Sunday, February 27, 2011


We all have the enzyme myeloperoxidase, (MPO), in our bodies. But as plaque inside our blood vessel walls becomes more likely to rupture, we produce even more MPO at that site. The increased amounts of MPO, which can be measured in the blood causes erosion of the plaque. When the plaque in the blood vessel erodes enough, it ruptures. There a micro-clot forms to patch the weak spot. Platelets (formed elements) in the blood cells flowing by the clot start participating in growing and firming up this coagulated mass. If that clot blocks blood flow to the heart or brain, a heart attack or stroke usually occurs. A high level of MPO is a signal that a person is in risk of having a catastrophe. This is so even though the cholesterol levels and blood pressure are perfect as in almost fifty percent of these incidents. The MPO oxidizes the LDL cholesterol, modifying so it is more delectable to the certain white cells (macrophages) that reside within the wall of our arteries. These ingest the LDL particles, get sick, die and spill their fatty guts thus enlarging the existing fatty streaks to form an inflammatory plaque. This is the generator of all atherosclerosis. Unbeknownst to most doctors is that Acetaminophen blocks the activity of MPO and stops the transformation of the bad cholesterol (LDL) that is available for the macrophages to ingest.

And Aspirin stops the platelets in our blood from getting sticky, preventing the clump. The basis for the use of low dose aspirin lies in its unique inhibitory effect on a key enzyme, COX-1 (cyclooxygenase-1). In low doses, 81 mg (a child’s aspirin) twice a day, the platelets are less tacky and not as likely to coalesce together to coagulate. However, in higher amounts such as 650 mg (2 adult Aspirins) it affects the arterial walls making them sticky and more likely to initiate a clot on the rough plaque.

A personal friend of mine, Professor Gary Merrill, of Rutgers' department of cell biology and neuroscience, demonstrated significant improvement in acetaminophen-treated hearts compared with non-treated hearts following periods of induced ischemia (reduced blood flow) attributed the rapid post-ischemia recovery of heart muscle and circulation to the antioxidant properties of acetaminophen. This research as part of a growing body of evidence supporting the positive effects of acetaminophen on the cardiovascular system. His findings, together with those of Dr. Addison Taylor of Baylor College of Medicine, Houston, and Professor Phillip Greenspan of the University of Georgia College of Pharmacy, indicate that acetaminophen prevent the damaging effects of LDL cholesterol. Taylor and Greenspan separately conducted investigations showing acetaminophen may protect against the life-threatening condition, hardening of the arteries. The bad press that Acetaminophen has recently had makes this well studied drug almost a curse word. It is true in very high doses like over 6,000 mg a day it can negatively affect the liver and perhaps the kidney, but 1000mg/day is positively healthy for all who want protect their blood vessels.

After the discovery, the Cleveland Clinic, through Cleveland Heart Lab started doing the MPO test. Blood samples, are overnighted to them from the doctors offices, for MPO and four other valuable markers. They include urinary Isoprostain and Microalbumin; a pro-oxidant and an arterial disrupter, HsCRP; indicating lining damage, and Plac2; a predictor of plaque rupture. Many insurance companies and Medicare now cover the test. And for those who don't have coverage, the cost is relatively inexpensive: $189 for MPO and the other tests conducted with it.

If none of the above makes sense to you, still do yourself a favor. Betwixt and between Aspirin and Acetominophen will keep the artery clean-and YOU healthy! If you are a male over the age of 45 or a female over 50-PLEASE take one each of 81 mg Aspirin and 500 mg Acetominophen (Tylenol), both twice a day, it will keep the heart attack and stroke away!!


The enzyme myeloperoxidase, (MPO), in our bodies played a role in the past as a defense. But in modern civilization it causes our demise. This intra White Cell enzyme generates reactive oxidants that kills invading microbes. In modern times it hastens plaque build up inside our blood vessel walls. Three mechanisms have been elucidated by the scientists. The MPO oxidizes the LDL cholesterol, modifying it so it is atherogenic. This now bad, bad cholesterol is rapidly ingested by the macrophages that reside within the inside wall (endothelium) of our arteries. These ingest the LDL particles, get sick, die and spill their fatty guts thus enlarging the existing fatty streaks to form an inflammatory plaque. The second mechanism is it oxidizes the endothelial Nitric Oxide that normally keeps these cells healthy. Then this nefarious enzyme weakens the fibrous cover of the plaque, which makes it rupture. There, along with the platelets already in the blood and another enzyme, Plaq2, a micro-clot forms to patch the weak spot. If that clot does not spontaneously dissolve, it blocks blood flow to the heart or brain, a heart attack or stroke usually occurs.

The increased amounts of MPO can be measured in the blood. If greater than 723 pmol/L, there is a 5-fold increase of a catastrophic event even in the absence of other cardiovascular risk factors. But if other risk factors are present a high value makes it much more dangerous. MPO is also used clinically in the Emergency Room to determine if the acute chest pain that the patient is having is a heart attack or not. Another emerging use is that it predicts the severity of heart failure (inability of the heart to pump enough blood) and the prognosis. It is also used to determine the rate of narrowing of the carotid arteries.

Statins decrease MPO levels and Acetaminophen blocks its activity, which stops the transformation of the bad cholesterol (LDL) that is available for the macrophages to ingest. This important test can be done by the Cleveland Clinic, through Cleveland Heart Lab by a special arrangement with a local physician. Blood samples, are overnighted to them for MPO and four other valuable markers. They include urinary Isoprostain and Microalbumin; a pro-oxidant and an arterial disrupter, HsCRP; indicating lining damage, and Plac2; a predictor of plaque rupture. Many insurance companies and Medicare now cover the test. And for those who don't have coverage, the cost is relatively inexpensive: $189 for MPO and the other tests conducted with it.

Monday, February 21, 2011


One size does not fit all! There is as much genetic variation in the metabolism of drugs, foodstuffs and ingested pollutants as there is in the countenance of humans. Other than identical twins, we each have our facial individual identity and, similarly, each of us metabolizes differently both quantitatively and qualitatively. Our technology has advance to the point that medical science can detect many of the nuances that make us uniquely distinct. This is particularly important so that a physician can prescribe an exact dose of a given drug and particularly when several other medications are given coincidently.

Not only does age, sex, weight, intestinal flora, general health, liver and kidney function alter a patient's response to drugs, but genetic factors must be considered. This information is crucial. Prescription Drug Fatality is the fourth leading cause of death after heart disease, cancer, and stroke. The major determinant involved in the metabolism of drugs, toxins and our hormones is the Cytochrome (CYP) P450 enzymes. The most important of these are CYP2D6, CYP2C9, CYP2C19, NAT2, UGT1A1, DPD, 5HTT, and CYP1A2. The'CYP's is a host of enzymes that use iron to oxidize organic molecules, as part of the body's preparation to dispose of potentially harmful substances by making them more water-soluble. The capital letter indicates the superfamily, and the number before and after, the subfamily.

In humans, CYP3A represents one of the most important subfamilies of the P450 superfamily. The CYP3A subfamily is the most abundantly expressed P450 in human liver, and CYP3A is involved in the biotransformation of approximately 50% of drugs that are metabolized. As a result, drug-drug interactions associated with modulation of CYP3A-mediated metabolism can be of substantial consequence. In the past, it was a trial and error of the dose and the drug we would use. To err could cause not only great harm, but even death of a patient. With this new tool, doctors can take the guess work out of prescribing and do it scientifically.

In addition to our hereditary, the CYPs can be both up-regulated (induced) or down-regulated (inhibited) by other chemicals making it on occasion a complexed proposition for drug deposition. When several competing drugs are use for the same CYP enzyme an Adverse Drug Interaction occurs. At times there are multiple CYPs that work on a drug. For example, adding a hydroxyl group to a medication is the body's strategy to get rid of it and is often followed by joining them to other molecular groups such as glucuronide to increase the solubility even further. Most of the CYP in man is found in the liver, the main organ involved in drug and toxin removal, but a fair amount is also in the small intestine. CYP usually is found in the 'microsomal' part of the cytoplasm (endoplasmic reticulum).

We determine the dose and interaction of not only prescribed drugs, but OTC (over-the-counter) and herbal medicines including those used to treat depression, anxiety, seizures and psychoses; heart disease, cancer, diabetes, and pain. These include medications as Coumadin (warfarin), Prozac, Zoloft, Paxil, Effexor, hydrocodone, Amitriptyline, Claritin, Cyclobenzaprine,, Metoprolol, Tagamet, Tamoxifen, Valium, Carisoprodol, Dilantin, Premarin, and Prevacid (and the over-the-counter drugs, Allegra, and the several NSAIDS).

Almost half of us have genetic variations that affect how we process these drugs. There are four different types of metabolizers, and we all fall into one of these categories for the unpredictable pathways in Cytochrome P450 system. The first type which is the norm, and therefore that person would be an NORMAL Metabolizer and medications prescribed in the usual doses will be handled well by your body. The second type, you would be an INTERMEDIATE metabolizer. This means that you to metabolize the medications more slowly. In this case a lower dosage is needed, and there is a chance of medications building up in your system causing adverse effects. It is especially important to monitor medications if you are in this category. Intermediate metabolizers through the 2C9 pathway, for instance, have an increased risk of bleeding incidences when taking the common blood thinner Coumadin or warfarin. For this reason, screening for CYP2C9 variants may reduce the risk of adverse drug reactions in these patients. The third type is a POOR metabolizer. This type of metabolizer is potentially very dangerous, as there is a great chance for the medication to build up in your system making one very sick, or even death.For example, a poor metabolizer of phenytoin, a common antiepileptic would not be able to process the drug and would actually have toxicity if prescribed this drug. The fourth type of metabolizer is ULTRA EXTENSIVE. In this instance, one would very rapidly excrete the medication. If you were an Ultra Extensive Metabolizer through the 2D6 pathway and one were prescribed a narcotic, there may not be any pain relief because the medication would be metabolized so fast that it would have little or no effect.


A. PM poor metabolizer, absent or greatly reduced ability to clear or activate drugs. 
B. IM intermediate metabolizer. Heterozygotes for normal and reduced activity genes.
C. EM EuMetabolizer or the Normal Metabolizer. The expected result.
D. UM Ultra Metabolizer. Greatly increased activity accelerating clearance or activation.

CYP2D6 10% 35% 48% 7%
CYP2C9 2-4% >35% ~60% N/A
CYP2C19 2-20% 24-36% 14-44% 30%

Currently Available Tests:

CYP2D6(cytochrome P450 2D6) acts on one-fourth of all prescription drugs, including the selective serotonin reuptake inhibitors (SSRI), tricylic antidepressants (TCA), betablockers such as Metoprolol and many of the antiarrhythmics. Approximately 10% of the population has a slow acting form of this enzyme and 7% a super-fast acting form. Thirty-five percent are carriers of a non-functional 2D6 allele (half of the gene), especially elevating the risk of ADVERSE DRUG REACTION when these individuals are taking multiple drugs. Drugs that CYP2D6 metabolizes include Prozac, Zoloft, Paxil, Effexor, hydrocodone , amitriptyline, cyclobenzaprine (Flexeril), Coreg, Tagamet, Tamoxifen, and the over-the-counter diphenylhydramine (Benadryl) drugs, Allegra and Claritin. CYP2D6 is responsible for activating the pro-drug codeine into its active form and the drug is therefore inactive in CYP2D6 slow metabolizers.
CYP2C9(cytochrome P450 2C9) is the primary route of metabolism for Coumadin (warfarin). Approximately 10% of the population are carriers of at least one allele for the slow-metabolizing form of CYP2C9 and may be treatable with 50% of the dose at which normal metabolizers are treated. Other drugs metabolized by CYP2C9 include Amaryl, Isoniazid,, Amitriptyline, Dilantin, Hyzaar, THC (tetrahydrocannabinol), NASAIDS, and Viagra.
CYP2C19(cytochrome P450 2C19) is associated with the metabolism of Carisoprodol (Soma), Aprazolam, Dilantin, and Prevacid.
CYP1A2(cytochrome P450 1A2) is associated with the metabolism of Amitriptyline, Resperone, Duloxetine(Cymbalta), Theophylline, Caffeine, Diazepam, Sex Hormones Tamoxifen, and Cyclobenzaprine. Amongst other problems these folks have arrhythmias or get jittery when drinking coffee. Lycopene found in tomatoes reduces the effect of the above drugs and hence need more of a dose.
NAT2(N-acetyltransferase 2) is a secondary drug metabolizing enzyme that acts on Isoniazid, Demnerol, and Azulfidine. The frequency of the NAT2 "slow acetylator" in various worldwide populations ranges from 10% to more than 90%.
DPD (Dihydropyrimidine dehydrogenase) is responsible for the metabolism of Fluorouracil (5-FU), one of the most successful and widely used chemotherapy drugs.
UGT 1A1 (UDP-glucuronosyltransferase) variations can lead to severe even fatal reactions to the first dose of Camptosar (irinotecan).
5HTT (Serotonin Transporter) helps determine whether people are likely to respond to SSRIs, a class of medications that includes Citalopram(Celexa), Fluoxetine(Prosac), Paroxetine(Paxil) and Sertraline

With this tool, no longer is it a trial and error proposition as to what drug and its dose to prescribe, We can now do it scientifically with a much better outcome for the patient. Since our CYP genes do not change, this study is done only once in a lifetime. Although, there are several labratories that do this work. the best and the one that we use is the Seattle based GENELEXR . The test is paid for by most medical insurances and archived on a computer registry to be use with the patient’s permission by their current and future doctor and pharmacist. As a doctor with this science, 21st Century medicine can be practice with a far better outcome than the primitive approach we had taken in the past. Please embrace this technology; it can save your life!

Monday, February 14, 2011


BREAD is not only bad for celiac disease, gluten intolerance; bromide (lowers our iodide levels) but has Malted Barley Flour as an ingredient, typically the second one–which means it’s the second most prevalent ingredient. It has the amino acid glutamate, an excitotoxin like mono sodium glutamate. It causes headaches, fuzzy thinking, neuropathies, and the pins and needles pain that seems to have no explanation. Malted barley flour supposedly improves the taste of bread. It is also in some beers, with the same effects.

Also azodicarbonamide (ADA) is added to most bread flour. It’s a pesticide from China that’s added to speed up the bleaching process. Pesticides are linked to cancer, reproductive and developmental problems, and nerve damage. It also causes coughs, headaches that can last for days, shortness of breath, wheezing, swollen nasal cavities, burning throat and breathing problems. The United Kingdom, Singapore, Australia and most of Europe ban ADA. The FDA and World Health do not think it a problem yet.

To add insult to injury bread is fortified with iron. Unless you are deficient in this mineral, it increases the incidence of liver cancer and causes hardening of the arteries. To make matters even worse most commercial breads contain high fructose corn syrup, which raises triglyceride levels, leads to obesity and diabetes, and elevates uric acid levels causing hypertension and cardiovascular disease.

Can Death and Disability be Prevented by GlycoMark ?

You Bet!! According to the American Diabetes Association, monitoring of glycemic (blood sugar) status is the cornerstone of diabetes care. Many doctors and most patients use a Fasting Blood Sugar to determine not only if diabetes is present but how they were doing with their treatment. For the last eight years I have used a better test, the Hemoglobin A1C the average glucose, encompassing both hyperglycemia and hypoglycemia of all blood glucose levels over three months – invaluable information, to be sure. But it doesn’t show after meal spikes, which can affect 40% of patients who otherwise appear to have their diabetes under control.

GlycoMark® is a blood test, FDA approved in 2003, and now available. It is a new generation test that specifically targets glucose response above the renal threshold (about 175) over one to two weeks to give a window on postprandial (after-meal) glucose peaks. That is critical information! This knowledge can improve patient care by targeting the spikes with specific treatments that also have become available. This will prevent dangerous cardiovascular complications in patients who had previously these undetected postprandial serum glucose spikes. It allows patients to seek medical intervention in a more timely manner and when to start or change therapy, empowering them to achieve and maintain control of their disease. . The currently available markers, A1C and fructosamine (like A1C but a two week window) only reflect average glucose, potentially missing the most important hyperglycemic (high blood sugar) excursion that is balanced out by normal or slightly low sugars. The GlycoMark is an alternative marker that acurately reflects postprandial elevations. It is these sudden spikes of glucose that hit hard the sensitive endothelium (lining) of our blood vessels damaging them to form plaque. It is the plaque that not only narrows the vessel but encourages clot formation.

The test uses a natural “in serum” molecule, 1,5-anhydroglucitol (Glycomark) which like glucose, we ingest, is obviously in our blood. During normal blood sugars, the Glycomark is maintained at constant steady state level due to a large body pool and unlike glucose is not metabolized. Normally, in the kidneys, the Glycomark is filtered and completely reabsorbed and therefore neither raised or lowered in our blood under normal conditions. However, with elevated serum glucose concentrations (about 175 – the average renal threshold for glucose), glucose is not completely reabsorbed by the kidney, and serum Glycomark unlike glucose falls due to competiton of renal tubular reabsorption by glucose. Therefore the change in Glycomark depends on both the duration and amount of glucosuria (sugar in the urine). The Glycomark has been shown to reflect daily glycemic excursions in patients with A1Cs at or near goal. Even though the A1C has been validated as marker of risk of both micro- and macrovascular complications, the Glycomark is even better.

Monday, February 7, 2011


Our Body gets its energy from the three macronutrients (Carbohydrates, Protein, and Fats) we consume. As humans we do not need any carbs to survive. But carbs in today’s culture are a way of life. If we must eat carbs, then let us consume the least harmful rather than the detrimental ones, the CRAPOHYDRATES! These lousy carbs score high on the glycemic index, which assigns each food a numerical value based on how quickly it raises a person's blood sugar levels. (To develop this index, researchers spent years assessing the potential of various carbohydrates to raise blood sugar.) Therefore if the glycemic index is greater than 50, it is a crapohydrate rather than an eatable carb. Crapohydrates ( high-glycemic carbs) not only include the bad “whites” like sugar and starches, but white bread, white potatoes, white rice and most pastas! The better carbs, which include berries and vegetables, cause a more gradual rise in blood sugar leading to a slower release in the hormone insulin, which moves glucose out of the bloodstream and into cells where it's used as fuel if the individual excercises shortly after eating or stored as fat in a sedentary person. Not eating crapohydrates limits wreckage to cells triggered by elevated blood sugar thus protecting against heart disease, diabetes, and other ills. Not only is the metabolic Syndrome reversed, but a new study adds to previous research showing that following a low-glycemic, non-crapohydrate diet, type 2 diabetes had better control over their blood sugar and needed less or no medications than those who ate crapohydrates. As a fringe benefit my practice has demonstrated that switching to low-glycemic carbs causes successful weight loss forever. A discovery that has revolutionized my concept of an enduring winning diet is NUTRITIONAL KETOSIS.

After two days, when our liver glycogen is depleted, body fats and proteins are metabolized to produce energy. The fats are broken down into fatty acids that are used as fuel. In the absence of carbohydrate, the fatty acids are incompletely oxidized yielding ketone bodies and is called nutritional ketosis. Prolonged total fasting is unsafe, because it causes the body to begin to digest proteins from its muscles, heart, and other internal organs. Therefore low glycemic carbohydrate diets produce ketosis, and if properly designed, enable the body's nutritional needs to be met by dietary protein, and fat as well as unsightly stored body fat, so that our vital structures remain healthy. As the nutritional ketosis begins, there is a diuretic (water loss) effect, healping the dieter to feel that significant weight reduction is taking place. However, most of the early loss is water rather than fat; the lost water is regained quickly when if the dieter resumes eating crapohyrates, as would also occur, with resumption of a so called “balanced diet”. The appetite, is reduced during ketosis, which also returns when a regular diet is resumed. Current thinking suggest that appetite reduction and weight loss has to do with the balancing of pancreatic hormones, insulin and glucagon. The most widely publicized low-carbohydrate diet has been the one advocated by the late Robert C. Atkins, M.D., of New York City. His 1972 book Dr. Atkins' Diet Revolution sold millions of copies within the first two years! Bob Atkins, with whom I had the privilege and pleasure having supper, will go down in history as one of the greatest influences in medical health of the Twentieth Century.

Needs are necessary for human existence but wants are desires that may or may not be the best for the person. Humans have both a need and a want for food. In ancient times they were almost the same. But in modern times they are vastly deviating. To determine the difference for any given meal, eat only five bites of the beginning course then leave the table. Return a half hour later and eat all you want. Ninety percent of the time you really will not want to eat any more. Therefore your need was only for the five bites, but if you continued to eat after the initial bites, it was only for your wants. There are four easy ways to determine if you are in ketosis. 1. A simple urine Ketostix test of which you can buy and do yourself, or we could do in the office. 2. A characteristic breath odor. 3. Successful weight and appetite loss. 4. A sensation of grittiness or roughness on the back of the front teeth with the tongue. Do not get confused between healthy nutritional ketosis and damaging KETO-ACIDOSIS or METABOLIC-ACIDOSIS. The nutritional one indicates fat loss and the others an illness. It is the fat loss and all its beneficial properties such as normalizing blood sugars, lipids and pressure we want and nutritional ketosis will do it for us. And crapohydrates will make us sick and tired as well as decrease our life span. So say No to Crapohydrates!

Friday, February 4, 2011


Say hello to this Amazing Starch which is a carbohydrate (carbon, hydrogen, and oxygen)-forming glucose in which a large number of these molecules are joined together. Starch is a polysaccharide, which is naturally produced by all green plants as an energy store. It is contained in such foods as potatoes, wheat, maize (corn), and rice. Amylopectin and amylose are the two kinds of arrangement in the starch. Amylose is the most simple containing glucose, one molecule after another in long chains numbering into the thousands. Amylopectin has a more complex configuration in which the chains are off to the sides in several directions. Until the last century, we obtained our starch from the vegetable itself. But now it is added unnaturally to foodstuffs. It is also in the stripped cereal grains we use as the staff of life: bread. (“EAT BREAD AND YOU’RE DEAD” said one of my dying patients).

Pure starch is a white, tasteless and odorless powder that is insoluble in cold water and is tremendously caloric, even more so than plain sugar (sucrose). When dissolved in warm water, it is used as a slightly sweetening, thickening, stiffening or gluing agent. In our bodies the enzyme, amylase, starts breaking apart this large molecular structure to the subunit, glucose. The digestion starts in the mouth, but is mostly completed in the small intestine and what is left is finished by our colonic bacteria. The glucose is rapidly absorbed and used for short-term energy if the person is excercising or, if not, stored as fat. Resistant starches, on the other hand, resist digestion and pass through to the large intestine where they act like dietary fiber instead of being absorbed for instant use or stored energy as fat. There are four categories of Resistant Starch: RS1, RS2, RS3 and RS4. RS2, the resistant starch that occurs in its natural, granular form in foods such as uncooked potato, green banana flour and high amylose corn, is the healthiest. Hi-MAISE is the commercial form of this, costing less than $ 3.00 a pound. Studies have confirmed that different types of resistant starches deliver different effects. The benefits demonstrated by Hi-maize cannot be extrapolated to the other types of resistant starches R1, R3 and R4.

Hi-maize selectively increases the beneficial, while suppressing harmful bacteria. It is food for the good gut flora and, as such, is referred to as a prebiotic or a fiber that not only feeds but also sweeps the gut clean. Research on the health benefits of natural Hi-maize, including 300 peer-reviewed nutritional studies carried out over the last 20 years reveal its benefits that range from weight management, glycemic (blood sugar) management, colon cancer and cardiovascular protection as well as regularity. The fermentation of Hi-maize increases Short Chain Fatty Acid production (butyrate is particularly important for colon health), which reduces intestinal pH, potentially harmful secondary bile acids, ammonia and harmful phenols. Importantly, lipid oxidation is decreased by Hi Maise starch which burns lipid and leads to lower fat accumulation and weight loss.

Studies suggest continual exposure to elevated levels of insulin as a result of a high glycemic diet (sugars and starches) contributes to reduced sensitivity by cells to the insulin (insulin resistance) and a higher risk of diabetes. As insulin resistance increases, the body produces more insulin to maintain adequate blood sugar control. With rising resistance, even more insulin is required, and the body can not keep up or the pancreatic cells producing insulin may stop functioning and hence diabetes. Consumption of natural resistant starch decreases glycemic response in healthy individuals, reduces glycemic response in diabetics, increased insulin sensitivity with the prevention of the Metabolic Syndrome which in some form is present in 38% of our Americans today. The Metabolic Syndome is an abdominaly obese person with a crease in the lower part of the ear lobe, the top Blood Pressure reading higher than 136 and slightly abnormal blood studies. This includes a fasting blood suger and triglyceride higher than 100, and a HDL (Healthy) cholesterol lower than 45. Resistant starch can act as a replacement for wheat products in foods that are required to be gluten-free.

Our biotome, the 6 pounds of gut flora, can be divided into Bacteroidetes whose growth is favored by Resistant starch over the Firmicutes, causes weight/fat loss.
More Firmicutes, results in increased ‘energy-harvest’ or caloric extraction from our diet. Firmicutes are predominantly Clostridium, but include some Lactobacillus spieces, of which are in the probiotics we unknowingly doctors recommend! If Firmicutes outnumbers Bacteroidetes, partially digested complex carbohydrates are broken down to simple carbs rather than metabolized or eliminated through the stool. These, then, form the sugars that are easily absorbed into the blood stream. Also a special chemical is elaborated by this bacterial digestion that encourages the sugar to be directly made into triglycerides by the liver and preferentially stored by fat cells rather than burned! Additionally certain stains within the Bacteroidetes such as PL 60, are thought to produce a lipid digesting enzyme. The net result of having more Bacteroidetes and less Firmicutes is a decrease ‘energy-harvest’ or caloric extraction from the diet and a loss of 100 calorie a day which represents 12 pounds a year just by having the right ratio of the B/F. There have been some specific bacteria of the Bacteroidetes group such as Lactobacillus rhamnosus PL60 which produces conjugated linoleic acid and in itself has anti-obesity effects.

The combination of pre- and probiotics, known as Synbiotic, has been proposed to make a functional food with interesting nutritional properties that make these compounds candidates for a weight loss program. HI Maize, the high-amylose-resistant cornstarch laced with Lactobacillus rhamnosus, PL60, and other Bacteroidetes spiecies will soon be available. Some advanced practitioners have even proposed to rid the gut of most of the Firmicutes with the wonder antibiotic, Xifaxan and then repopulate with Bacteroidetes and feed it with Hi Maize RS2. Why wait another 10 years to be healthy, contact your health practitioner now. Armed with this information, you may be able to transform yourself NOW, rather than to remain overweight and unhealthy!