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.
Sugar, vegetable oils, and grains — in my more than 20 years of experience, I have never seen a type 2 diabetic patient that didn’t have this unholy trifecta.
The root cause of the obesity, prediabetes, and type 2 diabetes epidemic is this combination of acellular carbohydrates, industrial seed oils, and refined carbohydrates.
When every species gets the same disease, is it an epidemic or a pandemic? Reversing the obesity, prediabetes, and type 2 diabetes epidemic is today’s most important public health challenge.
Every single species exposed to the standard American diet becomes overweight, pre-diabetic, or diabetic type 2. It takes a conscious effort to prevent and reverse this. Something in our nutritional intake is defeating our normal regulatory mechanisms.
Less than 12.2% of the population is metabolically healthy. If any other disease or impending catastrophe were going to injure nearly 88% of the US population, I guarantee that someone would have declared a true national emergency.
Our dietary intake will bankrupt the healthcare system.
People wonder what weight has to do with experiencing pain and its treatment. I am an interventional pain physician, and sometimes I get the question, “Why are you so worried about a patient’s metabolic function? Why worry about their weight? Just treat the pain.”
However, almost all of the patients in our clinics are overweight, and when we evaluate their biochemical markers, they have prediabetes and metabolic inflammation. Even the ones who aren’t overweight have elevated GGT and evidence of fatty liver and insulin resistance. Clinical studies in Europe have found that “increased risk of adverse cardiovascular outcomes associated with type 2 diabetes does not begin at the diagnostic cutoff for plasma glucose (or HbA1c) at which the condition is diagnosed. Rather, there appears to be a continuum of increased microvascular and macrovascular risk that extends to levels of glycemia well below these cutoffs.”
Therefore, treating metabolic inflammation is treating the pain. and treating metabolic inflammation early, before the patient requires insulin, is the key to treating and managing chronic pain. The omega-6 pro-inflammatory pathway is the common link.
Hopper I, Billah B, Skiba M, Krum H. Prevention of diabetes and reduction in major cardiovascular events in studies of subjects with prediabetes: a meta-analysis of randomized controlled clinical trials. Eur J Cardiovasc Prev Rehabil. 2011;18:813–823.
For years, fat has been targeted as one of the main causes of obesity, but fat in someone’s diet isn’t what makes someone fat. The diet-heart hypothesis falsely attributed eating fat with the development of atherosclerotic heart disease. This anti-lipid agenda led to the low-fat craze, which replaced fat with tasty acellular carbohydrates, paradoxically resulting in a dramatic rise in the obesity rate and a worsening of heart disease, obesity, and diabetes.
Reducing fat intake is not the key to reducing obesity. Re-examining macronutrients in the diet as well as understanding satiety (feeling full) and controlling food intake is the key.
Replacing carbohydrates with avocado increased feelings of satiety, and this was caused primarily by PYY, a peptide hormone secreted by cells lining the ileum and the colon. PYY decreases food intake by inhibiting gut motility, acting as an “ileal brake” to cause a sense of satiety. According to the National Institutes of Health, “replacing carbohydrate with fats and fibers derived from avocados without increasing energy or energy-density enhanced the satiety value of meals in overweight and obese individuals as evidenced by greater hunger suppression.”
Conclusion:
Fat is a potent stimulator of PYY, enhancing satiety and reducing motivation to eat, keeping you full for 6-8 hours. By contrast, carbohydrates increase motivation to eat and don’t significantly increase PYY. Carbohydrates increase insulin, and in obese individuals cause reactive hypoglycemia, making them hungry in 2-3 hours.
That’s why people on whole natural food diets that are higher in fat tend to weigh less and have less heart disease and diabetes.
Lanjun Zhu, et al. Nutrients, 2019; 11 (5): 952
In the United States, we have a malnutrition crisis, but it’s not caused by people not having enough to eat. Just as assuredly people died of famine in the past, they now die of excess eating. It’s just not as compelling to put an 85-pound four-year-old in an advertisement for Save the Children.
This malnutrition from excess is a leading cause of poor health and spiraling health care spending and causes nearly 1,000 deaths each day in the United States from heart disease, stroke, or diabetes. The conservative estimates of direct and indirect costs of chronic diseases as a result of obesity were $1.72 trillion in 2016 — almost 10 percent of the nation’s GDP. Just as a comparison, total healthcare expenses were approximately $3.5 trillion or 17.6% of GDP; diseases of obesity are over half of the healthcare expenses.
Additionally, obesity is the greatest contributor to the burden of chronic diseases in the US, accounting for 47.1 percent of the total cost of chronic diseases nationwide.
JAMA. 2017;317(9):912-924. doi:10.1001/jama.2017.0947
https://www.milkeninstitute.org/publications/view/944
https://www.cms.gov/research-statistics-data-and-systems/statistics-trends-and reports/nationalhealthexpenddata/nhe-fact-sheet.html
The standard advice of dietitians and physicians to those who want to lose weight is simple: eat less, move more. However, this advice doesn’t actually produce favorable odds for losing and maintaining a healthy weight.
Using the standard calorie reduction approach recommended by the dietitians produces a probability of attaining a normal weight at 1 in 167. Following this standard advice of eating less, move more generates a greater than 99% failure rate, and explains why most people don’t get sustainable weight loss.
These odds are not in your favor. They favor obesity, prediabetes, and diabetes. These odds favor expensive and chronic medication management.
It’s time to follow a new path to health.
Fildes A et al. Probability of an Obese Person Attaining Normal Body Weight: Cohort Study Using Electronic Health Records. Am J Public Health. 2015;105: e54–e59.
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.
Research shows that patients in the prediabetic range need to be treated in order to prevent tissue damage. The HbA1c test has a significant tendency to miss cases of diabetes as compared to the oral glucose tolerance test (OGTT)
Patients should be treated in the prediabetic range because macrovascular tissue damage is occurring from HgBA1C of 5.7 to 6.5. Reversing diabetes while it is still prediabetes is safe, cost-effective, and disease-modifying.
Increased cardiovascular risk begins prior to the development of persistent hyperglycemia, due to insulin resistance (Stern, 1996; Haffner and D’Agostino,1999). Macrovascular damage has already occurred with the onset of insulin resistance, while microvascular damage increases with the onset of hyperglycemia. The United Kingdom Prospective Diabetes Study (UKPDS) analyzed more than 4,000 types 2 diabetes patients who were aggressively treated and followed for up to 15 years. Those in the intensely treated group had a significantly lower rate of progression of microvascular complications than did patients receiving standard care. Rates of macrovascular disease were only reduced in the metformin-monotherapy area, where the risk of myocardial infarction was significantly decreased.