DIABETES
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The Metabolic Score for Insulin Resistance (METS-IR) is a metabolic index developed with the aim to quantify peripheral insulin sensitivity in humans; it was first described under the name METS-IR by Bello-Chavolla et al in 2018. METS-IR is a novel score to evaluate cardiometabolic risk in healthy and at-risk subjects and a promising tool for screening of insulin sensitivity.
METS-IR levels are significantly associated with pre-HTN or HTN in normoglycemia individuals in Gifu, Japan.
METS-IR is calculated as Ln((2*G0)+TG0)*BMI)/(Ln(HDL-c)) (G0: fasting glucose, TG0: fasting triglycerides, BMI: body mass index, HDL-c: high-density lipoprotein cholesterol).
METS-IR also predicts visceral fat content, subcutaneous adipose tissue, fasting insulin levels and ectopic fat accumulation in liver and pancreas.
Ketoanalogues of amino acids (KAs) are nitrogen-free analogs of essential amino acids. Studies have demonstrated that the benefits of ketoanalogues (KA) supplementation on mortality and renal outcomes in CKD patients undergoing dietary protein restriction are controversial [7,8,9,10,11]. The effects of KA on patients with advanced CKD with an Low Protein Diet (LPD) are unclear [8,9,10,11]. Basically, the ketoanalogues help to prevent protein wasting and deficiencies.
In the human body, ketoanalogues capture nitrogen and convert it into amino acids, which are the building blocks of protein. Providing ketoanalogues like Ketosteril prevents malnutrition because the body is still able to build protein. In addition, because ketoanalogues use excess nitrogen, the kidneys do not have to work as hard to excrete nitrogen-containing waste. This may slow the progression of chronic kidney disease and postpone dialysis.
Till date, the effects of KA on advanced CKD patients with DM have not been examined yet through randomized controlled trials. In a 2020 study, KA supplementation increased the risk of long-term dialysis in the subgroup of advanced CKD patients with DM but not in the subgroup of advanced CKD patients without DM.
Ketosteril
Ketosteril is a calcium-based ketoanalogue. It includes the following ingredients:
- Calcium-3-methyl-2-oxovaleric acid
- Calcium-methy-2-oxovaleric acid
- Calcium-2-oxo-3-phenylpropionic acid
- Calcium-3-methyl-2-oxobutyric acid
- calcium-DL-2-hydroxy-4-(methylthio)-butyric acid
- L-lysine acetate
- L-threonine
- L-tryptophan
- L-histidine
- L-tyrosine
Other ingredients include corn starch, crospovidone, povideone, talc, highly dispersed silicon dioxide, magnesium stearate, macrocol 6000, colouring agents E104, E171 alkaline polymethacrylate, glycerol triacetate.
The total nitrogen content per tablet is about 36 milligrams. Total calcium content is 0.05 grams.
The table shows a summary correlating the therapeutic class and the dose adjustment based on creatinine clearance.
| Class and Medication | Dose Adjustment Based on eGFR |
|---|
Biguanide |
||
| Metformin | USA prescribing information: contraindication for men with serum creatinine ≥1.5 mg/dL and women with serum creatinine ≥1.4 mg/dL UK guideline allows metformin in patients with eGFR >30 mL/min/1.73 m2 KDIGO recommends metformin in patients with eGFR >45 mL/min/1.73 m2 | |
Sulfonylureas |
||
| Glipizide | No dose adjustment required | |
| Glimepiride | Initiate conservatively at 1 mg daily Avoid use if eGFR <60 mL/min/1.73 m2 | |
| Gliclazide | Reduce dose if eGFR <30 mL/min/1.73 m2. Not recommended if eGFR <15 mL/min/1.73 m2 | |
| Glyburide or glibenclamide | Avoid use in patients with eGFR <60 mL/min/1.73 m2 | |
Meglitinides |
||
| Repaglinide | Initial dose of 0.5 mg before meals when eGFR <30 mL/min/1.73 m2 | |
| Nateglinide | Caution when used with eGFR <30 mL/min/1.73 m2. Initiate with 60 mg before meals | |
a-Glucosidase inhibitors |
||
| Acarbose | Avoid if eGFR <30 mL/min/1.73 m2 | |
| Miglitol | Avoid if eGFR <30 mL/min/1.73 m2 | |
TZDs (Glitazones) |
||
| Pioglitazone | No dose adjustment required. Use with caution in patients with CKD and hypervolemia | |
GLP-1 receptor agonists |
||
| Exenatide | Avoid if eGFR <30 mL/min/1.73 m2. When eGFR between 30 and 50 mL/min/1.73 m2 dose should not exceed 5 mcg | |
| Lixisenatide | Avoid if eGFR <50 mL/min/1.73 m2 | |
| Liraglutide | Avoid if eGFR <60 mL/min/1.73 m2 | |
DPP-4 inhibitors |
||
| Sitagliptin | 100 mg daily if eGFR <50 mL/min/1.73 m2 | |
| 50 mg daily if eGFR 30–50 mL/min/1.73 m2 | ||
| 25 mg daily if eGFR <30 mL/min/1.73 m2 | ||
| Saxagliptin | 5 mg daily if eGFR <50 mL/min/1.73 m2 | |
| 2.5 mg daily if eGFR <50 mL/min/1.73 m2 | ||
| Alogliptin | 1.25 mg per day when eGFR 30–60 mL/min/1.73 m2, and for those patients with eGFR <30 mL/min/1.73 m2 or hemodialysis, the dose should not exceed 6.25 mg/day | |
| Linagliptin | No dose adjustment required | |
SGLT2 inhibitors |
||
| Canagliflozin | No dose adjustment required if eGFR <60 mL/min/1.73 m2 | |
| 100 mg daily if eGFR 45–59 mL/min/1.73 m2 | ||
| Dapagliflozin | Avoid use if eGFR <60 mL/min/1.73 m2, and discontinue use if eGFR <45 mL/min/1.73 m2 | |
Impaired wound healing in Diabetes is triggered by hyperglycemia, chronic inflammation, micro- and macro-circulatory dysfunction, hypoxia, autonomic and sensory neuropathy, and impaired neuropeptide signaling.
The normal wound healing includes four programmed phases: hemostasis, inflammation, proliferation, and remodeling, though these phases are continuous and overlapped. However, diabetes results in delayed wound healing via multifarious biological mechanisms, which affect the transition of the organized phases. A series of mechanisms comprising disordered growth factor production, impaired angiogenesis, imbalanced lymphocyte proliferation, and macrophage dysfunction may contribute to the delayed diabetic wound healing.
Conventional therapeutic strategies of diabetic wound include glucose and infection control, debridement, wound off-loading, dressings, and revascularization. However, many of diabetic wounds are refractory to current treatments and fail to heal, persist for months or years, ultimately lead to amputation.
So, delayed wound healing in Diabetes is not only due to Hyperglycemia. Risk factors include include oxygenation, infection, age and sex hormones, stress, diabetes, obesity, medications, alcoholism, smoking, immunosuppression, nutritional status, radiation therapy, and vascular insufficiencies.
The Most Important Factors Affecting Wound Healing
Advanced age
As you get older, hormonal changes and the cumulative effects of photoaging (sun damage) combine to leave your skin drier, thinner, more delicate, and less elastic. Besides leaving your skin more susceptible to injury, these age-related changes can substantially slow the healing process; older tissues simply don’t repair and regenerate as quickly as younger tissues.
Excess body weight
People who are very overweight or obese are more likely to experience delayed wound healing as well as wound complications, including infection. Being overweight places more pressure on the wound itself, effectively decreasing the amount of nutrients and oxygen it receives to fuel the healing process. Wounds that occur within skin folds also tend to heal more slowly due to continuous friction and tissue breakdown.
Chronic illness
Chronic conditions are a major factor in impaired wound healing for many people. Although the mechanisms at play tend to be numerous and varied, most persistent illnesses delay healing by interfering with one or more aspects of the immune system response. Diabetes can slow the healing process by making white blood cells less effective. Diabetes, cardiovascular disease, and other conditions that give rise to poor circulation may also make it harder for your body to deliver oxygen, nutrients, and reparative cells to an injured area.
Stress
Stressors, such as anxiety and depression can impair wound healing by deregulation of the immune system. Psychological stress has been found to have profound effects on the hypothalamus, psychological responses (health-damaging behaviors), and autonomic nervous system. Cortisol, a stress-induced hormone can also impair wound healing by interfering with the production of pro-inflammatory cytokines.
Obesity
The accumulation of fatty or adipose tissue in obese persons can impair the rate of wound healing. According to data from the CDC, obesity had a prevalence of 42.2% among adults in the United States between 2017 and 2018. It is known to increase the risk of many health conditions, including coronary heart disease, hypertension, and cancer, and also contributes to diabetes. Higher levels of glucose in the blood promote vasoconstriction, which results in low perfusion to the lower extremities.
Medication
Use of certain medications, such as chemotherapy drugs and Non-steroidal Anti-inflammatory Drugs (NSAIDs) may interfere with wound healing processes, such as platelet formation or inflammatory responses. Chemotherapy drugs, used for the treatment of cancer, can cause venous irritation, delayed cellular migration, and lower collagen synthesis and fibroblast proliferation. Moreover, research suggests that NSAIDs like aspirin and Ibuprofen commonly used for pain relief can have a negative effect on wound healing.
Poor nutrition
Optimal wound healing requires optimal nutritional support. People who eat an unhealthy diet that doesn’t meet their basic nutritional needs are more likely to experience the kind of slow or delayed healing that can lead to chronic wounds or injuries that take longer than three months to heal completely.
Lack of Hydration
A lack of moisture at the surface of a wound can halt cellular migration, decrease blood oxygenation, and seriously delay wound healing. Dehydration caused by either a depletion of sodium or water can delay all aspects of the healing process.
Poor Blood Circulation
Since blood delivers the necessary components to tissue for the wound healing process to take place, people with low blood pressure or vascular disease can have problems with delayed healing. Blocked or narrowed blood vessels or diseases of the heart, kidneys and lungs can also cause issues in the body delivering vital wound healing components, including white blood cells and adequate oxygen, to wounded tissues.
Edema
While most traumatic injuries cause some tissue swelling, excessive edema can increase the pressure on blood vessels, resulting in poorer blood circulation in the wound area. Tissue swelling can be caused by heart conditions or blood vessel problems. Compression therapy is often effective at transporting fluids back into the circulatory system to reduce edema so proper healing can occur.
Repeated Trauma
Wounds that continue to be reinjured due to shear force or pressure against a surface can have their healing process delayed or even stopped. Repetitive trauma often occurs with bed-bound patients and can be treated by careful repositioning on a regular schedule or use of offloading or protective devices under the supervision of a health care professional.
Unhealthy habits
People who smoke cigarettes and drink alcohol are more likely to experience slower healing rates than those who don’t smoke or drink. Both habits inhibit wound healing by suppressing your body’s inflammatory response and restricting the flow of blood, oxygen, nutrients, and reparative cells to the injured area. Other patient behaviors that can affect wound healing are a lack of adequate sleep, failure to elevate the affected area, not properly cleaning the wound, using inadequate wound dressing procedures, not keeping the wound moist and not moving enough.
When there isn’t enough insulin or cells stop responding to insulin, too much blood sugar stays in the bloodstream. When glucose doesn’t move into the cells, the body thinks it is starving and finds a way to compensate. It creates energy by burning fat and muscle at a fast pace. This is what leads to unexplained weight loss in people with diabetes.
Most of the time, this occurs in cases of Type 1 diabetes, although Type 2 diabetes can cause unexplained weight loss, too. This type of unexplained weight loss could be a sign of undiagnosed diabetes. It could also stem from a host of other conditions, including thyroid issues, celiac disease, Crohn’s disease, cancer, and more.
If blood sugars are high in a diabetes patient, it can make them urinate frequently, and this results in dehydration as a possible cause of weight loss. As sugar leaves your body, so do calories and weight loss may occur. Similarly, high blood sugars can also result in muscle breakdown and hence weight loss.
On the flip side, people who have diabetes may experience weight gain as a side effect of insulin therapy. Although insulin help regulates their glucose levels, it also promotes fat storage in the body.
Blood glucose fluctuation is often thought of as the first cause of fatigue in diabetes. But the authors of a study of 155 adults with type 2 diabetes suggested that blood glucose was the cause of fatigue in only 7 percent of participants. These findings suggest that diabetes fatigue may not be necessarily linked to the condition itself, but perhaps with other symptoms of diabetes.
As in other conditions, fatigue in people with diabetes may be caused by a variety of lifestyle, nutritional, medical, psychological, glycemic/diabetes-related, endocrine, and iatrogenic factors.
Non-Endocrine Diabetes fatigue syndrome (DFS)
Lifestyle-Related Causes
Non-endocrine factors that may contribute to DFS include an unhealthy lifestyle, inappropriate diet, and suboptimal mental health. Lack of physical conditioning, poor sleep hygiene, substance abuse (including excessive alcohol, caffeine), and drug withdrawal may lead to DFS.
Nutritional Causes
Unhealthy diets, which may lead to macronutrient or micronutrient malnutrition or starvation ketosis, can also precipitate DFS.
Medical Causes
Common medical conditions, such as anemia, dyselectrolytemia, and multiple vitamin deficiencies, are also characterized by fatigue. Anemia is not caused by diabetes, but it frequently occurs in people with diabetes and is a common cause of fatigue. A history of breathlessness on exertion, excessive blood loss, worm infestation, and pallor on examination suggest anemia. People with diabetes are at increased risk for thyroid diseases, especially hypothyroidism. A sluggish thyroid together with diabetes can be another cause. Dyselectrolytemia usually leads to neurological symptoms and signs. Proximal muscle weakness, together with musculoskeletal aches, pains, and easy fatigability, implies vitamin D deficiency.
Psychological Causes
At times, DFS may be worsened by psychological impairment. Diabetes distress is defined as an emotional response, characterized by extreme apprehension, discomfort, or dejection due to a prescribed inability to cope with the challenges and demands of living with diabetes. This adjustment disorder is characterized by a discomfort disorder that in turn is characterized by discomfort, and it may be reported as fatigue, possibly contributing to, overlapping with, or mimicking DFS. Yet another differential diagnosis of fatigue may be major depressive disorder.
Endocrine Diabetes fatigue syndrome (DFS)
If lifestyle, nutritional, and medical causes are ruled out, a targeted gluco-endocrine evaluation must be done to pinpoint the cause of DFS.
Diabetes-Related Causes
Diabetes-related causes include poor glycemic control, diabetic complications, and concomitant endocrinopathies. A suboptimal gluco-phenotype, involving any or all of the glycemic hexad (hyperglycemia, hypoglycemia, excessive glycemic variability), can lead to DFS.
Some evidence suggests that acute glycemic excursions are associated with fatigue. During an in-depth analysis of common hyperglycemic symptoms, 361 insulin-treated diabetics were asked to list their most common symptoms and report the blood glucose level at which those symptoms occurred. Tiredness was ranked fifth of the 16 most commonly reported symptoms. A mean symptom inventory score was computed for each subject based on the 16 symptoms. There was only a slight association between mean symptom inventory score and chronic glucose control measured by hemoglobin A1c (r = 0.149, p < 0.003). However 85% of the subjects were able to estimate a hyperglycemic threshold for the onset of their symptoms (including tiredness). The mean blood glucose threshold was 274 mg/dl, suggesting that acute elevations of blood glucose were more predictive of symptoms, including tiredness. Subjects also reported tiredness during lower levels of hyperglycemia, prior to osmotic symptoms such as thirst or increased urination.
Findings from an epidemiological study of 1,137 general practice patients with newly diagnosed type 2 diabetes revealed that fatigue was present in approximately 61% of patients at the time of diagnosis and was significantly associated with fasting plasma glucose (FPG) levels, but not hemoglobin A1c. It is possible that the average hemoglobin A1c may be falsely low in this group because their blood glucose level may not have been elevated the full three months. Similar findings were reported in 430 adults with newly diagnosed type 2 diabetes, prior to enrolling in the United Kingdom Prospective Diabetes Study (UKPDS). A high number of symptom complaints (including fatigue) was significantly associated with FPG, body mass index (BMI), and female gender. There was no association between symptom complaints and hemoglobin A1c, again suggesting a stronger association between fatigue and acute, rather than chronic, hyperglycemia.
Chronic hyperglycemia has long been assumed to cause fatigue; however, few data support this relationship. One cross-sectional study examined the relationship between glucose control and physical symptoms, moods, and well-being. The study included 188 Dutch patients with type 2 diabetes, and fatigue was measured using two different instruments: the Diabetes Symptom Checklist-Type 2 (DSC-Type 2) and the Profile of Mood States (POMS). Slight, but statistically significant, correlations between HbA1c and fatigue were noted using both instruments (DSC-Type 2 r = 0.14, p < 0.05; POMS r = 14, p < 0.05), suggesting that chronic hyperglycemia may contribute to fatigue.
In contrast, there was no association between hemoglobin A1c and fatigue symptoms as measured by the DSC-Type 2 during a two-year prospective study examining the initiation of insulin therapy in Dutch adults with type 2 diabetes. The authors reported a significant relationship of every unit increase of insulin dose with DSC-Type 2 total symptom complaint scores (which included a fatigue subscale) and POMS anger, displeasure, and fatigue scores, suggesting increased emotional fatigue possibly related to increased hypoglycemic events and the burden of daily injections.
In a study of patients with type 2 diabetes and restless leg syndrome, hemoglobin A1c was associated with sleepiness (as measured by the Epworth Sleepiness Scale), but not fatigue (as measured by the Fatigue Severity Scale).
Glucose variability may also cause psychological fatigue.
Similarly, fatigue may be the presenting symptom, or it may herald an insidious onset of vascular complications, such as heart failure and nephropathy. Lesser known comorbidities of diabetes, including chronic venous disease and Alzheimer’s disease, may also present with fatigue.
Endocrine Causes
Persons with diabetes, especially type 1 diabetes, are more prone to endocrinopathy. Diseases such as hypothyroidism, Addison’s disease, Cushing‘s syndrome, and hypothyroidism, if left unrecognized and/or untreated, may worsen DFS. The symptoms, sign, and laboratory anomalies specific to these diseases, coupled with a high index of clinical suspicion, help in their identification.
Iatrogenic Causes
At times, DFS may be iatrogenic. Drugs such as corticosteroids, beta blockers, diuretics, and statins are known to cause fatigue. Their use must be looked into during the evaluation of DFS.
Using individual patient data (IPD) and meta-regression methodology, researchers sought to indirectly compare the effectiveness of once-weekly (OW) semaglutide 1 mg vs once-daily (OD) empagliflozin 25 mg in patients with type 2 diabetes (T2D) inadequately controlled on metformin monotherapy. IPD for patients with T2D receiving metformin monotherapy and randomized to OW semaglutide 1 mg (SUSTAIN 2, 3, 8 trials), or to OD empagliflozin 25 mg (PIONEER 2 trial) have been involved. Findings revealed that baseline features were comparable between OW semaglutide (n = 995) and empagliflozin (n = 410). According to this indirect comparison, OW semaglutide 1 mg gives superior declines in HbA1c and body weight vs OD empagliflozin 25 mg in patients with T2D when added to metformin monotherapy.
This indirect comparison suggests that OW semaglutide 1 mg provides superior reductions in HbA1c and body weight vs OD empagliflozin 25 mg in patients with T2D when added to metformin monotherapy.
https://academic.oup.com/jcem/advance-article/doi/10.1210/clinem/dgaa577/5896001
The TyG index predicts future major adverse cardiovascular events (MACE) in patients with diabetes and acute coronary syndrome (ACS) independently of known cardiovascular risk factors, suggesting that the TyG index may be a useful marker for risk stratification and prognosis in patients with diabetes and ACS.
The triglyceride glucose index (TyG) was found to be an independent marker for predicting subclinical coronary artery disease (CAD) in individuals with no traditional cardiovascular risk factors (CVRFs).
The TyG index is an independent predictor of coronary artery calcification (CAC) progression, especially in adults without heavy baseline CAC.
TyG-index is significantly associated with incident Nonalcoholic fatty liver disease (NAFLD).
TyG index cut-off point of >4.44 was established for IR prediction.
TyG is superior to discriminate diabetes status, showing no inferior ability compared to the HOMA-IR. One important strength of TyG is a lower cost compared to HOMA-IR, as the cost of a fasting insulin level measurement is about six times higher than the cost of a triglyceride test. Therefore, we suggest the use of LAP and TyG as accurate, convenient and cost-effective diagnostic measurements for the early detection of prediabetes/diabetes in the general population.
Sulfonylureas and Meglitinides are oral hypoglycemic drugs directly stimulate release of insulin from pancreatic beta cells. Meglitinides act on the same β-cell receptor as sulphonylureas, but have a different chemical structure with a few major differences.
For example, meglitinides bind to the sulfonylurea receptor in beta cells (the insulin-producing cells of the pancreas), but at a different part of the receptor than the sulfonylureas do. The interaction of the meglitinides with the receptor is not as “tight” as that of the sulfonylureas, translating to a much shorter duration of action and a higher blood glucose level needed before the drugs produce insulin secretion from the pancreas. So, Meglitinides need to be taken more often than sulfonylureas because they work for a shorter amount of time.
In head-to-head comparisons with sulfonylureas, metiglinides failed to demonstrate better glucose control and led to a similar number of hypoglycaemic events. No significant differences were observed in terms of lipid profile and body weight reduction.
Meglitinides may be used in individuals allergic to sulfonylureas and in older adults unable to take insulin when the goal is to avoid hypoglycemia (McCulloch, 2015). Another advantage of meglitinides is their flexibility compared with sulfonylureas because of their faster onset and shorter duration of action (Pfeiffer & Klein, 2014).
The cost of meglitinides is relatively high. Similar to sulfonylureas, meglitinides lose their effectiveness as beta cell function declines over time (Marino, 2014). These agents are metabolized by the liver and, therefore, should be avoided in workers with liver dysfunction and used cautiously if renal dysfunction is present (Novartis, 2013; Novo Nordisk, 2011) although repaglinide has little renal clearance (McCulloch, 2015).
Sulfonylureas are usually taken once or twice a day, in the morning and/or evening, depending on the brand:
- Chlorpropramide is taken once a day (typical daily dose: 100 mg to 500 mg)
- Glipizide is taken once or twice a day (typical daily dose: 5 mg to 40 mg)
- Glyburide is taken once or twice a day (typical daily dose: 1.25 mg to 20 mg)
- Glimepiride is taken once a day (typical dose: 1 mg to 4 mg; maximum 8 mg daily)
Meglitinides are usually taken 15-30 minutes before each meal:
- Repaglinide is taken at doses ranging usally from 0.5 mg to 4 mg with each meal
- Nateglinide is taken at doses ranging usually from 60 mg to 120 mg
SGLT2 inhibitors, also called gliflozins, are a class of medications that inhibit reabsorption of glucose in the kidney and therefore lower blood sugar.[1] They act by inhibiting sodium-glucose transport protein 2 (SGLT2).
The gliflozins are used to treat type 2 diabetes mellitus but are most often used as second- or third-line agents instead of first-line because there are other medications on the market that have much longer safety record and are less expensive than gliflozins. These drugs may help improve insulin resistance and obesity, but for now, they’re approved only for people with type 2 diabetes.
These are the known members of the gliflozin class:
- Canagliflozin was the first SGLT2 inhibitor to be approved for use in the United States. It was approved in March 2013 under the brand name Invokana and it was also marketed throughout the EU under the same name.[16][17]
- Dapagliflozin is the first SGLT2 inhibitor approved anywhere in the world, it happened in 2011 by the EU. It was approved for use in the United States under the brand name Farxiga by the Food and Drug Administration in January 2014.[18]
- Empagliflozin, approved in the United States in August 2014 under the brand name Jardiance by Boehringer Ingelheim.[19] Of the gliflozins, empagliflozin and tofogliflozin have the highest specificity for SGLT2 inhibition.[1] It is the only oral medicine for type 2 diabetes that has been shown to reduce the risk of cardiovascular death.[20]
- Ertugliflozin was approved in the United States under the brand name Steglatro in December 2017.[21]
- Ipragliflozin, produced by the Japanese company Astellas Pharma Inc. under the brand name Suglat, approved in Japan January 2014.[22][23]
- Luseogliflozin was approved in Japan March 2014 under the brand name Lusefi and was developed by Taisho Pharmaceutical.[24]
- Remogliflozin etabonate was commercially launched first in India by Glenmark in May 2019.
- Sergliflozin etabonate discontinued after Phase II trials.[25]
- Sotagliflozin is a dual SGLT1/SGLT2 inhibitor in phase III trials under the brand name Zynquista. Developed by Lexicon pharmaceuticals. If approved, sotagliflozin would be the first oral treatment in combination with insulin to treat type 1 diabetes mellitus.[26]
- Tofogliflozin was approved in Japan March 2014 under the brand names Apleway and Deberza developed by Sanofi and Kowa Pharmaceutical[27]
According to the drugs’ labels, the most common SGLT2 side effects are vaginal yeast infections, yeast infections of the penis, stuffy or runny nose, and changes in urination. These common side effects occurred in two percent or more of clinical trial participants.
- Urinary tract infection
- Female and male genital yeast infections
- Upper respiratory tract infections
- Increased urination
- Dyslipidemia (increase in cholesterol)
- Joint pain
- Nausea
- Thirst
- Back pain
- Constipation
- Flu
- Painful urination
While clinical trials show the most common side effects are relatively minor, FAERS shows the most reported adverse events are more serious. The top three most-reported events in FAERS are diabetic ketoacidosis — a condition where a lack of insulin causes acid to build up in the blood— fungal infections and kidney injuries.
In 2015, the FDA released a Drug Safety Communication warning about the risk of ketoacidosis — also called diabetic ketoacidosis — and serious urinary tract infections (UTIs). The agency required drug companies to add warnings to SGLT2 medication labels.
In the same communication, the FDA warned about the risk of urinary tract infections that could turn into life-threatening blood infections (urosepsis) and kidney infections (pyelonephritis). The agency identified 19 cases of blood and kidney infections that began as urinary tract infections.
In August 2018, the FDA released a Drug Safety Communication warning that SGLT2s may cause a rare but serious genital infection called necrotizing fasciitis of the perineum — also known as Fournier’s gangrene. The disease can be life-threatening. Symptoms include tenderness, redness or swelling of the genitals and fever.
From 2014 to Sept. 30, 2018, the FDA received reports of 41 cases of bladder cancer and bladder neoplasms (possible cancerous growths) in people who took Farxiga (dapagliflozin). One person died.
In 2017, the FDA required Johnson & Johnson and Janssen Pharmaceuticals to add a black box warning to Invokana, Invokament and Invokamet XR for lower limb amputations. The agency based its decision on the results of two large, randomized, placebo-controlled trials that found amputations occurred twice as often in people who took canagliflozin versus a placebo, according to the FDA’s Drug Safety Communication.
The FDA urges people who suffer from leg or foot pain or tenderness, sores or ulcers, or infections to contact their doctor. From 2016 to Sept. 30, 2018, the agency received 236 reports of amputation in people who took Invokana. Two cases resulted in death.
In 2016, the FDA warned medications containing canagliflozin and dapagliflozin may harm kidneys. The agency required the drugs’ makers to strengthen warnings on the medication inserts.
From March 2013 to October 2015, the FDA identified 101 reported cases of kidney injury in users of canagliflozin and dapagliflozin. Some people needed to be treated in the hospital with dialysis. About half of these cases occurred within one month of starting either of the drugs.
More recent FAERS data shows people reported 1,614 cases of kidney injury with all SGLT2s from 2013 to Sept. 30, 2018 — including 54 deaths.
SGLT2 inhibitors may help people with type 2 diabetes who already have heart disease, according to an empagliflozin study published in November 2015 in The NEJM and a canagliflozin study published in August 2017 in The NEJM. Both studies suggested the drugs may reduce the likelihood of having another heart attack, stroke, or dying from heart disease. The American Diabetes Association’s guidelines, published in January 2019 in the journal Diabetes Care, recommend SGLT2 inhibitors for people with diabetes who have been diagnosed with heart disease or who are at high risk for heart disease.
A review of 10 studies, published in January 2019 in Postgraduate Medicine, found that in people without kidney disease, taking an SGLT2 inhibitor was associated with lower levels of protein in the urine — a symptom of kidney disease — and a lower risk of developing this symptom.
But there are downfalls with SGLT2 inhibitors.
The most common side effects of SGLT2 inhibitors include genital yeast infections, flu-like symptoms and a sudden urge to urinate. SGLT2 Inhibitors May Increase Risk for Urinary Tract Infections. We know that, the incidence of urinary tract infections is about 50 perent greater in people with diabetes compared with people without diabetes. Moreover, SGLT2 inhibitors may increase the risk of genital infections.
In late August 2018, US Food and Drug Administration (FDA) issued a warning about necrotizing fasciitis of the perineum, also known as Fournier gangrene with the class of type 2 diabetes medicines called sodium-glucose cotransporter-2 (SGLT2) inhibitors. The SGLT2s affected by the warning include canagliflozin, dapagliflozin, empagliflozin, ertugliflozin, and their combinations. Fournier gangrene remains very rare, but is more common in people using sodium-glucose cotransporter (SGLT)2 inhibitors compared with other diabetes medications and has severe consequences, shows research.
Also, risk of increasing breast and bladder cancer remains a safety issue of SGLT2 (sodium glucose cotransporter type 2) inhibitors.
People have reported more than 28,100 adverse events for the four main SGLT2 drugs. Invokana has more serious adverse events than all the other drugs combined. But it was also the first drug in the class approved for sale, and it also averages more prescriptions per year.
Adverse Events Reports in FAERS
| DRUG | TIME PERIOD | TOTAL ADVERSE EVENTS | SERIOUS EVENTS | DEATHS |
|---|---|---|---|---|
| Invokana | 2013 – September 2018 | 18,131 | 10,796 | 255 |
| Farxiga | 2014 – September 2018 | 3,923 | 1,119 | 62 |
| Jardiance | 2014 – September 2018 | 6,046 | 3,100 | 116 |
| Steglatro | January 2018 – September 2018 | 59 | 7 | 0 |
The drugs’ labels warn about common side effects such as yeast infections and nausea. The FDA has also released several Drug Safety Communications about more rare but serious side effects such as flesh-eating genital disease, lower limb amputations with Invokana, kidney problems, ketoacidosis and bone fracture risks. In addition, Farxiga may increase the risk of bladder cancer.
People who suffered serious side effects after taking the drugs have filed lawsuits against SGLT2 inhibitor manufacturers, alleging the companies knew of the dangers but failed to warn the public.
While clinical trials show the most common side effects are relatively minor, FAERS shows the most reported adverse events are more serious. The top three most-reported events in FAERS are diabetic ketoacidosis — a condition where a lack of insulin causes acid to build up in the blood— fungal infections and kidney injuries.
In 2015, the FDA released a Drug Safety Communication warning about the risk of ketoacidosis — also called diabetic ketoacidosis — and serious urinary tract infections (UTIs). The agency required drug companies to add warnings to SGLT2 medication labels.
In the same communication, the FDA warned about the risk of urinary tract infections that could turn into life-threatening blood infections (urosepsis) and kidney infections (pyelonephritis). The agency identified 19 cases of blood and kidney infections that began as urinary tract infections.
In August 2018, the FDA released a Drug Safety Communication warning that SGLT2s may cause a rare but serious genital infection called necrotizing fasciitis of the perineum — also known as Fournier’s gangrene. The disease can be life-threatening. Symptoms include tenderness, redness or swelling of the genitals and fever.
From 2014 to Sept. 30, 2018, the FDA received reports of 41 cases of bladder cancer and bladder neoplasms (possible cancerous growths) in people who took Farxiga (dapagliflozin). One person died.
In 2017, the FDA required Johnson & Johnson and Janssen Pharmaceuticals to add a black box warning to Invokana, Invokament and Invokamet XR for lower limb amputations. The agency based its decision on the results of two large, randomized, placebo-controlled trials that found amputations occurred twice as often in people who took canagliflozin versus a placebo, according to the FDA’s Drug Safety Communication.
The FDA urges people who suffer from leg or foot pain or tenderness, sores or ulcers, or infections to contact their doctor. From 2016 to Sept. 30, 2018, the agency received 236 reports of amputation in people who took Invokana. Two cases resulted in death.
In 2016, the FDA warned medications containing canagliflozin and dapagliflozin may harm kidneys. The agency required the drugs’ makers to strengthen warnings on the medication inserts.
From March 2013 to October 2015, the FDA identified 101 reported cases of kidney injury in users of canagliflozin and dapagliflozin. Some people needed to be treated in the hospital with dialysis. About half of these cases occurred within one month of starting either of the drugs.
More recent FAERS data shows people reported 1,614 cases of kidney injury with all SGLT2s from 2013 to Sept. 30, 2018 — including 54 deaths.
When compared in a cursory manner, DPP-4 inhibitors and sulfonylureas seem to be totally different classes of drugs. However, we should be mindful of two important aspects here:
- Both DPP-4 inhibitors and sulfonylureas are insulin secretagogues; the key difference is that DPP-4 inhibitors act indirectly on the beta cell, via the incretin pathway, while sulfonylureas act directly to increase insulin secretion.
- Not all sulfonylureas are alike. Modern sulfonylureas, such as gliclazide modified release (MR) and glimepiride, have different molecular structures, binding sites and pharmacokinetics to the older formulations, which allow for much safer glucose control.
DPP-4 inhibitors vs modern sulfonylureas: Not so different?
When DPP-4 inhibitors are compared with modern sulfonylureas alone, multiple similarities become more obvious, as highlighted in the table below:
| Characteristic | DPP-4 inhibitors | Modern sulfonylureas |
| Affected by weight | Weight-neutral and cause less hypoglycemia. | Weight-neutral, have low risk of hypoglycemia. |
| Demographic suitability | Can be used in the elderly and those who fast. | Can be used safely in prolonged fasting such as during Ramadan. |
| Cardio-renal benefit and safety | Linagliptin, sitagliptin, and alogliptin have proven cardiovascular safety; however, saxagliptin is associated with an increased risk of hospitalization for heart failure. Linagliptin has been shown to have renal benefits in terms of albuminuria reduction | Gliclazide MR has been shown to have cardiovascular and renal benefits in the ADVANCE and ADVANCE-ON studies. |
| Dose adjustment requirement | Linagliptin does not require dose adjustment. | Require dose titration. |
From a nationwide cohort in Korea (2008–2013), 23,674 patients with type 2 diabetes treated with DPP4i plus metformin or SU plus metformin showed that DPP4i therapy did not increase the overall risk of major cardiovascular and renal outcomes compared to SU therapy. However, the DPP4i-associated risk of hospitalization for heart failure (HHF) remained significant.
The dipeptidyl peptidase (DPP)-4 inhibitor linagliptin and the sulfonylurea glimepiride have similar cardiovascular safety profiles, show the results of the CAROLINA trial. The findings of the CAROLINA trial, which is the first cardiovascular outcomes trial to use an active comparator medication, may remove cardiovascular risk from the list of sulfonylureas’ drawbacks. The two medications produced similar glycemic control, with glycated hemoglobin levels deteriorating in both groups after initial improvements, and although bodyweight changes favored linagliptin, the difference was only modest – around 1.5 kg on average.
The McAuley index is a handy surrogate measure of insulin resistance. It basically estimates rather than measures your likelihood of being insulin resistant.
It only needs 2 things, fasting insulin and fasting triglycerides [1]. Such fasting indexes are usually not very useful because they have a high false-positive rate (i.e. it says you’re insulin resistant when in fact you’re not). However, the McAuley index is an exception to this rule. The problem with most fasting indexes is that they only capture a snapshot: the measurement in this very moment, which can be influenced by many factors, such as quality of sleep the night before or what you have eaten.
The reason why the McAuley index is more reliable is because it includes fasting triglycerides. Glucose and insulin levels don’t directly influence triglycerides, it is rather indirect and delayed in time. The fasting triglycerides value is, therefore, more stable over several hours, which makes it more reliable than standard fasting indexes. It is a shame that it is hardly known and under-used.
Because chronically elevated insulin levels and insulin resistance create this big fat storage problems, it is fair to say that hyperinsulinemia is toxic. Insulin toxicity increases the risk of atherosclerosis, cardiovascular diseases, and cancer [1,2,3,4].
It has been believed for a long time that glucose toxicity alone explains the increased risk of these conditions. This isn’t correct, insulin and other factors play a role too [5]. Case in point, controlling blood glucose levels by injecting insulin does not decrease the heart disease risk [6]. In fact, the opposite is true! Increased levels of insulin from injections further increase the net risk, despite lowering blood glucose sugars.
Diabetes is actually five separate diseases,” reports BBC News on a study looking at nearly 9,000 people with diabetes in Sweden and Finland.
The American Diabetes Association classifies diabetes into four major categories: type 1 diabetes (insulin deficient), type 2 diabetes, gestational diabetes (diabetes in pregnancy), and specific types of diabetes due to other causes, such as maturity-onset diabetes of the young (MODY), disease of exocrine pancreas, latent autoimmune diabetes in adults (LADA).
Short answer: Yes. Long answer: It depends – and even when possible, it may be difficult.
increasingly research finds that in some instances diabetes may be reversed, or – to use the parlance more commonly associated with cancer – a person may be able to achieve remission. That is, in some people previously diagnosed with diabetes, their blood sugar is now back in a non-diabetic range without medication.
That’s exactly what happened for more than one-third (36%) of participants randomly assigned to a weight management program, according to a two-year follow-up of a trial published in The Lancet Diabetes & Endocrinology in March. The most recent follow-up of the Diabetes Remission Clinical Trial, or DiRECT, assessing the impact of intensive weight management in primary care concluded, “Sustained remission was linked to the extent of sustained weight loss.” Nearly half (or 46%) of those in the intervention group had achieved and sustained remission at one-year, according to previous follow-up research published in The Lancet in 2018. The research involved individuals 20 to 65 years old who’d had diabetes for less than six years at the outset of the study.
Precisely who may be able to bring diabetes into remission and when it’s possible – let alone achievable for most individuals – remains unclear. Given that lack of clarity around when, and to what extent diabetes remission is possible, controversy still exists around how to discuss diabetes reversal. But, experts say that the early-going in the disease course seems to offer the best opportunity for potentially reversing the disease. And some clinicians and researchers say this should be more of an aim in primary care for patients who are newly diagnosed with the disease.
“It’s not impossible at all to reverse diabetes,” says Dr. Peter Arvan, chief of the division of metabolism, endocrinology and diabetes at the University of Michigan. Certainly, though, experts are quick to point out that often what it takes to do so, such as wholesale changes to completely alter the way one eats and shifting one’s schedule to prioritize exercise, can be challenging to say the least.
Although there’s no guarantee that you’ll reverse diabetes with weight loss and lifestyle changes, either, there’s no downside to making healthier choices. And to manage the disease – whether it’s possible to achieve remission or not – you’ll want to work closely with your health care team.
Although weight loss is probably the most important part of a diabetes reversal program, We believe that the best approach is to consider the whole person when selecting a reversal strategy. Not only should we identify ways to decrease the fat in the liver and pancreas and prevent further accumulation, but we need to consider increasing healing nutrients in the diet, getting the proper amount and the proper timing of exercise; we need to increase the amount of fiber in the diet, drink adequate water, have a good way to manage stress; we need to get plenty of sleep and avoid unnecessary snacking; we also need a strong support system, and an effective way to handle stress; we need to have a strong spiritual practice; and we need to regularly set realistic health goals and then work diligently to achieve them. This multi-dimensioned approach will give us our best hope for reversal.
Chronic Metformin use results in vitamin B12 deficiency in many diabetic patients. A potential consequence of B12 deficiency is that it could directly result in neuropathy or exacerbate diabetic neuropathy. Arms and feet could tingle or feel numb due to depletion of Vitamin B12, which is critical for nerve insulation. Our nerves are like electric wires and we need Vitamin B12 to keep the protective sheath of the nerves healthy. Metformin interferes with B12 absorption in the body. This leads to nerves becoming extra sensitive, almost like having a short circuit. If nerves get deadened instead, one could feel numbness or that ‘pillow walking’ feeling diabetics often complain about.
Additionally, Metformin increases homocysteine levels as well as methylmalonic acid levels, both contributing factors to neuropathy.
Because peripheral neuropathy is such a major complication of diabetes, people using metformin be screened for vitamin B12 deficiency or supplemented with vitamin B12. Also, anyone already diagnosed with peripheral neuropathy who uses metformin should be screened for vitamin B12 deficiency.
Atherogenic index of plasma (AIP) was found to be one of the strongest markers in predicting the cardiovascular disease (CVD) risk.
Atherogenic Index of Plasma and Triglyceride/High-Density Lipoprotein Cholesterol Ratio Predict Mortality Risk Better Than Individual Cholesterol Risk Factors.
Atherogenic index of plasma (AIP) is a strong predictive indicator of coronary artery disease in postmenopausal women.
Higher Atherogenic Index of Plasma level is positively and strongly associated with obesity.
Atherogenic Index of Plasma and Mean Platelet Volume regardless of ischemic etiology, were significantly higher in heart failure compared with controls. Both AIP and MPV are independent predictors of ejection fraction and have cut-off values for diagnosis of HF.
In type 2 diabetes mellitus patients; mean FBG, mean HbA1c and mean atherogenic index values were significantly higher in those patients having poor glycemic control than in those patients having good glycemic control. Also, atherogenic index is positively correlated with FBG and HbA1C.
Atherogenic Index of Plasma is calculated as Log (TG/HDL-C). Triglycerides and HDL-cholesterol in Atherogenic Index of Plasma (AIP) reflect the balance between the atherogenic and protective lipoproteins.
Usually Atherogenic Index of Plasma (AIP) values of < 0.1 are associated with low, 0.1 to 0.24 with medium and above 0.24 with high Cardio Vascular risk.
Because, Metformin makes your body think it’s working out and additional exercise is difficult.
A study just published in Aging Cell reports that metformin blunts the benefits of exercise training: Metformin inhibits mitochondrial adaptations to aerobic exercise training in older adults.
Participants, average age 62, were randomized to either metformin or placebo, and undertook aerobic exercise training for 12 weeks. This isn’t a surprise, since it’s already known one way in which metformin works is by inhibition of Complex 1 in mitochondria. (Ref) By inhibiting mitochondria, the powerhouses of the cell, less ATP is formed, which activates AMPK, an energy sensor. In turn, AMPK activates many processes that contribute to better metabolism, including lower insulin and glucose and increased fat burning.
The blunting effect of metformin on exercise was not small either. Increase in VO2max in the metformin group was only about 50% that of the placebo group. The improvement in whole-body insulin sensitivity in the metformin group was zero, compared to a significant increase in the placebo group.
Another study, “Metformin and Exercise in Type 2 Diabetes”, determined the effects of metformin on the metabolic response to sub-maximal exercise, the effect of exercise (relevant to activity patterns of type 2 diabetics) on plasma metformin concentrations, and the interaction between metformin and exercise on the response to a standardized meal. There is evidence that suggests that the benefits of exercise and metformin aren’t cumulative. In a study whose results were noted in this one, the reductions in diabetic risk were similar in a lifestyle that combined metformin and lifestyle modifications to the metformin or lifestyle alone groups. And in fact, the two adjustments may have contradictory effects on diabetes. First, metformin reduces blood glucose levels. But exercise tends to increase levels of glucagon, the hormone that deals with low blood sugar. When the two are combined, glucagon concentrations become significantly higher as the body tries to compensate for the effect of metformin. Second, by increasing the heart rate, metformin has the potential to lower some patients’ selected exercise intensity, which means it could lead to the prescription of lower exercise workloads than are commonly recommended. So, the combination of exercise and metformin, both common prescriptions for diabetics, is likely less effective at lowering the glycemic response to a meal than metformin alone.
The cancer research suggests that Metformin reduces any gains in insulin sensitivity that normally would be achieved from exercise.
According to one study, physical exercise can increase insulin sensitivity by up to 54% in insulin resistant individuals, unless of course, they are taking Metformin. Metformin abolishes any increased insulin sensitivity gained by exercise. Metformin also reduces peak aerobic capacity, reducing performance and making exercise more difficult.
Metformin reduces mitochondrial ATP production in skeletal muscle by as much as 48%. Sit with that one for a moment, a 48% reduction in cell fuel. Imagine functioning at only half capacity. This would make basic activities difficult at best and exercising to lose weight a very unlikely proposition. Moreover, despite claims to the contrary, Metformin does not appear to be an especially effective tool for weight loss, netting a reduction of only 5-10 pounds over 4-8 months. Regular exercise and a healthy diet net on average a loss of 5-10 pounds per month for most people and are significantly more effective at reducing diabetes and associated health complications without the potential side effects.
Metformin abolishes the improvement in mitochondrial respiration after aerobic exercise training. Metformin attenuates the improvement in physiological function after aerobic exercise training. The study reasoned that the cellular energy sensor AMPK would have increased activity due to the energetic stress of metformin preventing the increase in mitochondrial respiration in response to the energetic demands of exercise training.
Since cardiorespiratory fitness is one of the strongest factors for survival into old age, and since it decreases with age, the effect of metformin on this factor is concerning.
Surprisingly, a study in rats found little evidence for additive effects of combining metformin and aerobic exercise training on outcomes of obesity, type 2 diabetes, and NAFLD and actually suggest potential impairments in exercise-induced hepatic mitochondrial adaptations.
A study showed that, for individuals undergoing intensive lifestyle therapy, background metformin therapy conferred little additional benefits.
When cells are exposed to mitochondria damage, a central cellular fuel gauge, the enzyme AMPK, sends an emergency alert to mitochondria instructing them to break apart into many tiny mitochondrial fragments. Interestingly, AMPK is activated by the widely used diabetes therapeutic metformin, as well as exercise and a restricted diet.
Metformin is the most widely prescribed drug for the treatment of diabetes. Although, the exact molecular mechanism of action of metformin remains partly unknown despite its use for over 60 years and more than 17,000 articles in PubMed, its main mechanism of action is widely recognized as inhibition of mitochondrial complex I, increasing the glycolytic pathway through reduction of OXPHOS. Due to lower production of mitochondrial ATP, the AMP/ATP index increases and activates AMPK which further inhibits mTOR. Used at high doses it may produce lactic acidosis due to increased lactic acid production. Phenformin is metformin’s predecessor with similar effects on lactic acid production, but is a more powerful inhibitor of the mitochondrial respiratory chain which entails an increased risk of lactic acidosis. This adverse effect led to the withdrawal of this drug from the market.
The primary target of metformin is the inhibition of mitochondrial complex I→ low ATP → high AMP/ADP (energetic stress) → activation of AMPK (an enzyme that senses low energy levels and activates numerous pathways to restore the intracellular ATP)→ increased glucose transport into cells and glucose metabolism (increased insulin sensitivity). Basically, Metformin is a kind of mitochondrial “poison” that, as a result, reduces ATP production and, thus, activates AMPK. This, of course, stimulates nutrient catabolism, lowering glucose, which lowers insulin, etc.
Cells treated with metformin become energetically inefficient, and display increased aerobic glycolysis and reduced glucose metabolism through the citric acid cycle. So, cancer cells exposed to metformin display a greater compensatory increase in aerobic glycolysis than nontransformed cells, highlighting their metabolic vulnerability.
Preasbsorptive metformin activates AMPK in gastrointestinal cells, which indirectly lowers blood glucose by reducing the amount of glucose that goes into the bloodstream.
Metformin activates AMPK in liver cells, which inhibits gluconeogenesis and the liver excretes less glucose.
Pretty smart, yes?
Metformin also activates AMPK in skeletal muscle, and we know that when AMPK is activated by ATP depletion, AMPK switches on catabolic pathways that generate ATP while switching off anabolic pathways and other ATP-consuming processes, which restores the energy balance. So it is not rocket science, that Metformin blunts the benefits of exercise by reducing mitochondrial ATP production in skeletal muscle by as much as 48%. In simple terms, Metformin abolishes the improvement in mitochondrial respiration after exercise training.
Since cardiorespiratory fitness is one of the strongest factors for survival into old age, and since it decreases with age, the effect of metformin on this factor is concerning.
A study of over 7,000 patients with Alzheimer’s disease showed that, metformin increased the risk of developing Alzheimer’s . No large clinical trials have confirmed whether metformin is beneficial in non-diabetic Alzheimer’s patients. In a cohort study that followed about 9300 patients with T2DM in Taiwan for up to 12 years, the risk for Parkinson’s disease (PD) or Alzheimer’s dementia was more than double during a 12-year period for those who took metformin vs those who did not — even after adjusting for multiple confounders. The use of metformin may be associated with an increased risk for dementia in older African Americans with diabetes. This research was presented at the 2018 Alzheimer’s Association International Conference, held July 22-26, 2018 in Chicago, Illinois.
Imagine reductions in ATP production were observed in the brain or the heart or the GI tract which leads to neurocognitive decline, psychiatric instability, neuropathy, heart rate, rhythm and blood pressure abnormalities, along with gastrointestinal distress to name but a few. Underlying all of these symptoms, and indeed, all mitochondrial dysfunction, is an overwhelming sense of fatigue and malaise.
Metformin is excreted almost entirely unchanged in urine so reduced kidney function may lead to accumulation of both metformin and lactate and therefore, a metformin-associated lactic acidosis (MALA). So it’s not a secret that, Metformin may have an adverse effect on renal function in patients with T2D and moderate CKD. Mild to moderate renal impairment is common among metformin initiators. Even, FDA recommends against starting metformin therapy in patients with estimated glomerular filtration rate (eGFR) between 30 and 45 mL/min/1.73m2
By the way, Metformin alters immune reactivity first by damaging the mitochondrial ATP factory and reducing energy production capacity and then by inhibiting the signaling cascades that would normally respond to the danger signals.
So, what gives? Is metformin healthy and anti-aging, or not?
When we contrast the reduction in glucose mediated by Metformin with the damage this medication does to the mitochondria and immune signaling, along with its ability to leach vitamin B12, block insulin sensitivity and reduce aerobic capacity, one cannot help but wonder if we are causing more harm than good.
Although metformin is not often acutely toxic, the underlying mechanisms manipulated by this drug suggest that it is likely to induce and not prevent, as is so frequently suggested, chronic illness.
Long-term use of the diabetes medication metformin may increase the risk for neurodegenerative disease in patients with type 2 diabetes mellitus (T2DM), new research suggests.
A study of over 7,000 patients with Alzheimer’s disease showed that, metformin increased the risk of developing Alzheimer’s . No large clinical trials have confirmed whether metformin is beneficial in non-diabetic Alzheimer’s patients.
In a cohort study that followed about 9300 patients with T2DM in Taiwan for up to 12 years, the risk for Parkinson’s disease (PD) or Alzheimer’s dementia was more than double during a 12-year period for those who took metformin vs those who did not — even after adjusting for multiple confounders. The use of metformin may be associated with an increased risk for dementia in older African Americans with diabetes. This research was presented at the 2018 Alzheimer’s Association International Conference, held July 22-26, 2018 in Chicago, Illinois.
Additionally, Metformin is associated with low vitamin B12 levels and people with profoundly low vitamin B12 levels can have significant cognitive impairment.
The pancreas, which is responsible for making and releasing the hormone insulin, is especially sensitive to melatonin levels. While melatonin levels are high during nighttime hours, insulin levels are at their lowest. Melatonin binds to receptors in the pancreas and cause a slowdown in insulin production while you’re asleep. This makes sense when you think about the role of insulin.
And, since you’re in a period of fasting during sleep, low levels of insulin at night actually help keep blood sugar levels stable, preventing hypoglycemia, until you eat again the next day.
If melatonin levels are low, then the suppression of insulin activity at night is also decreased. This means your pancreas doesn’t get a nightly rest from producing insulin.
When insulin levels are elevated around the clock, your pancreas can become inefficient at making enough insulin and/or the cells in the rest of your body can become desensitized in response to exposure to too much insulin. This is known as insulin resistance. It results in increased blood sugar levels and is a major risk factor in developing type 2 diabetes.
Many patients who are ultimately diagnosed with diabetes first go to their doctor with concerns about unexplained weight loss. Weight loss can occur as a consequence of high blood sugar, dehydration, muscle breakdown and problems with your thyroid.
High Blood Sugar
Although both type 1 and type 2 diabetes can involve fairly dramatic weight loss over several days at the onset of the disease, it tends to be more common among people with type 1. In both cases, the cause is that your body fails to adequately deal with insulin. The job of insulin is to transport glucose from the foods you eat into your cells to provide energy for all the work that’s required to keep you alive. However, most type 1 diabetics don’t produce insulin. Type 2 diabetics either don’t produce enough insulin or their bodies don’t respond to it properly. Consequently, even if you eat normally, that blood sugar simply builds up and gets excreted in your urine. This causes weight loss, but it could also damage your organs if you don’t receive treatment. If you experience an unexplained weight loss, surpassing 5 percent of your body weight within days, see your health care provider as soon as possible.
Dehydration
Another symptom of diabetes associated with weight loss is frequent urination. When you urinate more frequently and don’t drink enough to replace the lost fluid, you become dehydrated. Urination increases in diabetes, because your kidneys have to work harder to filter the excess glucose building up in your system. The increased glucose in the urine draws fluid from your tissues. When you lose glucose through your urine, you’re also losing calories. This, as well as dehydration, can lead to rapid weight loss.
Muscle Breakdown
Poorly controlled diabetes can cause weight loss through muscle wasting, according to a report published in the “British Medical Journal.” Scientists in this study found that the insulin deficiency found in diabetes both decreases muscle synthesis and increases its breakdown. In a later meta-analysis published in the “Journal of Nutrition,” these findings were confirmed, with the report saying that insulin replacement helps diminish this effect of the disease. However, as muscle makes up up to 36 percent of an average woman’s weight and up to 45 percent of a man’s weight, muscle wasting can lead to weight loss through diabetes.
Hyperthyroidism
People with diabetes have a higher prevalence of thyroid disorders than people without diabetes, according to Dr. Patricia Wu. The thyroid is a hormone-producing gland inside your neck that sits above your collarbone, just underneath your skin. The thyroid helps set your metabolic rate. With hyperthyroidism, the glands makes too much hormone and causes weight loss. Wu explains that this dysfunction can worsen blood sugar control and require that you take more insulin. It also makes your liver produce more blood sugar and is linked to greater insulin resistance. In fact, says Wu, excessive amounts of thyroid hormone in the bloodstream might reveal latent diabetes. A major sign of hyperthyroidism is weight loss. It also speeds up your heart rate and causes sweating and tremors, symptoms that look a lot like low blood sugar. Your health care provider will advise you on how to monitor your blood sugar to understand the effects of hyperthyroidism and blood sugar fluctuations.
In 1986, the World Health Organization helped to fund the China Da Qing Diabetes Prevention Outcomes Study, a randomized controlled trial of lifestyle interventions lasting over twenty years. During the first six years of active intervention of diet and exercise, the incidence of diabetes was reduced by 43%. This benefit persisted over the extended follow up period of twenty years. Onset of type 2 diabetes had been delayed by an average of 3.6 years with diet and exercise.
Similar randomized, controlled studies of lifestyle interventions have shown exactly the same benefit around the world. In the United States, the Diabetes Prevention Program reduced the incidence of type 2 diabetes by 58% while maintaining an average weight loss of 5% over 4.8 years. Ten-year follow up continued to show a substantial 34% benefit. The Indian Diabetes Prevention Programme used lifestyle modifications to reduce the incidence of type 2 diabetes by almost 30%. The Finnish Diabetes Prevention Program reported a 58% reduction. A Japanese trial was able to reduce progression by 67%.
The one factor of over-riding important to note is that all these successful prevention studies use lifestyle changes. Type 2 diabetes is overwhelmingly a lifestyle disease, so lifestyle interventions are required, not medications. You can’t use drugs to prevent a dietary disease.
You can do a lot to reduce your chances of developing type 2 diabetes. Here are some things you can change to lower your risk:
- Lose weight and keep it off. You may be able to prevent or delay diabetes by losing 5 to 7 percent of your starting weight. For instance, if you weigh 90 kg, your goal would be to lose about 5-10 kg.
- Move more. Get at least 30 minutes of physical activity 5 days a week. If you have not been active, talk with your health care professional about which activities are best. Start slowly to build up to your goal.
- Eat healthy unprocessed foods most of the time.
- Drink water instead of sweetened beverages.
- Adopt Time Restricted Eating habit. An example of time-restricted eating is if you choose to eat all your food for the day in an 8-hour period, such as from 10 a.m. to 6 p.m. The remaining 16 hours each day are the fasting period, during which no calories are consumed.
Apart from Dawn effect, a second possible cause of high blood sugar levels in the morning is the Somogyi effect, sometimes also called rebound hyperglycemia. It was named after the doctor who first wrote about it.
If your blood sugar drops too low in the middle of the night while you are sleeping, your body will release hormones in an attempt to “rescue” you from the dangerously low blood sugar. The hormones do this by prompting your liver to release stored glucose in larger amounts than usual. But this system isn’t perfect in a person with diabetes, so the liver releases more sugar than needed which leads to a high blood sugar level in the morning. This is the Somogyi effect.
How is it determined if the dawn phenomenon or Somogyi effect is causing the high blood sugar levels?
Your doctor will likely ask you to check your blood sugar levels between 2 a.m. and 3 a.m. for several nights in a row. If your blood sugar is consistently low during this time, the Somogyi effect is suspected. If the blood sugar is normal during this time period, the dawn phenomenon is more likely to be the cause.
Some additional clues that the Somogyi effect may be the cause include nightmares, restless sleep and overnight sweating as these are all signs of low blood sugar levels.
“The dawn phenomenon, sometimes called the dawn effect, is an early-morning (usually between 2 a.m. and 8 a.m.) increase in blood sugar (glucose) which occurs to some extent in all humans, more relevant to people with diabetes.”– from Wikipedia, the free encyclopedia.
When you wake up in the morning, the body needs to shift gears. When you’re sleeping, your body is in rest and repair mode, called parasympathetic function. When the sun comes up and you start your day, you shift into sympathetic function. The body gives us a little burst of energy from various hormones, which raise blood sugar and activates our muscles, and senses. Without this, most of us would be too weak and foggy-brained to get out of bed and get going.
People who don’t have diabetes are, of course, at an advantage, because as their blood glucose increases, so does insulin, and their livers are sensitive and responsive to that insulin. People with diabetes and blood sugar problems don’t properly respond to insulin, so their early morning blood glucose levels can rise dramatically.
If these early morning blood sugar spikes aren’t caused by food, what is the cause?
Although the exact underlying causes of the dawn phenomenon are still unclear, it is known that hormones, including adrenaline, cortisol, glucagon, and growth hormone, play a large part. These hormones follow a circadian rhythm, or a daily cycle, and tend to be found in higher concentrations in the blood in the morning to help prepare us for the day ahead.
The hormones that promote glucose release into the blood include:
- Adrenaline: Known as the “fight or flight” hormone, adrenaline increases blood flow to the muscles and promotes the release of glucose into the blood.
- Cortisol: Known as the “stress hormone”, cortisol also plays a role in increasing blood glucose.
- Glucagon: Signals the liver to release glucose into the blood.
- Growth Hormone: Important for repair and regeneration and promotes the release of glucose into the blood.
Two key processes occur in the liver overnight that result in the release of glucose into the bloodstream and contribute to increased morning blood glucose:
1) Glycogenolysis, the breakdown and release of stored glucose (a.k.a. glycogen)
2) Gluconeogenesis, the creation of glucose from components of protein (i.e. certain amino acids) or fat (i.e. glycerol)
One more hormone that plays an important role is insulin. When blood glucose rises, insulin is released and helps move glucose out of the blood and into cells for energy use or storage.
Does the dawn phenomenon occur only in people with prediabetes and type 2 diabetes?
The physiological processes that underlie the dawn phenomenon occur in everyone regardless of whether they have diabetes or not. The difference lies with insulin and how our bodies react to it. Healthy individuals secrete enough insulin and are insulin sensitive enough to counteract a rise in morning blood glucose. However, someone with prediabetes or type 2 diabetes is insulin resistant and/or may not secrete enough insulin, which allows blood glucose to rise. This may be further compounded in the early morning hours because our body is more insulin resistant compared to the rest of the day, causing an elevated fasting glucose to remain elevated longer. Progression of prediabetes and type 2 diabetes is likely to result in a worsening of the dawn phenomenon as insulin function and sensitivity continue to diminish.
“Eat many, small meals to stoke the metabolic flame.” Many people believe that eating small meals more frequently keeps your metabolism humming, prevents hunger, and controls blood sugar. As a result, your body burns more calories overall. Sound good, right? Except it may not work that way.
The idea that eating more frequent, smaller meals will boost your metabolism is a persistent myth and research shows that this is simply not true. While this idea sounds legit in theory, most studies have found no link between meal frequency and increased TEF. In fact, after examining four separate studies (in which people split the same total caloric intake among anything from one to seven meals), the International Society of Sports Nutrition found that increasing the number of meals consumed per day did not improve resting metabolic rate or 24-hour energy expenditure.
It is true that the body expends a certain amount of energy digesting and assimilating the nutrients in a meal. This is termed the Thermic Effect Of Food (TEF), and amounts to about 20-30% of calories for protein, 5-10% for carbs and 0-3% for fat calories. On average, the thermic effect of food is somewhere around 10% of the total calorie intake.
However, what matters here is the total amount of calories consumed, not how many meals you eat. And for the most part, research shows that eating more frequently doesn’t appear to boost weight loss.
Eating six 500-calorie meals has the exact same effect as eating three 1000-calorie meals. Given an average thermic effect of 10%, it is 300 calories in both cases.
This is supported by numerous feeding studies in humans, showing that increasing or decreasing meal frequency has no effect on total calories burned.
BOTTOM LINE: There is no difference in calories burned if you eat more frequently. Total calorie intake and macronutrient breakdown is what counts.
In the study, published October 9, 2018, in the journal BMJ Case Reports, intermittent fasting, in which eating is limited during certain times of the day or week, reportedly helped three middle-aged men with type 2 diabetes lose weight, get off their insulin, and reduce or get off their oral medication.
“Everyone has a physician inside him or her; we just have to help it in its work. The natural healing force within each one of us is the greatest force in getting well. Our food should be our medicine. Our medicine should be our food. But to eat when you are sick is to feed your sickness.” – Hippocrates
A recent study published in the journal cell in 2017 shows how a fasting diet can trigger the pancreas to regenerate itself, which works to control blood sugar levels and reverse symptoms of diabetes.
Mark Mattson, one of the foremost researchers of the cellular and molecular mechanisms underlying multiple neurodegenerative disorders, like Parkinson’s and Alzheimer’s disease, has shown through his work that fasting can have a tremendous effect on the brain, and could prevent or even reverse the symptoms of multiple neurodegenerative disorders. You can watch a great TEDx talk he gave on the topic here.
The problem is we don’t treat diabetes as a dietary problem; we treat it with a lot of drugs, and that never addresses the root problem of the diabetes. Since type 2 diabetes is merely excessive glucose in the body, burning it off will reverse the disease. Fasting is the simplest and fastest method to force your body to burn sugar for energy. Glucose in the blood is the most easily accessible source of energy for the body. Fasting is merely the flip side of eating — if you are not eating you are fasting. When you eat, your body stores food energy. When you fast, your body burns food energy. If you simply lengthen out your periods of fasting, you can burn off the stored sugar. The answer for Type 2 diabetes is to stop feeding your body sugar and burn off the sugar already in your cells, and the most effective way to do this is fasting, which less than inexpensive — it’s free.
While it may sound severe, fasting has been practiced for at least 2000 years. It is the oldest dietary therapy known. Literally millions of people throughout human history have fasted without problems.
STANDARD MEDICATIONS FOR type 2 diabetes represent a trade-off between glucotoxicity and insulin toxicity. Insulin, TZDs, and SUs all increase insulin or its effect to reduce hyperglycemia. The effect of the increased insulin becomes clinically obvious as weight gain. The price of better glucose control has been higher insulin dosage, so there is no net benefit. These medications simply trade lower glucotoxicity for higher insulin toxicity.
Metformin and DPP-4 medications use mechanisms other than raising insulin to lower blood glucose. But they do not lower insulin either, so the result is neither weight gain nor weight loss. Reducing glucotoxicity while keeping insulin neutral produces minimal benefits. Clinically, these medications are weight neutral, but also neutral with regard to cardiovascular risk or benefits.
Meta-analyses reviewing all the available literature up to 2016, including twenty randomized controlled trials, could only conclude that “there is no significant evidence of long term efficacy of insulin on any clinical outcome in T2D (type 2 diabetes). A similar review in the Journal of the American Medical Association that included all relevant trials up to March 2016 found that none of the drug classes considered, including metformin, SUs, TZDs, and DPP-4 inhibitors, reduced cardiovascular disease or other complications. Importantly, these older medications did not reduce the hyperinsulinemia that is the root problem, or indeed, made it worse. Again, diabetes will continue unless we treat the root cause.
While the scientific evidence is crystal clear, diabetes guidelines are slow to reflect this new reality. Dr. Victor Montori of the Mayo Clinic discovered that 95 percent of published guidelines endorsed the use of diabetes drugs despite their nonexistent benefits. Why would you take medications that have no benefits? Worse, why would you take medications that have no benefits and make you fat?
The classic medical treatment, which relies almost exclusively on pharmaceuticals to reduce blood glucose, can therefore best be described as how not to treat type 2 diabetes. By contrast, newer agents, which can reduce both blood glucose and insulin levels, show proven benefits to reduce heart and kidney complications of type 2 diabetes. Nevertheless, these medications, while an important step forward, are clearly not the answer; they do not reverse the root cause of type 2 diabetes—our diet.
DIABETES, AS WELL as obesity and prediabetes, increases the risk of many different types of cancer, including breast, colon, endometrial, kidney, and bladder cancers. This suggests that factors other than increased blood glucose play a major role in the development of cancers, further disproving the glucotoxicity paradigm as the major cause of disease.
Insulin, a hormone well known to promote growth, can drive tumor growth, and women with the highest insulin levels carry a 2.4-fold higher risk of breast cancer. Obesity may be a contributing factor, but hyperinsulinemia is associated with an increased risk of cancer, independent of weight. Lean and overweight women, when matched for insulin level, exhibit the same risk of breast cancer.
The intimate link between insulin and cancer is reinforced by the discovery of a single mutation in the PTEN oncogene that significantly increases the risk of cancer. What’s the connection? This mutation increases the insulin effect. It lowers the blood glucose and reduces the risk of diabetes, but increases the risk of obesity and cancer.
Similarly, medications that raise insulin toxicity are associated with higher rates of cancer. Insulin use increases the risk of colon cancer by approximately 20 percent per year of therapy. The UK General Practice Database revealed that insulin increased the risk of cancer by 42 percent compared with a glucose-lowering drug that did not raise insulin. And a review of the newly diagnosed diabetics in the Saskatchewan population disclosed that use of insulin raised the risk of cancer by 90 percent.
It’s simple to understand why high insulin levels should favor cancer cell growth. First, insulin is a known hormonal growth factor. Second, cancer cells are highly metabolically active and need large supplies of glucose to proliferate. Insulin increases the risk of cancer, and once cancer has been established, high blood glucose enables it to grow faster.
While the lifespan of people with type 1 diabetes has increased progressively since the advent of insulin therapy, these patients still experience premature mortality, primarily from cardiovascular disease (CVD). However, a subgroup of those with type 1 diabetes survives well into old age without significant morbidity.
Early glycaemic control is an important factor in preventing CVD in type 1 diabetes and it might be expected that hyperglycaemia plays a major role in explaining the increased incidence of CVD and mortality, but it is apparent that good glycaemic control alone cannot explain why some patients with type 1 diabetes avoid fatal CVD events. For example, the Golden Years Cohort Study followed 400 patients with type 1 diabetes who lived for over fifty years with their disease. They had beaten the odds and survived. What was their secret? Well, it certainly was not tight blood glucose control. Their average A1C was 7.6 percent, with some as high as 8.5 to 9.0 percent, which is well above the standard recommended target of 7.0 percent. In fact, not a single Golden Years Cohort patient had an A1C in the normal range, ruling out glucotoxicity as a major player. The entire Golden Years Cohort of survivors had suboptimal blood glucose control and yet their health was excellent.
The common factor was a low insulin dosage. Obesity, high blood pressure, and other manifestations of hyperinsulinemia were notably absent.
In addition, a number of other publications have shown only a weak correlation between long-term glycaemic control, CVD and mortality.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4058732/
With a FBG of 90 and an HbA1c of 10, what is likely happening is that the person has sufficient insulin functionality to bring glucose into control during the night when no food has been consumed for the fasting period, BUT that when food is ingested blood sugar is rising VERY high, insulin production is badly failing to keep up, the liver may actually TURN ON glucose production making the problem worse, and EVENTUALLY insulin catches up bringing blood glucose down. If this happens every time the person eats, their long term average blood glucose (HbA1c) will be very high, but fasting glucose can be low.
On the other hand, it may indicate that the blood sugar levels were totally out of control in the previous three month period and now there is better control.
Both Sitagliptin and Linagliptin are a class of oral hypoglycemics that block DPP-4 (DPP-IV). They can be used to treat diabetes mellitus type 2. Linagliptin is good add-on medicine for controlling your blood sugar, but may cause body aches.
Drugs belonging to this class are:
- Sitagliptin[6] (FDA approved 2006, marketed by Merck & Co. as Januvia)
- Vildagliptin[7] (EU approved 2007, marketed in the EU by Novartis as Galvus)
- Saxagliptin (FDA approved in 2009, marketed as Onglyza)
- Linagliptin (FDA approved in 2011, marketed as Tradjenta by Eli Lilly and Company and Boehringer Ingelheim)[8]
- Gemigliptin (approved in Korea in 2012, marketed by LG Life Sciences)[9] Marketed as Zemiglo
- Anagliptin (approved in Japan in 2012, marketed by Sanwa Kagaku Kenkyusho Co., Ltd. and Kowa Company, Ltd.)[10]
- Teneligliptin (approved in Japan in 2012[11])
- Alogliptin (FDA approved 2013, marketed by Takeda Pharmaceutical Company)
- Trelagliptin (approved for use in Japan in 2015)
- Omarigliptin (MK-3102) (approved in Japan in 2015,[12] developed by Merck & Co.; research showed that omarigliptin can be used as once-weekly treatment and generally well-tolerated throughout the base and extension studies[13])
- Evogliptin (approved for use in South Korea[14])
- Gosogliptin (approved for use in Russia[15])
- Dutogliptin (being developed by Phenomix Corporation), Phase III[16]
Side effects of Linagliptin include:
-
back pain,
-
lung infection,
-
cough,
-
headache,
-
joint pain.
Side effects of Sitagliptin include:
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abdominal pain,
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diarrhea,
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the common cold.
Taking insulin and Drugs that increase insulin production for Type 2 diabetes is about the worst thing you can do.
What happens when you give insulin is that insulin lets your body use all that glucose, and when there’s too much glucose, it’s just going to [turn it into] fat. So, all these patients gain weight. And they always come back and say, ‘Whoa doc, you’ve told me I need to lose weight, then you give me insulin and I’ve gained 10 kilograms. How is that good?
And the answer is that it’s not. As you gain more weight your diabetes gets worse, which means you need to take more insulin, which means you’re going to gain more weight. They can see themselves spiraling down the drain, and the doctors do nothing but give them more insulin. It doesn’t even make any sense because the underlying issue is the hyperinsulinemia and insulin resistance. That is, if you look at Type 2 diabetes, insulin levels are very high.
So [why give] more insulin in a situation where you have too much insulin already? If you have hyperthyroidism, if you have too much thyroid hormone, you don’t give more thyroid hormone. If you have an alcoholic, you don’t give more alcohol. It’s the exact wrong thing to do. In fact, if your levels of insulin are too high and that’s your disease, you need to lower insulin. By giving insulin, you’re actually making the fundamental problem much worse.
There are two types of diabetes, Type 1, or insulin dependent diabetes, and Type 2 diabetes, which is lifestyle related. Type 2 diabetes accounts for 90 to 95 percent of all diabetes cases and is the topic of this particular discussion. Prevalence of Type 2 diabetes started to rise in the 1980s, at a time when obesity had yet to become a significant trend. However, as obesity became more prevalent, so did Type 2 diabetes.
But the fundamental underlying problem of Type 2 diabetes, which is insulin resistance, is actually much more widespread than that. The innovative thing Dr Joseph R Kraft did was that he took a standard glucose tolerance test, and measured blood insulin levels instead of blood glucose. Because if you think about what’s happening, when you ingest 75 grams of glucose [the amount administered prior to the test], your blood glucose may stay normal.
But, your body may be producing a huge amount of insulin to really shove that glucose into the cell. Because one of the functions of insulin is to move the glucose from the blood into the cell. Insulin resistance refers to the fact that blood glucose is simply not getting in there. So, if your body needs to produce two, three, four, five times the amount of normal insulin to get that glucose in there, you have a problem, which is not detectable if you just measure blood glucose.
Because, yes, you are shoving all that glucose into the cell, but it took you a huge amount of effort to do so. And by [using the] Kraft assay, which looks at how much the insulin goes up, you can detect [insulin resistance] at a much earlier stage. This is important because there are things we can do about reversing … insulin resistance, and the sooner we get to it, the sooner we can get on the path to wellness.”
Ultimately, diabetes is just one symptom. Insulin resistance, which results in mitochondrial dysfunction, is also at the heart of cancer, heart disease, Alzheimer’s and other degenerative diseases, and it all starts because your body is unable to burn fat as a primary fuel. When your body relies primarily on sugar instead, more reactive oxygen species (ROS) are generated, which damage the mitochondria in your cells.
A review from the Cochrane Collaboration, the most respected group that reviews scientific studies concluded that among people who have had type 2 diabetes for more than one year and aren’t using insulin the effect of testing “is very small.” And when they have diabetes longer it makes even less difference. Even worse: no evidence shows that testing “affects patient satisfaction, general well-being, or general health-related quality of life.”
Many experts believe that Type 2 Diabetes is a chronic disease, so it may be more accurate to use the term remission rather than cure, particularly when considering the cause of type 2 diabetes and the fact that relapse is always possible.
DiRECT (short for Diabetes Remission Clinical Trial) has been testing a new approach to putting Type 2 diabetes into remission in just over 300 people with Type 2 diabetes.
The study found there was a close link between remission and total weight loss. 86% of people who lost more than 15kg on the programme put their Type 2 diabetes into remission after a year. As did 57% of those who lost 10 to 15kg, along with 34% of those who lost 5 to 10 kg. In the comparison group, where people with Type 2 diabetes received standard care, only 4% achieved remission.
What’s Type 2 diabetes remission? Remission doesn’t mean that Type 2 diabetes is gone for good. It means that blood glucose levels have returned to a healthy range again. In this trial, the team defined remission as having blood glucose levels (HbA1c) below 6.5% (48mmol/mol) after 12 months, with at least two months without any Type 2 diabetes medications.
Even American Diabetes Association admits that, Type 2 Diabetes Remission Without Surgery Does Happen—But Very Rarely.
In a consensus statement issued by the American Diabetes Association (ADA), remission is defined based on the following:
- Partial remission: Maintenance of blood glucose below diagnostic levels without diabetes medication for at least one year.
- Complete remission: Normal blood glucose without diabetes medication for at least one year.
- Prolonged remission: Complete remission for at least five years duratio
All types of carbohydrates will raise your blood insulin levels to some degree at least. That is the reason why type 2 diabetes is a form of “carbohydrate intolerance”.
Protein also has a tendency to raise the levels but to a much lesser degree compared to carbohydrate. The only kind of macronutrient which keeps your insulin levels constant and your blood sugar stable is Fat.
Nevertheless, if you are willing to reduce the insulin levels, all you need to reduce is the amount of carbohydrates and replace them instead with healthy, natural fats.
There are a lot of effects which is raised as the insulin level increases. Some of the effects are as follows:
- It causes water and salt retention, which causes raised blood pressure.
- You become at risk of atherosclerosis (“furring of arteries”), which can lead to heart attacks.
- Increase in insulin levels raises very low-density lipoprotein (VLDL), a kind of blood fat and one of the worst forms of cholesterol.
- Can drive the growth of certain cancer cells.
- In women, it can cause the ovaries to produce more testosterone, which is associated with Polycystic Ovarian Syndrome.
- It also increases your risk of having type 2 diabetes.
निरन्तर रुपमा तनावको महसुस भयो भने रगतमा चिनीको मात्रा बढ्नुका साथै धेरै प्रकारका शारिरिक समस्याहरु हुन्छन् ।
प्याक गरिएका खानेकुराहरुमा धेरै चिनी र नुन हालिन्छ । लागु औषध वा चुरोटहरु जस्तै यि खानेकुराहरुले केही समयका लागि आनन्द दिन्छन् । तर पछि स्वास्थ्य खराब हुन्छ ।
खाद्य कम्पनीहरुले तिनीहरुका उत्पादनहरु विज्ञापन गर्दा यस्तो खानेकुरा स्वस्थ छ भनेर ढाँट्दछन् पनि । तिनीहरुको उद्देश्य त स्वस्थ बनाउने नभई पैसा कमाउने मात्र हुन्छ ।
गुलियो मिसाइएका चिसो पेय पदार्थहरु हानीकारक छन् । यसमा धेरै चिनी भएकोले रगतमा चिनीको मात्रा बढाइदिन्छन् । फलफूलका जुसहरुमा समेत धेरै चिनी हुन्छ । त्यसको सट्टामा चिनी नभएको पानी वा चिया पिउनुपर्छ । प्रत्येक हप्ता थोरै मात्रामा घटाउँदै तपाईंको चिया वा कफीमा कम चिनीसँग बानी पार्न सक्नुहुन्छ । वढी सुगन्धका लागि पानी वा चियामा पुदिनाका पाताहरु वा कागती मिसाउन सकिन्छ । फलफूलको जुसको सट्टामा सिंगै फलफूल खानु मधुमेहका लागि राम्रो हुन्छ किनकी फलफूलमा भएको फाइवरले फाइदा गर्छ । जाँड, रक्सि र अल्कोहलयुक्त पेय पदार्थहरु समेत शरिरमा चिनीमा परिणत हुन्छन्, तसर्थ यस्ता वस्तु नखानु नै जाति हुन्छ ।
मधुमेह र उच्च रक्तचाप जस्ता मुटु सम्वन्धि समस्याहरुले विशेष गरी धनी मुलुकहरुका जनतालाई असर गर्दथ्यो । अहिले न्यून आय भएका मुलुकहरुमा समेत यि समस्याहरु छन् । परम्परागत जिवन पद्धतीमा आएको परिवर्तन र परिवारको विघटन सँगै यि समस्याहरु आउँदछन् । पत्रु खाना, नयाँ रसायनहरु, अस्वस्थ जिवनशैली र कम ब्यायामले गर्दा तिनले मधुमेह र अन्य जीर्ण रोगहरुको जोखिम बढाइदिन्छन् । नेपालमा अहिले युवा अवस्थामा नै मधुमेह देखिने कारण नै अस्वस्थकर भोजन र हिंडाई एवं व्यायामको कमी हो ।
अहिले शहरमा बसाइसराइ गरेपछि माइक्रोबस, ट्याम्पुको सुविधा छ, त्यसैले मानिसहरु धेरै हिंड्दैनन् । काम पनि धेरैजसो बसेर नै गर्छन् र खाना पनि पत्रु खाना खान्छन् ।
हाम्रो खानेकुरा र हाम्रो जिवनशैली सँगै केही रसायनहरुले पनि मधुमेह गराउँदछन् । तल उल्लेखित रसायनहरुको संशर्गमा आउँदा, खाँदा, पिउँदा वा श्वासप्रश्वास गर्दा मधुमेहको जोखिम बढ्न सक्दछ । तल दिइएका कुनै पनि रसायनहरुसँग काम गर्दा, खाँदा, सास लिंदा मधुमेहको जोखिमलाई बढाउँछ ।
- डाइअक्सिनहरु किरा मार्ने विषादीहरु एवं कागज बनाउँदा र प्लाष्टिकहरु जलाउँदा उत्पन्न हुन्छन् ।
- पि.सि. वि. हरु उद्योगमा इन्सुलेसन र चिल्लो पार्ने काम (लुब्रिकेशन) का लागि प्रयोग गरिने एक प्रकारका रसायनहरु हुन् ।
- Phthlates प्रायःजसो शरीरको हेरचाहमा प्रयोग हुने क्रिम र तेलहरुमा पाइन्छ ।
- Bisphenols’ वोतलयुक्त पानी, जुस र सोडामा प्रयोग हुने प्लाष्टिक बोतलहरुमा पाइन्छ ।
- गहुँगों धातुहरु (लिड, मर्करी, आर्सेनिक र क्याड्मियम जस्ता) तेल ड्रिलिङ (प्वाल पार्ने) र रिफाइनिङ (शुद्ध बनाउने), माइनिङ (खानी उत्खनन) र अन्य किसिमका उद्योगबाट वातावरणमा छोडिन्छन् ।
यि रसायनहरुबाट जोगिन तिनको प्रयोग सकेसम्म गर्नुहुँदैन । यदि कसैको कार्यस्थलमा यस्ता रसायनहरु छन् भने तिनबाट सुरक्षित रहन अनुहारमा लगाउने मास्क र अन्य सुरक्षा दिने लुगा लगाएर हातहरु वेलावेलामा पखाल्नुपर्छ ताकी खानेकुरा र मुखमा रसायनहरु प्रवेश नगरुन् ।
रसायनहरु हाम्रो वरीपरि सबैतिर छन् । सकेसम्म जिवनाशक विषादीहरु नछरिएका खानेकुराहरु खानुपर्छ । रसायनहरु नभएका वा थोरै मात्र भएका घरायसी सरसफाई सामग्रीहरु (क्लिनर्स) को प्रयोग गर्नुपर्छ ।
पिसावको जाँचले पनि ब्यक्तिलाई मधुमेह भएको देखाउन सक्दछ । पिसावको जाँचमा strips प्रयोग गरिन्छ । पिसावमा चिनी भएमा रङ परिवर्तन गर्दछ । व्यक्तिले पिसाव गर्ने बित्तिकै जाँच गर्नुपर्छ । जाँचका लागि भोको बस्नुपर्दैन
तर पिसावको जाँच गर्दा मधुमेह छ की छैन पूर्ण थाहा पाईंदैन किनकी पिसावमा चिनीको मात्रा देखाउन रगतमा चिनीको तह धेरै माथि बढ्नुपर्दछ (१० mmol/l अथवा १८० mg/dl) । यदि पिसावको जाँच गर्दा मधुमेह नदेखिएपनि मधुमेह हुने सम्भावना छ भने रगतको जाँच गराउनुपर्छ ।
मधुमेह निगरानी परीक्षणमा क्रमशः निम्न टेस्टहरु पर्दछन्:
१. फास्टिङ तथा पोस्ट प्रान्डल ब्लड ग्लुकोज लेवल परीक्षण
२. ग्लाइकोसिलेटेड हेमोग्लोविन परीक्षण
३. लिपिड प्रोफाइल
४. पिसाब माइक्रो आल्बुमिन्युरिया र अन्य
५. बल्ड युरिया नाइट्रेड
६. क्रियाटिनन
७. मुटु परीक्षण (इको, टीएमटी, इसिजी)
८. आँखा परीक्षण
९. मृगौला परीक्षण (किटोन बडी, ब्लड युरिया नाइट्रेट, क्रियटिन, माइक्रो आल्वुमेन्यरोया)
१०. खुट्टा परीक्षण
डायबेटिक रेटिनोपैथीका लक्षणहरु मधुमेह भएलगत्तै सुरुमै देखिँदैन त्यसैले पनि सचेत हुन जरुरी छ। मधुमेह भएको धेरैपछि पनि समयसमयमा आँखा जाँच नगराउँदा झनै जोखिम बढ्दै जाने हुन्छ। दृष्टि क्षमता कम हुँदै गएको आभास हुने, धमिलो देखिने, आँखाको अगाडि कालो थोपा ( भुसुना) जस्तो देखिने, आँखाअगाडि छायाँ देखिने, आदि लक्षणहरु देखापर्न सक्छन्।
आँखाको दृष्टि पर्दालाई रेटिना भनिन्छ जसमा आउने समस्या नै रेटिनोप्याथी हो। बढ्दो उमेर, उच्च रक्तचाप र मधुमेहले रेटिनामा बिस्तारै असर पुर्याउँदै गइरहेको हुन्छ। मधुमेहले आँखाको पर्दामा पार्ने असरलाई डायवेटिक रेटिनोप्याथी भनिन्छ। जसको कारणले दृष्टि धमिलो हुनुका साथै दुष्टि गुम्न पनि सक्दछ।
नेपालमा मधुमेहका रोगीहरुको बढ्ने क्रमसँगै मधुमेहसँग जोडिएको डायबेटिक रेटिनोप्याथी पनि बढेको देखिएको छ। मधुमेह रोग लागेपछि आँखाको जाँच पनि गराउनुपर्छ भन्ने धेरैलाई थाहा छैन। मधुमेहको औषधी मात्र खाएर बसिरहेका छन्, जसका कारण डायबेटिक रेटिनोप्याथी बढेको छ। मधुमेह भएका व्यक्तिमा आँँखाको समस्या दुई गुणाले बढी हुन्छ।
समयमै उपचार नभए अत्यधिक रक्तस्राव हुने, पर्दा खुम्चिने, उप्कनेजस्ता समस्याले आँखाको दृष्टि सधैंका लागि गुम्ने खतरा हुन्छ । टाइप वान मधुमेह भएको २० वर्षमा प्रायः सबैलाई र टाइप टु भएका करिब दुई तिहाइ बिरामीको आँखाको रेटिनामा असर परिसकेको हुन्छ । मधुमेहले आँखामा सुख्खापन आउने, आनो आउने, फुलोपन तथा अन्धोपन ल्याउन सक्छ । आँखामा धेरै असर गरिसकेपछि मात्र रोगबारे थाहा हुन सक्छ । तर, त्यतिखेरसम्म उपचार गरे पनि पहिलेकै जस्तो दृष्टि फर्काउन गाह्रो हुन्छ । समयमै उपचार भयो भने अन्धोपनबाट बँच्न सकिन्छ । त्यसकारण मधुमेह भएको थाहा पाएलगत्तै आँखा परीक्षण गरिहाल्नु पर्छ ।
जबकि मध्यम मात्रामा मदिरा सेवनले रगतमा सुगरको लेभल बढन सक्छ, तर अधिक मात्रामा मदिरा सेवनले वास्तवमा तपाईंको रगतमा सुगरको लेभल कम गर्न सक्छ।
जुन व्यक्तिले हप्तामा तीन देखि चार पटकसम्म मदिरा सेवन गर्छन् उनीहरुलाई कहिल्यै मदिरा सेवन नगर्ने व्यक्तिहरुलाई भन्दा टाईप २ मधुमेह रोग लाग्ने सम्भावना कम रहेको डेनमार्कका अनुसन्धानकर्ताहरुले जनाएका छन्।
रगतमा चिनीको मात्राको व्यवस्थापन गर्ने सम्भावनाका कारण खासगरि वाइनको सेवन फाइदाजनक हुनसक्ने डायवेटोलोजियामा प्रकाशित उक्त अध्ययनमा भनिएको छ।
अनुसन्धानकर्ताहरुले ७० हजार मानिसहरुलाई उनीहरुले सेवन गर्ने मदिराको परिमाण र उनीहरुले कतिचोटी पिउँछन् भन्ने बारे सोधपूछ गरेका थिए।
तर विशेषज्ञहरुले यसलाई तोकिएको परिमाण भन्दा बढी मदिरा सेवन गर्न अनुमती मिलेको रुपमा नलिन भनेका छन्।
मदिरामध्ये विशेषगरि रेड वाइनमा हुने पोलीफेनल्स पदार्थका कारण त्यसको सेवनले रगतमा चिनीको मात्रा व्यवस्थापन गर्न फाइदाजनक हुनसक्ने बताइएको छ।
हप्तामा कम्तिमा एउटा वियर खाने पुरुषको तुलनामा ६ वटासम्म वियर सेवन गर्ने पुरुषलाई मधुमेहको जोखिम २१ प्रतिशतले घटेको तथ्य अध्ययनवाट फेला परेको छ। तर महिलाहरुमा भने यसको त्यस्तो कुनै प्रभाव देखिएन।
नेपाल सरकारले मधुमेह रोगका विरामीलाई भनेर छुट्टै कार्यक्रम ल्याउन सकेको छैन । मधुमेह रोगको रोकथामका लागि सरकारी स्तरमा थुप्रै कामहरु गर्नु पर्ने देखिन्छ । ग्रामीण क्षेत्रका मानिसमा अझै मधुमेह रोगबारे उचित चेतना अभिवृद्धी गर्न सकिएको छैन ।
उदाहरणका लागि, गर्भावस्थामा हुने मधुमेहको नियन्त्रणका लागि सरकारले प्रत्येक अस्पताल तथा प्रसुती गृहले मधुमेह विशेषज्ञको बन्दोबस्त गर्नुपर्छ ।
नेपाल सरकारले मधुमेह न्यूनिकरण गर्न स्वास्थ्य मन्त्रालयसँग समन्वयगरी जनचेतनामुलक कार्यक्रम सञ्चारमाध्यमबाट प्रचार प्रसार गर्नुपर्छ ।
नेपालमा पछिल्लो समय महिलामा पुरुषलाई भन्दा मधुमेह अर्थात सुगरको रोग बढ्दै गएको तथ्याङ्कले देखाएको हो । ४१ प्रतिशत पुरुषलाई मधुमेह देखिंदा महिलामा यो ५८ प्रतिशत छ ।
२०७४ सालको तथ्यांकअनुसार हाल नेपालमा कुल जनसंख्याको १० प्रतिशत अर्थात करिव २५ लाख मानिसमा मधुमेहको समस्या रहेको अनुमान छ ।
ग्लोबल हेल्थ एक्सनमा प्रकाशित डा. ज्ञवाली एण्ड अल गरेको एक अध्ययन अनुसार नेपालमा कुल ३० हजार जनसंख्यामध्य करिब ४१ दशमलव ५ प्रतिशत पुरुष तथा ५८ दशमलव ५ प्रतिशत महिला मधुमेह रोगबाट पिडित छन् ।
त्यस्तै, मधुमेहको जाखिम शहरी क्षेत्रमा ८ प्रतिशत तथा ग्रामिण भेगमा एक प्रतिशत रहेकोमा मधुमेहमध्य पनि टाइप २ मधुमेहको जोखिम १ दशमलव ४ प्रतिशतदेखि १९ प्रतिशतसम्म रहेको पाइएको छ ।
नेपालमा १० लाख मानिसमा मधुमेह रोग रहेको विश्व स्वास्थ्य संगठनले जनाएको छ । पछिल्लो समयमा नेपालमा करिब ५१ प्रतिशत बिरामी नसर्ने रोगका रहेका र त्यसमा मधुमेह रोगका बिरामी १५ प्रतिशत हुने गरेका छन् ।
मधुमेह भएका रोगीलाई मस्तिष्कघात, हृदयघात, अन्धोपन, स्नायुसम्बन्धी समस्या र मिर्गाैलासम्बन्धी समस्या निम्त्याउन सक्छ
- परिवारका सदस्यमा मधुमेह भएको अवस्थामा ।
- शरीरको तौल बढी भएमा वा बी.एम.आई. (शरीरको तौल, केजी, उचाइ (मिटर) २) २२.९ भन्दा कम बढी भएमा ।
- कम्मरको गोलाई पुरुषको ९०. से.मि (३५.५) र महिलाको ८० से.मि (३१.५) भन्दा बढी भएमा ।
- निष्क्रिय जीवनशैली एवम् शारीरिक व्यायाममा कमी भएमा ।
- गर्भवती अवस्थामा मधुमेह भएमा ।
- रगतमा चिल्लोको मात्रा बढी भएमा ।
- उच्च रक्तचाप भएमा ।
- मानसिक तनाव एवम् चिन्ता बढी भएमा ।
जापानस्थित टोकियो विश्वविद्यालयका शोधकर्ताहरुद्धारा गरिएको नयाँ अध्ययनलेे दिउँसो नसुत्ने मानिसको तुलनामा ६० मिनेट भन्दा बढी समयसम्म सुत्ने मानिस र ४५ प्रतिशत टाइप २ मधुमेहको बीच सम्बन्ध फेला पारेको थियो जुन ४० मिनेट भन्दा कमको सुत्ने मानिसमा नभेटिएको बताउँछन् ।
निद्राको गडबढी, सामाजिक जीवनशैली तथा व्यस्त जीवनले पनि टाइप २ मधुमेहको जोखिम बढाउन सक्छ । तर यसका बाबजुद यो पनि सम्भावना छ कि जो मानिस कम स्वस्थ्य छ तथा मधुमेहको प्रारम्भिक चरणमा छन्, उनीहरु दिउँसोको समयमा धेरै सामयसम्म सुत्न रुचाउँछन् । त्यसको विपरित थोरै समयको सुताईले शरीरमा सतर्कता तथा स्फुर्तीको वृद्धि गराउने उक्त अध्ययनलेे बताउँछन् ।
मोटोपन हटाऔं, क्रियाशील बनौः स्वस्थ्यकर वजन राख्नाले रक्तचाप कम हुने र मुटुलाई कम काम गर्ने बनाउँदछ, यसले कोलेस्ट्रोल घटाउँदछ र मधुमेहको विकास हुने जोखिमलाई कम गराउँदछ ।
फलफूल र सब्जी र स्वास्थ्यकर खानपिनले मधुमेहको जोखिमलाई कम गर्दछ ।
धूमपान छोडौः धूमपानले विभिन्न किसिमका क्यान्सर, श्वासप्रश्वास, उच्च रक्तचाप र मुटुको रोगलाई निम्त्याउछ । धूमपान त्याग्नु नै स्वास्थ सुधार्नु हो ।
उच्च रक्तचाप नियन्त्रण गरौः मधुमेह भएको मान्छेलाई प्रायशः उच्च रक्तचाप हुने गर्दछ । यसलाई नियन्त्रण गर्नु जरुरी छ । चिन्तालाई कम गरौः चिन्ता अहिले संसारमा मान्छेको स्वास्थ्यमा जोखिम बढाउने प्रमुख कारण हो ।
रगतमा उच्च ग्लुकोज लेभल भएपछि रगत बाक्लो र टाँसिने हुनपुग्छ । त्यसैले शरीरभरि रगत पम्प गर्न मुटुलाई भार पर्छ । यसले आर्टरीको भित्तामा असर गर्दछ । चिल्लो जम्ने क्रमको विकास गर्न सक्दछ । मुटु रोगका जोखिमका तत्ववहरू धूमपान, उच्च रक्तचाप र रगतमा उच्च कोलेस्ट्रोलबाट हुने नोक्सानलाई मधुमेहले अरू बढाउँदछ । टाइप २ मधुमेह भएको मान्छेको प्रायः ट्राइग्लिसराइड बढी र एचडीएल कोलेस्ट्रोल कम हुन्छ । मधुमेह भएको मान्छेलाई रक्तचाप हुने बढी सम्भावना हुन्छ । मधुमेहले मुटुको मांसपेशीलाई असर गर्न सक्छ र रगत पम्प गर्ने क्षमतामा ह्रास आउन सक्छ । मधुमेहले मुटुको स्नायुलाई असर पार्न सक्छ । त्यसैले एन्जाइनाको लक्षणहरूमा फरक पर्न सक्छ । यसले इन्जाइना र हृदयाघात पत्ता लगाउन ढिलो हुन सक्छ ।
गर्भावस्थाका सुरुकै दिनहरूमा मधुमेह नियन्त्रित नभएमा शिशुको शारीरिक बनावटमा असर हुन्छ । मधुमेहकै कारण विकलांग बच्चा जन्मिने खतरा हुन्छ । बच्चाको मुटु, दिमाग र ढाडमा सीधै असर गर्न सक्छ ।
गर्भवती महिलामा मधुमेह लाग्दा गर्भपात हुने सम्भावना अत्यधिक हुन्छ । गर्भावस्थाका पछिल्ला महिनाहरूमा शिशुलाई पोषण अत्यधिक बढी भएर शारीरिक तौल बढ्न पुग्छ । बच्चा सामान्यभन्दा बढी तौलको हु“दा प्रसवकालमा चोटपटक लाग्ने, सामान्य तरिकाले जन्मिन नसकेर अप्रेसन गर्नुपर्ने तथा शिशुको मृत्यु नै हुन सक्ने जोखिम रहन्छ ।
मधुमेह रोग लागेका महिलाको पेटमा भएको बच्चा जन्मिएपछि पनि मृत्यु हुन सक्ने खतरा रहन्छ । समय नपुग्दै बच्चा जन्मिने सम्भावना बढी हुने भएकाले मृत्युको खतरा उच्च हुन्छ । जन्मिनेबित्तिकै नवजात शिशुमा चिनीको मात्रा धेरै घटेर कम्पन हुने वा बेहोस हुने हुन्छ ।
मधुमेहरोगी आमाको पेटमा रहेको बच्चा जन्मिनेबित्तिकै श्वासप्रश्वासमा पनि समस्या देखिन सक्छ । यस्ता शिशुलाई कृत्रिम श्वास दिनुपर्ने हुन सक्छ । यस्तो समस्या धेरैजसो समय नपुग्दै जन्मिने बच्चामा देखिन्छ ।
गर्भवती महिलालाई मधुमेह भएमा बच्चालाई हुने प्रवल सम्भावना भएकाले आउने पिढीको भविष्य अन्धकार हुनबाट बचाउन सरकारले आफ्नो स्वास्थ्य कार्यक्रममा यसका बारेमा प्रभावकारी जनचेतनामूलक कार्यक्रम ल्याउनुपर्छ
किनकि यि औषधिहरूले हामीले हेर्न सक्ने ठाउँबाट (रगत) हेर्न नसक्ने ठाउँमा (सम्पूर्ण शरीर) चिनी सार्छ र हामी चिन्ता नलिकन धुक्क सँग बस्छौ।
यदि रगतमा चिनी विषाक्त हुन्छ भने, यो किन शरीर भित्र विषाक्त हुँदैन?
हुनसक्छ, किनकि यि औषधिहरूले शरीरलाई जबर्जस्ती चिनी थुपार्न बाध्य गर्छ, जस्तै सानो बच्चालाई धम्काएर, फकाएर जबर्जस्ती खान बाध्य गर्छौ?
रगतमा भएको चिनीको मात्रा घटाउने औषधिहरूले शरीरलाई जबर्जस्ती चिनीलाई बोसो को रुपमा थुपार्न बाध्य गर्छ, र तिनीहरूले त्यो बोसोलाई ऊर्जाको रूपमा प्रयोग गर्ने क्षमतालाई बन्द गर्छ।
हुनसक्छ, किनकि यि औषधिहरूले सम्पूर्ण शरीरमा जबर्जस्ती ग्लुकोज धकेलेर थुपार्न बाध्य गर्छ, जस्तै धकालने मान्छेहरु लाई काममा लगाएर रेलगाडी भित्र यात्री हरुलाई जबर्जस्ती छिराउन खोज्छ।
हुनसक्छ, किनकि यि औषधिहरूले शरीरमा ऊर्जा संकट सिर्जना गरेर ब्लड सुगर घटाउँन बाध्य गराउन्छ। उदाहरणका लागि मेटफर्मिनले शरीरमा ऊर्जा उत्पादन गर्ने कारखानालाई क्षति पुर्याउँछ र फलस्वरूप
ऊर्जा उत्पादन गर्ने क्षमता घटछ (लोड शेडिंग)। कलेजोलाई ग्लुकोज उत्पादन (धेरै ऊर्जा खर्च हुने प्रक्रिया) कम गर्न बाध्य हुन्छ र फलस्वरूप रगतमा सुगर को मात्रा घटछ
किनभने शरीर मा इन्सुलिन हुँदा हुँदै पनि शरीर का कोषहरु ले इन्सुलिन प्रति आवश्यक प्रतिक्रिया जनाउन सक्दैनन् । टाइप टू मधुमेह, इन्सुलिनको प्रतिरोध का कारण उत्पन्न हुने समस्या हो । जब हामी (दोस्रो प्रकारको मधुमेह) टाइप 2 डायबिटीजको मुल कारण इन्सुलिन प्रतिरोध (धेरै बर्ष रगतमा इन्सुलिनको मात्रा बढ्नाले) हो भन्ने जान्छौ, तब हामी मधुमेह बाट मुक्त हुने बाटोमा यात्रा सुरु गर्न सक्छौ।
यदि, मधुमेहलाई रगतमा रहेको चिनीको समस्याको रूपमा मात्र हेर्ने हो भने, न त यो रोगको चाँडै निदान (डायग्नोसिस्) गर्न सकिन्छ, न निर्मुल पार्न सकिन्छ।
किनभने, इन्सुलिन टाइप 2 डायबिटीजको (दोस्रो प्रकारको मधुमेह) कारण हो र इन्सुलिनले टाइप 1 डायबिटीजको उपचार गर्छ ।
टाइप १ मधुमेहको रोगिको हकमा प्याक्रियाज ले इन्सुलिन उत्पादन नै नगर्ने वा न्युन मात्रै गर्ने भएकोले बाह्य इन्सुलिन को माध्यम बाट नै उपचार गर्नु पर्ने हुन्छ ।
यदि तपाईं आफ्नो मधुमेह पूर्ण रुपमा निर्मूल गर्न चाहनुहुन्छ भने, तपाईंले आफ्नो इन्सुलिनको मात्रा थाहा पाउनु र नियन्त्रण गर्नुपर्छ।
इन्सुलिनले टाइप 1 डायबिटीजबाट बचाउछ। इन्सुलिन टाइप 2 डायबिटीजको कारण हो।
किनभने टाइप 1 मधुमेहमा इन्सुलिनको मात्रा एकदम कम हुन्छ र टाइप 2 मधुमेहमा इन्सुलिनको मात्रा धेरै हुन्छ। लक्षण एउटै हो, तर रोगका कारण विपरीत छन। त्यसोभए एउटै किसिमको उपचार कसरी दुवै अवस्थामा फाइदाजनक हुन सक्छ?
के हामी निष्क्रिय(hypothyroidism) र अधिक सक्रिय(hyperthyroidism) थाइरोइडको लागि एउटै किसिमको उपचार गर्दछौं? के हामी गर्मीमा र जाडोमा एउटै किसिम को लुगा लगाउँछौ?
सकिन्दैन, किनभने टाइप 2 डायबिटीजमा शरीरले धेरै इन्सुलिन उत्पादन गर्छ। के रक्सि बढि सेवन गर्नाले, रक्सिको लत हटाउन सकिन्छ?
किनभने यिऔषधिहरूले मधुमेहको कारण लाई सम्भोदन नगरिकन लक्षण लाई मात्र सम्भोदन गर्छ। के तपाईले कहिले सुन्नु भएको छ, वास्तवमा कसैको स्वस्थ सप्रेको जब एकपटक उनीहरु मधुमेह औषधिहरू प्रयोग गर्न थालेपछी, पूरा औषधि निर्भरता को बाहेक?
यसैले पारंपरिक डाक्टरहरूले यो रोग लागि सकेपछि रोगीको आयु बढाउने अर्थात् यो रोगको व्यवस्थापन गर्ने विकल्प मात्र बाकि रहन्छ भन्छन । यो झूट छ ।
किनकी, सख्त ग्लुकोज नियन्त्रण भन्दा इन्सुलिनको मात्रा कम हुनुपर्छ। बेलायतमा टाइप १ मधुमेह रोग लागेपछि ५० वर्ष भन्दा बढी बाच्ने रोगिहरुको औसत HbA1C 7.6% छन र केहिको 8.5-9.0% छन।
सन २००८ मा ACCORD (मधुमेहमा हृदय रोग जोखिम नियन्त्रण गर्ने) अध्ययनको परिणामले बिल्कुल स्पष्ट भयो, रगतमा ग्लूकोज कम गर्ने औषधिहरु मधुमेह रोग भन्दा बढी खतरनाक हुन्छ!
किनकी, हामी अझै पनि रगतको ग्लूकोज कम गर्नमा मात्र ध्यान दिन्छौ। किनकी, सख्त ग्लुकोज नियन्त्रण भन्दा इन्सुलिनको मात्रा कम हुनुपर्छ।
मधुमेहले ५ वटा दीर्घकालीन प्राणघातक परिणाम जन्माउन सक्दछ । ती हुन् हृदयाघात (हर्ट अट्याक),मस्तिष्कघात (स्ट्रोक
मधुमेह एक दिर्घ रोग हो जुन रगतमा ग्लुकोजको मात्रा निरन्तररुपमा सामान्य भन्दा बढि हुनगई मुटु, रक्तनली, आँखा, मृगौला तथा नशाहरुमा गम्भिर असर पुग्दछ ।
लामो अवधिसम्म रहने जटिलताहरूमा मुटु तथा रक्तनलीका रोगहरू (कार्डियोभास्कुलर डिजिजेज), स्ट्रोक, मिर्गौलाको खराबी, खुट्टामा हुने अल्सर तथा आँखामा खराबी आउने जस्ता समस्याहरू पर्दछन्।
Researchers are still trying to pan out the details, but in general, LADA is known to:
- develop in adulthood
- have a slower course of onset than type 1 diabetes
- often occur in people who are not overweight
- often occur in people who don’t have other metabolic issues, such as high blood pressure and high triglycerides
- result in a positive test for antibodies against the islet cells
The symptoms of LADA are similar to those of type 2 diabetes, including:
- excessive thirst
- excessive urination
- blurred vision
- high levels of sugar in the blood
- high levels of sugar in the urine
- dry skin
- fatigue
- tingling in the hands or feet
- frequent bladder and skin infections
In addition, the treatment plan for LADA and type 2 diabetes are similar at first.
It is not possible for type 2 diabetes to turn into type 1 diabetes, because the two conditions have different causes.
A pervasive myth suggests that people with type 2 diabetes can develop type 1 diabetes when they take insulin. This is not true.
The Triglycerides/Glucose (TyG) index is a simple, cost-effective surrogate marker of insulin resistance among adolescents compared with HOMA-IR.
The TyG index is calculated as: [triglycerides (mg dl−1) × fasting glucose (mg dl−1)/2]. IR was defined using HOMA-IR >95th percentile for age and sex. The cut-off of the TyG index for diagnosis of insulin resistance was 8.18.
With the increasing prevalence of obesity, type 2 diabetes, and related metabolic disorders, NAFLD has become an important public health concern in Asia.
The Fatty Liver Index is a simple and accurate predictor of nonalcoholic fatty liver disease (NAFLD) in in the general population. The “fatty Liver index” (FLI) is accurate and easy to employ as BMI, waist circumference, triglycerides and GGT are routine measurements in clinical practice.
A recent Korean study indicates that Fatty Liver Index , a simple surrogate measure of hepatic steatosis, is a useful and easily accessible tool for identifying individuals at high risk for DM.
Generally, a Fatty Liver Index < 30 ruled out and a Fatty Liver Index ≥ 60 ruled in hepatic steatosis as detected by ultrasonography. A chinese study in 2015 validated the accuracy of the Fatty Liver Index for predicting NAFLD in a large general Chinese population, and determined that the optimal cut-off point of the Fatty Liver Index for NAFLD was 30 in middle-aged and elderly Chinese.
The formula that calculates the probability of fatty liver disease occurrence is:
FLI = (e 0.953*loge (triglycerides) + 0.139*BMI + 0.718*loge (ggt) + 0.053*waist circumference – 15.745) / (1 + e0.953*loge (triglycerides) + 0.139*BMI + 0.718*loge (ggt) + 0.053*waist circumference – 15.745) x 100
Visceral obesity is a major risk factor for diabetes; therefore, it is crucial to identify visceral adiposity. Visceral obesity, is associated with an increased risk of metabolic diseases, such as dysglycemia (pre-diabetes and type 2 diabetes), dyslipidemia, hypertension, and cardiovascular disease.
Magnetic resonance imaging (MRI) and computed tomography (CT) are the gold standard for determining visceral obesity. However, they are unsuitable for clinical practices because they are time-consuming, costly and harmful.
Visceral Adiposity Index can replace imaging procedures with the advantages of reduced economic burden and can be used as screening tool for surveillance of cardiometabolic risk in Indian population.
The simplicity of WC and BMI measurement and TG and HDL assessment, make Visceral Adiposity Index an easily applicable index to estimate visceral adiposity.
Visceral Adiposity Index is calculated as following (both TG and HDL-C expressed in mmol/L):
Males: VAI=(WC/39.68+(1.88×BMI))×(TG/1.03)×(1.31/HDL−C)
Females:VAI=(WC/36.58+(1.89×BMI))×(TG/0.81)×(1.52/HDL−C)
Chinese VAI, a better index is calculated by the following formula:
Males: CVAI=−267.93+0.68×age+0.03×BMI+4.00×WC(cm)+22.0×Log10TG−16.32×HDL−C;
Females: CVAI=−187.32+1.71×age+4.23×BMI+1.12×WC(cm)+39.76×Log10TG−11.66×HDL−C.
Yes, definitely. Apart from weight loss, you can expect to be free from the typical longer term complications of diabetes such as strokes, heart attack, erectile dysfunction, renal failure, nerve pain, blindness, foot sores, ulcers and amputations.
Sadly, it is a widely held belief that just controlling the blood sugar levels will avoid diabetes complications. Keep in mind most doctors only have medications and surgery as the 2 tools in their ‘toolbox’. Unless they have been trained in Lifestyle Medicine, they have nothing much else to offer.
All Six Major Studies Show Harm from Aggressive controlling the blood sugar levels
- The Diabetes Control and Complications Trial (DCCT) is one of the largest studies done to show the effects of drug therapy on diabetics. Six and a half years of treatment with intensive insulin therapy for type-1 diabetics resulted in more weight gain as well as higher cholesterol, LDL (bad) cholesterol, triglycerides, and blood pressure compared to people treated less As expected from the rise in cholesterol, there was an increase in the risk of heart disease and stroke for the intensively treated patients.
- The Veterans Affairs Cooperative Study in Glycemic Control and Complications in NIDDM study showed an increase in cardiovascular events in those receiving intensive Diabetic patients with a history of a heart attack were studied, and those treated with insulin and/or other diabetic medications had an increased risk of death.
- In the large European TRAndolapril Cardiac Evaluation (TRACE) study, investigators found diabetic patients with a history of heart attacks treated with insulin and/or other diabetic medications had almost twice the death rate as those diabetics treated with diet alone. Diabetics treated without medications (diet only) had the same death rate as people without.
- The ACCORD study (Action to Control Cardiovascular Risk in Diabetes) showed that intensive treatment of diabetics increases the risk of dying compared to those patients treated less On February 6, 2008 the National Heart, Lung, and Blood Institute (NHLBI) stopped the ACCORD study 17 months early because of adverse effects, including more death. Patients in the intensive- treatment group were oftentimes taking four shots of insulin and three pills daily, and checking their blood-sugar levels four times a day.
- The ADVANCE (Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation) study found no reduction in heart attacks or strokes, deaths from cardiovascular causes, or death from any cause with intensive Hypoglycemia was more common, as always, for those people receiving more drugs.
- The Veterans Affairs Diabetes Trial (VADT) found the intensive-therapy group reduced their hemoglobin A1c levels to 6.9% compared to 8.4% in the standard- therapy group. A weight gain of 18 pounds occurred with the intensive-treatment compared to 9 pounds with standard-therapy. There were 102 deaths from any cause in the intensive-therapy group and 95 in the standard-therapy group (sudden death was three times higher).
Do you want a “quick fix” to control blood sugar, or would you like to improve the quality of health and reverse your diabetes?
If your desire is to improve the quality of health and reverse type 2 diabetes, you have no choice but to learn the principles that will allow you to restore the quality of health you have lost, because the medical establishment has little to offer. The primary role of a traditional medical doctor is to diagnose and treat disease with medical drugs, surgery and any other form of treatment that has been approved by the orthodox medical establishment.
what
If you follow our Diabetes Reversal Program and are currently on medications for diabetes, hypertension (high blood pressure) and/or cardiovascular disease, you should expect at a minimum to greatly reduce your medication dosage and lose weight. Based on our previous results, the majority of clients have been medication free in a matter of months. Results can vary though and are dependent on compliance and persistence in working together to develop a plan that achieves a positive outcome for you. You cannot fail if you commit with a long term mindset. Because we are so confident that our plans work, we back ourselves with a 100% money back guarantee.
Provided you STRICTLY follow the agreed plan, we will refund all the money, if you are not satisfied with your results.
Pre-diabetes is a condition in which blood glucose levels are higher than normal, but not high enough to be classified as full-blown diabetes. Actually, it is called ‘pre-diabetes’ in order to emphasize the fact that this is the same disease as Type 2 Diabetes, but not to the same degree.
It also subtly reinforces the notion that Type 2 Diabetes is a chronic and progressive disease and that eventually, you will become diabetic. However, this is only a lie. It is like saying my son is ‘pre-Doctor’ or ‘pre-Engineer’ or ‘pre-Pilot’. It seems to imply that these things are inevitable even if they are not.
Conventionally, a fasting blood sugar level from 100 to 125 mg/dL (5.6 to 7.0 mmol/L) is considered prediabetes. This result is sometimes called impaired fasting glucose. A fasting blood sugar level of 126 mg/dL (7.0 mmol/L) or higher indicates type 2 diabetes.
Because, one of the biggest lie in the treatment of type 2 diabetes is that ‘it is all about controlling blood sugar’.
Actually, it makes virtually no difference at all. The disease of type 2 diabetes is excessive insulin resistance. It is this insulin resistance that leads to high blood sugars. In order to treat/ cure diabetes, you must reverse the insulin resistance. The high blood sugar is only the symptom, not the disease. Therefore, treating the symptom alone is useless.
Imagine that you have a life threatening infection. The infection causes a high fever. But instead of treating the infection with antibiotics, you treat the symptom of fever with paracetamol. It is not useful. You must treat the disease and not the symptom. The same is true in type 2 diabetes. This is a disease of too much insulin resistance resistance. Yet we treat the symptom of high blood sugars. Medications don’t even attempt to reverse the underlying insulin resistance.
If it was all about controlling blood sugar, then why do diabetics die earlier and face heart attacks, stroke, blindness, kidney failure and other serious complications, if they religiously control blood sugar by medications?
The ACCORD Study proves that, aggressive lowering of blood sugar to the level of HbA1C to 6% for 3.5 years with multiple drugs killed people compared to fewer/less medication and did not reduce major cardiovascular events.
To cure a disease would usually mean to bring back to normal the underlying abnormal body function of the disease. To reverse a disease is usually taken to mean to bring about improvement to the underlying cause, signs and symptoms and potential complications of the diseases.
Diabetes, like most other chronic diseases, is not a absolutely curable disease as opposed to most infectious diseases for eg. where it can be cured, that is one either has the infection or not. A person with a bacterial infection treated by antibiotics may be cured of the infection as compared to diabetic, who after undertaking a guided comprehensive lifestyle modification programme, successfully improve his/her condition to extent of being able to achieve good blood glucose control (for eg. good HbA1c levels) to the extent of being able to adjust the need for or dosage of their diabetes medication – in the latter example, we could only say the person has reversed the severity of his/her diabetic condition and could not say he/she has ‘cured’ his/her diabetes.
So we cannot completely cure type 2 diabetes. But Type 2 Diabetes can go into remission. When diabetes is in remission, you have no signs or symptoms of it.
As Diabetes is A Major Risk Factor for Kidney Disease. On the other hand, despite the contraindication for metformin use in diabetic patients with moderate to severe renal impairment (eGFR < 60 mL/min/1.73 m2), metformin is often used off-label in patients with moderate renal impairment.
So it is necessary to perform kidney function tests.
GFR values can be classified as follows:
Normal: 100-140 mls/min,
Mild Kidney Failure < 90 mls/min,
Moderate Kidney Failure < 60mls/min,
Severe Kidney Failure < 30 mls/min, and
End-stage Kidney Failure < 15mls/min, which is incompatible with life, without dialysis or transplantation.
An estimate of the normal value for your GFR can be obtained by using the equation: GFR = 140 – [your age]. For example, if you are a fit, healthy 30 yr old, your GFR should be approximately 110mls/min.
Observational studies usually show some measures of liver function, such as ALT, ALP and GGT, associated with higher risk of cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). Among these liver enzymes, GGT is most strongly positively associated with both CVD and T2D, although GGT is a non-specific marker of liver function. ALT is more clearly positively associated with T2D than with CVD while the role of ALP is unclear.
Recent 2017 study on hepatic Involvement in Nepalese Subjects with Type 2 Diabetes Mellitus observed marginal, yet statistically significant increase of serum ALT (26.6±0.84 (diabetic) vs 20.0±0.69 (control), p=0.003) and GGT (40.4±1.51(diabetic) vs 21.2±1.1(control), p<0.001) in the diabetic patients compared to healthy controls. Because of marginal elevation of liver enzymes within normal range in diabetic patients, estimation of liver enzymes is highly recommended for patients with T2DM for early detection of liver dysfunctions.
Both ALT and GGT have been shown in cross sectional studies to be modestly associated with the presence of fatty liver, whereas AST is not related. Significant elevation of ALT but not AST may be due to the reason that ALT is more specific serum liver marker. The usual observed biochemical pattern in hepatic steatosis due to NAFLD is of increased levels of transaminases, with alanine aminotransferase (ALT) levels exceeding those of aspartate aminotransferase (AST). Hepatic steatosis due to alcohol excess is often associated with an AST:ALT ratio >1.5, unlike non-alcoholic fatty liver disease.
Elevated uric acid levels are associated with rising blood pressure; any program you adopt to address your hypertension needs to normalize your uric acid levels as well8,9
You may already know that elevated uric acid levels cause gout. Uric acid has proven emerging roles in various diseases such as gout, renal dysfunction, hypertension, hyperlipidemia, diabetes and obesity. Serum uric acid is more closely related to early-phase mechanisms in the development of type 2 diabetes mellitus than late-phase mechanisms, because uric acid concentration rises prior to diagnosis of diabetes and then declines with diabetes duration. In addition, serum UA, a by-product of oxidation of purines that is filtered by glomeruli in the kidney and reabsorbed by the proximal tubule, may promote insulin resistance by inhibiting endothelial cell function.
Uric acid has antioxidant capacities extracellularly and can be responsible for 2/3 of the total plasma antioxidant capacity, where it chelates metals and scavenges oxygen radicals. However, intracellularly, it has pro-inflammatory and pro-oxidant activity.
It has been shown that uric acid is a circulating marker for oxidative damage in conditions like ischemic liver, atherosclerosis, diabetes, and chronic heart failure.
But did you know uric acid can serve as a marker for fructose toxicity?
Fructose, when over-consumed, is very taxing to your body’s metabolic processes. One of the by-products of fructose metabolism is uric acid, so when you consume too much sugar—particularly concentrated fructose—your uric acid levels may rise. Fructose turns you into a uric acid factory! Elevated uric acid is thought to explain much of the damage fructose causes in your body.
The safest range for uric acid is between 3 and 5 mg/dl, and there appears to be a steady relationship between uric acid levels and blood pressure and cardiovascular risk, even down to the range of 3 to 4 mg/dl. This is a noninvasive and cost-effective method to diagnose and monitor metabolic syndrome and its components.
You show no insulin resistance if:
- TG: HDL ratio is near 1 (0.5 -1.9)
- Fasting insulin is between 1.5–5 uIU/mL
- HOMA-IR is near 1 (.5–1.5).
You show insulin resistance (Pre-diabetes) if:
- TG: HDL ratio is greater than 2.
- Fasting insulin is greater than 5 uIU/mL
- HOMA-IR is greater than 1.5.
You show severe insulin resistance (type 2 Diabetes) if:
- TG: HDL ratio is greater than 4.
- Fasting insulin is greater than 12 uIU/mL
- HOMA-IR is greater than 3.
If you have a diagnosis of type 2 diabetes, it also means that you currently express severe insulin resistance.
Elevated gamma-glutamyl transferase (GGT) is strongly associated with obesity and excess deposition of fat in the liver, which is thought to cause hepatic insulin resistance and to contribute to the development of systemic insulin resistance and hyperinsulinemia.
The normal range of GGT is 0-45 U/L. However, the level of GGT exceeds 20 U/L , then the risk for chronic disease increase significantly.
A key thing to remember is that high levels of GGT correlate proportionately with low levels of glutathione (GSH). Note that GGT is a significantly more powerful in predicting new cases of diabetes than obesity alone, even when BMI is above 30 or 35. Note also that elevated GGT increases the risk of diabetes in normal weight people by 3 fold.
In patients with raised alanine aminotransferase (ALT) or γ glutamyltransferase (GGT) levels or with hepatic steatosis noted on ultrasonography, non-alcoholic fatty liver disease (NAFLD) should be suspected in those with risk factors (increased body weight, raised fasting glucose or HbA1c, modestly raised triglycerides, low high density lipoprotein cholesterol, and AST:ALT ratio <0.8) and with daily alcohol intake <20 g in women and <30 g in men.
The GGT test is currently the most sensitive enzymatic indicator of liver damage and disease. This damage is often caused by heavy use of alcohol or other toxic substances, like drugs or poisons. GGT is used to screen for chronic alcohol abuse, because it will be elevated in about 75% of chronic drinkers.
BEWARE! CRP test is NOT hs-CRP test
Type 2 diabetes is an inflammatory atherothrombotic condition associated with a high prevalence of cardiovascular disease. In patients with type 2 diabetes, low grade inflammation is reflected by increased plasma levels of several biomarkers of inflammation such as C-reactive protein (CRP).
C- Reactive Protein is a marker of chronic inflammation and is an independent predictor of all cause cardiovascular mortality.
In cross-sectional studies, highly sensitive – CRP has been found to correlate with increased triglyceride, decreased HDL, increased blood pressure and increased fasting plasma glucose concentrations, suggesting its association with increased prevalence metabolic syndrome associated with insulin resistance and signals an increased risk for practically all degenerative disorders, including cardiovascular disease, cancer, nephropathy progression, diabetes and more.
In a cross-sectional study involving 125 MetS patients recruited at Department of Biochemistry of B P Koirala Institute of Health Sciences, Nepal, rise of hs-CRP, uric acid, or both tends to associated with increased risk for hypertension, hyperglycemia and low HDL cholesterol. Similarly, combined rise of hs-CRP and uric acid is associated with the increase in severity of MetS. Thus, hs-CRP and uric acid may be used to assess severity of MetS.
One study in Pokhara, Nepal concludes that the increase in serum hs-CRP value in type 2 diabetic patients increase the risk of diabetic nephropathy and thus increase the value of serum creatinine level. And there is no correlation of both serum hs-CRP and creatinine level with the risk factors especially sex and family history of type 2 diabetes. The significance of these findings emphasizes to choose these associations for early screening and staging of diabetic nephropathy.
Therefore, we ask our patients to get their C-Reactive Protein (CRP) levels checked during the course of their diabetes reversal program.
Values greater than 3.0 mg/L suggest an increased likelihood of developing cardiovascular disease or ischemic events.
The risk of developing cardiovascular disease is quantified as follows :
- Low risk: hs-CRP level under 1.0 mg/L
- Average risk: between 1.0 and 3.0 mg/L
- High risk: above 3.0 mg/L
- Very high risk: 5-10 mg/L
- Above 10 mg/L – clinically significant inflammatory states
It’s important to order the High-sensitivity CRP or hs-CRP test.
The standard CRP test is ordered for people with symptoms of serious bacterial infection or chronic inflammatory disease. It measures CRP in the range from 10 to 1000 mg/L, while hs-CRP test measures CRP in the range from 0.3 to 10 mg/L.
The “routine” CRP reference range is 0.0-0.7 mg/dL (mg/DECILITER). If a “routine” CRP has been used as an inflammatory marker and a hs-CRP is performed, the results can in most cases be compared by simply dividing the hs-CRP value by 10 as this converts the value from mg/L to mg/dL.
CRP levels increase with age (R,R).
CRP can be elevated in pregnancy (median value of 4.8 mg/L, interquartile range of 0.63 – 15.7 mg/L), and these elevations are evident from even the earliest gestational ages and can persist throughout gestation. Fluctuations are common (R).
Viral infections and any mild inflammation elicit a smaller increase in CRP level (10–40 mg/L), while bacterial infection, as well as active inflammation, can elicit much higher responses of between 40–200 mg/L. In some severe bacterial infections and burns, the level can increase more than 200 mg/L (R).
CRP peaks at about 15:00 hours each day, with a 1% variation in CRP level attributed to the daily and seasonal effects. Very small changes occur during the menstrual cycle in females (R).
A lack of CRP elevation in inflammation may be seen with liver failure, as well as during flares of conditions such as systemic lupus erythematosus (R).
Elevations of CRP in the absence of clinically significant inflammation can occur in renal failure (R).
CRP is positively correlated with BMI, waist circumference, blood pressure, triglycerides, cholesterol, LDL cholesterol, blood glucose, and fasting insulin, and it was inversely correlated with HDL cholesterol and insulin sensitivity (R).
Strong associations are observed between CRP levels, central obesity, and insulin resistance (R).
Additionally, CRP in the setting of MetS confers an increased risk of future cardiovascular events (R).
Of the lipid panel, triglycerides tend to be the most specific marker of insulin resistance. High blood levels of insulin cause the liver to produce very low-density lipoprotein triglyceride (VLDL-TG). If TG are high in the fasting state, this indicates insulin resistance, and when triglycerides are too high their transfer to the HDL particles causes the HDL count to drop. Because the natural range of TG is fairly wide and context-dependent, the value of this single measurement is disputed, fasting TG/HDL ratio is taken as the more sensitive marker.
Perhaps TG/HDL ratio is the most cost effective marker, which can be used as a surrogate for insulin resistance along with a healthy dose of common sense!
The fasting TG/HDL ratio is highly correlated with 2-hour insulin (insulin levels 2 hours after consuming glucose) and, with a higher cut off, is also predictive of fasting hyperinsulinemia. Elevation in the ratio of TG to HDL-c was the single most powerful predictor of extensive coronary heart disease among all the lipid variables examined.
People with the highest TG/HDL levels are 16 times more likely to suffer a heart attack.
So, calculating this ratio is not only a simple trick to measure insulin resistance but also a more-accurate heart disease risk assessment.
Ideally, you want no more than a 2:1 ratio of triglycerides to HDL cholesterol. So, if your triglycerides are 100 mg/dl, your HDL cholesterol should be 50 mg/dl.
Some insulin resistance: 2.0–3.0
Significant insulin resistance and heart disease risk is found at ratios >3.0
A completely free yet accurate marker of insulin resistance is the waist to height ratio. Waist to height ratio is an indicator of your risks for obesity, heart disease, diabetes, stroke, and hypertension. It is obtained by dividing waist size by height. Men and women should keep their waist circumference, no more than half their height. Waist/Height Ratio (WHtR) is a far more accurate way of measuring healthy weight than the traditional Body Mass Index (BMI).
Waist to height ratios over 0.5 are considered to be exceptionally risky when it comes to metabolic health.
Waist Circumference is considered a risk factor for heart disease, irrespective of height and build, in the following cases:
Men: Over 94 cm (approximately 37 inches)
Women: Over 80 cm (approximately 31.5 inches)
Your waist measurements are the most accurate just after you wake up from 7-8 hours of sleep.
The homeostasis model assessment-estimated insulin resistance (HOMA-IR), developed by Matthews et al. [1] has been widely used for the estimation of insulin resistance in research. Compared with the “gold” standard euglycemic clamp method for quantifying insulin resistance [2], quantification using HOMA-IR is more convenient. It is calculated multiplying fasting plasma insulin (FPI) by fasting plasma glucose (FPG), then dividing by the constant 22.5, i.e. HOMA-IR = (FPI×FPG)/22.5 [3].
HOMA-IR tells us how hard the body is working to keep blood glucose from getting dangerously high. In other words, it tells us how much insulin pancreas has to produce in order to maintain blood glucose at a certain level.
Pre-diabetes can exist for a long time in your body without triggering the most common outward signs of diabetes (continual thirst, frequent urination, blurred vision, etc). And standard methods of detecting insulin resistance or pre-diabetes using glucose tolerance tests or an HbA1C percentage often show false negatives.
Here are some examples:
Patient A
Fasting glucose: 90 mg/dL
Fasting insulin: 4 μIU/mL
HbA1C: 4.8%
HOMA-IR: (90 x 4) / 405 = 0.88
Patient B
Fasting glucose: 82 mg/dL
Fasting insulin: 14 μIU/mL
HbA1C: 4.5%
HOMA-IR: (82 x 14) / 405 = 2.83
A1c = (46.7 + average_blood_glucose) / 28.7
Patient A’s fasting glucose is higher than Patient B’s, but Patient A’s insulin is much lower. By taking both glucose and insulin into account, the HOMA-IR scores show us that even with a lower fasting glucose, Patient B is at greater risk for metabolic complications down the road.
Because of the wide variation in insulin levels during a GTT, most endocrinologists evaluate the fasting insulin level only.
A simple test of blood sugar measured after an overnight fast, this is a measure particularly good at picking up diabetes. Levels above 5.5 mmol/L (99 mg/dl) indicate a higher chance of diabetes. There are however many, many individuals with normal fasting glucose who have significant insulin resistance and pre-diabetes.
The Oral Glucose Tolerance Test is commonly prescribed to detect diabetes, yet again it will rarely be able to detect insulin resistance or hyperinsulinemia. Many patients with insulin resistance will have completely normal glucose tolerance tests and passing this test does not mean your metabolism is healthy!
In PCOS, a condition where high levels of insulin cause the ovarian theca cells to release high levels of testosterone and other androgenic hormones, it is helpful to know the degree to which hyperinsulinemia is present. Often, women with PCOS have completely normal blood sugar levels, and can often have low blood sugar levels as well. Yet, their metabolisms may be significantly impaired.
If your answer is “Yes” to any of the questions below, testing for insulin resistance is highly recommended.
- Are you overweight or do you have a difficult time losing weight?
- Do you carry weight around your central abdomen?
- Do you frequently crave carbohydrates and sweets?
- Were you overweight as a child?
- Did you have gestational diabetes during pregnancy?
- Do you have polycystic ovarian syndrome, or suspect that you might (i.e. have irregular periods, carry weight around the middle, and have acne)?
- Do you feel bloated and sleepy after a high-carbohydrate meal?
- Do you have High blood pressure?
- Do you have thinning hair (not explained by low iron or low thyroid function), skin tags, acne and large pores on the face or fatty liver?
- Do you have a brown to black, poorly defined, velvety hyperpigmentation of the skin (Acanthosis nigricans)? It is usually found in body folds, such as the posterior and lateral folds of the neck, the armpits, groin, navel, forehead, and other areas.
- Do you look puffier? You can experience fluid retention anywhere on your body, such as your fingers, face, legs, ankles and abdomen.
- Do you have Elevated uric acid? People who are insulin resistant are sensitive to fructose and convert too much of it into uric acid. Elevated uric acid can raise the risk of gout and kidney stones.
Criteria for diabetes remission
- Buchwald criteria (FPG <100 mg/dl [< 5.6 mmol/l] or A1c <6 %)
- American Diabetes Association (ADA) complete (FPG <100 mg/dl plus A1c <6 % maintained for at least 1 year in the absence of pharmacologic therapy), ADA partial (FPG <125 mg/dl (5.6-6.9 mmol/l) with A1c <6.5 % maintained for at least 1 year in the absence of pharmacologic therapy.
- Fasting Plasma Glucose: <6.1 mmol / L (110 mg / dl) maintained for at least 6 months in the absence of pharmacologic therapy.
- Glycated hemoglobin (HbA1c): <6.5% (48 mmol / mol) maintained for at least 6 months in the absence of pharmacologic therapy.
Here are some examples:
Patient A Patient B
Fasting glucose: 90 mg/dL Fasting glucose: 82 mg/dL
Fasting insulin: 4 μIU/mL Fasting insulin: 14 μIU/mL
HOMA-IR: (90 x 4) / 405 = 0.88 HOMA-IR: (82 x 14) / 405 = 2.83
Patient A’s fasting glucose is higher than Patient B’s, but Patient A’s insulin is much lower. By taking both glucose and insulin into account, the HOMA-IR scores show us that even with a lower fasting glucose, Patient B is at greater risk for metabolic complications down the road.
Unless people with diabetes are taking insulin, they waste their time and money when they test their blood sugar.
It’s important to recognize and diagnose insulin resistance, because it is the root cause of type 2 diabetes and most heart attacks, and Alzheimer’s disease (Type 3 Diabetes). Insulin resistance usually occurs 10 to 15 years before type 2 diabetes is diagnosed. Alzheimer’s and other forms of dementia are characterized by brain insulin resistance.
Insulin and leptin resistance causes your blood pressure to increase.
What this means is that, if testing for insulin resistance began as part of a standard physical examination, we could catch people who are at high risk of developing diabetes at a stage where it is reversible. This is truly proactive and preventative medicine.
Besides having a predisposition to diabetes, insulin-resistant people may have other health issues, too, including high blood pressure, high cholesterol, heart disease, and polycystic ovarian syndrome (PCOS), a leading cause of infertility issues. And finally, insulin resistance is associated with increased risk of developing cancers, including breast, prostate, and pancreatic cancer. It’s no surprise that hyperinsulinemia is a risk factor for most, if not all cancers.
Unfortunately, there is no home test for insulin, or insulin resistance, and we cannot judge them from our blood glucose levels.
You don’t have to get it perfect, you just have to get it going. Babies don’t walk the first time they try, but eventually they get it right. The 5 step process we have developed has been shown to work time and time again. We don’t know your case and everyone is different. Yet, everyone we have worked with has seen decreases in their A1C and reductions in their insulin resistance. However, not everyone is starting from the same place and not everyone gets the same results in the same amount of time. Your results will depend on your level of insulin resistance and what lifestyle shifts you choose to implement. The great news about our 5 step process is that during Step 1 the testing and review will give you a clear picture of what to expect individually before starting to make the lifestyle shifts.
Sometimes it’s ok, not to follow the program. But, tomorrow it’s back to the program. There’s no right/wrong and you’re not going to undo everything by having an off day. Moreover, sometimes changing the daily routine keeps your body from adapting a new eating habit. Keep the body guessing! Keep it positive
It’s just our nature, that before embarking on any journey, its seems like the first question that pops into our minds is, “How long will the journey take?”
The first phase of any journey is deciding where it is you want to go.
Do you want a “quick fix” to control blood sugar, or would you like to improve the quality of health and reverse your diabetes?
If your desire is to improve the quality of health and reverse type 2 diabetes, you have no choice but to learn the principles that will allow you to restore the quality of health you have lost, because the medical establishment has little to offer. The primary role of a traditional medical doctor is to diagnose and treat disease with medical drugs, surgery and any other form of treatment that has been approved by the orthodox medical establishment.
Since it took decades to bring the quality of your health to the level it presently is, logic dictates that it will take work and time to reverse it. If you understand the science and pathology of diabetes, then, you will realize that you can’t reverse diabetes in 30 days or less! For example, it takes a minimum of 100-120 days to turn over your red blood cells and get rid of the damaged red blood cells, which have been glycated and damaged by the glucose molecules.
If we were to say that you could enjoy optimum health in a certain number of weeks, of course that wouldn’t be realistic.
There is no guarantee of specific results. Results can vary. Each individual determines for him or herself, the length of time for total reversal. The factors that make this determination is comprised of personal dedication, desire and the willingness to be consistent in following the program. When a person is diligent and consistent in following the program, it is possible to reverse type 2 diabetes within 6 months. Less diligence requires more time.
What matters most is to just begin, and to work at a pace that is most comfortable for you. Like a large pile of dirty dishes, the work gets done when you do it!
As a bonus, you’ll find that our program also prevents you from developing or experiencing heart disease, high blood pressure and obesity. In addition, it lessens the likelihood of cancers of the breast, prostate and colon, which are often linked to poor eating habits.
How hard is it to live with diabetes or pre-diabetes? Compared to that, it’s not hard at all. But like most things in this life, it’s all up to you and your motivation.
Are you willing to commit to yourself and take on a temporary challenge in order to vastly improve the rest of your life? Imagine the possibility of living a life of vibrant health, a life full of the energy you need to accomplish all of your goals and enjoy simply being alive. Of course it’s a change. But unlike the “change” that has you on the path of pre-diabetes and diabetes, this one is positive. And you will be supported along your journey and meet others on a similar path.
When you start seeing results and feeling better than you ever realized was possible, change becomes easy and fun.
Because diabetes is a systemic disease that, over a period of years, attacks and causes major cellular damage to all of your tissues and organs!
Let’s take a car that has not had an oil change or engine tune-up and has been running on cheap fuel for several years. If you switch from the cheap fuel to a higher-octane “super” fuel, the car may run a little better, but it will still run sluggish. Once you change the oil and air filters and tune up the engine, the car will run even better.
The same principle applies to the human body – if you clean the filters (the kidneys and liver), then, this will help them to remove the buildup of toxins and waste and kill the pathogenic bacteria and parasites so that the body will run better.
If you are overweight by more than 10 kg, more than likely, you are carrying as much as 3 kg of fecal matter packed in your colon.
If you are also struggling with high cholesterol or high blood pressure, then, your body is carrying extra fluid/waste in your cells and tissues.
Consequently, cleansing the liver and kidneys, your body’s primary filters, will help the body to better release this extra fluid/waste.
This will thin out the blood, hydrate cells, break down fats, absorb protein, convert glycogen to glucose, turn on the body’s natural healing mechanisms, and, in most cases, lower blood pressure, inflammation, cholesterol, glucose levels, and body weight.
- Eating “live” super foods is one of the best ways to help your body with the cleansing and detoxification until your body is healthy enough to perform the cleansing and detoxification on its own. If you want to further accelerate the detoxification process, you should drink at least 1 cup of raw vegetable juices preferably 30 minutes before meals.
- Use ZenMet (Ayurvedic Rasayana) to nourish the colon, liver, gall bladder, lymph nodes, and kidneys while protecting them from oxidative damage during the cleansing/ detoxification process.
- Exercising on a consistent basis is another way to help accelerate the cleansing/detox process.
- Detox your mind by using meditation (e.g. yoga), prayer, laughter, helping others, showing gratitude, forgiving others, and using self-affirmations, and tapping into your inner spirit. If your mind is full of negative thoughts and full of hopelessness, you are not going to be motivated to change and stick with those changes to your diet and lifestyle.
Type 2 diabetes is a disease of insulin resistance and hyperinsulinemia. When a person becomes insulin resistant, it’s not a disease of blood sugar at all, it’s a disease of insulin signaling. So why focus on lowering blood glucose, which is only the symptom? Isn’t that useless? Yes. Yes it is. You need to lower insulin, not glucose, because the disease is about too much insulin.
Obviously, having elevated blood sugars is not healthy. But how you lower the blood sugars is very important. We don’t want to substitute a worse evil than the elevated blood sugar. If you’re lowering sugar by raising insulin level or by increasing insulin sensitivity artificially (PPAR agonists), then you’re mimicking the conditions that cause diabetes in the first place. When cells become insulin resistant, they’re not being stupid. Cells become very smart because they let less sugar in.
The mainstream media is picking up the fact that our current drug therapies for type 2 diabetes don’t seem to be of much use to anybody.
Insulin in excess is proinflammatory, pro-infections, pro-cancer, pro-premature aging, and pro-degenerative disorders and yet insulin tests are seldom, if ever, done by most doctors.
TYPE 2 DIABETES is really just advanced insulin resistance. Rather than a condition that develops overnight, the onset of type 2 diabetes is a lengthy process that takes many, many years to manifest. It begins with insulin resistance, often starting decades before the high blood sugar levels characteristic of a diabetic emerge.
Insulin resistance is characterized by hyperinsulinemia – the secretion of higher than normal amounts of insulin either after eating, or continuously even when fasting. The clinical manifestations of IR apart from hyperinsulinemia include hyperglycemia, hyperlipidemia, increased circulating inflammatory marker levels, and diminished plasma adiponectin levels.
The first grievous error of considering insulin insufficiency as the cause of TYPE 2 DIABETES has misled generations of doctors, leading to the mistreatment of hundreds of millions of people with prediabetes and TYPE 2 DIABETES. In reality, hyperinsulinism predates TYPE 2 DIABETES for five to ten or more years.
Insulin resistance is one of the key factors in the development of type 2 diabetes. Thus, it is very important to measure the level of insulin resistance.
Insulin testing has several other possible uses. Insulin testing may be used to help:
- Diagnose an insulinoma (insulin production from a tumor), verify tumor removal has been successful, and/or to monitor for recurrence.
- Diagnose the cause of hypoglycemia (low blood sugar) in an individual with signs and symptoms
- Identify insulin resistance
- Monitor the amount of insulin produced by the beta cells in the pancreas (endogenous); in this case, a C-peptide test may also be done. Insulin and C-peptide are produced by the body at the same rate as part of the conversion of proinsulin to insulin in the pancreas. Both tests may be ordered when a health practitioner wants to evaluate how much insulin in the blood is made by the body and how much is from outside (exogenous) sources such as insulin injections. The test for insulin measures insulin from both sources while the C-peptide test reflects insulin produced by the pancreas.
- Determine when a type 2 diabetic might need to start taking insulin to supplement oral medications.
- Determine and monitor the success of an islet cell transplant intended to restore the ability to make insulin, by measuring the insulin-producing capacity of the transplant.
Reference range is a term that is given to Doctors who practice an incredibly basic way of diagnosing, managing and treating disorders.
They simply look to see if your lab values fall inside the reference range of the lab results, and if they do, you are considered to be normal. Anything outside of this reference range is typically labeled as “high” or “low” in bold font.
Even if you are in the bottom 5% of that reference range, you are still normal. And that is a huge problem. Disease doesn’t start as soon as you go outside of that range. You’re either trending toward disease, outside of the reference range, or you’re trending toward optimal health.
There are a lot of people who go to their doctor to find out why they’re struggling with health issues, and their labs come back “normal.” They’re told there is nothing wrong with them and left with no answers or solutions.
There is a big difference between being “normal” and being “optimal”. There’s also a huge difference in what being “optimal” means between different individuals!
Because, there is No Perfect Thyroid Test. Thyroid blood tests are not completely accurate and usually do not tell what the cause of the condition is. What is the value of solely using TSH, T3, T4 or even Reverse T3 and antibodies as one’s diagnostic yard-stick, when this health issue goes far beyond simply a thyroid gland dysfunction or failure?
This is a big reason why most endocrinologists and other types of medical doctors simply recommend thyroid hormone for people with hypothyroidism and Hashimoto’s Thyroiditis, or anti-thyroid drugs/RAI for people with hyperthyroidism and Graves’ Disease. They simply are not taught how to find the cause of most thyroid conditions and so the only thing they know is give their patients prescription drugs to manage the symptoms, or radioactive iodine in hyperthyroid conditions to obliterate the thyroid gland.
When you are driving into unfamiliar territory you probably use a GPS, right? The first thing the GPS needs to know is your current location. Without knowing your current location, the GPS can’t plot a course for you.
Blood sugar numbers only tell half of the story. You need to know your level of insulin resistance and other measurable parameters in order to know how to proceed on your journey. If by controlling blood glucose level diabetes will go away, then no one should be diabetic today.
Like a GPS device, these test results plot where you are right now. It is your job to understand how to plan a course that will best take you from your current location to where you want to go. Future tests will reveal your progress and whether or not the changes you’ve made are keeping you on the right path. It’s our job to be your guide.
Typically the tests in the standard model of care diagnose a disease so that it can be matched with a corresponding pharmaceutical drug. The labs your doctor runs are adequate if he’s just prescribing medications. Comprehensive tests look at underlying causes, imbalances and dysfunctions, give amazing insight into these often overlooked pieces of your health puzzle.
We will show you how to decipher the meaning of your own test results. It will become clear to you why there is no “magic bullet,” like a miracle pill to reverse Type 2 Diabetes. The only real magic bullets We know of are your curiosity, your will, and our ability to respond to what you learn, making the necessary corrections to stay on course along the way.
The main blood tests are fasting Insulin, fasting Glucose, High Sensitivity C-Reactive Protein (hsCRP), Hemoglobin A1c (HbA1c), Triglycerides(TG), HDL Cholesterol (HDL).
We also recommend testing ALT, AST, GGT, Urea, Uric Acid, Creatinine for liver and kidney functions.
The most important tests are fasting Insulin and glucose (for determining level if insulin resistance HOMA-IR,), HsCRP (for determining the level of systemic inflammation) and HbA1c.
The answer is simple. We don’t treat symptoms we identify the root CAUSE. Once we understand type 2 diabetes, then the solution becomes pretty obvious. If we have too much sugar in the body, then get rid of it. Don’t simply use medications to hide it away so we can’t see it. Currently, if you are in a pharmacological model, you’re being treated for symptoms and/or lab values and are being given medication to cover up the symptoms which are just going to bully your body’s physiology to make your labs look normal. Diabetes can neither be prevented nor reversed by focusing on blood glucose levels. By addressing the underlying causes of Diabetes, we design unique, personalized healing plans that Conventional Medicine literally doesn’t have the tools, training, or the time for.
We treat the person who has the disease rather than the disease the person has and we look beyond the laundry list of symptoms, we take the whole person into account.
The human body is not a single being, but a vast and beautiful community of various cells and bacteria, all working in harmony towards the continued survival of the being. The key to wellness, slowing down aging, reversing diabetes and heart disease and increasing overall longevity are all dependent on the accurate and effective communication between the different parts of the body; the harmonious unification of the universe inside each of us. Through our program, we aim to improve that communication between trillions of separate cells, bring them together to function as a whole and uncover the happy and healthy person within us all.
It’s quite possible that, the right tests haven’t been run in your case. Diabetes is not a disease of blood sugar, osteoporosis is not a disease of calcium and heart disease is NOT a disease of cholesterol. So first of all we try to seek and explain the cause of your diabetes via running some specific tests.
Our Diabetes Solutions is focused on supporting and enabling your long-term success in a sustainable lifestyle.
We are your partners in wellness, committed to empower you with the knowledge and skills you need to take back control of your overall wellness with a high level of trust, mutual respect and friendship. We literally participate in the process, that slow transition from illness to wellness.
We are committed to your success.
We strongly believe that, life is about relationships, not accomplishments.
The only thing current drugs do is to help lower blood glucose, which has virtually no influence on the long-term damage due to type 2 diabetes. Most of the damage is caused by elevated insulin levels.
To reverse type 2 diabetes, our primary objective is to lower both blood sugar and insulin levels by making insulin work better. For individuals with pre-diabetes with insulin toxicity but without high blood sugar levels, our goal is to lower blood insulin levels by increasing insulin efficiency.
Diabetes is not a blood sugar disease. So, drugs that focus on the symptom of elevated blood sugar, rather than addressing the underlying cause, are doomed to fail in most cases.
Because the current treatment approach for type 2 diabetes is based on the blood glucose paradigm and views Type 2 diabetes (T2D) as a chronic condition that can be managed but cannot be reversed. Under this paradigm, most of the toxicity of T2D is due to the high blood sugar (hyperglycemia). Therefore, it follows that lowering blood glucose will ameliorate the complications even though we are not directly treating the T2D itself (high insulin resistance).
While clinicians may be increasingly more aware that T2D can be reversed, most think it is only possible through drastic means like bariatric surgery.
The first grievous error of considering insulin insufficiency as the cause of T2D has misled generations of doctors, leading to the mistreatment of hundreds of millions of people with prediabetes and T2D. In reality, hyperinsulinism predates T2D for five to ten or more years. T2D is really just advanced insulin resistance.
Insulin in excess is proinflammatory, pro-infections, pro-cancer, pro-premature aging, and pro-degenerative disorders and yet insulin tests are seldom, if ever, done by most doctors.
We must shift from our previous paradigm with its monocular focus on control of blood glucose and HbA1c, to one of control of blood glucose plus preventing cardiovascular disease and death from cardiovascular causes.
Sugar doesn’t cause diabetes. Sugars are the most important nutrient for the human body. Sugar is to the body what gasoline is to a car—the central source of energy. So sugars are not the problem. It’s the intake of excessive quantities of sugar, in combination with proteins and certain types of fats, that contributes to disease both directly and indirectly—by activating aging-related genes, creating insulin resistance, and triggering hyperglycemia.
Much progress has been made in standardizing and improving the accuracy of the A1c test thanks to the National Glycohemoglobin Standardization Program (NGSP). Results from a non-NGSP certified lab may not be as reliable. Depending on the machine, a single A1c test can have up to a 0.5% margin of error, which means the “true” value might be 0.5% higher or lower than the measured A1c. For example, if a lab report shows an A1c value of 7.0%, the actual A1c value might range from 6.5% and 7.5%.
The main problem is that there is actually a wide variation in how long red blood cells survive in different people. This study, for example, shows that red blood cells live longer than average at normal blood sugars. Researchers found that the lifetime of hemoglobin cells of diabetics turned over in as few as 81 days, while they lived as long as 146 days in non-diabetics. This means diabetics and those with high blood sugar will test with falsely low A1c levels.
Another condition that affects hemoglobin A1c levels is anemia. People who are anemic have short-lived red blood cells, so like diabetics, they will test with falsely low HbA1c levels.
If you have diabetes, it’s also important to take the perspective that A1c is not a “grade” on diabetes management, but rather a helpful measurement tool that you and your healthcare providers can use to guide decisions and assess the risk of complications.
Non-glycemic factors that can affect A1c:
While there are many unsuspecting factors that can impact A1c, the information in the table below is not meant to invalidate the A1c test. Rather, knowing how certain conditions and factors can change A1c levels is a key part of using A1c as one measure of diabetes management.
Many of the conditions that affect A1c results are related to changes in the turnover of red blood cells, and thus notably, types of anemia. Correction of anemia by treatment can also affect A1c results.
|
Condition |
What is the impact on A1c? |
How to test for this condition |
|---|---|---|
|
Untreated anemia due to:
|
Untreated anemia can misleadingly increase A1c values due to decreased production of red blood cells. (If anemia is treated, A1c can go down.) |
To test for anemia, ask your healthcare provider about taking a complete blood count (CBC) test. |
|
Asplenia: decreased spleen function |
The spleen is involved in the production and removal of red blood cells. Decreased spleen function, which may be caused by surgical removal, congenital disorders, or other blood disorders such as sickle cell disease. This may lead to misleadingly increasedA1c. |
Asplenia can be identified by MRI, echocardiogram, chest X-ray, or a screening test.
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Blood loss and blood transfusions |
The body’s response to recent blood loss (create more blood cells) or blood transfusion can misleadingly lower A1c, but the next A1c test should return to a more representative reading. |
Let your healthcare provider know if you have recently received a blood transfusion. |
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Cirrhosis of the liver: chronic liver damage that leads to scarring |
Cirrhosis, in addition to affecting response to glucose-lowering medications – including insulin – may misleadingly lower A1c values. |
Ask your healthcare provider about a liver examination. |
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Genetic blood disorders
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Depending on the abnormal form of hemoglobin, hemoglobinopathy can result in either increased or decreased A1c values. Thalassemia can misleadingly lower A1c values due to early destruction of red blood cells. |
Tell your healthcare provider if you have any known family members that have had thalassemia, and ask for a Complete Blood Count test. |
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Hemolysis: rapid destruction of red blood cells
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Hemolysis may misleadingly lower A1c values due to the shortened red blood cell lifespan. This condition may be caused by an inappropriate immune response and artificial heart valves. |
Ask your healthcare provider about taking a Complete Blood Count (CBC) test. |
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Untreated hypothyroidism: low levels of thyroid hormone |
Hypothyroidism may misleadingly increase A1c, while treatment with thyroid hormone can lower A1c.
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Ask your healthcare provider about taking blood tests that measure the level of thyroid-stimulating hormone, which helps determine if there are thyroid gland problems. |
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Pregnancy |
Decreased red blood cell lifespan and increase in red blood cell production may misleadingly lower A1c values in both early and late pregnancy. |
Ask about taking an oral glucose tolerance test, which is used to diagnose gestational diabetes. A common practice for pregnant people with diabetes is to use CGM. To learn more about managing diabetes during pregnancy |
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Uremia: high levels of waste (normally filtered by kidneys) in the blood |
Untreated uremia may misleadingly increase A1c values. Dialysis is used to treat uremia – in this case, A1c is not a suitable test. |
Ask your healthcare provider about taking a blood test to detect uremia or abnormal kidney function. |
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Medications |
Medications that may misleadingly increase A1c include:
Medications that may misleadingly lower A1c include:
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Always discuss appropriate use of opioids for pain and their possible effect on A1c as well. Tell your healthcare provider if you are taking any of these medications prior to your A1c test. |
For people without diabetes, the normal range for the hemoglobin A1c level is between 4% and 5.6%. Hemoglobin A1c levels between 5.7% and 6.4% mean you have a higher change of getting of diabetes. Levels of 6.5% or higher mean you have diabetes.
The American Diabetes Association provides a calculator that shows how A1C levels correlate to glucose levels.
HbA1C measures the amount of hemoglobin in the blood that has glucose attached to it. Hemoglobin is a protein found inside red blood cells that carries oxygen to the body. Hemoglobin cells are constantly dying and regenerating, but they have a lifespan of approximately three months.
Glucose attaches, or glycates, to hemoglobin, so the record of how much glucose is attached to your hemoglobin also lasts for about three months. If there’s too much glucose attached to the hemoglobin cells, you’ll have a high HbA1C. If the amount of glucose is normal, your HbA1C will be normal.
Analysis of glycated hemoglobin (HbA1c) in blood provides evidence about an individual’s average blood glucose levels during the previous two to three months, which is the predicted half-life of red blood cells (RBCs).1 The HbA1c is now recommended as a standard of care (SOC) for testing and monitoring diabetes, specifically the type 2 diabetes.
The American Diabetes Association has recommended glycated hemoglobin (HbA1c) as a possible substitute to fasting blood glucose for diagnosis of diabetes. HbA1c test may continue to be implemented as part of the diagnostic and prognostic tool, leading to better patient care and successful clinical outcomes.
Symptoms of low blood sugar can occur suddenly. They include:
- blurry vision
- rapid heartbeat
- sudden mood changes
- sudden nervousness
- unexplained fatigue
- pale skin
- headache
- hunger
- shaking
- dizziness
- sweating
- difficulty sleeping
- skin tingling
- trouble thinking clearly or concentrating
- loss of consciousness, seizure, coma
People with hypoglycemic unawareness do not know their blood sugar is dropping. If you have this condition, your blood sugar can drop without you noticing it. Without immediate treatment, you can faint, experience a seizure, or even go into a coma.
Yes. Low blood sugar can happen in people with Type 2 Diabetes who take medicines that increase insulin levels in the body. Drinking alcohol when you’re on these medications can also lead to low blood sugar, especially if it replaces food.
Symptoms of hypoglycemia include:
- shaking
- dizziness
- hunger
- headache
- sweating
- trouble thinking
- irritability or moodiness
- rapid heartbeat
If you are on medicines that increase the amount of insulin in your body, be sure you know how to treat low blood sugar.
Regular exercise has a significant benefit on insulin sensitivity, which may persist for 72 hours or longer after the last training bout.
Latest findings suggest that short periods of inactivity (e.g., 72 hours) may not result in a loss of insulin sensitivity, and this may reflect chronic adaptations to the underlying pathophysiology. Therefore, clinicians should reinforce the importance of regular exercise to manage insulin sensitivity as these chronic benefits may ensure that short-term periods of inactivity will not negate the therapeutic effect from generally regular exercise participation.
Diabetes is a well-known cause of ED, with prevalence rates approaching 50% in both type 1 and type 2 diabetes. Men who have diabetes are 3 times likelier to have erectile dysfunction than men who don’t have diabetes. Among men with ED, those with diabetes may experience the problem as much as 10 to 15 years earlier than men without diabetes.
Why does this happen? High blood sugar levels affect blood vessels and nerves that are crucial for achieving or maintaining an erection. Complications progress when diabetes is left unchecked, much like the case in diabetic neuropathy. One common symptom among the two of these complications is that diabetic men lose sensation in the feet, or feel like they are walking on pillows.
Itching of the genitals or around the penis is yet another symptom of diabetes in men. Elevated blood sugar levels weaken the immune system, making diabetics more prone to yeast infections. The kidneys try to excrete excess sugar from the body via urine. Bacteria and yeast thrive on sugar, so this environment is perfect for them to multiply.
- Increased thirst.
- Increased hunger (especially after eating)
- Dry mouth.
- Frequent urination.
- Unexplained weight loss (even though you are eating and feel hungry)
- Fatigue (weak, tired feeling)
- Blurred vision.
- Headaches.
In cases where medication is thought to be the primary cause of diabetes, this may be termed as drug induced diabetes.
A number of drugs have been linked with an increased risk development of type 2 diabetes.
- Corticosteroids
- Thiazide diuretics
- Beta-blockers
- Antipsychotics
- Statins
The scientific consensus is that people have genetic predisposition to Type 2 diabetes, as it tends to run in families, but environment also has a significant role in triggering this condition, and apparently triggering genes to change their behaviors. However, this increased risk does not necessarily mean you will develop Type 2 diabetes; it only means that you are susceptible to it, but can beat it by reducing lifestyle and environmental risk factors.
A Swedish study trying to research on Clinical risk factors, DNA variants, and the development of type 2 diabetes found that “compared with clinical risk factors alone, common genetic variants associated with the risk of diabetes had a small effect on the ability to predict the future development of type 2 diabetes.
But, there is growing evidence that epigenetics plays a role in the way genes interact with the environment. There are increasing signs that epigenetics plays a role in the development of Type 2 Diabetes, and also contributes to the complications of diabetes. For example, babies conceived during times of famine switch on hundreds or thousands of genes in anticipation of having to survive after birth in an environment of extreme scarcity. If these babies then grow up in a world of abundant food and little need to exercise, those switched-on genes become dangerously dysfunctional, leading to obesity, diabetes and other problems.
Most statistics are done assuming that we tend to eat and live the way our parents did. So if your parent’s poor lifestyle choices resulted in Type 2 Diabetes, take a good, hard look at your current lifestyle. Are you making the same mistakes as your parents which are increasing your risk factors for developing Type 2 Diabetes?
Type 2 diabetes usually begins with insulin resistance, a condition in which muscle, liver, and fat cells do not use insulin well. As a result, your body needs more insulin to help glucose enter cells. At first, the pancreas makes more insulin to keep up with the added demand. Over time, the pancreas can’t make enough insulin, and blood glucose levels rise.
Obesity is the major risk factor for type 2 diabetes and appears to drive tissue insulin resistance in part via gain of ectopic fat, with the best-studied organ being the liver. However, ectopic fat in the pancreas may contribute to β-cell dysfunction. The majority of people who are obese will never develop type 2 diabetes – a fact that exposes the statement “obesity causes diabetes” as absurd.
People have different tolerance levels of fat in the liver and pancreas. It is only when a person has more fat than they can handle, while type 2 diabetes develops. In other words, once a person crosses your personal threshold of fat, sugar type 2 diabetes develops. After they successfully pass below their threshold personal fat in the liver and pancreas, diabetes disappears.
Some people can tolerate a BMI of 40 or more without getting diabetes. Others cannot tolerate a BMI of 22 without diabetes appearing, as their bodies are set to function normally at a BMI of, say 19. This explains why South Asian Indians are notoriously more prone to develop type 2 diabetes without obesity. South Asians are less able to store fat under the skin, so will accumulate fat a lot earlier on in their liver than white people. The risk of South Asian Indians and Nepalese developing type 2 diabetes at a BMI of 22 is the same as that for white people with a BMI of 30.
At the moment, type 1 diabetes cannot be reversed. Type 1 diabetes is an autoimmune disease, and reversing it would require a method of preventing the body’s immune system from attacking its own insulin-producing cells.
Because it leads to the following complications:
• cardiovascular disease (heart attacks and strokes), the most common cause of death in the developed worlds.
• kidney damage, which can result in kidney failure.
• nerve damage, which can result in chronic numbness and pain in the legs and feet.
When diabetes gets reversed many of these severe complications are also reversed.
The term ‘diabetes reversal’ means that it is not a complete cure, but a change in the direction of the condition, to a clinical condition where blood glucose levels, as ascertained by a variety of tests including the hemoglobin A1C (below 6.5%), are in the normal range and do not require diabetes medications. Reversing diabetes is a term that usually refers to a significant long-term improvement in insulin sensitivity in people with type 2 diabetes. This also known as putting diabetes into remission, which is a very realistic condition to aspire to for most type 2 diabetics.
This is exactly the opposite of what was thought to be the inescapable progression of a disease that puts patients at high risk for so many complications, including cardiovascular disease, blindness, renal failure, and amputations.
Medications can make your ‘blood sugar level’ look good. However, in the background, your insulin sensitivity is worsening and you are heading for a worsening of the dreaded complications of diabetes like blindness etc.
Many people do not think it’s possible to reverse Type II Diabetes. That really depends on the method of treatment. The traditional/conventional treatments that only focus on symptom care are not successful at reversing the disease. These treatments seek to slow the progression.
When the cause(s) of the disease (insulin resistance) is addressed using comprehensive testing and the appropriate individualized treatment plan is followed, then Type 2 diabetes can be successfully reversed. It is possible to not only reverse Type 2 diabetes, but to stay free of the condition long term.
A recent scientific study done at the University of Newcastle showed that Type 2 diabetes is a potentially reversible condition. In this early study, a number of participants with Type 2 diabetes were able to achieve continuing remission of diabetes for at least 6 months – through a robust and sustainable weight loss program following a low-calorie diet.
For obese patients, bariatric surgery is a potentially curative treatment for type 2 diabetes.
In a study published in the Journal of the American Medical Association researchers found that type 2 diabetes remission is possible with intensive lifestyle intervention. Individuals in the study were instructed to exercise for 175 minutes a week, limit their calories to 1,200 to 1,800 per day, and attend weekly counseling and education sessions on these lifestyle changes.
Within a year, over 11% of the lifestyle intervention participants had partial or complete remission of diabetes and were able to come off their diabetes medications. Moreover, rates of any remission were notably higher (15%–21%) among individuals with substantial weight loss or fitness change, less severe or newly diagnosed diabetes, and those not using insulin.
Type 1 diabetes is a chronic condition in which the pancreas produces little or no insulin, a hormone essential to allow sugar (glucose) to enter cells to produce energy.
Type 2 diabetes, on the other hand, is a non-insulin dependent diabetes which means that you have become insulin-resistant, and your body does not function properly with the regular insulin you secrete. Type 2 diabetes is not insufficient insulin production, but insulin resistance.
They are both deadly diseases. If you have Type 1 diabetes, you can die in a few hours if you get low, in a couple of days if you get too high. Type 2 diabetes can evolve to the level where you are as almost as insulin dependent as if you had Type 1. In both cases, you are at very high risk of kidney failure, heart diseases, blindness and other severe complications.
Till date Type 1 Diabetes is not fully curable and is required daily insulin injections. But, Type 2 diabetes is an entirely reversible disease. However, taking medications will not reverse Type 2 diabetes.
T2D is actually a form of accelerated aging. Diabetic patients develop the diseases of aging (cardiovascular disease, cataracts, osteoporosis, Alzheimer’s disease etc.) at a much earlier age than most of us.
T2D is not only a blood sugar issue. If you simply define diabetes by blood sugar levels going high, which is how it’s done today by most doctors, then getting fat becomes a healthy event because it prevents our blood sugar from going too high. As long as you can make fat out of the sugar, it keeps the sugar levels low and keeps you from becoming a diabetic.
A crucial point is that individuals have different levels of tolerance of fat within liver and pancreas. Only when a person has more fat than they can cope with does type 2 diabetes develop. In other words, once a person crosses their personal fat threshold, type 2 diabetes develops. Once they successfully lose weight and go below their personal fat threshold, diabetes will disappear.
Some people can tolerate a BMI of 40 or more without getting diabetes. Others cannot tolerate a BMI of 22 without diabetes appearing, as their bodies are set to function normally at a BMI of, say 19. This is especially so in people of South Asian ethnicity.
When fat cells get resistant to insulin, they can no longer make more fat out of the sugar, then blood sugars do start to go up, and that’s when someone is diagnosed as a diabetic. But in reality, the actual diagnosis of diabetes is preceded by decades when muscle cells and liver cells get insulin resistant prior to when fat cells get resistant to insulin.
गर्भावस्थामा मधुमेह देखिनु असामान्य अवस्था हो। यस्तो बेलामा करिब ५-१० प्रतिशत गर्भवतीमा मधुमेह देखिने गरेको छ। यसरी गर्भावस्थामा मधुमेह देखिनुलाई जेस्तेसनल मधुमेह भनिन्छ। यो मधुमेहले आमा र पेटमा भएको शिशुको स्वास्थ्यमा नकारात्मक असर पर्न सक्छ। यो मधुमेह धेरैजसोमा सुत्केरी भएपछि हराउने गर्छ। गर्भवती हुनुअघि नै यो रोग नियन्त्रणमा नआए बढी समस्या उत्पन्न हुन सक्छ। साधारण व्यक्तिमा देखिने मधुमेह र गर्भवतीमा देखिने मधुमेहमा केही फरक हुन्छ । गर्भावस्थामा हुने मधुमेह साधारणतया बच्चा जन्माइसकेपछि हराएर जाने गर्दछ। त्यस्ता महिलामा पुनः मधुमेह हुने सम्भावना भने उच्च हुन्छ।
विश्व स्वास्थ्य सङ्गठनको आँकडाअनुसार नेपालमा अहिलेसम्म मधुमेहपीडित कति छन् भन्ने तथ्याङ्क नै छैन तर सन् २०१६ मा गरेको एक सर्वेक्षणले ९ दशमलब १ प्रतिशत नेपालीमा मधुमेह रहेको उल्लेख छ । त्यसमा १० दशमलब ५ प्रतिशत पुरुष र ७ दशमलब ९ प्रतिशत महिला मधुमेह पीडित रहेको देखाएको छ ।
त्यस्तै, मधुमेहको जोखिम शहरी क्षेत्रमा ८ प्रतिशत तथा ग्रामिण भेगमा एक प्रतिशत रहेकोमा मधुमेहमध्य पनि टाइप २ मधुमेहको जोखिम १.४ देखि १९ प्रतिशतसम्म रहेको पाइएको छ । नेपालमा मधुमेह हुने अधिकांश व्यक्तिमा मोटोपनाका कारण यो रोग लाग्ने गरेको एक तथ्याङ्कले देखाएको छ । नेपालमा १६ दशमलब ७ प्रतिशत मोटोपनका कारण मधुमेह हुने गरेको पाइएको हो ।
मधुमेहको लक्षण देखाएको कम्तीमा १० वर्षपछि मात्र मृगौलामा समस्या देखा पर्छ । प्रकार १ मधुमेह भएको बिरमीमा १५–२० वर्षपछि मृगौलाको समस्या देखा पर्नसक्छ तर प्रकार २ मामधुमेह भएको सुरुकै अवस्थामा मृगौलामा असर गरिसकेको हुनसक्छ । सामान्यरुपमा हेर्ने हो भने १०–१५ वर्षमा धेरै बिरामीमा मृगौलामा असर देखिएको छ । मृगौलामा ९० प्रतिशत रोग लागिसक्दा पनि थाहा नहुँने भएकोले प्रत्येक वर्ष परीक्षण गराउनुपर्छ । मधुमेह पहिचान गर्न ढिला भएको खण्डमा भने बिरामीले चाडैँ नै ज्यान गुमाउने जोखिम हुन्छ । सबै मधुमेहको बिरामीलाई मृगौलामा समस्या हुँदैन। दोस्रो प्रकारको मधुमेह लाग्नुको मुख्य कारण शरीरमा बोसोको मात्रा धेरै हुनु हो।
मोटोपनले पनि मधुमेह हुने भएकाले यसबाट मुक्त हुनुपर्छ । जंकफूड खानुहुदैन । घरमै बनाइएको रेशायुक्त खानेकुरा खानुपर्छ । दिनमा कम्तीमा पनि आधा घण्टा हिँडडुल गर्नुपर्छ । खानपान तथा जीवनशैलीमा सुधार ल्याउनुपर्छ । वंशाणुगत कारणले पनि मधुमेह हुने भएकाले समय–समयमा सुगर जाँच गराइरहनुपर्छ ।
मधुमेह भएकाले सबै खानेकुरा खान हुन्छ तर खानाको मात्रा कम गर्नुपर्छ । थोरै खाना पटक–पटक खानुपर्छ । यसैगरी चिनी हालेको चिया, कोल्ड ड्रिंक्स, जुस तथा चिल्लो कुरा खानुहुँदैन । फलफूल भने दिनमा एउटासम्म खान सकिन्छ । अण्डाको पहेलो भागले कोलेस्ट्रोल बढाउने भएकाले सेतो भाग मात्र खानु उपयुक्त हुन्छ । अन्न समूहका खानेकुरा, प्रोटिन तथा चिल्लो पदार्थ सीमित मात्रामा खानुपर्छ ।
कतिपयलाई कुनै लक्षणविना नै मधुमेह देखिन सक्छ । कतिपयलाई भने मुख सुक्ने, तिर्खा लाग्ने, थकाइ लाग्ने, आलस्य हुने, छिनछिनमा पिसाब लाग्ने, खुट्टामा कमिला हिँडेजस्तो हुने, भोक धेरै लाग्नेजस्ता लक्षण देखा पर्छन् । त्यसका साथै छातीमा संक्रमण हुने, हातखुट्टा झमझम गर्ने तथा पोल्ने समस्या पनि हुन्छ ।
स्वस्थ मानिसको शरिरमा सुगरको मात्रा खाली पेटमा ९० भन्दा कम र खानापछि १ सय ४० भन्दा कम भए उपयुक्त मानिन्छ ।
टाइप–१ मधुमेह शरीरमा इन्सुलिनको कमीले गर्दा हुन्छ । यो मधुमेह बालबालिकामा धेरै पाइएको छ । वंशाणुगत कारणले पनि मधुमेह हुन्छ । टाइप–१ मधुमेहमा जीवनभर इन्सुलिन लगाइरहनुपर्छ । यसैगरी टाइप–२ मधुमेह ३५ वर्षको उमेर वा त्यो भन्दा अघिदेखि हुनसक्छ । यसका लागि औषधी सेवन गर्नुपर्छ । औषधीले काम गर्न छोडेको अवस्थामा भने इन्सुलिन नै दिनुपर्छ ।
यो रोग हरेक उमेरकालाई लाग्छ । सामान्यत: ३५ वर्षमाथिका व्यीक्तलाई टाइप–२ मधुमेह हुन्छ । यद्यपि हिजोआज बालबालिकामा समेत मधुमेह देखा परेको छ । बालबालिकालाई टाइप–१ मधुमेह हुने गरेको छ ।
मधुमेह मानिसको शरीरमा इन्सुलिनको अभाव भएर लाग्ने रोग हो । रगतमा चिनीको मात्रा बढ्नु नै मधुमेह हो ।
— जुन औषधिको effect हुन्छ, त्यसको side effect पनि हुन्छ l यदि side effect गर्दैन भने त्यसले effect पनि गर्दैन l सबै side-effects हरु हामीले बाहिरबाट हेरेर थाह पाउने होइन र सबै खाले side effects हरु महसुस गरिने पनि होइन l side effect गरेको छ छैन, कुन अंगमा गरेको छ भन्ने कुरा विभिन्न अंगले उत्पादन गर्ने तत्वहरु (जस्तै hormone, enzymes आदि ) जांच गरेर, बिभिन्न अन्य टेस्ट र स्क्यान् गरेर मात्र शरीरका भित्रि अंगले गर्नु पर्ने काम ठिक तरिकाले गरेको छ छैन भनेर थाह हुन्छ l
— यदि Type II मधुमेह हो र सुगरको जांच प्रत्यक दिन जस्तो गर्न सकिन्छ भने जडीबुटी र आयुर्वेदिक औषधिको प्रयोग गर्न सकिन्छ l
पहिलो कुरा Type II मधुमेह कहिले सुरु भएको भन्ने कुरा थाह पाउन गार्हो हुन्छ l भर्खर पत्ता लागेको मात्र हो l बर्षौं सम्मको निरन्तर अधिक क्यालोरी सेवन, कम शारीरिक काम आदिले गर्दा मधुमेह भएको हो l एक दुई दिनमा हुने कुरो होइन l बर्षौं सम्मको अज्ञानताले वा हेल्चक्राइंले मोटोपन बढ्ने, पेटको साइज बढ्ने; बर्षौंसम्म शरीरलाई चाहिने भन्दा धेरै क्यालोरी खानाले इन्सुलिन उत्पादन अत्याधिक मात्रामा हुन गई शरीरका कोषले इन्सुलिन को प्रतिरोध गरिदिंदा यस्तो अवस्था सिर्जना भएको हो l नखाएर सुगरको मात्रा घट्दैन बरु कलेजो (liver) बाट स्टोर भएको सुगर झन् बढी उत्पादन हुन्छ (निस्कन्छ) जसले गर्दा कलेजोले अर्को पटक खाना खाँदा झन् धेरै सुगर स्टोर गर्न थाल्छ l बरु स्वस्थ कुरा खाने तर शारीरिक कामहरु, ब्यायाम आदि गरेर सुगरलाई प्रयोगमा ल्याउनु पर्छ l शरीरलाई आवस्येक पर्ने खाने कुरा जस्तै फलफुल, हरियो सागपात, तरकारी आदि नखाईदिंदा शरीर झन् थाक्ने, केहि गर्न मन नलाग्ने, मासु र हड्डी कम्जोर हुने आदि समस्या हरु आउनेछन l
यो औषधि Type II मधुमेह लाई मात्र काम गर्छ l Type II मधुमेह हुने कारणहरु मध्ये (एक) कलेजो (Liver) ले चाहिने भन्दा धेरै सुगर उत्पादन गरिदिनु (जुन पछि आवस्येक परेको बेलामा चाहिन्छ कि भनेर स्टोर गरेर राख्ने गरको हुन्छ); अर्को Pancreas ले उत्पादन गरेको इन्सुलिन सोहि कलेजो (liver) र मांसपेशीमा काम नगरिदिनु l जसले गर्दा कोषमा भित्र छिरेर शरीरलाई काम गर्न शक्ति दिनु पर्ने ठाउँमा बाहिरै रगतको नलीमा बसिदिनु l यस्ता दुई थरि अवस्थाले सुगर बढेको भए metformin ले काम गर्छ l तर समस्या कलेजो (liver) मा नभई pancreas ले नै इन्सुलिन को उत्पादन गर्न कम गरेको, खानु पर्ने क्यालोरी भन्दा धेरै गुना बढी खाएको, वा उत्पादन भएको इन्सुलिन शरीरको कोषले उक्त इन्सुलिन पूर्ण रुपमा नलिइदिने/प्रतिकार गरिदिने भएको भए metformin ले काम गर्दैन l यस्तो अवस्थामा अर्को खाले औषधि जसले इन्सुलिन उत्पादन गर्न सहयोग गर्छ वा खाएको खानाबाट सुगरमा परिबर्तन गर्न रोक लगाउँछ त्यस्तो खाले औषधिको समेत खानु पर्छl
— Type I को हकमा तत्कालै हुन सक्ने आपातकालीन समस्या भनेको यदि इन्सुलिन लिइएन वा प्रयाप्त भएन भने जति खाना खाए पनि शरीरको कोषले सुगर पाउन सक्दैन l कोषहरु भोकै भएपछी शक्तिको लागि शरीरको आफ्नै अन्य कोषहरु (मांसपेशी, बोसो) नस्ट गर्न थाल्छ l यस्तो असामान्य परिस्थितिले शरीरमा ketones भन्ने तत्व धेरै उत्पादन गरिदिन्छ र रगतमा सुगरको मात्रा पनि बढ्दै जान्छ l जसले गर्दा बान्ता हुने, पिसाब धेरै लाग्ने, स्वास छिटो फेर्नु पर्ने, शरीरमा पानीको मात्रा कम हुने, बेहोस हुने र ज्यानै समेत जान सक्छ l
— Type II मा समयमा औषधि नलिंदा वा औषधिको मात्रा नपुग्दा रगतमा सुगरको मात्रा धेरै हुन्छ l जसले गर्दा धेरै पिसाब लाग्न गई शरीरमा पानीको मात्रा कम भएर रिंगटा लाग्ने, बेहोस हुने आदि हुन सक्छ र किड्नीमा समेत समस्या ल्याउन सक्छ l
— Type I र Type II दुबैमा, बर्षौसम्म रगतमा सुगरको मात्रा धेरै भयो भने धेरै दिर्घकालिन समस्या देखिन्छन् l धेरै सुगरको कारण रगत औसत भन्दा धेरै बाक्लो र गरुङ्गो बन्न जान्छ (जस्तै सफा पानी आउने पाइपमा लेदो गरुङ्गो तत्वहरु आएर पाइप नै जाम भए झैँ ) l रगतले नियेमित गर्ने काम जस्तै oxygen ओसार्ने काम लगाएत अन्य धेरै काममा बाधा परिरहेको हुन्छ l रगत बाक्लो र गरुङ्गो भएकै कारण नसाको भित्रिभागमा पनि क्षति पुर्याउछ, स-साना नसामा रगत छिर्न सक्दैन l रगत पुग्नु पर्ने ठाउँमा समयमा रगत नपुग्दा शरीरका धेरै अंगका कोषहरु राम्रोसंग काम गर्न छाडछन् र मर्न थाल्छन् l त्यसपछि घाउ समयमा सन्चो नहुने, हात खुट्टा पोल्ने, झम झम्झम्याउने, आँखामा समस्या ल्याउने, किड्नीको समस्या, heart attack आदि हुन सक्छ l
— Type I मधुमेह भए इन्सुलिन नलीइ सुखै छैन l यस्तोमा खाने चक्कीले काम गर्दैन l
— Type II मधुमेह भएको भए तुरुन्त diet कन्ट्रोल गर्नुस् र कम्तिमा ५ केजी तौल तत्काल घटाउनुस, पेटको साइज घटाउनुस l हप्तामा कम्तिमा २ पटक सुगर चेक गर्दै गर्नुस् l खाना र ब्यायेमको सन्तुलन मिलाउनुस, पानी सकेसम्म धेरै पिउनुस l तर याद गर्नुस् सुगर बढेर रिंगटा लाग्ने बेहोस हुने जस्ता आपातकालीन समस्याहरु पनि आउन सक्छन् l बरु सुरुमा औषधि खाने अनि सुगर कन्ट्रोल गर्दै गएर डाक्टर को प्रत्यक्ष निगरानीमा औषधिको मात्रा घटाउँदै जानु बेस हुन्छ l
सुगर चेक गर्दा fasting (बिहान उठ्ने बित्तिकै केहि नखाएको बेलामा वा दिउँसो कम्तिमा ८ घण्टा केहि पनि नखाएको अवस्थामा) १२६ भन्दा धेरै भएको वा random (कुनै पनि बेलामा) २०० भन्दा धेरै भएको वा खाना खाएको २-३ घण्टा पछि २०० भन्दा धेरै भएको अवस्थामा मधुमेह भएको मानिन्छ l तर कम्तिमा दुई फरक दिनमा सुगर चेक गर्नु पर्छ l एक दिनको मात्रले हुँदैन l HbA1C ६.५ भन्दा बढी भएको भए पनि मधुमेह भएको मानिन्छ l HbA1C ले गएको करिब ३ महिनामा रगतमा औसत कति सुगर थियो भनेर पत्ता लगाउँछ l चिन्ता, पिडा, त्रसित भएको अवस्था, अन्य रोग ब्याधि लागेको अवस्था आदिमा पनि कहिले काहीं छोटो समयका लागि (केहि दिन) सुगर बढ्ने गर्छ l त्यसैले HbA1C जांच गर्नु निकै आवस्येक हुन्छ l
— Type I र Type II दुबैमा: अति धेरै पिसाब लाग्ने, अति धेरै तिर्खा लाग्ने र अति धेरै भोक लाग्ने l
— Type I मा तौल घट्न सक्छ र Type II मा अलि बढी आलस्य हुने, थकाई लाग्ने हुन सक्छ तर सबैमा यस्तो नहुन पनि सक्छ l
— Type I सानै उमेर देखि लाग्ने गर्छ भने Type II (प्राय) अलि ठुलो भएपछी शरीरलाई चाहिने भन्दा धेरै खाना खाएर वा अस्वस्थ कुरा धेरै खाएर शरीरमा बोसो धेरै लाग्न थालेपछि देखिन्छ l
— सरल भाषामा भन्नु पर्दा धेरै दिनसम्म रगतमा हुनु पर्ने भन्दा सुगरको मात्रा धेरै भएको अस्वस्थालाई मधुमेह (मधुमेह) भनिन्छ l हामीले खाने प्राय सम्पूर्ण खानाहरु अन्तिममा सुगर बनेर रगतसम्म पुग्छ l रगत नलीले त्यो सुगरलाई शरीरको प्रतेक अंगको (प्राय) प्रत्येक कोषमा पुर्याउछ l उक्त कोष भित्र सुगर पुगेपछि मात्र भोक लाग्न छोड्छ l अनि शरीरका अंगले गर्नु पर्ने कामहरु गर्न थाल्छन् l साना र ठुला खाले रगत नली हुँदै आएको सुगर शरीरको अंगको प्रत्येक कोषभित्र छिर्न (घरको ढोका भित्र छिर्न चाबी अवास्येकता भए झैं) इन्सुलिन को प्रयोग गर्छl इन्सुलिन चाहिं pancreas बाट उत्पादन हुन्छ l
— मधुमेह लाग्ने मुख्य गरि दुई कारण हुन्छन्:
(एक) Pancreas ले इन्सुलिन उत्पादन गर्न नसक्नु जसले गर्दा शरीरको अंगको प्रत्येक कोष भित्र सुगर छिर्न सक्दैन l त्यसपछि खाना खाए पनि शरीर भोकै हुन्छ र सुगर रगतमा जम्मा भएर बसिदिन्छ l यस्तो अवस्थालाई Type I मधुमेह भनिन्छ l Type I मा Pancreas मा समस्या भै अब कहिल्यै पनि इन्सुलिन को उत्पादन हुँदैन र जिन्दगि भर इन्सुलिन injection नै लिनु पर्छ l Type II मधुमेह बिग्रिएर पनि Type I मा परिणत हुन सक्छ l
(दुई) उत्पादन भएको इन्सुलिन शरीरको कोषले नचिनिदिनु वा प्रतिकार गरिदिनु (चाबिले काम गर्न छाडेकाले ढोका भित्र छिर्न नसकेको जस्तो हुनु) वा यति धेरै खाना खाइयो कि त्यस खानाबाट बनेको सुगरलाई कोष भित्र लैजान इन्सुलिन प्रयाप्त नहुनु (कोठाको चाबिले काम त गरेको छ तर कोठामा जाने मानिस नै धेरै हुनु र धेरै जना बाहिरै बस्न पर्ने जस्तो हुनु) l यस्तो अवस्थालाई Type II मधुमेह भनिन्छ l
