Sorry for the confusion. The website for the International Evolutionary Health Conference changed when the venue changed from Boston to Virtual. Here is the correct website link which gives a list of speakers/topics and sign up information.
https://2023.evolutionaryhealthconference.com/
The previously published link will lead you to a site that says “canceled”. The conference is not cancelled, the venue has changed to virtual.
Dr. Bob
I’ve been asked to talk at the fourth International Evolutionary Health Conference on the topic of Cardiovascular Risk Assessment. This year the conference is virtual. Presenters include clinicians and researchers discussing many topics related to health. The underlying principle of this approach attributes modern degenerative and chronic diseases to mismatch between our evolutionary biology and present day life. You can sign up for this virtual event here.
https://2023.evolutionaryhealthconference.com/
9:45 AM – 10:00 AM
Opening remarks
Prof. Lynda Frassetto
10:00 AM – 10:30 AM
Maladaptive cognitive/emotional processing as the cause of the stress response
Prof. Igor Mitrovic
Physiologic reserve is spare capacity activated when demand exceeds baseline, causing stress. If demand surpasses reserve, it damages the system and leads to death. The brain predicts the future to a…
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10:30 AM – 11:00 AM
How breathing patterns affect health
Dr. Michael Mew
11:00 AM – 11:15 AM
Round table with Q & A (Moderator: Darryl Edwards)
Dr. Michael Mew
Prof. Igor Mitrovic
11:15 AM – 11:45 AM
Break and Poster session
If you would like to submit a poster, please contact us at evolution.conference@nutriscience.pt
11:45 AM – 12:15 PM
Decoding The Truth: Cancer, Carbs and Cure
Darryl Edwards, MSc
1. We will delve into the extensive evidence showcasing how higher levels of physical activity can reduce the risk of various cancers. 2. While awareness of the importance of exercise exists, we will…
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12:15 PM – 12:45 PM
Influential factors on sun-induced vitamin D synthesis
Pedro Bastos, PhD candidate
Ultraviolet B radiation is absorbed in the epidermis by 7-dehydrocholesterol, giving rise to previtamin D3 and subsequently to vitamin D3. In the liver, vitamin D is converted to one of the various c…
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12:45 PM – 1:00 PM
Round table with Q & A (Moderator: Prof. Lynda Frassetto)
Darryl Edwards, MSc
Pedro Bastos, PhD candidate
1:00 PM – 2:15 PM
Lunch Break
2:15 PM – 2:45 PM
How nutrition can impact microbiome composition/permeability/immune response
Prof. Alessio Fasano
Improved hygiene and reduced microorganism exposure are linked to the ‘epidemic’ of chronic inflammatory diseases (CID) in developed nations. This hygiene hypothesis suggests that lifestyle and envir…
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2:45 PM – 3:15 PM
Comprehensive cardiovascular risk assessment
Dr. Robert Hansen
Assessing insulin resistance is central to predicting CV risk. LDL-C and standard lipid profile is extremely limited in predictive value. A systems engineering understanding of atherosclerosis and ev…
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3:15 PM – 3:30 PM
Round table with Q & A (Moderator: Pedro Bastos)
Prof. Alessio Fasano
Dr. Robert Hansen
3:30 PM – 3:45 PM
Short Break
3:45 PM – 4:15 PM
Environmental influences on cellular senescence and aging
Prof. Peter Stenvinkel
Planetary health recognizes that human well-being depends on the health of ecosystems. Neglecting this concept has led to an anthropocentric world, causing increased greenhouse gas emissions, heat st…
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4:15 PM – 4:45 PM
Fueling a Bright Future: The Role of Diet in Preventing Childhood Obesity
Dr. Polina Sayess
Childhood obesity is a global health issue. In my presentation, I’ll explore its origins, classifications, and mitigation strategies. I’ll discuss the definitions and distinctions between “overweight…
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4:45 PM – 5:00 PM
Round table with Q & A (Moderator: Prof. Lynda Frassetto)
Prof. Peter Stenvinkel
Dr. Polina Sayess
5:00 PM – 5:30 PM
Final discussion with all speakers and moderators
Establishing future research and intervention directions.
5:30 PM – 5:45 PM
Closing remarks
Prof. Lynda Frassetto
Please join us if you can.
Dr. Bob
I have spent a few days watching lectures from various low-carb-healthy-fat meetings. There is an impressive amount of solid clinical data to support Very Low Carb (with healthy fat) diets to treat obesity, insulin resistance, diabetes, pre-diabetes, metabolic syndrome, and seizure disorders. Eric Westman MD, author, Associate Professor of Medicine, Past Chairman of the Obesity Medicine Association, and director of Duke University Lifestyle Medical Clinic gave an impassioned and authoritative talk on the success of LCHF in treating all of these disorders here.
Dr. Steven Phinney, Professor Emeritus UC Davis and presently Chief Medical Officer for VIRTA has given numerous talks on the beneficial effects of a ketogenic diet. He and Jeff Volek Ph.D. have done research for decades on the physiology of low carbohydrate diets. They elucidated the changes that occur in high level athletes as they adapt to burning fat as their major fuel source during and after a period of “fat adaptation”. It turns out that endurance athletes, after a period of 1 to 3 months of adaptation to a low carb-high fat diet (variable from person to person) perform at equal or higher levels as compared to their performance when previously on a high carbohydrate diet. In fact, because lean athletes have much greater energy stored in fat as compared to glycogen (carbohydrate) they can go for many hours longer than an athlete who is dependent on carbohydrate metabolism (not fat adapted). Glycogen is the starch source of energy that humans store in the liver (100 grams) and in muscle (400 grams). Compared to glycogen, fat stores in lean individuals, including buff athletes, can provide more than 10 times the amount of energy. Endurance athletes who are keto-adapted (fat burners) can ride a bike all day or run an ultra-marathon (100 miles) without taking in any energy source. (They must of course replace fluid and electrolytes). Whereas athletes who have followed a traditional high carb diet must start consuming calories after about 3 hours of moderate-high intensity exercise. Doctors Phinney and Volek have done clinical research on humans with obesity, pre-diabetes and diabetes and they have demonstrated superior results when compared to any other dietary approach.
You can learn about their work here:
And here:
So what is this all about? If carbohydrates are restricted to very low levels and instead we consume (healthy) fat as our major source of energy with moderate amounts of protein, then the human body starts to burn fat. This process results in the production of ketones (in the liver) which serve not only as a source of energy but also act as “signaling” molecules that turn on beneficial genes that fight inflammation and turn off genes that produce inflammation. When a well formulated ketogenic diet is followed under medical supervision, diabetics can often get off most or all of their diabetes medications within weeks to months as they lose weight. Improvements are seen quickly in blood pressure, fasting blood sugar, liver function tests, insulin sensitivity, inflammatory markers, subjective energy levels, mental clarity and mood. Triglycerides are reduced, HDL increases, and improvements are seen in the “atherogenic profile” with reductions in small dense LDL particles with a shift to large buoyant LDL particles. On a ketogenic diet humans spontaneously consume lower caloric intake because fat and protein are more satiating compared to carbohydrate. Circulating saturated fat in the blood DECREASES on a keto-genic diet. Refined carbohydrates and sugar (so prevalent in processed foods) produce increased circulating fat in the blood and increased fat storage throughout the body, often leading to fatty liver disease and the long list of chronic diseases caused by and associated with insulin resistance.
A ketogenic diet is also part of Dr. Dale Bredesen’s effective treatment program for early dementia (ReCoDe-Reversal of Cognitive Decline). I have discussed Dr. Bredesen’s approach before. Here is one of his discussions.
You can read Dr. Bredesen’s report of 100 patients who have reversed cognitive decline using a ketogenic diet as PART of the ReCoDe program here.
So what are the healthy fats in a low carb high fat diet?
They include fats found in whole foods such as nuts and avocados, pasture raised animals free of hormones and antibiotics, free range poultry and eggs, wild fish and seafood (avoiding large fish that have high mercury levels), extra virgin olive oil, avocado oil, butter from pastured grass-fed animals, and coconut oil. (yes butter is included despite that fact that strict paleo excludes dairy)
You should avoid all of the processed/refined oils that come from seeds, grains and legumes including soy oil, corn oil, cottonseed oil, canola oil, safflower oil, sunflower oil, sesame oil. You can learn why these (misnamed) “vegetable oils” are dangerous and how they were marketed to an unwitting public with the help and support of faulty science by listening to Nina Teicholz here:
There are many great lectures about the low-carb-high-fat ketogenic diet in addressing obesity, insulin resistance, pre-diabetes, metabolic syndrome, diabetes, seizures and more. Go to youtube and search “keto diet”, “low carb high fat”.
Before I sign off I will provide one more link:
Remember, this website offers educational information only. Consult your health care provider for medical advice.
Sleep well, exercise outdoors, laugh, love, engage in meaningful work, drink filtered water, eat clean, eat whole foods, get plenty of sunshine, spend time with those you love.
Doctor Bob
Ever wonder why the public is so confused about nutrition recommendations? Just follow the money and you will understand that most of the professional societies that publish nutrition articles are funded by big food companies that are trying to sell more sugar, refined carbs and junk food. I recently read an excellent post about this topic here:
The Vilest Villain: American Society of Nutrition
This theme is repeated by medical journals that are “The Official Journal of the Society of >>>>>>” Just fill in the blanks for just about any medical society. Funding comes from big pharmaceutical companies the same way that funding in the nutrition Journals comes from large (junk) “food” manufacturers.
Don’t get me wrong, there are plenty of very valuable, life-saving drugs out there.
But most chronic human disease in developed societies is generated by various combinations of poor nutrition, lack of exercise, disruption of circadian rhythm, inadequate restorative sleep, stress and lack of social support systems.
The obesity and diabetes epidemics continue to worsen yet the failed dietary advise of major health organizations is slow to respond to the data. Excess refined carbs (especially in the form of “food” made with flour) and added sugar (especially in the form of HFCS) are the major driving forces for obesity, diabetes and cardiovascular disease. Red meat is not the culprit, provided the meat is properly sourced (hormone and antibiotic free, grass fed) and cooked in a manner that does not create carcinogens and inflammatory mediators (cook with slow, low, moist heat, high temperature grilling and smoking cause problems, but that topic is for another post).
Americans consume an average 130 pounds per year of added sugar and 140 pounds per year of refined flour. Those are averages so there are many people who consume more. The added sugar is not the white stuff people put in their coffee. It comes in all sorts of forms but is found in energy drinks, soda, lattes and mochas, salad dressing, ketchup, canned soups, canned vegetables, white AND whole grain breads, pasta (even “whole grain”), crackers, breakfast cereal, just about any packaged food that has more than one ingredient on the label. These foods represent 70% of the American diet. The problems created by this situation are enormous and will bankrupt our “healthcare system”. This is a cultural and economic problem.
The solutions are simple but largely ignored in our society. We are creatures of habit and convenience.
Eat whole foods, nothing from a package that has more than one ingredient. Eat meat, seafood, poultry, fresh organic vegetables (6-9 servings per day), fresh organic fruits, and nuts. Meat should be hormone and antibiotic free (free range, grass fed). Seafood should be wild. Poultry should be free range and the eggs should come from free range chickens, ducks, geese.
Do not worry about eating fat as long as it comes from healthy animals and sources such as coconut oil, extra-virgin olive oil, avocado oil and clarified butter (ghee).
Do not use any “vegetable” oils (corn, soy, and other oils from grains or seeds) The vegetable oils are highly refined and inflammatory. They contain easily oxidized omega 6 fats that feed the production of inflammatory mediators in your body and create oxidized LDL leading to atherosclerosis.
Exercise daily, preferably outside in a green space. Twice per week spend 20-30 minutes doing resistance training (lift weights, work against the resistance of bands, use your own body weight doing pushups, pull-ups etc)
Reduce stress with mediation, yoga, tai chi, dancing, engaging in fun sports and social activities. Walk on the beach, by a lake, river or stream, in the woods, listen to music.
Get some sunshine regularly especially during the morning to get your circadian rhythm in order and to produce adequate amounts of vitamin D.
Spend time with family, friends and colleagues who are supportive and fun to be around.
Sleep in the dark.
Get at least 7 hours of sleep per night. Avoid TV, computer screens and other electronic devices for at least 2 hours before bedtime.
Unplug from the internet, email, etc on a regular basis.
We evolved as hunter-gatherers.
Peace
Bob Hansen MD
In January I attended the annual meeting of Physicians for Ancestral Health. There were great presentations on many topics related to lifestyle and health. Take a look at the website linked below to learn about many topics relating nutrition, exercise, and lifestyle to health.
Open Video Archives | Physicians for Ancestral Health
I presented a lecture titled “The Lipoprotein Retention Model, What’s Missing?” This discusses many factors (root causes) that contribute to the formation of plaque in arteries and what can be done to prevent this insidious process by adopting a “Paleo Lifestyle“.
Other videos include:
Paleopathology and the Origins of the Paleo Diet. Keynote speaker Michael Eades MD, author of several books and a well known website.
Medicine Without Evolution is like Engineering Without Physics– Randolph M Neese, MD Director of the Arizona State University Center for Evolution.
The Roles of Intermittent Fasting and Carbohydrates in Cancer Therapy– Dawn Lemanne, MD, MPH, integrative oncologist.
23 and Me: Practical First Steps-Deborah Gordon MD, discusses a practical approach to utilizing information from this genetic test.
Histamine Intolerance-Why (food) Freshness Matters– Georgia Ede MD.
Mood and Memory: How Sugar Affects Brain Chemistry-Georgia Ede, MD.
Systems Analysis and Multiple Sclerosis– Tommy Wood MD, author, blogger and lecturer, frequently interviewed on topics related to exercise and nutrition.
Cholesterol OMG– Jeffry Gerber, MD “The Diet Doctor” in Denver Colorado
Bob Hansen MD
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:
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
Erythrocyte fatty acid profiles can predict acute non-fatal myocard… – PubMed – NCBI
Low-density lipoprotein subclass patterns and risk of myocardial in… – PubMed – NCBI
Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis
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
Finally a quote from the Dali Lama (thanks to my cousin Diane for bringing this to my attention).
“Man. Because he sacrifices his health in order to make money. Then he sacrifices money to recuperate his health. And then he is so anxious about the future that he does not enjoy the present, the result being that he does not live in the present or the future, he lives as if he is never going to die, and dies having never really lived.”
Eat clean, live clean, sleep well, exercise wisely, rest often, enjoy the company of loved ones, spend time outdoors and live in the present.
BOB
The Duke University Lifestyle Medicine Clinic prescribes a nutritional program based upon a very simple concept, limit carbohydrate intake and multiple problems improve. This approach is so powerful in controlling blood sugar that diabetic patients must reduce their medication before adopting the nutritional program in order to avoid very low blood sugars.
Compared to a low-fat diet weight loss approach, it is better or equal on every measurement studied. Here is what happens on the carbohydrate restricted program when compared to a low fat diet (American Heart Association diet). The carbohydrate restricted diet results in
All of these beneficial effects are accepted by the medical community as reducing cardiovascular risk .
The improved metabolic outcome can occur even without weight loss simply by substituting fat for carbohydrate.
“The key principle is that carbohydrate, directly or indirectly through the effect of insulin, controls the disposition of excess dietary nutrients. Dietary carbohydrate modulates lipolysis, lipoprotein assembly and processing and affects the relation between dietary intake of saturated fat intake and circulating levels.” see here
Yet despite these proven effects, the proponents of low-fat diets refer to the carbohydrate restriction approach as a “fad diet”. In his excellent discussion of this term, Richard Feinman points out that historically, a carbohydrate restriction approach is actually the longest standing and proven approach to the treatment of obesity compared to a low-fat diet which is a relative newcomer. He describes how a low-fat diet more closely meets the dictionary’s definition of a “fad”.
Multiple Studies have compared carbohydrate restriction to low fat diet approaches and the results are consistent. In addition to the advantages cited above, carbohydrate restricted approaches when compared to low-fat diets reveal that symptoms of “negative affect and hunger improved to a greater degree” compared with those following a low fat diet”. (see here)
When one analyzes the carbohydrate restricted diet (CRD) approach employed by many centers, including the Duke Interventional Medicine Clinic, one finds great similarity to a paleolithic diet.
They both eliminate or dramatically reduce
Fruits under a CRD are limited to small amounts of berries initially and this is liberalized over time as weight loss is achieved and metabolic parameters are improved. This is consistent with a paleolithic approach that recognizes that fruits and vegetables grown today have been bred to provide much higher sugar and starch content compared to the pre-agricultural fruits and vegetables that early hominids consumed for hundreds of thousands of years.
A carbohydrate restricted nutritional approach to treat obesity, diabetes, or metabolic syndrome appears to be a valid and arguably superior remedy to a growing problem in the developed world. Yet despite this strong and convincing scientific data, dietary fat-phobia has impaired the utilization of this proven therapeutic modality.
Peace,
Bob Hansen M.D.
When I recommend to my patients that they should eat eggs and vegetables for breakfast rather than breakfast cereals (which have high sugar content and nasty gut inflaming gluten proteins) they often ask “well what about my cholesterol ?”. I tell them that eggs are a health food and that they do not need to worry about their cholesterol.
I first read about the man who ate 25 eggs per day for 15 years here.
He was 88 years old when some cholesterol fearing physicians studied his plasma lipids (HDL, LDL, triglycerides etc.) and other aspects of his health (blood pressure, weight, etc.) and discovered that he was very healthy at the ripe age of 88.
This article was published in 1991 and the authors concluded that this man was exceptional in lacking adverse health consequences from eating 25 fat and cholesterol laden eggs every day for 15 years. Since that time, many studies on the health effects of eggs have demonstrated that they are in fact a health food and do not increase cardiovascular risk. In fact they provide a nutrient dense assortment of important vitamins, minerals, fat, and protein. Perhaps most importantly they are very high in choline, an important nutrient which is not hard to come by. Eggs and liver provide an abundance of choline.
Choline is widely used in the human body for many important functions. These include:
You can read more about the importance of choline here:
Choline – Wikipedia, the free encyclopedia
Regular egg consumption has been demonstrated to improve insulin sensitivity and cardiovascular risk profiles in healthy individuals and in individuals with metabolic syndrome as demonstrated here:
Whole egg consumption improves lipoprotein profil… [Metabolism. 2013] – PubMed – NCBI
Daily egg consumption with modest carbohydrate restriction in that study resulted in:
They concluded that:
“Atherogenic dyslipidemia improved for all individuals”
In adults with metabolic syndrome (hypertension, insulin resistance, obesity, high triglycerides) three whole eggs per day with moderate carbohydrate restriction resulted in:
The authors concluded that:
“on a moderate carbohydrate background diet, accompanied by weight loss, the inclusion of whole eggs improves inflammation to a greater extent than yolk-free egg substitute in those with MetS.”
Effects of carbohydrate restriction a… [J Clin Lipidol. 2013 Sep-Oct] – PubMed – NCBI
In yet another study:
Daily intake of 3 whole eggs, as part of a CRD, increased both plasma and lipoprotein lutein and zeaxanthin. Egg yolk may represent an important food source to improve plasma carotenoid status in a population at high risk for cardiovascular disease and type 2 diabetes.
See for yourself:
Egg intake improves carotenoid status by increasi… [Food Funct. 2013] – PubMed – NCBI
In another study:
Consumption of 2 and 4 egg yolks/d for 5 wk increases macular pigment concentrations (lutein and zeazanthin) in older adults with low macular pigment taking cholesterol-lowering statins.
“Lutein and zeaxanthin may reduce the risk of dry, age-related macular degeneration because of their photo-oxidative role as macular pigment.”
Consumption of 2 and 4 egg yolks/d for 5 wk i… [Am J Clin Nutr. 2009] – PubMed – NCBI
Studies of the benefits of high-cholesterol egg consumption have been so convincing that even the American Heart Association has removed advice to avoid eggs.
“…there have been a number of epidemiological studies that did not support a relationship between cholesterol intake and cardiovascular disease. Further, a number of recent clinical trials that looked at the effects of long-term egg consumption (as a vehicle for dietary cholesterol) reported no negative impact on various indices of cardiovascular health and disease”
Exploring the factors that affect blood cholesterol… [Adv Nutr. 2012] – PubMed – NCBI
From an evolutionary medicine point of view, eggs and ample dietary cholesterol have been around a long time in the human diet.
“Paleoanthropologists suggest that dietary cholesterol has been in the human diet for millions of years (7–10). Sources included eggs, bone marrow, and organ meats. Stone Age intake of cholesterol is uncertain, but it may well have exceeded current dietary recommendations.
There are many important biological roles for cholesterol that span the spectrum from cell membrane structure to steroid hormone synthesis, bile acid synthesis, and others. The vital role of cholesterol in human metabolism and the well-established place of dietary cholesterol in the native human diet provide a robust theoretical challenge to the view that dietary cholesterol poses a threat to human health.
More important still are prospective, population-based studies that, when similarly scrupulous about variation in other dietary components, find no association between cholesterol intake in general, or egg intake in particular, and the risk of CVD (13).”
Exploring the factors that affect blood cholesterol… [Adv Nutr. 2012] – PubMed – NCBI
Here are more links to discover that eggs are a health food.
Egg consumption and endothelial function: a randomized controlled crossover trial.
Endothelial function testing as a biomarker of vascular disease.
Endothelial function testing as a biomarker of vascular disease.
Rethinking dietary cholesterol. [Curr Opin Clin Nutr Metab Care. 2012] – PubMed – NCBI
Endothelial function is the term used to describe how well the arteries can expand and contract to meet the needs of blood flow. It is considered an important tool for assessing cardiovascular risk and it is impaired in metabolic syndrome, diabetes and in patients with coronary artery disease. Compromise of endothelial function is part of the process of atherosclerosis and heart attacks.
“There is thus a case to be made that endothelial function is potentially a summative measure of overall cardiac risk status and at least a valuable addition to standard risk measures (45). The ever-expanding footprint of research in this area in the cardiology literature attests to its importance.”
Despite (or because of) their high fat and cholesterol content, eggs have not been found to have any negative effects on endothelial function.
Rethinking dietary cholesterol. [Curr Opin Clin Nutr Metab Care. 2012] – PubMed – NCBI
So far since launching this blog a few weeks ago we have discovered that saturated fat and cholesterol containing foods are not the villains portrayed by the media, doctors and professional organizations that give us nutritional advice.
We have reviewed evidence that added sugar, sweetened beverages, refined carbohydrates (especially flour foods), trans-fats, and excessive polyunsaturated omega six fats from processed “vegetable oil” are the culprits with regards to obesity, diabetes, heart attack and stroke. These culprit components of the modern Western diet were definitely absent from the diets of our paleolithic ancestors. We have not evolved to tolerate them. These modern manufactured and processed “foods” represent an unhealthy deviation from our evolutionary past.
There is so much more to discuss. In the spirit of more work ahead during this 50th anniversary week of John F Kennedy’s assassination. I will close with a quote from JFK’s favorite poet and friend, Robert Frost.
“I have promises to keep, / And miles to go before I sleep, / And miles to go before I sleep.”
Peace,
Bob Hansen MD
New guidelines published on Tuesday of last week widely expand the category of who should take statins.
Two physicians authored the article providing an excellent analysis and warning against implementation of the new guidelines which are unfortunately and again, not based on sound evidence or reasonable analysis.
” based on the same data the new guidelines rely on, 140 people in this risk group would need to be treated with statins in order to prevent a single heart attack or stroke, without any overall reduction in death or serious illness.”
“At the same time, 18 percent or more of this group would experience side effects, including muscle pain or weakness, decreased cognitive function, increased risk of diabetes (especially for women), cataracts or sexual dysfunction.”
“We believe that the new guidelines are not adequately supported by objective data, and that statins should not be recommended for this vastly expanded class of healthy Americans. Instead of converting millions of people into statin customers, we should be focusing on the real factors that undeniably reduce the risk of heart disease: healthy diets, exercise and avoiding smoking. Patients should be skeptical about the guidelines, and have a meaningful dialogue with their doctors about statins, including what the evidence does and does not show, before deciding what is best for them.”
History repeats itself, soon the AHA and ACA will want statins in the water. The 18% estimate of serious side effects in my opinion is understated. Every week in the pain clinic I diagnose statin myopathy and/or cognitive impairment on at least one patient. Here are some stories about patients that appeared in the comments section of the oped on-line.
Noreen stated:
I am a victim of statin “therapy.” At the age of 72, with just a moderately high LDL, Simvastatin was prescribed. I took it for approximately 2 weeks, and severe pain developed in my whole body, but, primarily in my lower legs. I read the side effects on line and stopped taking it.
The pain went away, but my legs were weak. After much investigation by neurologists at University of California, SFMC, I was diagnosed with statin-induced neuropathy. The calf muscle in both legs has totally gone — nothing left but sinew. My life has been severely damaged by an inability to walk properly. I cannot raise on my toes. It has been three years since I took this medication, and there is no further hope of recovery. Prior to taking Simvastatin I was an athlete all my life. At the time of this pharmaceutical invasion I was still, hiking, exercising regularly and downhill skiing. Shame of this hired committee of “experts.”
Here is how a physician/patient described his experience.
I agree with Abramson and Redburg that treating a numbers instead of the patient is wrong. I am in a high risk group and I would hope to prevent another heart attack (I had one in 2009), yet I cannot take statins as I repeatedly developed muscle pain and then progressive weakness and loss of balance with all the statins I tried. My cardiologists (including Mayo physicians) and internists continued to push trying different statins and other cholesterol lowering medications even though I complained of side effects. Although some of my loss of power is due to aging and not statins, I used to be able to hike 10 to 20 miles with up to 5 to 6,000 feet elevation gain in a day before my statin era and now I can barely manage 4-5 miles at a slow pace. I’ve seen this in others taking statins. Even though the percentage who develop weakness may be low compared to the majority, it is a real debilitating effect for some. Doctors are brain washed (and the lay public too by TV and other ad bombardment), by the pharmaceutical industry to treat numbers rather than individuals. The result is the standard of care is now to treat the lab test instead of the person. Statins are dangerous medications and should not be prescribed lightly. SD Markowitz, MD
George from CA describes his experience as follows.
I had been on statins for over 15 years. Slowly, I began experiencing cognitive dysfunction, balance issues, muscle weakness, etc. even though I exercised both my body and brain. I quit several months ago and have been feeling better all around every day with improvement in every area. I’d rather die feeling good in 10 or 20 years than be miserable for however long this terrible medicine might extend my life.
JR Hoffman MD from Los Angeles provided further insight.
Congratulations to Drs Abramson and Redberg for their outstanding editorial, and to the NYT for having the courage to print it. As the authors note, this new guideline’s major beneficiary will be the pharmaceutical industry, while the American people will likely be its primary victim.
The British Medical Journal has recently printed a series of papers (disclosure — I co-authored one of those papers) addressing the biases and distortions that enter far too many published clinical guidelines, because a large majority of panel members and panel chairs have a financial conflict of interest, and because panels are stacked to support viewpoints reflecting those conflicts, independent of the evidence. This is particularly true of guidelines from prominent medical specialty societies … societies which themselves receive major financial support from industry.
How many people targeted by the new guidelines would take one of these medicines if they were told that far more than 9 out of 10 (in fact probably more than 99%) would get no possible benefit whatever? And essentially none would get an overall reduction in major morbidity or mortality? And that this would come at a substantial cost in the side effects that a good many would suffer (not even considering the cost in dollars)?
If your physician tells you that you “need” a statin, please ask her for the details of how likely you as an individual are to benefit, and at what chance of harm.
Statin drugs interfere with the human production of many important substances. One of these is Coenzyme Q 10 also called uibiquinone. Co Q 10 functions as an important anti-oxidant and as an essential component of the apparatus inside every cell that produces ATP, the fundamental unit of energy that provides energy for every cellular function. Without ATP the cells in every organ shut down and cannot do any work.
Statin side effects can include not only muscle pain and weakness but also nerve damage, dementia, amnesia. Shortness of breath can be the only symptoms when the muscles of respiration are affected. Diabetes can be caused by any of the statin drugs and this can be permanent. Rarely, statins can cause death . This happens when a massive amount of muscle damage causes a flood of debris that overwhelms the body’s ability to clear the debris. Damage to muscles and nerves can be permanent without any recovery after the statin is stopped. A former astronaut and flight surgeon suffered transient global amnesia which fortunately cleared after stopping the statin drug. He has since published a few books about the dangers and inappropriate use of statins. Kidney failure requiring dialysis or kidney transplant is also a rare but potential result of statin medication.
Cardiologists and primary care physicians often ignore complaints about muscle pain, fatigue, weakness and forgetfulness in older patients and attribute it to old age. But even when these complaints are recognized as a side effect, rarely does a physician report it to the FDA. As a result, post marketing surveillance data underestimates tremendously the frequency of side effects.
Be careful out there. Read my first post about statin medications. it provides risk-benefit data. Remember, we do not know with certainty the frequency of side effects and permanent damage, but you can be sure it happens more often than the drug company states. It happens more often than most physicians realize.
Peace
Bob Hansen MD
My 85 year old mother-in-law was placed on a statin drug two years ago by her primary care physician. She had no risk factors for coronary disease other than age, she had a prior completely normal cardiac catheterization (coronary angiogram) and was totally without symptoms before being placed on the statin. Within weeks she developed muscle pain and weakness, suffered fatigue and overall felt poorly. I convinced her to stop the statin and within a few weeks she felt great. I see similar scenarios frequently in the pain clinic. I personally suffered severe statin induced myopathy pain from two different statins (in the days before enlightenment) and gratefully recovered when I stopped the drug each time. I have since learned more about coronary artery disease, cholesterol metabolism, statins, and related topics.
There is a great website that analyzes data from multiple studies to estimate the number of patients needed to treat in order to help and/or harm a patient. Two such analyses on this website are the NNT with statin drugs for five years to achieve certain results. They analyze data in patients without known coronary artery disease (primary prophylaxis) and in patients with known coronary artery disease (secondary prophylaxis).
Here is the website:
Here is the page for primary prophylaxis:
Statins for Heart Disease Prevention (Without Prior Heart Disease) | TheNNT
Here is the link to the page on secondary prophylaxis:
Statins for Heart Disease Prevention (With Known Heart Disease) | TheNNT
Here are the results for primary prophylaxis.
“In Summary, for those who took the statin for 5 years:
In Other Words:
Here are the results for secondary prophylaxis.
“In Summary, for those who took the statin for 5 years:
In Other Words:
If anything, the side effects (harm) are understated and the authors acknowledge this because many of the studies do not adequately report side effects and complications. (The studies were funded in part or in totality by the pharmaceutical company that makes the drug and that is a problem as discussed below)
Association of funding and conclusions in randomized dr… [JAMA. 2003] – PubMed – NCBI
It is rare that this sort of analysis would be presented to a patient in the physician’s office to help a patient decide whether the risks and benefits are acceptable. (I provide patients with this data on a multi-page handout with significant narrative and explanation when I diagnose statin myopathy.)
The obsession that American physicians have with cholesterol (another topic to be addressed in future posts) creates a knee-jerk reaction to a lab value that results too often in muscle damage and pain and sometimes cognitive impairment.
My experience in the pain clinic has been that the % of elderly with statin induced muscle damage and/or muscle pain is much higher. When I suggest that the patient stop the statin drug because they are suffering disabling pain and possibly permanent muscle damage they often return at the next visit to tell me they were started on a different statin drug. Most patients who suffer this complication will have a repeat of the same complication when placed on a different statin drug. This complication can cause permanent damage.
In the medical literature, many studies presented as “primary prophylaxis” are not truly primary prophylaxis because there are some patients included that have known diagnosed coronary disease. This tainted data is then presented as if it were a true primary prophylaxis study.
A more recent study purported to demonstrate once and for all that statins in primary prophylaxis can save lives. Unfortunately, there were problems with this study as well. Here is an excerpt from a commentary in the publishing journal:
“There are reasons to be cautious about the findings of the meta-analysis by Taylor and colleagues. As the authors note, all but 1 of the trials were partly or fully funded by pharmaceutical companies. Trials funded by for-profit organizations are more likely to recommend the experimental drug than are trials funded by nonprofit organizations (4). Further, adverse event reporting in the original trials was poor, with few details about type or severity, and quality of life was rarely assessed. Some adverse events, such as cognitive impairment, are rarer and not assessed.”
Disappointingly, the commentary failed to point out that the study data again included some patients with diagnosed coronary artery disease. (up to 10%).
Here are the authors own words.
“We included randomized controlled trials of statins versus placebo or usual care control with minimum treatment duration of one year and follow-up of six months, in adults with no restrictions on total, low density lipoprotein (LDL) or high density lipoprotein (HDL) cholesterol levels, and where 10% or less had a history of CVD.”
Once again we have a “primary prophylaxis” meta-analysis that is not really a primary prophylaxis study. It never seems to end.
When drug companies fund studies the conclusions often overstate the benefit and understate the risks. If you do not look for a side effect or complication, you will not find one. Here is an excerpt from a large study that look at the issue of bias in drug company sponsored research.
“CONTEXT:
Previous studies indicate that industry-sponsored trials tend to draw proindustry conclusions.
OBJECTIVE:
To explore whether the association between funding and conclusions in randomized drug trials reflects treatment effects or adverse events.
Conclusions in trials funded by for-profit organizations may be more positive due to biased interpretation of trial results. Readers should carefully evaluate whether conclusions in randomized trials are supported by data.”
Association of funding and conclusions in randomized dr… [JAMA. 2003] – PubMed – NCBI
There are many ways that authors can present data to give the appearance of success. A more recent study published in Lancet alleged to demonstrate benefit (death prevention) for statins in primary prophylaxis.
Here it is.
But when you drill down into the data you discover a mechanism of deception. The benefits reported in the paper applied only to patients whose cholesterol dropped significantly. Looking at all patients in the study who took the statin did not result in decreased death rates. Selecting those whose cholesterol dropped 40 points did show death prevention benefit. They presented risk reduction per unit of cholesterol reduction. From a scientific point of view this is less than honest. The authors simply demonstrated that patients who responded to the drug benefited.
DUH***All previous studies that simply compared patients on statins vs. those not on statins (primary prophylaxis) showed no prevention of death. This is an important distinction, The cost implications of putting low risk individuals on statins are enormous. Statins also rarely can cause death (from rhabdomyalysis) and frequently caused harm. One comment about this studies’ conclusions was titled “Statins for all by the age of 50 years?” That frightens me.
The mechanism of statin drug benefits are likely related to many known potentially beneficial physiologic effects, not from a reduction of cholesterol. As you will learn in future posts, cholesterol reduction in and of itself is almost meaningless. The amount of circulating cholesterol in your blood is not the problem. The problem is much more complex and relates in part to the oxidation of LDL particles, which has little to do with the amount of cholesterol carried in those particles. Other important factors include systemic inflammation and the response of the innate immune system to factors such as circulating LPS which in turn reflects intestinal permeability. I apologize for the sudden onslaught of abbreviations and medical terms but stay tuned and you will learn what they all mean.
Finally, in the secondary prophylaxis group, the benefits of statin drug use are equivalent to the benefits achieved with exercise-based cardiac rehabilitation following a heart attack. Cardiac rehab offers many benefits in addition to saving lives, produces no significant negative side effects, and improves quality of life and sense of well-being. Many patients on statins feel lousy.
Efficacy of exercise-based cardiac rehabilitation… [Am Heart J. 2011] – PubMed – NCBI
In my next post I will discuss saturated fat and coronary artery disease. This issue represents the crux of controversy in the heart-healthy diet debate which most physicians and the AHA consider clarified (eat less saturated fat). You already know generally what I have to say about that if you have read my Manifesto page. The next post will expand on the saturated fat section in the Manifesto. Subsequent posts will discuss cholesterol, LDL cholesterol, LDL particle number, oxidized LDL and glycated LDL (the last two are referred to as modified LDL)
Bob Hansen MD
Practical Evolutionary Health 