Successfully Treating Metabolic Conditions
Insulin Resistance and Diabetes
Insulin resistance and diabetes are more often than not the result of eating the wrong foods over time. Whether you have a poor diet or your body has autoimmune sensitivities to foods you include in your diet, the result is the same. Under ideal circumstances, the body is able to properly metabolize glucose at the cell level, creating the energy necessary for the brain and other organs to both function and repair themselves. Autoimmune issues and poor diet can both contribute to an environment wherein cells don’t metabolize glucose properly. This situation sets off a series of attempts by the brain to compensate (unsuccessfully) by sending out insulin and eventually increasing cortisol levels.
Failing to eliminate the causes that trigger this natural response in the body will lead to a cycle that has the potential of developing into type II diabetes, and other areas in your body begin functioning below desired levels. Fatigue, appetite, sleeping habits, stress management, and memory can all be affected by the increases in insulin and cortisol.
Through proper testing, we can determine the cause(s) of your symptoms that are pointing to insulin resistance and diabetes. We can then make diet and other lifestyle changes to help you better correct your glucose levels. Our patients don’t just strive to manage their condition when they do the work, we teach them to do they correct the underlying condition! This process leads to not only bringing blood sugar back into balance but it often leads the patient to a state of health they have not enjoyed in many years!
Check out our page on lab testing to get an idea of the process by which we start our evaluation and watch the video above to learn more about our approach to the correction of this major killer.
Stopping the Head Pain
The migraine headache is perhaps the best known special type of headache. A lot of things accompany this type of headache—all of them bad. Symptoms can include dizziness, visual problems, “spots” before the eyes, redness, swelling, tearing of the eyes, muscle contraction, irritability, nausea, vomiting, constipation, or diarrhea. These symptoms often arise before the headache hits. The headache itself may last for a few minutes to a few days, and the severity may range from minor discomfort to immobilizing agony. Migraine pain is most commonly felt in the temple, but it may be experienced anywhere in the head, face, and neck.
Another variety of headache, closely related to the migraine, is the cluster headache. Attacks come on abruptly with intense, throbbing pain arising high in the nostril and spreading to behind the eye on the same side. Sometimes, the forehead is also affected. The attacks tend to occur from once to several times daily in clusters lasting weeks, or even months. Without apparent reason, the cluster subsides as quickly as it began.
One more common type of headache is called a sinus headache. This frequently can present as atmospheric pressure changes occur if the individual has chronic inflammation in their sinuses cavities. This type of headache responds well to food sensitivity testing and dietary modification as well as in the moment of pain with laser therapies which can rapidly reduce the pressure in the sinuses.
One more that we see a lot of is the cervicogenic or “tension-type” headache which is caused by improper muscle firing patterns in the neck, head, and shoulders. This type is the most common cause of head pain and comprises a full 80% of the people who experience headaches. This is another type that responds fabulously to laser therapy as well as proper oxygenation and magnesium.
So what puts the ache in headache? The pain-sensitive structures of the head are the culprits. These are the arteries of the brain and skull, the tissues surrounding the head, the veins, the dura mater covering over the brain, and certain nerves called cranial nerves. When these parts are inflamed, stretched, pulled, or under pressure, any type of headache may be caused.
Migraine headaches can be classified into two types: classical and common. The classical migraine is a headache that follows an aura or some type of spontaneous events such as numbness or tingling. The aura may be flashes of light, squiggly lines, or a halo effect. The common migraine does not have an aura associated with it. Most people who suffer from migraines suffer from common migraines—usually at a 3:1 ratio.
Approximately 28 million Americans suffer from migraines, and millions go without treatment. Scientists once thought migraines were caused by abnormally dilated or enlarged blood vessels. Now, new imaging devices have allowed them to watch brains during migraine attacks, and scientists are discovering that sufferers have abnormally excitable neurons or brain nerve cells.
The latest migraine research has yielded a mechanism called cortical spreading depression, or CSD. Prior to the onset of pain in a migraine, researchers have observed a sudden burst of cortical activity that occurs most commonly in the occipital lobes (back part of the brain). The occipital lobe will increase in the frequency of firing, or have a burst of activity, and then there will be an episode of silence or depressed activity. The actual activity of the brain becomes depressed when compared to normal. The resulting pain comes from either the brain stem activation or from blood vessels inflamed by rapidly exchanging blood flow or both.
I take a different approach to the treatment and prevention of headaches and migraines. After a thorough neurological examination, I determine which part of the nervous system is not functioning properly, and if there is proper fuel delivery in the form of oxygen and glucose. In many headache and migraine patients, I may find a high mesencephalic output. There are three parts to the brain stem: top, middle, and lower. The mesencephalon is the top part of the brain stem. A high-output of the mesencephalon that is not dampened by the lower portions (the pons and medulla) will cause an increased pulse and heart rate, inability to sleep, or waking up from fitful sleep, urinary tract infections, increase warmth or sweating, and sensitivity to light. Often times, in these patients poor muscular firing patterns have developed that lead to chronic spasms in the involuntary muscles of the neck and shoulders. For these patients, utilizing laser therapies has been extremely successful at minimizing and sometimes removing one more trigger for their pain.
I think I must have had headaches all of my life, but the first time I remember asking a doctor about them was when I was 28. I got through them the next 35 years with over the counter drugs, and then I developed a bleeding ulcer and couldn’t take the O.T.C. meds any longer. 20 years ago I began getting headaches about 2-3 hours after I went to sleep, so I started on a quest to find an answer. I have done many protocols – infusions, hormone therapy, food allergies, and several different kinds of pillows. Recently my primary doctor sent me to Dr. Marquis. 3 weeks ago I started laser treatments, I have only taken 5 Maxalt in that time (I was taking 3 per day). Only 3 of the headaches in the past 3 weeks were at night. This has been the best 3 weeks of my life in 20 years!
Delphia R. Connella
There are metabolic triggers for head pain as well. A common one is the surprising array of food sensitivities. Many times, the culprit can be foods that are considered “healthy.” I have seen just as many headaches caused by dairy and bread as I have food dyes and flavorings. The best way to identify the individual trigger is through comprehensive metabolic blood testing. This is an invaluable tool that we use for most chronic conditions and are able to provide beneficial life-changing information once we gain the data. No matter what the condition, it is imperative that the doctor performs a thorough and comprehensive exam to determine the exact nature of the patient’s condition. If you would like to have more information or to set up a consultation and see how we can help you (or someone you know)
The functional medicine system of care has helped thousands of people across the country and is now available in the Central Coast.
Peripheral Neuropathy describes damage to the nervous system in your legs, feet, arms, or hands. This vast communications network transmits information from the brain and spinal cord (the central nervous system) to every other part of the body. Peripheral nerves also send sensory information back to the brain and spinal cord, such as a message that the feet are cold or a finger is burned. Damage to the peripheral nervous system interferes with these vital connections. Like a poor cell phone connection, peripheral neuropathy distorts and sometimes interrupts messages between the brain and usually the endings of nerves.
Patients with peripheral neuropathy experience a variety of symptoms such as chronic tingling, numbness, weakness, or even burning pain. They often find it difficult to walk or sense the type of surface under their feet. They often don’t even know if they have injured the affected area and are often miserable because of the chronic pain they experience.
Our approach is comprehensive in helping our patients with peripheral neuropathy. Not only do we treat the local area affected by using cutting edge therapy, addressing metabolic conditions (such as blood sugar problems) but we also treat areas in the brain responsible for receiving these messages from the body. Covering both the neurological and metabolic aspects of this disease is vital for any treatment to truly be successful. It is common that peripheral nerve damage will lead to functional changes in the brain! You MUST address all areas in order to get the BEST OUTCOMES.
Many people have seen images of the brain with our body superimposed over it displaying specific body parts and how they relate to the brain. There is a ‘road map’ in the brain of your entire body. Every body area (foot, hand, face, etc.) is represented in a part of the brain called the parietal lobe. If poor nerve signals come into the brain because of peripheral neuropathy, this can lead to problems in the brain itself. Allowed to progress and the brain actually changes over time and becomes less and less functional. This is termed neuroplasticity. This plasticity can work for us or against us depending on the information you provide the brain.
Although you might start out with peripheral neuropathy, the longer you have this condition the more likely you’ll experience issues higher up into areas of the brain. That is why damage to the peripheral nerves is just part of the story. And why treating the local area can lead to discouraging short-term results.
We Offer So Much More... a Unique Nondrug Approach
For peripheral neuropathy, our evaluation starts with a unique exam based on the Toronto Clinical Scoring System. Why? Because this exam scores the health or sickness or your nerves. In-depth laboratory analysis provides important details as to the CAUSE of your condition. Wouldn’t it be nice to objectively demonstrate where you are and how you are improving? Not just “I feel good today” but an exam that proves you are getting better. How is this accomplished? Through the unique combination of clinically proven therapies…
Treatment
We use a combination of brain-based therapy (BBT), laser and infrared therapy, spinal decompression when necessary, whole body vibration, Exercise with Oxygen Therapy (EWOT), The ReBuilder, and other brain-based therapies (BBT) geared toward your specific condition to address peripheral neuropathy in a very dynamic way.
On top of the brain-based therapies (BBT), we also support the nervous system using advanced metabolic and nutritional protocols designed to give you every chance possible to feel better. If you want to restore normal nerve communication, function, and health it is best to start healing from the inside out!
No matter what the condition, it is imperative that we perform a thorough and comprehensive exam to determine the exact nature of the patient’s condition.
While searching for better ways to help my patients, I was fortunate to learn of Dr. Datis Kharrazian, a pioneer in natural health care and author of the best selling book “Why Do I Still Have Thyroid Symptoms When My Thyroid Tests Are Normal?“ I have spent a great deal of time studying his work and in fact learning directly from him for quite some time now. On this page, you will have the opportunity to learn about some fundamental aspects of thyroid function and dysfunction. I highly recommend reading Dr. Kharrazian's book as well.
Introduction to Functional Thyroid Disorders
Functional thyroid disorders are incredibly common and often overlooked in our current health care model. Most patients that have functional thyroid imbalances do not have primary thyroid imbalances. In fact, 5 out of every 6 thyroid patients are suffering from an undiagnosed auto-immune problem driving their thyroid problem.
Thyroid problems are often misdiagnosed and mistreated... and women are often affected the most. Over 80% of our patients who have a thyroid problem are not being treated in a manner that will provide them long-term solutions and many are experiencing their problems worsen because the root cause has been overlooked.
See if this sounds familiar? Your labs come back “normal” and yet you still feel tired, achy, cold, depressed, and mentally sluggish. I can’t tell you how many people have been told…”go home, get some rest, your blood work looks normal, you are probably just overworked.” Or even worse, you are put on thyroid hormone replacement and you still have all the symptoms of hypothyroidism but your lab tests show that your thyroid levels are good. And worst of all it’s difficult to get anyone to listen to you. So now what do you do? You go through your day with any one or more of these symptoms (some poor souls have them all!).
Book by Dr. Kharrazian
It doesn’t have to be that way. I have found that most patients will have inadequate labs (often only two tests done: TSH and T4) to determine if they have a thyroid problem. These two tests offer a simple screening for thyroid function but they certainly don’t provide the complete picture! Did you know there are over 20+ ways that your thyroid can go bad? Fundamentally, there are 6 major categories for thyroid dysfunction and 24 subsets off of these 6. And only one of those ways will respond to typical replacement therapy. So, why is everyone treated with hormone replacement if only 1 out of 6 will actually be resolved with the medication? Not everyone fits into the replacement model of treatment. Modern approaches allow us to determine your specific needs and then let the body correct itself with proper neurological and metabolic support. Don’t go on feeling frustrated. We will always listen to your concerns and help you chart a course to get you back on track. You need comprehensive blood work (see our Laboratory Analysis page) and functional neurological analysis will help us determine the shortest path to getting you better.
If you are ready to reserve an appointment, please call
(805) 481-3499. Below you will find some core information on thyroid and the physiology of the gland.
Thyroid Physiology Review
Once the thyroid is stimulated by thyroid-stimulating hormone (TSH) from the pituitary, it produces thyroxine (T4) and triiodothyronine (T3) by transporting iodine into the thyroid and by stimulating Thyroid Peroxidase Activity (TPO). TPO is involved in the formation of T4 and T3 as it catalyzes the oxidation of iodine using hydrogen peroxide. The thyroid will produce 94% of the available T4 and 7% of the available T3. As we know, T4 is inactive and T3 is an active thyroid hormone. Therefore, the majority of hormone production at the thyroid is inactive T4. Once the thyroid has produced T4, it is metabolized peripherally from the thyroid into combination T3 hormones by the enzyme 5′ deiodinase, mostly at the liver. Under normal circumstances, about 40% of the available T4 is converted into T3, 20% is converted into reverse T3 (rT3), which is irreversibly inactive, and 20% is converted into T3 sulfate (T3S) and triiodothyroacetic acid (T3AC). T3S and T3AC are inactive thyroid hormones until they circulate into the gastrointestinal tract and are acted upon by intestinal sulfatase into active T3. Gastrointestinal sulfatase activity is dependent upon a healthy gut microflora.
So with most of your thyroid hormone conversion occurring in the liver and gut, what happens if your liver function is compromised or your have an inflamed gut. Do you know anyone with either or both of those problems? The funny thing is (and it's not really funny) that most people end up being told they have 3 distinct problems and never realize that their GI problems and toxic liver and thyroid dysfunction are all part of the same disease. This is why so many people are suffering and being medicated but not finding a resolution to their complaints. Looking at thyroid dysfunction requires a comprehensive metabolic and neurological approach. In this way no stone is left unturned and although the process generally takes time patients do finally find the relief they have been seeking.
Understanding Thyroid Markers and Panels
TSH: thyroid stimulating hormone (TSH) is also called thyrotropin. The pituitary releases this hormone after the hypothalamus releases TRH (thyrotropin-releasing-hormone). This is the most common marker used to assess thyroid function and it is also the most sensitive. The TSH levels increase when the T4 levels drop, and the TSH falls when T4 levels increase. This is the only test performed in the traditional health care model as a means to screen the patient for thyroid disorders; this is because they are only concerned for screening the thyroid for hormone replacement and not optimal physiological function. A TSH test alone does not consider thyroid pituitary feedback loops, peripheral thyroid metabolism, or potential or active risk factors as identified by antibody testing. A high TSH with or without changes in T4 or T3 is diagnostic to determine hypothyroidism. If the thyroid is not making enough T4, the pituitary will pump out TSH to stimulate its production. A low TSH is used to determine hyperthyroid activity. If the thyroid is overactive such as in Grave’s disease, the antibodies bind to active thyrotropin (TSH) receptors on the thyroid cells and stimulate T4 production without the influence of TSH. Please note that some antibodies may inhibit thyroid function by inactivating instead of stimulating thyrotropin receptors. This is called an autoimmune hypothyroid. These patterns will demonstrate a hypothyroid pattern (elevated TSH) with elevated thyroid antibodies.
Laboratory Reference Range: 0.5 – 5.5 (varies from one lab to another)
Functional Reference Range: 1.5-3.5
Total Thyroxine (TT4): The TT4 test measures both bound and unbound thyroxine levels, therefore, it does not give the activity of T4 when measured alone. This test is best completed with a T3 uptake. The free thyroxine index (FT4) can be calculated by using the T3 uptake and demonstrating a level of T4 activity. Total T4 levels can be altered by many drugs.
Free Thyroxine Index: As stated earlier, the total thyroxine and T3 uptake must be used together to calculate the FT4. The index is measured by multiplying the TT4 levels by the T3 uptake levels. The result is the FT4 and it determines the amount of active T4 available. The impact of drugs, as will be discussed, will always impact T4 and resin T3 uptake levels in opposite directions due to its impact on binding sites. If the TT4 level is depressed, then the T3 uptake is high; if the TT4 is elevated, the resin uptake is low. Please note that even if you are taking drugs that may impact thyroid-binding, the free thyroxine index should be within the normal range if your thyroid is functioning normally.
Free Thyroxine (FT4): The free thyroxine test is used to measure the amount of free or active T4 in the blood. All the factors such as drugs and physical conditions that may impact the TT4 do not impact the FT4. The level of T4 in the blood is high with hyperthyroidism or low with hypothyroidism. Please note that even a high TSH with normal T4 is enough to diagnose hypothyroidism. A rare pattern is an elevated T4 without hyperthyroidism, which may be related to a hereditary condition of thyroid resistance. Elevated Free T4 may also be caused by patients taking heparin or by an acute illness that may briefly cause the binding protein levels to suddenly fall. If an illness becomes severe and chronic, it may decrease the FT4 levels but it is not a thyroid disease.
Resin T3 Uptake: The resin T3 uptake measures the amount of sites for active (unbound) T3 to bind on thyroxine-binding proteins. This test is performed by mixing the blood with radioactive thyroid hormones. These radioactive hormones then combine with binding sites on thyroxine-binding proteins. The blood is then exposed to a substance called a resin that will bind the unbound thyroid hormones, and measure for radioactivity. The result can be expressed as the percent of radioactivity found on the resin compared to the original radioactivity that was added. The more binding sites that are open on the proteins, the lower the resin-uptake result will be, and vice versa. For example, anything that reduces the binding sites, such as elevated testosterone or testosterone replacement therapy, causes a low T4 measurement because it leaves very few binding sites for any more thyroid hormone to bind to it. If T3 is added to the sample of the blood, little T3 will be bound. This pattern would have low TT4 levels and high resin T3 uptake levels. On the other hand, anything that raises the binding sites, such as estrogen or birth control pills, would cause a pattern of high TT4 and low T3 uptake.
Free Triiodothyronine (FT3): This test measures the free T3 hormone levels. This test is rarely completed in traditional endocrinology. It is typically only used in a situation where the patient has hyperthyroid, yet the FT4 levels are normal. However, the FT3 test is the best marker to see what amount of active thyroid hormones is available for the thyroid receptor sites.
Reverse T3 or (rT3): This test measures the amount of reverse T3 that is produced. The production of rT3 typically takes place in cases of extreme stress such as major trauma, surgery, or severe chronic stress. It appears that the increased production of reverse T3 is due to the inability to clear rT3, as well as from elevated cortisol.
Thyroid Antibodies: Thyroid autoantibodies indicate that the body’s immune system is attacking itself. Production of thyroid autoantibodies may create a hypothyroid or a hyperthyroid state. Some antibodies attach to the TSH receptors but do not cause a response. Therefore, the patient will complain of low thyroid symptoms, however, the serum TSH may not be altered. It is just not able to cause a cellular change. On the other hand, some antibodies will bind to the receptor sites and cause over-activation of the thyroid. This will present as elevated T4 levels, a low TSH, and elevated thyroid antibodies.
Low Thyroid Symptoms
Low Thyroid Signs
Drugs That Influence Thyroid Metabolism
Drugs That Decrease TSH Secretion:
Drugs That Alter Thyroid Hormone Secretion by Decreasing Secretion:
Drugs That Alter Thyroid Hormone Secretion by Increasing Secretion:
Drugs That Decrease T4 Absorption:
Drugs That Alter T4 and T3 Transport in Serum by Increasing TBG Concentrations:
Drugs That Alter T4 and T3 Transport in Serum by Decreasing TBG Concentrations:
Drugs That Alter T4 and T3 Transport by Displacement Form Protein-Binding Sites:
Drugs That Alter T4 and T3 Metabolism by Increasing Hepatic Metabolism:
Drugs That Decrease T4 5′ Deiodinase Activity: