The Fasting Mimicking Diet: Benefits and Limitations

The fasting mimicking diet is made up of five days per cycle, which can be repeated once per month to see long-term results. For the first day, calories are slashed to 1,100 per day, and just 800 calories are allowed daily on subsequent days.

The diet is rich in nuts and olives to provide healthy fats. Other diet components include foods like vegetable soup or broth, puffed rice bars, nut bars, and tea.
Plant-based whole foods are emphasized on the diet along with minimal amounts of animal products. Carbohydrates should be from complex plant sources, and fats should be from healthy oils and nuts.
Alcohol is prohibited on the diet, and coffee intake should be limited to no more than one cup per day. Additionally, you should not exercise at all while doing this diet plan.
A typical fasting mimicking diet meal plan may include a handful of nuts with tea for breakfast, vegetable soup for lunch, olives as a snack and more soup for dinner.
It’s recommended to do one cycle of this diet per month for at least three months or even longer to help improve long-term health. Doing more than one cycle per month could lead to nutrient deficiencies and negative effects on health.

FMD Recipes
Although pre-made and pre-portioned products are available for convenience and ease, it can be pretty pricey. For a five-day fast, for example, the Prolon diet cost hovers around $300.
However, you can try making some FMD-friendly, cost-effective recipes of your own. Here are a few of the fasting mimicking diet (FMD) recipes that you can try at home:
• Paleo Nut Bars
• Weight Loss Vegetable Soup
• Simple Homemade Kale Crackers

Fasting Mimicking Diet History
The fasting mimicking diet was created by Dr. Valter Longo, the director of the Longevity Institute at the University of Southern California. For the past 20 years, Dr. Longo has been researching ways to slow and reverse aging to prevent chronic disease.
He became interested in how fasting had an anti-aging, rejuvenating effect on the body as well as the effects of regimens like alternate day fasting.
However, because fasting can be associated with negative side effects and risks, he created a new diet plan of his own: the fasting mimicking diet.
Since the inception of the diet, a multitude of studies have been released demonstrating the potential benefits of short-term caloric restriction, and more interest has generated on the possible health effects of the fasting mimicking diet.

 

The 5-day FMD is a low-protein, high-moderate-carb, moderate-fat diet.

The first day is 1090 calories, with 10% from protein (27 grams), 56% from fat (68 grams), and 34% from carbohydrates (93 grams).

The next four days are 725 calories, with 9% protein (16 grams), 44% fat (35 grams), and 47% carbohydrates (85 grams).

Most of the fat is polyunsaturated and monounsaturated. The protein is plant-based. The carbs come from nuts, seeds, legumes, and grains.

He even came up with a shelf-stable package of FMD food called ProLon. Instead of weighing and measuring your carrots and mac nuts and olives, you could just buy the 5-day supply of dry food and be on your merry way.

It’s certainly an attractive idea—a shortcut to fasting.

Does it live up to the hype? Does it truly improve lifespan in humans?

There’s certainly nothing wrong with it. Let’s get that off the table. It’s a fine idea. Certainly better than what most people do.

I just don’t know if it offers unique benefits to healthy people interested in extending their lives that other eating plans, like keto or Primal or intermittent fasting, don’t offer.

Let’s take a look at some of those benefits.

In rodents, the FMD has been shown to do some pretty cool things:

•Improve lipids numbers.

•Reduce body weight (and fat).

•Activate autophagy.

•Rejuvenate damaged organs, like the pancreas in type 1 diabetes.

•Reduce cancer occurrence.

•Extend life.

The one human trial, done last year, also got positive results.

•Improved lipids.

•Reduced body fat and body weight.

•Lower blood pressure.

•Lower fasting glucose.

•Reduced CRP, a marker of inflammation.

•Reduced IGF-1, insulin-like growth factor.

But there are some issues with the human study.

The subjects weren’t quite healthy at baseline. They were “generally” healthy, and there’s a difference. Over half were obese or overweight. The average body fat percentage was 34%. No one was about to keel over, but these weren’t lean, athletic types.

We don’t quite know what they ate before starting the trial, but the average American doesn’t have a great track record when it comes to dietary quality. They may very well have been going from a standard American diet full of junk food to the healthier approach promoted by the researchers.

They got healthier. They lost weight and body fat. Their biomarkers improved, suggesting a reduction in risk for some of the diseases that characterize aging. That’s real. But it’s also not unique to the fasting mimicking diet.

Furthermore, the people who were the most overweight and unhealthy at baseline reaped the greatest benefits. The lean, healthy people saw fewer benefits, which is understandable—they had fewer problems to solve.

The meatiest results came in rodent studies. The human study shows that overweight and obese folks can really benefit from the proprietary fasting mimicking diet, but that’s about it. It doesn’t show increased lifespan (study was too short). It doesn’t show organ rejuvenation (didn’t measure). It doesn’t show reversal of type 2 diabetes (didn’t try). All those things could very well happen in humans, and I wouldn’t be surprised—but for the time being, those effects have only been shown in rodents. We are not rodents, as I’ve made explicitly clear before and you can hopefully surmise from your own lived experience.

I see another major problem to Longo’s approach and the crux of his argument: It’s predicated on the idea that lower IGF-1 is a Good Thing.

Older folks with lower IGF-1 levels have a lower risk of cancer. That’s true. That’s important, assuming the connection is causal. There’s good reason to believe that it is.

IGF-1 participates in the etiology of ovarian cancer, is involved in breast cancer, helps sustain cancer cell viability, and affects the prognosis of non-small-cell lung cancer, just to name a few. As a growth-promoter, IGF-1 has the potential to promote the growth of cancer cells.

But IGF-1 levels also have a curious association with all-cause mortality. It’s U-shaped, meaning both super low levels and super high levels are linked to increased mortality risk, and that there’s a sweet spot somewhere between where IGF-1 is helping, not hurting. Lower isn’t always better. Somewhere in the middle is the best for longevity.

And for quality of life and overall health, IGF-1 does some good things after all. We don’t manufacture it in order to kill ourselves.

Resistance training, for example, spikes IGF-1. The increase in IGF-1 actually mediates the increase in strength—the beneficial adaptation to the training. Is Longo or any other longevity researcher going to suggest that lifting weights is bad for lifespan and health? (Oh, I’m sure there’s someone…)

IGF-1 counters age-related muscle wasting. I can’t think of a more important physical characteristic for older adults than lean muscle mass.

IGF-1 builds bone strength. Older women with higher IGF-1 levels have stronger bones, and IGF-1 is necessary for bone formation. This goes hand in hand with increasing muscle strength, as resistance training famously builds both muscle and bone.

IGF-1 is necessary for metabolic health. When you inject type 2 diabetic patients with IGF-1, their blood sugar drops, insulin sensitivity increases, and lipids improve.

Dying from cancer is awful. Dying in general, from any number of other maladies, is also bad. We can all agree that we want less of both types of death. We also want good muscle strength, bone mass, metabolic function, and all the rest.

 

For example, the IGF-1 goes way down, the glucose will go way down, the ketone bodies are greatly elevated. The reason is that the body starts burning fat … primarily the visceral fats. This is a really important point. We really did not see much of a significant difference in the subcutaneous fat.

We saw a significant difference in the abdominal fat, indicating that this is coming mostly from one source. Maybe this is the reservoir where the body goes first when the glucose is not coming in. I think the clearance of damaged cells is also very important.

We’ve shown this in a mouse and human preliminary multiple sclerosis trial, in which we were able to show that each cycle of the fasting-mimicking diet is able to kill some of the autoimmune cells and then turn on the stem cells and regenerate cells that are no longer autoimmune.

The human trial is still preliminary, but certainly it was very promising. Especially when you consider, like in the mouse [study], we saw a temporary reduction of the white blood cells in the patients. Over 70 percent of the patients had over 20 percent reduction in the white blood cell number. That told us it is probably working in people like it’s working in mice.

The system tries to … [kill] off white blood cells, turning on the hematopoietic stem cells. Then when you refeed, and only if you refeed, the stem cells are now giving rise to young and functional white blood cells … [The] human clinical trial supports the notion that this is happening everywhere in the human body.”

 

 

Longo also points out that when you inject stem cells, the stem cells lack the program that tells them what to do. When you fast, and the level of white blood cells drops, the refeeding phase automatically provides the instructions to rebuild everything that is missing. His book

 

 

 

 

 

 

 

 

 

 

 

 

“We published a paper1,2 … showing increased mortality in Americans, particularly cancer mortality in Americans, who had a high-protein diet. This makes sense. One of the reasons it makes sense is that proteins, in particular short amino acids (such as leucine and methionine) are central regulators of these growth factors, particularly mTOR and IGF-1 … and have a pro-aging and also pro-damage effect.

Cell Metabolism May 4, 2014; 19(3): 407-417

NIH.gov, March 17, 2014

The higher level of protein, the higher level these amino acids, the higher activity of TOR-S6 kinase pathway. As a consequence, we now have very clear evidence in many organisms that TOR accelerates aging and also accelerates mortality, meaning that all kinds of organisms will die earlier and develop many more diseases when they maintain this pathway

 

 

 

 

The way insulin works is not by driving glucose into the cells, which is what’s conventionally taught. Insulin actually works by stopping the liver’s ability to produce glucose (hepatic gluconeogenesis). If you have very low levels of insulin, you’re not going to be able to suppress hepatic gluconeogenesis. Paradoxically, your blood sugar will rise pretty dramatically, even though you’re not having any carbohydrates.

 

Five health benefits of the fasting mimicking diet

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Animal models allow researchers to analyze a wider range of health outcomes, such as the regeneration of tissues. Mice are among the most commonly used animal models for studying FMD and are typically given two four-day-long FMD cycles per month, with ad libitum (unrestricted) intake between cycles. In the remaining part of this section, we’ll explore the evidence for FMDs in animal studies.

Metabolic disorders and diabetes

In one mouse study, FMD cycles had profound effects on visceral fat, glucose, and IGF-1 levels. IGF-1 is an endocrine hormone produced primarily in the liver. IGF-1 signaling has been associated with biological aging in some organisms, but whether high levels are good or bad is somewhat controversial (5). After return to an ad libitum (eat as desired) diet, both glucose and IGF-1 levels returned to baseline, but visceral fat remained lower. Mice also showed evidence of significant liver and muscle regeneration as a result of FMD (4). In another study published in February 2017, FMD cycles were shown to reverse late stage Type 2 and even Type 1 diabetes! The FMD triggered epigenetic changes that resulted in expression of prenatal development genes in the adult pancreas. This led to pancreatic β cell regeneration and the return of insulin secretion (6).

Cognitive function

An FMD has been shown to promote hippocampal neurogenesis and improve motor learning and memory in old mice (4). In a mouse model of Alzheimer’s, protein restriction cycles have been shown to alleviate the age-dependent impairment in cognitive performance and reduce levels of phosphorylated tau, a protein that forms the tangles characteristic of Alzheimer’s and several other neurological diseases (7).

Autoimmune disease

In a mouse model of multiple sclerosis, FMD reduced clinical severity in all mice and completely reversed symptoms in 20 percent of animals (8). At the molecular level, FMD increased corticosterone levels and regulatory T cells and promoted remyelination in axons. FMD also reduced levels of pro-inflammatory cytokines and immune cells involved in promoting inflammation.

Cancer

FMD has been shown to rejuvenate the immune system and protect against cancer in mice. One study found a 45 percent reduction in neoplasia incidence in the FMD group relative to the control group. Cycles of FMD beginning at middle age also delayed tumor onset and reduced the number of lesions, which may indicate a switch from malignant to benign tumors. FMD has also been shown to reduce the number of tissues with inflammation and protect against inflammation-associated skin lesions (4).

Aging

Immunosenescence is the age-associated decline in hematopoiesis (the creation of new blood cells), resulting in diminished or altered production of adaptive immune cells. FMD causes a rejuvenation of the blood profile and a reversal of this decline by increasing the number of hematopoietic and mesenchymal stem and progenitor cells. Four months of FMD cycles resulted in a significant increase in RBC count and hemoglobin levels compared to baseline. FMD also increased median lifespan of mice by 11 percent and either attenuated age-dependent bone mineral density loss or induced bone regeneration in mice.

Interestingly, there were some contraindications to fasting in older mice. The authors suggest that in older animals, a less severe low-calorie and low-protein diet may be preferable to continue to provide beneficial effects while minimizing malnourishment (4).

FMD: human clinical trials

While most studies on FMD have been done in animal models, there have been a few clinical trials in humans. In one of the most substantial studies to date, performed by Wei et al. (9), they had 71 subjects complete three FMD cycles. Each FMD cycle lasted for five days, and was repeated once every month. During the five-day period, subjects in the FMD group consumed about 34 to 54 percent of their normal caloric intake. The diet composition was approximately 9 to 11 percent protein, 43 to 47 percent carbohydrate, and 44 to 46 percent fat by energy.

The researchers measured several markers in the blood after three FMD cycles, some of which were maintained after returning to their normal diet:

•Subjects who completed three full FMD cycles and returned to their normal diet for five to seven days had significantly reduced body weight, total body fat, trunk fat, absolute lean body mass, waist circumference, IGF-1, systolic and diastolic blood pressure, total cholesterol, LDL, and HDL.

•The effects of FMD on body weight, BMI, waist circumference, IGF-1, and diastolic blood pressure persisted for at least three months after the final FMD cycle.

FMD was found to have especially profound effects in patients at high risk for cardiovascular, metabolic, and age-related disease.

•Individuals who had high baseline levels (>1 mg/liter) of C-reactive protein, a potent marker of inflammation, had significantly lower CRP levels three months post-FMD.

•Subjects with low baseline HDL showed significantly increased three-month follow-up HDL levels.

Altogether, these data suggest that FMD causes many beneficial changes in risk factors for chronic, age-related diseases in both animals and humans. Further studies will only contribute to our understanding of the mechanism behind these changes.

When to prescribe a fasting mimicking diet

FMD clearly has numerous health benefits, as I have outlined in this article. However, it should be noted that fasting does have the potential to make some patients worse, depending on their condition.

Patients who are good candidates for FMD include: those who are fighting chronic infections or trying to lose weight; those who have a weak immune system, neurological issues, type 2 diabetes, or other metabolic problems; and those who are healthy and are simply trying to optimize longevity.

Patients who are typically not good candidates for FMD include: those who are pregnant or have HPA axis dysregulation (“adrenal fatigue”), an eating disorder, or thyroid problems. Fasting is also not usually recommended for children or teens.

Always be sure to monitor patients closely when they start to implement FMD or any type of fasting. If patients start to exhibit symptoms of HPA-D or hypothyroidism, you will need to reconsider their fasting schedule. Remember that each patient will respond to fasting differently.

The FMD, as studied, is currently available from Prolon as a specific package of prepared foods and micronutrients intended to be administered under a doctor’s supervision.

It’s likely that a “homemade” version with similar macronutrient ratios and foods would have the same effects, but this hasn’t yet been studied in a clinical trial.

 

 

 

 

 

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