The Nutrition Debate #53: On the Digestion and Absorption of Food

Food digestion physiology varies between individuals and with the composition and size of a meal. There are other factors, but a primer on what is most common and universal will be useful to understanding the various processes and their effect on our biological systems. This digest (note the pun) should provide some enlightenment.

Digestion, the hormonal process, has three phases. The cephalic phase begins when receptors in the head are stimulated by an emotional state (thought of food), sight, smell, taste and chewing. The cerebral cortex, the medulla oblongata and the hypothalamus are all involved. The vegus nerve is the messenger, triggering various enzymatic and hormonal activities. The gastric phase starts with distension, acidity, and the presence of amino acids and peptides in the stomach. The intestinal phase is initiated by distension, acidity, and osmolarity of digestive products in the intestine (we’ll explain).

Digestion, the mechanical and chemical process, begins with chewing. Chewing breaks food down to smaller units that are in turn broken down by enzymes to the smallest units to permit them to be absorbed, mostly in the small intestine, into the blood. Saliva containing mucus and the enzyme amylase is secreted from three pairs of salivary glands located in the mouth cavity. Mucus moistens the food and amylase partially digests polysaccharides (starches) into a disaccharide called maltose. About 30% of starch is broken down in the mouth (optimum pH: 6.8 or weakly acidic).

In addition, papillae on the surface of the tongue secrete the enzyme lingual lipase which begins the process of breaking down some fats from triglycerides into diglycerides. Long chain triglycerides cannot be absorbed unless completely broken down to monoglycerides, so the process starts here and continues in the stomach. As much as 30% of fat is broken down within 1 to 20 minutes of ingestion by lingual lipase alone, according to Wikipedia.

Food then passes through the pharynx and descends the esophagus to the stomach, a sac that stores and mixes and processes the food into a milky solution called chyme. Glands lining the stomach secrete hydrochloric acid, which is necessary for protein digestion by the enzyme pepsin. The stomach’s high acidity (optimum pH 1.8) inhibits the breakdown of carbohydrates within it, but it does produce a small amount of the enzyme lipase to continue the digestion of fats. So far, although the breakdown of food particles by enzymatic and mechanical action is continuing apace, virtually no absorption of nutrients into the bloodstream has occurred. The exceptions are water, some simple sugars, and other small molecules like alcohol that are absorbed in the stomach, passing through the membrane of the stomach and entering the circulatory system directly.

The final stages of digestion and most of the nutrient absorption occur in the next portion of the tract: the small intestine. The small intestine is divided into three segments – duodenum, jejunum and ileum. The duodenum in turn is connected to the hepato-pancreatic duct which connects to the liver and the gall bladder (to store and supply bile) and to the pancreas. These organs and glands provide digestive enzymes and an alkaline fluid (pH 8.5) to neutralize the acid being emptied from the stomach.

In the duodenum, dipeptides from protein in the stomach are broken down to amino acids by enzymes from the pancreas. The enzymes break down the disaccharides maltose, lactose and sucrose into the monosaccharides glucose, fructose and galactose.  The major portion of fat digestion, the breakdown of diglycerides by lipase into free fatty acids and glycerol, also happens here.

Absorption of nutrients occurs mostly in the jejunum and ileum. Amino acids (from protein) and the monosaccharides (glucose, fructose and galactose, all from carbohydrates) are water soluble nutrients and enter the blood directly through the villi and microvilli in the endothelial layer of the small intestine wall. The surface area of these many small structures (imagine a shag carpet) increases the absorption interface by 600 times, roughly equivalent to the surface of a tennis court. However, the products of fat digestion, fatty acids and glycerol, are not water soluble and therefore enter the circulation through the lymph system by a process called passive diffusion in which no energy is required.

Passive or simple diffusion requires no energy input from the body because it is driven by concentration. Fats, water and some minerals simply cross the membrane barrier because the concentration of the substance (fat, water, etc.) is lower on the other side. It is an equalization process. The small intestine is full of nutrients and the blood is not, so they cross over. This equalization process is also called osmosis, ergo ‘osmolarity of digestive products’ referred to above. 

Fructose is transported across the membrane barrier by a process called ‘facilitated diffusion,’ which means it may need a little help depending on the concentration gradient. Glucose and galactose, the other monosaccharides, as well as amino acids, also require energy for active transport, which occurs against a concentration gradient. See The Nutrition Debate #52, “The Thermic Effect of Foods,” for the energy requirements of protein digestion as compared to carbohydrates, especially of processed foods.

Finally, gastric emptying, which is the rate that food leaves the stomach to enter the small intestine, is tightly controlled. Liquids are emptied much more quickly than solids, and carbohydrates are emptied first, followed by protein, fat and fiber. Gastric emptying has attracted medical interest as “rapid gastric emptying is related to obesity and delayed gastric emptying syndrome is associated with Type 2 diabetes, aging and gastroesophageal (acid) reflux or GERD.” But that’s another subject. Next week: Paleo book reviews. 

© Dan Brown 5/20/12

The Nutrition Debate #52: The Thermic Effect of Food

Thermogenesis is the process of heat production in organisms, and heat is a form of expended energy. The unit of measurement is a calorie. Human metabolism is comprised of three components of energy expenditure: 1) the energy expended by the basal metabolic rate (to keep the resting organism “going,” i.e. alive), 2) the energy expended through exercise (motion), and 3) the energy expended due to the “cost” of processing food for storage and use. This last component is known as the thermic effect of food.  It is also sometimes called Diet-Induced Thermogenesis (DIT).

It is estimated that the thermic effect of food is about 10% of the caloric intake of any given meal, “though the effect varies substantially for different food components,” according to Wikipedia. Of the three food components (called macronutrients), fat has minimal thermic effect. Carbohydrates, especially simple sugars and carbs in highly processed, manufactured foods, are very easy to process and have very little thermic effect. Proteins, on the other hand (and whole food, complex carbohydrates to a lesser extent) are harder to process and have a much larger thermic effect. The ratio of protein to carb energy expenditure is generally between 2:1 and 3:1, depending on how “simple” the carb is.

So, for total daily energy expenditure there's a resting metabolic rate component (60-70% of total), the physical activity component (15-30% of total), and the thermic effect of food component (~10%). While 10% is a small percentage, if the energy expended to digest, absorb and eliminate protein is two or more times the amount required for carbs and fat, wouldn’t replacing carbs with protein in an isocaloric diet thus increase the metabolic rate and help to burn more calories including stored fat? And if the difference in the burn rate was even greater for the simple sugars and processed carbs made easier to digest by manufacturing, couldn’t that account for why our metabolisms burn less on today’s modern processed-food diets? Thus, to naturally increase our metabolic rate, we should 1) increase the amount of protein in our diet and 2) replace simple sugars and processed-foods in the diet with whole foods, that is, unprocessed, complex carbohydrates. Note that 2) above assumes that you don’t already have insulin resistance (IR), pre-diabetes, or full-blown Type 2 diabetes, or are obese. It you are, you should severely restrict/limit the carbohydrates in your diet.

The typical American (or for my international readers, Western) diet currently gets about 15% of calories from protein. The Standard American Diet (SAD for short), espoused by the FDA and promoted on food packages in the Nutrition Facts Panel, is 10% protein. (On a 2,000 calorie diet, 50g/day x 4 cal/g = 200 cal.) I get about 25% of my calories from protein.

So, who’s looking at this? Barr SB and Wright JC, that’s who, in their paper, “Postprandial energy expenditure in whole-food and processed-food meals: implications for daily energy expenditure,” published online July 2010 in The Journal of Food and Nutrition Research. The abstract on PubMed explains: “Empirical evidence has shown that rising obesity rates closely parallel the increased consumption of processed foods (PF)… in the USA. Differences in postprandial thermogenic responses to a whole-food (WF) meal vs. a PF meal may be a key factor in explaining obesity trends, but currently there is limited research exploring this potential link.” And their conclusion: “Ingestion of the particular PF meal tested in this study decreases postprandial energy expenditure by nearly 50% compared with the isoenergetic WF meal. This reduction in daily energy expenditure has potential implications for diets comprised heavily of PFs and their associations with obesity” (Italics added by me).

The processed food meal decreased energy expenditure by nearly 50%. Wow! That’s a big difference in thermic effect. And the meals they were comparing were “either ‘whole’ or ‘processed’ cheese sandwiches; multi-grain bread and cheddar cheese were deemed whole, while white bread and processed cheese product were considered processed.” Imagine if they had chosen a real whole food instead of ‘multigrain bread’ which is a far, far cry from a real whole food as readers here know. And what if it had been a protein food instead? The authors explained, “A more strict WF would be one devoid of any processing, such as a specific fruit, vegetable, or meat. However, for the present study, we sought to compare two meals that were familiar to the Western diet, and could be easily interchangeable.”And while the much higher thermic effect of protein is probably too small to have a noticeable effect on weight loss in the short term, over a period of months or years this difference becomes significant. Have I discovered another cause for the obesity epidemic? Just joking, folks. I am just your humble commentator bringing you the insights of the cognoscenti.                   

© Dan Brown 5/13/12

The Nutrition Debate #51: Dietary Cholesterol

Pay attention - dietary cholesterol is the cholesterol you eat. Serum cholesterol is the cholesterol in your blood. They are not only distinct; they are largely independent of each other. The following excerpt from Wikipedia gets “into the weeds” a bit, but is necessary to provide a framework.

“While the absolute production quantities vary with the individual, group averages for total human body content of cholesterol, with the U.S population, commonly run about 35,000 mg (assuming lean build; varies with body weight and build) and about 1,000 mg/day ongoing production. Dietary intake plays a smaller role, 200-300 mg/day being common values; for pure vegetarians, essentially 0 mg/day, but this typically does not change the situation very much because internal production increases to largely compensate for the reduced intake.”

Assuming a “lean (body) build” for the U.S. population is a dubious proposition, as must be patently obvious to even the casual observer. My body is certainly not lean. Neither do I eat just 200-300mg/day of dietary cholesterol. I typically average 600-650 mg/day. I know this from the days (years, actually) when I tracked carefully. But, the HHS/USDA Dietary Guidelines for Americans age 2 and older urge us to eat no more than 300mg daily (200mg with CVD risk factors). Does this make any sense when we consider that most societies wean at 3 or 4, and breast milk is 55% fat, mostly saturated, and loaded with cholesterol? “Mother's milk is especially rich in cholesterol and contains a special enzyme that helps the baby utilize this nutrient. Babies and children need cholesterol-rich foods throughout their growing years to ensure proper development of the brain and nervous system,” says Dr. Mary Enig, the doyenne of lipid chemistry and the author of the definitive biochemistry guide, “Dietary Fats.”

“The brain is the most cholesterol-rich organ in the body, most of which comes from in situ synthesis,” begins the abstract of a paper, “Diabetes and insulin in regulation of brain cholesterol metabolism,” from the Joslin Diabetes Center and Harvard Medical School published in Cell Metabolism (2010 Dec 1; 12(6):567-79).Yet, many people have deprived themselves for decades of cholesterol-laden foods (shrimp, eggs, butter, cream, liver, even a marbled steak) in an effort to comply with the government’s public health guidelines. What a pity (for them)!

Perhaps the most telling statement in the quoted paragraph, however, is that vegetarians have serum cholesterol levels similar to omnivores “…because internal production increases to largely compensate for the reduced intake.” Vegetarians have avoided eating cholesterol-loaded foods altogether “but this typically does not change the situation very much.” Admittedly, they completely gave up eating animal-based foods – meaning they ate absolutely no cholesterol – for a different reason, but they did not thereby lower their serum cholesterol “very much.”

The reason, as the numbers In the Wiki-quoted paragraph above note, is that most cholesterol, typically 80-90% within the body, is created and controlled by internal production by all the cells in the body, with typically slightly greater relative production by hepatic (liver) cells. As described in The Nutrition Debate #24 cell structure relies on fat membranes to separate and organize intracellular water, proteins and nucleic acids, and cholesterol is one of the components of all animal cell membranes. More on cholesterol within this blog can be found at The Nutrition Debate #25 , “Understanding Your Lipid Panel,” and The Nutrition Debate #45 , “Do You Need to Lower Your Cholesterol?”

But get this: “For many,” the Wikipedia entry on atherosclerosis continues, “especially those with greater than optimal body mass and increased glucose levels, reducing carbohydrate intake (especially simple forms), not fat and cholesterol, is often more effective for improving lipoprotein expression patterns (i.e. cholesterol), weight and blood glucose values. For these reasons, medical authorities much less frequently promote the low dietary fat concept than was common prior to about the year 2005.” That’s certainly been true for me, as I have reported here with my own example (n = 1). Since switching to a high fat/high cholesterol, moderate protein and very low carbohydrate diet about 10 years ago, my HDL has doubled and my triglycerides have dropped by two-thirds, while my LDL has been constant and my T. Chol. has risen only slightly. Remember the common laboratory formula for serum cholesterol: T. Chol. = LDL + HDL + TG/5.

Finally, Ancel Keys, the father of the (infamous) Lipid (saturated fat/heart disease) Hypothesis, is equally famous in some circles for having said later in life, according to Malcolm Kendrick, author of “The Great Cholesterol Myth,” “There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along.”

Given that we were born to drink mother’s milk, and our brain is mostly cholesterol, it strikes me as pretty natural and healthy to eat cholesterol rich foods. As the ‘70s margarine commercial said, “It’s not nice to fool Mother Nature.”

© Dan Brown 5/6/12

The Nutrition Debate #50: Free Radicals and Oxidative Stress

In The Nutrition Debate #46, we posited that oxidative stress was one of the three prime contributors to cardiovascular disease, along with inflammation and imbalances in blood sugar and insulin. But, what is oxidative stress and what causes it? Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to neutralize them. Thus, a delicate balance is required. Too many reactive oxidizing species or too few (or ineffective) anti-oxidant defenses produce oxidative stress. And oxidative stress can lead to atherogenesis, etc., etc.

Free Radicals are one of the most common ROS. They have an unpaired electron that makes them highly reactive chemically, but also generally short-lived. The long-lived free radicals can be dangerous, depending on their stability. According to Wikipedia, “Excessive amounts of these free radicals can lead to cell injury and death, which may contribute to many diseases such as cancer, stroke, myocardial infarction and diabetes. Many forms of cancer are thought to be the result of reactions between free radicals and DNA, potentially resulting in mutations that can adversely affect the cell cycle and potentially lead to malignancy.”

Some of the symptoms of aging such as atherosclerosis are also attributed to free-radical induced oxidation of many of the chemicals in the body. In addition, free radicals contribute to alcohol-induced liver damage, perhaps more than alcohol itself. Radicals in cigarette smoke are implicated in the process that promotes the development of emphysema.

But, free radicals play an important role in a number of biological processes, and “some of these are necessary for life such as the intracellular killing of bacteria by… macrophages,” according to Wikipedia. See column #48. So, because some free radicals are necessary for life, the body produces a number of enzymes to minimize free radical-induced damage and to repair damage that does occur. In addition, antioxidants play a key role in these defense mechanisms. Research is underway to determine the relative importance and interactions between antioxidants. In the meantime the use of antioxidant supplements to prevent disease is very controversial; real food sources are probably the best choices and very tasty too.

Antioxidants are classified into two broad divisions, depending on whether they are water soluble or fat soluble. These compounds may be synthesized in the body or obtained from the diet or through supplementation. Some are mostly present within cells, while others, such as uric acid, are more evenly distributed. In fact, human blood has a high concentration of water-soluble uric acid. Antioxidants are found in vegetables, fruits, grains, eggs, meat, legumes, and nuts. Herbs and spices are particularly high in antioxidants.

·         Vitamin C (ascorbic acid): Bell pepper, parsley, broccoli, Brussels sprouts, cauliflower, kale (see list here).

·         Vitamin E (tocopherols, tocotrienols): green leafy vegetables, almonds, asparagus, papaya (see list here).

• Polyphenolic antioxidants (flavonoids): tea, coffee, fruit, olive oil, chocolate, red wine, and herbs and spices  (top 10 list here).  Also, see this 2002 Science Daily reprint from the American Chemical Society.

·         Carotenoids (lycopene, carotenes, lutein): sweet potatoes, spinach, tomatoes,  and chili peppers (see list here).

In general, processed foods contain fewer antioxidants than fresh and uncooked foods, since generally the preparation process exposes the food to oxygen.

Again, Wikipedia: “The paradox in metabolism is that, while the vast majority of complex life on Earth requires oxygen for its existence, oxygen is a highly reactive molecule that damages living organisms by producing reactive oxygen species. Consequently, organisms contain a complex network of antioxidant metabolites and enzymes that work together to prevent oxidative damage to cellular components such as DNA, proteins and lipids. In general, oxidant systems either prevent these reactive species from being formed, or remove them before they can damage vital components of the cell. However, reactive oxygen species also have useful cellular functions, such as redox signaling. Thus the function of antioxidant systems is not to remove oxidants entirely, but instead to keep them at an optimum level.” The oxidative challenge in biology is to maintain proper cellular homeostasis -- a balance between reactive oxygen production and consumption. Diet and lifestyle play a large role in this complex system… and you are in charge.

 © Dan Brown 4/29/12

The Nutrition Debate #49: The Dietary Causes of Inflammation

Do you have syphilis? Or snort cocaine, or smoke tobacco, or have a bacterial infection or periodontal disease that causes overproduction of cholesterol that accumulates in the arteries? If none of these “insults” apply to your body, the cause of chronic inflammation, and therefore the cause of atherosclerotic plaque in your arteries, is likely to be dietary.

The relationship between dietary fat and atherosclerosis, however, is a contentious field. The USDA, in its food pyramid and Dietary Guidelines for Americans, promotes a low-fat diet, based largely on the view that fat in the diet is atherogenic. The American Heart Association, the American Diabetes Association and the National Cholesterol Education Program make similar recommendations. Especially singled out are saturated fats, dietary cholesterol and trans fats.  Trans fats are one of the few consensus points in nutrition as everyone thinks these are very bad for your health. But could all of these authorities be wrong about the role of saturated fats and dietary cholesterol?

In a word, “yes.” Writing in Science, multiple award-winning science writer Gary Taubes says that political considerations played into the recommendation of government bodies. Gary Taubes broke onto the scene with his 2002 exposé in the New York Times Sunday magazine cover story, “What if it’s All Been a Big Fat Lie?” Later he wrote a tome for serious readers, “Good Calories – Bad Calories” and later still a more readable “Why We Get Fat – And What to Do About It.”

Professor Walter Willett, of the Harvard School of Public Health and Principal Investigator of the second Nurse’s Health Study, recommends much higher levels of dietary fat than the public health establishment, and especially of monounsaturated and polyunsaturated fat. Once again, there is growing unanimity that monounsaturated fats, such as are found in olive oil, are healthy. But polyunsaturated fats, such as are found in vegetable and seed oils, are coming under increasing scrutiny. Soy bean oil and corn oil are the most widely used, accounting for over 90% of food oils used in the U.S.

Unfortunately, polyunsaturated fats are not particularly stable. They become damaged or oxidized very easily. Oxidized or rancid fats play a very troubling role. Feed rancid fats to lab rats and they will develop atherosclerosis. In another study, rabbits fed atherogenic diets containing various seed and grain oils showed the largest increase in oxidative susceptibility of LDL. In a study involving rabbits fed heated soybean oil, “grossly induced atherosclerosis and marked liver damage were histological and clinically demonstrated,” as per Wikipedia.

Rancid fats and oils taste and smell very bad even in small amounts and people avoid eating them. But, in the United States, the majority of oils consumed are refined, bleached, deodorized and degummed by manufacturers. The resultant oils are colorless, odorless, tasteless, and have a longer shelf life than their unrefined counterparts. This extensive processing makes fully oxidized, rancid oils much more elusive to detection via human senses.

To properly protect polyunsaturated fats (vegetable and seed oils) from oxidation, it is best to keep them cool and in a dark and oxygen free environment. And don’t overheat or use them repeatedly, such as in deep fat frying. I keep my Omega-3 fish oil capsules and Flax Oil (very high in Omega-3s) in the refrigerator. I also keep Safflower Oil, another polyunsaturated fatty acid (PUFA), which I use with olive oil and coconut oil to make mayonnaise, in the refrigerator.

So, if atherosclerosis is defined by Wikipedia as “a chronic inflammatory response in the walls of arteries, promoted by LDL…without adequate removal of fats and cholesterol…by…HDL,” then we should be concerned about the quality and quantity of LDL in our arteries – lest it become oxidized LDL. Likewise, we should be concerned if our circulating HDL in not high enough to transport any oxidized-LDL back to the liver the way it is supposed to.

Why do these two conditions (high LDL and low HDL) co-exist in so many of us today? It’s the diet of course. To avoid oxidized LDL, we can begin by eating far fewer polyunsaturated fats, especially ones that are hydrogenated, oxidized, or overheated. We can also take supplementary Omega-3s to help us regain a better Omega 6/Omega 3 balance. Then, we can significantly raise our HDL so they can do their job. See The Nutrition Debate #34 for “Foods that Raise HDL.”

The oxidized-LDL hypothesis posits that, “Once inside the vessel wall, LDL molecules become susceptible to oxidation by free radicals and become toxic to the cells.” (See The Nutrition Debate #48) Free radicals cause the oxidative stress that “triggers a cascade of immune responses which over time can produce an atheroma, the characteristic nodule in the artery wall that is the start of atherosclerosis. “Free Radicals and Oxidative Stress” is the subject of the next column.                           

 © Dan Brown 4/21/12

The Nutrition Debate #48: Inflammation and Atherosclerosis

“Atherosclerosis…is a condition in which an artery wall thickens as a result of the accumulation of fatty materials such as cholesterol. It is a syndrome affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries, caused largely by the accumulation of macrophage white blood cells and promoted by low-density lipoproteins (LDL) -- plasma proteins that carry cholesterol and triglycerides -- without adequate removal of fats and cholesterol from the macrophages by…high-density lipoproteins (HDL)” (all italics added).  So begins the Wikipedia entry on Atherosclerosis.

Atherosclerosis is a chronic disease that remains asymptomatic for decades. Atherosclerotic lesions, or plaques, cause narrowing (stenosis) of the artery and, if unstable, can rupture and induce a thrombus (blood clot, attached or motile). A thrombus, in place or more likely downstream, can cause an occlusion of the lumen of the artery, stopping blood flow (ischemia), resulting in the death of tissues fed by the artery. This catastrophic event is called infarction. Thrombosis in the coronary artery is a myocardial infarction (heart attack). Stroke is often caused by a clot in the carotid artery.

These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. What’s “new” in the understanding of atherosclerosis, however, is an appreciation of the role of inflammation in atherosclerosis. The 2002 abstract of a paper titled “Inflammation and Atherosclerosis” begins, “Atherosclerosis, formerly considered a bland lipid storage disease, actually involves an ongoing inflammatory response.” The full paper was published in Circulation (2002; 105:1135-1143), the Journal of the American Heart Association, under the banner “Clinical Cardiology: New Frontiers.”

The main cause of atherosclerosis is yet unknown, but a considerable body of experimental evidence points to oxidized LDL. This hypothesis posits that the inflammatory processes in the artery wall are initiated in response to retained low-density lipoprotein (LDL) molecules. The LDL molecule is globular shaped with a hollow core whose purpose is to carry cholesterol throughout the body. Once inside the vessel wall, LDL molecules become susceptible to oxidation by free radicals, and become toxic to the cells. The damage caused by the oxidized LDL molecules triggers a cascade of immune responses which over time can produce an atheroma, the characteristic nodule in the artery wall.

The body’s immune system responds to the damage to the artery wall by sending specialized white blood cells (macrophages and T-lymphocytes) to absorb the oxidized-LDL forming specialized foam cells. These white blood cells are not able to process the oxidized-LDL, and ultimately grow, then rupture, depositing a greater amount of oxidized cholesterol into the artery wall. This triggers more white blood cells, continuing the cycle, according to the theory. The primary documented driver of this process is therefore oxidized-LDL particles within the artery wall.

According to Wiki, various anatomic, physiological and behavioral risk factors for atherosclerosis are known. They can be divided into the categories modifiable or not. The points labeled ‘+’ in the list below form the core components of Metabolic Syndrome, discussed in multiple columns in The Nutrition Debate, starting with column #9.

Modifiable

·         Diabetes or Impaired glucose tolerance (IGT) +

·         Dyslipoproteinemia (unhealthy patterns of serum proteins carrying fats and cholesterol, such as) +

o   High LDL (bad if elevated and small/dense particles) and/or High VLDL

o   Low HDL (protective if large/fluffy particles and high enough)

o   An LDL:HDL ratio great than 3:1

·         Elevated serum C-Reactive Protein concentrations

·         Hypertension +, on its own increasing risk by 60%

·         Vitamin B₆ deficiency

·         Tobacco smoking, increases risk by 200% after several pack years

·         Periodontal disease

Non-modifiable risk factors include advanced age, male sex, having close relatives who have some complication of atherosclerosis (e.g. coronary heart disease or stroke), and genetic abnormality, e.g. familial hypercholesterolemia.

Other lesser or uncertain risk factors for atherosclerosis includes obesity +, a sedentary lifestyle, hypercoagulability, post-menopausal estrogen deficiency, high intake of saturated fat (may raise total and LDL cholesterol), intake of trans fats (may raise total and LDL cholesterol while lowering HDL), high carbohydrate intake, elevated triglycerides +, homocysteine, uric acid, or fibrinogen or lipoprotein(a) concentrations, chronic systemic inflammation, as reflected by upper normal WBC concentrations, elevated hs C-reactive protein or serum insulin levels +, stress or symptoms of clinical depression, hyperthyroidism (over-active thyroid), short sleep duration and Chlamydia pneumoniae infection. That only leaves dietary causes of inflammation that cause atherosclerotic plaque, the subject of the next column.

© Dan Brown 4/15/12

The Nutrition Debate #47: Testing for Heart Disease Risk

“Key tests can reveal problems with a person’s blood sugar and insulin, inflammation level, level of folic acid, clotting factors, hormones and other bodily systems that affect your risk of cardiovascular disease,” says Mark Hyman, MD, the Lennox, MA, practitioner, on a May 2010 blog post.  This last-of-three column on that post will discuss some of these tests and zero in on these prime markers for cardiovascular disease.

“There’s no doubt about it,” Dr. Hyman says, “Inflammation is a key contributor to heart disease. A major study done at Harvard found that people with high levels of a marker called C-Reactive Protein (hs-CRP) had higher risks of heart disease than people with high cholesterol. Normal cholesterol levels were NOT protective to those with high CRP. The risks were greatest for those with high levels of both CRP and cholesterol.”

“Another predisposing factor to heart disease is insulin resistance or metabolic syndrome, which leads to an imbalance in the blood sugar and high levels of insulin. This may affect as many as half of Americans over age 65. Many younger people also have this condition, which is sometimes called pre-diabetes,” says Dr. Hyman.

“Although modern medicine sometimes loses sight of the interconnectedness of all our bodily systems, blood sugar imbalances like these impact your cholesterol levels too. If you have any of these conditions, they will cause your good cholesterol to go down, while your triglycerides rise, which further increases inflammation and oxidative stress. All of these fluctuations contribute to blood thickening, clotting, and other malfunctions – leading to cardiovascular disease.”

“What’s more, elevated levels of a substance called homocysteine (related to our body’s levels of folic acid and vitamins B6 and B12) appear to correlate to cardiovascular illness. Where problematic levels occur, they can be easily addressed by adequate folic acid intake, along with vitamins B6 and B12.” My own internist, who is also a board-certified cardiologist, has had me on a supplement called Homocysteine Modulators (Solgar brand), as well as CoQ_10, for years.

“So, heart disease is not only about cholesterol. It is important to look at many factors that contribute to your overall risk.” Dr. Hyman notes, “It seems that insulin and blood sugar imbalances and inflammation are proving to be more of a risk than cholesterol.” If you want to test your overall risk, consider asking your doctor to perform the following tests:

·         Cardio (hs) CRP (C-Reactive Protein): There can be many causes of inflammation in the body, but this marker of inflammation is essential to understand in the context of overall risk. Your CRP should be less than 1.0.

·         Standard Lipid Panel: Total cholesterol, HDL cholesterol, LDL cholesterol and triglycerides. Pay particular attention to your HDL and triglycerides and the TC/HDL and TG/HDL ratios and work to improve them.  Pay less attention to lowering Total Cholesterol by lowering LDL, an outcome shown to be of dubious value alone. Your doctor can’t write a script for raising HDL and lowering triglycerides. You have to do it yourself by the food choices you make each and every meal.

·         VAP cholesterol test: directly measures LDL (vs. calculated as in the standard lipid test above), also VLDL, LP(a), and LDL particle size and characteristics (small, dense vs. large, fluffy).

·         Hemoglobin (Hb) A1c: This measures your average blood sugar over the last 6 weeks to 3 months. Anything over 5.5 is high. Dr. Richard K. Bernstein, the glucose self-testing guru and leading diabetes expert, considers 5.8 to be full-blown diabetes. Alas, the ADA considers 6.5 (formerly 7.0) to be diabetes and 6.0 to be pre-diabetes. Studies show that CVD risk doubles from an A1c of 5.5 to 6.0.

·         Glucose Insulin Tolerance Test: Measurements of fasting and 1 and 2 hour levels of glucose AND insulin helps identify pre-diabetes and excessively high levels of insulin. Most doctors just check blood sugar and NOT insulin, which is the first thing to go up. By the time your blood sugar goes up, “the train has left the station.”

·         Homocysteine: Your homocysteine measures your folate status and should be between 6 and 8.

·         Fibrinogen: Looks at clotting factors in the blood. It should be less than 300.

And, most importantly, know your test results. Take charge of your health. It’s your life. Make the most of it.

© Dan Brown 4/8/12