Author Archives: Bob Hansen MD

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About Bob Hansen MD

I am a practicing physician, board certified in Anesthesiology and Internal Medicine with Certificate of Special Qualifications in Critical Care. My interests include the effects of lifestyle on health and health care policy.

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

Stomach bacteria can cause and worsen heart disease

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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

Fat consumption, Fat circulating in your blood, Heart Disease

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Peace,

Bob Hansen MD

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Thai Red Curry Coconut Ginger Basil Chicken Soup

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This delicious recipe will warm your soul, tingle your tongue, enhance your immune system, and enhance athletic performance. Use fresh organic ingredients, free range chicken for the healthiest soup.

  • 3-4  pounds whole chicken, organic, free range
  • fresh garlic, as much as you want, usually I press 4-6 cloves
  • two large yellow onions, sliced
  • one yam or sweet potato, peel and slice
  • two-three fresh beets with greens, peel and thinly slice, cut the greens into one inch pieces
  • one head kale, chop stems into one inch pieces
  • one head chard, chop stems into one inch pieces
  • 1/2 red cabbage, sliced
  • 1/2 cauliflower, slice
  • one quart coconut milk, full fat, not the light stuff
  • 4 carrots, whole
  • 2-4 TBS Thai red curry paste (how hot do you want it?)
  • one large piece (4-5 inches long) of fresh ginger root, grate it fresh
  • one tube of lemon grass (4 ounces, usually you can find this by fresh produce/herbs)
  • Thai or regular basil, as much as you want
  • 3 oz of lime juice
  • one orange sliced (include the skin)

Simmer chicken in water or chicken broth for 45-60 minutes or until fully cooked with onion and garlic, grated ginger, red thai curry paste and lemon grass.

Remove chicken from broth and let it cool off

While the chicken is cooking, saute the pieces of chard stems and kale stems in organic extra virgin coconut oil with cover on pan for 10 minutes,  then add to broth after the chicken is cooked and removed from the broth.

Add all the root vegetables to the broth and simmer until cooked to your preference of firmness or softness. Then add the greens and basil and lime juice, simmer for two minutes, then add the coconut milk and turn off the heat.

Cut up the chicken and add to the soup.

Optional,  cut up fresh fish into small 1 inch pieces and add to simmering broth at end of recipe, takes only 2 minutes to cook, You can also try scallops, shrimp, and squid (calamari) and use some fish or seafood stock.

The following is paraphrased from Jo Robinson’s Eating on the Wild Side, so I have placed it in quotations.

“Most red-colored fruits and vegetables get color from anthocyanins or lycopenes. Beets get their red from phytonutrients called betalains. Beet juice in a test tube blocked proliferation of human cancer cells of the pancreas, stomach, prostate, lung, and brain by 85-100%. A dietary survey revealed that people who eat beets regularly have a lower risk of cancer, cardiovascular disease, diabetes, obesity, and diseases of the GI tract.

Beets contain nitrates that enhance cardiovascular function. British athletes in the 2012 Summer Olympics drank beet juice rather than Gatorade before their events. Mo Farah did that and won the fold medal for the men’s five and ten-kilometer races. Sedantary volunteers who consumed beet juice required 12 percent less effort to walk a given distance compared to when they drank a placebo juice.”

Langley, K et.al., Dietary Nitrate Supplementation Reduces the O2 Cost of Walking and Running: A Placebo-Controlled Study. 2012 Journal of Applied Physiology 110: 591-600

Murphy, Margaret, et al., 2012 Whole Beetroot Consumption Acutely Improves Running Performance. journal of the Academy of Nutrition and Dietetics 112: 548-52

Reynolds, Gretchen 2012 Looking for Fitness in a Glass of Juice. New York Times, August 8.

For information on the potential health benefits of ginger here are a selected few results of a PubMed search using “ginger AND inflammation”, “ginger AND cancer”.

Anti-inflammatory effects of zingiber officinale in type 2 diabetic patients.

Antioxidant, anti-inflammatory and antinociceptive activities of essential oil from ginger.

Anti-neuroinflammatory capacity of fresh ginger is attributed mainly to 10-gingerol.

Protective effects of ginger-turmeric rhizomes mixture on joint inflammation, atherogenesis, kidney dysfunction and other complications in a rat model of human rheumatoid arthritis.

Influence of ginger and cinnamon intake on inflammation and muscle soreness endued by exercise in Iranian female athletes.

Effects of ginger and its constituents on airway smooth muscle relaxation and calcium regulation.

Antioxidant activity and protecting health effects of common medicinal plants.

Enterohepatic re-circulation of bioactive ginger phytochemicals is associated with enhanced tumor growth-inhibitory activity of ginger extract.

[6]-Gingerol Prevents Disassembly of Cell Junctions and Activities of MMPs in Invasive Human Pancreas Cancer Cells through ERK/NF- κ B/Snail Signal Transduction Pathway.

Of course, the kale, chard, carrots, onions, garlic, coconut, orange, lime juice, and free range chicken also provide some great nutrients.

Most importantly, this tastes great and is easy to make.

Enjoy.

BOB HANSEN MD

The Ornish Low Fat Vegetarian Diet, does it work?

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

Let’s review what this study did.

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

The intensive lifestyle change group followed this program:

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Peace,

BOB Hansen MD

REFERENCES:

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

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

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

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

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

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

7. Adrenocortical activity during meditation.

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

9. Polyunsaturated fat, Saturated fat and the AHA

10, Lose weight, control blood sugar, reduce inflammation

11. Sugar, a serious addiction

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

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

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

15. saturated fat | Practical Evolutionary Health

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

Intestinal Permeability, Food and Disease

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

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

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

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

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

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

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

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

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

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

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

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

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

Do dietary lectins cause disease?

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

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

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

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

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

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

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

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

Peace,

Bob Hansen MD

Over-diagnosis and Over-treament, Less is sometimes more

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There have been many books published recently by physicians concerned about over-diagnosis and over-treatment. One very emotional area that caused great controversy when new prevention guidelines were published (regarding mammograms) relates to early detection and treatment of cancer. It would seem intuitively obvious that early detection and early treatment of cancer would save lives but it turns out this is not always so straight forward. Some cancers are very slow growing and early detection and treatment can cause more harm than good. This has been argued relative to screening for breast cancer, cancer of the uterus and prostate cancer, among others. For these particular cancers the screening tests are mammograms, pap smears and PSA blood test. To understand how and why less could be better you should read  Overdiagnosed.

If a cancer is diagnosed by a screening test 3 years before symptoms would have resulted in a diagnosis, but the early treatment does not change the course of the illness compared to treatment latter, it gives the appearance that the patient lived three years longer as a result of early treatment simply because the patient carries the diagnosis for three years longer. This actually turns out to be the case in many situations. Despite this knowledge our emotional response as physicians and as patients refuses to adapt to new data and we continue to follow old habits such as annual pap smears even though the data suggests that pap smears every three years would be equally  effective in saving lives and would actually prevent unnecessary, expensive and anxiety producing follow up procedures and testing. The exception to this recommendation would be for “high risk” individuals that still benefit from more frequent screening.

It turns out that in the US we likely over-diagnose and over-treat many conditions. The benefits of treatment are sometimes not justified by the side-effects and complications of the treatment. As a result of this concern the  Choosing Wisely campaign was created by a consortium of more than 30 Medical Specialty Societies with a goal of avoiding unnecessary testing and treatment. This is similar to the   Too much medicine campaign | BMJ

Medical testing can cause harm directly (complications of the test itself) but also indirectly. False positive results can lead to further invasive testing which can have complications and create anxiety for the patient.

Beyond screening tests for patients without symptoms there are many drugs now being marketed to treat “conditions” that may not need treatment. (read my posts on statins as an example) Big money is behind over-treatment and it is hard to stem the tide. Dr. Malcolm Kendrick | Scottish doctor and author of ‘The Great Cholesterol Con’

The BMJ (formerly the British Medical Journal) has been much more active in addressing these concerns as stated below:

“Has modern medicine undermined the capacity of individuals and societies to cope with death, pain, and sickness? Has too much medicine become a threat to health? Yes, argued Ray Moynihan in a BMJ theme issue in April 2002. He accused the pharma industry of extending the boundaries of treatable disease to expand markets for new products. Barbara Mintzes http://www.bmj.com/content/324/7342 blamed direct to consumer advertising of drugs in the US for portraying a dual message of “a pill for every ill,” and “an ill for every pill.” Elsewhere in the issue, doctors were accused of colluding in and encouraging medicalisation. Leonard Leibovici and Michel Lièvre http://www.bmj.com/content/324/7342/866 wrote : “The bad things of life: old age, death, pain, and handicap are thrust on doctors to keep families and society from facing them.”

Useful links:

Treatment of GERD with prolonged use of a Proton-pump inhibitor results in increased risk of pneumonia and increased risk for vitamin B12 deficiency http://jama which can result in permanent nerve damage, anemia and other ailments. This class of drug has many other potential complications. They cause decreased intestinal absorption of minerals and other nutrients and likely alter the mix of important health-promoting bacteria in your gut. They can lead to  Small intestinal bacterial overgrowth in 35% of patients who use them. They also likely contribute to increased risk of osteoporosis,  fractures and a four-fold increase in certain heart  rhythm disturbances. These drugs are now available as non-prescription medications as well as prescription medications and they are often indiscriminately used for prolonged periods of time.

Sleeping pills are another example of over-prescribed medications. The FDA has approved the use of many of these drugs for just a few weeks at a time but I see patients frequently on these medications for years. They can  lead to addiction within a few weeks, can cause dizziness, drowsiness, memory problems, confusion , hallucinations, and other side effects, and should not be used with alcohol. Sleep walking, sleep eating, sleep driving, and other abnormal-dangerous behaviors have been reported with many sleep medications. In addition to these concerns:

“An analysis of data of clinical trials submitted to the FDA concerning the drugs zolpidem, zalepon, and eszopiclone (Ambien, Sonata, and Lunesta) found that these sedative hypnotic drugs more than doubled the risks of developing depression compared to those taking placebo pill. All studies have been funded by the drug companies without independent research.”

Examples such as this abound in the US, the only developed country that permits direct to consumer advertising of drugs on TV.

Why do we pay almost twice per capita for health care in the US compared to other developed countries while ranking between 20 and 30 on various measures of public health? Over-diagnosis and over-treatment in my opinion, are big factors.

I would encourage you to explore some of the links above to learn more about over-diagnosis and over-treatment so that you can make more informed health-care decisions.

Peace

Bob Hansen MD

Unnecessary Cardiac Stents and Angioplasty Procedures

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Acute Coronary Syndrome is a very dangerous situation. If a patient with this problem reaches a well-equipped and well-staffed hospital on time, a balloon angioplasty,  placement of a coronary stent or emergency bypass surgery can prevent a death, limit the size of heart muscle damage, and reduce complications of a heart attack. But what if a person is found to have some coronary artery disease (blockages in the arteries that supply blood and oxygen to the heart muscle and heart valves) but is considered “stable”.

Multiple studies have demonstrated that such stable patients do not benefit from having an angioplasty or having one or more stents placed in heart arteries that have partial blockages from plaque.  Despite the fact that over one dozen studies have demonstrated that stents placed in coronary arteries for patients with stable coronary artery disease do not prevent deaths, heart attacks or other problems associated with atherosclerosis, an estimated 50% of the 700,000 coronary stents placed each year in the US are placed in patients who have stable disease. Deaths Linked to Cardiac Stents Rise as Overuse Seen – Bloomberg

By 2012 the excessive utilization of angioplasty and stents had become such a large problem that Bill Boden MD, a cardiologist on the faculty of SUNY wrote an editorial in Archives of Internal Medicine titled Mounting Evidence for Lack of PCI Benefit in Stable Ischemic Heart Disease:What More Will It Take to Turn the Tide of Treatment?:  Comment on “Initial Coronary Stent Implantation With Medical Therapy vs Medical Therapy Alone for Stable Coronary Artery Disease”

In this editorial Dr. Boden explains that while angioplasty and/or placement of stents (Percutaneous Coronary Intervention) is beneficial for acute coronary syndrome, it has never been demonstrated to benefit patients with stable coronary artery disease compared with standard medical management.

Since that editorial was published a more recent review of the medical literature draws the same conclusion.

Cardiologists are paid an average $1,000 (range about $600 to $2500) for this procedure and hospitals and surgery centers receive about $25,000 for this procedure. If only half of the stents placed in patients with stable coronary disease are unnecessary the cost for the procedure alone amounts to $26,000 times 150,000 procedures per year in the US for stent placement. That is $390 million dollars a year in the US. If all of the stents placed in stable patients are unnecessary the direct cost totals $780 million per year.

But there is more cost than that. Patients who receive a stent must take potent blood thinning agents such as Plavix

Use of drugs like Plavix can result in costly and life threatening complications such as gastrointestinal bleeding (2% annually), cerebral hemorrhage resulting in stroke (0.1 to 0.4 % annually) severe drop in infection fighting white blood cells (1/2000) and other complications.

The placement of a coronary stent or performance of an angioplasty in a stable patient is also associated with complications that can result in death. What Are the Risks of Having a Stent? – NHLBI, NIH

So if you are not in the middle of a heart attack, what options are available to treat or prevent the complications of coronary artery disease? Optimal nutrition, exercise,  stress reduction and medications. This combination approach offers as much benefit with much less risk than having a coronary artery stent placed or an angioplasty performed.

Peace

Bob Hansen MD