Do you want to make yourself immune to chronic disease?
If so, you need to prevent and reverse insulin resistance.
Good news and bad news. Which first? Okay bad news…
Insulin resistance is related to almost every chronic disease:
It may not cause them all. But at the very least, persistently high insulin levels exacerbates them.
Good news: you can reverse insulin resistance. And reversing it is one of the most important things you can do for your health.
Learn more below about why insulin resistance is bad and the 8 simple steps to reversing it.
What is Insulin?
Our cells generate energy from three different sources: protein, fats, and carbohydrates. Protein is a minor player. Most of our energy comes from carbohydrates and fat.
When Ancel Keys brainwashed us into fearing saturated fats, we needed to replace fat with carbohydrates. According to the CDC, from 1971 to 2000 American’s increased carbohydrate consumption by 25%. Fat was also reduced to less than 30% of calories.
Today animal products only constitute ~10% of calories in a standard American’s diet.
Despite both being macronutrients, carbohydrates and fats produce very different chemical reactions when consumed. When we eat a carbohydrate, this leads to a complex chain reaction, which can take a toll on us.
At any given time, your body only has a very small amount of sugar in your blood — around one teaspoon in your entire circulatory system.
When you digest carbs, you break them down into glucose. For example, when you drink soda, your body will quickly break that down into glucose, and dump 5-10 teaspoons of sugar into your bloodstream. Five times more than the existing amount.
Your body, rightfully so, freaks out.
Your body (specifically your pancreas) responds by secreting insulin, which drives glucose into cells to ensure blood glucose levels stay constant. If this process doesn’t work, you’d have an instant case of diabetes.
How responsive blood glucose is to insulin is your insulin sensitivity. The more effective insulin is, the more insulin sensitive. The less effective, the more insulin resistant.
However, most people don’t need all the energy they just consumed. At rest, your body burns at most 50 kcal of glucose per hour, so a lot of the new glucose goes into storage as glycogen [*].
Your body can only store so much glycogen, and when it exceeds these levels, the glucose is turned into fat. This process is called lipogenesis [*].
The glycemic index, which you have probably heard of, measures how much blood sugar rises and lowers after certain foods.
What is Insulin Resistance?
Over time your body can become less responsive to insulin’s signal.
How does it happen? Insulin resistance is an energy overload problem.
It’s a result of maxing out all your fat cells. The simplest way to put it is that you’ve exceeded your ability to store energy, but there’s still abundant energy in your blood that your pancreas is trying to force into the fat cells.
Think of it like a packed elevator and somebody is running for the door. You, the fat cell, don’t want to let them in even though you make eye contact. It’s an awkward situation…
Your cells don’t want more energy and are giving the middle finger to the rest of your body. They refuse to let energy in and start fighting with your pancreas.
Your pancreas pumps out insulin, but your cells become less and less responsive to it. This is insulin resistance.
What Causes Insulin Resistance?
The biggest cause is consuming too much carbohydrates and fat together.
Because excess glucose gets stored as fat it doesn’t make sense to simultaneously burn fat. So glucose and fat are burned reciprocally.
Our bodies are too efficient to both burn and create fat at the same time.
Instead, your body physically blocks fat from entering the cell to be converted to energy when insulin is present.
If carbohydrates are eaten occasionally and they are lower glycemic, your insulin levels will normalize and your body will burn fat as fuel. But, as we all know too well, most people eating carbs aren’t doing so occasionally.
According to a new research by Dr. David Ludwig, when insulin is present:
“Our rapidly growing fat cells take up too many calories, leaving too few for the rest of the body. That’s why we get hungry. And that’s why metabolism slows down if we force ourselves to eat less.” [*]
So, to summarize, when you eat carbs, a chain reaction occurs:
- Blood sugar spikes
- Pancreas secretes insulin
- Insulin secretion shuts off fat burning
- Excess sugar gets turned into glycogen and fat for storing
Because you’re not burning fats, your cells get more and more packed. But you simultaneously have new energy in your bloodstream – the carbs and newly synthesized fats – that need to get in.
In response to the elevated glucose levels in your bloodstream, your pancreas pumps out more and more insulin to push the energy into your cells.
The efficacy of the insulin drops over time until your cells become resistant to its secretion.
Basically, to summarize: so many carbs are around that you can’t ever burn fat.
Carbs and Fat Together Make You As Fat As Possible
And because sugar and fat are burned reciprocally, if you combine them it makes you as fat as possible. All the fat just goes straight to storage.
Nutritional scientists have discovered this and actually use this methodology to fatten up rats. Researchers created an “obesogenic rat chow” made up of 14% protein, 45% fat and 40% carbohydrates.
Well, thanks to the USDA, our basic dietary recommendations are basically the same obesogenic rat chow.
The fat and sugar accumulate in your bloodstream, causing more futile insulin secretion. When your insulin levels are chronically elevated, this is called hyperinsulinemia.
Unsubstantiated evidence led experts to substitute saturated fats for poisonous carbohydrates. Now hundreds of millions of people around the globe are insulin resistant today.
Every time you eat carbohydrates — especially refined, high glycemic carbs — your body goes to war with itself. And you lose.
Ancel Keys’ Junk science has destroyed your health.
Hyperinsulinemia & Insulin Resistance Causes More Death Than WW1 and WW2 Combined
When you’re more insulin resistant, your body requires MORE insulin from your pancreas to push glucose and energy into cells.
High insulin may not cause all chronic disease. But at the very least it exacerbates them. Having persistently high fasting insulin levels is called hyperinsulinemia. It usually goes hand in hand with insulin resistance.
If you have insulin resistance, you’re at risk for chronic disease. There’s no chronic disease that’s not related to insulin resistance:
- Heart disease [*]
- 62% higher cancer mortality [*]
- 160% higher gastrointestinal cancer mortality [*]
- Prostate cancer [*]
- Alzheimer’s disease [*]
- Aging [*]
- Inflammation: Elevated CRP and IL-6
- Acne [*]
Think of chronic diseases like a tree. The fertilizers and starch, grain and sugars. And insulin resistance is one of the strongest roots.
Signs That You May Have Insulin Resistance
Below are some signs that you may have insulin resistance.
- Sugar & carbohydrate cravings
- Persistent belly fat
- Fatty liver disease
- Skin tags
- Trouble concentrating
- Elevated blood sugar
- Getting “hangry” when you don’t eat for 2 or 3 hours
- Anxiety & Moodiness: Insulin is master hormone controller and leads to a glucose roller coaster
- Gum disease [*]
- A waist larger than 35” for women or 40” for men
- A fasting insulin level above 5
8 Actionable Steps to Reverse Insulin Resistance
The opposite of insulin resistance is insulin sensitivity. You want your body to only release small amounts of insulin and for it to be very effective.
How can you become more insulin sensitive?
If you have insulin resistance, your body is at war with yourself. Your pancreas is willing to blow up everything to win. And your cells are extremely stubborn, have shut the door and are not giving up. They can’t give up because they’re full!
The loser of the battle: your health.
You’re calling for the white flag. Below are some ways to reverse it and end this futile war.
1. Cut Out Highly Glycemic Carbs
Shocker: the best way to reduce high insulin levels is to stop eating the crap that raises it!
The amount of times I’ve seen someone with type 2 diabetes continue to eat carbohydrates is sickening. You’d think that this would be the obvious first step, but unfortunately it isn’t because it can open doctors to lawsuits.
According to diabetes Dr. Bernstein, MDs prescribe a high-carb diet to their diabetic patients just so that they don’t get sued.
Even though this leads to blindness & amputation, it prevents hypoglycemia, the 1 thing they can be sued for [*].
Carbohydrates are one of the main reasons why insulin exists. Most are highly insulinogenic. And they’re non essential (i.e. you don’t need ’em).
They’re providing nothing for you other than satisfying your carb addiction. If you’re insulin resistant you need to cut out carbs and fuel yourself from fat ASAP.
In this study, participants on Keto:
- Ate 30% fewer calories
- Lost 4 lbs in 14 days
- Decreased hemoglobin A1c levels from 7.3% to 6.8%
- And most importantly….improved insulin sensitivity by 75%
This is in just 14 days!
The Ketogenic diet will reduce your insulin needs. It also will increase your metabolic rate, which frees up your fat cells to burn energy like they’re supposed to.
Subjects of this study burned more energy just by having lower insulin levels. That’s the magic of reducing insulin.
Lastly, carbohydrates cause oxidative stress, which worsen insulin resistance and inflame your entire body [*].
If you want to optimize your health, cut out these inflammatory, unnecessary carbs.
2. Stop Eating Fructose
I know I rail out against carbs and glucose frequently. But somehow fructose is even worse. It’s like glucose’s evil twin.
Glucose and fructose metabolism are different. Almost every cell in the body can use glucose for energy. But only the liver can metabolize fructose.
Fructose is like a nuclear bomb headed straight for your liver every time you eat it. It is 20x more likely to cause fatty liver than glucose alone.
And fatty liver can lead directly to insulin resistance.
In this study, subjects were given 25% of their calories as kool-aid, sweetened with fructose or glucose for 8 weeks [*]. High school me would have been the first to sign up for this test….
It may seem like a lot, but actually this diet isn’t too different from an American’s diet today.
The fructose group was more insulin resistant and developed pre-diabetes after just 8 weeks.
3. Cut Out Vegetable Antinutrients
Vegetables aren’t here for human survival. They don’t want to be eaten.
Turns out those “innocent and healthy” veggies are quite devious after all. To prevent predators from eating them, vegetables all have chemical weapons and booby traps set.
They’re all like Kevin McAllister in Home Alone. Innocent looking, but destructive. Don’t judge a book by its cover…
One of those groups of anti nutrients are lectins. They’re found primarily in grains, nuts, legumes and nightshades.
And they wreak absolute havoc on your body, especially in high doses. This study found that when lectins they reach the bloodstream, they can bind insulin receptors and thereby interfere with insulin’s action [*]
Just one more reason to cut out vegetables and eat meat like we’re made to.
4. Cook With Saturated Fats Instead of Vegetable Oils
Removing vegetable oils is one of the most important things you can do for your health. Not only are they directly linked to cancer and Alzheimer’s, they also cause insulin resistance.
In this study, mice were placed on a high fat diet [*]. One group consumed olive oil and the other consumed vegetable oils.
The group of mice consuming vegetable oils developed insulin resistance.
Another study showed that vegetable oils damage the GLUT4 transporter, which ultimately reduces the efficacy of insulin [*]
Instead, cook with natural fats like beef tallow, butter and ghee.
5. Eat Protein and Highly Nutritious Meat
What are you supposed to eat now that I’ve attacked your sacred vegetables and carbohydrates?
The carnivore diet is the best way to reverse insulin resistance. Why? It maximizes nutrient density and cuts out all of the crap that causes insulin resistance in the first place.
To reverse insulin resistance and achieve optimal health, you need to center your diet around highly nutritious meat and animal products.
Animal products have the most nutrient density and in the context of a low carbohydrate diet, do not raise insulin.
Humans are carnivores. We’re made to eat meat. That’s why our body responds so well to it. And why we develop chronic disease when we avoid it in favor of all the nutritional sludge we’ve invented in the last 10k years.
This allows you to maximize nutrient intake, while minimizing energy. Remember, insulin resistance is an energy overload problem. So you want to give your cells a chance to expend energy, rather than take it in.
This study showed that patients on a high protein diet — 30% of their calories — completely reversed type 2 diabetes [*]. If this were a drug, doctors would be raving about it…
But it’s the only thing more magical. And that is red meat.
Protein also improves satiation and will reduce hunger. And protein tends to be correlated with low insulin foods.
Another study below showed that a high fat diet will reverse ALL coronary heart disease risk factors — including insulin — vs a low fat diet.
And if you want to eat the most nutrient dense animal food possible, you need to try beef liver.
6. Get Off Your Ass and Exercise
If you want to be healthy, you need to get off of your ass. You need to try to mimic your hunter gatherer ancestors as much as possible. But still continue to follow me on Twitter, even though they didn’t…
Unfortunately, most people today are sitting down and eating all day. Most people are cramped in a cubicle surrounded by snacks. You want to do the exact opposite. Move around as much as possible throughout the day.
And most importantly for insulin resistance, conduct high intensity exercise.
Other than consuming red meat, exercise is the fastest way to reduce insulin resistance. Just one single bout of high intensity training can increase insulin sensitivity 40% [*]
This study below showed that just 6 weeks of training, with one set of 8 exercises improved insulin sensitivity. You don’t need to go out and run a marathon.
Just lift heavy weights.
Steak + deadlifts are a magical combination.
Obesity is also highly correlated to insulin resistance, which rises linearly with BMI [*]. If you’re insulin resistant and obese, you need to cut your BMI.
Lastly, lean muscle mass is associated with better insulin sensitivity [*]. Lean muscle is like a glucose sink. It sucks up any and all glucose available in your blood stream.
7. Start Intermittent Fasting.
Dietary recommendations have destroyed your health by changing both
(1) what we eat and
(2) when we eat.
If you want to restore your health, you need to restore both to your evolutionary ways.
We’ve already covered what to eat. What about when to eat?
In the early to mid 1900s, most people only ate 3 meals a day. But in the late 1900s, people started to eat 6-7 times a day. Doctors recommended many small meals to “speed up your metabolism”.
Guess what? The only thing that’s speeding up is how fast you give money to big cpg and big pharma companies. And how fast you develop insulin resistance.
You can only get energy from two sources: Food or body fat. But you can’t get energy from both at the same time. When you’re getting energy from food, this is called the fed state. When you’re getting your energy from body fat, this is called the fasted state. Insulin regulates this process.
When you eat insulin levels increase, which signals to your cells to suck in energy from your bloodstream. And when you sleep, insulin falls, telling your body to use stored energy to run your vital organs. This is why you don’t die when you sleep.
But most people are eating all day, and not giving their body enough time to lower these insulin levels and burn body fat. In fact, it takes ~12 hours to lower insulin far enough to actually burn body fat. But instead, most people shut this natural process off by eating a high carb meal first thing in the morning.
“Breakfast is the most important meal of the day!”
This is the biggest load of bull shit….Almost worse than the advice to avoid saturated fats.
When you first wake up in the morning, your insulin levels are low and you’re just about to enter the fasted state.
The worst thing to do is to eat a big meal and change that. And what makes it even worse is that most people are eating dessert for breakfast…
No, they’re not eating a cake. But I’d consider something like cheerios with 33g of sugar dessert. This shuts off fat burning, spikes insulin as high as possible and drives all of that additional fat right into storage.
And we all know what comes after a big spike….an even bigger fall. 3 hours later you’re going to be HANGRY, starving for another meal.
Instead, start intermittent fasting. Leverage your 8 hours of sleep time fasting and skip breakfast. Eat in an 8 hour window and fast from dinner to lunch time.
Over time, you can work up to 18 to 24 hours of fasting. According to Ted Naiman, this is where the sweet spot is.
But after 12 hours, you’ll still get immense benefits.
There are also many other benefits of intermittent fasting you can look forward to, according to Ted Naiman.
(Check with your doctor before fasting. This is especially important if you’re on meds and are diabetic)
8. Get Sleep
Most people think insulin resistance is just a result of macro nutrient composition. But sleep plays a major role.
Researchers found that one single night of sleep deprivation decreased insulin sensitivity by 25% [*].
An additional study showed that just two nights of 4h of sleep reduced insulin response by 30% [*]
This is also in healthy individuals! No matter how healthy you eat, you can become insulin resistant if you’re not sleeping well.
What’s likely happening is that the beta cells in your pancreas become less responsive after you don’t sleep well [*]. They’re groggy, just like you are.
Make sure to get your shut eye.
Reversing insulin resistance is the most important thing you can do for your health. And frankly, it’s not even that hard.
Just 24hr of a fast makes insulin drop by half.
But instead, doctors tell patients to continue eating carbs throughout the day and pump themselves full of drugs.
Reverse this trend. The carnivore diet is the best way to reverse insulin resistance.
It has long been known that polycystic ovarian syndrome (PCOS) is driven largely by chronically elevated insulin (hyperinsulinemia). PCOS is the most common endocrine abnormality among reproductive age women, affecting as much as 10% of the population (1). But if insulin is primarily a “blood sugar hormone,” why would chronic hyperinsulinemia affect female fertility? Why would it contribute to irregular or absent menstrual periods, facial hair, acne, and other signs and symptoms of PCOS?
The answer is that insulin is not just a blood sugar hormone. In fact, insulin has such surprising and far-reaching effects throughout the whole body that lowering blood sugar might actually be one of the least notable things this hormone does.
In a past KetoDiet post exploring chronic hyperinsulinemia, I mentioned that high insulin plays a driving role in such diverse issues as hypertension, skin tags, gout, and migraines. A quick flip through a biochemistry or endocrinology textbook shows that hormones don’t exist in a vacuum. They interact with and influence each other in complex ways, with multiple control mechanisms and feedback loops, so that changing the levels of one inevitably causes changes in the levels of others, too.
If hyperinsulinemia produces multiple hormonal abnormalities in women leading to PCOS, might it also produce hormonal abnormalities in men? Is there a male equivalent to PCOS?
Insulin Isn’t the Enemy; Chronically High Insulin Is
Insulin has gotten a very negative reputation in the keto community. But by itself, insulin isn’t a bad thing. Insulin is an essential hormone that performs numerous critical functions.
Insulin is only a problem when there’s too much of it in the bloodstream too often. Just like water, or even oxygen, it’s possible to get too much of a good thing. Insulin isn’t the enemy. For example, if you want to put on healthy muscle mass, you need insulin. But you don’t need a flood of it circulating in your body all the time. Keeping it pulsatile—that is, rising now and then for short periods of time—is sufficient for this purpose. What we want to avoid are prolonged periods of sustained high insulin.
Association Versus Causation
In medical research, the phrase “associated with” is often used when researchers are wary of using the term “causes.” It’s not always straightforward to establish cause and effect between two things with absolute certainty, so when things tend to occur together, it’s more scientifically responsible to say those things are “associated,” rather than declaring that one or more of them causes the others. However, in the case of PCOS, researchers believe that chronic hyperinsulinemia is a causative factor:
“Hyperinsulinemia associated with insulin resistance has been causally linked to all features of the syndrome, such as hyperandrogenism, reproductive disorders, acne, hirsutism and metabolic disturbances.” (2)
In fact, this causal link between hyperinsulinemia and PCOS is so well-known and so powerful that metformin — which is best known as a diabetes drug — is among the frontline pharmaceutical interventions for PCOS. As we’ll see soon, metformin and other diabetes drugs are also now being used for certain men’s health issues for the same reason — these issues stem from chronically elevated insulin.
The signs and symptoms of PCOS are driven by the underlying hormonal disturbances, which, apart from elevated insulin, include increased adrenal androgen synthesis (higher levels of testosterone and/or DHEA), decreased sex hormone binding globulin, increased luteinizing hormone (LH), and decreased follicle stimulating hormone (FSH). All of these features have also been observed in men, leading researchers to believe that yes, there is indeed a male hormonal equivalent of PCOS, and it has interesting repercussions for men of all ages (3).
And while many women with PCOS are overweight or obese, as many as 50% of PCOS patients are not (4). So it stands to reason that men with the male equivalent of PCOS won’t all be overweight, nor will they be diabetic, as defined by high blood sugar level. In PCOS and the male equivalent — just as in so many other chronic conditions — high blood glucose isn’t the driving factor; it’s high insulin.
Let’s look at three men’s health issues that seem to be coming from chronic hyperinsulinemia:
- Androgenetic alopecia (a.k.a. “male pattern baldness”)
- Erectile dysfunction
- Benign prostate hypertrophy (enlargement of the prostate gland)
Male-Pattern Baldness: Does Insulin Affect Hair Loss in Men?
Why do so many men lose their hair? Is it solely genetic? If someone comes from a long line of men who lost their hair, are they destined to lose theirs, too? If so, what would the evolutionary advantage to this be?
After all, many genetic conditions that have persisted throughout the ages are believed to have conferred a survival advantage in the distant past. For example, the sickle-shaped red blood cells produced by the genes responsible for sickle cell anemia also offer some degree of protection against malaria, so it makes sense that even though there’s a drawback to these genes in the modern age, in the past, it offered a distinct advantage. If there is an evolutionary advantage to men losing their hair, it hasn’t been identified yet. What has been identified, however, is a role for chronic hyperinsulinemia in contributing to male pattern baldness.
At first glance, you might think of male balding as an aesthetic issue and not a health problem. And no one could blame you for thinking it’s solely about appearance, rather than an underlying health issue. But looking at the role of insulin here tells us that for men losing their hair, things are more than “skin deep.”
The role of chronically elevated insulin as a contributor to male pattern baldness seems especially pronounced in young men. In fact, some researchers believe that in some men, hair loss might be the only warning sign of hyperinsulinemia.
An analysis of hormonal profiles in young men with early-onset androgenetic alopecia (AGA) (5) showed that compared to men without alopecia, young men with the condition had higher fasting insulin, HOMA-IR (a measurement of insulin resistance), and triglycerides, with slightly higher BMI, and lower HDL. All of these indicate that the men with AGA were affected more strongly by insulin. The study authors wrote, “Early-onset AGA might represent a phenotypic sign of the male PCOS-equivalent.”
In a case-control study of young men (age 19-30) presenting with AGA and 32 controls (men without AGA), mean fasting insulin levels were only slightly higher in the men with AGA than in those without it. However, compared with the controls, the men with AGA had significantly higher mean levels of testosterone, DHEA-sulfate and luteinizing hormone, with decreased mean levels of FSH and SHBG — precisely some of the same observations seen in women with PCOS.
The study conclusion couldn’t have said it better: “Men with early AGA could be considered as male phenotypic equivalents of women with PCOS. They can be at risk of developing the same complications associated with PCOS, including obesity, metabolic syndrome, IR [insulin resistance], cardiovascular diseases, and infertility.”(6)
It seems early male pattern baldness is more of a metabolic issue than a cosmetic one. The conclusion could have been written differently, though, with the arrow of causality pointing in the other direction: rather than saying men with AGA are at greater risk for metabolic syndrome and IR, it might be more educational to say that men with insulin resistance and metabolic syndrome are at greater risk for early baldness.
But how does this work? Is the connection between insulin resistance and early onset AGA merely an “association,” or is there a plausible mechanism by which causation can be established?
According to a paper written (7) by well-known Paleo diet authority Loren Cordain, PhD, along with low-carb advocates Drs. Michael and Mary Dan Eades, authors of Protein Power:
“Male balding clearly has a genetic component. However, it is well established that male pattern balding also is an androgen-dependent trait that occurs from elevated androgenesis after puberty. Consequently, any environmental factor or factors that would elevate serum androgen levels would promote increased balding, particularly in genetically susceptible individuals. High-glycemic-load carbohydrates, by inducing hyperinsulinemia, along with a concomitant elevation of serum androgens and reduction in SHBG represent a likely environmental agent that may in part underlie the promotion of male vertex balding.”
So it seems there is a genetic component to male balding. Obviously, not all men with hyperinsulinemia lose their hair, and not all men who are balding are hyperinsulinemic. Among young men with a genetic propensity for alopecia, chronic hyperinsulinemia simply increases the chances that they’ll lose their hair, compared to men of the same age who also have this genetic propensity but who are not hyperinsulinemic. The oft-uttered phrase regarding modern non-communicable health issues seems apropos here: “Genetics loads the gun, but diet and lifestyle pull the trigger.”
Other researchers have proposed a mechanism more specific to hair follicles, themselves, rather than a downstream effect of altered androgen hormone levels. The contend that insulin resistance “plays a pathogenetic role in the miniaturization of hair follicles.”(8) They go on to say that hyperinsulinemia causes alterations in blood vessel function that result in adverse effects on local circulation affecting the hair follicles, leading to a shrinking of follicles and eventual hair loss.
Another case/control study comparing groups of young men with early-onset AGA (9) and unaffected controls showed that compared to the men without hair loss, the men with AGA had higher fasting glucose, insulin, HOMA-IR, triglycerides, and blood pressure, all of which are suggestive of chronic hyperinsulinemia (10).
Unfortunately, the two groups were not matched for weight. Waist circumference, body weight, and BMI were all higher in the men with alopecia. This might have confounded the findings in that the higher weights could have been a contributing factor, but it could just as easily be true that higher insulin in the affected men was driving the higher body weight and waist circumference. That is, higher insulin may have been responsible for the higher weight, larger waist circumference, and the alopecia.
In case you needed another bit of evidence that there’s at the very least a correlation between male pattern baldness and insulin resistance, another study found that HOMA-IR was significantly higher in cases of men with early onset AGA than in men without alopecia (11).
For a nice change of pace, the authors of this one recognized the important implications: they recommend that young men with AGA be screened for insulin resistance and cardiovascular disease, writing, “Epidemiological studies have associated androgenetic alopecia (AGA) with severe young-age coronary artery disease and hypertension, and linked it to insulin resistance.” Of course, it would be wiser to simply make fasting insulin a standard part of routine bloodwork, right along with fasting glucose, which would then provide the HOMA-IR as well.
Men shouldn’t have to wait until they lose their hair before they’re told they’re at risk for the very serious complications of metabolic syndrome — including cardiovascular disease.
As just discussed, researchers believe young men with early onset male pattern baldness are at increased risk for coronary artery disease and hypertension, and suggest they should be screened for cardiovascular disease (CVD). With this in mind, it’s crucial to note that erectile dysfunction (ED) doesn’t result from lack of sexual desire. It’s not a libido problem, it’s a cardiovascular problem. And cardiovascular problems are largely insulin problems. CVD is not driven by high cholesterol or dietary saturated fat! (12)
Chronically high insulin — even when blood glucose is normal — is very damaging to the blood vessels. When combined with high blood glucose levels, it’s the perfect storm. Damage to the microscopic blood vessels in the eyes and the kidneys leads to the retinopathy and nephropathy that are well known consequences of poorly managed type 2 diabetes. But it’s not just those tiny blood vessels that suffer. The larger ones — major arteries — take a beating, too. In fact, cardiovascular disease is the number one cause of death in people with type 2 diabetes (13).
Impaired circulation also affects blood flow to the male genitalia. In fact, physicians informed on the hyperinsulinemic basis of blood vessel disfunction posit that ED may be the first sign of insulin resistance and endothelial dysfunction (14). This is especially true among younger men, who would not otherwise be suspected of having poor cardiovascular health. Make no mistake: erectile dysfunction and cardiovascular disease are different manifestations of the same underlying pathology (15). ED can be considered an early warning indicator of CVD.
Additionally, insulin resistance has been shown to reduce the synthesis and release of a compound called nitric oxide. Nitric oxide is a “vasodilator” — it helps blood vessels dilate so they can accommodate increased blood flow. In the vessels that supply blood to the penis, no dilation and no increased blood flow means no erection.
A systematic review looking at the association between erectile dysfunction and cardiovascular disease concluded, “ED and CVD should be regarded as two different manifestations of the same systemic disorder.” (15) And signs point to that systemic disorder being chronic hyperinsulinemia.
For a young man with no other signs and symptoms of metabolic derangement, erectile dysfunction could be the canary in the coalmine — an early warning sign that something is awry long before severe cardiovascular disease or type 2 diabetes have developed. One study found that in men under 40, compared to men without ED, those with ED had significantly higher HOMA-IR and systolic blood pressure. The researchers wrote, “Subclinical endothelial dysfunction and insulin resistance may be the underlying pathogenesis of ED in young patients without well-known etiology.” (16) In other words, for young men dealing with ED that has no known cause, insulin resistance should be suspected.
If the man/men in your life experience ED that has no obvious cause (such as depression, chronic stress, or physical trauma), or you are a man experiencing unexplained ED, a fasting insulin test might be warranted.
The incidence of various cardiovascular risk factors in 283 young ED patients (ages 18-45, with ED history at least 6 months). Insulin resistance (IR) is the most prevalent risk factor for ED in this study population. (17)
Metformin for Erectile Dysfunction: Why a Diabetes Drug?
It’s noteworthy that metformin — mainly a diabetes drug — has been shown to improve erectile function among insulin resistant men with ED who are not diagnosed diabetics (18). Why would a diabetes drug have any influence on erectile function if there was no connection to insulin or blood glucose? In a randomized, double-blind trial, compared to placebo, metformin led to significant improvements in HOMA-IR and erectile function. These two things are not unrelated! Based on the research we’ve explored here, it makes sense that better insulin management leads to better erectile function.
Benign Prostate Hypertrophy/Hyperplasia (BPH)
BPH is likely another condition with a surprising foundation in chronic hyperinsulinemia, but most men and even their physicians are unaware of this connection. Men are told, “You’re just getting older. This is normal.” It may be common, but that doesn’t mean it’s normal.
Insulin is a growth-promoting hormone. It stimulates growth of adipose tissue (fat cells), muscle tissue, and even the aforementioned skin tags and ovarian cysts. Another tissue insulin promotes growth of is the prostate gland (19). This finding, which is well documented in the scientific literature, has not yet made its way to the offices of many primary care physicians.
This is unfortunate, because these doctors are the ones most likely to encounter men complaining of the associated signs and symptoms, which include frequent or urgent need to urinate, waking up during the night to urinate, pain or straining during urination, or inability to completely empty the bladder.
One study showed that among men with BPH, fasting insulin levels were positively correlated with annual increase in growth rate of the prostate gland: the higher the insulin, the faster the growth (20). Prostate growth was faster in men with type-2 diabetes, hypertension, and obesity, all signs of hyperinsulinemia. In another study that compared 90 BPH patients and 90 men without the condition, levels of insulin and two other hormones, IGF-1 and estradiol, were higher in the cases compared to the controls. (Insulin may upregulate an enzyme called aromatase, which converts testosterone to estrogen/estradiol.) The researchers found that insulin and the related hormonal imbalances predicted the prostate size in patients with BPH: the higher the insulin, the larger the prostate (22).
Diabetes Drugs for BPH
As shown for erectile dysfunction, metformin has a therapeutic role in BPH. In rats with prostate enlargement induced by hyperinsulinemia (which is telling in itself—they gave rats insulin for the express purpose of enlarging their prostates!), treatment with the diabetes drug pioglitazone reduced insulin levels and prostate weight (23).
In a study looking at cultured human prostate cells in vitro, metformin substantially inhibited the proliferation of human prostate epithelial cells (24). Since these were a rat study and an in vitrostudy, we can’t be sure the same effects would be seen in human males, but the findings can still provide some insights.
Again, the fact that drugs primarily used for diabetes are effective for things as seemingly unrelated as PCOS, erectile dysfunction, and BPH, suggests these three conditions share a common origin: chronic hyperinsulinemia.
Take Home Message
It’s time to realize that type 2 diabetes and obesity are merely the tip of a much bigger iceberg of modern health issues rooted in chronically high insulin. Maybe it’s even time for a new acronym: MIRS—male insulin resistance syndrome.
If you’re a man dealing with problems known or suspected to be driven by chronic hyperinsulinemia, consider adopting a ketogenic diet or low-carb diet to bring your insulin levels down. Considering the amazing keto-friendly food you can eat when you reduce your carb intake, getting healthy never tasted so good!
Intermittent fasting is another strategy that can help improve insulin levels, and regular exercise may also be beneficial (25).
Source: Article by Amy Berger, MS, CNS, NTP (https://ketodietapp.com/Blog/lchf/hyperinsulinemia-and-mens-health-is-there-a-male-equivalent-to-pcos)
Give your brain a break—eat smarter by lowering your consumption of the starchiest (and most prevalent!) carbs. Try eliminating bread, cereal, pasta, rice, etc. from your diet for one week and eating more natural fats from animal and fruit (e.g. olives, avocados, coconuts) sources and see how your headaches change.
More common than most other neurological disorders, migraine headaches affect roughly 18% of adults in the US. A study of middle-aged women found that insulin resistance is associated with a two-fold greater likelihood of regularly experiencing a migraine.
A separate study in men and women found that insulin levels were significantly higher in people who experience migraines compared with non-migraine controls.
The Diet/Migraine Connection
Despite its association with insulin resistance, very few researchers have sought to determine whether carbohydrate restriction is effective in the treatment of migraine headaches and the limited evidence that supports the role of ketogenic diets in migraine therapy is almost an afterthought.
For example, one study reports that two sisters, who, in an effort to lose weight, adopted a carbohydrate-restricted, high-fat diet. However, both sisters reported often suffering from severe migraines (5–7 per month, over 72 hours, often accompanied with vomiting) and, with adherence to the diet, the migraines resolved. However, the migraines returned when the diet was stopped.
Importantly, this diet-migraine connection occurred independently of weight loss, which by itself is known to help reduce migraine severity.
Furthermore, an interesting case study reported the experience of the wife of a physician who had experienced migraines since childhood. For reasons unrelated to her headaches, she began a high-fat, carbohydrate-controlled diet and noticed almost immediate resolution of her migraines.
Does this seem like new information? It must be. That’s why you’ve never heard it before, right? Remarkably, there are published reports from 1928 and another larger report from 1930 of improvements in migraine headaches with carb-restricted, high-fat diets!
Regardless of your strict adherence to a low-carb, high-fat diet, there still may be validity in scrutinizing carbohydrate consumption. People with insulin resistance who experience migraine headaches (remember—you may not know you’re insulin resistant) have a 75% improvement in migraine frequency and severity simply by restricting sugar in their diet.
Give your brain a break by managing your insulin. You’ll never know how much it may help you until you try.
Source: Article by Ben Bikman (https://www.insuliniq.com/insulin-resistance-and-migraine-headaches/)