Addressing Accurate Diagnosis And The Significance of Patient Compliance
We are surrounded by pre-diabetes (PD), insulin resistance (IR) or syndrome X—all names for the same thing. While we all may know what to look for, it can still sometimes be difficult to see.
Below are some of the hallmark symptoms of PD.
· Central obesity.
People with elevated insulin will store every extra calorie they eat as central fat. On days they are trying to be “good” by skipping meals or starving themselves (a bad idea) they will burn muscle and not fat. The result is an overweight trunk with thin legs and arms.
· Constant hunger.
When a person with PD eats a high glycemic index (GI) food, the blood glucose (BG) rises, followed by an exaggerated insulin release, resulting in reactive hypoglycemia, which in turn results in hunger. If he “fixes” hunger with another high GI food, the cycle will start all over again.
· Blurred vision
BG is a major component of the osmotic pressure in the blood. With swings in BG come swings in osmotic pressure, causing a distortion of the lens and cornea of the eye, which results in blurred vision.
· Fatigue.
In PD, insulin receptors are insensitive to insulin. This results in low muscle concentrations of available carbohydrate and inefficient energy metabolism.
· Depression.
The metabolic derangement resulting from PD has many psychological effects. Depression may arise from the same type of energy metabolism inefficiencies seen in fatigue.
· Brain fog.
The brain is the most prolific consumer of glucose of any organ. With problems in glucose metabolism and transport, brain fog seems to arise.
Many clinical tests exist to diagnose PD, but some are more accurate than others.
· Fasting blood glucose (FBG). FBG is a late indicator of pre-diabetes. The metabolic disorders known as PD may exist for 3 to 5 years prior to diagnosis if done by FBG. A fasting blood sugar level between 100 and 125 mg/dL is considered pre-diabetes. Optimal blood sugars are significantly lower—some say as low as 70.
· Postprandial blood glucose (PBG) and glucose/insulin tolerance testing (GITT). PBG is a better indicator of pre-diabetes because it is more like a stress test of the glucose metabolism system. I generally do a GITT with a fasting insulin and FBG, then a 75 gram glucola followed by a 2-hour postprandial insulin level and BG. I look for fasting insulin less than 10 and FBG less than 95 (some say 85). The postprandial limits are insulin less than 3 times the fasting level and not greater than 30, the BG not greater than 140 (although I think that is too high).
· Lipids. Lipid levels are another early indicator of PD. We know that those with PD have elevated triglyceride and low HDL levels. An ideal triglyceride to HDL ratio (THR) is less than 2. A THR greater than 4 is worrisome and probably represents PD. A THR of 6 or more is a significant risk factor for heart disease.
Maintaining a high index of suspicion for pre-diabetes is key to the diagnosis. Following proper diagnosis, one of the key challenges with treatment is patient compliance.
The treatment of PD is primarily a lifestyle issue. While there are pharmacological treatments available, studies have shown them inferior to lifestyle management. The primary problem with lifestyle management is compliance. In my early practice I had a “my way or the highway” type of approach to lifestyle. With age comes some humility, accompanied by greater empathy for my patents.
Whether the treatment plan features a low glycemic index diet, increased activity, or various nutrients such as fish oil or lipoic acid, theadvice is sound. What fascinates me is how we often do not do what we know is good for us. I am trained in functional medicine. This means I assess the biochemical individuality of the patient, consider his current lifestyle, and then determine whether the two are ideally compatible. Once this is accomplished I set up a program with follow-up visits. It is not uncommon for the subsequent visits to reveal a lack of follow-through with the program. In days gone by I would have been quite irritated by this. I now see it as the therapeutic moment.
The therapeutic moment is when you have an opportunity to understand and intervene in noncompliance. Understanding why a patient was not able to comply with a plan is far more important than the noncompliance itself. Sometimes it is time, sometimes money, and sometimes preference. Often it is a deeper issue, like food as comfort and companion. Creating a therapeutic alliance with the patient and exploring these issues is often magical, not just for the patient but for the provider as well.
Tom Sult, MD, is a residency trained and board certified family doctor. He is boarded in Holistic medicine and on the faculty of the Institute for Functional Medicine (IFM). Dr Sult’s practice is in Central Minnesota were he has a consultative, tertiary care clinic for Functional Medicine. He primarily sees autism, Lyme disease, autoimmune disorders, environmental illness and other chronic complex disease. Dr Sult teaches GI and Toxicology for IFM. His primary interest is addressing the underlying causes of illness and addressing the interplay of genetic predisposition with lifestyle and environmental change.
http://www.naturalmedicinejournal.com/pdf/NMJ_OCT09_CR.pdf
http://www.depsyl.com/
http://back2basicnutrition.com/
http://bionutritionalresearch.olhblogspace.com/
Showing posts with label Reversal of Pre-Diabetes. Show all posts
Showing posts with label Reversal of Pre-Diabetes. Show all posts
Thursday, January 20, 2011
Wednesday, January 19, 2011
Diagnosis and Possible Reversal of Pre-Diabetes #3
Chronic Inflammation With Two Key Dietary Supplements
Many of my colleagues no longer support a pre-diabetes diagnoses, believing instead that any consistent fasting blood sugar (FBS) over 100 should be considered type 2 diabetes (albeit a milder form) and must be treated. Diabetes is most reversible in the earliest stages, when FBS is less than 125, which is the general range of the term “pre-diabetes.” Effective early identification of underlying causes is critical to the successful treatment of this condition.
While the etiology of pre-diabetes is multifactorial, one consistent hallmark is chronic inflammation. This potential underlying cause is often not considered as fully as it should be in clinical practice. In a self-perpetuating, destructive cycle, hyperglycemia and insulin resistance beget inflammatory changes. According to one recent study, “insulin receptor substrates serine phosphorylation is a time-controlled physiological feedback mechanism in insulin signaling that is hijacked by metabolic and inflammatory stresses to promote insulin resistance.”1 FBS consistently above normal and not contributable to non-diabetic factors is evidence of this process in action. In simpler terms, inflammation promotes insulin resistance, insulin resistance promotes hyperglycemia, and hyperglycemia promotes inflammation.
It is important that this cycle be interrupted or pre-diabetes will evolve to diabetes in the majority of patients thus diagnosed. Two scientifically substantiated potent anti-inflammatories to consider clinically are curcumin and omega 3 fatty acids.
Curcumin has been examined for its ability to prevent oxidative stress, modulate the immune system, and reduce inflammation—all of which has a positive impact on pre-diabetes. However, one area of particular interest is curcumin’s ability to inhibit and modulate specific kinases called c-Jun N-terminal kinases (JNKs, also called “stress-activated kinases” or SAPKs). JNKs modify the activity of certain proteins that are especially important in the development of insulin resistance, which is clinically the earliest stage in the development of type 2 diabetes.2 Curcumin is a known inhibitor of JNKs and therefore could be a powerful tool in reversing the metabolic processes that lead to insulin resistance and subsequent prediabetes.3
Biochemistry aside, from a treatment perspective, curcumin has been shown quite efficacious in the prevention of cardiovascular disease, one of the unfortunate potential sequela of diabetes as well as diabetic retinopathy, a leading cause of blindness.4,5 Preliminary research indicates that curcumin may help prevent diabetic neuropathy.6
Omega 3 fatty acids also have proven anti-inflammatory properties. In a recent study, 148 men with impaired glucose tolerance and/or impaired fasting blood glucose were followed for 12 months after counseling in dietary fat quality. At the end of the study, 92 subjects reverted to normal glucose levels and 56 remained in prediabetic status. None of the participants progressed to full diabetes. Additionally, it was noted that subjects in the highest tertile of omega-3:omega-6 fatty acid ratio showed the highest chance of improving glucose disturbances (2.51, 1.01-6.37).7 Therefore, incorporating more fatty fish into the diet and/or supplementing with omega 3 fatty acids can have a profound impact on ameliorating blood sugar changes associated with type 2 diabetes, and studies indicate a higher omega 3:omega 6 ratio is protective against progression to diabetes.
Given the strong correlation between inflammation and pre-diabetes, I feel it is imperative that clinicians address this issue in this patient population. The scientific literature provides us with enough substantiation to incorporate curcumin and omega 3 fatty acids into the dietary supplement program of the pre-diabetic patient, along with applicable dietary and lifestyle counsel.
References
1 Tanti JF, Jager J. Cellular mechanisms of insulin resistance: role of stress-regulated serine kinases and insulin receptor substrates (IRS) serine phosphorylation. Curr Opin Pharmacol. 2009 Aug 13.)
2 Kaneto H. The JNK pathway as a therapeutic target for diabetes. Expert Opin Ther Targets. 2005;9(3):581-92.
3 Moon DO, Jin CY, Lee JD, et al. Curcumin decreases binding of Shiga-like toxin-1B on human intestinal epithelial cell line HT29 stimulated with TNF-alpha and IL-1beta: suppression of p38, JNK and NF-kappaB p65 as potential targets. Biol Pharm Bull. 2006;29(7):1470-5.
4 Wongcharoen W, Phrommintikul A. The protective role of curcumin in cardiovascular diseases. Int J Cardiol. 2009;133(2):145-51.
5 Kowluru RA, Kanwar M. Effects of curcumin on retinal oxidative stress and inflammation in diabetes. Nutr Metab (Lond). 2007;4:8.
6 Osawa T. Nephroprotective and hepatoprotective effects of curcuminoids. Adv Exp Med Biol. 2007;595:407-23.
7 Sartorelli DS, Damião R, Chaim R, Hirai A, Gimeno SG, Ferreira SR. Dietary omega-3 fatty acid and omega-3: omega-6 fatty acid ratio predict improvement in glucose disturbances in Japanese Brazilians. Nutrition. 2009 Jul 30.
Cheryl Myers, RN, is recognized as an expert in the health and dietary supplement field. She writes, gives public appearances, and is in charge of scientific affairs and education for EuroPharma, Inc. Cheryl graduated from Purdue University, and also has clinical certifications in oncology and gerontology, and has a second degree in psychology. Cheryl’s nationally published articles have addressed a variety of health applications for natural products, and Cheryl has been a featured guest on radio shows, and is frequently interviewed by a variety of periodicals, including the New York Times, Wall Street Journal, Prevention Magazine, and Healthy Living.
http://www.naturalmedicinejournal.com/pdf/NMJ_OCT09_CR.pdf
http://www.depsyl.com/
http://back2basicnutrition.com/
http://bionutritionalresearch.olhblogspace.com/
Many of my colleagues no longer support a pre-diabetes diagnoses, believing instead that any consistent fasting blood sugar (FBS) over 100 should be considered type 2 diabetes (albeit a milder form) and must be treated. Diabetes is most reversible in the earliest stages, when FBS is less than 125, which is the general range of the term “pre-diabetes.” Effective early identification of underlying causes is critical to the successful treatment of this condition.
While the etiology of pre-diabetes is multifactorial, one consistent hallmark is chronic inflammation. This potential underlying cause is often not considered as fully as it should be in clinical practice. In a self-perpetuating, destructive cycle, hyperglycemia and insulin resistance beget inflammatory changes. According to one recent study, “insulin receptor substrates serine phosphorylation is a time-controlled physiological feedback mechanism in insulin signaling that is hijacked by metabolic and inflammatory stresses to promote insulin resistance.”1 FBS consistently above normal and not contributable to non-diabetic factors is evidence of this process in action. In simpler terms, inflammation promotes insulin resistance, insulin resistance promotes hyperglycemia, and hyperglycemia promotes inflammation.
It is important that this cycle be interrupted or pre-diabetes will evolve to diabetes in the majority of patients thus diagnosed. Two scientifically substantiated potent anti-inflammatories to consider clinically are curcumin and omega 3 fatty acids.
Curcumin has been examined for its ability to prevent oxidative stress, modulate the immune system, and reduce inflammation—all of which has a positive impact on pre-diabetes. However, one area of particular interest is curcumin’s ability to inhibit and modulate specific kinases called c-Jun N-terminal kinases (JNKs, also called “stress-activated kinases” or SAPKs). JNKs modify the activity of certain proteins that are especially important in the development of insulin resistance, which is clinically the earliest stage in the development of type 2 diabetes.2 Curcumin is a known inhibitor of JNKs and therefore could be a powerful tool in reversing the metabolic processes that lead to insulin resistance and subsequent prediabetes.3
Biochemistry aside, from a treatment perspective, curcumin has been shown quite efficacious in the prevention of cardiovascular disease, one of the unfortunate potential sequela of diabetes as well as diabetic retinopathy, a leading cause of blindness.4,5 Preliminary research indicates that curcumin may help prevent diabetic neuropathy.6
Omega 3 fatty acids also have proven anti-inflammatory properties. In a recent study, 148 men with impaired glucose tolerance and/or impaired fasting blood glucose were followed for 12 months after counseling in dietary fat quality. At the end of the study, 92 subjects reverted to normal glucose levels and 56 remained in prediabetic status. None of the participants progressed to full diabetes. Additionally, it was noted that subjects in the highest tertile of omega-3:omega-6 fatty acid ratio showed the highest chance of improving glucose disturbances (2.51, 1.01-6.37).7 Therefore, incorporating more fatty fish into the diet and/or supplementing with omega 3 fatty acids can have a profound impact on ameliorating blood sugar changes associated with type 2 diabetes, and studies indicate a higher omega 3:omega 6 ratio is protective against progression to diabetes.
Given the strong correlation between inflammation and pre-diabetes, I feel it is imperative that clinicians address this issue in this patient population. The scientific literature provides us with enough substantiation to incorporate curcumin and omega 3 fatty acids into the dietary supplement program of the pre-diabetic patient, along with applicable dietary and lifestyle counsel.
References
1 Tanti JF, Jager J. Cellular mechanisms of insulin resistance: role of stress-regulated serine kinases and insulin receptor substrates (IRS) serine phosphorylation. Curr Opin Pharmacol. 2009 Aug 13.)
2 Kaneto H. The JNK pathway as a therapeutic target for diabetes. Expert Opin Ther Targets. 2005;9(3):581-92.
3 Moon DO, Jin CY, Lee JD, et al. Curcumin decreases binding of Shiga-like toxin-1B on human intestinal epithelial cell line HT29 stimulated with TNF-alpha and IL-1beta: suppression of p38, JNK and NF-kappaB p65 as potential targets. Biol Pharm Bull. 2006;29(7):1470-5.
4 Wongcharoen W, Phrommintikul A. The protective role of curcumin in cardiovascular diseases. Int J Cardiol. 2009;133(2):145-51.
5 Kowluru RA, Kanwar M. Effects of curcumin on retinal oxidative stress and inflammation in diabetes. Nutr Metab (Lond). 2007;4:8.
6 Osawa T. Nephroprotective and hepatoprotective effects of curcuminoids. Adv Exp Med Biol. 2007;595:407-23.
7 Sartorelli DS, Damião R, Chaim R, Hirai A, Gimeno SG, Ferreira SR. Dietary omega-3 fatty acid and omega-3: omega-6 fatty acid ratio predict improvement in glucose disturbances in Japanese Brazilians. Nutrition. 2009 Jul 30.
Cheryl Myers, RN, is recognized as an expert in the health and dietary supplement field. She writes, gives public appearances, and is in charge of scientific affairs and education for EuroPharma, Inc. Cheryl graduated from Purdue University, and also has clinical certifications in oncology and gerontology, and has a second degree in psychology. Cheryl’s nationally published articles have addressed a variety of health applications for natural products, and Cheryl has been a featured guest on radio shows, and is frequently interviewed by a variety of periodicals, including the New York Times, Wall Street Journal, Prevention Magazine, and Healthy Living.
http://www.naturalmedicinejournal.com/pdf/NMJ_OCT09_CR.pdf
http://www.depsyl.com/
http://back2basicnutrition.com/
http://bionutritionalresearch.olhblogspace.com/
Tuesday, January 18, 2011
Diagnosis and Possible Reversal of Pre-Diabetes #2
Diagnosis and Possible Reversal of Pre-Diabetes
Early And Accurate Diagnosis is Critical
Commentary by Mona Morstein, ND
The medical diagnosis of pre-diabetes (PD) includes both standard evaluations, as well as a unique naturopathic test. The goal of early and accurate diagnosis is to determine if the patient is in a mild, moderate, or severe state of pre-diabetes. Early and accurate diagnosis helps determine how aggressive the treatment needs to be, and how much damage PD may have already caused the body.
PD is often associated with metabolic syndrome, which is defined similarly by various organizations. The basic definition based on the American Heart Association (AHA)/Updated National Cholesterol Education Program (NCEP) consists of having three or more of the following traits:
..Elevated waist circumference (men >40 inches; women >35 inches; lower for Asian populations)
..Hypertriglyceridemia (>150 mg/dl)
..Reduced HDL (men <40 mg/dl; women <50 mg/dl)
..Hypertension (>130/85 mmHg)
..Fasting hyperglycemia (>100 mg/dl)
Not all pre-diabetic patients have metabolic syndrome; however, simply having a fasting glucose level of 101–125 mg/dl can identify a patient as pre-diabetic. When I have a patient with a pre-diabetic glucose number, I reflex to a more comprehensive analysis of glucose regulation, which is justified in scientific literature. The Oral Glucose Tolerance Test is a standard lab test consisting of having a patient fast 12 hours, get a fasting glucose level, and then drink 75–100 g of a glucose drink, with repeated glucose blood draws over the next one, two, and three hours. I have personally adapted this test to a different format. I have patients fast for 12 hours and then test their fasting glucose and insulin levels. I then have them eat—preferably at a local fast food restaurant—one pancake with syrup and one hash brown. This gives the patient 100 g of refined sugar and grain carbohydrate, as well as saturated fat—the two top food groups that initiate insulin resistance. I am more interested in seeing what actual food does to people than just a glucose drink. I then have the patient return to the clinic 1.5 hours after eating for a second blood draw of glucose and insulin. Some other naturopaths at my clinic have patients get postprandial draws of one, two, and three hours, but I find that is very difficult for many patients, and it is time-consuming. For my interpretation of the patient’s condition, it also does not seem to help more than the solo 1.5-hour postprandial reading.
Insulin levels are vital for understanding how much insulin resistance is occurring. How much insulin that is secreted, analyzed in combination with glucose levels, gives the clinician a very accurate way of determining if the patient’s insulin resistance and pre-diabetes status is mild, moderate, or severe.
I also do a comprehensive CMP/CBC, including TSH/FT3/FT4, vitamin D (25OHVD), ferritin (to check for early liver inflammation indicating fatty liver), and A1C. It might be wise to also include fibrinogen to check on blood clotting risk, HS-CRP to analyze inflammation, and homocysteine to check for L-methylfolate bioavailability.
The initial physical exam should include vitals, heart/lung evaluation, thyroid exam, search for skin tags or acanthosis nigricans, height, weight, waist circumference with BMI, body fat percentage (via scale such as Tanita or Bio-Impedance device), foot exam including edema/pulses/lesions/neuropathy (using standard monofilament check), and abdominal exam to check for hepatomegaly.
The patient should be instructed to fill out a week-long diet diary to track eating habits, accurately recording everything she/he eats and drinks for all meals/snacks. Bowel movement frequency, symptoms, and sleeping habits should also be recorded.
Regarding the treatment of pre-diabetes, some clinicians fail to emphasize the importance of sleep in this patient population. Several well-designed studies, including a recent one this year from the Journal of Clinical Endocrinology,1 have clearly demonstrated that lack of sleep causes insulin resistance and weight gain. Sleep directly affects the two main hormones that regulate human appetite: leptin and ghrelin. Leptin is made in the adipocytes and instructs a person to eat less food. When a person gets enough sleep, it raises leptin levels, which decreases the desire to eat. Conversely, low amounts of sleep lower leptin levels and can thus cause increased appetite. Ghrelin is another appetite hormone made in the stomach. Opposite to leptin, ghrelin tells the brain to eat more food. When people don’t get enough sleep, ghrelin levels increase and people crave high carbohydrate foods.
Less sleep also causes an increase in cortisol output at night, which can cause hyperglycemia and initiate insulin resistance, another factor in abdominal weight gain and developing pre-diabetes and diabetes. Lastly, sleep is also needed for growth hormone (GH) to be fully secreted. Adult patients with low GH secretion are insulin resistant, due to several not wholly understood factors.
If a patient presents with PD symptoms and has sleep problems, a sleep study should be performed. Instituting sleep hygiene is a necessary aspect of pre-diabetes treatment and includes turning off most lights in the house so melatonin output can be enhanced; establishing the same bedtime routine each night; not watching disturbing TV shows or even news at night before bed, which may cause mental/emotional upset; spending some time reading before bed to initiate sleep; ensuring the mattress and room temperature is conducive to the patient’s body; addressing problems such as partner snoring or restless legs that may be interrupting the patient’s sleep; urging the use of a continuous positive airway pressure (CPAP) if apnea is diagnosed; dealing with hormonal imbalances thaymay be causing sleeping problems, such as elevated nighttime cortisol, or menopausal night sweats; using guided relaxation DVDs (or other stress relaxation techniques) to help induce sleep; and recommending occasional sleep aids, but avoiding nightly addiction to them.
References
1 Nedeltcheva AV, Kessler L, Imerial J, Penev PD. Exposure to recurrent sleep restriction in the setting of high caloric intake and physical inactivity results in increased insulin resistance and reduced glucose tolerance. J Clin Endocrinol Metab. 2009 Sep; 94(9):3242-51. Epub 2009 Jun 30.
http://www.naturalmedicinejournal.com/pdf/NMJ_OCT09_CR.pdf
http://www.depsyl.com/
http://back2basicnutrition.com/
http://bionutritionalresearch.olhblogspace.com/
Early And Accurate Diagnosis is Critical
Commentary by Mona Morstein, ND
The medical diagnosis of pre-diabetes (PD) includes both standard evaluations, as well as a unique naturopathic test. The goal of early and accurate diagnosis is to determine if the patient is in a mild, moderate, or severe state of pre-diabetes. Early and accurate diagnosis helps determine how aggressive the treatment needs to be, and how much damage PD may have already caused the body.
PD is often associated with metabolic syndrome, which is defined similarly by various organizations. The basic definition based on the American Heart Association (AHA)/Updated National Cholesterol Education Program (NCEP) consists of having three or more of the following traits:
..Elevated waist circumference (men >40 inches; women >35 inches; lower for Asian populations)
..Hypertriglyceridemia (>150 mg/dl)
..Reduced HDL (men <40 mg/dl; women <50 mg/dl)
..Hypertension (>130/85 mmHg)
..Fasting hyperglycemia (>100 mg/dl)
Not all pre-diabetic patients have metabolic syndrome; however, simply having a fasting glucose level of 101–125 mg/dl can identify a patient as pre-diabetic. When I have a patient with a pre-diabetic glucose number, I reflex to a more comprehensive analysis of glucose regulation, which is justified in scientific literature. The Oral Glucose Tolerance Test is a standard lab test consisting of having a patient fast 12 hours, get a fasting glucose level, and then drink 75–100 g of a glucose drink, with repeated glucose blood draws over the next one, two, and three hours. I have personally adapted this test to a different format. I have patients fast for 12 hours and then test their fasting glucose and insulin levels. I then have them eat—preferably at a local fast food restaurant—one pancake with syrup and one hash brown. This gives the patient 100 g of refined sugar and grain carbohydrate, as well as saturated fat—the two top food groups that initiate insulin resistance. I am more interested in seeing what actual food does to people than just a glucose drink. I then have the patient return to the clinic 1.5 hours after eating for a second blood draw of glucose and insulin. Some other naturopaths at my clinic have patients get postprandial draws of one, two, and three hours, but I find that is very difficult for many patients, and it is time-consuming. For my interpretation of the patient’s condition, it also does not seem to help more than the solo 1.5-hour postprandial reading.
Insulin levels are vital for understanding how much insulin resistance is occurring. How much insulin that is secreted, analyzed in combination with glucose levels, gives the clinician a very accurate way of determining if the patient’s insulin resistance and pre-diabetes status is mild, moderate, or severe.
I also do a comprehensive CMP/CBC, including TSH/FT3/FT4, vitamin D (25OHVD), ferritin (to check for early liver inflammation indicating fatty liver), and A1C. It might be wise to also include fibrinogen to check on blood clotting risk, HS-CRP to analyze inflammation, and homocysteine to check for L-methylfolate bioavailability.
The initial physical exam should include vitals, heart/lung evaluation, thyroid exam, search for skin tags or acanthosis nigricans, height, weight, waist circumference with BMI, body fat percentage (via scale such as Tanita or Bio-Impedance device), foot exam including edema/pulses/lesions/neuropathy (using standard monofilament check), and abdominal exam to check for hepatomegaly.
The patient should be instructed to fill out a week-long diet diary to track eating habits, accurately recording everything she/he eats and drinks for all meals/snacks. Bowel movement frequency, symptoms, and sleeping habits should also be recorded.
Regarding the treatment of pre-diabetes, some clinicians fail to emphasize the importance of sleep in this patient population. Several well-designed studies, including a recent one this year from the Journal of Clinical Endocrinology,1 have clearly demonstrated that lack of sleep causes insulin resistance and weight gain. Sleep directly affects the two main hormones that regulate human appetite: leptin and ghrelin. Leptin is made in the adipocytes and instructs a person to eat less food. When a person gets enough sleep, it raises leptin levels, which decreases the desire to eat. Conversely, low amounts of sleep lower leptin levels and can thus cause increased appetite. Ghrelin is another appetite hormone made in the stomach. Opposite to leptin, ghrelin tells the brain to eat more food. When people don’t get enough sleep, ghrelin levels increase and people crave high carbohydrate foods.
Less sleep also causes an increase in cortisol output at night, which can cause hyperglycemia and initiate insulin resistance, another factor in abdominal weight gain and developing pre-diabetes and diabetes. Lastly, sleep is also needed for growth hormone (GH) to be fully secreted. Adult patients with low GH secretion are insulin resistant, due to several not wholly understood factors.
If a patient presents with PD symptoms and has sleep problems, a sleep study should be performed. Instituting sleep hygiene is a necessary aspect of pre-diabetes treatment and includes turning off most lights in the house so melatonin output can be enhanced; establishing the same bedtime routine each night; not watching disturbing TV shows or even news at night before bed, which may cause mental/emotional upset; spending some time reading before bed to initiate sleep; ensuring the mattress and room temperature is conducive to the patient’s body; addressing problems such as partner snoring or restless legs that may be interrupting the patient’s sleep; urging the use of a continuous positive airway pressure (CPAP) if apnea is diagnosed; dealing with hormonal imbalances thaymay be causing sleeping problems, such as elevated nighttime cortisol, or menopausal night sweats; using guided relaxation DVDs (or other stress relaxation techniques) to help induce sleep; and recommending occasional sleep aids, but avoiding nightly addiction to them.
References
1 Nedeltcheva AV, Kessler L, Imerial J, Penev PD. Exposure to recurrent sleep restriction in the setting of high caloric intake and physical inactivity results in increased insulin resistance and reduced glucose tolerance. J Clin Endocrinol Metab. 2009 Sep; 94(9):3242-51. Epub 2009 Jun 30.
http://www.naturalmedicinejournal.com/pdf/NMJ_OCT09_CR.pdf
http://www.depsyl.com/
http://back2basicnutrition.com/
http://bionutritionalresearch.olhblogspace.com/
Monday, January 17, 2011
Is Reversal of Pre-Diabetes Possible?
Diagnosis and Possible Reversal of Pre-Diabetes
Comprehensive Supplementation is a Key to Successful Treatment
At least 92% of diabetes cases can be attributed to lifestyle choices, with 8% attributable to genetics. The fact is, diabetes is extremely expensive, can be very deadly, and is almost completely avoidable. Pre-diabetes (PD) is the antecedent to diabetes. The causes of pre-diabetes are:
· lack of an essential nutrient,
· environmental toxin exposure,
· distress that impairs stress responsive hormones and neuro-chemicals,
· autoimmune attack on the insulin production centers or insulin receptors, and
· being sedentary
The consequences of PD range from obesity to insulin resistance, also known as metabolic syndrome and syndrome X. The health ramifications of unmanaged PD that leads to diabetes include heart attacks, coronary artery atherosclerosis, arteriosclerosis, and stroke.
I will use a recent successful outcome study in pre-diabetes that I had the opportunity to lead as an example of what can be done using an innovative comprehensive approach.1
The goals of our study were to improve sugar insulin performance and remove obstacles to recovery. This meant that we wanted to reduce the glucose/insulin ratio to healthier levels. We also wanted to confirm this by reduction in hemoglobin A1c as an independent risk marker. Because of the role of stress hormones in PD risk, we also measured cortisol and DHEA stress hormones to assess how they changed over the six weeks of the program. We are highly encouraged that all markers improved and the improvement was statistically significant. Statistically, we found significance below the 0.001 level. This makes the outcome highly likely to be real and unlikely to be due to coincidence. We were also pleased to report that compliance was high and dropout rates below expectation.
In the outcome study, we
· restored tolerance in the immune defense and repair system;
· corrected essential nutrient deficits;
· improved detoxification of environmental toxins;
· reduced excess distress and restored neurohormone balance; and
· identified deficits in digestion or other systems and improve function, structure and resilience.
The following supplements proved effective in this program:
1. Novel nutrients and herbs in standardized form in 100% rice bran oil with phosphatides to improve uptake and components that improve insulin function:
· Chromium as citrate 250–1,000 mcg/day
· Vanadium ascorbate 250–1,000 mcg/day
· French lilac (Galega) 150–600 mg/day
· Bitter melon (Marah) 150–600 mg/day
· Huckleberry/Bilberry 100–400 mg/day
· Agnus Castus•• 250–1,000 mg/day
2. L-carnitine as the fumarate, 500–2,500 mg/day; GABA, 200–1,000 mg/day; and alginate, 50–250 mg/day in MCT oil for better uptake.
3. Fully buffered 100% L-ascorbate with potassium, calcium, magnesium, and zinc.
4. Polyphenolics as quercetin dihydrate 250–5,000 mg/day and soluble OPC 5–100 mg/day.
5. Exercise in the form of walking measured with a pedometer with the goal of 10,000 steps per day.
6. Stress management, mindfulness, and relaxation response practices, 20 minutes twice daily.
7. Good hydration based on drinking at least eight 8-ounce glasses of water daily, sufficient to stimulate 3 to 6 urinations per day.
Our successful outcome study in people with PD confirms the hope that people can feel and function better at lower net costs when enough of the essential protective and repair factors are provided.
http://www.naturalmedicinejournal.com/pdf/NMJ_OCT09_CR.pdf
http://www.depsyl.com/
http://back2basicnutrition.com/
http://bionutritionalresearch.olhblogspace.com/
Comprehensive Supplementation is a Key to Successful Treatment
At least 92% of diabetes cases can be attributed to lifestyle choices, with 8% attributable to genetics. The fact is, diabetes is extremely expensive, can be very deadly, and is almost completely avoidable. Pre-diabetes (PD) is the antecedent to diabetes. The causes of pre-diabetes are:
· lack of an essential nutrient,
· environmental toxin exposure,
· distress that impairs stress responsive hormones and neuro-chemicals,
· autoimmune attack on the insulin production centers or insulin receptors, and
· being sedentary
The consequences of PD range from obesity to insulin resistance, also known as metabolic syndrome and syndrome X. The health ramifications of unmanaged PD that leads to diabetes include heart attacks, coronary artery atherosclerosis, arteriosclerosis, and stroke.
I will use a recent successful outcome study in pre-diabetes that I had the opportunity to lead as an example of what can be done using an innovative comprehensive approach.1
The goals of our study were to improve sugar insulin performance and remove obstacles to recovery. This meant that we wanted to reduce the glucose/insulin ratio to healthier levels. We also wanted to confirm this by reduction in hemoglobin A1c as an independent risk marker. Because of the role of stress hormones in PD risk, we also measured cortisol and DHEA stress hormones to assess how they changed over the six weeks of the program. We are highly encouraged that all markers improved and the improvement was statistically significant. Statistically, we found significance below the 0.001 level. This makes the outcome highly likely to be real and unlikely to be due to coincidence. We were also pleased to report that compliance was high and dropout rates below expectation.
In the outcome study, we
· restored tolerance in the immune defense and repair system;
· corrected essential nutrient deficits;
· improved detoxification of environmental toxins;
· reduced excess distress and restored neurohormone balance; and
· identified deficits in digestion or other systems and improve function, structure and resilience.
The following supplements proved effective in this program:
1. Novel nutrients and herbs in standardized form in 100% rice bran oil with phosphatides to improve uptake and components that improve insulin function:
· Chromium as citrate 250–1,000 mcg/day
· Vanadium ascorbate 250–1,000 mcg/day
· French lilac (Galega) 150–600 mg/day
· Bitter melon (Marah) 150–600 mg/day
· Huckleberry/Bilberry 100–400 mg/day
· Agnus Castus•• 250–1,000 mg/day
2. L-carnitine as the fumarate, 500–2,500 mg/day; GABA, 200–1,000 mg/day; and alginate, 50–250 mg/day in MCT oil for better uptake.
3. Fully buffered 100% L-ascorbate with potassium, calcium, magnesium, and zinc.
4. Polyphenolics as quercetin dihydrate 250–5,000 mg/day and soluble OPC 5–100 mg/day.
5. Exercise in the form of walking measured with a pedometer with the goal of 10,000 steps per day.
6. Stress management, mindfulness, and relaxation response practices, 20 minutes twice daily.
7. Good hydration based on drinking at least eight 8-ounce glasses of water daily, sufficient to stimulate 3 to 6 urinations per day.
Our successful outcome study in people with PD confirms the hope that people can feel and function better at lower net costs when enough of the essential protective and repair factors are provided.
http://www.naturalmedicinejournal.com/pdf/NMJ_OCT09_CR.pdf
http://www.depsyl.com/
http://back2basicnutrition.com/
http://bionutritionalresearch.olhblogspace.com/
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