Tag Archives: atherosclerosis

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

Yesterday I posted a comment on Medscape after reading an article Longtime Dietary Fat Advice Unsupported by Data: Analysis . Medscape is a website with articles and news written for physicians and other health professionals. Anyone can access this information by creating a user name and password, there is no fee.

Here is my comment. It is long and technical. I will provide an explanation in lay terms after quoting myself.

Sugar, especially HFCS (high fructose corn syrup), used in so many foods is more inflammatory than saturated fat. Grass fed meat from ruminants has a fatty acid mix that is exactly the same as wild game, which we evolved to eat, along with tubers, green leafy vegetables, and fruit in season. Excess refined fructose intake AND use of modern refined “vegetable oils” along with non-healthy grains combine to cause excess caloric intake, NAFLD (non-alcoholic fatty liver disease), obesity, metabolic syndrome and CAD (coronary artery disease). N6 PUFA (omega six polyunsaturated fatty acids) are easily oxidized. N3 PUFA (omega 3 fatty acids) despite greater number of double bonds are protected from oxidation in cell and Lipoprotein membranes by plasmalogens as opposed to linoleic acid which is not easily incorporated into plasmalogens. The PUFA in vegetable oils (linoleic acid) is the FA (fatty acid) that is oxidized on LDL particles and remnant particles, stimulating monocytes to transform to macrophages and then foam cells. The USDA, ADA and AHA have had it upside down for decades and they still fail to admit folly. We evolved for > 1 million years without grains and they have contributed to disease. Per calorie fresh vegetables have five times the amount of fiber compared to whole grains. We do not need grains and would be better without them. They contain anti-nutrients and wheat, hybridized in the 1980s to a storm resistant dwarf plant, now has 50 times more gluten/gliadin than the old wheat. This has generated more gluten intolerance and celiac. Our greatest nutritional threats to public health include refined sugar, carbohydrates predominantly from grains and refined vegetable oils. Vegetable oils are not healthy, we did not evolve to eat them. N3 FAs are anti-inflammatory but have been competing in our diets with a sea of inflammatory N6 PUFA from unnatural refined and easily oxidized “vegetable oils”. Even though PUFA can reduce LDL-C they wreak havoc by creating ox-LDL particles which initiate the cascade of atherosclerosis. Substituting SFA (saturated fatty acids) with PUFA results in increased levels of Lp(a) and oxLDL in humans, not a good thing. Close the feed lots, stop government subsidy of corn, wheat, dairy and soy, eat meat from grass fed ruminants, wild seafood, fresh organic vegetables and fruits in season. Nibble on tree nuts. Stop creating carcinogens with high dry heat cooking methods and we will watch obesity, insulin resistance, metabolic syndrome and atherosclerosis melt away.

That was my comment. Here is some explanation.

I have previously discussed the pro-inflammatory nature of refined “vegetable oils”. “Vegetable oils” are actually not from vegetables, they are from grains, seeds and legumes. The two major sources of excess omega six polyunsaturated fats in the American diet are corn oil and soy oil marketed by various brand names such as Wesson. They are major components of margarine and other butter substitutes and are present in most salad dressings. Most salad dressings sold in our supermarkets contain high levels of easily oxidized unhealthy refined “vegetable oils” and HFCS. The use of these salad dressings converts a healthy salad into a vector for disease.

The major source of caloric sweeteners in our food and beverages is high fructose corn syrup. Both corn (oil and sugar) and soy predominate our processed food supply because they are cheap. They are cheap because our tax dollars subsidize their production. This subsidy started during the Nixon administration. Once a food subsidy is put in place it is very difficult to eliminate, Big Agriculture provides a deep pocket for lobby money and our elected officials from the mid-west bread-basket respond to $$.

Another major source of disease causing elements in the standard American diet is highly refined flour from wheat. Doctors Davis and Perlmutter discuss the problems associated with wheat-flour foods in their books Wheat Belly and Grain Brain respectively. The production of wheat has also been subsidized since the Nixon administration.

Wheat is not what it used to be. A new dwarf hybrid wheat has predominated the US market since the 1980s. Bread and pasta are not what they used to be when great grand-mother made her own bread and pasta in the kitchen from coarsely ground whole flour. But even if we all went back to making our own whole-grain bread and pasta from locally ground pre-1980s wheat, bread, pasta and pastry would still present a health risk because of issues related to intestinal permeability, auto-immune disease (now epidemic in the USA), and the presence of nasty lectins and phytates (discussed in my manifesto and previous posts).

The Medscape comment quoted above describes adverse consequences caused by replacing saturated fat in the diet with “vegetable oils”. This is a complex subject and I will try to be brief for now but promise to expand on this in a future post.

Many factors contribute to atherosclerosis, heart attack and stroke. Sedentary lifestyle, stress, inadequate restorative sleep, smoking and poor dietary choices top the list. These factors also contribute to obesity, diabetes, metabolic syndrome, insulin resistance and many cancers.

DIETARY FACTORS:

The combination of sugared foods and beverages (predominantly sweetened with HFCS), refined flour foods, and excess consumption of the PUFA in “vegetable oils” TOGETHER contribute to the formation of plaque in the walls of our arteries (atherosclerosis).

How does this happen?

LDL (low density lipoprotein) is a particle that transports cholesterol and triglycerides through our blood to our organs. This particle is comprised of a core and a surrounding membrane. Here is a picture.

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

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

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

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

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

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

But back to LDL.

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

The short version is as follows.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Now here is another twist.

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

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

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

The simple answer is no.

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

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

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

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

In summary:

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

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

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

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

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

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

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

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

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

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

Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis

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

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

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

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

Modulation of Endothelial Glycocalyx Structure under Inflammatory Conditions

Oxidized Lipoproteins Degrade the Endothelial Surface Layer

S1P Control of Endothelial Integrity

Mechanical control of the endothelial barrier. – PubMed – NCBI

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

The Fats of Life, Dr. Glen Lawrence

Functions of plasmalogen lipids in health and disease

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

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

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

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

BOB

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

Amputations, Gangrene and Carbohydrates

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

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

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

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

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

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

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

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

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

Peace, health, and harmony.

BOB

1. Type 2 Diabetes

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

3. Nutrition Science on Pinterest

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

And Many More:

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

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

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

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

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

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

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

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

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

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

Weight Gain, Another Reason to Avoid Statins

2 Replies

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

Fat consumption, Fat circulating in your blood, Heart Disease

1 Reply

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)

Studies that evaluated the association between dietary consumption of different kinds of fat and cardiovascular disease (heart attack and stroke)
Studies that evaluated the association between levels of different kinds of fat circulating in the blood and cardiovascular disease
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

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.
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

The Ornish Low Fat Vegetarian Diet, does it work?

Unnecessary Cardiac Stents and Angioplasty Procedures

1 Reply

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

Lose weight, control blood sugar, reduce inflammation

1 Reply

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

Greater reduction in weight and body fat
Greater reduction in fasting blood sugar
Reduction in the amount of saturated fat circulating in the blood despite a higher intake than a low fat diet
Greater reduction in insulin with improved insulin sensitivity
Reduction in small LDL (low fat diets increase small LDL which is considered to be associated with more heart attacks and strokes)
Increase in HDL (low fat diets decrease HDL, decreased HDL is associated with increased risk of heart attack and stroke)
Greater reduction in Triglycerides
Reduction in the ApoB/ApoA-1 ratio (low fat diets do the opposite, and the opposite is considered to increase risk of heart attack and stroke).
Reduction in multiple markers of inflammation
Spontaneous reduction in caloric consumption without counting or restricting calories (people automatically eat less as a result of restricting carbohydrates, low-fat diets require counting and restricting calories in order to lose weight)
Increased consumption of non-starchy vegetables

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

sugar-sweetened foods and beverages,
grains, flour foods and cereal foods
legumes (paleo completely, CRD to a large extent)
processed-refined vegetable oils
dairy (paleo completely, CRD to a large extent)

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.

Statin Guidelines, one step forward, two steps backwards

10 Replies

The new statin guidelines published jointly by the AHA (American Heart Association) and ACC (American College of Cardiology) present some good news but also allot of bad news.

The good news (one step forward) is that the guidelines acknowledge the following:

1. None of the cholesterol lowering drugs (except for statins) have ever demonstrated the ability to save lives by lowering cholesterol.

2. The ability of statin drugs to save lives (after a heart attack) is independent of whether and by how much the cholesterol is lowered.

This acknowledgement is very important because it sheds light on the fact that statins work primarily by effects independent of how much cholesterol is circulating in the blood. This is a fact that is not well understood by many physicians or patients. This fact will create some confusion because the American public has been misinformed for many years by physicians, the media and professional organizations all using terms like “good cholesterol” and “bad cholesterol”. These terms are meaningless, confusing, and counter-productive.

The new guidelines are two steps backwards for a few reasons:

1. They expand the number of patients under the guidelines in the US by tens of millions of people who will not benefit from their use and implementation of the guidelines will likely harm many.

2. The guidelines continue to assume and quote unrealistically low and inaccurate complication rates.

3. The risk assessment tool that accompanies the guidelines over-estimates risk for heart attack and stroke by 75-150%. This calculation of the over-estimate is based upon application of the guidelines to a huge database of real patients. This analysis has been published in a Peer Reviewed Journal and this analysis has already been discussed by the lay-press to the embarrassment of the AHA and ACC. This particular concern was communicated to the guideline committee one year ago by a prominent research cardiologist and statistician on the faculty of Harvard Medical School, but ignored by the guideline committee.

4. The guidelines have lowered the recommended 10 year risk threshold for use of statins from the previous 10-20% level to a 7.5% level (thereby tremendously increasing the number of people who would be placed on statins). And since the risk calculator, as discussed in #3 above, greatly inflates the risk it essentially would apply the statin guidelines in reality to individuals with only a 3.75 to 4% risk of a cardiovascular event in the next 10 years. This shifts the risk/benefit ratio to a much higher level than the already high risk/benefit ratio of the previous guidelines.

Gratefully the excessive use of statins as well as the folly of the previous and new guidelines have been brought to the public arena and the debate has finally drawn attention. Perhaps some reasonable discussion will ensue and perhaps the medical community at large will finally think about the bias represented in policy statements and guidelines as well as the bias presented in the many review articles that have been published on this topic.

Here are links to some reading of recent articles in the lay press.

Cholesterol Guidelines Under Attack – NYTimes.com

New Cholesterol Advice Startles Even Some Doctors – NYTimes.com

Risk Calculator for Cholesterol Appears Flawed – NYTimes.com

“After the guidelines were published, two Harvard Medical School professors identified flaws in the risk calculator that apparently had been discovered a year ago but were never fixed, as Gina Kolata reported in The Times on Monday.

In a commentary to be published Tuesday in The Lancet, a leading medical journal, the professors estimate that as many as half of the 33 million do not actually have risk thresholds exceeding the 7.5 percent level. Other experts who have tested the calculator found absurd results; even patients with healthy characteristics would be deemed candidates for statins.”

Be careful out there.

Peace,

Bob Hansen MD

Don’t Give More Patients Statins

3 Replies

On November 14, the following editorial was published in the New York Times.

Don’t Give More Patients Statins

By JOHN D. ABRAMSON and RITA F. REDBERG

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

Practical Evolutionary Health

How food, exercise, sleep and stress affect your health, longevity, and happiness. How have we deviated from our evolutionary makeup?

Tag Archives: atherosclerosis

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

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

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

Amputations, Gangrene and Carbohydrates

Weight Gain, Another Reason to Avoid Statins

Fat consumption, Fat circulating in your blood, Heart Disease

The Ornish Low Fat Vegetarian Diet, does it work?

Unnecessary Cardiac Stents and Angioplasty Procedures

Lose weight, control blood sugar, reduce inflammation

Statin Guidelines, one step forward, two steps backwards

Don’t Give More Patients Statins

On November 14, the following editorial was published in the New York Times.

Don’t Give More Patients Statins

By JOHN D. ABRAMSON and RITA F. REDBERG

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On November 14, the following editorial was published in the New York Times.

By JOHN D. ABRAMSON and RITA F. REDBERG

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