It seems that the medical community is always focusing on glucose levels when perhaps more upstream thinking (root cause) should focus on insulin levels. We could perhaps prevent extensive damage to our bodies and avoid type II diabetes, obesity and a range of diseases if we took preventative measures to test for unusually high insulin, instead of the normal blood glucose levels all the time. After a meal, blood-glucose levels increase and our pancreas responds by secreting insulin.
In youth, there is a delicate balance where insulin drives glucose into cells mostly for energy production but also for fat storage if there is an over abundance of sugar available. Once blood-glucose levels drop to a fasting range, insulin production subsides.
With age, a sedentary lifestyle, and a diet featuring refined carbohydrates and simple sugars, our cells become insulin resistant, which allows blood-glucose levels to rise. There are a couple of factors that cause this resistence in scientific literature: 1)toxic fat (ceremides) accumulation 2) habituation (after continual stimulation of excess levels of Insulin, cellular sensitivity decreases and therefore it takes more insulin to get the same effect)
Rising glucose levels trigger the pancreas to release more insulin to counter the glucose—creating a vicious cycle. These factors promote weight gain and other metabolic disturbances.
As weight accumulates, fat cells pour out cytokines or inflammatory messengers, which generate inflammation throughout the body. It sets the stage for age-related diseases like atherosclerosis, hypertension, lipid abnormalities, type II diabetes, obesity, Alzheimers and cancer.
Since insulin is required to sustain life, the public mistakenly sees this hormone in a favorable light. Too much insulin not only contributes to weight gain, but to a multitude of diseases associated with obesity. Excess blood levels of the hormone insulin occur in response to poor dietary choices, lack of physical activity and normal aging.
The medical term that defines the pancreas over-secreting insulin is hyperinsulinemia.
Excess insulin remaining in the blood after a meal has been identified as a major cause of nonalcoholic fatty liver disease.
Hyperinsulinemia is an independent risk factor for kidney disease among metabolic syndrome patients. High insulin blood levels are predictive of type II diabetes and strongly associated with obesity. In a study on variables that are associated with Alzheimers, the number one association was with a particular gene called ApoE4. Number two was, drum roll please...high insulin levels. Number three was age. That is a shocker! That means you can get Alzheimers at any age with the wrong diet and lifestyle choices (over consumption of carbs and sugar).
Link Between Elevated Insulin and Cancer
A number of published studies indicate that high insulin levels drive the development and progression of many types of malignancies.
Human studies implicate high insulin levels in at least seven common cancers:
Colorectal cancer: 17% to 42% greater risk of precancerous adenomas; Breast cancer: 2- to 3-fold higher risk; Stomach cancer: 69% to 101% higher risk; Endometrial cancer: 45-fold greater risk for type I endometrial (uterine lining) cancer; Ovarian cancer; Prostate cancer: 2.55-fold risk of malignancies; and a 5.62-fold risk of locally advanced tumors; Liver cancer: 2.4-fold risk among those with both hepatitis B and high insulin levels.
Elevated insulin levels are associated with the development of more aggressive and metastatic cancers that carry a grim prognosis.
These alarming figures have inspired researchers to find out why there’s such a close connection between high insulin levels and cancer. And in just the past few years, researchers have uncovered mechanisms behind this deadly insulin/cancer connection.
Why Insulin Promotes Cancer
High levels of insulin trigger rapid cell division, while at the same time elevated blood sugar and fat levels provide metabolic fuel for tumor expansion.
In response to chronically elevated insulin/glucose some cells lose control of their DNA regulatory genes—which is the hallmark of malignancy. This sequence of events is believed to promote cancer, at least in colon cells and possibly in those throughout the body.
By its very nature, insulin is a growth factor, which means it naturally stimulates cell growth. The problem is that once a cancer cell has emerged, too much insulin results in overstimulation. This results in greater proliferation, migration, and invasiveness of cancer cells—all of the factors that make them so deadly.
These cancer-promoting effects of insulin were shown vividly when scientists injected colon cancer cells into mice and then fed them either a normal or high-calorie diet. The high-calorie-diet mice had elevated levels of insulin and other growth-promoting molecules. As a result, their tumors grew to twice the size of tumors in the normal-diet group—in just 17 days.
Another reason excess insulin promotes cancer is because it causes damaging oxidative stress. When researchers applied a small amount of insulin to cell cultures, enough oxidative stress was generated from just a single exposure to damage DNA strands. When they extended the exposure to six days, the amount of insulin required to induce similar damage was reduced by a factor of 10. This demonstrates how chronically elevated insulin rapidly escalates DNA damage.
Studies have also revealed a close relationship among body size, type II diabetes, and many cancers. A diet rich in readily digested sugars and carbohydrates, for example, has been shown to increase the risk of developing a common form of breast cancer (estrogen receptor-negative) by 36%-41%.
The connection between high insulin levels and cancer adds a strong rationale to suppress after-meal insulin and glucose surges or even better, eat low carb. Eating low carb means avoid flour products, eliminate sugar (use stevia or monk fruit as substitutes), and consume lots of less starchy vegetables.
What You Need to Know. In an article from Life Extension:
Block After-Meal Insulin and Glucose Surges
Modern medicine’s reliance on fasting plasma-glucose tests for yearly examinations means that lethally high after-meal insulin and glucose levels are often missed for years. By the time glucose abnormalities are caught, excess insulin has likely already caused immense damage. Fortunately, maqui-berry extract has been verified in human studies to delay glucose absorption—crushing after-meal insulin by up to 56% and glucose by 15%—and to lower HbA1c readings by 0.3% (from 5.65% to 5.35%). Additionally, human research demonstrates that a natural clove extract inhibits hepatic glucose release, reversing after-meal glucose within two hours.
Maqui-Berry Extract Slashes After-Meal Insulin and Glucose
Maqui-berry extracts have been shown to decrease after-meal rises in both glucose and insulin.
Research suggests that a proprietary extract of maqui berries contains potent compounds known as delphinidins.
Delphinidins stimulate a peptide that lowers after-meal blood glucose and can help moderate insulin spikes. The peptide stimulated by maqui-derived delphinidins is glucagon-like peptide-1 (GLP-1).
GLP-1 slows and delays stomach-emptying, so glucose from a meal reaches the absorptive tissue in the small intestine later, and in lower quantities, than it would otherwise.39,40
In a human trial, ten volunteers were enlisted whose fasting glucose levels were normal (under 100 mg/dL) but whose after-meal glucose levels, after a standard white rice meal, were between 100 mg/dL and 125 mg/dL (considered altered glucose tolerance).
Participants took either a placebo or 200 mg of maqui-berry extract 30 minutes before eating a small meal of 75 grams (about 2.5 ounces) of white rice, calculated to produce a rise in after-meal glucose levels.
The placebo group’s after-meal glucose levels peaked after one hour, at about 115 mg/dL.
By contrast, the after-meal glucose levels in the maqui-berry group had only risen to 98 mg/dL after one hour, a 15% difference. As an added benefit, their glucose levels did not peak for a full two hours after the meal. Even then, they reached a high of about 107 mg/dL.
The effect on insulin levels was more dramatic. After the meal, insulin concentrations in the placebo group rose steadily until they reached an average of 25.33 µIU/ml after one hour. In sharp contrast, the maqui-extract group’s insulin levels increased much more slowly, reaching an average of only 11.22 µIU/ml after an hour—a compelling 56% lower insulin level!
In fact, insulin levels in the maqui-extract group did not peak until a full hour and a half after the meal. Even then, it peaked at a much lower level than the placebo group.
Maqui-Berry Extract Reduces Long-Term Glucose Levels
A separate study showed that maqui-berry extract can impact chronically elevated glucose levels as well.
For the study, a group of newly identified prediabetic individuals took 180 mg of standardized maqui-berry extract every morning for 90 days. Follow-up tests occurred at 30, 60, and 90 days.
On follow-up testing days, researchers measured the participants’ hemoglobin A1c (HbA1c) blood levels. Unlike an after-meal glucose reading, which tells you what your glucose levels are at that moment in time, the HbA1c measures how high glucose has been over the past three to four months. The normal value for HbA1c is 5.6% or lower.
The researchers documented that maqui-berry extract reduced HbA1c levels by 0.3% (from 5.65% to 5.35%).
No serious adverse events were observed in either of these clinical trials.
Clove Extract Prevents Glucose Spikes
Clove extract is an excellent complement to maqui berry because of its impressive ability to control after-meal blood glucose.
In an exciting study, investigators found that a water-soluble extract of the clove flower bud (Syzygium aromaticum) reduced after-meal blood sugar.
Clove extract contains polyphenols that can regulate glycogen phosphorylase, the enzyme responsible for releasing glucose into the bloodstream that is stored in the liver and muscles in the form of glycogen.
This typically happens under stress or low nutrient availability, But with aging, too much stored glucose is often chronically released from liver stores.
Inhibiting glycogen phosphorylase with clove can help block excess glucose release into the bloodstream.
These benefits were seen when clove extract was given to diabetic mice, where it suppressed both blood-glucose elevations and HbA1c readings.
But would it reduce after-meal glucose spikes in humans as well?
To answer that question, scientists divided a group of healthy volunteers into two groups according to baseline glucose levels: one with normal glucose levels and one with high-glucose. All subjects received 250 mg of clove extract daily for 30 days.
Random blood-glucose levels were measured before supplementation, and again on days 12, 24, and 30. Additional blood draws were done two hours after a typical lunch.
For both groups, glucose readings fell significantly at day 12—and they continued to drop throughout the study until the after-meal glucose values were about the same level as the before-meal values!
The high-glucose group showed greater improvement, indicating greater benefit for this at-risk population. No one experienced abnormally low blood-glucose, making clove extract safer than hypoglycemic drugs that can trigger dangerously low readings.
Summary
With aging, a sedentary life, and ingestion of sugars and starch, after-meal insulin and glucose spikes can escalate to a chronic state of hyperinsulinemia, a risk for multiple age-related diseases including cancer.
Most individuals rely on a fasting blood glucose test from annual physical exams, but high after-meal insulin levels can be missed for many years.
When glucose abnormalities are finally detected, severe insulin-driven damage has likely already occurred.
Human studies have validated two plant extracts that can reverse this trend.
Maqui-berry extract has been shown to slash after-meal insulin up to 56%, glucose by 15%, and HbA1c by 0.3% (from 5.65% to 5.35%).
And clove extract reverses after-meal glucose surges within two hours.
Inasmuch as excess insulin and glucose levels promote disease and accelerate aging, these two plant extracts provide powerful support for a healthy longevity program.
Now lets think about this terms of low carb or Ketogenic diets.
As a byproduct of low carb or high fat diets that might drive you into a fat burning state called ketosis, you are getting very low insulin levels. So there are really two benefits at the same time, the inherent benefits of added ketones to your blood stream (I will do a whole separate blog on this) and lowered/stable insulin levels. But there is another hormone in play here and that is glucagon. Insulin suppresses glucagon so when insulin rises, glucagon lowers. Insulin is produced by the beta cells in the pancreas and glucagon is secreted by the alpha cells in the pancreas, and for some reason, no one ever talks about glucagon. Glucagon causes three things, fat lipolysis or destruction and use of energy stored in fat, gluconeogenisis or the creation of glucose use by some cells that can only burn sugar for fuel, like your red blood cells, and mitochondria creation (your energy factories). So, when you are low in sugar, insulin decreases and glucagon goes to work, decreasing your fat storage and spreading that energy around your system for use and creation of just enough glucose for the cells that must have it. Or said another way, according Dr Ben Bickman as interviewed on the Mike Mutzel show:
Our red blood cells need glucose. When we need gluconeogenesis, glucagon will be elevated. If you are low carb, exercising in a fasted state, or you are fasted, you need gluconeogenesis. Glucagon will be elevated and insulin, which inhibits gluconeogenesis, will be low. People may be confusing gluconeogenesis with an insulinogenic effect. If you are low carb, gluconeogenesis happens only as much as you need it. If you have ketogenesis happening, you have gluconeogenesis. Fat is used for fuel, and in parallel, we have the need for new essential glucose to be produced.
Glycogen is stored sugar in our muscle and liver tissue. Depleting glycogen is a necessary event before ketogenesis kicks in. True clinical hypoglycemia is remarkably uncommon. If you are insulin resistant, and your brain has been depending upon high glucose and has had no time to adapt to using ketones for fuel, glucose levels can get low. Your body senses this and panics, causing you to eat even more carbs and sugar, a nasty circle of high carbs, raising insulin levels chronically in your system and slowly destroying your body. In fact, there is more than enough glucose, you just have get through those low periods, avoid those sugar cravings by eating more good fats or protien instead of sugar. Eventually your body will adapt to low sugar and your cravings will disappear. To help you get into fat burning, you need to enter a fasted state for around 16 hours. There are two phases of hunger. The first phase is hunger from empty guts. It is passing. The second phase of hunger is when your body says that there is a genuine deficiency of energy and you want to eat anything and will do anything to get it. As long as you have sufficient salt and water consumption, you are good for exercise in a fasted state. If you have food in your gut, your body is conflicted about sending blood to your muscles or your guts. So it is better to exercise in a fasted state. Glucagon is catabolic of fat tissue only. There are not many glucagon receptors in muscle. If you are low carb or fasted and you need gluconeogenesis, there is no appreciable increase in insulin from the protein, yet a substantial increase in glucagon.
Just FYI, Acetyl-CoA is the branch point of all metabolic processes in the liver and most other cells. It can be used for creating new glucose, activating gluconeogenesis, create lipids through lipogenesis and it can be used to move sugar into the citrate cycle and be used for energy, creating ATP, or it can be used for ketogenesis. All of this is dependent upon insulin. Catecholamines and glucagon counter insulin, but insulin reigns supreme.
Earlier I mentioned that one of the reasons for insulin resistance was toxic fats or lipotoxicity. Consuming meat or saturated fat does not create lipotoxicity, nor insulin resistance.
In animal and human studies of saturated fat, fat was administered intravenously. Elsewhere it was tested against muscle tissue in the lab, which does not reflect the complex systems of the body, especially the influence of insulin. Both of these formats helped to form our mechanistic thinking of how saturated fat can cause insulin resistance. What we see in whole body function is that saturated fat that we eat is changed by the liver into non saturated fat components before it enters the blood stream, decreasing the harmful effects of consuming saturated fats. But I do think the science of the harmful effects of saturated fats still has a long way to go to help us understand the potential dangers of which saturated fats are bad for us because there are many versions of saturated fat out there.
It is easier to induce insulin mediated lipotoxicity with a vegan diet than a ketogenic diet due to the high carb content. We produce a certain amount of ceramides naturally and would not survive without them. But excess ceremides can cause insulin resistance. There are more ceramides in sedentary, obese, insulinemic individuals. They also have higher levels of circulating fatty acids. This is because the liver is making more fat or the adipocytes are becoming increasingly insulin resistant. Thus adipocytes are spilling lipid into the blood. The lipids switch from inert triglycerides to ceramides.
Alpha cells that produce glucagon become insulin resistant because of a ceramide accumulation. We have a microenvironment in the pancreas. Butted up against each other, you have an alpha cell that releases glucagon and a beta cell that releases insulin. Insulin from the beta cell tells the alpha cell not to make glucagon. Within this environment is a greater amount of insulin than in our circulatory system. This means that the alpha cell is getting hundreds, maybe thousands of times more insulin than other tissues.
In type 1 diabetes, where you are not making insulin in the microenvironment, too much glucagon is produced, elevating glucose. An insulin resistant person, who’s insulin levels have been climbing over the decades, but there is enough to keep glucose in check, remains clinically silent, meaning that they are below the radar in terms of showing signs of diabetes. Viewing diabetes as an insulin disease results in better treatment and earlier. But eventually, glucose levels rise and you are a type 2 diabetic. This could be when the alpha cells become insulin resistant. Insulin tells the alpha cell to make less glucagon, unless the alpha cell becomes insulin resistant and glucagon climbs. This signals the liver to start pumping out glucose.
Interestingly, both insulin and glucagon are high in type 2 diabetics. It should be one or the other. Weight gain results from insulin therapy for both type 1 and type 2 diabetics, even if caloric consumption remains the same. That is because insulin causes the body to store fat from sugar or glucose.
Glucagon also activates processes that are involved in mitochondrial biogenesis. This is a good thing. We all need as many functional mitochondria as possible to keep our energy levels high and our body working well.
Just as a reference point, if you are trying to get into ketosis, meaning converting to using fat for fuel instead of sugar for fuel, the definition of ketosis had been arbitrarily set at .5 mml. It is being considered to start at .3 mml due to the body’s efficiency shifts in fat adaptation. Once ketones are detectible from a low carb diet (and not exogenous ketones or MCT), metabolic pathways have been activated and insulin is low. You will be catabolic of your fat tissue.
Love to have your inputs on this very important subject and let me know what you thought about this post in your comments so I can continue to bring you worthwhile information..