Functional Medicine

It is critical hormone therapy is monitored properly. To obtain only serum or salivary levels of hormones is not adequate. You must know how your hormones are being metabolized by your body based on numerous epigenetic factors, such as diet, exercise, genetics, environmental toxins, and medication. For example, estradiol (estrogen) does not cause cancer! It is how you metabolize to various metabolites that increase your risk of cancer. We measure the metabolites by the DUTCH test and adjust the results to the more beneficial metabolite not associated with cancer.

Erectile dysfunction is not a Viagra deficiency! Extensive evaluation is carried out to determine the cause.

Insulin, a hormone made by the pancreas, allows cells to absorb glucose so it can be used as energy. The cells of individuals with insulin resistance are unable to use insulin effectively. Insulin levels increase in an attempt to force glucose in the cells. Elevated insulin levels are associated with central body weight gain, cancer, heart disease, depression, and Alzheimer’s, just to name a few! Insulin resistance is an epidemic worldwide.

Salivary levels are determined throughout the day and if they are abnormal, the question is always, “WHY?”

A complete evaluation is performed to determine the cause of depression, anxiety, manic depression, and other disorders.

Organic acids are chemical compounds excreted in the urine of mammals that are products of metabolism. Metabolism is the sum of chemical reactions in living beings by which the body builds new molecules and breaks down molecules to eliminate waste products and produce energy.

Organic acids in urine are often present at 100 times their concentration in the blood serum and thus are more readily detected in urine. This is why organic acids are rarely tested in blood or serum. The number of organic acids found in urine is enormous. Over 1,000 different organic acids have been detected in urine since this kind of testing started. The results are invaluable in determining the cause of an individual’s problems.

Fungi are able to grow on almost any surface, especially if the environment is warm and wet. Inner wall materials of buildings, wall paper, fiber glass insulation, ceiling tiles, and gypsum support are all good surfaces for fungi to colonize. These fungi then release mycotoxins into the environment, causing symptoms of many different chronic diseases. Diseases and symptoms linked to mycotoxin exposure include fever, pneumonia-like symptoms, heart disease, rheumatic disease, asthma, sinusitis, cancer, memory loss, vision loss, chronic fatigue, skin rashes, depression, ADHD, anxiety, and liver damage.

MycoTOX screens for 11 different mycotoxins, from 40 species of mold, in one urine sample.

The Comprehensive Stool Analysis detects the presence of pathogenic microorganisms such as yeast, parasites, and bacteria that contribute to chronic illness and neurological dysfunction. It provides helpful information about prescription and natural products effective against specific strains detected in the sample. The test also evaluates beneficial bacteria levels, intestinal immune function, overall intestinal health, and inflammation markers.The Comprehensive Stool Analysis detects the presence of pathogenic microorganisms such as yeast, parasites, and bacteria that contribute to chronic illness and neurological dysfunction. It provides helpful information about prescription and natural products effective against specific strains detected in the sample. The test also evaluates beneficial bacteria levels, intestinal immune function, overall intestinal health, and inflammation markers.

Many chronic disorders come from digestive problems and inadequate nutrient absorption. Proper gastrointestinal function is needed to eliminate toxic substances, pathogenic microbes, and undigested food particles from the body to prevent health problems. Nutrients require a specific internal environment to be properly digested and transported throughout the body.

Abnormal intestinal microorganisms in the GI tract are widely known to cause disease. Research shows a relationship between the GI tract and the neurological, hepatic, and immune systems. For example, excessive yeast produces toxic substances that can pass through the blood-brain barrier and alter neurological functioning causing “brain fog,” behavior problems, and learning difficulties.

THE COMPREHENSIVE STOOL ANALYSIS INCLUDES:

• Parameters for digestion and absorption
• Cultures for bacteria and yeast
• Parasite testing
• Sensitivity panels
• Inflammatory markers
• Stool metabolic markers
• Infectious pathogens

The gastrointestinal tract harbors a tremendous diversity of microbial life. These microbes, known collectively as the “microbiome,” are directly involved in digestion and immune function, and appear to also play a role in multiple additional human biologic processes. Intestinal dysbiosis refers to an abnormality of the gut microbiota, either due to low microbial diversity, suboptimal levels of commensal microbes, or an abundance of pathogenic microbes. Alterations to the microbiome have been linked to a variety of disorders, including gastrointestinal diseases, diabetes, kidney disease, and cardiovascular disease.

Glyphosate is the world’s most widely produced herbicide and is the primary toxic chemical in Roundup™, as well as in many other herbicides. In addition, it is a broad-spectrum herbicide used in more than 700 different products from agriculture and forestry to home use. Glyphosate was introduced in the 1970s to kill weeds by targeting the enzymes that produce the amino acids tyrosine, tryptophan, and phenylalanine. The enzymes of many bacteria are also susceptible to inhibition by this chemical, thus altering the flora of many animals. Usage of glyphosate has since amplified after the introduction of genetically modified (GMO) glyphosate-resistant crops that can grow well in the presence of this chemical in soil.

Recent studies have discovered glyphosate exposure to be a cause of many chronic health problems. It can enter the body by direct absorption through the skin, eating foods treated with glyphosate, or drinking water contaminated with glyphosate. A recent study stated that a coherent body of evidence indicates that glyphosate could be toxic below the regulatory lowest observed adverse effect level for chronic toxic effects, and that it has teratogenic, tumorigenic, and hepatorenal effects that can be explained by endocrine disruption and oxidative stress, causing metabolic alterations, depending on dose and exposure time. The World Health Organization International Agency for Research on Cancer published a summary in March 2015 that classified glyphosate as a probable carcinogen in humans. Possible cancers linked to glyphosate exposure include non-Hodgkin lymphoma, renal tubule carcinoma, pancreatic islet-cell adenoma, and skin tumors. Studies have also indicated that glyphosate disrupts the microbiome in the intestine, causing a decrease in the ratio of beneficial to harmful bacteria.

Thus, highly pathogenic bacteria such as Salmonella entritidis, Salmonella gallinarum, Salmonella typhimurium, Clostridium perfringens, and Clostridium botulinum are highly resistant to glyphosate, but most beneficial bacteria such as Enterococcus faecalis, Enterococcus faecium, Bacillus badius, Bifidobacterium adolescentis, and Lactobacillus spp. were found to be moderately to highly susceptible. The relationship between the microbiome of the intestine and overall human health is still unclear, but current research indicates that disruption of the microbiome could cause diseases such as metabolic disorder, diabetes, depression, autism, cardiovascular disease, and autoimmune disease.

Many studies have shown that people with higher (vs. lower) Omega-3 Index levels are at decreased risk for a variety of diseases, including heart disease, stroke, dementia, and depression, to name a few. These people even live longer than those with lower levels. Raising your Omega-3 index and keeping it up should help reduce your risk these conditions. Omega-3 fatty acids are found primarily in fish, especially “oily” fish. The two most important Omega-3 fatty acids are EPA and DHA. It should be noted that Omega-3 fatty acids from flaxseed oil (alpha-linolenic acid, or ALA) will have little to no effect on your Omega-3 Index. Therefore, ALA is not an effective substitute for EPA and DHA. To make sure your Omega-3 Index remains in the target range you should re-check it every six months.Many studies have shown that people with higher (vs. lower) Omega-3 Index levels are at decreased risk for a variety of diseases, including heart disease, stroke, dementia, and depression, to name a few. These people even live longer than those with lower levels. Raising your Omega-3 index and keeping it up should help reduce your risk these conditions. Omega-3 fatty acids are found primarily in fish, especially “oily” fish. The two most important Omega-3 fatty acids are EPA and DHA. It should be noted that Omega-3 fatty acids from flaxseed oil (alpha-linolenic acid, or ALA) will have little to no effect on your Omega-3 Index. Therefore, ALA is not an effective substitute for EPA and DHA. To make sure your Omega-3 Index remains in the target range you should re-check it every six months.

FATTY ACID BENEFITS (EPA, DHA, GLA)

• Lowers LDL and increases HDL cholesterol; decreases blood clotting time
• Anti-arrhythmic, anti-inflammatory effect that benefits heart tissue
• Structural in brain and retinal tissue; improves learning and memory
• Critical in fetal and infant development
• Improves hyperactivity in children and depression in adults
• Treatment for autoimmune disorders, kidney disease, PMS, RA, MS
• Improves skin integrity

One of the earliest manifestations of endothelial dysfunction is nitric oxide (NO) deficiency, which promotes atherosclerosis. ADMA (asymmetric dimethylarginine) and SDMA (symmetric dimethylarginine), its structural isomer, are metabolites of L-arginine, an amino acid that is catalyzed to L-citrulline and NO by nitric oxide synthase (NOS). One of the earliest manifestations of endothelial dysfunction is nitric oxide (NO) deficiency, which promotes atherosclerosis. ADMA (asymmetric dimethylarginine) and SDMA (symmetric dimethylarginine), its structural isomer, are metabolites of L-arginine, an amino acid that is catalyzed to L-citrulline and NO by nitric oxide synthase (NOS). 

Both ADMA and SDMA have distinct pathophysiologies and manifestations. ADMA is a competitive inhibitor of NOS, thereby reducing NO production and promoting endothelial dysfunction. SDMA also interferes with NO production, but does so indirectly by reducing the cellular availability of arginine. ADMA is primarily cleared through enzymatic degradation in the bloodstream and identifies subclinical cardiovascular disease. Conversely, SDMA is primarily excreted in the urine and identifies reduced renal function.

Clinical Use

ADMA/SDMA may be measured in individuals with multiple risk factors for the development of cardiovascular disease. Fasting is recommended, but not required. 

Clinical Significance / Cardiovascular Significance

Elevated ADMA levels are associated with the presence of hypertension1, insulin resistance1, and hyperlipidemia.

Elevated ADMA levels are associated with subclinical atherosclerosis. Elevated ADMA concentrations correlate with internal carotid artery bulb intimal media thickness, a hemodynamically unstable region vulnerable to nitric oxide deficiency and plaque formation.

Elevated ADMA in young adults has been associated with increased coronary artery calcification (CAC) score.

Individuals with established coronary artery disease and elevated ADMA levels have more than twice the risk for adverse events (MI, stroke) than those with normal ADMA levels6. 

Renal Significance

Elevated SDMA levels positively correlate with reduced renal function as measured by eGFR.

Gut microbes live symbiotically within the human digestive tract and play important roles in host defense, immunity, and nutrient processing and absorption. This diverse community is unique to each person and influenced by both acute and chronic dietary exposures to various food sources. Gut microbes live symbiotically within the human digestive tract and play important roles in host defense, immunity, and nutrient processing and absorption. This diverse community is unique to each person and influenced by both acute and chronic dietary exposures to various food sources. 

Nutrients such as phosphatidylcholine (also known as lecithin), choline, and L-carnitine are abundant in animal-derived products such as red meat, egg yolk, and dairy products. When consumed, these nutrients are processed by gut bacteria, resulting in the release of various metabolites, including TMA (trimethylamine), into the blood. TMA is then transported to the liver where it is converted into TMAO (trimethylamine N-oxide). TMAO has been shown to regulate various physiological processes which are involved in the development of atherosclerosis, as well as reverse cholesterol synthesis and platelet function. 

Clinical Use

TMAO may be measured in individuals with one or more risk factors for the development of cardiovascular disease and/or individuals who may benefit from intensive dietary intervention. 

Clinical Significance

There is a dose-response relationship between TMAO and atherosclerotic burden and major adverse cardiovascular events incidence (MACE: MI, stroke or death).  In stable individuals undergoing elective cardiac evaluation, elevated TMAO levels are associated with increased risk of cardiovascular disease1 and MACE5.  Increased plasma L-Carnitine (a dietary precursor to TMAO) is associated with cardiovascular risk only when TMAO is simultaneously elevated via the metabolism by specific gut microbes.

In subsets of this population considered low risk (<65 years old, <100mg/dL LDL-C, normal blood pressure, non-smokers, low levels of MPO), elevated TMAO remained a significant predictor of MACE risk.

Elevated TMAO increases 7-year mortality risk in patients admitted to the ER who presented with acute coronary syndrome as well as 5-year mortality risk in patients with CAD receiving optimal therapy and PAD patients.