ARTICLE SUMMARY
- Chronically high insulin—hyperinsulinemia—is the culprit in many serious health problems, even when blood glucose is normal. There’s almost no organ, gland or tissue system not adversely affected by chronically high insulin.
- Blood glucose measurements may appear “normal” because glucose is being kept in check by sky-high insulin. Normal glucose due to high insulin is much more common than is recognized.
- Although insulin resistance is often associated with being overweight or obesity, millions of people at a “normal” body weight may have chronically high insulin and be at risk for serious health problems.
- Insulin testing isn’t part of routine bloodwork, reflecting a blind spot in doctors’ ability to identify people at risk for major health complications long before these develop.
- When testing insulin levels, it’s possible to have a fasting insulin level in the optimal range but have high insulin throughout most of the rest of the day. If the fasting level is normal, but the body is giving clear signs of high insulin, a Kraft test (a variation on the oral glucose tolerance test) should be considered.
- Not everyone needs to follow a very low-carb diet to stay metabolically healthy, but if someone already has one or both feet in the door of metabolic syndrome, it’s a highly effective way to go.
- Sleep is important. Sleep deprivation is recognized as a risk factor for metabolic syndrome and type 2 diabetes, owing to reduced insulin sensitivity and changes to levels of hormones that regulate appetite and energy expenditure.
- Intermittent fasting allows insulin levels to normalize and can give the body more time in a lower insulin state.
Modern medicine is finally catching on to the fact that elevated blood sugar is a major driving force behind the tsunami of chronic, noncommunicable diseases plaguing much of the world. For example, high blood sugar is the sine qua non of type 2 diabetes (T2D). Long-term complications from poorly managed type 2 diabetes include blindness, limb amputation, kidney failure, nerve damage and cardiovascular disease, with the latter being the number one cause of death among those with T2D.
Research indicates that health can become compromised even when blood sugar is below the diabetes and pre-diabetes cutoffs but is still higher than normal. Something that’s far less appreciated, however, is that it’s possible to have perfectly normal blood sugar yet still be at risk for severe health problems. When it comes to blood glucose control, glucose alone doesn’t tell the whole story. In fact, the single-minded focus on glucose has eclipsed what may be an even more important part of metabolic health: insulin.
If you’re used to thinking of insulin solely as a “blood sugar hormone,” hang on to your hat. Insulin has many other roles, almost to the point that lowering blood sugar is one of the least impressive things it does. If you follow what you think is a healthy diet yet still experience bothersome symptoms or serious issues your doctor has been unable to explain—joint pain, acne, infertility, hypertension, erectile dysfunction, migraines, skin tags—chronically high insulin might be the culprit.
HYPO- AND HYPERGLYCEMIA
A healthy, well-regulated body keeps blood glucose (BG) within a relatively narrow range. When BG is 99 milligrams per deciliter (mg/ dL), the equivalent of 5.5 millimoles per liter (mmol/L), there’s only about a teaspoon—one teaspoon—of glucose in your entire bloodstream. When BG drops too low, or drops very quickly from a previously high level, signs and symptoms of hypoglycemia may occur, such as feeling shaky, dizzy, light-headed or nauseated. Other symptoms include sweating or having a racing heart. In very severe cases, seizures or unconsciousness can result.
On the other hand, hyperglycemia—blood sugar that’s very high—causes damage slowly and silently, over a long period of time, until the damage is so severe or widespread that a person begins to show signs and symptoms. Common complications from T2D show us the harmful effects of chronically high blood glucose. These mostly involve damage to both small and large blood vessels, leading to eye damage (retinopathy), nerve damage (neuropathy), kidney damage (nephropathy), stroke, cardiovascular disease, poor or slow wound healing and more.
With these things in mind, it’s obvious why maintaining a healthy blood glucose level is important. But as strange as it might sound, there’s a lot more to blood glucose than just blood glucose!
FLAWED DIAGNOSIS OF T2D
There’s a major flaw with how T2D is traditionally diagnosed. When doctors suspect a patient has T2D, blood glucose typically is the only thing measured. This is illustrated in Table 1, which lists the American Diabetes Association’s diagnostic criteria1 and shows that the three tests used for diagnostic purposes— fasting BG, the hemoglobin A1c test (HbA1c) and the oral glucose tolerance test (OGTT)—are all measures solely of blood glucose. HbA1c is generally taken to represent a three- to four-month average BG level, although there is some controversy regarding how accurate this is. An OGTT involves taking a measurement of BG, then drinking a liquid containing seventy-five to one hundred grams of glucose and measuring BG again at intervals afterward (typically at thirty, sixty and one hundred twenty minutes.)
There is a key reason why these tests are problematic. For many people, the tests will show normal blood glucose measurements, but they’re only normal because glucose is being kept in check by sky-high insulin. And a large body of research shows that chronically high insulin is the culprit in many serious health problems, even when glucose is normal.
Dr. Joseph Kraft, MD, coined the term “diabetes in situ” or “occult diabetes” to describe this situation.2 Occult means hidden: the diabetes (defined as high glucose) is hidden by the high insulin. For many people, fasting glucose and HbA1c are the last things to rise. They are late indicators of metabolic dysfunction, becoming elevated only after one of two things has happened:
- The pancreas can no longer pump out the extraordinary amounts of insulin required to keep blood glucose within a safe range (sometimes called “beta cell burnout”).
- The pancreas still secretes large amounts of insulin, but some of the body’s cells no longer respond to it properly, resulting in high blood glucose. (These cells become resistant to the presence of insulin.)
This explains why many people are surprised by a diagnosis of T2D or prediabetes. They—and their doctors—had been fooled into a false sense of security by glucose measurements that fell within normal ranges for years, perhaps decades, because insulin wasn’t being measured. Kraft’s research indicates that this situation—normal glucose due to high insulin—is much more common than is recognized. And as we’ll soon see, the long-term effects of chronically elevated insulin are staggering. T2D is merely the tiny exposed tip of an enormous iceberg of devastating metabolic dysfunction that remains hidden to the conventional allopathic medical world.
CHRONICALLY HIGH INSULIN
Having come from a checkup where their fasting glucose and HbA1c were normal, many people get a clean bill of health with regard to risk for T2D. But what if they know something isn’t right? They struggle to lose weight despite exercising and eating a healthy diet—or what they think is a healthy diet. They have skin tags. Some women experience infertility or amenorrhea due to polycystic ovarian syndrome (PCOS); men may be dealing with erectile dysfunction or an enlarged prostate gland. What about high blood pressure in those who think they are doing the right thing by dutifully avoiding sodium, or high triglycerides in those who embrace the dogma to follow a lowfat diet religiously? These are all signs and symptoms of chronically elevated insulin, independent of blood glucose levels. High insulin is called hyperinsulinemia.
Gerald Reaven, MD, was one of the first physicians to recognize that several seemingly unrelated issues clustered together in patients. He hypothesized that because they clustered together, they likely had the same underlying cause. The issues often found together were abdominal obesity, high triglycerides, low HDL cholesterol, elevated blood pressure and elevated fasting blood glucose.
Not knowing what the underlying cause was, Dr. Reaven coined the term “syndrome X.”3 Over time, research revealed the unifying factor to be elevated insulin, and the name changed from syndrome X to metabolic syndrome. It could just as easily be called high insulin syndrome, and some doctors quite rightly call it “insulin resistance syndrome.”4 Unlike “metabolic syndrome,” which is a nebulous and unclear term to most laypeople, calling it “insulin resistance syndrome” hammers home loud and clear that the main problem is insulin.
In order to trigger a diagnosis of metabolic syndrome, a person has to show at least three of the five criteria shown in Table 2.5 The criteria pertain to waist circumference, triglycerides, HDL, blood pressure and fasting glucose. However, the astute observer will notice that something is missing—something important— the official diagnostic criteria for metabolic syndrome (aka insulin resistance syndrome) do not include elevated insulin! In other words, the underlying factor driving the condition is not even taken into consideration.
SIGNS AND SYMPTOMS OF CHRONIC HYPERINSULINEMIA
Keep in mind that with regard to metabolic syndrome, it’s not necessary to have all five issues above to be diagnosed. Having three or more, or using medication to control them, is sufficient to prompt the diagnosis. However, even if you have just one or two, it’s worth assessing whether you have chronically high insulin. Here are some of the many conditions associated with chronic hyperinsulinemia, even when glucose is normal—and remember, this is only a handful of them!
- Hypertension6
- Obesity7
- Cardiovascular disease8
- PCOS9-12
- Gout13,14
- Erectile dysfunction15
- Benign prostate hypertrophy/hyperplasia16
- Skin tags17,18
- Migraines19,20
- Vertigo, tinnitus, Ménière’s disease21,22
- Alzheimer’s disease23-25
Something else to keep in mind is that while insulin resistance is often associated with being overweight or obesity, millions of people at a “normal” body weight or with a healthy body mass index (whatever that even means!) may have chronically high insulin and be at risk for serious health problems. Researchers even have names for situations when there are clear signs and symptoms of metabolic dysfunction in people at a normal body weight: “normal weight obesity” or “metabolically obese, normal weight.”26,27 Thus, while a slim and trim physique might look nice on the outside, it’s no guarantee of health on the inside. (You might even have heard this casually called “TOFI”— thin outside, fat inside.28) After all, not everyone with cardiovascular disease, gout, migraines, hypertension or an enlarged prostate is obese. What individuals with these conditions do likely have, however, is chronically high insulin.
Obesity is often considered a risk factor for developing T2D or metabolic syndrome, but this orientation ignores the millions of type 2 diabetics and metabolic syndrome patients who are not obese, nor even overweight. All of the other conditions listed above occur in people of all body sizes, and more progressive medical professionals are beginning to see excess body weight as a symptom, rather than a cause, of metabolic dysfunction.
Here, too, insulin is a key player. Insulin is an anabolic hormone: it facilitates tissue growth, including growth of adipose tissue—fat cells. It’s also directly anti-lipolytic—it inhibits the breakdown of stored body fat. This is why some people find it extremely hard to lose weight even on a low-calorie diet: if most of those calories come from carbohydrates, people who have inordinate insulin secretion in response to dietary carbohydrates might find themselves trapped in a futile cycle of eat carbs, burn carbs, eat carbs, burn carbs, with burning fat never entering the equation. Think of chronically high insulin like a security guard outside the fat cells, ensuring that no fat can escape.
WHY IS HYPERINSULINEMIA OVERLOOKED?
The simple answer to this question is that, unlike fasting blood glucose, fasting insulin is not a routine part of standard bloodwork. It’s a more complex and expensive assay, but considering the frequency with which far more complex and costly tests and procedures are performed, it’s unlikely that expense is the issue. The most likely explanation for why annual checkups and routine blood tests don’t include insulin is that most doctors simply aren’t aware of the wide-ranging and powerful effects of insulin.
The unfortunate fact is that, even today, insulin is considered little more than a blood sugar hormone, despite decades of research showing the undeniable influence of insulin on kidney function, the cardiovascular system, reproductive function, fuel metabolism and more. As is true for glucose, there’s almost no organ, gland or tissue system not adversely affected by chronically high insulin.29 Insulin’s role in the etiology of so many illnesses has led researchers to say that hyperinsulinemia is the cornerstone of “a unifying theory of chronic disease.”30
It’s not a meaningless oversight that insulin testing isn’t part of routine bloodwork. Rather, it’s a gaping hole of a blind spot in doctors’ ability to identify people at risk for major health complications long before these develop. In the case of T2D, insulin might be elevated for decades before glucose budges into territory diagnostic for diabetes. The same may be true of Alzheimer’s disease, now regularly referred to as “type 3 diabetes” or “brain insulin resistance.” If health providers tested insulin more routinely, these conditions could be dealt with when there’s only some smoke, rather than waiting until they’re raging, out-of-control fires.
Several conditions often considered idiopathic—meaning, no one knows what causes them—can be directly tied to chronic hyperinsulinemia. One of these is essential hypertension. Insulin inhibits renal sodium excretion:13,31 as the kidneys retain more sodium, more water is retained as well, increasing the blood volume and raising blood pressure. Hyperinsulinemia also impairs healthy blood vessel function, making the vessels less pliant and accommodating, which also contributes to higher blood pressure. As if that weren’t enough, insulin also has effects on the sympathetic nervous system that may raise blood pressure.32 For most people, salt consumption has little to no effect on blood pressure, and dietary sodium is not a contributor to hypertension.
Another condition that fits this description—misattribution to a wrongly demonized dietary factor—is gout. Animal protein in general, and red meat, in particular, typically take the blame for gout, with alcohol—beer, especially—a close second. Gout occurs when a compound called uric acid builds up in the body and precipitates into crystals that lodge in the joints. The big toe is most commonly affected, but gout attacks can affect other joints. Uric acid comes from the breakdown of purines, which are concentrated in animal proteins but are also found in plant foods. Uric acid isn’t a problem in a healthy body that excretes it properly. It’s only problematic when it accumulates and solidifies, and the primary driver of this is high insulin. Just as with sodium, hyperinsulinemia inhibits excretion of uric acid.13,31 The answer isn’t to reduce dietary purines (which would mean cutting back on some of the most nutrient-dense foods available); the answer is to reduce insulin levels.
Simply stated, health providers fail to identify chronic hyperinsulinemia as the primary driving factor in many chronic noncommunicable diseases because insulin testing isn’t performed anywhere near as often as it should be. A great deal of morbidity and early mortality could be prevented if people were made aware that their seemingly inexplicable issues actually have a very clear explanation, and it’s something fairly easy to correct.
MEASURING INSULIN
The easiest way to assess insulin status is with a fasting insulin test. You can request one from your doctor, but if you find your physician uncooperative, you can order a fasting insulin test from directlabs.com (in the U.S.). Reference ranges vary among different laboratories. According to the Mayo Clinic, the reference value for fasting insulin is 2.6-24.9 µIU/mL.33 However, most physicians who are well-informed regarding metabolic syndrome and insulin resistance prefer to see fasting insulin below 10 µIU/mL, and some would say that below 5 µIU/mL is ideal. If your fasting insulin is in the double digits and you experience any of the issues mentioned earlier, it’s too high.
Another helpful measurement of insulin sensitivity is HOMA-IR (homeostatic model assessment of insulin resistance). This is a helpful tool because it takes into account both glucose and insulin. It tells you how much insulin your body has to produce in order to keep your glucose at a certain level: that is, how hard your pancreas has to work to maintain homeostasis— a glucose level that’s neither too high nor too low. Table 3 shows how HOMA-IR is calculated. As with fasting insulin, reference ranges and opinions on what is optimal vary. Physicians who use reduced carbohydrate diets to treat metabolic syndrome gauge insulin sensitivity with the following parameters for HOMA-IR:
- Excellent insulin sensitivity: ≤ 1
- Average insulin sensitivity: 1.75
- Insulin resistant: ≥ 2.75
There are many reasons why fasting glucose might be slightly higher than expected, and because it’s not necessarily indicative of a problem, HOMA-IR is a much more informative indicator than fasting glucose alone. The two examples in Table 4 can serve to illustrate HOMA-IR in action. 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 that even with a lower fasting glucose, Patient B is at greater risk for metabolic complications down the road. Patient B’s body has to work harder and the person requires much more insulin to maintain a healthy glucose level. If Patient B’s doctor persists in testing only glucose and not insulin, the patient will remain dangerously unaware of serious metabolic trouble brewing.
THE KRAFT TEST
If your fasting insulin is in the high double digits, it’s a sure sign something is awry. However, if your fasting insulin is normal, it doesn’t automatically mean that all is well. As with blood glucose, in some people, the fasting level is normal, but it rises very high after meals and takes a long time to come back down to the baseline level. In some people, it might not even come down fully before the next meal. In such cases, it’s possible to have a fasting insulin level in the optimal range but have high insulin throughout most of the rest of the day.
In most people living with signs and symptoms of hyperinsulinemia, fasting insulin will be elevated and no further assessment will be needed. However, if your fasting level is normal, yet your body is giving you clear signs that you have high insulin, you may want to consider the Kraft test. The test is a variation on the oral glucose tolerance test and is named for Dr. Joseph Kraft, the physician mentioned earlier who pioneered the research identifying the harms of chronic hyperinsulinemia in people with normal glucose.
Unlike with the conventional two-hour OGTT, which only measures glucose, the Kraft test also measures insulin and is extended to five hours. This is where the Kraft test shines—with these two small changes, the Kraft test provides valuable information that you won’t get from a standard OGTT. It was through performing thousands of these modified OGTTs that Dr. Kraft uncovered the staggering scope of diabetes in situ—the result of dangerously high insulin in people with normal glucose levels.
The Kraft test is not recommended if you feel well and are satisfied with your health and body composition. However, if you’re not happy with your health—if you feel like you’re doing “all the right things,” yet you still struggle with signs and symptoms of a condition known to be driven by high insulin—it might be worth seeing your glucose and insulin in action together, especially if your fasting levels for both are normal. If you decide to have this test performed, consider skipping drinking the glucose glug and do the test in response to a typical meal instead. Consume whatever you might normally eat and drink for breakfast or lunch, so that the test measures your insulin response to the foods and beverages you eat “in the real world.”
WHAT TO DO ABOUT HYPERINSULINEMIA
If your insulin is high, there are many strategies to lower it. Reducing dietary carbohydrate intake is extremely effective for this purpose, to the point that researchers have said this should be the “default treatment” and “first approach” for metabolic syndrome and T2D.34,35 However, as Weston A. Price Foundation (WAPF) members know, and as Sally Fallon Morell explores in her latest book, Nourishing Diets, healthy, robust and long-lived people all over the world thrive on highly varied diets, some of which include substantial amounts of starchy vegetables and grains. It would be myopic to insist that everyone, everywhere, cut back to extremely low, ketogenic levels of carbohydrate consumption to prevent chronic hyperinsulinemia and the resulting metabolic derangement.
However, once someone is already down the disease path and is dealing with a condition known to stem from high insulin, he or she would likely benefit from an intervention more drastic than the strategy a healthy person would follow to remain healthy. That is, what’s required to reverse an illness isn’t necessarily required to prevent it from happening in the first place. With the increased popularity of ketogenic diets, carbs are getting a bad reputation. Not everyone needs to follow a very lowcarb diet to stay metabolically healthy, but if you already have one or both feet in the door of metabolic syndrome, it’s a highly effective way to go. Using a reduced carbohydrate diet to lower insulin levels means cutting way back on even the carbohydrates we might otherwise consider nutritious, such as potatoes, properly prepared grains, beans and fruit. (The fructose portion of fruit doesn’t affect insulin as powerfully as glucose does, but large amounts of fructose contribute to the buildup of fat in the liver, leading to adverse effects on metabolic health.)
If you’ve been following a low-carb or ketogenic diet for a while, but you still have signs and symptoms of hyperinsulinemia and you’d like to do a Kraft test out of curiosity, you will need to “carb up” for a few days beforehand. Your body has to become reacclimated to metabolizing a large amount of glucose. Without this adjustment period, you might get a false result: you’ll look like you have out-of-control diabetes when you’re actually perfectly healthy. Low-carb-savvy physicians recommend consuming one hundred to one hundred and fifty grams of carbohydrate per day for seven days before doing the test.
Some people find that they need a very low-carb diet for some period of time to restore healthy metabolic function, after which they can reintroduce small amounts of starches and grains. They might never get to a point where they can partake of bottomless breadsticks and gargantuan bowls of pasta at their favorite Italian restaurant, but they won’t have to live on fatty meats, avocados and cheese forever—not that there’d be anything wrong with that! (If you reintroduce bread, do it WAPF-style: with enough butter that you can see your teethmarks in it! And if you have morning oatmeal, make it luxurious with cream.)
Carbohydrate intake has arguably the largest effect on insulin levels, but it’s not the only factor. Exercise and physical activity in general improve insulin sensitivity, as does getting an adequate amount of good quality sleep. Sleep deprivation is now recognized as a risk factor for metabolic syndrome and T2D, owing to reduced insulin sensitivity and changes to levels of hormones that regulate appetite and energy expenditure.36-38 Eating regular meals that are nourishing and satisfying—as opposed to grazing all day—can also help promote healthy insulin levels. The last thing someone with chronic hyperinsulinemia should do is snack all day. Even if the snacks are low in carbohydrates, insulin rises in response to all food (except for small amounts of pure fat), so it’s best to space meals with a significant time in between.
Fasting or “time-restricted feeding” may also help reduce insulin levels, even in the context of a high carbohydrate intake. Simply going longer without eating gives the body more time for insulin to come back to normal. This doesn’t mean fasting for multiple days at a time; beneficial effects can be experienced by simply skipping breakfast or dinner and having two meals a day instead of three, or eating within a compressed window of time. One popular method is fasting for sixteen hours and consuming food only during the other eight hours; for example, you would have breakfast at 10:00 AM, dinner at 6:00 PM and not eat again until breakfast the next morning. There are many different options for implementing intermittent fasting; the point is to extend the amount of time you go without eating to allow your insulin level to normalize and give your body more time in a lower insulin state.
SUMMARY
When it comes to metabolic health and proper gluco-regulation, blood glucose tells only part of the tale. Even when blood glucose is normal, chronically high insulin exerts a powerful influence over just about every organ and tissue system in the body: the kidneys, the brain, the reproductive and cardiovascular systems and more. Don’t let a normal glucose level trick you into thinking everything’s fine if you know you don’t feel your best. To stay on top of your long-term health, have your insulin level checked periodically.
SIDEBARS
HOME TESTING? NOT YET
Regrettably, something insulin doesn’t have in common with glucose is availability of convenient home testing. Unlike the handheld glucometers diabetics use to test their blood glucose, the complexity of the chemical assay needed to measure insulin means there are no home insulin meters. No doubt enterprising engineers are working on one, because it’s a zillion-dollar idea.
The Kraft Test
If you’d like to see detailed images of the Kraft test insulin and glucose patterns, Meridian Valley Lab has a nice overview.39 For those interested in learning more about Dr. Kraft’s fascinating work in uncovering the massive scope and underappreciated consequences of chronic hyperinsulinemia, I highly recommend his book, Diabetes Epidemic & You.2
DRUGS DON’T FIX DIETARY DISEASES
That chronic hyperinsulinemia is under-recognized as the primary driver of so many otherwise “idiopathic” (unexplained origin) health issues has consequences more far-reaching than just the psychological effects of having troublesome symptoms that interfere with quality of life. Probably the most powerful consequence is that health care providers use pharmaceutical drugs to treat conditions that are driven almost entirely by diet and lifestyle.
Hyperinsulinemic conditions—such as hypertension, gout, skin tags, erectile dysfunction and type 2 diabetes—are warning signs from the body that something has gone awry. Using drugs to treat individual symptoms without addressing the underlying cause opens up a can of worms that leads to increased dysfunction. When we ignore the fundamental cause of a health issue and mask the red flags with drugs, the underlying cause continues wreaking havoc, typically resulting in a need for higher doses of drugs or introduction of additional drugs when the ones initially used are no longer up to the task of holding back the snowballing tide of metabolic dysfunction.
Very few pharmaceutical drugs are without unpleasant and even harmful side effects:
• Drugs for hypertension, such as diuretics, may result in electrolyte imbalances, leading to headaches, muscle cramps, dizziness, arrhythmias and hypo- or hyperkalemia (too little or too much potassium in the blood). Beta-blockers may cause dizziness, fatigue, drowsiness, headache, dry mouth and constipation or diarrhea. Calcium channel blockers may cause drowsiness, slower heart rate, increased appetite, lightheadedness, fluid retention in the lower legs (swollen feet, ankles and legs) and constipation.
• Drugs for type 2 diabetes come with varying side effects depending on their mechanisms of action, but may include weight gain, upset stomach, hypoglycemia, increased hunger, water retention, chest pain, eyesight problems, urinary tract infections and conditions as severe as diabetic ketoacidosis and kidney failure.
• Drugs for gout may cause liver damage, life-threatening skin rash, drowsiness, vomiting, headache and muscle pain.
None of these drugs does anything to address the actual cause of the illness for which they’re prescribed. Because they don’t address the fundamental drivers of metabolic derangement, not only do the unfortunate individuals who take them have to deal with a laundry list of side effects, but they will eventually need even more medication, as the underlying problem continues to get worse. Using drugs to treat dietary diseases creates an endless downward spiral, inevitably leading to ever more severe derailment of health, not to mention an increasing financial burden. It’s like putting a piece of electrical tape over your car’s check engine light: You can’t see the light anymore, but that doesn’t mean you fixed the problem that was making it go on. You cannot medicate away dietary diseases.
REFERENCES
1. American Diabetes Association. Diagnosing diabetes and learning about prediabetes. http://www.diabetes.org/are-you-at-risk/prediabetes/. Accessed July 10, 2018.
2. Kraft JR. Diabetes Epidemic & You. Bloomington, IN: Trafford Publishing; 2008.
3. Reaven GM. Syndrome X: a short history. Ochsner J 2001;3(3):124-125.
4. Sarafidis PA, Nilsson PM. The metabolic syndrome: a glance at its history. J Hypertens 2006;24(4):621-626.
5. Mayo Clinic. Metabolic syndrome. https://www.mayoclinic.org/diseases-conditions/metabolicsyndrome/
diagnosis-treatment/drc-20351921. Accessed July 10, 2018.
6. Ferrannini E, Haffner SM, Stern MP. Essential hypertension: an insulin-resistant state. J Cardiovasc Pharmacol 1990;15(Suppl 5):S18-S25.
7. Kahn BB, Flier JS. Obesity and insulin resistance. J Clin Invest 2000;106(4):473-481.
8. Reaven GM. Insulin resistance, the insulin resistance syndrome, and cardiovascular disease. Panminerva Med 2005;47(4):201-210.
9. Diamanti-Kandarakis E. Insulin resistance in PCOS. Endocrine 2006;30(1):13-17.
10. Baptiste CG, Battista MC, Trottier A, Baillargeon JP. Insulin and hyperandrogenism in women with polycystic ovary syndrome. J Steroid Biochem Mol Biol 2010;122(1-3):42-52.
11. Diamanti-Kandarakis E, Dunaif A. Insulin resistance and the polycystic ovary syndrome revisited: an update on mechanisms and implications. Endocr Rev 2012;33(6):981-1030.
12. Dunaif A, Segal KR, Futterweit W, Dobrjansky A. Profound peripheral insulin resistance, independent of obesity, in polycystic ovary syndrome. Diabetes 1989;38(9):1165-1174.
13. Quiñones-Galvan A, Ferrannini E. Renal effects of insulin in man. J Nephrol 1997;10(4):188-191.
14. Perez-Ruiz F, Aniel-Quiroga MA, Herrero-Beites AM et al. Renal clearance of uric acid is linked to insulin resistance and lower excretion of sodium in gout patients. Rheumatol Int 2015;35(9):1519-1524.
15. Yao F, Liu L, Zhang Y et al. Erectile dysfunction may be the first clinical sign of insulin resistance and endothelial dysfunction in young men. Clin Res Cardiol 2013;102(9):645-651.
16. Vikram A, Jena G, Ramarao P. Insulin-resistance and benign prostatic hyperplasia: the connection. Eur J Pharmacol 2010;641(2-3):75-81.
17. Sari R, Akman A, Alpsoy E, Balci MK. The metabolic profile in patients with skin tags. Clin Exp Med 2010;10(3):193-197.
18. Shaheen MA, Abdel Fattah NS, Sayed YA, Saad AA. Assessment of serum leptin, insulin resistance and metabolic syndrome in patients with skin tags. J Eur Acad Dermatol Venereol 2012;26(12):1552-1557.
19. Fava A, Pirritano D, Consoli D et al. Chronic migraine in women is associated with insulin resistance: a cross-sectional study. Eur J Neurol 2014;21(2):267-272.
20. Bhoi SK, Kalita J, Misra UK. Metabolic syndrome and insulin resistance in migraine. J Headache Pain 2012;13(4):321-326.
21. Kraft JR. Hyperinsulinemia: a merging history with idiopathic tinnitus, vertigo, and hearing loss. Int Tinnitus J 1998;4(2):127-130.
22. Kaźmierczak H, Doroszewska G. Metabolic disorders in vertigo, tinnitus, and hearing loss. Int Tinnitus J 2001;7(1):54-58.
23. Neumann KF, Rojo L, Navarrete LP et al. Insulin resistance and Alzheimer’s disease: molecular links & clinical implications. Curr Alzheimer Res 2008;5(5):438-447.
24. Craft S. Insulin resistance and Alzheimer’s disease pathogenesis: potential mechanisms and implications for treatment. Curr Alzheimer Res 2007;4(2):147-152.
25. Watson GS, Craft S. Modulation of memory by insulin and glucose: neuropsychological observations in Alzheimer’s disease. Eur J Pharmacol 2004;490(1-3):97-113.
26. Oliveros E, Somers VK, Sochor O et al. The concept of normal weight obesity. Prog Cardiovasc Dis 2014;56(4):426-433.
27. Ding C, Chan Z, Magkos F. Lean, but not healthy: the “metabolically obese, normal-weight” phenotype. Curr Opin Clin Nutr Metab Care 2016;19(6):408-417.
28. Zdrojewicz Z, Popowicz E, Szyca M et al. TOFI phenotype—its effect on the occurrence of diabetes. Pediatr Endocrinol Diabetes Metab 2017;23(2):96-100.
29. Fung J, Berger A. Hyperinsulinemia and insulin resistance: scope of the problem. Journal of Insulin Resistance 2016;1(1):a18.
30. Crofts C, Zinn C, Wheldon M, Schofield G. Hyperinsulinemia: a unifying theory of chronic disease? Diabesity 2015;1(4):34-43.
31. Reaven GM. The kidney: an unwilling accomplice in syndrome X. Am J Kidney Dis 1997;30(6):928-931.
32. Landsberg L. Insulin and the sympathetic nervous system in the pathophysiology of hypertension. Blood Press Suppl 1996;1:25-29.
33. Mayo Clinic. Mayo Medical Laboratories. Insulin, Serum. https://www.mayomedicallaboratories.
com/test-catalog/Clinical+and+Interpretive/8664. Accessed July 10, 2018.
34. Feinman RD, Volek, JS. Carbohydrate restriction as the default treatment for type 2 diabetes and metabolic syndrome. Scand Cardiovasc J 2008;42(4):256-263.
35. Feinman RD, Pogozelski WK, Astrup A et al. Dietary carbohydrate restriction as the first approach in diabetes management: critical review and evidence base. Nutrition 2015;31(1):1-13.
36. Morselli L, Leproult R, Balbo M, Spiegel K. Role of sleep duration in the regulation of glucose metabolism and appetite. Best Pract Res Clin Endocrinol Metab 2010;24(5):687-702.
37. Nedeltcheva AV, Scheer FAJL. Metabolic effects of sleep disruption, links to obesity and diabetes. Curr Opin Endocrinol Diabetes Obes 2014;21(4):293-298.
38. Chaput JP, McNeil J, Després JP et al. Short sleep duration as a risk factor for the development of the metabolic syndrome in adults. Prev Med 2013;57(6):872-877.
39. Meridian Valley Lab. http://meridianvalleylab.com/Kraft-prediabetes-profile-patterns-overview.
This article appeared in Wise Traditions in Food, Farming and the Healing Arts, the quarterly magazine of the Weston A. Price Foundation, Fall 2018.
🖨️ Print post
Danna C Seevers says
Wow!!! Excellent article!! So glad to have this information as I see elevated insulin in the presence of normal fasting glucose and HbA1c in my practice all the time.
DrJim says
Thank you for this little treasure. This article is a major contribution to my understanding the vast field that is natural health. Dr. Michael Cutler has a great book on this same subject & feels insulin is our master control hormone & the one trigger of all disease (The Insulin Factor).
Peggy says
This was a very comprehensive article on exactly what I needed to know. I have been afraid of going on high fat, low carb diet because I am fat. My love for carbs is undeniable and low carb will be quite a challenge. But I have to do something, my weight is over 200 lbs, my waist is 49 inches, taking BP and cholesterol meds. I’m having symptoms of hypoglycemia: sweaty, shaky and hungry after I eat. My memory is not what it should be for 67 years old. I will start intermittent fasting and Adkins type diet asap. Thank you for possibly prolonging my life.
Kassia says
This was very informative and helpful, thank you. I’ve been intermittent fasting (eating in a 6-8 hour window) for the past 5 months. My weight went down 12 lb, fasting insulin went from 20 to 11, fasting glucose from 105 to 88, and A1C from 5.7 to 5.4. I lost a few inches around my waist too. I’m very encouraged BUT my weight loss has stalled for the past 2 months. This article has me feeling ready to try a low carb approach again and see if it helps me make more progress back to health!!
Wayne Taylor says
Excellent article about metabolic syndrome! After reading the book “Diabetes Code” I am convinced that hyperinsulinemia is the root cause of the metabolic mayhem many of us experience. Your article perfectly aligns with Dr. Fung’s book. I was diagnosed with T2D on December 29 and prescribed Glimiperide to bring down my my blood sugar (A1C at diagnosis was 12.6, fasting blood sugar was 285). I did a lot of research on T2D (thank God for the internet) as well as reading Dr. Fung’s book. I am now in week three after diagnosis. I took the Glimiperide as prescribed and it did bring my blood sugar down, but I concluded that I was only treating the symptom (high blood sugar) and not the underlying disease. I went VERY LOW CARB/HIGH FAT starting the day I was diagnosed. I quit taking the Glimiperide two days ago and my blood sugar is averaging about 115 with just the VLCHF diet. I have also done a couple of 24 hour fasts and my blood sugar levels usually retreats to about 80 at the end of the 24 hour fast period. I will continue this regimen until my next doctor appointment at the end of March (it is now January 18) to see where my A1C is then. I intend to ask for an insulin level test then.
wendell says
I read this article in 2018 and visited a doctor in cummings, ga who did insulin test on me and I was at 29. next year I was 81. Checked out a book called: The Insulin resistance solution, by dr. rob thompson and dana carpender and learned the how and read amy’s book: reversing alzheimer’s and got the why. lost 20 lbs since dec-29th and insulin fell to 47. A1c fell from 6.7 to 6.2. triglycerides fell from 277 to 167 and cholesterol, which I wasn’t worried about is total of 160. plan to continue this eating program, not diet, because I eat all the food I want, don’t have food cravings and eat just two meals a day and I’m full and satisfied each day. walking 2 miles every other day.
Sandra says
So profound from the viewpoint of western metabolic diseases. Studying Diabetes management now, and after forty years of conventional understanding, this is in deed food for thought. Thank you and I will definitely be mindful of this evidence in my practice.
Ed from Scott AFB says
Thanks for this wonderful detailed article on hyperinsulinemia. This information is not easy to find. It is very useful to me. I am retired Air Force as well. Struggling with FI of 15.6 , HOMA of 3.5 and a number of the associated conditions including CVD and BPH. Trying to bring it down with diet and fasting. It took me a long time to figure out the problem. My doctors have been zero help. Actually my doctors have been in the way of progress. Best to you!!
MW Martin says
Good article. I would also mention the work of Prof Jim Johnson at UBC which highlighted the fact that raised Insulin can precede obesity. It was ,for so long, widely taught that obesity causes insulin problems, (it doubtless worsens it) whereas it has always made more sense that insulin problems should precede obesity as it raises food intake and inhibits the use of fat as a fuel. Blaming and stressing the patient has never been helpful.
John St.Hilaire says
IT appears as though, at some point in the past, someone should have INSISTED on SCREENING OF INSULIN LEVELS; SADLY, MOST OF US WERE NOT TALKED TO ABOUT OUR INSULIN, JUST BLOOD GLUCOSE AND A1C. NEGLIGENCE DEFINITELY COMES TO MY MIND. JUST DAMN DISGUSTING TO THINK OF HOW MANY MILLIONS OF LIVES LOST AS A RESULT OF NOT PERFORMING THIS KIND OF SCREENING.
Kim says
I’m 52 and after my doctor retired last year my new doctor ordered fasting insulin test. It was 48.1, which is insanely high. I have in range glucose and A1C but my pancreas is working overtime. I took Mounjaro and after 7 months my fasting insulin is 4.1, which is optimal range. It is incredible to me that the medical community hasn’t or won’t acknowledge that treatment needs to begin when insulin resistance is found. I feel like I have my life back after 25 years…that’s a lot of lost time.
Thomas says
Could you share your thoughts on the reduced first-phase insulin response in people affected with Type 2 diabetes? Which is restored with fat loss in the pancreas.