut microbiota affect… [J Physiol. 2014] – PubMed – NCBI

(6) Metabolic tinkering by the gut microbiome: Impl… [Gut Microbes. 2014] – PubMed – NCBI

(7) The gut-brain axis rewired: adding a functional vaga… [FASEB J. 2014] – PubMed – NCBI

(8) Cesarean versus vaginal delivery: long-term infant outcomes and the hygiene hypothesis.

(9) Probiotics for prevention of necrotizing enterocolitis in preterm infants.

(10) Preventing atopy and allergic disease.

(11) Gut microbiota and allergic disease: new findings.

(12) Clostridium Difficile Colitis ,

(13) Gut microbiome, obesity, and metabolic dysfunc… [J Clin Invest. 2011] – PubMed – NCBI

(14) Fecal microbiota transplantation: indications, methods, evidence, and future directions.

(15) Fecal microbiota transplantation: past, present and future.

(16) Therapeutic potential of fecal microbiota transplantation.

Here are the NPR and other links.

Interview: Martin Blaser, Author Of ‘Missing Microbes’ : NPR

FDA Backs Off On Regulation Of Fecal Transplants : Shots – Health News : NPR

Human Microbiome Project – Home | NIH Common Fund

Staying Healthy May Mean Learning To Love Our Microbiomes : Shots – Health News : NPR

Gut Bacteria Might Guide The Workings Of Our Minds : Shots – Health News : NPR

Worried That Your Baby’s Sick? There May Be An Upside : Shots – Health News : NPR

Addendum to lose weight, control blood sugar, decrease inflammation

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To those of you who have subscribed to my blog by e-mail, I must apologize that I hit the “publish button” by mistake before I completed the finished article. So if you would like to read the full article, please go to the website for the updated and completed version.

Thanks

Bob Hansen MD

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