CARBOHYDRATE ADDICTION

The Basic Problem

   At the root of the physiological dysfunction responsible for this poorly understood and underestimated form of addiction is an insulin imbalance which can assume far-reaching and life-threatening proportions.  Though known since 1983, most of the research into the mechanisms involved in carbohydrate addiction have been focused on the weight problems this disorder leads to.  While carbohydrate addiction is related to rapid weight gain and obesity, it is also intimately involved in serious, life-threatening disorders of the cardiovascular system.  Of special interest are its dangerous effects on the formation of plaques in the coronary arterial system and its role in strokes. 

   Carbohydrate addiction is clearly related to abnormal levels of neuro-regulators like serotonin and abnormal levels of hormones such as insulin.  Carbohydrate addicted subjects exhibit an abnormal early insulin response to food intake that can lead to obesity, impulsive eating, subconscious hunger, dissatisfaction hunger, specific cravings and abnormally intense general hunger.  These abnormal hunger states are associated with changes in insulin sensitivity and responsiveness. 

   This review is intended to acquaint you with carbohydrate addiction and provide you with relevant information regarding this complex and poorly understood form of addiction.  The focus of the review is not on obesity, but instead on the relation of carbohydrate addiction to diseases of the cardiovascular system, especially the coronary arteries and atherosclerosis. 

What Normally Happens When Carbohydrates are Consumed?

   Carbohydrates are essentially sugars and starches.  Some are called simple sugars (e.g. cane or beet sugar, also known as sucrose and corn syrup which contains the common sugar fructose).  These types of simple sugars are found in fruits, fruit juices, table sugars and honey.  Complex carbohydrates are also referred to as starches.  Starches are most commonly found in breads, cereals, vegetables, rice, pasta, peas and beans. 

   Digestion breaks carbohydrates down into glucose which is absorbed from the small intestine into the bloodstream and distributed to the muscle cells for fuel and to the liver and fat cells for storage.  Glucose is the body's fuel.  It provides energy to run the millions upon millions of cells that make up your body.   

   The pancreas plays a role in controlling this fuel.  When carbohydrates are eaten, blood sugar (glucose) begins to rise.  When the pancreas detects the rise in blood sugar, it responds by releasing insulin into the bloodstream.  This insulin goes throughout the entire body and binds with receptor sites on the membranes of the cells and thereby increases their ability to absorb glucose from the blood stream.  In other words, insulin is the "key" to unlock the door to the cell so that glucose can get in. 

   Insulin "unlocks" and "opens" the doors to muscle cells so your muscles can work.  It also unlocks and opens the doors to fat cells as well.  In this way, by unlocking and opening all these millions of doors, the body's cells can effectively lower the glucose levels in the bloodstream.   Some of the absorbed glucose provides immediate energy, some of it is stored in the form of glycogen and triglycerides (fats) for later production of energy. 

   But insulin also acts on the brain.  There it tells your brain to stop eating.  Insulin does this through some complex mechanisms that involve neuro-regulators such as norepinephrine, serotonin and mesolimbic dopamine.  In simple English, this means that insulin alerts the brain to release serotonin after each meal.  Serotonin is a neurotransmitter that tells you you're no longer hungry.  It also is the neurotransmitter that makes you feel sleepy after eating high levels of carbohydrates. 

   Under normal circumstances, the pancreas releases just enough insulin to allow the cells to receive the right amount of glucose for immediate and intermediate energy needs.  This insulin also helps convert the excess glucose into glycogen (the animal equivalent of starch) and triglycerides (animal fat) for use at a later time.  All of this happens at a time when insulin has also told the brain that you are full.

   In normal people and in carbohydrate addicts, there is no difference in the body's ability to release insulin.  The body releases insulin in two phases, the first of which is called the preload phase.  The preload phase begins within minutes of eating carbohydrates.  The second phase of insulin release begins about 75 to 90 minutes after eating. 

Preload Phase Insulin Release

   Within minutes of eating foods rich in simple and complex sugars (i.e.  carbohydrates), the pancreas releases a fixed amount of insulin regardless of how much carbohydrate has been eaten.  The amount of insulin released at this time is determined by the amount of carbohydrates eaten in earlier meals.  It's like the pancreas has a memory of its own.  So it doesn't matter whether you have only just eaten one slice or five slices of cake, the preload phase release of insulin will be a set amount that was influenced by what your carbohydrate pattern had been, not by what you have just eaten.  In other words, the more carbohydrates eaten at earlier meals, the more insulin is released.

Second Phase Insulin Release

   About 75 to 90 minutes after eating carbohydrates the pancreas releases another round of insulin into the bloodstream depending on how much carbohydrate you actually ate.  The body is able to determine whether the amount of insulin released in the preload phase is sufficient to handle the carbohydrates you ingested.  This phase simply adjusts your insulin production and release in response to the total volume of carbohydrates eaten at that particular meal.  If you indeed ate five  slices of chocolate cake, then your body will probably have to release more insulin to take care of this increased carbohydrate load.

What Happens in the Carbohydrate Addict?

   In the carbohydrate addict these mechanisms fail to operate properly.  A number of studies reveal that serum levels of insulin are higher in overweight people than normal individuals.  Such overweight people are therefore said to exhibit hyperinsulinemia (sustained high levels of insulin in the blood). 

   Sustained, high levels of insulin in the blood have several important consequences.  High levels of insulin somehow decrease the number of insulin receptor sites on muscle and fat cells.  High levels of insulin also decrease the sensitivity of these insulin receptor sites to insulin.  Think of it as having fewer locks that the key (insulin) has to open and that these locks somehow get frozen, corroded or gummed up so they don't work as easily.  This is called insulin resistance -- fewer responsive sites; diminished responses to insulin.        

   This means that when we eat too much carbohydrates we cause our pancreas to produce too much insulin which remains in our bloodstream for too long and we become hyperinsulinemic.  As a result, our cells become more insulin resistant meaning that less insulin is able to enter the cells and unlock the glucose entry doors.  The longer the insulin remains high, the greater becomes the decrease in the number of insulin receptor sites.  

   Insulin stimulates fat synthesis, which means then that if your blood levels of insulin remain high, this insulin actually causes more fat to be manufactured. Indeed, animals repeatedly injected with insulin become obese.  And in humans many studies have shown that hyperinsulinemia can be genetically linked and leads to obesity.  High insulin levels are routinely found in obese people who also show abnormally high levels after glucose intake.   

   The reduced sensitivity to insulin is not just a phenomenon that occurs in our bodies (i.e. arms, legs and bellies).  Certain brain cells that regulate eating loose their sensitivity to insulin and fail to respond properly also.  Thus, just like the body, the brain exhibits insulin resistance also as a function of hyperinsulinemia.  As a result the carbohydrate addict continues to eat because the brain has lost its "satiety thermostat" (due to insulin resistance) and the sensation of being satisfied is never delivered. 

   When this happens the result is a relatively continuous feeling of hunger usually accompanied by intense cravings for carbohydrates.  This combination is the result of control mechanisms that have gone haywire. 

   When the control mechanisms go haywire, a positive feedback loop of sorts is established which results first in too much insulin circulating in the bloodstream which creates intense hunger, usually characterized as intense cravings for carbohydrates.  Intense cravings for chocolates is one form of this addiction. In some people the disorder manifests itself as an inability to eat a meal without bread, in others it manifests as an intense desire for pasta-type dishes or desserts.  

   The body attempts to satisfy this state of intense craving by eating more bread, chocolate, sugar loaded foods, candy, pasta, fruits, potatoes, beans, etc., which leads the body to produce and release even more insulin in the preload and second, adjustment phases.  This then makes the hyperinsulinemia worse and this then contributes to increased weight gain and continued, increased carbohydrate hunger.

   Remember, the preload phase of insulin release is determined by the amount of carbohydrates eaten at previous meals.  Thus, the more this vicious cycle operates, the greater the carbohydrate ingestion becomes and the greater becomes the preload phase release of insulin.  Research studies clearly demonstrate that obese people release significantly more insulin during the preload phase than non-obese, normal weight people. 

Mount Sinai Medical Center Studies

   The experience of hunger and weight gain were studied in carbohydrate addicts and non addicted subjects when both groups were instructed to eat comparable foods during two, month-long studies.  During one half of the study, the carbohydrates were distributed equally across breakfast, lunch and supper meals.  In the other half of the study, the carbohydrates were confined and consumed in one meal daily.  Here's what happened:

   Hunger and weight change were measured in both groups.  Both groups were affected but carbohydrate addicts got hungrier and gained more weight than did the non addicted subjects when the carbohydrates were spread throughout the day.  In fact when the sugars and starches were spread throughout the day, the carbohydrate addicts showed more intense hunger and greater weight gain than the non addicts.  When carbohydrates were available at only one meal, the carbohydrate addicts reported greatly reduced hunger and significantly greater weight loss. 

What Does This Mean for You? 

   If you are a carbohydrate addict, you need to limit your carbohydrate intake to one meal per day because: 

(1)  This will lower your insulin production and release thereby creating an increase in insulin receptor sites which will then lead to an increase in the rate at which insulin is taken up by the cells of the body and thereby removed from the blood.  

(2)  If you are a carbohydrate addict, by limiting your carbohydrate intake to only one meal per day you will reduce your cravings for all carbohydrates.  At the same time you will dramatically increase your tendency for weight loss! 

(3)  If you are a carbohydrate addict, your carbohydrate addiction may very likely lead to abnormal triglyceride and cholesterol levels in the blood as well as to severe disorders in the metabolism of these products, and

(4)  If you are a carbohydrate addict your chances of having or developing severe coronary artery and other vascular diseases are much greater because carbohydrate addiction is known to affect triglyceride production and LDL cholesterol levels.  More about this later. 

Addiction Triggers

   A number of factors can cause or intensify the desire to eat.  A wide variety of emotional factors trigger carbohydrate addiction and include emotions such as anger, anxiety, loss of emotional control, depression, excitement, frustration, guilt and self-blame.  But there are other factors which can trigger this addiction.  Relatively benign changes in your home life or working conditions can cause changes in your eating habits which can lead to carbohydrate addiction.  Exercise, illnesses, pregnancies, premenstrual changes, smoking and quitting smoking and stress of any kind can all affect carbohydrate consumption. 

   Dieting can also trigger carbohydrate addiction.  This is especially common in people that subject themselves to extreme dieting or fasting.   

   Of course, high carbohydrate foods can trigger the addiction process.  The best trigger foods are bread and grain products including bagels, rolls, donuts, cookies, crackers, cereals (both man-made and natural), cakes, and pastries of all types. 

   But foods we usually think of as very healthy are equally potent triggers.  Fruits of all kinds including the dried varieties and their juices are potent triggers.  This is because all of the fruits are full of sugars which trigger the release of insulin.

   Snack foods such as popcorn, potato chips, pretzels, cheese puffs, and candies are potent triggers.    

Carbohydrate Addiction and Cholesterol

   Cholesterol is a vitally important chemical manufactured by our bodies.  It is a waxy type substance that also happens to be one of the most perfect lubricants known to man.  Cholesterol lubricates the lining of our arteries.  It's what we do to our bodies and what we feed our bodies that ultimately causes the problems with cholesterol.

   You no doubt have had your cholesterol checked by a medical laboratory.  But do you know what the report you got back means?  Probably not.  So you need to understand a few terms.

   Lab reports may mention cholesterol, HDL, LDL, or HDL-cholesterol or LDL-cholesterol, triglycerides and on some reports you will find the terms Lp(a) and VLDL.  The total cholesterol value on the lab report is simply the sum total of the LDL, the HDL, the Lp(a) and the cholesterol that is carried with the triglycerides which is known as VLDL.  Of the various cholesterols found in your blood, only a few are bad actors.       

Villains and Heroes

   VLDL, LDL and Lp(a) are bad actors or villains while HDL is your hero that has probably saved your life more often than you will ever know.  What do these terms mean?

   LDL stands for low-density lipoprotein.  It is also referred to as LDL-cholesterol.  An easy way to remember which is the deadly form of cholesterol is to remember that the "L" could also stand for "lethal."  Numerous studies now clearly indicate that it's the LDL cholesterol that's associated with coronary artery disease.  Understanding atherosclerotic plaque formation and buildup requires an understanding  of  LDL metabolism.

   A large number of studies show that when LDL levels are lowered through dietary manipulations, the progression of coronary artery disease is dramatically reduced.  In fact, in some studies it has been shown that when LDL levels were reduced for long periods of time, the clogged arteries actually showed signs of clearing.  But that's not all of the story.

Oxidized LDL   

   A great deal of hard evidence is accumulating that strongly suggests, if not clearly proves, that it is actually oxidized LDL that is accumulated in the plaques that ultimately obstruct our arteries.  Thus, LDL can turn bad on us just as Crisco and other vegetable oils can become rancid when left out or used too much for cooking.  In both cases oxidation is to blame.  In the case of Crisco or other cooking oils, simply reducing their contact with oxygen and air will reduce the amount of oxidation.  But in the case of LDL circulating in our bloodstream, we need the presence of antioxidants to protect the LDL from being oxidized.  Potent antioxidants include vitamins C and E, selenium, beta carotene and other vitamins and minerals.      

   The best approach is to lower the LDL levels in the blood and at the same time protect them from oxidation with antioxidants. 

HDL-Cholesterol

   HDL stands for high-density lipoprotein and your lab report may call it HDL-cholesterol.  HDL is a hero because it actually protects our heart's arteries by carrying LDL away from the arterial wall before it gets hopelessly entangled in the plaque. 

   This is the reason that study after study has shown that HDL levels are inversely related to heart disease.  When HDL carries away LDL, this process is referred to as reverse cholesterol transport. 

   HDL carries LDL back to the liver where it is dumped into the bile, subsequently injected into the small intestine and ultimately eliminated through bowel movements. 

   In addition to its role in reverse cholesterol transport, HDL may also be involved in the early shrinkage of fatty streaks -- the earliest signs that a plaque formation has begun. 

Formation of Arterial Fatty Streaks

   When LDL-cholesterol is oxidized, it appears to become capable of penetrating the walls of our arteries.  When it penetrates the arterial walls it attracts monocytes, a form of white blood cells.  Monocytes will actually follow oxidized LDL right into the arterial wall according to some scientists because of their strong attraction to this lethal form of lipoprotein.  It has been suggested that oxidized LDL is recognized by the monocytes as a foreign substance, thereby triggering a powerful immune response. 

The Creation of Obese Monocytes

   The monocytes' job is to track down oxidized LDL.  And they are too good at this for our own good because once they begin to attack the oxidized LDL in our arterial walls, the monocytes continue to consume or eat oxidized LDL until they become so fat they can't work themselves free from inside the artery's wall.  They eat and eat until they become simply obese with oxidized LDL.  Now, monocytes that have lost their mobility because they are trapped inside a particular tissue are referred to as macrophages.  In this case, our monocytes-turned-macrophages are now called foam cells because that's what they look like under a microscope. 

   As these foam cells begin to grow in the artery walls, one begins to see the formation of fatty streaks that eventually become arterial plaque.  LDL-cholesterol is NOT accumulated in such plaques; only oxidized LDL is involved along with fatty debris and other substances including calcium and perhaps heavy metals such as lead. 

   Recent research on coronary arteries obtained from autopsies revealed another interesting inclusion in plaque -- mast cells.  While mast cells were found in 50 percent of supposedly normal artery sections, mast cells were present in 84 percent of sections where fatty streaks were present and in a whopping 95 percent of the tissues comprising the shoulder areas of the plaque.  Shoulders are those areas where hardened and capped plaque deposits join the normal arterial wall.  Shoulders are rupture prone and easily damaged by angioplasty and other procedures such as stent implantation.  When these areas are damaged, these cracks appear to release enzymes that dissolve collagen and other components of the plaque's so-called cap -- a protein layer that grows over the plaque. 

   Mast cells are capable of spewing out copious quantities of enzymes that literally melt the plaque caps and which also release histamine. 

   Histamine can actually make matters worse because histamine constricts coronary arteries.  If the crack at the shoulder should create the formation of a clot, the histamine-narrowed vessel could become completely occluded, thus leading to catastrophic results.  

Lp(a)

   This is a unique molecule -- a molecule that is half-LDL and half-clotting factor.  Just like LDL, Lp(a) can be oxidized as well and in this state enhances the clotting ability of blood. 

   Lp(a), pronounced "L, p little a" is perhaps the worst of the bad actors.  The clot promoting portion of this molecule resembles plasminogen.  Because Lp(a) blocks circulating Tissue Plasminogen Activator (TPA), any clots that are formed are not broken down very easily. 

   Linus Pauling along with Matthias Rath, advanced the theory that Lp(a) is perhaps the most important of all the risk factors.  In species that cannot manufacture vitamin C, a powerful antioxidant, the Lp(a) becomes a patch of sorts that attaches to the arterial wall.  In reality, the atherosclerotic plaque is comprised of Lp(a) along with other ingredients.  The work of Dr. Pauling suggests that vitamin C might be of value in lowering this risk factor.  The B-vitamin niacin (nicotinic acid) is the only known agent that can consistently lower Lp(a) levels.  Estrogen and anabolic steroids may also have actions on Lp(a) levels. 

Triglycerides

    The liver produces triglycerides.  And as we discussed earlier, the production of triglycerides is related to insulin levels.  The prolonged presence of insulin as in hyperinsulinemia, the more pronounced the production of triglycerides.

   Triglycerides are generally packaged with LDL in the liver.  This combination of triglycerides and cholesterol (or fatty-cholesterol) is known as VLDL.  A number of reports show that VLDL is highly toxic to arterial walls. 

The Need to Reduce Homocysteine

   Recent research clearly demonstrates that too much homocysteine can cause heart disease.  Homocysteine is an amino acid that is normally present in the blood at very low concentrations.  Nevertheless, much evidence suggests that homocysteine is an exceptionally dangerous byproduct or metabolite of methionine. 

   The effects of homocysteine on our arteries is complex.  Homocysteine blocks the production of a relaxing factor that is manufactured by the endothelium lining the walls of our arteries.  This relaxing factor is called Endothelium-Derived Relaxing Factor (EDRF).  Under normal circumstances the amino acid arginine is used by arterial endothelial cells to manufacture nitric oxide.  Studies show that EDRF is nitric oxide.  Arginine is known to be deficient in patients with coronary artery disease, especially in those with elevated levels of cholesterol.

   EDRF completely shuts down the process of atherosclerosis through a series of complex mechanisms including: relaxation of the walls of the arteries; through inhibiting the binding of monocytes and oxidized LDL-cholesterol on and within the arterial walls.

   High levels of homocysteine may also be directly involved in the conversion of LDL-cholesterol into oxidized LDL-cholesterol.  But that's not all.  

   High levels of homocysteine cause the rapid proliferation of arterial smooth muscle  in and around plaque-prone areas.  When coronary and other arteries are damaged (as in angioplasty) or inflamed (as a result of an immune response), smooth muscles cells in that area proliferate rapidly.    

   Homocysteine also increases the risk of blood clotting.  Thus, this dangerous metabolite can not only cause heart attacks, but strokes as well. 

The Necessity of B-vitamins

   Since homocysteine is one of the byproducts of the metabolism of methionine, a sulfur-containing essential amino acid, it's relatively easy to prevent its production.  In the absence of vitamin B-6, B-12 and folic acid, methionine is converted into dangerously high levels of homocysteine.  When vitamin B-12 and folic acid are present, homocysteine is converted back to methionine.  In the presence of B-6, homocysteine is converted into cysteine.  These facts are supported by literally hundreds of studies which clearly show that when homocysteine levels are high, levels of vitamin B-6, B-12 and folic acid are low and arteries begin to plug up.

L-Carnitine             

Methionine is also a precursor for another amino acid -- L-carnitine.  This strange amino acid is not used in the production of protein.  Instead, it seems to be a primary carrier of fatty acids into cells.  That is important because fat is a high energy form of cellular fuel.  In fact, most of the energy produced in our hearts comes from the burning of fatty acids.  

L-carnitine is also an antioxidant.  It will lower LDL-cholesterol levels as well as triglycerides.  L-carnitine also raises blood levels of HDL-cholesterol. 

Chromium

   Trivalent chromium plays an important role in the prevention and reversal of coronary artery disease through its relationship with Glucose Tolerance Factor (GTF).  Trivalent chromium is normally bound to niacin and certain amino acids within the GTF complex.  A number of studies show that chromium within GTF exerts powerful effects on cells to dramatically increase their sensitivity to insulin.  When GTF is not available, or when trivalent chromium is deficient in the diet (thereby reducing the effective levels of GTF), the circulating insulin is profoundly reduced in terms of potency.  When the body's sensitivity to insulin is reduced, the body responds by making more insulin.  However, in the continued absence of GTF and/or trivalent chromium, the blood sugar still continues to rise.  This is by definition "adult onset" or "Type II" diabetes.

            Excess insulin is associated with accelerated atherosclerotic plaque formation.  Supplementing the levels of  trivalent chromium in the diet (with  chromium picolinate or chromium polynicotinate) will lower blood glucose levels and lower blood insulin levels dramatically within several weeks. 

   Patients suffering from hyperinsCARBOHYDRATE ADDICTIONulinemia due to chromium deficiency also show high levels of triglycerides as well as low levels of HDL-cholesterol.  Insulin drives the triglycerides higher while severely lowering the levels of HDL-cholesterol.

Beta-Blockers, Plaque and Chromium

   If you suffer from coronary artery disease and have been under the care of a cardiologist, chances are good that you have been prescribed beta-blockers.  You should know that among the many side effects of beta-blockers is their profound ability to lower HDL-cholesterol.  Adding chromium picolinate to the diet can drive HDL-cholesterol back up while lowering LDL-cholesterol.  Some studies have observed chromium-induced lowering of total cholesterol and triglycerides.  In fact, at least one study in rabbits shows that adding chromium actually reversed arterial blockages.        

Sugar

   One hears so much these days about low fat or zero fat products it's easy to forget that ordinary sugar, a prime ingredient in the plethora of low fat or zero fat products lining the supermarket shelves, is exceptionally capable of inducing coronary artery disease.  Sugar is at the heart of carbohydrate addiction and for good reason.  As we have seen above, sugar elevates triglyceride levels, knocks down HDL-cholesterol and raises insulin levels.  But sugar also raises LDL-cholesterol and increases platelet stickiness.  This raises serious questions about placing all of the blame for coronary artery disease on fats.