This post is all about the question: does a sweet taste really cause an insulin release? What does the science say? I have some links at the end of this blog post that you can go to in order to draw your own conclusions. Please do, in fact. I will always believe that it is best to examine the science yourself rather than blindly believe what I say about it.
If this is the first you are hearing about this concept, and you aren’t sure why it matters, check out my blog post about the importance of a clean fast. It is locatedhere. Personally, I believe the key to long-term intermittent fasting success is the clean fast. I’ve experienced it both ways, and the difference is night and day.
The “sweet taste and insulin” debate is one of the biggest sticking points for many people, and there are people out there who ridicule the concept completely. I actually got a comment today on my coffee blog post from a guy who tried to prove to me that the science shows sucralose (Splenda) is actually fine during the fast, because it doesn’t raise insulin. He had a study (his study is linked here) that “proved it”. Well, I went to his link and read his study, and the sucralose was administered through something called “intragastric infusion.”
What does that mean? The sucralose was inserted DIRECTLY INTO THE STOMACH. That is what “intragastric infusion” means.
So, what did we learn from that study? If you would like to insert sucralose directly into your stomach through intragastric infusion, this study shows it’s absolutely fine to do that. Indeed, it does not appear that will cause you to secrete insulin.
The elephant in the room is that in real life, we are NOT inserting anything directly into our stomachs. We drink beverages through our mouths, and we taste them. In the insulin response theory, it’s the TASTE of the sweetness that is the problem. All of the studies that I link in my books and blog posts about insulin release relate to the sweet TASTE of something you ingest tricking the brain into thinking that you need insulin to handle whatever sweet thing you are consuming. According to the sweetness/insulin response theory, the body doesn’t understand that it’s actually a zero calorie sweet taste. The body is ready for the calories it associates with sweetness, hence the insulin release. Clearly, inserting something directly into the stomach bypasses the taste receptors, which is what the study about intragastric infusion illustrates.
This is such a confusing topic for many, and this is why: as with MANY topics, you can find studies (and resulting opinions) that contradict one another. That’s right! You can find studies that show there IS an insulin response to sweet tastes, and you can also find studies that show there is NOT an insulin response to sweet tastes! I could “prove” there is NOT an insulin response to you by referencing some studies that came to that conclusion, but I could also “prove” there IS an insulin response by selecting other studies that determined the opposite to be the case. This is called “cherry picking” data: only looking at information that agrees with what you believe to be true, and ignoring any that don’t match what you believe.
So, what do we do when faced with contradictory information? Of course, I personally want to err on the side of caution. If there is a possibility something is going to cause me to release insulin during the fast, I am going to avoid it. Trust me. NO ONE wanted to have Stevia during the fast more than I did. I searched and searched for a rationale that would allow me to keep it in my coffee. Once I decided to eliminate it, it changed the way I experienced intermittent fasting and made the process truly effortless.
Here are some links if you want to dig in for yourself. Note: “CPIR” stands for “Cephalic Phase Insulin Response”.
1. This one, from 2008, was performed on humans (not rats), and it is the one that finally convinced me to drop the stevia: https://www.ncbi.nlm.nih.gov/pubmed/18556090 *Key takeaway: “A significant increase of plasma insulin concentration was apparent after stimulation with sucrose and saccharin. In conclusion, the current data suggest that the sweeteners sucrose and saccharin activate a CPIR even when applied to the oral cavity only.” Even if I read ten studies that had a different outcome, this one would make me stay away from anything sweet during the fast. Better safe than sorry.
2. https://www.ncbi.nlm.nih.gov/pubmed/17510492 *This is a rat study, but it is fascinating because: “The non-nutritive sweetener saccharine elicited CPIR. However, starch, which is nutritive but non-sweet, did not elicit CPIR although rats showed a strong preference for starch which is a source of glucose. In addition, we studied whether CPIR was related to taste receptor cell activity. We carried out the experiment in rats with bilaterally cut chorda tympani nerves, one of the gustatory nerves. After sectioning, CPIR was not observed for sweet stimulation. From these results, we conclude that sweetness information conducted by this taste nerve provides essential information for eliciting CPIR.” What that means is that when the scientists cut the nerves from the tongue to the brain, and the rats could not TASTE the sweetness, there was no insulin release. It was related to the taste only.
3. https://www.ncbi.nlm.nih.gov/pubmed/28899680 *Key takeaway: “The results indicate the presence of a significant CPIR in a subset of individuals with overweight or obesity after oral exposure to sucralose, especially when present in solid food form.” Don’t miss this important conclusion: while the beverage form had a smaller insulin spike than the food form, there still was an insulin response to the sweet beverage.
4. https://www.ncbi.nlm.nih.gov/pubmed/8246776 *Key takeaway: “obese subjects exhibited significantly greater CPIR than normal-weight subjects.” This implies that when you are overweight, your body has MORE of an insulin response than someone of normal weight.
5. https://www.ncbi.nlm.nih.gov/pubmed/3289998 *Another rat study. Key takeaway: “We conclude that saccharin (through taste) appears to elicit parasympathetic (insulin release) and sympathetic (HGP increase) reflexes in lean and obese rats. These taste-induced changes in plasma insulin and glucose turnover are exaggerated in the obese rats and may participate in obesity and in insulin resistance of the overall syndrome.” Again, the obese animals had a HIGHER insulin response than the lean ones.
Those last 2 studies imply that if you are overweight, you need to be even more careful than others about what you ingest during your fast. I think that is important to understand.
In conclusion: you are an adult, and you are making your own decisions here. I will continue to believe that if you are looking for the best possible results from an intermittent fasting lifestyle, you want to avoid all sweet tastes during the fast. Yes, I cherry-picked the studies that support my conclusion and I didn’t link to any that imply that the sweet tastes are a-okay. But, if you want to err on the side of caution, that is what you would do.
Not everyone is going to agree with my conclusions, and I’m okay with that. Remember, there are groups of people who still believe the earth is flat, and that scientists are lying to us with the whole “earth is round” nonsense. Boy, do I wish I was kidding. https://www.livescience.com/24310-flat-earth-belief.html If we can’t come to 100% consensus on the shape of the earth, then I’m pretty sure the complex issue “does a sweet taste cause an insulin response” is never going to be “settled” for everyone. (Spoiler alert: I do believe the earth is round. Thank goodness.)
And for everyone who remains unconvinced about sweet tastes and insulin: I would like to issue a challenge to you. Fast clean for at least two weeks, with nothing but black coffee and unflavored/unsweetened still and sparkling water. Then, reintroduce whatever it is that you believe is not a problem. Pay attention to how you feel. I’ll be very surprised if you don’t notice that the fast is notably easier when you fast clean. That’s what most people discover, and it is what I found personally. Try it and see! What do you have to lose?
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:
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/)
At any given moment, your body is either burning fat or storing it. Which of the two states you are in, depends on the hormones, insulin, and glucagon.
Energy metabolism is principally managed by the actions of two very important hormones, called insulin and glucagon. Insulin is the main storage hormone, the one that stimulates fat to accumulate in fat cells, whereas glucagon does the opposite, it makes stored energy available for use.
How do these hormones manage the processes of weight loss and weight gain? How do they impact on appetite control? More importantly, how can you manage your appetite and weight, by managing your metabolic hormones?
When is insulin released?
Insulin is a hormone secreted by the pancreas in response to glucose. All carbohydrates in the diet, like starches and sugars, are eventually converted to glucose. Different types of carbohydrates affect the amount of insulin that is released by the pancreas, following a meal or a snack.
Protein also stimulates insulin release, but how much insulin is released by protein, largely depends on the other components of the meal. The more carbohydrate there is in the meal, the more protein will contribute to increasing the insulin response to the meal. If carbohydrate is limited in a meal, then protein appears not to illicit a significant insulin response.
Fat in the diet does not stimulate insulin release, and the combination of fat and protein in a meal also does not appear to have a significant impact on blood concentrations of insulin when compared to carbohydrate, with or without the presence of protein.
Dr. Benjamin Bikman has a PhD in Bioenergetics and in this video he does a wonderful job at explaining why we should have a healthy respect for insulin. It is fairly technical, but it is well worth anyone’s time.
The work of insulin: Storage mode
When the insulin in your blood is raised, your body is saving up the energy for later, and this is a very normal process. The two main processes are called glycogenesis (glycogen storage, the way glucose is stored in muscle and liver cells) and lipogenesis (fat storage).
Think of insulin is the “master anabolic hormone”. When insulin is released, it stimulates uptake of glucose into liver, muscle and fat cells, where the glucose is converted to glycogen or to fat. Insulin places your body in storage mode. It also stimulates muscle growth, which is why it is a hormone often stimulated (and abused) by body builders.
Insulin also suppresses a the circulating concentrations of the hormone glucagon, which does the opposite of insulin. Insulin stops all fat burning and processes, and tells the body to utilise or store the incoming energy from the diet.
Insulin has other important functions too, like stimulating the release of leptin, the main satiety hormone. Leptin is produced and secreted by fat cells in the body. When everything works normally with your carbohydrate metabolism, you will have a meal, the meal will raise your insulin, the body will use what it can immediately and store the rest of the energy for later. It will signal your hypothalamus with leptin, that you have eaten and that your are no longer hungry. You may read more on the technical details in this academic publication.
When is glucagon released?
Following a meal, the energy that was immediately available has either been used directly by muscle cells, or stored successfully for later use. Following the storage phase, as the body requires energy for regular maintenance or physical activity, the concentration of insulin decreases and the concentration of glucagon starts to increase. Insulin has already done its job, made sure that the energy has been stored in all the right places, if you are healthy.
As the concentration of insulin decreases after a meal, glucagon starts increasing more and more, as your body progresses towards a fasted state. This is your body’s natural mechanism to make sure that it has enough energy available for normal metabolism or during exercise.
The work of glucagon: Freeing up stored energy
Glucagon does the opposite of insulin. It signals the liver, muscle and fat cells to utilise the stored glycogen and fat for energy. The body can only store a limited amount of glycogen (glucose), but it can store unlimited amounts of fat.
At rest, the muscle cells consume the majority of the available energy and it prefers fat as its primary fuel and it also uses a lot of fat when we do endurance exercise. The ratio between how much fat we use during endurance training and how much carbohydrate, is determined by your medium term dietary profile.
As the insulin levels continue to normalise to fasting levels, the glucagon levels will continue to rise to their fasting levels, or higher if physical activity demands it.
The hormonal similarities between fasting and exercise
During exercise the body requires stored energy to be released in order to meet the energy demand of the physical activity. During exercise, glucagon continues to liberate stored energy for utilisation and insulin remains low.
The same process occurs as you approach a fasted state after eating, albeit slower than when you are performing physical exercise. The hormonal processes are extremely similar.
The simple thing to remember here is that glucagon is the hormone that you need when you are trying to liberate stored energy. When you are trying to lose weight.
Your body spends most of the day relatively idle, and its preferred source of energy in this state, is fat. In order to utilise fat, you need glucagon to signal the body to make sure that there is fat available for energy.
Turning on glucagon, means turning off insulin
Glucagon is not controlled by us or our diets directly, but rather indirectly via the action of insulin. In order to increase glucagon, we need to limit insulin secretion. It is important to understand that these hormones exist in equilibrium. Their relative ratios change in response to eating, exercising or fasting, but neither ever disappears from circulation completely.
Insulin secretion is the primary signal to change the ratios between insulin and glucagon in the favour of insulin. Glucagon only rises again after insulin starts going down. Think about glucagon this way: “When the cat is gone the mouse comes out to play”.
The amount of insulin that is secreted, is a response to the amount- and type of food consumed. There are several ways by which we can shift the equilibrium of these two hormones in the favour of glucagon, more frequently and for longer periods of time, which is what we want for losing weight.
Reduce the frequency of insulin secretion (that is why intermittent fasting has become such a popular and effective method for weight control), reduce snacking during the day, etc.
Reduce the extent of insulin secretion after a meal — This is achieved by selecting meals and food combinations that will limit the amount of insulin that is secreted. The smaller the amount of insulin that is secreted, the quicker the body will get back to increasing the glucagon and start using stored energy.
That sounds simple! What’s the catch?
The problem for most of us is that if it were that simple to eat less, both in volume and frequency, we would not be having this problem.
I have explored the concept more extensively here, but the essence of it is that appetite is the result of your diet, a consequence, not an inherent feature of you, or your metabolism.
How much carbohydrate we can process safely, is different for every person. When we eat more carbohydrate than we can process safely, we dramatically shift the hormonal balance in favour of insulin.
If we do this too often and for too long, we reach a point that our muscle, liver, kidney and fat cells don’t respond to insulin quite the way they used to and our bodies respond by secreting more and more insulin, to deal with the increased glucose in our blood. Our bodies become resistant to the effect of insulin.
The insulin resistance snowball effect
When our bodies start becoming insulin resistant, we start to see a few things develop, gradually at first.
We eat more in order to satisfy our hunger — Insulin promotes the secretion of leptin, a hormone that tells the hypothalamus that we are satiated. As we become resistant to insulin, we become resistant to the effect of leptin and our hypothalamus is no longer the receiving the signal for satiety as clearly as it used to. We tend to need to eat more carbohydrates to generate the “full” signal. The fat cells are the ones responsible for making leptin, and as the insulin resistance increases, the leptin secretion increases, but the hypothalamus is not listening, so we keep increasing the leptin to get ourselves to stop eating. Meanwhile, the fat cells are still receiving the “storage” signal, loud and clear!
We get hungry more frequently— As we need more and more insulin to get our blood glucose under control, the high insulin levels cause the blood sugar to drop unexpectedly (called reactive hypoglycemia) and when this happens, our bodies go into a state of panic. The is when hunger anxiety strikes. We get hangry. We become irritable and the need to eat something feels urgent.
We gain weight — We find ourselves in storage mode all the time and the only reprieve we have from the storage mode, is when we go to the gym, or when we sleep. The persistent storage mode we enter into, coupled with the frequent blood sugar crashes that sends us running for our lunchboxes at 10:00AM, makes us lethargic, makes feel unmotivated and reduces the chances that we will even make it to the gym.
The first step to gaining control of your appetite is to recognise that you have to get your body to stop turning on the master storage hormone so frequently and so aggressively.
You can control your weight by controlling your appetite. You can control your appetite by controlling your insulin. When glucagon is elevated, it will suppress your appetite and as the body starts using its own fat for energy, you will start gaining real control of your appetite and your cravings.
You do not have to starve yourself
Eat when you are hungry. Don’t ever go hungry. But have a healthy respect for insulin. Remember these facts.
Dietary fat does not cause insulin to increase.
Protein + fat does not cause insulin to increase remarkably.
Carbohydrates cause insulin to increase.
Protein increases the magnitude of the insulin response when eaten alongside carbohydrate.
Carbohydrate + fat will put your appetite into overdrive by putting you into ultra storage mode. This is what junk food does to us.
The basics of appetite
It is extremely important to understand that feeling hungry is NOT equal to losing weight. When people think about losing weight, the very first thing they think about, the anxiety around how hungry they are going to feel.
You are losing weight when you aren’t hungry.
I will repeat.
You will lose weight when you aren’t hungry.
Think about it, next time you are in the gym. Before you start, you may be extremely hungry, but 10 minutes into your session, you start forgetting about food and you are focusing on your burning legs. During your last set, you are not thinking about food. Maybe you are tired, but you aren’t hungry. That is the feeling you should have when you haven’t eaten for several hours. Not the feeling that you get when it is 12:30PM and you have already had your lunch sandwiches at 10:00AM.
When you are in a healthy fasted state, you are not going to experience hunger in the same, a way that frightens you or makes you anxious. There is no point to being hungry. Later on when you gain control of your appetite, you will start to experience hunger completely differently and you will be able to delay eating. That is something else entirely. That is when people start telling you about it, like CrossFitters. How they haven’t eaten in 20 hours and aren’t hungry. They aren’t (only) rubbing your face in it, they are sincerely ecstatic about the fact their their appetites are no longer dominating their every routine.
What does that mean for your eating habits?
The easiest way to achieve reduced insulin levels, is a low carbohydrate, high fat diet. It takes care of all the details.
Avoid carbohydrates and sugar. And not pretend-avoid for three days out of the week. You will have to make a real effort. This is where you need to be disciplined. There are several resources out there to help with a journey of that sort.
If you want control of your appetite, take control of your insulin, by taking control of your carbohydrate consumption.
Accept it, you cannot have your cake and keto too.
Source: Article by Philip Marais (https://medium.com/@finmn/cannot-have-your-cake-and-keto-too-60c4e50d51dc)
Here’s a startling truth. I can make you fat. Actually, I can make anybody fat. How? I simply prescribe insulin injections. Giving people extra insulin inevitably leads to weight gain. In type 1 diabetes, when insulin levels are extremely low, patients lose weight no matter how many calories they eat. Give insulin – gain weight. No insulin – lose weight (even to the point of death). The implication is clear. Insulin causes weight gain. Knowing this is crucial, because if insulin causes weight gain, then losing weight depends upon lowering insulin. But instead, we’ve been told to focus obsessively on calories.
The standard (failed) weight loss advice is to restrict a few calories every day by reducing dietary fat and eating multiple times per day. This does not lower insulin much since dietary fat has little insulin effect and eating frequently constantly stimulates insulin secretion. This ‘caloric reduction as primary’ advice has an estimated failure rate of 99.5%. So, if you have tried calorie restriction to lose weight and failed, understand this. You were expected to fail.
If you have tried calorie restriction to lose weight and failed, understand this. You were expected to fail.
So here’s the situation. ‘The Man’ tells you that obesity is a caloric balance and that you should eat less and move more. ‘The Man’ tells you to eat a low-fat diet, and to eat 10 times a day. This advice fails virtually everybody. When you fail, ‘The Man’ tells you it’s your own damned fault for being such a lazy-assed, floppy-willed person. His advice was good, ‘The Man’ tells you. You were just a failure. That’s what ‘The Man’ wants you to believe.
Imagine, though we have a classroom of 100 pupils. One fails. It’s likely his fault. Maybe he played too many video games. But if 99 students fails, then it’s not a problem with the students. The problem is with the teacher. In obesity, the problem of rampant obesity means that it is very obviously not the fault of the people. The fault lies with the official dietary advice.
Understanding that obesity is a hormonal disorder, not a caloric imbalance (as discussed in our last post) means that we must instead focus on the insulin effect rather than the number of calories to successfully lose weight. Reducing insulin depends mostly upon 2 things:
What you eat
When you eat
We often think and talk about the first problem, but both are equally important in lowering insulin levels.
What to eat
The three different macronutrients stimulate insulin to different degrees. Carbohydrates, particularly refined carbohydrates raise insulin the most. Protein also raises insulin significantly, although blood glucose remains stable. Animal proteins stimulate more insulin release compared to plant proteins. Dietary fat raises neither glucose nor insulin.
Most natural foods contain varying combinations of the three macronutrients and therefore raise insulin to varying degrees. For example, refined carbohydrate-rich foods like cookies have the greatest effect on raising insulin and glucose. Fat-rich foods like salmon have little effect on insulin. This differing ability to stimulate insulin means that foods also differ in their fattening effect. This is only common sense. 100 calories of cookies, is far more fattening than 100 calories of salmon, despite what all the obesity ‘experts’ claim.
100 calories of cookies, is far more fattening than 100 calories of salmon, despite what all the obesity ‘experts’ claim.
The overlap between calories and insulin effect is what causes the confusion between the hormonal (insulin) hypothesis of obesity and the caloric hypothesis of obesity. Many people say that ‘A calorie is a calorie’, which is, of course, true. But that’s not the question I asked. The question is ‘Are all calories equally fattening’? To which the answer is an emphatic no. Insulin-stimulating foods like glucose are more fattening than non-insulin stimulating foods like kale, even if you have the same number of calories.
Certain factors increase insulin which encourages weight gain. The most important factors raising insulin are refined carbohydrates, animal proteins, and insulin resistance. Fructose, from added sugar and fruits can directly cause fatty liver and insulin resistance. This leads the body to increase insulin secretion to compensate.
Other factors decrease insulin, protecting against weight gain. Acids found in fermented foods (sauerkraut, kimchee) and vinegar lowers the insulin effect of foods. Animal protein causes secretion of incretin hormones that slows absorption of foods thus lowering insulin. Thus meat has both pro- and anti- insulin effects. Fibre also has this same effect of slowing absorption and insulin effect.
Thus, the main principles for lowering insulin and losing weight would include the following, as detailed in The Obesity Code.
Rules for ‘What to Eat’
Avoid added sugar – causes insulin resistance and high insulin
Eat less refined grains – High insulin effect
Moderate protein – excessive consumption can be fattening
Don’t be afraid of eating natural fats – Low insulin effect
Eat real unprocessed foods – refining increases insulin effects
Funny. That’s precisely the sort of no-nonsense advice your grandmother would have given.
When to eat
The second and equally important part of lowering insulin is understanding the question of ‘when to eat’. All foods can raise insulin, which leads to obesity. But there is another important contributor to high insulin levels outside of food – insulin resistance. This refers to the situation where normal insulin levels are unable to force the blood glucose into the cells. In response, the body raises insulin in a knee-jerk reaction to ‘overcome’ this resistance, and these high levels will drive obesity. But how did insulin resistance develop in the first place?
Our body follows the biologic principle of homeostasis. If exposed to any prolonged stimulus, the body quickly develops resistance. A baby can sleep soundly in a crowded restaurant because the noise is constant, and the baby has become noise ‘resistant’. But that same baby, in a quiet house, will wake instantly at the slightest creak of the floorboards. Since it has been quite, the baby has no ‘resistance’ against noises and thus awakens quickly.
If you listen to loud music constantly, you will become slightly deaf. This ‘resistance’ to loud noises protects the ear from damage. Raising the volume to ‘overcome’ this resistance works but only temporarily. Volume increases and you become progressively more deaf (resistant to loud noise), which leads you to raise the volume again. The solution is not to keep raising the volume, but to shut it off.
Think about the story of the boy who cries wolf. Raising the alarm constantly may work at first but eventually leads to the villagers becoming resistant to the signal. The more the boy cries, the less effect it has. The solution is to stop crying wolf.
Insulin resistance is simply a reaction to too much insulin. The body compensates by raising insulin, but that only makes things worse because higher insulin levels lead to more resistance. This is a vicious cycle.
High insulin leads to insulin resistance.
Insulin resistance leads to higher insulin.
The end result is higher and higher insulin levels, which then drives weight gain and obesity. Therefore, a high insulin level depends on 2 things.
High insulin levels
Persistence of those high levels
Providing extended periods of low insulin levels can prevent the development of insulin resistance. How to provide those low levels? A daily period of fasting.
This may sound strange, but this is the way we used to eat. Suppose you eat breakfast at 8 am and dinner at 6 pm. You eat for 10 hours of the day and fast for 14 hours. This happens every single day, and the reason we use the word ‘break-fast’. This is the meal that breaks our fast implying that fasting is simply a part of everyday life. The body spends roughly equal portions of every day in the fed (insulin high, storing fat) and the fasted state (insulin low, burning fat). Because of this nice balance, weight tends to stay stable over time. Up until the 1980s, this was pretty standard practice and obesity was not a big issue.
Somehow, we moved away from this traditional way of eating and now eat constantly. We are hounded to eat something the minute we get out of bed in the morning whether we are hungry or not, believing that eating white bread and jam is better than eating nothing at all. We are pestered to eat throughout the day and not stop until it is time for bed. Large surveys show that most Americans eat 6-10 times per day. Now our body spends the majority of time in the fed state, and we wonder why we can’t lose weight.
Large surveys show that most Americans eat 6-10 times per day. Now our body spends the majority of time in the fed state, and we wonder why we can’t lose weight.
Eating constantly does not provide the critical period of very low insulin to balance the high insulin periods. Persistently high insulin leads to insulin resistance, which leads only to higher insulin. This is the vicious cycle of weight gain that we must break with fasting.
For the boy who cried wolf, which is the better strategy? Stop crying wolf for a month, and then cry loudly once, or cry wolf constantly, but a little more softly? Similarly, to start burning body fat, you must allow prolonged periods of time of low insulin.
Rules for ‘When to Eat’
Don’t eat all the time (time-restricted eating or intermittent fasting). Stop snacking.
If you want to lose more weight – increase the fasting periods
We often obsess about the foods we should or should not eat, the question of ‘what to eat’. But we often ignore the equally important question of ‘when to eat’. By attacking the insulin problem on both fronts, we have a far higher chance of successfully losing weight.
Source: Article by Dr. Jason Fung (https://www.dietdoctor.com/what-and-when-to-eat-to-reduce-insulin)