Summary: Accumulation of amyloid-beta appears to play a central role in the development of Alzheimer’s. However, researchers have a limited understanding of the production of amyloid protein in brain cells. But new studies show that the production of amyloid-beta protein is increased in those with higher cholesterol synthesis by astrocytes (supporting cells in the brain) and its transportation with the help of apoE protein. It means that regulating the production and transportation of cholesterol by astrocytes may help prevent amyloid-beta overproduction and plaque formation. Thus, it could be a way to prevent Alzheimer’s or slow down its progress.

It could also mean that the accumulation of amyloid-beta could be a surrogate marker of disease, with accumulation due to localized inflammation and lack of clearance.

Keywords: amyloid-beta, brain, Alzheimer’s, astrocytes, cholesterol, apoE

Alzheimer’s is the leading cause of dementia in older adults. Despite numerous studies for more than 100 years, many things about this disease are poorly understood. Researchers know that in the disease, there is an increased accumulation of amyloid-beta and tau proteins.

However, researchers are not sure why this accumulation of amyloid and tau plaques occurs. They are unsure if the formation of these plaques is the leading cause of Alzheimer’s or formation of these plaques happens as a result of something else. Demystifying this puzzle may help find the treatment of the condition.

Researchers know that many metabolic disorders result from changes in lifestyle that occurred in the last century or so. They also know that it has led to the dysregulation of cholesterol metabolism, causing a higher prevalence of heart diseases and stroke. However, now a new study shows that cholesterol may play a role in Alzheimer’s, too.

Researchers have also studied the role of the most abundant cells in the brain: astrocytes. They almost tile the whole brain and are about five times more than neurons. They are needed for the working of brain cells neurons. They provide brain cells with vital support. Nonetheless, when we talk about the brain, we often forget about them, only considering neurons1.

It is known that the brain requires lots of cholesterol, as a considerable part of the brain is made of cholesterol. However, as people grow older, neurons start losing their ability to produce cholesterol. Thus, in adults, most of the cholesterol is produced by astrocytes. These brain cells then transport the cholesterol to neurons with the help of a protein called apolipoprotein E (apoE).

Early studies showed that those with apoE defects due to genetic reasons have a higher rate of Alzheimer’s. But researchers did not know why a defect in apoE, the transporter protein, increases the risk of Alzheimer’s2.

The researcher found that increased apoE resulted in increased cholesterol transportation to the neurons in the new finding. Cholesterol is needed by brain cells to produce amyloid protein. However, a high supply of cholesterol may also result in the overproduction of amyloid protein, resulting in the formation of amyloid plaques. It means that astrocytes and their greater supply of cholesterol to neurons may result in the formation and growth of amyloid plaques, thus causing Alzheimer’s.

Studies show that cholesterol levels are high in the brain of those living with Alzheimer’s. It means that suppression of cholesterol production by astrocytes may also help lower the production of amyloid protein. Further, it may be good to suppress apoE, the major transportation protein for cholesterol, to prevent amyloid plaque formation.

In the experimental study, researchers found that reducing the activity of transporter protein apoE resulted in less supply of cholesterol and thus lesser formation of amyloid plaques.

Thus, researchers think that astrocytes and their increased production and transportation of cholesterol to neurons may be causing amyloid-beta accumulation and Alzheimer’s. Tests in animal models show that suppressing the ability of astrocytes to produce cholesterol in the brain or reducing their ability to transport cholesterol may help prevent Alzheimer’s3.

Further, researchers think that reducing the overproduction of cholesterol may be the right way of preventing Alzheimer’s. Although amyloid-beta accumulation ultimately causes Alzheimer’s, suppressing its production is not an option. The brain tightly controls the production of amyloid protein due to its high importance in brain health. It means suppressive amyloid production directly may have unforeseeable results. Moreover, researchers do not have much understanding of how amyloid protein is produced in brain cells. It could also simply be that cholesterol over production is a reactive phenomenon due to underlying metabolic inflammation, and that the amyloid-beta protein tangles accumulate because the clearance mechanism is inhibited.

To conclude, controlling the production and transportation of cholesterol by astrocytes may be a key to preventing Alzheimer’s or slowing down its progress.

References

1. Sofroniew MV, Vinters HV. Astrocytes: biology and pathology. Acta Neuropathol. 2010;119(1):7-35. doi:10.1007/s00401-009-0619-8

2. Yamazaki Y, Painter MM, Bu G, Kanekiyo T. Apolipoprotein E as a Therapeutic Target in Alzheimer’s disease: A Review of Basic Research and Clinical Evidence. CNS Drugs. 2016;30(9):773-789. doi:10.1007/s40263-016-0361-4

3. Wang H, Kulas JA, Wang C, Holtzman DM, Ferris HA, Hansen SB. Regulation of beta-amyloid production in neurons by astrocyte-derived cholesterol. PNAS. 2021;118(33). doi:10.1073/pnas.2102191118

We have been looking at metabolic inflammation and its role in the development of obesity, diabetes and other chronic diseases. Does overnutrition contribute to metabolic inflammation? How?

1. Some background on overnutrition….

It is estimated that by 2020, two-thirds of the global burden of the disease will be due to chronic non-communicable diseases, most of which are associated with diet. While hunger is a tremendous global health concern that cannot be minimized, overnutrition should similarly be given concentrated attention. Malnutrition affects up-to 1 billion people. Even though undernutrition is the main cause of malnutrition, people who are overweight could also be malnourished.

The “double burden of malnutrition” is a term coined by the World Health Organization (WHO) to describe a situation which is characterized by “the coexistence of undernutrition along with overweight and obesity, or diet-related non-communicable diseases, within individuals, households and populations, and across the life course. Globally, the problem is not the availability of food resources, but the allocation and consumption of food.

1. What is overnutrition?

Overnutrition is defined as the overconsumption of nutrients and food to the point at which health is adversely affected. Overnutrition can develop into obesity, which increases the risk of serious health conditions, including cardiovascular disease, hypertension, cancer, and type-2 diabetes.

Until recently, overnutrition had been viewed as a problem that only affected developed nations. However, this has been reviewed to affect most populations. The prevalence of obesity is increasing in developing countries with the introduction of fast food and refined sugars.

While once considered the disease of the rich, low-income groups in richer countries are also being affected by this condition.

2. What is overnutrition induced inflammation?

Inflammation is a biological response launched by the immune system against dangerous assaults that threaten the integrity and normal physiology of an organism. Chronic nutrient overload causes an increase in adipose irregularities in that, if adipose tissue expandability is low, there will be an increased presence of thickened tissue. This condition would lead to a pro-inflammatory state that can trigger insulin resistance, the release of macrophage chemoattractant proteins, and in chronic inflammation, even the death of the thickened adipose tissue itself. This creates cyclic an action that extends the insulin resistance to all adipose tissue.

An important characteristic of overnutrition-induced diseases is chronic low-grade inflammation caused by nutritional excess. Overnutrition-induced inflammation is thought to occur in the brain and thus plays an extensive and steering role in overnutrition-induced diseases.

3. Overnutrition and the metabolic syndrome

The metabolic syndrome is a constellation of metabolic risk factors including high cholesterol, elevated blood pressure, insulin resistance, and elevated serum glucose, a pro-inflammatory state, and a prothrombotic state.

Most persons with metabolic syndrome are obese and usually have abdominal obesity. Generally, obesity is a reflection of overnutrition. A current view is that when adipose tissue fails to store all excess nutrients as triglyceride, lipid begins to accumulate in various tissues (eg, muscle, liver, pancreas, and heart). The foundation of the metabolic syndrome thus appears to be overnutrition, that is, more nutrient intake than can be safely disposed of by lipid oxidation.

When obesity is present, adipose tissue becomes inflamed. This inflammation may result in a pro-inflammatory state, which could contribute to both ASCVD and diabetes.

4. What is carbohydrate overnutrition?

Most evidence supports the concept that fatty acids represent the final common pathway to tissue nutrient overload. Less attention has been given to the possible negative effects of excessive intake of carbohydrates.

Chronic overstimulation of insulin secretion induced by dietary carbohydrates could have the following adverse effects:

• The β-cell function may be impaired by chronic glucotoxicity
• Carbohydrate-induced hyperinsulinemia may suppress muscle insulin sensitivity.

Furthermore, high-carbohydrate intakes can prompt lipogenesis in the liver; fatty acids produced in this way can feed into the final common pathway of ectopic lipid accumulation. There is thus a need to look further into the role of carbohydrate overnutrition in the development of the metabolic syndrome.

5. What factors Contribute to Overnutrition?

Obesity in the United States has reached startling heights. The National Center for Health Statistics at the Centers for Disease Control and Prevention (CDC) estimated that in 2015-2016, the prevalence of obesity in the United States was 39.8% in adults and 18.5% in youth.

While obvious factors including genetics, drugs, and other medical conditions may contribute to obesity, the behavior is perhaps the most common contributor. Healthy weight on an individual level is associated with a healthy diet and regular physical activity. Restaurants serve incredibly caloric meals, with some meals containing as much as 2,000 calories. The sedentary lifestyle practiced by most adds to the epidemic.

Unfortunately, this obesogenic culture has spread to other nations, including many developing countries. China, for example, now has more than 5,000 Kentucky Fried Chicken (KFC) restaurants in 1,100 cities. Similarly, McDonald’s expects to have 4,500 restaurants in China by 2022, up from 2,500 in 2017. A growing number of Chinese households also own television sets, personal vehicles, and other technologies that reduce physical activity and facilitate weight gain.

It is of note that economic inequality in developing nations is a primary cause of both overnutrition and undernutrition. Studies conducted in India show that income inequality had the same effect on the risk of being overweight as it did on the risk of being underweight; specifically, for each standard deviation increase in income inequality, the odds of being underweight increased by 19% and the odds of being obese increased by 21%.

While some people have the resources to purchase amounts of food beyond their daily caloric requirements, others cannot meet their recommended caloric intake. However, increasing numbers of poor people are becoming overweight in more nations, as these individuals consume affordably, yet highly caloric meals, such as fast food and processed foods.

6. What then should be done to avoid overnutrition?

An approach to understanding the effects of overnutrition on the metabolic profile is through overfeeding studies. These indicate that overnutrition produces a deterioration of metabolic status. Variability in individual response is, however, is expected. Such investigations are potentially useful for identifying those who are particularly susceptible to the development of metabolic risk factors.

The host of genetic factors likely acts at tissue levels to influence the response to nutrient excess. Different people may react differently to the accumulation of fat. However, overnutrition is generally considered to trigger metabolic disorders and predispose one to chronic conditions like Type 2 Diabetes. When choosing what to eat, one should be careful to ensure they choose balanced meals rich in fiber and nutrients and avoid the modern-day fast-food craze, as there cost of bad eating is too high.

References

1. Unite for Sight (2018): Module 4: Overnutrition. Retrieved from http://www.uniteforsight.org/hunger/module4
2. NCBI (2009): From chronic overnutrition to insulin resistance: the role of fat-storing capacity and inflammation. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19171470
3. NCBI(2013): Neuroinflammation in Overnutrition-induced Diseases. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4389772/
4. American Federation for Medical Research (2016): Overnutrition, ectopic lipid, and metabolic syndrome. Retrieved from https://jim.bmj.com/content/jim/64/6/1082.full.pdf 
5. NCBI (2009): From chronic overnutrition to insulin resistance: the role of fat-storing capacity and inflammation. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/19171470

Obesity has become rampant in recent times. It is said to affect almost 50% of the American population. It has been credited with being a leading cause of chronic illness and ill health. The carnivore diet has become very popular as the new way to lose weight, maintain a healthy lifestyle and ward off diseases. A major proponent of this diet is its ability to melt away the fat. How effective is it in the management of obesity? Do its effects last? In this article we will explore the role this diet can play in the curbing of obesity.

1. What is obesity?

Obesity is a complex disease involving an excessive amount of body fat. Obesity isn’t just a cosmetic concern. It is a medical problem that increases your risk of other diseases and health problems, such as heart disease, diabetes, high blood pressure and certain cancers. There are many reasons why some people have difficulty avoiding obesity. Usually, obesity results from a combination of inherited factors, combined with the environment and personal diet and exercise choices.

2. What is the Carnivore diet?

The Carnivore Diet is a restrictive diet that only includes meat, fish, and other animal foods like eggs and certain dairy products. It excludes all other foods, including fruits, vegetables, legumes, grains, nuts, and seeds. Its proponents also recommend eliminating or limiting dairy intake to foods that are low in lactose — a sugar found in milk and dairy products — such as butter and hard cheeses.

A good number of people who have adopted the carnivore diet report faster weight loss, improved mental clarity, healthier digestion, and even improved athletic performance. Some have also reported remarkable relief from debilitating chronic health problems where conventional means did not succeed.

1. What does one eat on the carnivore diet?

This is what you are likely to eat if you are on the carnivore diet:

–Below is the Green List that is, food you should be eating all the time with an emphasis on fattier cuts of meat to take in enough calories:

• Meat: beef, chicken, turkey, organ meats, lamb, pork, etc.
• Fish: salmon, mackerel, sardines, crab, lobster, tilapia, herring, etc.
• Other animal products: eggs, lard, bone marrow, bone broth, etc.
• Low-lactose dairy (in small amounts): heavy cream, hard cheese, butter, etc.
• Water

Generally, salt, pepper, and seasonings with no carbs are allowed.

– Below is the RED list of what you should NOT be eating:

• Vegetables: broccoli, cauliflower, potatoes, green beans, peppers, etc.

• Fruits: apples, berries, bananas, kiwi, oranges, etc.
• High-lactose dairy: milk, yogurt, soft cheese, etc.
• Legumes: beans, lentils, etc.
• Nuts and seeds: almonds, pumpkin seeds, sunflower seeds, pistachios, etc.
• Grains: rice, wheat, bread, quinoa, pasta, etc.
• Alcohol: beer, wine, liquor, etc.
• Sugars: table sugar, maple syrup, brown sugar, etc.
• Beverages other than water: soda, coffee, tea, fruit juice, etc.

While some people incorporate some of these foods, a true Carnivore Diet does not permit them:

• Milk
• Yogurt
• Cheese

Coffee and tea: These may be plant-based, but some people keep these in the diet.

The carnivore diet can be considered to be a fad. Is there evidence that any traditional populations practiced the carnivore culture?

3. What effect might the carnivore diet have on obesity?

When on a carnivore diet, all you consume is meat, meat and more meat…Occasionally you could have some eggs and cheese and maybe a cup of coffee. What about this diet at a glance could help in combating obesity?

How does the carnivore diet work?

1. Cutting out sugar and carbohydrates

The absence of sugar and carbohydrates cause rapid and sustained fat loss without the need to count calories. Carbohydrates are hard to store and actually harmful if left to circulate in your system too long, so your body always wants to use them up first.

Your body releases insulin to shuttle blood sugar into muscles. To make sure the sugar gets used up first, insulin also tells your fat cells to store any fat you consume and to not release stored body fat for hours afterwards. If you eat a lot of easily-absorbed carbohydrates, your body releases a ton of insulin in response. Excess insulin can then remove too much sugar from your blood stream, resulting in hypoglycemia. The quickest way to restore blood sugar levels is to eat more carbs, which puts people on the carb roller coaster to weight gain.

The carnivore does away with all this by totally eliminating sugar and carbohydrates from your diet.

2. Eating a lot of protein suppresses appetite

One way that protein controls appetite is through the amino acid phenylalanine. Consumed protein is broken down into amino acids so it can be absorbed by the body. Multiple studies have shown how phenylalanine suppresses appetite and even improves mood and helps you burn stored fat. One study found that phenylalanine increases the release of an intestinal hormone called cholecystokinin in humans. This hormone signals the brain to feel satiated after eating and causes a reduction in subsequent food intake. A mouse study found that a single dose of phenylalanine caused an increase in another satiety hormone called GLP-1, it reduced levels of the hunger-hormone ghrelin.

3. Increase in dopamine

Protein foods are made from the building blocks of amino acids (including tyrosine), which are essential to the production of dopamine. It has therefore been suggested that upping protein intake may also boost dopamine production without increasing appetite. Dopamine is considered the reward-hormone and increasing its levels in your brain is helpful for making your weight loss diet less unpleasant.

4. The carnivore diet “imposes” time restricted eating

The carnivore diet tends to make people naturally adopt time-restricted eating patterns. Studies show that eating at night is a common cause of obesity. Junk food actually causes you to prefer late-night eating. Sugar and fat together, act as a trigger that cements the unhealthy habit of late-night eating. Worse yet, your body runs on an internal clock called circadian rhythms. These do more than set your sleep and wake times; they also determine your digestion and energy usage times. We’re meant to eat during the day and sleep at night. When you eat at night, your body doesn’t want to process those calories and instead they sit and cause metabolic dysfunction.

Protein does not seem to trigger a desire for late-night eating so the carnivore diet also helps curb that unhealthy practice. Late-night eating also reduces the quality of your sleep and poor sleep leads to poor eating the next day. Reduced sleep also increases stress and anxiety, so removing late-night eating not only improves weight loss, but helps your mood and overall feeling of well-being.

5. Does the carnivore diet stave off obesity?

There is a link between the Carnivore diet and sustained weight loss. In the absence of carbohydrates, fat can be kept off for long periods of time. The question becomes how safe it is to do the carnivore diet long term. More studies on this need to be carried out but in the meantime, this diet is one of the best in keeping obesity, and its associated diseases at bay.

References

1. Mayo Clinic (2019): Retrieved from https://www.mayoclinic.org/diseases-conditions/obesity/symptoms-causes/syc-20375742

2. NCBI (1994):L-phenylalanine releases cholecystokinin (CCK) and is associated with reduced food intake in humans: evidence for a physiological role of CCK in control of eating. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/8201963

3. NCBI (2012):The Carnivore Connection Hypothesis: Revisited, Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3253466/

4. Lolo (2018):Carnivore Diet: Fad or the Future? Retrieved from http://unity.lolofit.com/blog/posts/carnivore-diet-fad-or-miracle-diet

5. Healthline (2019):All You Need to Know About the Carnivore (All-Meat) Diet. Retrieved from https://www.healthline.com/nutrition/carnivore-diet

Cellular metabolic overactivity leads to metal inflammation.

The immune system protects us from infections and tumors. the linkage between metabolism and inflammation, which seems clinically evident, has been elusive to demonstrate from a biochemical pathway perspective.

Researchers demonstrated that the metabolic activity in the immune cells of primary immunodeficiency disorders (PID) patients is significantly up-regulated, with resulting increased cellular respiration. This then signaled the cells to produce inflammatory mediators.

This study identified the pathway for pathological mitochondrial retrograde signaling leading to metal inflammation.

SDHA gain-of-function engages inflammatory mitochondrial retrograde signaling via KEAP1–Nrf2. Nature Immunology, 2019

Time Restricted Feeding | Reverse Diabetes MD from Gurpreet Padda on Vimeo.

Time-restricted feeding.

Time-restricted feeding can help people move into a healthier lifestyle and reverse insulin resistance as well as maintain a healthy weight. Most people eat from the time they wake up until the time they go to bed; typically, they eat three main meals, multiple snacks, and often soda in between.  This pattern leads to chronic high insulin production, which fatigues the insulin receptors.  In addition, insulin is a fat storage hormone, and elevated insulin levels lead to fat accumulation in the liver, creating metabolic inflammation.

Your metabolism exists in two states – the “fed” (insulin high) state and the “fasted” (insulin low) state. Either we are storing food energy (increasing storage), or we are burning stored energy (decreasing storage or fat lysis).  If we start eating the minute we roll out of bed and do not stop until we go to sleep, we spend almost all our time in the fed state. Over time, we gain weight, because we have not allowed our body time to burn stored food energy.

Time-restricted feeding shortens the time window that a patient eats, shortening the “fed” state and lengthening the “fasted” state.  This reduces the total amount of insulin produced for the day.  Insulin is a fat-storage hormone, and a high level of insulin production leads to insulin resistance.  Time-restricted feeding is considered a type of fasting and has extraordinary benefits, including weight and body fat loss, lowered blood insulin and sugar levels, and a reversal of type 2 diabetes. Other possible benefits include improved mental clarity and concentration, a reduction in the risk of Alzheimer’s disease, activating of cellular cleansing by stimulating autophagy, and reduction of inflammation.

Time-restricted feeding is a type of fasting; it is not starvation.  Starvation is the involuntary absence of food for a long time, leading to severe suffering or even death. Starvation is not deliberate or controlled.  Fasting is the voluntary withholding of food. It’s done by someone who is not underweight and thus has enough stored body fat to live off. When done right, intermittent fasting should not cause suffering.  Food is easily available, but you choose not to eat it. You may begin a fast at any time of your choosing, and you may end a fast at will, too. You can start or stop a fast for any reason or no reason at all.  Any time that you are not eating, you are intermittently fasting. For example, you may fast between dinner and breakfast the next day, a period of approximately 12-14 hours. In that sense, intermittent fasting should be considered a part of everyday life.

The mere presence of insulin increases fat storage, and the absence of insulin permits lipolysis or fat usage as energy.

Lifestyle changes are key to managing obesity and Type 2 Diabetes, but by themselves don’t always control blood glucose levels. Bariatric surgery (gastric band or bypass) is effective but has significant risk. Drugs often manage the symptoms and may stave off complications, but don’t reverse the disease.

Time-restricted feeding has the potential to fill this gap in obesity and diabetes care by providing calorie restriction and the hormonal benefits of bariatric surgery without invasive surgery. Time-restricted feeding is defined as the controlled and voluntary abstinence from all calorie-containing food and drinks for a specified period of time.  During the fasting periods, patients are allowed to drink unlimited amounts of very-low-calorie fluids such as water, coffee, tea, and even bone broth. A general multivitamin supplement is encouraged to provide adequate micronutrients.

Metabolic flexibility:

Time-restricted feeding, or meal-timing strategy, reduces swings in hunger and alters fat and carbohydrate burning patterns, which may help with losing weight and improving insulin sensitivity.  It does not necessarily affect how many total calories patients burn but reduces the daily hunger swings and increases fat burning at night. It improves metabolic flexibility, which is the body’s ability to switch between burning carbs and burning fats.  Metabolic flexibility is the ease with which the body transitions between two different and opposing states, “fed” and “fasted,” without cravings or hunger pangs.

During feeding, insulin is elevated, which signals your body to store excess calories as fat. In the presence of insulin, the burning of fat is halted, while the body burns glucose instead.  In the fasted state, insulin is low (while glucagon and growth hormone increase), so the body mobilizes stored body fat from your fat cells and burns this fat for energy (instead of glucose).  You can only burn stored body fat while in the fasted state, and you can only store more body fat while in the fed state.

Most overweight patients live in a constant fed state, and rarely in a fasted state.  They continually burn glucose rather than fat at the cellular level. They have insulin resistance, caused by chronically high insulin levels, which promote fat storage and suppress fat mobilization.

When overweight “sugar burners” stops eating for even a few hours, they quickly run out of glucose from their last meal, instead of transitioning to the fasted state and burning stored body fat.  This causes acute brain signals of hunger and cravings for immediate sugar.  They spend most of the day trapped in a cycle of eating every few hours, spiking glucose, and then becoming hungry when blood sugar drops.  They may even develop low blood sugar and feel jittery; this is called reactive hypoglycemia.  This is a big clue that a patient lacks metabolic flexibility.

Fat-adapted energy use:

Your metabolic flexibility is determined by your mitochondria, the tiny energy factories inside the cells.  The mitochondria can burn both glucose (sugar) or fat for fuel, and over time they will develop a preference for one over the other; “sugar burners” have increased the pathways in the mitochondria that burn glucose and decreased pathways for burning fat.  As you become more metabolically flexible, the fat burning pathways will predominate, and you will become “fat adapted.”

Becoming fat adapted takes time and practice, and your body has to do a number of things to slowly up-regulate (or increase) your fat-burning pathways.  This includes improving insulin sensitivity to lower insulin and promote fat mobilization into free fatty acids and upregulating the fat-burning pathways at the cellular level (in the mitochondria).

Ways to improve fat adaptation include:

• Low-carbohydrate diets: A low-carb, high-fat (LCHF) diet improves the body’s ability to utilize fat for energy rather than glucose, as there is more fat and less glucose, even in the fed state.
• Exercise: High-intensity exercise depletes glucose and glycogen rapidly, forcing the body to switch to fat for fuel. Exercise also improves insulin sensitivity.
• Caloric restriction: Eating fewer calories also equals less glucose available for fuel, forcing the body to rely on stored body fat for fuel.
• Intermittent fasting forces the body to spend more time in the fasted state, giving the body more “practice” at burning fat.
• Supplementation: Ketone supplementation may be useful when first starting out. Ketones are breakdown products of fat, and when you first start out, ketones can reduce your hunger and provide energy for your mitochondria.

Patient education and engagement is the key to remission and curtailing the use of pharmacological interventions.  Morrison et al, also found that more frequent interactions with a provider led to markedly rapid reductions in serum glucose, HbA1C, and low-density lipoprotein cholesterol levels, followed up with the treating physician on average every 2 weeks.

How to do time-restricted feeding:

Our protocol can reverse obesity and Type 2 Diabetes (in individuals who still have the capacity to produce some insulin) by resensitizing the insulin receptor and restoring normal cyclical insulin production.  We restore the normal ebb and flow pattern of insulin, so the receptors are re-sensitized, and the constant high level of circulating insulin is reduced, reducing the fat storage action of insulin.

Time-restricted feeding is a type of intermittent fasting that limits your food intake to a certain number of hours each day.  An example of time-restricted eating is if you choose to eat all your food for the day in an 8-hour period, such as from 11 a.m. to 7 p.m., providing an 8-hour feeding window.  The remaining 16 hours are the fasting period, during which no calories are consumed.  This same schedule would be repeated every day.

Restricting feed times to a shorter window each day, starting at 8 hours/day and reducing by 1 hour per week down to 4-6 hours/day is highly effective in reversing diabetes and weight loss.  Medications must be clinically adjusted to prevent unintentionally low glucose levels or changes in blood pressure, which can be life-threatening.  To have success with this technique, cravings should be prevented.  Satiety is the key; you should not be hungry, or this will not be sustainable.  Food choice drives satiety.

Steps to success

Step 1

Before you start a time-restricted feeding schedule, you should talk to your doctor or health care provider. Get medical advice from a professional who is aligned with your health goals.

You may have medical conditions that need close monitoring. Likewise, you may be on medications that may need to be adjusted. It is important to have a strong understanding of your medical history and the medications you take prior to initiating a fasting program. Please talk to your doctor or healthcare provider.

Step 2

Stop all sugars, including all artificial sweeteners. Many sugars and processed carbs just aren’t satiating. Stop all sugar and artificial sugar sweetened beverages. Before you start your protocol, you should eliminate sugars and processed carbohydrates.

Stop all sources of vegetable oil and replace with healthy natural oil and real butter.  Replacing industrial seed oil with real oils is easy if you are not eating processed foods.  It even makes the food taste better.

Stop all processed foods.  Processed foods are engineered to make you eat again and again and again, every 2-3 hours.

Step 3

Focus on protein and healthy fats. Focus on getting meals that are rich in protein and healthy fats. Eat all types of meat like beef, fish, chicken, eggs, lamb, and seafood. Yogurt and cheeses are also nutritious and filling. Fill up on low-sugar vegetables like olives, peppers, cucumbers, and avocado, and eat as many green leafy vegetables as you please.  This approach will help you get better adapted to fat metabolism and may make fasting easier to adopt.

Step 4

Start slow.   This metainflammation didn’t happen in one day, and it won’t go away in a day. Consider a liberal 8-hour eating window on your first day to see how it feels. Eat as you please during your 8-hour time frame and see how your body and appetite feel during the remaining hours of the day.

Then, slowly narrow your eating window. As you feel more comfortable assessing your hunger and understanding the nature of hunger pangs, you can slowly decrease your daily feeding window. Consider decreasing by one hour a week, until you reach a 4-hour window.

Things to think about:

If you haven’t made adjustments to your diet beforehand to include more satiating foods filled with protein, healthy fat and fiber, you may notice hunger pangs. If you are experiencing hunger pangs, consider drinking some hot tea, coffee, water or seltzer. This will fill your stomach up and give you enough time to realize that maybe you really aren’t as hungry as you initially thought.  Some people use lemon in seltzer water.

This should be a fun experience, not a miserable experience.  If you are having a miserable experience, something has been overlooked.  Remember that time-restricted feeding is a  great way to limit snacking. Eating satiating real food during your eating window will restore and realign your hormone system.

Patients can reverse their diseases without the worry of side effects and financial burden of many pharmaceuticals, as well as the unknown long-term risks and uncertainty of surgery, all by means of time-restricted feeding.

Some practical tips:

• Don’t use time restricted feeding as an excuse to eat junk food when you are eating—continue to avoid processed foods.
• When you first start time-restricted feeding, you might have to supplement with a fast-mimicking substance like a ketone supplement.
• Check with your doctor before starting time-restricted feeding, especially if you are diabetic and on diabetes medications!
• You can generally take any vitamins or supplements you want while fasting as long as they don’t have calories, but you don’t need any supplements as you will be eating plenty of nutrient-dense foods every day. You may have to increase salt intake.
• You don’t have to worry about losing muscle from lack of protein during your fast, as long as you eat adequate protein at the meals before and after fasting. A LCHF (low-carb, high-fat) diet pairs nicely with intermittent fasting, as both improve fat adaptation a great deal.
• Exercising with time restricted feeding, either cardio or lifting weights (lifting weights is better), is acceptable. You will not lose muscle while fasting as long as you are exercising regularly.
• Drink plenty of water and non-caloric beverages while fasting; coffee and tea in the morning make fasting considerably more enjoyable in addition to health and fat-burning benefits and are highly recommended. You may have to increase salt intake.
• Skipping your morning meal gives your body more time to burn fat for energy. Hunger is lowest in the morning, so it may be easiest to skip it and break your fast later in the day.

Time-restricted feeding has many benefits but remains controversial. Diabetes medications will need to be adjusted. Discuss any changes in medication and relevant lifestyle changes with your doctor.  People who should not use time-restricted feeding include those who are underweight or have eating disorders, pregnant or breastfeeding women, and children under the age of 18.

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Additional references:

Suleiman Furmli, Rami Elmasry, Megan Ramos, Jason Fung. Therapeutic use of intermittent fasting for people with type 2 diabetes as an alternative to insulin. BMJ Case Reports, 2018; bcr-2017-221854 DOI: 10.1136/bcr-2017-221854

Morrison F , Shubina M , Turchin A . Encounter frequency and serum glucose level, blood pressure, and cholesterol level control in patients with diabetes mellitus. Arch Intern Med 2011;171:1542–50.doi:10.1001/archinternmed.2011.400

Duke S-AS , Colagiuri S , Colagiuri R . Cochrane Metabolic and Endocrine Disorders Group. Individual patient education for people with type 2 diabetes mellitus. Cochrane Database Syst Rev 2009;22.doi:10.1002/14651858.CD005268.pub2

Brethauer SA , Aminian A , Romero-Talamás H , et al . Can diabetes be surgically cured? Long-term metabolic effects of bariatric surgery in obese patients with type 2 diabetes mellitus. Ann Surg 2013;258:1.doi:10.1097/SLA.0b013e3182a5034b

Pucher PH , Lord AC , Sodergren MH , et al . Reversal to normal anatomy after failed gastric bypass: systematic review of indications, techniques, and outcomes. Surg Obes Relat Dis 2016;12:1351–6.doi:10.1016/j.soard.2016.01.030

Shoar S , Nguyen T , Ona MA , et al . Roux-en-Y gastric bypass reversal: a systematic review. Surg Obes Relat Dis 2016;12:1366–72.doi:10.1016/j.soard.2016.02.023

The University of Alabama at Birmingham. “Time-restricted feeding study shows promise in helping people shed body fat.” ScienceDaily. ScienceDaily, 6 January 2017. www.sciencedaily.com/releases/2017/01/170106113820.htm

Intermittent versus daily calorie restriction: which diet regimen is more effective for weight loss? K. A. Varady. https://onlinelibrary.wiley.com/doi/full/10.1111/j.1467-789X.2011.00873.x

Moro, T., Tinsley, G., Bianco, A., Marcolin, G., Pacelli, Q. F., Battaglia, G., … Paoli, A. (2016). Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males. Journal of translational medicine, 14(1), 290. doi:10.1186/s12967-016-1044-0. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5064803/

Gabel, K., Hoddy, K. K., Haggerty, N., Song, J., Kroeger, C. M., Trepanowski, J. F., … Varady, K. A. (2018). Effects of 8-hour time restricted feeding on body weight and metabolic disease risk factors in obese adults: A pilot study. Nutrition and healthy aging, 4(4), 345–353. doi:10.3233/NHA-170036. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6004924/