We Could Do Better!
Beating cardiovascular disease is achievable when you aim at the correct targets, but I believe that most clinicians are aiming at the incorrect targets related to cardiovascular disease. When I talk to clinicians across the country before my presentation and ask them, “What do you target when trying to prevent cardiovascular disease in your patients?” Most of the physicians questioned about their cardiovascular target of evaluation and care respond by stating that they keep LDL low and work hard on their lipid management. Occasionally some clinicians add comments about their treatment of hypertension and diabetes when questioned about their targets of care when trying to prevent cardiovascular disease. I then go on to teach about how I discovered that there are eight primary inflammatory disease states that lead toward cardiovascular disease. We could do better with the elimination of cardiovascular disease if clinicians everywhere would cast their diagnostic net out further and look beyond just lipids, hypertension, and diabetes! Most patients with cardiovascular disease have 3-4 of the 8 inflammatory disease states at the same time, and missing even one diagnosis causes inflammation to continue to hurt our patients. We have chronic inflammatory biomarkers that give us clues when we have missed a diagnosis, so routinely checking these advanced cardiovascular biomarkers could be a major “game-changer” in our cardiovascular outcomes. I have stated for years that, “Spending money on the front end by doing aggressive preventive care will save us much more money on the back end, making up for the front end costs related to regular advanced cardiovascular biomarker testing.” Everyone wins when good preventive care in medicine is performed. The patients win with great patient outcomes! The insurance carrier wins by ultimate cost savings when they don’t have to pay for expensive care related to heart attacks, strokes, stents, CABG surgery, carotid endarterectomies, and dialysis! Clinicians win by getting to see the patients that they care for diligently enjoying a healthy, productive life!
Diabetes
Diabetes is one of the most important reasons people today have cardiovascular disease. Insulin resistance of Diabetes Type 2 leads to the lowering of the carbohydrate tolerance of each diabetic and prediabetic patient. When the insulin resistant patient overeats their carbohydrate capacity, they experience problems with recurrent liver-pancreas-intraabdominal fat cell inflammatory responses that don’t stop for 4 days. Overeating the carbohydrate capacity also causes a 4 day penalty by the liver synthesizing small dense LDL particles that are usually proatherogenic. This 4 day production of oxidized small dense LDL particles along with the 3 organ inflammatory response caused by excess carbohydrate intake is the number one reason people have cardiovascular disease today! Approximately 64% of people within the United States > 20 years of age are insulin resistant. An independent study carried out within my office demonstrated that insulin patients do not tolerate > 25 grams of carbohydrates each 4 hours. Patients that are not insulin resistant appear to tolerate approximately 90 grams of carbohydrates every 4 hours. Thus it is vital that each patient know if they are insulin resistant, and the only good way that insulin resistance is going to be apparent is by advanced cardiovascular biomarker testing. It is easy to overeat the 90 gram carbohydrate limit of the patient that is not insulin resistant so apparently no one is safe when it comes to diet intake if they are eating fast food or processed food on a regular basis. Carbohydrates have become a “poison” that gradually leads to cardiovascular disease far too often!
When you ask most clinicians what their primary goal of diabetes treatment is they will respond by saying that they are focussing primarily on HgbA1C results or mean blood sugar results. The problem with focussing on HgbA1C or mean blood glucose is that the blood sugar is not the real problem in diabetes! Blood sugar is the friend to cells, as blood sugar (AKA glucose) is the energy form that cells rely on for functionality. The real problem for patients with Diabetes Type 2, the most common form of diabetes, is that they are having problems with insulin resistance that leads to a great deal of inflammation. Insulin is attempting to get the glucose into the cell and the insulin is meeting resistance to glucose transport across the cell membrane. Thus, the real problem with Diabetes Type 2 is not the blood sugar! The real problem with Diabetes Type 2 is the inflammation related to the insulin resistance causing the blood sugar to have problems getting into the cell! The cardiovascular disease that results from Diabetes Type 2 stems from inflammation related to problems associated with insulin resistance. The clinician that is going to make a major difference with their Diabetes Type 2 patients is going to be the physician that identifies insulin resistant patients very early in their disease state and then does something to lessen that insulin resistance! Ultimately, the clinician that is going to help their patients avoid complications of diabetes such as peripheral neuropathy, nephropathy, retinopathy, heart attack, stroke, and CHF, needs to focus not only on eliminating insulin resistance, but also the ability to rejuvenate pancreatic beta cell function. Diabetes Type 2 is potentially reversible, and the Diabetes Type 2 plan of care needs to include a strategy that allows for disease state reversal. Allowing Diabetes Type 2 to progress means that any of the complications of Diabetes Type 2 is now possible. We could do better if we used advanced biomarkers related to diabetes to better evaluate glycemic control, insulin resistance, pancreatic beta cell function and inflammatory changes related to diabetes. We could do better if we educated patients across the country about the need to limit their carbohydrate intake whether they are diabetic or not. We could do better if we focussed more on the inflammation related to diabetes and not the blood sugar only!
There are 4 types of diabetes with most clinicians only focussing on 2 of the 4 types of diabetes. Diabetes Type 1 and Diabetes Type 2 are the primary emphasis of the average clinicians taking care of diabetics today. That means that patients that have Diabetes Type 1.5 and Diabetes Type 3 are being overlooked in most cases.
Missing a case of Diabetes Type 1.5 means that you are going to allow a slowly progressing autoimmune response to gradually destroy the pancreatic beta cell function over a 5 -12 year period due to a slow autoimmune destruction of those beta cells. Much of the autoimmune destruction of Diabetes Type 1.5 is potentially avoidable by early use of analogue basal insulin, pioglitazone, and a GLP-1 agonist medication. We could do better if we would recognize Diabetes Type 1.5 regularly by using an advanced diabetes panel that includes evaluation of the antibody responses seen in Diabetes Type 1.5. The anti-GAD antibody is the most common antibody response seen in Type 1.5 diabetics, albeit these patients could also be seen with Islet Cell Antibodies, Tyrosine Phosphatase Insulin Antibody-2 (1A-2A), and Insulin Auto-Antibodies (1AA).
If Diabetes Type 3 is present and missed by the clinician, it appears that the patient is at risk of going on to become an Alzheimer’s patient. In 2005, the National Institute of Health (NIH) reported on one of their research projects that showed evidence of a new form of diabetes correlating with brain insulin resistance. The NIH funded research found that Alzheimer’s patients lacked intracellular glucose and insulin growth factor in their frontal cortex, hypothalamus, and hippocampus while the adjacent cerebellum had normal amounts of intracellular glucose and insulin growth factor. Alzheimer’s syndrome specifically involves a shrinkage of the frontal cortex, hypothalamus, and hippocampus, and now it appears that the shrinkage of this brain matter relates to a form of insulin resistance that focusses on the brain specifically! Diabetes Type 2 is insulin resistance of the body from the neck down and Diabetes Type 3 is insulin resistance of the brain. The genetic expression of Diabetes Type 2 and Diabetes Type 3 appear to be distinctly different from one another. When a patient is becoming insulin resistant in their brain, they are also becoming Leptin resistant making Diabetes Type 3 identifiable. A patient with an elevated Leptin level or an elevated Leptin:BMI ratio is likely to be a patient with Diabetes Type 3. There are other potential biomarkers being studied that might also help us identify patients with Diabetes Type 3. This research related to Diabetes Type 3 is in it’s infancy, so there are still many unanswered questions. One important unanswered question is “How long does it take from the time Diabetes Type 3 turns on until the patient begins developing problems with Alzheimer’s syndrome? Do all patients that become Leptin resistant alway become Alzheimer’s patients eventually? If you treat a patient that already has Alzheimer’s syndrome with Diabetes Type 3, can you slow down or halt the progression of their Alzheimer’s disease state?” Until the studies related to these questions become available, I think the focus of Diabetes Type 3 management has to be on down regulating the genetic expression that is leading to this form of brain insulin resistance seen by an elevated Leptin level or elevated Leptin:BMI ratio. The combination of pioglitazone (Actos) with a GLP-1 agonist (i.e. Byetta, Victoza, Bydureon, Tanzeum, and Trulicity) often is enough to down regulate the Diabetes Type 3 genetic expression, but occasionally an analogue basal insulin needs to be added to the regimen to completely stop this diabetes from causing brain damage. The decision related to adding analogue basal insulin to the Diabetes Type 3 patient’s treatment regimen corresponds to whether the fasting insulin level or the proinsulin:C-peptide ratio is elevated significantly regardless of the HgbA1C level. We could do better if we would identify patients with Diabetes Type 3 early in it’s disease state so that we could limit the amount of brain matter that is lost because of Diabetes Type 3! Using advanced cardiovascular biomarkers to identify developing Diabetes Type 3 makes good sense as these advanced biomarkers are the only way we will be able to identify anyone with Diabetes Type 3!
In summary, we could do better with diabetes management by focussing more on the inflammation related to insulin resistance rather than aiming at the blood sugar control only. It is the insulin resistance that causes the inflammation related to CV disease, and there are multiple biomarkers that relate to insulin resistance. Detecting the insulin resistance earlier in our physical exam workups could lessen complications of Diabetes Type 2 substantially by early intervention in the disease process. Detecting when your Diabetes care is controlling inflammation to the six key organ areas related to diabetes ultimately decides when your diabetes care is complete! Furthermore, consideration of Diabetes Type 1.5 and Diabetes Type 3 in our routine workups will help each patient avoid serious preventable complications that would include loss of pancreatic beta cell function and Alzheimer’s syndrome.
Dyslipidemia
Most clinicians within the United States look at cardiovascular disease as a problem related to lipids primarily. I often hear clinicians say, “If I can just get my patient’s lipids under control, I can make cardiovascular disease go away,” but nothing can be further from the truth! Cardiovascular disease is caused by inflammation, and the lipids are influenced by inflammation to cause plaque and plaque rupture which is the basis of cardiovascular disease.
Truth be told, there are problems with the way we look at lipids! Most clinicians use the traditional lipid profile to evaluate lipids but the “old school” lipid profile has some terrible flaws. For starters, the “C” in LDL-C stands for “cholesterol,” meaning the measurement of LDL-C in a standard lipid profile relates to the measurement of the cholesterol within LDL content in blood. Approximately 64% of people over the age of 20 within the United States are insulin resistant and insulin resistance drastically changes the content of cholesterol within LDL. As a person becomes insulin resistant, LDL-C begins to lose cholesterol, replacing the cholesterol with triglycerides. The insulin resistant patient has LDL-C that measures artificially low because of the trade of cholesterol for triglycerides as the patient overeats their carbohydrate capacity. We have heard for years about insulin resistant patients having small dense LDL-C (sdLDL-C), but maybe you haven’t realized that the smaller, denser, LDL-C comes from this transfer of cholesterol for triglycerides making the LDL smaller and denser. This conversion of LDL-C to the smaller denser form of LDL-C means that the sdLDL-C production leads to an artificially low LDL-C. The problem with this is that an LDL-C of 65 mg/dl could correlate with a LDL-P of 1900 nmol/L. The LDL-C at 65 mg/dl is low and seems normal, while the LDL-P represents a patient at the 95th percentile of highest LDL levels within the United States. The LDL-C is seemingly low because the prolonged insulin resistance and the repetitious overeating of carbohydrates has made the cholesterol leave the LDL-C while replacing the cholesterol with triglycerides. Physicians need to order LDL-P with each patient as insulin resistance is too common to trust our clinical decision making to a LDL-C level.
While lipids are not the cause of cardiovascular disease, lipids do participate in the production of plaque and plaque rupture. When you make your lipid treatment decisions based on the false information of the LDL-C, you can make the wrong decision regarding if the LDL needs to be treated or not. It should make sense that insulin resistance creates a disconcordance between LDL-C and LDL-P, and this differing information will always favor the advanced cardiovascular biomarker LDL-P. It should be apparent by now that since insulin resistance is so common all across the U.S., all clinicians should be ordering advanced cardiovascular lipid panels!
Hypertension
When a patient presents with hypertension in the United States, a clinician will often use 1,2, or 3 medications to bring hypertension down to the normal level. The problem with hypertension care in the United States is that usually hypertension is treated with the appropriate number of medications that lead to BP control, then over time BP gets worse. Normal “Standard of Care” hypertensive treatment leads to a gradual increase of plaque, and a gradual further increase of BP. We often see that the patient treated by standard of care often gets another BP medication several times until eventually this person has a heart attack or a stroke. Proper treatment of the hypertensive patient means using 1,2, or 3 BP medications to gain adequate BP control in the patient. After initially establishing adequate control of BP, it is important to control the blood vessel inflammatory state and the circulating lipids. Plaque regression is made possible when the inflammation and the lipids are controlled satisfactorily for a season of time. Controlling LDL-P < 900 and Apo B < 50 usually provides the lipid control needed for plaque regression. The hs-CRP is a good advanced biomarker to decide if you have less inflammation entering the bloodstream than you have leaving the bloodstream with the ideal hs-CRP being < 1.0 mg/L. It is good to see the fibrinogen level < 390 mg/dl as this represents how regularly the patient is doing what is necessary to remove inflammation since fibrinogen responds to internal inflammatory changes rapidly. As a patient develops plaque regression with control of BP, inflammation, and lipids, the patient gradually gets off one BP medication after another. Ultimately the patient treated holistically for BP, inflammation, and lipids, gets off of all their BP medications and regains cardiovascular health. Treating BP without treating the associated causes of inflammation and dyslipidemia makes no logical or physiological sense. We could ultimately do better by paying more attention to inflammatory changes and lipid changes while we treat hypertension!
Sleep Disorders
Sleep is a vital part of life, as it is during sleep we make brain chemicals that are vital to an enjoyable life filled with energy, good moods, robust memory and concentration. There are 5 stages of sleep, stages 1,2,3,4, & REM. Brain chemistry is produced during stages 3 and 4 of sleep, and it is important that 25% of each night’s sleep time is spent in stages of 3 and 4 of sleep. When a patient has all the chemical substrates needed to make the various brain chemicals (i.e. methylfolate, vitamin D, and omega-3), and they spend 25% of their night in stages 3 and 4 sleep (AKA N3 sleep), they will make plenty of chemicals needed to carry out all the upcoming days activity. When these substrates of the brain chemicals are deficient or there is very little sleep time spent in N3 sleep, the patient will then wake up tired due to a lack of needed brain chemicals. Cardiovascular disease begins to develop when patients don’t have the needed brain chemicals as adrenaline will now have to take charge of activating brain neurons. Adrenaline is a rather inefficient means of helping the neurons do their job as it may take 10 - 15 signals sent across the neuron before the neuron is activated by adrenaline “jumpstarting” the neuron at the postsynaptic membrane (back side of the nerve). The patient waking up with very limited brain chemicals will have to circulate high levels of adrenaline 24 hours per day, 7 days per week, and this prolonged exposure of the blood vessels, heart, kidney, and brain to high levels of adrenaline all day is inflammatory in nature. The persistently high levels of adrenaline leads to the development of plaque within blood vessels that ultimately can cause clogged arteries or plaque rupture. The persistently high levels of adrenaline can also cause problems with the heart stiffening leading to the potential for developing congestive heart failure. Adrenaline in high levels circulating all day long is also caustic the kidneys as well leading to progressively worsening chronic kidney disease (CKD). This marked elevation of adrenaline around the clock may even trigger the Diabetes Type 3 activation that ultimately leads to brain tissue damage.
For the most part sleep disorders are getting overlooked across the United States. In 2000, CMS reports that 90% of primary care physicians (PCP’s) did not make one diagnosis of obstructive sleep apnea (OSA) in their Medicare patient population. It would be essentially impossible for a physician taking care of a modest number of Medicare patients to not have a single diagnosis of OSA in at least one patient. In a practice with 35% Medicare patient population, it would be unlikely to not have at least 5 cases of OSA per week. Thus one thing we could do better is begin to identify who has OSA in our practice! A good physical exam will often tell you who has OSA as there are three findings that make OSA likely. When looking for evidence of OSA on the physical exam, look for: 1) a drooping soft palate, 2) an enlarged or elongated tongue, and 3) bilateral intranasal airway obstruction.
When sleep disorder diagnoses are missed such as obstructive sleep apnea, we are exposing patients to much higher risks of cardiovascular disease. Once we diagnose OSA in a patient, it is important that we work aggressively with their use of CPAP or BiPAP. Approximately 70% of patients that have OSA never acquire the ability to wear the CPAP or BiPAP treatment that is prescribed! If each clinician got more acquainted with sleep medicine, they would be better at helping patients acquire the skills needed to adapt to CPAP or BiPAP use. It is obviously very unnatural to wear a device on your face to go to sleep but this is a life and death issue! Many things in life are acquired tastes (i.e. people who smoke acquired the taste to smoke as the first cigarette smoked was likely not a good experience) and the CPAP and BiPAP are no different. With the proper guidance by the well trained clinician, each patient can learn how to acquire the skills to use the CPAP or BiPAP proficiently. Well-trained CPAP and BiPAP patients often tell me that if their house was ever on fire, the first thing that they would grab on the way out of the house is their CPAP or BiPAP. If you are having difficulty getting your patient comfortable with CPAP or BiPAP, you might consider ordering a “PAP Nap” which is a procedure done at the sleep lab to evaluate the patient over a 2-3 hour period to find out what works and doesn’t work to make them able to use the CPAP. You may have to consider giving the claustrophobic patient a 1-2 month prescription for lorazepam (Ativan) to help them get more accustomed to use of the CPAP or BiPAP. It is vital that every PCP office be able to download sleep card information at each office visit as this is your only way to keep up with how well the patient is using their CPAP or BiPAP as well as assessing how well the CPAP or BiPAP are working. Most medical supply companies that sell CPAP/BiPAP equipment to your patients are glad to assist you in acquiring the smart card readers and showing you how to use the equipment.
There are 3 primary sleep disorders: 1) Obstructive Sleep Apnea, 2) Restless Leg Syndrome (RLS), and 3) Narcolepsy. While obstructive sleep apnea is by far the most common of the sleep disorders, it is important not to forget about RLS and narcolepsy! Restless Leg Syndrome can cause a rather large number of nightly arousals and these arousals cause a deficiency of N3 sleep. Narcolepsy patients tend to bypass N3 sleep as they go from stage I, stage II, to REM sleep quickly, bypassing N3 sleep! Since N3 sleep is where the brain chemicals are made, restless leg syndrome and narcolepsy patients end a night’s sleep just like obstructive sleep apnea patients without their needed brain chemicals.
A better history might help the Restless Leg Syndrome patient get detected. Usually the RLS patient goes to bed with the covers in place and they often wake up with their bed covers out of place. If the RLS patient is married their spouse will often discuss how often their legs move during the night, as the RLS patient is often very actively moving around the bed.
Narcolepsy is definitely more common than we think! I diagnosed 4 cases of narcolepsy during the first 26 years of my career and during the last 2 years I have diagnosed 26 cases of narcolepsy. The advanced biomarkers will help you make the narcolepsy diagnosis! I learned several years ago that the patient with essentially no chronic inflammation has a Lp-PLA2 level of 80 ng/ml and a Myeloperoxidase (MPO) of 100 pmol/L. When you have patients well-treated for all known inflammatory disease states that cause chronic inflammation, and your Lp-PLA2 and MPO remain elevated significantly, a diagnosis has been overlooked. When narcolepsy is that missed diagnosis, the patients will tell you about their rather significant problem with fatigue and drowsiness. Narcolepsy patients often have rather disrupted sleep at night and may sleep often at unnatural times during the day. Questions to ask the possible narcolepsy patient include: 1) Do you have rather vivid dreams that you remember for days and weeks later? (hypnogogic hallucinations), 2) Do you have episodes of sudden weakness in your upper or lower extremities that might cause you to fall or drop things? (cataplexy), and 3) Do you ever wake up and find yourself paralyzed for a few minutes? (sleep paralysis). The persisting chronic inflammation levels attributed to Lp-PLA2 and MPO have caused me to pick up more cases of narcolepsy than any of the other sleep specialists in the city where I live, making me further appreciate the value of advanced cardiovascular biomarkers!
Chronic Kidney Disease (CKD)
The “standard of care” clinician uses the findings of the regular metabolic profile (i.e. BUN, Creatinine, and Albumen) to calculate the estimated glomerular filtration rate (eGFR) of their patients. There are two primary methods of calculating the eGFR using the “standard of care” methodology, namely the Modification of Diet in Renal Disease (MDRD) calculation or the Cockcroft-Gault calculation. Both the MDRD calculation and the Cockcroft-Gault calculation are inaccurate at identifying chronic kidney disease (CKD) at the early stages (stages I and II). Most labs using either the MDRD or the Cockcroft-Gault calculations to estimate glomerular filtration rate report normals as > 60 ml/min/1.73m2. This means that clinicians using the “standard of care” methods of measuring estimated GFR (eGFR) are not detecting that the patient has problems until that patient is at stage III CKD. There is an advanced biomarker, Cystatin C, that can help you detect CKD at stage II which represents an eGFR of 60-90 ml/min/1.73m2. There are only 5 stages of CKD, so this makes identifying CKD earlier rather important as CKD is a significant cardiovascular disease risk factor! Once you get to CKD stage III, you have an eGFR of 30-59 and erythropoietin deficiency becomes an issue. People deficient of erythropoietin become rather anemic and their bone marrow will not produce significant red blood production leading to significant anemia. CKD patients having severe anemia due to erythropoietin deficiency require expensive injections of erythropoietin medication to maintain an adequate blood supply to avoid left ventricular hypertrophy development. If every physician started checking Cystatin C levels we would have information on the patient as they entered the early CKD states, lowering the risk that the patient will develop left ventricular hypertrophy due to erythropoietin deficiency related anemia. Millions of dollars in medical expense money could be avoided if the CKD patient is caught early! We could do better if every PCP started checking Cystatin C levels in their routine lab panels to begin improving cardiovascular risk reduction, while they will also be lowering overall medical costs!
Mental Health Disorders
Mental health disorders have a correlation with brain chemical substrates (i.e. brain food) and sleep quality, yet so few clinicians taking care of mental health disorders are are evaluating brain chemical substrates or sleep. The main substrates of note are methylfolate, vitamin D, and omega-3, all measurable by a blood test. The area of sleep interest is stage N3 sleep, also known as stages 3 and 4 of sleep.
The MTHFR genetic abnormality affects the ability to break down folic acid into the fifth breakdown product, methylfolate. We need methylfolate to synthesize 4 important brain neurochemicals: serotonin, melatonin, dopamine, and norepinephrine. People that are homozygously effected by the MTHFR genetic abnormality can only produce a 35% capacity for production of these 4 brain neurochemicals at birth causing these patients to have Attention Deficit Disorder symptomatology in early childhood. By age 30 these homozygously impaired MTHFR genetic abnormality patients are hardly producing any of these 4 neurochemicals at all, surviving primarily on high circulating levels of adrenaline to make their neurons respond to signaling (adrenaline can jumpstart the neurons by attaching to the post-synaptic membrane of a neuron). Patients with heterozygous MTHFR genetic abnormalities act similarly to the homozygous patient effected by the MTHFR genetic abnormality, except the heterozygous MTHFR patients are just 30 years behind them with their symptoms. At 30 years of age the heterozygous MTHFR genetic abnormality patient is beginning to have Attention Deficit Disorder type symptoms and by 50 years of age the heterozygous MTHFR genetic abnormality patient is often withdrawing from society, just going out to do what they have to and then retreating to their homes hoping everyone will leave them alone. Little things get on the nerves of MTHFR genetic abnormality patients and major things often take MTHFR genetic abnormality patients to a bad place mentally. If clinicians providing care for mental health patients would begin testing each mental health patient for the MTHFR genetic abnormality, we could make an enormous improvement in both mental health and cardiovascular outcomes! When the adult patients are recognized with a MTHFR genetic abnormality, they should be prescribed Deplin 15 mg daily forever. The MTHFR 677 genetic abnormality patient usually responds quickly to the Deplin prescription, improving significantly by week 8 of treatment but not maximally improved until about 18 months after treatment has begun. The MTHFR 1298 genetic abnormality patient responds more slowly to treatment with Deplin 15 mg daily dosing noticing improvement in 4 stages: 1) by the end of month 3, patients notice that their sleep has improved, 2) by the end of month 6, patients are noticing that their memory is getting better as is their ability to focus on a project, 3) by the end of month 12, their energy is beginning to improve but not enough to write home about, and 4) by the end of month 18, these MTHFR 1298 genetic abnormality patients usually sleep well, have good focus and concentration skills, moods are improved, and energy is now substantially better. With 60% of the U.S. population having at least one copy of the MTHFR genetic abnormality, we could really improve mental health substantially by universally ordering the MTHFR 677 and 1298 genetic tests on all of our patients!
Vitamin D and Omega-3 deficiencies effect mental health by their participation in the synthesis of serotonin, a very important brain neurochemical that effect mood, memory, concentration, energy, and pain control. It is very easy to measure both Vitamin D and Omega-3 levels and effectively make sure that you have enough of both of these substrates so that serotonin production is not limited by their deficiencies.
When attempting to help mental health patients, it is vital that we consider their sleep quality and quantity, as it is during sleep that the majority of brain neurochemicals are made. There are 5 stages of sleep, stages 1,2,3,4, and REM, and our brain neurochemicals are synthesized during stages 3 and 4 of sleep. When looking at these sleep stages on a sleep study, you will find that stages 3 and 4 of sleep are called N3 sleep, since both stages behave very similarly. We need to make sure that our patients get at least 25% N3 sleep to assure that the patients are capable of making adequate brain neurochemicals to perform the next day’s activities.
When we make sure that our patients have adequate amounts of substrates (methylfolate, vitamin D, and omega-3) as well as adequate amounts of N3 sleep, then we can observe what their baseline mental state is. If the patient continues to exhibit mental health issues such as anxiety, depression, or bipolar characteristics after the substrates and sleep are managed properly, then these patients will respond to most of the appropriate type mental health medications used. Mental health patients treated in this manner feel better, enjoy life more, and have much better cardiovascular outcomes! We could do better with mental health care if all clinicians managing mental health care would measure all levels of “brain food” while also measuring the amount of time spent in N3 sleep!
Genetics
Historically, I think many clinicians as well as patients have thought of genetics as simply their “lot” in life and accepted that their fate could not be altered in this area of genetics. We now can use genetic testing to make amazing changes in patient outcomes! A good example of using genetic information to make a positive change in outcome is the treatment of MTHFR genetic abnormality patients with daily Deplin intake. We use Actos as a prescription means to down-regulate the genetic expression of patients with Diabetes Type 2 and Type 3. Pharmacogenomics testing is becoming more popular to better understand how each patient metabolizes medications through the Cytochrome p450 system, making it possible to improve patient medication outcomes with less adverse drug reactions. Apo E testing is used to identify what to expect from a patient in the cardiovascular arena. Knowing that a patient has an Apo E4 gene might make a clinician be more aggressive with medical management as Apo E patients tend to have more problems with developing atherosclerosis and inflammatory problems. It appears that identifying the entire human genome sequence has given us the potential to make amazing improvements in patient outcomes, as many more genetic tests are likely to be offered in the future due to the continue genetic research ongoing. We could do better if more clinicians were actively taking advantage of the genetic information that is available today!
Inflammatory and Autoimmune Disease States
Since inflammation is at the core of cardiovascular disease, it should not come to a surprise to anyone that inflammatory and autoimmune disease states cause increases in cardiovascular disease. Inflammatory factors related to the illness spill over into the bloodstream setting the stage for plaque development, plaque rupture, heart stiffening, and kidney damage. The goal of treatment for each of these inflammatory and autoimmune disease states is to modify the disease state into remission, but disease modification of these inflammatory and autoimmune disease states is not often easy to accomplish. At any given time, our body’s immune system is carrying out work at many fronts with other disease states while also trying to deal with inflammatory and autoimmune disease states. It stands to reason that we need to quieten all the extraneous inflammatory disease states when dealing with an autoimmune illness, so the immune system can focus as much energy to the autoimmune illness treatment as possible. For instance, when an insulin resistant patient overeats carbohydrates there is an immunologic reaction within the liver, pancreas, and intraabdominal fat cells. Patients with an autoimmune condition such as rheumatoid arthritis taking disease modifying medication in hopes to place the RA in remission should be extra careful about how they are eating carbohydrates to avoid the added stress to the immune system that comes from liver, pancreas, and intraabdominal fat cell response to excess carbohydrate intake. I often see patients struggling with their RA get remarkably better with their disease modification treatment after I place the patient on Actos (down-regulating the insulin resistance patient’s genetic expression that is making them insulin resistant) and teaching them how to follow a low carbohydrate/reduced saturated fat diet. Where we could do better in our treatment of inflammatory and autoimmune disease states would be to cast a “wider net” over inflammatory disease states and simultaneously attempt to lessen immune system workload which is in essence, ending the “divide and conquer” problems that our present inflammatory/autoimmune patients often have to deal with today!
