Metabolic syndrome is an early indicator of diabetes even among people of normal weight, and it’s important to take steps to prevent and treat it. During the early phase of metabolic syndrome, the body is compensating for insulin resistance by increasing insulin production to maintain near-normal blood glucose levels. However, when the pancreas and liver overflow with fat from the chronic high insulin levels (the fat-storage hormone), there is a sudden change. Hyperinsulinemia can no longer keep up with the pace of insulin resistance, and the pancreatic beta cells, responsible for insulin production, are also unable to keep up. As this compensatory mechanism fails, the blood glucose rises quickly. It takes only two years or so before the beta cells begin to fail and full-blown type 2 diabetes is diagnosed.
The diagnosis of type 2 diabetes exists on a spectrum. It goes from healthy to metabolic syndrome (with or without obesity) to prediabetes to diabetes. Almost all individuals who are type 2 diabetic for a period of time and treated with insulin become obese due to the fat storage caused by insulin and remain so until they get a secondary complication. However, the metabolic syndrome that precedes the frank diagnosis of diabetes can exist even in normal-weight individuals. The key is preventing metabolic syndrome, whether caused purely by carbohydrate overconsumption or by vegetable oil omega-6 consumption because it will eventually lead to Type 2 Diabetes.
This protocol is relevant for patients who have metabolic syndrome with or without obesity, as they are both risk factors for type 2 diabetes.
Time-restricted feeding can reduce high insulin levels, which can reverse type 2 diabetes. It’s important to understand some facts about insulin and how it works.
First, insulin is fat storage and a growth hormone. It reduces circulating glucose by converting it to glycogen storage first, which then overflows to fat storage. Eating carbohydrates causes insulin release and thereby increases fat storage, especially in the liver. The more fat you store in the liver, the more insulin resistant you become, which can lead to prediabetes and increase the likelihood of becoming obese. Constant feeding (three meals and two snacks per day) keeps your insulin levels high and causes you to gain weight. You release insulin even if you eat artificial sugars, and the circulating glucose causes fat storage.
By contrast, time-restricted feeding reduces constant high insulin levels, permitting the liver to stop storing fat, and resensitizes the liver to insulin, which reverses fatty liver and reverses type 2 diabetes.
There are other things, but it’s literally that simple: The higher your insulin level and the longer the time period it is high for, the fatter you get. The more insulin resistant you get, the more fatty liver you get.
This is true whether you are producing your own insulin by eating all the time, or you are injecting insulin. Type 1 diabetics, who don’t produce any insulin, are thin until they start getting injectable insulin.
Nearly the worst advice we give to patients is “six small meals.” In reality, time-restricted feeding is the key to lowering insulin. Lowering insulin production immediately stops fat storage and decompresses the liver. The easiest way to do this is to eliminate one meal and at other meals eat food that is satiating, higher in fat and protein.
The nutritional and informational value of food is often ignored by conventional medicine, and ignoring it can lead to severe and expensive chronic diseases.
Unfortunately, most currently practicing physicians received less than 16 hours of education on nutrition during medical school. Often, dietary guidelines and recommendations were delegated to the dietitians. Unfortunately, the dietitians were heavily sponsored by Big Food, and the guidelines promote high frequency of feeding (six small meals), carbohydrate-oriented consumption (>150 g/D), grain orientation, and omega-6 industrial seed oils.
These guidelines don’t take into consideration the role of processed foods. Ignoring a lifetime of subsidized ultra-processed food leads to severe expensive chronic diseases.
Low-fat food doesn’t always mean healthy, and looking at fat negatively can actually lead to insulin resistance and weight gain. Demonizing fat because it has more calories per gram ignores the information transmitted in food to your body and encourages consumption of ultra-processed foods.
If it says “low-fat” and you think it’s healthy, think again. You have fallen prey to Big Food and Ancel Keys.
Focusing simply on calories in and calories out produce an inherent bias against high-fat food, which may actually protect against obesity and related diseases. The simplistic calorie focus results in dietary guidelines that support replacing fat with starch and sugar, which promotes insulin resistance.
Malhotra A, DiNicolantonio JJ, Capewell S. It is time to stop counting calories, and time instead to promote dietary changes that substantially and rapidly reduce cardiovascular morbidity and mortality. Open Heart 2015;2(1) doi: 10.1136/opener-2015-000273 [published Online First: Epub Date|.
Fructose and glucose are both sugars, but they are not the same. High-fructose corn syrup was invented in the 1970s and began to replace regular sugar around 1975. The obesity epidemic coincides with the use of HFCS, and vegetable oils and ultra-processed grain also increased in the mid-1970s. The per capita consumption of HFCS — the mainstay of soft drinks and other sweetened beverages — has increased from 38.2 pounds in 1980 to 868 pounds in 1998. In 1942, the annual U.S. production of soft drinks was 90 8-oz. servings per person; in 2000, it was 600 servings.
Like glucose, fructose is absorbed directly into your bloodstream from the small intestine. However, fructose is 20 times more likely to cause fatty liver (the key problem of insulin resistance) compared to glucose alone. In fructose feeding studies, replacing glucose with a calorically equal amount of fructose results in a documented 5x increase in de novo lipogenesis and increased liver fat by 38% within eight days. Fructose induces insulin resistance in less than eight weeks, even at typical consumption doses.
Fructose increases the hunger hormone ghrelin, which makes you feel less full after eating, increasing consumption. It also preferentially activates the reward pathways.
Glucose activates the cortex, the basal ganglia, certain other parts, but not the limbic system, and results in a sensation of serotonin-induced happiness. By contrast, fructose stimulates the limbic system and is associated with increased dopamine release in the nucleus acumens, similar to other addictive drugs (glucose does not stimulate the nucleus acumens). Fructose results in a sensation of dopamine-induced pleasure.
Ask yourself why soda companies would spike HFCS with extra fructose, at an additional cost.
Can anxiety and depression unexpectedly improve when treating insulin resistance with metformin? I am an interventional pain physician in the urban core. More than 90% of my patients with chronic unrelenting pain also have metabolic syndrome with insulin resistance, and more than 90% also have significant anxiety and depression. I had always assumed that the anxiety and depression were related to socioeconomic conditions or comorbidity of chronic pain — until I started aggressively treating their insulin resistance.
Undertreatment, I found that lifestyle modification and interventional techniques certainly improved their pain, but their anxiety seemed to persist. However, when I added metformin to treat insulin resistance and metabolic syndrome, the anxiety and depression seemed to immediately improve, unexpectedly. A recent mouse study sheds light on why this might be.
People with diabetes are known to have an increased risk for mood disorders such as depression and anxiety; the underlying mechanisms may be the neurotransmitter serotonin, or it may be an issue of gut-induced vagal signaling with reduced heart rate variability. Tryptophan is a necessary precursor for serotonin, and if tryptophan’s entry into the brain is reduced, it also reduces serotonin production. This mouse study demonstrated that metformin reduced the amino acids that impair the entry of tryptophan into the brain, increasing tryptophan entry and subsequently increasing serotonin. Additionally, metformin’s antidepressant-like effects were accompanied by improved neurotransmission in the hippocampus.
J Zemdegs, et al. The Journal of Neuroscience, 2019; 2904-18.
Satiety, or the feeling of feeling full, is the key to maintaining a healthy weight and living a healthy life long-term. Instead of calories, people should focus on eating real food. It’s easier to track not eating sugars and artificial sugars than actually counting their calories. Tracking and reliving the calories of carbohydrates you didn’t eat stimulates ghrelin, the hunger hormone.
It’s easier to track pounds of steak, fish, shrimp, and chicken than calories. A calorie is a calorie only if it is incinerated in a bomb calorimeter, and the heat is given off is measured. Biologically derived calories from different foods have entirely different metabolic effects on the human body.
It’s irrelevant how many calories a food portion contains because equal calorie portions of sugar, alcohol, meat or olive oil have widely differing effects on hormonal systems. These effects include insulin as well as satiety signals such as cholecystokinin or peptide YY. What matters is how our body responds to the ingestion and absorption of those calories, how they are metabolized, and the resulting level of satiety.
Our weight depends on a variety of factors, but one secret to a healthy weight is found in awareness of the role the hormone insulin plays in fat storage.
It is wrongly assumed that consuming excessive calories is the root cause of obesity. However, a calorie of food energy has different metabolic fates depending upon the hormonal stimulation. That same calorie may be used to generate body heat or stored as body fat. It can also act as a signaling molecule to trigger a secondary response. The gut microbiome then interacts with the consumed molecules first and creates its own signaling to the human host and affects metabolic pathways, increasing or decreasing nutrient availability.
Obesity is a disease of failed energy partitioning, not one of total energy intake, and one of the primary drivers of this partitioning is the hormone insulin. Insulin is specifically a fat storage growth hormone. The mere presence of insulin causes an immediate metabolic shift from using fat as a fuel source, to storing circulating glucose to glycogen for a total of about 500 grams. Once the initial glycogen stores are full, then glucose is converted to fat storage, a nearly unlimited storage capacity.
Insulin is specifically a fat storage growth hormone. The higher your insulin and the more often your insulin spikes determine your fat storage, not the number of calories you eat.
Metformin, an anti-diabetic drug, can protect the heart in pre-diabetic patients.
Even without a frank diagnosis of type 2 diabetes, normotensive or hypertensive patients with insulin resistance can develop left ventricular hypertrophy (LVH) and coronary artery disease (CAD). Insulin resistance (IR) is implicated in the development of LVH. Dysglycaemia is very common in patients with CAD and is linked to IR. Left ventricular hypertrophy is regarded as one of the strongest independent predictors of CV outcome, and LVH regression reduces future CV events irrespective of BP changes.
Metformin is an anti-diabetic drug and has been shown to safely improve insulin sensitivity and reduce IR. A recently published randomized clinical trial involving 68 patients who did not have diabetes, but had insulin resistance, received a 2000-mg daily dose of metformin or a placebo. In this 12-month trial, metformin reduced left ventricular mass. Metformin also reduced body weight, systolic blood pressure, and biomarkers for oxidative stress. The results suggest that metformin acts to reverse insulin resistance and is cardioprotective.
This study should be taken in the context that macrovascular damage to vessel walls accumulates in the pre-diabetic stage,so it is untenable to ignore patients with insulin resistance with the HgBa1C range of 5.6 to 6.5. Future evaluation with ultrasound carotid intimal wall thickness measurement and coronary calcium score would be fascinating.
We should strive to reverse diabetes before it becomes established, and certainly before patients develop LVH and progression of coronary calcification.
Individuals experience significantly different changes in blood glucose levels (as shown by using a continuous glucose monitor) after eating the same foods. Some patients with normal blood glucose levels experience after-meal glycemic spikes that are in the diabetic range.
A person’s gut microbiome more accurately predicts the individual spike in blood glucose after eating than just knowing a food’s calories or carbohydrates. Eran Segal and Eran Elinav from the Weizmann Institute of Science, Rehovot, Israel, developed an algorithm, described in the journal Cell, that used microbiome data as well as other factors, such as age, sex, height, hip circumference, and physical activity, to predict after-meal glycemic responses in people who did not have diabetes.
In essence, food labeling remains a mythical beast. It is the personalized dietary intervention that drives the individual insulin response.
DOI:https://doi.org/10.1016/j.cell.2015.11.001